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We usually think of bacteria as organisms so small they can be seen only through a microscope. But scientists discovered a giant white bacterium lurking on rotting leaves in the brackish waters of a red mangrove swamp in Guadeloupe in the Lesser Antilles.It’s so large it can be seen easily with the naked eye. But size isn’t the only astonishing trait of this long, filamentous microbe; it has a more complex structure than any other bacterium previously discovered, and, unlike most, it stores its DNA in tidy little packets.Previously discovered giant bacteria, some of which can also form centimeters-long filaments, are composed of hundreds to thousands of cells. But the newfound bacteria, which is roughly the shape and the size of an eyelash, is a single bacterial cell. “Realizing that a filamentous bacteria of that size is actually just a single bacterium was an aha moment,” says Jean-Marie Volland, a marine biologist at the Lawrence Berkeley National Laboratory who led the research, in an interview with National Geographic.The scientists have named the microbe Thiomargarita magnifica for its size and the pearl-like beads of sulphur found inside the cell. T. magnifica is not only more than a thousand times bigger than a typical bacterium, it’s also longer than many multicellular animals such as fruit flies. In a news conference on Tuesday Vollard said that “Discovering this bacterium is like encountering a human being that will be as tall as Mount Everest.”“The discovery of this new Thiomargarita bacterium makes us appreciate the incredible diversity of the microbial world, and the intricate structural and genomic adaptations of bacteria that allow them to grow towards cell sizes that nobody would have expected,” says Andreas Teske, a marine biologist at the University of North Carolina at Chapel Hill. Teske co-discovered the previous size record-holder, Thiomargarita namibiensis.It’s a stunning illustration that bacteria are much more complex, organized, and versatile than we expect, says Chris Greening, a microbiologist at Monash University, Australia, who was not involved in the discovery. “Bacteria keep defying textbook descriptions of them.”Bacteria are not simple In 1999, Teske and other scientists discovered the strikingly large bacterium that they called Thiomargarita namibiensis, or the “Sulfur Pearl of Namibia.” Until now that bacterium—which grows as a string of white beads, occasionally reaching the size of three-fourths of a millimeter and is large enough to be visible to the naked eye—held the record for the largest bacterium. But the Caribbean bacterium is more than 50 times larger.Petra Anne Levin, a microbiologist at Washington University in St. Louis, who was not involved in the discovery isn’t surprised by its size. “The main take-home message is that we shouldn't underestimate bacteria as simple organisms because that definition is outdated,” she says. “Bacteria are endlessly adaptable, and we should expect to see them in a wide variety of sizes.”Bacteria belong to the branch of life called prokaryotes, which are the most basic living creatures. They are often described, though not accurately, as a bag of enzymes surrounded by a single membrane. What makes bacterial prokaryotic cells different from eukaryotic cells—which include animal, plant, and fungal cells—is that they don't have a nucleus, which is a separate compartment where the DNA is housed, explains Danny Ionescu, an aquatic microbiologist at The Leibniz Institute of Freshwater Ecology and Inland Fisheries in Germany. “There are many other functional physiological differences, but this is the one that makes them different than the eukaryotes, such as us.”The newly discovered bacterium defies this definition because it packages its genetic material in compartments surrounded by membranes that resemble a primitive nucleus.This newly characterized bacterium was first spotted by Olivier Gros, a mangrove biologist at the University of the French Antilles in Guadeloupe. “I spend a lot of time in the water looking at different things in the mangrove sediments. One time I saw these long white filaments, so I just collected them out of curiosity,” he says.The scientists in Gros’s lab tried to characterize these filaments, which they originally thought were a fungus or some other multicellular organism. But their early analyses hinted that these microbes probably belonged to the family of giant Thiomargarita bacteria. “But we were not so confident about that,” Gros says.Volland, who was a postdoctoral fellow in Gros’s lab joined Shailesh Date, founder and chief executive officer of the Laboratory for Research in Complex Systems in Menlo Park, to continue the quest to characterize this strange specimen. Date’s lab is a nonprofit corporation that partners with academic institutions for transdisciplinary research.“It was very apparent right away to everyone that what we had was a big bacterium, and it was a single cell,” Date says. But the challenge was how to figure out what else was special about the microbe. Using a range of molecular biology techniques, Volland, Date, and colleagues created high-magnification, three-dimensional photographs of these long specimens. That allowed them to see every one of these super large cells that made up a filament.Size limitsIt has long been thought that bacterial cells could not become very big for reasons that come down to basic physics. For example, the larger a cell becomes, the greater the surface area required to absorb the nutrients and energy needed to sustain such a large organism.“This bacterium breaks these rules by having a sophisticated organization similar to the more advanced animal and plant cells,” Greening says.Vollard’s team shows that the structure of the bacterium is subdivided into numerous compartments that perform different functions and dramatically increase available surfaces. This complexity may help the organism overcome the predicted limits for bacterial cell size.“We scientists try to define boundaries and say, okay, bacteria cannot reach this or that size, because of certain theoretical limits,” Ionescu says. “And apparently, bacteria do not read our textbooks.”The new bacterium stores its DNA in membrane-bound compartments which the scientists have named “pepins” because they look like pips, the small seeds in fruits such as watermelon.The structure of these pepins further blurs the distinctions between bacterial and eukaryotic cells because separating genetic material from everything else in the cells allows more sophisticated control and greater complexity, Greening says.Thiomargarita magnifica is also unique because, although all bacterial giants carry multiple copies of their genomes, it carries more than 700,000 copies of its genetic blueprint in a single cell.This bacterium will help us figure out why eukaryotic genomes, like those in animal and plant cells, have been getting bigger and bigger, Yoichi Kamagata and Hideyuki Tamaki of National Institute of Advanced Industrial Science and Technology in Japan wrote in an email.While Vollard and his colleagues probe the specimens collected from the mangroves, their next goal is to grow the bacteria in the lab. Growing it in a lab will allow scientists to understand how it reproduces and how it maintains its large stash of genetic material.“Discoveries await when people take a closer look and take notice,” Teske says. “T. magnifica has been hiding in plain sight in a very common coastal habitat, waiting for a microbiologist to stop by and wonder, Hey, could this be a new kind of Thiomargarita?”Bacteria don't have as complex an organization with as many compartments as eukaryotes, says Vollard. “They don't form tissues that are organized in organs to make complex organisms.” But he points out, “They are way more complex in terms of biochemistry. They can fix carbon, they can use sugars, they can grow on all kinds of substrates, they can communicate, they can do signaling, all kinds of complex mechanisms, they are also capable of social behavior, and some of them have complex life cycles. So, it is not true that bacteria are simple, and eukaryotes are complex.” | Biology |
Two common respiratory viruses can fuse to form a hybrid virus capable of evading the human immune system, and infecting lung cells – the first time such viral cooperation has ever been observed.Researchers believe the findings could help to explain why co-infections can lead to significantly worse disease for some patients, including hard-to-treat viral pneumonia.Each year, about 5 million people around the world are hospitalised with influenza A, while respiratory syncytial virus (RSV) is the leading cause of acute lower respiratory tract infections in children under five years old, and can cause severe illness in some children and older adults.Although co-infections – where a person is infected with both viruses at the same time – are thought to be relatively common, it was unclear how these viruses would respond if they found themselves inside the same cell.“Respiratory viruses exist as part of a community of many viruses that all target the same region of the body, like an ecological niche,” said Dr Joanne Haney from the MRC-University of Glasgow centre for virus research, who led the study.“We need to understand how these infections occur within the context of one another to gain a fuller picture of the biology of each individual virus.”To investigate, Haney and her colleagues deliberately infected human lung cells with both viruses and found that, rather than competing with one another as some other viruses are known to do, they fused together to form a palm tree-shaped hybrid virus – with RSV forming the trunk, and influenza the leaves.“This kind of hybrid virus has never been described before,” said Prof Pablo Murcia, who supervised the research, published in Nature Microbiology. “We are talking about viruses from two completely different families combining together with the genomes and the external proteins of both viruses. It is a new type of virus pathogen.”Once formed, the hybrid virus was also able to infect neighbouring cells – even in the presence of antibodies against influenza that would usually block infection. Although the antibodies still stuck to influenza proteins on the hybrid virus’s surface, the virus merely used neighbouring RSV proteins to infect lung cells instead. Murcia said: “Influenza is using hybrid viral particles as a Trojan horse.”As well as helping the viruses evade the immune system, joining forces may also enable them to access a wider range of lung cells. Whereas influenza usually infects cells in the nose, throat and windpipe, RSV tends to prefer windpipe and lung cells – although there is some overlap.Possibly, it could increase the chances of influenza triggering a severe, and sometimes fatal, lung infection called viral pneumonia, said Dr Stephen Griffin, a virologist at the University of Leeds. Although he cautioned that more research was needed to prove that hybrid viruses are implicated in human disease. “RSV tends to go lower down into the lung than the seasonal flu virus, and you’re more likely to get more severe disease the further down the infection goes,” he said.“It is another reason to avoid getting infected with multiple viruses, because this [hybridisation] is likely to happen all the more if we don’t take precautions to protect our health.”Significantly, the team showed that the hybrid viruses could infect cultured layers of cells, as well as individual respiratory cells. “This is important because the cells are stuck to one another in an authentic way, and the virus particles will have to go in and out in the right way,” said Griffin.The next step is to confirm whether hybrid viruses can form in patients with co-infections, and if so, which ones. “We need to know if this happens only with influenza and RSV, or does it extend to other virus combinations as well,” said Murcia. “My guess is that it does. And, I would hypothesise that it extends to animal [viruses] as well. This is just the start of what I think will be a long journey, of hopefully very interesting discoveries.” | Biology |
Making stem cells from a patient’s adult cells – rather than human embryos – is one of the holy grails in modern medicine treatments. New research brings us two steps closer. Biomedical engineers and medical researchers at UNSW Sydney have independently made discoveries about embryonic blood stem cell creation that could one day eliminate the need for stem cell blood donors.
The achievements are part of a move in regenerative medicine towards the use of ‘induced pluripotent stem cells’ to treat disease, where stem cells are reverse engineered from adult tissue cells rather than using live human or animal embryos.
But while we have known about induced pluripotent stem cells since 2006, scientists still have plenty to learn about how cell differentiation in the human body can be mimicked artificially and safely in the lab for the purposes of delivering targeted medical treatment.
Read more: Scientists are a step closer to developing 'smart' stem cells - and they're made from human fat Two studies have emerged from UNSW researchers in this area that shine new light on not only how the precursor blood stem cells occur in animals and humans, but how they may be induced artificially.
In a study published today in Cell Reports, researchers from UNSW School of Biomedical Engineering demonstrated how a simulation of an embryo’s beating heart using a microfluidic device in the lab led to the development of human blood stem cell ‘precursors’, which are stem cells on the verge of becoming blood stem cells.
And in an article published in Nature Cell Biology recently, researchers from UNSW Medicine & Health revealed the identity of cells in mice embryos responsible for blood stem cell creation.
Both studies are significant steps towards an understanding of how, when, where and which cells are involved in the creation of blood stem cells. In the future, this knowledge could be used to help cancer patients, among others, who have undergone high doses of radio- and chemotherapy, to replenish their depleted blood stem cells.
Emulating the heart
In the study detailed in Cell Reports, lead author Dr Jingjing Li and fellow researchers described how a 3cm x 3cm microfluidic system pumped blood stem cells produced from an embryonic stem cell line to mimic an embryo’s beating heart and conditions of blood circulation.
She said that in the last few decades, biomedical engineers have been trying to make blood stem cells in laboratory dishes to solve the problem of donor blood stem cell shortages. But no one has yet been able to achieve it.
“Part of the problem is that we still don’t fully understand all the processes going on in the microenvironment during embryonic development that leads to the creation of blood stem cells at about day 32,” Dr Li said.
“So we made a device mimicking the heart beating and the blood circulation and an orbital shaking system which causes shear stress – or friction – of the blood cells as they move through the device or around in a dish.” The microfluidic device that emulated an embryo's heartbeat and blood circulation. The cell seeding channels are filled with red food dye, while the heart ventricular contraction control channels and circulation valve control channels are filled with blue and green food dye respectively. Photo: UNSW/Jingjing Li These systems promoted the development of precursor blood stem cells which can differentiate into various blood components – white blood cells, red blood cells, platelets and others. They were excited to see this same process – known as haematopoiesis – replicated in the device.
Study co-author Associate Professor Robert Nordon said he was amazed that not only did the device create blood stem cell precursors that went on to produce differentiated blood cells, but it also created the tissue cells of the embryonic heart environment that is crucial to this process.
“The thing that just wows me about this is that blood stem cells, when they form in the embryo, form in the wall of the main vessel called the aorta. And they basically pop out of this aorta and go into the circulation, and then go to the liver and form what's called definitive haematopoiesis, or definitive blood formation.
“Getting an aorta to form and then the cells actually emerging from that aorta into the circulation, that is the crucial step required for generating these cells.”
“What we've shown is that we can generate a cell that can form all the different types of blood cells. We've also shown that it is very closely related to the cells lining the aorta – so we know its origin is correct – and that it proliferates,” A/Prof. Nordon said.
The researchers are cautiously optimistic about their achievement in emulating embryonic heart conditions with a mechanical device. They hope it could be a step towards solving challenges limiting regenerative medical treatments today: donor blood stem cell shortages, rejection of donor tissue cells, and the ethical issues surrounding the use of IVF embryos.
“Blood stem cells used in transplantation require donors with the same tissue-type as the patient,” A/Prof. Nordon said.
“Manufacture of blood stem cells from pluripotent stem cell lines would solve this problem without the need for tissue-matched donors providing a plentiful supply to treat blood cancers or genetic disease.”
Dr Li added: “We are working on up-scaling manufacture of these cells using bioreactors.”
Mystery solved
Meanwhile, and working independently of Dr Li and A/Prof. Nordon, UNSW Medicine & Health’s Professor John Pimanda and Dr Vashe Chandrakanthan were doing their own research into how blood stem cells are created in embryos.
In their study of mice, the researchers looked for the mechanism that is used naturally in mammals to make blood stem cells from the cells that line blood vessels, known as endothelial cells.
“It was already known that this process takes place in mammalian embryos where endothelial cells that line the aorta change into blood cells during haematopoiesis,” Prof. Pimanda said.
“But the identity of the cells that regulate this process had up until now been a mystery.”
Read more: Baby mice have a skill that humans want – and this microchip might help us learn it In their paper, Prof. Pimanda and Dr Chandrakanthan described how they solved this puzzle by identifying the cells in the embryo that can convert both embryonic and adult endothelial cells into blood cells. The cells – known as ‘Mesp1-derived PDGFRA+ stromal cells’ -– reside underneath the aorta, and only surround the aorta in a very narrow window during embryonic development.
Dr Chandrakanthan said that knowing the identity of these cells provides medical researchers with clues on how mammalian adult endothelial cells could be triggered to create blood stem cells – something they are normally unable to do.
“Our research showed that when endothelial cells from the embryo or the adult are mixed with ‘Mesp1 derived PDGFRA+ stromal cells’ – they start making blood stem cells,” he said.
While more research is needed before this can be translated into clinical practice – including confirming the results in human cells – the discovery could provide a potential new tool to generate engraftable haematopoietic cells.
“Using your own cells to generate blood stem cells could eliminate the need for donor blood transfusions or stem cell transplantation. Unlocking mechanisms used by nature brings us a step closer to achieving this goal,” Prof. Pimanda said. | Biology |
Consider the possibility of alien plants. After all, plenty of exoplanets likely have conditions friendly to the development of plants, even if evolution there never makes it as far as complex organisms and animals. But if moss, algae, and lichen envelop lush exoplanets in the faraway realms of the Milky Way, those worlds and the stars they circle could be completely different than our own. Extraterrestrial flora could be nothing like we’ve ever seen before.Most of the rocky exoplanets discovered so far orbit red dwarf stars, the most abundant type of star in the galaxy. They give off fainter, redder light than the sun. “It’s natural to ask, if photosynthesis happens in a range of visible light— 400 to 700 nanometers—and you take a star that’s fainter, cooler, and redder, is there enough light to support photosynthesis?” says Thomas Haworth, a physicist at the Queen Mary University of London. His tentative answer to that question, recently published in the Monthly Notices of the Royal Astronomical Society, is a “yes, sometimes.” His team’s conclusion, that conditions around red dwarf stars aren’t a deal breaker for life, is encouraging. But life might have adapted very differently to the light of redder suns. Most plants on Earth, including leafy vegetation, mosses, and cyanobacteria, use photosynthesis to turn sunlight and carbon dioxide into energy and oxygen. Plants use chlorophyll pigments to transform that solar energy into chemical energy. Chlorophyll gives plants their green color, and it’s tuned to absorb sunlight in the part of the spectrum that goes from violet-blue to orange-red. But astrobiologists have noted that there’s a “red edge” for vegetation, meaning that chlorophyll doesn’t absorb many photons at longer, redder wavelengths beyond 700 nanometers. Those are precisely the wavelengths at which these small red dwarf stars give off most of their light. That seems to pose a problem for photosynthetic species. So along with his colleague, biologist Christopher Duffy, Haworth tried to envision how extraterrestrial photosynthesis might work, even under unusual conditions. “We wanted to develop a general model of photosynthesis that wasn’t tied to any particular species,” Duffy says. In particular, they modeled light-harvesting antennae—pigment-protein complexes that all photosynthetic organisms have—which collect photons and channel the light energy down to a reaction center that carries out the photochemistry needed to turn it into chemical energy.They concluded that organisms with extremely efficient antennae could indeed absorb dim light redder than 700 nm, but that oxygenic photosynthesis might be a struggle. In that scenario, organisms would have to invest lots of their energy just to keep the photosynthetic machinery running. Evolutionarily, this might limit them to remaining, say, pond-dwelling green-blue bacteria, not structures that could colonize land. And although green plants, with their reliance on chlorophyll and sunlight, dominate the Earth, neither biology nor physics requires it to work that way. We already know of species on our own planet that follow different rules. There are subterranean microbes that make “dark oxygen” in the absence of light. And there are purple bacteria and green sulfur bacteria that conduct photosynthesis without oxygen, using different pigments and gases, especially sulfur. They rely on infrared light for energy, between 800 to 1,000 nanometers. That’s well within the range of red dwarfs’ starlight.Duffy and Haworth speculate that on remote planets, communities of purple bacteria could swell in black sulfurous oceans, or spread in films around local sources of hydrogen sulfide. If they evolved into plants that could survive on land, like Earth plants they would still angle their light-absorbing surfaces toward their star, but they might be purple, red, or orange, depending on the wavelengths of light they are attuned to. They’d still have clumps of cells that coax nutrients from the ground, but they would be seeking different nutrients. (For plants on Earth, nitrates and phosphates are critical.)If these scientists are correct that botanical life could arise in red dwarf systems, astronomers then need to figure out where to point their telescopes to find it. To start, scientists typically focus on the habitable zone around each star, also sometimes called a “Goldilocks” region because it’s neither too hot nor too cold for liquid water on a planet’s surface. (Too hot and water will evaporate away. Too cold and it will permanently turn to ice.) Since water is likely necessary for most kinds of life, it’s an exciting development when astronomers find a rocky world in this zone—or in the case of the TRAPPIST-1 system, multiple worlds.But University of Georgia astrophysicist Cassandra Hall says perhaps it’s time to rethink the habitable zone in a way that emphasizes not just water but also light. In a study earlier this year, Hall’s group focused on factors like starlight intensity, the planet’s surface temperature, the density of its atmosphere, and how much energy organisms would need to expend for mere survival, rather than growth. Considering these together, they estimated a “photosynthetic habitable zone” that lies a bit closer to a planet’s star than the traditional habitable zone for water. Think of an orbit more like Earth’s and less like Mars’.Hall highlights five promising worlds that have already been discovered: Kepler-452 b, Kepler-1638 b, Kepler-1544 b, Kepler-62 e and Kepler-62 f. They’re rocky planets in the Milky Way, mostly a bit larger than Earth but not gas giants like “mini-Neptunes,” and they spend a significant fraction of their orbits, if not the entire orbit, within their star’s photosynthetic habitable zone. (Astronomers found them all within the past decade using NASA’s Kepler Space Telescope.) Of course, the hard part is trying to spot clear signs of life from more than 1,000 light-years away. Astrobiologists look for particular chemical signatures lurking in exoplanets’ atmospheres. “Generally, you’re looking for signs of chemical disequilibrium, large amounts of gases that are incompatible with each other because they react with each other to form different things,” Hall says. These could indicate life processes like respiration or decay. A combination of carbon dioxide and methane would be a prime example, since both can be given off by life forms, and methane doesn’t last long unless it’s constantly being produced, such as from the decomposition of plant matter by bacteria. But that’s no smoking gun: Carbon and methane could just as well be produced by a lifeless, volcanically active world. Other signatures could include oxygen, or its spin-off, ozone, which is generated when stellar radiation splits oxygen molecules. Or perhaps sulfide gases could indicate the presence of photosynthesis without the presence of oxygen. Yet all of these can come from abiotic sources, such as ozone from water vapor in the atmosphere, or sulfides from volcanoes.While Earth is a natural reference point, scientists shouldn’t limit their perspective to only life as we know it, argues Nathalie Cabrol, an astrobiologist and director of the SETI Institute’s Carl Sagan Center. Seeking just the right conditions for oxygenic photosynthesis could mean narrowing the search too much. It’s possible life isn’t that rare in the universe. “Right now, we have no clue if we have the only biochemistry,” she says.If alien plants can survive or even thrive without oxygenic photosynthesis, that ultimately could mean expanding, rather than tapering, the habitable zone, Cabrol says. “We need to keep our minds open.” | Biology |
Topline
An “all-in-one” vaccine currently in development could protect people from future Covid-19 variants, as well as SARS, MERS and new strains of other coronaviruses from other animals, a study by researchers at the California Institute of Technology found. Image courtesy of Wellcome Leap, Caltech, and Merkin Institute Image courtesy of Wellcome Leap, Caltech, and Merkin Institute Key Facts The study, published Thursday in the journal Science, was done by scientists at Caltech and the University of Oxford who are working on developing the mosaic-8 vaccine, which aims to offer protection to a variety of coronaviruses Researchers tested mice vaccinated with the Covid-19 shots as well as the mosaic-8 vaccine and found unvaccinated mice died when infected with SARS or Covid-19, while mice vaccinated only against Covid-19 survived the virus, but not SARS, and mice given the mosaic-8 vaccine survived both viruses. The mosaic-8 vaccine uses 60 fragments of eight strains of coronaviruses, including Covid-19, which was shown to induce a “broad spectrum” of antibodies in primates and genetically-engineered mice with human-like cell receptors to target coronavirus “spike proteins.” The nanoparticle development has the potential to mitigate viral infection caused by known and future Covid-19 variants and other “viral spillovers,” according to the study. Caltech, which conducted the research in collaboration with WellCome Leap, is expected to start phase-one clinical trials over the next year using $30 million from the Coalition for Epidemic Preparedness Innovations. Key Background
A similar experiment conducted at Caltech last year showed that the mosaic-8 vaccine induces mice to produce antibodies that react to a variety of coronaviruses in a lab dish. The research comes nearly two months after a study in JAMA Network Open found immunity against the omicron variant fades rapidly after a second and third dose of the Pfizer and BioNTech vaccine. A study published in April by researchers at Johns Hopkins University found booster shots did not stop coronavirus spike proteins from binding to cells as well in omicron cases as it did with other strains. Two weeks ago, however, clinical data on Moderna’s vaccine booster – aimed at the original Covid-19 and the omicron strain – found the booster provided a “potent” antibody response against two omicron subvariants. Crucial Quote
Caltech biology professor Pamela Bjorkman said in the study, “We can’t predict which virus or viruses among the vast numbers in animals will evolve in the future to infect humans to cause another epidemic or pandemic.”
What To Watch For
Pfizer and Moderna are waiting for final approval from the Food and Drug Administration on omicron-specific boosters, which they intend to release this fall. Last week, the FDA announced any new boosters need to protect people from the newest omicron-related strains. Pharmaceutical companies Sanofi and GlaxoSmithKline also announced last month they intend to launch a vaccine later this year to target the omicron variant, after studies showed it had a 65% efficacy rate when used as a first and second shot, and a 5% rate on adults who had previously been infected.
Big Number
20 million. That’s how many people Covid-19 vaccines are estimated to have saved during the first year the vaccines were released, according to a study published two weeks ago in The Lancet Infectious Diseases. Further Reading
Nanoparticle Vaccine Protects Against a Spectrum of COVID-19-causing variants and Related Viruses (Caltech)
A New Covid Vaccine That’s Effective Against Omicron Could Hit The Market This Year (Forbes)
Full coverage and live updates on the Coronavirus | Biology |
Monk parakeets shown to lose social standing during an absence
Monk parakeets take that saying to heart, according to new research by the University of Cincinnati.
These loud and gregarious parrots risk losing their hard-won social standing if they are absent from their flock for just eight days, biologists found. And the highest-ranking birds lose the most status during their brief absence, researchers found.
The study was published in the journal Behavioral Ecology.
UC scientists studied three groups of captive monk parakeets in 2021 and 2022. The study, led by postdoctoral researcher Annemarie van der Marel, focused on testing whether social history was a critical component in structuring how the parakeets gained and maintained their ranks within their groups. Researchers were able to identify each bird's status in the flock's dominance hierarchy by observing their interactions and quantifying rank using networks of aggression.
Van der Marel, a former postdoctoral researcher at UC, is now a postdoctoral fellow at the Pontifical Catholic University of Chile where she is conducting research on social mammals. But monk parakeets are never far from her mind. Feral parakeets nest outside her home in Santiago.
"They're loud. They are very affiliative toward some members of the group but can be quite grumpy towards others. There's a lot of social drama," van der Marel said.
The field crew recorded 100,000 fights over two years of experimentation. They recorded a lot of data on the birds' efforts to increase or defend their social standing, said Elizabeth Hobson, a behavioral ecologist and assistant professor in UC's College of Arts and Sciences.
"Monk parakeets are very feisty. They fight all the time," Hobson said. "They generally don't have knock-down, drag-out fights, they're just constantly squabbling."
Typically, an aggressor will sidle up to another bird and threaten to peck it. Often, the other bird flees before the interaction becomes physical.
"We call it a displacement. It's clear who the winners and losers are," Hobson said
Once the hierarchy had formed in the social groups, the researchers removed birds of different social standing for eight days before returning them and observing their reintegration to the flock.
"We predicted that if there was something intrinsic about the bird that gave it high rank, it should have been able to waltz back in and easily retake its former rank," Hobson said.
Unlike some animal societies where the biggest individual is often dominant, researchers found that size doesn't matter as much among monk parakeets. Instead, they get ahead through sheer force of will.
"It's really striking to see a bird that had risen all the way to the top of the hierarchy have their rank fall so dramatically after being absent from the group for only about a week," Hobson said. "Because this loss of rank isn't associated with anything we measured about the birds, we think that rank loss is more likely the result of a change in social history, possibly because the removed birds were absent and couldn't fight to hang onto their spot in the hierarchy."
The new study also found that high-ranked birds had a much more difficult reintegration into their former groups. While lower-ranked birds also experienced a decline in status, it was not nearly as dramatic as in higher-ranked birds.
"The group treats them very differently," Hobson said. "In general, when we reintroduce the top-ranked bird, the group responds with a lot of aggression towards that reintroduced bird. A lot of bullying happens.
"But when we reintroduced a middle- or low-ranked bird, we didn't see nearly the kind of focused aggression on that bird as we saw in the top-ranked bird," she said.
Hobson said it's possible members of the flock don't perceive the lower-ranked birds as a threat to their own standing.
"When we take a bird out, there's a power vacuum and everything shifts to accommodate it," co-author and UC doctoral student Chelsea Carminito said. "When that bird suddenly comes back, the birds at the top don't want to relinquish their top rank and will defend their position."
Carminito is studying the behavior of monk parakeets to learn ways to improve their care and the care of other social birds in captivity and zoos and research centers.
"My interest is how to reduce stress in captive situations when you have to remove a bird," she said.
Van der Marel said the flock's social structure adapted quickly to the absence or loss of a single bird. In the wild, flocks occasionally lose individuals to predators or disease, so the remaining birds may be adaptable. Less common, she said, is when a high-status bird would return to the flock after a prolonged absence, perhaps from injury. These reintroductions seem to cause more havoc in the social group than removals.
"Monk parakeets have a very complex social system and demonstrate a lot of cognitive complexity," van der Marel said.
From Hobson's previous studies, researchers learned that monk parakeets in captive groups can have a keen understanding of their social order and can use this to be selective in picking which birds to target with aggression.
"They spend a lot of time and energy watching each other's fights and remembering the outcomes," Hobson said. "They appear to be aware of their ranks and the position of others in these hierarchies."
In dominance hierarchies, higher rank often confers better access to food and other resources. Hobson said it's not clear what advantages rank affords monk parakeets in the wild, where it's more difficult to study the social birds.
Hobson studied several dozen wild birds she captured and tagged in Argentina, but they would congregate with many others, making it difficult to identify where they fit in the greater social structure.
"In Argentina, people call the parakeets 'la plaga," which means the plague," Hobson said. "There are thousands and thousands of them.."
In her biology lab, Hobson is using bobwhite quail as a model system to study the formation of relationships and social structure. This year she also added aquariums of colorful bettas, which may also be able to use social information to structure their social interactions and aggression.
"The more similar we can make the experiments and analytical approach, the more potential we have to compare sociality in an apples to apples way across species," Hobson said.
More information: Annemarie van der Marel et al, Perturbations highlight importance of social history in parakeet rank dynamics, Behavioral Ecology (2023). DOI: 10.1093/beheco/arad015
Journal information: Behavioral Ecology
Provided by University of Cincinnati | Biology |
Researchers at The University of Queensland have found an anti-ageing function in a protein deep within human cells.
Associate Professor Steven Zuryn and Dr Michael Dai at the Queensland Brain Institute have discovered that a protein called ATSF-1 controls a fine balance between the creation of new mitochondria and the repair of damaged mitochondria.
Mitochondria, with their own DNA, produce energy within cells to power biological functions but the toxic by-products of this process contribute to the rate at which the cell ages.
“In conditions of stress, when mitochondrial DNA has been damaged, the ATSF-1 protein prioritises repair which promotes cellular health and longevity,” Dr Zuryn said.
As an analogy, Dr Zuryn likened the relationship to a race car needing a pitstop.
“ATSF-1 makes the call that a pitstop is needed for the cell when mitochondria need repairs,” he said.
“We studied ATFS-1 in C. elegans, or round worms and saw that enhancing its function promoted cellular health, meaning the worms became more agile for longer.
“They didn’t live longer, but they were healthier as they aged.”
“Mitochondrial dysfunction lies at the core of many human diseases, including common age-related diseases such as dementias and Parkinson’s.
“Our finding could have exciting implications for healthy ageing and for people with inherited mitochondrial diseases.”
Understanding how cells promote repair is an important step towards identifying possible interventions to prevent mitochondrial damage.
“Our goal is to prolong the tissue and organ functions that typically decline during ageing by understanding how deteriorating mitochondria contribute to this process,” Dr Dai said.
“We may ultimately design interventions that keep mitochondrial DNA healthier for longer, improving our quality of life,” Dr Dai said.
This research was published in Nature Cell Biology.
Media: QBI Communications, [email protected], Merrett Pye +61 422 096 049; Elaine Pye +61 415 222 606. | Biology |
Scanning electron micrograph of a human T lymphocyte (also called a T cell) from the immune system of a healthy donor. Credit: NIAID Using new machine learning techniques, researchers at UC San Francisco (UCSF), in collaboration with a team at IBM Research, have developed a virtual molecular library of thousands of "command sentences" for cells, based on combinations of "words" that guided engineered immune cells to seek out and tirelessly kill cancer cells. The work, published online Dec. 8, 2022, in Science, represents the first time such sophisticated computational approaches have been applied to a field that until now has progressed largely through ad hoc tinkering and engineering cells with existing—rather than synthesized—molecules. The advance allows scientists to predict which elements—natural or synthesized—they should include in a cell to give it the precise behaviors required to respond effectively to complex diseases. "This is a vital shift for the field," said Wendell Lim, Ph.D., the Byers Distinguished Professor of Cellular and Molecular Pharmacology, who directs the UCSF Cell Design Institute and led the study. "Only by having that power of prediction can we get to a place where we can rapidly design new cellular therapies that carry out the desired activities." Meet the molecular words that make cellular command sentences
Much of therapeutic cell engineering involves choosing or creating receptors, that when added to the cell, will enable it to carry out a new function. Receptors are molecules that bridge the cell membrane to sense the outside environment and provide the cell with instructions on how to respond to environmental conditions. Putting the right receptor into a type of immune cell called a T cell can reprogram it to recognize and kill cancer cells. These so-called chimeric antigen receptors (CARs) have been effective against some cancers but not others. Lim and lead author Kyle Daniels, Ph.D., a researcher in Lim's lab, focused on the part of a receptor located inside the cell, containing strings of amino acids, referred to as motifs. Each motif acts as a command "word," directing an action inside the cell. How these words are strung together into a "sentence" determines what commands the cell will execute. Many of today's CAR-T cells are engineered with receptors instructing them to kill cancer, but also to take a break after a short time, akin to saying, "Knock out some rogue cells and then take a breather." As a result, the cancers can continue growing. The team believed that by combining these "words" in different ways, they could generate a receptor that would enable the CAR-T cells to finish the job without taking a break. They made a library of nearly 2,400 randomly combined command sentences and tested hundreds of them in T cells to see how effective they were at striking leukemia.
What the grammar of cellular commands can reveal about treating disease Next, Daniels partnered with computational biologist Simone Bianco, Ph.D., a research manager at IBM Almaden Research Center at the time of the study and now Director of Computational Biology at Altos Labs. Bianco and his team, researchers Sara Capponi, Ph.D., also at IBM Almeden, and Shangying Wang, Ph.D., who was then a postdoc at IBM and is now at Altos Labs, applied novel machine learning methods to the data to generate entirely new receptor sentences that they predicted would be more effective. "We changed some of the words of the sentence and gave it a new meaning," said Daniels. "We predictively designed T cells that killed cancer without taking a break because the new sentence told them, 'Knock those rogue tumor cells out, and keep at it.'" Pairing machine learning with cellular engineering creates a synergistic new research paradigm. "The whole is definitely greater than the sum of its parts," Bianco said. "It allows us to get a clearer picture of not only how to design cell therapies, but to better understand the rules underlying life itself and how living things do what they do." Given the success of the work, added Capponi, "We will extend this approach to a diverse set of experimental data and hopefully redefine T-cell design."
The researchers believe this approach will yield cell therapies for autoimmunity, regenerative medicine and other applications. Daniels is interested in designing self-renewing stem cells to eliminate the need for donated blood.
He said the real power of the computational approach extends beyond making command sentences, to understanding the grammar of the molecular instructions. "That is the key to making cell therapies that do exactly what we want them to do," Daniels said. "This approach facilitates the leap from understanding the science to engineering its real-life application." More information: Kyle G. Daniels et al, Decoding CAR T cell phenotype using combinatorial signaling motif libraries and machine learning, Science (2022). DOI: 10.1126/science.abq0225. www.science.org/doi/10.1126/science.abq0225 Citation: How AI found the words to kill cancer cells (2022, December 8) retrieved 10 December 2022 from https://phys.org/news/2022-12-ai-words-cancer-cells.html This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only. | Biology |
Nano plumbing: An artistic rendering showing how DNA nanotubes could connect artificial cells. (Courtesy: Schulman Lab, Johns Hopkins University) Synthetic cells, engineered to mimic some of the functions performed by living cells, hold promise for applications in biotechnology and medicine. Even the smallest biological cells, however, are extremely complex and the construction of living artificial cells faces numerous roadblocks. Researchers in the Schulman Lab at Johns Hopkins University have recently made progress towards one of these challenges: the exchange of matter and information across cell boundaries.
Writing in Science Advances, the researchers – working in collaboration with the Aksimentiev Group at the University of Illinois Urbana-Champaign – demonstrate the leak-free transport of small molecules through engineered DNA nanochannels across unprecedented distances. In the future, their work may help in the construction of artificial cells, and also aid the study and manipulation of living tissue.
Cells within multicellular organisms need to exchange matter and communicate to ensure their collective survival. Since each cell is surrounded by a lipid membrane that is impenetrable to many biological molecules, evolution has produced mechanisms by which this barrier can be traversed. Signalling receptors, transporters and pores relay information and allow the passage of molecules between cells and their exterior, while cell contacts such as gap junctions directly connect the interior of neighbouring cells and enable cell-to-cell diffusion of small molecules.
To mimic these processes in artificial systems, “researchers have developed synthetic cells positioned next to each other that can communicate through protein pores on their membranes” explains first author Yi Li, who co-led the study. “However, developing synthetic cell systems where cells can communicate and exchange materials across longer distances is still a challenge.”
The protein structures that facilitate cell-to-cell communication in biology are built “bottom-up” from amino acids – the information encoded in their sequence translates into a structure. Another biological macromolecule, DNA, is mainly used for information storage in cells; but due to its ease of synthesis and potential to form high-level structures, the field of DNA nanotechnology has gone far beyond its first proof-of-concept some 30 years ago. Scientists have since assembled ever more sophisticated 2D and 3D structures from DNA, including lattices, tubes, geometric bodies and even artistic renderings of smiley faces, in efforts referred to as DNA origami.
In their study, the Schulman Lab researchers combined DNA origami nanopores, which bridge the membranes of cell-like vesicles and create small openings for molecules to cross, with engineered self-assembling DNA nanotubes. By quantifying the flux of a dye molecule into the vesicles, they showed that short nanopores made the membrane permeable to the dye. They also validated that the speed of this transport is consistent with diffusion and found that a specially designed DNA cap can block the pores and stop the dye from entering.
First author: Yi Li in the laboratory at Johns Hopkins University. (Courtesy: Yi Li)
The team then extended this work to DNA nanotubes with a median length of 700 nm and a maximum of over 2 µm. Again, experiments showed that dye influx is enhanced in the presence of the DNA constructs, and that the cap can arrest permeation. The implication, says Li, is that “small molecules can pass through the tubes without leaks, and we expect large molecules, such as proteins, can also be transported through these nanotubes”.
Members of the Aksimentiev Group conducted Brownian dynamics computer simulations of the nanopore–dye system. These illustrated that for molecules below a threshold size, leakage through the side wall of the DNA tube dominated influx, while for larger molecules, end-to-end diffusion becomes the preferred mechanism .
Li explains that such simulations are complementary with experiments in two ways. “They can be used as design tools to help researchers design nanoscale structures that have specific functions”, he says, for example by “simulating the self-assembly kinetics of our DNA nanostructures”, but they also help to “validate experimental results and provide additional insights into the physical processes”. Read more Do-it-yourself DNA design Rebecca Schulman – who co-led the research – draws an analogy to pipes. “This study suggests very strongly that it’s feasible to build nanotubes that don’t leak using these easy techniques for self-assembly, where we mix molecules in a solution and just let them form the structure we want. In our case, we can also attach these tubes to different endpoints to form something like plumbing.”
The lab has ambitious plans for application of these nanotubes. “Future developments include connecting two or more artificial cells with our DNA nanotubes and showing molecular transport among them. We can potentially show [that] the transport of signalling molecules from one cell can activate/deactivate the gene expression in another cell,” Li tells Physics World. The team also hopes to “use nanotubes to control the delivery of signalling molecules or therapeutics to mammalian cells, either to study cell signalling behaviours or to develop a drug delivery strategy”. | Biology |
Adélie penguins need an optimal level of sea ice to breed—too much, and access to food is threatened.Image: Louise Emmerson/Australian Antarctic ProgramAs the fervor of Fat Bear Week rages on, a different corner of the animal kingdom is in trouble: The Antarctic penguin community. Australian researchers studying Adélie penguins point to a plunging population.OffEnglishResearchers from the Australian Antarctic Division’s Department of Climate Change, Energy, the Environment and Water are reporting a startling dip in the population of Adélie penguins in eastern Antartica—a whopping 43%. The research was published by seabird ecologists Louise Emmerson and Colin Southwell this week in Global Change Biology. “We think this population decline was initially triggered by five years of extensive summer sea ice adjacent to the colony in the mid-2000s, which hampered access to the adults’ foraging areas and saw virtually no chicks survive,” said Emmerson in a press release. “The frequency of these unfavourable breeding conditions subsequently remained high, and fledgling survival also began to decrease. These two processes together resulted in a more rapid population decline than would be expected if they had been acting in isolation.”The location of Mawson research station.Image: Gizmodo/DatawrapperThe loss of penguins is specifically occurring on the eastern side of the continent near Mawson research station. The researchers liken the rate of decline in this location to that of the Adélie penguins on the Antarctic peninsula, where populations are subject to the human-related pressures of commercial fishing, climate change, and human activity. Emmerson and Southwell, however, suspect that the Mawson population is seeing a decline due to environmental conditions creating a feedback loop within the population—more specifically, an increase in near-shore sea ice has made breeding less successful as hunting for food is more difficult. The researchers further propose that the smaller this population gets, the harder it will be for it to survive as it faces less defense from predators and less success in navigating and hunting. “Whether this Mawson penguin population stabilizes, continues to decline, or recovers, remains to be seen. It is clear from this study though that where possible, we are better off preventing impacts in the first place, or trying to alleviate them before population decline is well-established, or the processes causing the decline become confounding and result in rapid population declines,” said Emmerson.According to Emmerson, the next step in this research is to continue monitoring the Adélie population to more thoroughly understand the mechanisms that allow the fledgling members of the species to survive amidst this ongoing feedback loop. | Biology |
Forest growing season in eastern U.S. has increased by a month
Warming changed timing of budburst, coloration in past century
The growing period of hardwood forests in eastern North America has increased by an average of one month over the past century as temperatures have steadily risen, a new study has found.
The study compared present-day observations of the time span from budburst to peak leaf coloration in seven tree species to similar documentation that was collected by an Ohio farmer at the turn of the 20th century.
An analysis of changes in those leaf patterns along with decades of temperature data for northwest Ohio showed a clear connection between increased warming during winter and spring and an extended period of tree growth.
The implications of the longer growing period – both positive and negative – remain unknown. But the simple fact that leaves stay on trees about 15% longer than they did 100 years ago is an “obvious indicator that temperatures are changing and shows that things are not the way they used to be – they are profoundly different,” said lead author Kellen Calinger-Yoak, assistant professor of evolution, ecology and organismal biology at The Ohio State University.
“An entire month of growing season extension is huge when we’re talking about a pretty short period of time for those changes to be expressed,” she said.
Wauseon, Ohio, farmer Thomas Mikesell recorded temperatures, precipitation and observations of seasonal changes to trees and other plants from 1883 to 1912 – creating what may be the only comprehensive dataset of pre-warming tree growing patterns in all of North America, Calinger-Yoak said.
For this study, Calinger-Yoak traveled to Wauseon multiples times per week in the spring and fall between 2010 and 2014 to make her own observations of seven species: American elm, black walnut, white oak, black oak, eastern cottonwood, staghorn sumac and sassafras trees, all of which are hardy species that grow well across most of the United States. The researchers also used monthly temperature and precipitation data from the U.S. Historical Climatology Network’s Wauseon station to calculate long-term trends.
Though species did not respond to changing temperatures in exactly the same way – some budded early and most kept their leaf color longer into the fall – Calinger-Yoak said two patterns stood out in the analysis: Average mid-winter and spring temperatures in the region have increased by up to 5 degrees Fahrenheit since 1892, with six of the 10 warmest years in November and December occurring since 1990, and leaves’ longer life spans into autumn indicated when most of the growing season extension took place – because foliage coloration was delayed.
Calinger-Yoak used the dates of peak coloration, rather than when leaves fell to the ground, to determine the end point of the growing season to tie in with each tree’s peak period for photosynthesis. As leaf colors fade, trees become much less efficient at taking in carbon dioxide and water to obtain the sugars that sustain them.
While extended growing likely increases trees’ absorption of carbon dioxide from the atmosphere, the mix of overall warming and extreme temperature fluctuations can stress trees in ways this research couldn’t detect. Overall, though, there was quite a bit of variety in the species’ responses to changing temperatures – which is a red flag for a biologist.
“If you’re exposing organisms to the exact same environmental pressures and you see radically different responses, chances are that one of those responses is going to be better in the long term than the other,” Calinger-Yoak said. “Time will tell who the long-term winners and losers will be, and what that means for how different forests will end up looking if some species are consistently underperforming because they can’t handle the extremes we’ve introduced to the system.”
These findings point to the need for even more species-specific research to improve models designed to predict how forests, and their valuable carbon-absorption service, will respond as the climate continues to change, she said.
“We are invested in making the bad effects of global warming less horrible, and are wondering how much benefit we can get from trees we already have and from potentially planting more trees – that’s really important,” she said. “When we’re thinking about a relatively low-cost mitigation strategy, planting a whole bunch of trees that suck CO2 out of the air is a really good strategy, but to promote those activities you also have to have evidence of the level of benefit you’d derive from it.” | Biology |
Adult albatrosses on a remote island are being attacked and eaten by an aggressive invasive species — mice.
Invasive mice have been wreaking havoc on the ecosystem of Marion Island — located about halfway between South Africa and Antarctica — for decades, chowing down on native invertebrates and the chicks of many seabirds that breed there. But the latest discovery is the first time they've been documented attacking adult albatrosses on the island.
"If the mice are starting to attack the adults, that's becoming really problematic," Maëlle Connan, a researcher at Nelson Mandela University in South Africa, told Live Science.
At 115 square miles (298 square kilometers), Marion Island is about half the size of Chicago but is home to an impressive array of wildlife, including king penguins, elephant seals and seabirds like wandering albatrosses (Diomedea exulans), one of the world's largest flying birds. The island wasn't home to any non-marine mammals until about the 19th century, when house mice (Mus musculus) were introduced by humans via ships.
Since then, mice have decimated many of the invertebrates and plant species that live there. But in recent decades, the local mouse population has boomed, likely as a result of warmer and drier weather due to climate change.
As the mouse population has grown, so has their appetite — and in 2003, researchers discovered that the mice had started eating the chicks of wandering albatrosses on the island.
Now, it seems the mice have begun feasting on adult birds. In April, researchers found the bodies of eight adult wandering albatrosses that had died within weeks of each other.
The carcasses showed evidence of mouse attacks, such as wounds on their elbows, Connan said. News of this discovery was first reported in Nature Africa. Blood patterns suggest the injuries were inflicted while the birds were still alive, the report said.
Wandering albatrosses have a 10-foot (3 meters) wingspan so are significantly bigger than mice, but they evolved to live on islands without any mammalian predators and have no defense mechanisms against the invasive rodents, Anton Wolfaardt a seabird researcher with The Mouse-Free Marion Project told Live Science. The project is an initiative of the South African government and the nonprofit organization BirdLife South Africa.
It's not clear exactly how the albatrosses died, but it could have been due to infection from the mouse bites or even starvation if the birds were too injured to go out to sea and find food, Wolfaardt said. Long-term, this predation could have a significant impact on the global wandering albatross population — about a quarter of which lives on Marion Island.
Mice have also recently been observed attacking adult albatrosses in other seabird hotspots, such as Tristan albatrosses (Diomedea dabbenena) on Gough Island in the South Atlantic and Laysan albatrosses (Phoebastria immutabilis) on Midway Atoll in the Pacific. That's a worrying trend for this threatened group of birds — of the 22 species of albatross worldwide, nine are listed as endangered or critically endangered.
On Marion, there's a plan to fight back. The Mouse-Free Marion Project is planning to spread rodenticide all over the island, which the conservationists hope will kill off all the mice, Wolfaardt said.
The local native seabirds mostly look for food in the ocean, and the native invertebrates aren't affected by rodenticide, he said, so this technique would only target the invasive mice living on the island. If it's successful, the Marion Island ecosystem may finally start to heal.
"Once those introduced predators, invasive species, are removed," Wolfaardt said, "you can really then kind of start the process of turning back the clock."
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Ethan Freedman is a science and nature journalist based in New York City, reporting on climate, ecology, the future and the built environment. He went to Tufts University, where he majored in biology and environmental studies, and has a master's degree in science journalism from New York University. | Biology |
Neural networks, a type of computer system loosely modeled after the organization of the human brain, are the basis of many artificial intelligence systems for applications such as speech recognition, computer vision and medical image analysis.
In the field of neuroscience, researchers often use neural networks to try to model the same kinds of tasks that the brain performs, in the hope that the models could suggest new hypotheses about how the brain itself performs those tasks. However, a group of researchers at MIT insist that more caution should be exercised when interpreting these models.
In an analysis of more than 11,000 neural networks trained to simulate the function of grid cells — important components of the brain’s navigation system — the researchers found that neural networks only produced grid cell-like activity when given very specific constraints that do not occur. for biological systems.
“This suggests that to obtain a result with grid cells, the researchers train the models needed to bake those results in with specific, biologically unlikely implementation choices,” said Rylan Schaeffer, a former senior research associate at MIT.
Without those limitations, the MIT team found that very few neural networks generated grid cell-like activity, suggesting that these models don’t necessarily generate useful predictions about how the brain works.
Schaeffer, who is now a graduate student in computer science at Stanford University, is the lead author of the new study, which will be presented this month at the 2022 conference on neural information processing systems. Ila Fiete, a professor of brain and cognitive sciences and a member of MIT’s McGovern Institute for Brain Research, is the senior author of the paper. Mikail Khona, an MIT graduate student in physics, is also an author.
Model grid cells
Neural networks, which researchers have used for decades to perform various computational tasks, consist of thousands or millions of processing units connected together. Each node has connections of different strengths to other nodes in the network. Because the network analyzes massive amounts of data, the strengths of those connections change as the network learns to perform the desired task.
In this study, the researchers focused on neural networks designed to mimic the function of the brain’s grid cells, which are found in the entorhinal cortex of the mammalian brain. Together with place cells, found in the hippocampus, grid cells form a brain circuit that helps animals know where they are and how to navigate to another location.
Place cells have been shown to fire when an animal is in a specific location, and each place cell can respond in more than one location. Grid cells, on the other hand, work very differently. When an animal moves through a space such as a room, grid cells fire only when the animal is on one of the vertices of a triangular grid. Different groups of grid cells create grids of slightly different sizes, overlapping each other. This allows grid cells to encode a large number of unique positions with a relatively small number of cells.
This type of location coding also makes it possible to predict an animal’s next location based on a particular starting point and a speed. In several recent studies, researchers have trained neural networks to perform the same task, known as path integration.
To train neural networks to perform this task, researchers enter a starting point and a speed that varies over time. The model essentially mimics the activity of an animal wandering through a space and calculates updated positions as it moves. As the model performs the task, the activity patterns of different units within the network can be measured. The activity of each unit can be represented as a firing pattern, similar to the firing pattern of neurons in the brain.
In several previous studies, researchers have reported that their models produced units with patterns of activity that closely mimic the firing patterns of grid cells. These studies concluded that grid cell-like representations would naturally appear in any neural network trained to perform the path integration task.
However, the MIT researchers found very different results. In an analysis of more than 11,000 neural networks they trained for path integration, they found that while nearly 90 percent of them successfully learned the task, only about 10 percent of those networks generated patterns of activity that could be classified as grid cell-like. This also applies to networks in which even one unit achieved a high net score.
According to the MIT team, the previous studies were more likely to generate cell-like activity because of the limitations researchers build into those models.
“Previous studies have put forward this story that if you train networks to integrate, you get grid cells. What we found is that instead you have to pick this long set of parameters, which we know don’t align with biology, and then you get the result you want in a little bit of those parameters,” Schaeffer says.
More organic models
One of the limitations found in previous studies is that the researchers needed the model to convert the speed to a unique position reported by one network unit corresponding to a place cell. For this to happen, the researchers also required that each place cell correspond to only one location, which isn’t how biological place cells work: Studies have shown that place cells in the hippocampus can respond to up to 20 different locations, not just one.
When the MIT team modified the models so that place cells looked more like biological place cells, the models were still able to perform the pathway integration task, but they no longer produced grid cell-like activity. Grid-cell-like activity also disappeared when the researchers instructed the models to generate different types of location output, such as location on a grid with X and Y axes, or location as a distance and angle from a home point.
“If all you ask of this network is path integration, and you impose a set of very specific, non-physiological demands on the readout unit, then it is possible to obtain grid cells,” says Fiete. “But if you loosen any of these aspects of this readout unit, it greatly deteriorates the network’s ability to produce grid cells. In fact, they usually don’t, even though they’re still solving the path integration task.”
Therefore, if the researchers had not already known about the existence of grid cells and guided the model to produce them, it would be very unlikely that they would appear as a natural consequence of the model training.
The researchers say their findings suggest more caution is needed when interpreting neural network models of the brain.
“When you use deep learning models, they can be a powerful tool, but you have to be very careful when interpreting them and determining whether they really make de novo predictions, or even shed light on what the brain is optimizing.” , says Fiet.
Kenneth Harris, a professor of quantitative neuroscience at University College London, says he hopes the new study will encourage neuroscientists to be more careful about what can be demonstrated by analogies between neural networks and the brain.
“Neural networks can be a useful source of predictions. If you want to know how the brain solves a calculation, you can train a network to perform it and then test the hypothesis that the brain works the same way. Whether the hypothesis is confirmed or not, you will learn something from it,” said Harris, who was not involved in the study. “This paper shows that ‘postdiction’ is less powerful. Neural networks have many parameters, so it’s not that surprising to have them replicate an existing result.”
When using these models to make predictions about how the brain works, it’s important to consider realistic, known biological constraints when building the models, the MIT researchers say. They are now working on models of grid cells that they hope will generate more accurate predictions about how grid cells work in the brain.
“Deep learning models will give us insight into the brain, but only after you inject a lot of biological knowledge into the model,” Khona says. “If you use the right constraints, the models can give you a brain-like solution.”
The research was funded by the Office of Naval Research, the National Science Foundation, the Simons Foundation through the Simons Collaboration on the Global Brain, and the Howard Hughes Medical Institute through the Faculty Scholars Program. Mikail Khona was supported by the MathWorks Science Fellowship. | Biology |
Using microbes to get more out of mining waste
Researchers have developed a new mining technique which uses microbes to recover metals and store carbon in the waste produced by mining. Adopting this technique of reusing mining waste, called tailings, could transform the mining industry and create a greener and more sustainable future.
Tailings are a by-product of mining. They are the fine-grained waste materials left after extracting the target ore mineral, which are then stacked and stored. This method is called dry-stack tailing.
Over time, mining practices have evolved and become more efficient. But the climate crisis and rising demand for critical minerals require the development of new ore removal and processing technologies.
Old tailings contain higher amounts of critical minerals that can be extracted with the help of microbes through a process called bioleaching. The microbes help break down the ore, releasing any valuable metals that weren't fully recovered in an eco-friendly way that is much faster than natural biogeochemical weathering processes.
"We can take tailings that were produced in the past and recover more resources from those waste materials and, in doing so, also reduce the risk of residual metals entering into local waterways or groundwater," said Dr. Jenine McCutcheon, an assistant professor in the Department of Earth and Environmental Sciences.
In addition to improving resource recovery, the microbes capture carbon dioxide from the air and store it within the mine tailings as new minerals. This process aids in offsetting some of the emissions released while the mine was active and helps stabilize the tailings.
Microbial mineral carbonation could offset more than 30 per cent of a mine sites annual greenhouse gas emissions if applied to an entire mine. In addition, this microbial-driven technique gives value to historical mine tailings that are otherwise considered industrial waste.
"This technique makes better use of current and past mine sites," McCutcheon said. "Rethinking how future mine sites are designed in order to integrate this process could result in mines that are carbon neutral from the get-go rather than thinking about carbon storage as an add-on at the end.
McCutcheon further believes that the microbial-driven processes could help the industry move towards carbon-neutral or carbon-negative mining, but industry engagement is critical to move this technology towards large-scale deployment.
Dr. McCutcheon published this research with co-author and associate professor Ian Power of Trent University in the peer-reviewed journal PLOS Biology.
More information: Jenine McCutcheon et al, Microbially mediated carbon dioxide removal for sustainable mining, PLOS Biology (2023). DOI: 10.1371/journal.pbio.3002026
Journal information: PLoS Biology
Provided by University of Waterloo | Biology |
Study uncovers a unique, efficient method of copper delivery in cells
A new study has uncovered a unique way in which the anti-cancer drug elesclomol enables copper delivery in cells, aiding in the search for treatments for copper deficiency disorders such as Menkes disease.
Menkes disease is an extremely rare hereditary copper-deficiency disorder in infants. It is characterized by progressive neurological injury culminating in death, typically by the age of three.
A Texas A&M AgriLife Research team led by Vishal Gohil, Ph.D., associate professor in the Department of Biochemistry and Biophysics in Texas A&M's College of Agriculture and Life Sciences, Bryan-College Station, first discovered the therapeutic potential of elesclomol for treating copper deficiency disorders. Additionally, previous research by Gohil's team showed that elesclomol could be used effectively in a mouse model to treat Menkes disease.
The new study, "FDX1-dependent and independent mechanisms of elesclomol-mediated intracellular copper delivery," was recently published in the Proceedings of the National Academy of Sciences, a peer-reviewed journal of the National Academy of Sciences. The research was led by Gohil, with Mohammed Zulkifli, Ph.D., a research scientist in the same department, as the first author of the study.
The study was conducted in collaboration with scientists from the University of Houston, Oregon Health and Science University, University of Missouri and the Advanced Photon Source at Argonne National Laboratory, a U.S. Department of Energy multidisciplinary science and engineering research center.
Elesclomol and copper deficiency
Genetic defects in copper transport to copper-containing enzymes, referred to as "cuproenzymes," result in fatal disorders such as Menkes disease. No effective treatment is currently available for these copper deficiency disorders.
"To realize the full potential of elesclomol, it was necessary to gain a mechanistic understanding of how this drug makes copper available to different cellular cuproenzymes," Gohil said. "We needed to look at the mechanism by which copper brought into cells by elesclomol is released and delivered to cuproenzymes present in different subcellular compartments."
He said the study used a combination of biochemistry, cell biology and genetics to demonstrate that the release of copper from elesclomol occurs both inside and outside mitochondria.
Copper and human health
Copper is an essential trace element required for the activity and stability of several cuproenzymes involved in a wide array of physiological processes.
"Copper is an essential micronutrient, and genetic mutations that prevent copper transport across cellular membranes or its delivery to cuproenzymes can result in lethal human disorders such as Menkes disease," Gohil said.
Currently, no Food and Drug Administration-approved therapies are available for treating Menkes disease. Additionally, direct administration of hydrophilic copper salts has shown limited efficacy in clinical trials.
"We hypothesized that this limited efficacy was likely due to inefficient copper delivery across cellular membranes, so there was an unmet need to identify compounds that can safely and effectively transport copper across biological membranes and restore cellular copper balance," Gohil said.
The study
Previous research had shown that ferredoxin 1, FDX1, a mitochondrial enzyme, was the protein target of elesclomol. In the current study, Gohil and his team showed that FDX1 releases copper bound to elesclomol by reducing it to a form of copper cells can use. The study also showed that even when FDX1 was absent, elesclomol could still bring some copper into cells in other unknown ways.
Zulkifli said FDX1 can also help release copper from other clinically used copper-transporting drugs, but compared with elesclomol, these drugs are much less dependent on FDX1 to make the copper bioavailable to cuproenzymes.
"These modes of copper release by elesclomol are distinct from those of other currently used copper-transporting drugs," Zulkifli said. "This may explain the high potency of elesclomol in rectifying copper deficiency."
Building on past research
Previous studies by Gohil and his team have highlighted the therapeutic potential of elesclomol in treating diseases of copper deficiency. Some of this previous research also showed that elesclomol can restore the levels of cytochrome c oxidase protein complex, a critical copper-dependent enzyme required for mitochondrial energy production.
The Gohil lab also demonstrated that elesclomol improves copper deficiency in yeast, zebrafish and mouse models by delivering copper to mitochondria and restoring the function of the cytochrome c oxidase.
Additionally, the use of elesclomol to treat copper deficiency disorders is at the center of a licensing agreement between The Texas A&M University System, managed through the Intellectual Property and Commercialization office of Texas A&M AgriLife Research, and California-based Engrail Therapeutics.
More information: Mohammad Zulkifli et al, FDX1-dependent and independent mechanisms of elesclomol-mediated intracellular copper delivery, Proceedings of the National Academy of Sciences (2023). DOI: 10.1073/pnas.2216722120
Journal information: Proceedings of the National Academy of Sciences
Provided by Texas A&M University | Biology |
Celiac disease, also called celiac sprue, is a condition that affects mostly the small intestine, although it can have consequences throughout the body. People with celiac disease experience digestive symptoms and potential long-term tissue damage as a result of the immune system attacking the inner lining of the small intestine (opens in new tab).
In nearly all cases, this immune reaction is triggered by the ingestion of gluten, a group of proteins present in grains such as wheat, rye and barley.
Related: What is gluten?
What causes celiac disease?
Celiac disease occurs mostly in people who have a genetic predisposition (opens in new tab) to the condition, due to abnormalities in the human leukocyte antigen (HLA) genes (opens in new tab) that are located on chromosome 6. These genes code for HLA proteins, whose function is to bind bits of infectious pathogens, like viruses, and alert the immune system to the invaders' presence. Mutations in these genes can cause the body to mistake its own tissues as a threat and attack them.
Two HLA gene abnormalities, called HLA-DQ2 and HLA-DQ8, are linked to celiac disease, such that the presence of one or both of them makes a person genetically predisposed to the disease. These individuals experience a hypersensitive reaction to the presence of gluten in the gastrointestinal tract, meaning their immune systems respond inappropriately and excessively to the substance.
In celiac disease, the hypersensitivity is classified as a type IV hypersensitivity reaction (opens in new tab), or delayed hypersensitivity. Type IV hypersensitivity is mediated by the interaction of immune cells called T lymphocytes, monocytes and macrophages, which, in turn, trigger additional immunological events. In celiac disease, this immunological cascade occurs in the small intestine and changes the histology (the microscopic anatomy) of the inner lining of the organ, leading to symptoms and complications.
Typically, these changes in the small intestine reverse, and the symptoms abate, when gluten is removed completely from the diet. But in rare cases, known as refractory celiac disease, the disease process can continue even in the absence of gluten (opens in new tab), due to the celiac immune process going into a kind of autopilot.
Meanwhile, the disease process in the small intestine leads to the malabsorption of food and the release of mucus, and often blood, into the gastrointestinal tract. All of this produces diarrhea, gas and bloating, nausea and, over the long term, malnutrition.
Celiac disease risk factors
The prevalence of celiac disease depends greatly on a genetic predisposition (opens in new tab) involving the HLA-DQ2 and HLA-DQ8 genes, but there is notable variation among countries and ethnic groups.
In North America, celiac disease affects about 0.71% of people (opens in new tab), or about 1 in 141. The disease is a little more common in white people, with 1 case per every 100 individuals. In Europe, about 1 in 100 people has celiac disease, but the prevalence is higher in certain countries, notably Finland, where 2.4% of people (opens in new tab) have the disease.
Celiac disease is also about as common in India, North Africa and the Middle East (opens in new tab) as it is in Europe.
While the aforementioned genetic factors constitute risk factors, people are not often tested for the presence of the HLA-DQ2 and HLA-DQ8 gene variants. Thus, practically speaking, the main risk factor for celiac disease is having a first-degree relative (parent, sibling, child) who is known to have the condition. Additionally, type 1 diabetes has been found to be a potential risk factor (opens in new tab) for celiac disease.
What are the symptoms of celiac disease?
People with celiac disease experience a constellation of symptoms, including the following:
- Diarrhea
- Abdominal pain
- Nausea and vomiting
- Bloating and gas
- Constipation
- Fatigue
- Weight loss
- Constipation
In people diagnosed with celiac disease, both the short- and long-term symptoms tend to be very severe. However, it is not uncommon for people with a family history of celiac disease to experience any of the above symptoms at milder levels, even if diagnostic tests, including serology tests, do not show indications of celiac disease.
Abatement of the above symptoms following the withdrawal of gluten from the diet can support a diagnosis of celiac disease, but such a diagnosis cannot be made based solely on how a person responds to a gluten-free diet. One major reason for this is that foods that lack gluten also lack various other components that could potentially cause gastrointestinal distress. Such components include fiber, as well as fermentable oligosaccharides, disaccharides and monosaccharides and polyols (FODMAPs) (opens in new tab), which will be discussed later in this article.
How is celiac disease diagnosed?
Diagnosing celiac disease can be complex (opens in new tab), but it should begin with a thorough patient history and physical examination. A combination of any of the following suggests celiac disease:
- A long history of diarrhea
- Tummy pain
- Bloating
- Sores in the mouth
- Weight loss
- Bleeding of the GI tract, due to immune attack in the lining of the small intestine
- Bruising and bleeding outside the GI tract, due to nutritional deficiencies
- Bone fractures, which are made more likely by malnutrition
In many cases, celiac disease can be difficult to confirm, because other serious gastrointestinal conditions, such as inflammatory bowel disease and ulcers, cause similar symptoms. These other diseases can be ruled out through additional testing, which can include the checking of stool samples for signs of blood, as well as imaging tests.
If a patient does not suffer from malnutrition, doctors should consider that the person's gastrointestinal problems might be the result of a very common condition called irritable bowel syndrome (opens in new tab), which frequently results from intolerance to one or more FODMAPs (opens in new tab). One particular FODMAP to which people are often intolerant is lactose, the kind of sugar that's in milk, but there are other types of FODMAP intolerance that cause dietary distress following the ingestion of other things, such as beans and grains.
Although dietary fiber is healthy because it helps move food and waste through the gastrointestinal tract and can have beneficial effects on cholesterol levels in the blood, eating a lot of high-fiber foods also can also produce gas and gastrointestinal distress.
A family history of celiac disease in one or more close relatives points to the possible presence of celiac disease. After a doctor takes this history, the next step is to perform "serology testing," meaning doctors will screen a patient's blood samples for various antibodies (opens in new tab). Classically, serology testing centered on what doctors call anti-gliadin antibodies (AGA), which react to gliadins, a component of gluten. These antibodies come in two flavors: IgA and IgG.
If a patient tests positive on one or more of these tests, experiences gastrointestinal distress, and has a family history of celiac, doctors may diagnose the disease without further tests.
In many cases, however, the diagnosis will not be made until there is also proof of abnormal histology in the lining of the small intestine. This requires a test called endoscopy, in which a gastroenterologist uses an instrument to look at the inside of the small intestine from the inside and to obtain a sample called a biopsy. Positive serology plus a positive biopsy (opens in new tab) confirms a celiac disease diagnosis.
Sometimes people will be referred for an endoscopy even if their serology testing is negative. In cases when the serology is negative and yet the endoscopy demonstrates histology resembling that of celiac disease, such patients will be diagnosed with a different intestinal disorder.
While genetic testing can reveal the HLA-DQ2 and HLA-DQ8 gene variants, whose presence correlates extremely well with celiac disease, in practice, celiac diagnosis is usually made on the basis of serology and endoscopic biopsy. On the other hand, because nearly everybody with celiac disease has one or both of the aforementioned gene variants, doctors often use genetic testing to rule out celiac disease. For example, in pediatrics, when a sibling or parent of a child is found to have celiac disease, that child might be offered genetic testing. If it comes out negative, the child can avoid going through the usual celiac workup.
Complications of celiac disease
If not recognized and treated, celiac disease can lead to severe malnutrition (opens in new tab) due to an inability of the small intestine to absorb nutrients. In particular, this can include deficiencies of micronutrients, such as iron, magnesium, vitamin B12, folic acid, vitamin D, zinc, calcium, niacin and riboflavin.
Deficiency of calcium and vitamin D can lead to osteopenia and osteoporosis, in which bone loses density and becomes more susceptible to fractures. Iron deficiency leads to iron deficiency anemia, while B12 deficiency and folate deficiency each lead to another type of anemia called megaloblastic anemia. B12 deficiency also causes very serious neurological problems. Celiac disease also may raise the risk of other medical conditions (opens in new tab), including lymphoma and fertility problems.
Additionally, changes to the intestinal lining in celiac disease can cause lactose intolerance. As noted above, this is an inability to digest milk sugar (lactose). Since lactose intolerance is very common outside of celiac disease, this particular complication can complicate the diagnosis of celiac disease.
Treatment of celiac disease
When celiac disease is diagnosed, the first treatment attempted is a gluten-free diet (opens in new tab). This diet must include fiber as well as certain micronutrients, such as folic acid and other B vitamins, which are present in whole grains. If implemented correctly, a gluten-free diet works in almost all cases, but the caveat is that such a diet is not always easy to implement.
Studies have revealed that it is not uncommon for people on gluten-free diets to still unwittingly ingest some amount of gluten. Occasionally, this results from patients being ill-informed about dietary sources of gluten, but there may be a societal factor at play, particularly when it comes to cross-contamination in restaurants (opens in new tab). One 2019 study suggested that approximately one-third of food items (opens in new tab) designated as gluten-free on restaurant menus actually contained substantial quantities of gluten.
Given this reality, in cases when patients don't improve on a gluten-free diet, they may have to work with a dietitian to confirm that their diet is truly gluten-free before receiving a diagnosis of refractory celiac disease (opens in new tab). It's also important for doctors to check that the patient doesn't have another gastrointestinal condition alongside celiac disease, as this could also explain the lack of response to a gluten-free diet.
As noted above, there are some rare cases in which celiac disease does not resolve after a switch to a gluten-free diet. The reasons for this are not fully understood but may involve the immune system continuing to attack the small intestinal lining in the absence of gluten. Alternatively, the disease may have progressed to a point at which intestinal damage is not reversible.
To treat these tough cases, scientists are working on new treatments, including regimens that may involve gradual, controlled exposure to progressively larger amounts of gluten-like protein (opens in new tab). This treatment is aimed at deconditioning the immune system from its harmful response.
This article is for informational purposes only and is not meant to offer medical advice.
David Warmflash is a medical researcher, astrobiologist, science communicator, and author, located in Portland, Oregon. He holds an MD from Tel Aviv University Sackler School of Medicine and has conducted research in astrobiology, space biology, and space medicine during research fellowships at NASA's Johnson Space Center, the University of Pennsylvania, and Brandeis University, and in collaboration with The Planetary Society and the Israeli Aerospace Medicine Institute. | Biology |
Species known as marine habitat-forming species -- gorgonians, corals, algae, seaweeds, marine phanerogams, etc. -- are organisms that help generate and structure the underwater landscapes. These are natural refuges for other species, and provide biomass and complexity to the seabeds. But these key species in marine ecosystems are currently threatened by climate change and other perturbations derived from human activity. Now, a study published in the journal Global Ecology and Biogeography warns that even in the marine protected areas (MPAs) the genetic diversity of structural species is not protected, although it is essential for the response and adaptation of populations to changes that alter the natural environment.
The study was carried out by Laura Figuerola-Ferrando, Cristina Linares, Ignasi Montero-Serra and Marta Pagès-Escolà, from the Faculty of Biology of the University of Barcelona and the Biodiversity Research Institute of the UB (IRBio); Jean-Baptiste Ledoux and Aldo Barreiro, from the Interdisciplinary Centre of Marine and Environmental Research (CIIMAR) in Portugal, and Joaquim Garrabou, from the Institute of Marine Sciences (ICM-CSIC).
Genetic diversity is also a component of biodiversity
Traditionally, marine biodiversity management and conservation plans have considered factors such as species richness. Genetic diversity -- another major component of biodiversity -- reflects the genetic variation that exists among organisms of the same species and is a determining factor in the adaptive capacity of populations and their survival. Despite its importance, genetic diversity has so far been overlooked in management and conservation plans.
"Genetic diversity plays a key role in enhancing the ability of species, populations and communities to adapt to rapid environmental changes resulting from climate change and thus increase their resilience," says researcher Laura Figuerola-Ferrando, first author of the study.
"However, -- she continues -- so far, the vast majority of marine protected areas are implemented based on the presence of several species and habitats, without considering their genetic diversity. Another example would be the red list of the International Union for Conservation of Nature (IUCN), which does not consider genetic diversity either."
"In recent years, the need to focus conservation efforts on the protection of genetic diversity has been reinforced. Technological progress in the massive development of different techniques to determine genetic diversity (for example, through the use of microsatellites or small DNA fragments), as well as their affordable cost, can help to include genetic diversity in management and conservation plans," says the researcher from the Department of Evolutionary Biology, Ecology and Environmental Sciences of the UB.
From the northwest Atlantic to the Gulf of Guinea
The study applies macrogenetic techniques to identify general genetic patterns of diverse marine species at large spatial scales. The authors have analyzed data from a global database containing genetic diversity information (based on microsatellites) for more than 9,300 populations of 140 species in different marine regions around the globe.
The results outline a reference scenario of genetic patterns in marine habitat-forming species (corals, macroalgae, marine phanerogams, etc.) of potential interest for improving marine life management and conservation plans.
The northwest Atlantic provinces and the Bay of Bengal are the regions where the highest genetic diversity in marine landscape species has been identified. Quite high values (above the global average) have also been identified in the Mediterranean. In contrast, the marine provinces with the lowest values of genetic diversity are the Gulf of Guinea and the southwest Atlantic.
The findings also indicate a positive correlation between genetic diversity and species richness of both animal and plant marine habitat-forming species. However, the paper warns of a worrying result: the Network of Marine Protected Areas (RAMP) in the large oceanic ecoregions does not preserve areas where the genetic diversity of marine habitat-forming species is highest.
"What we have seen is that what is not being protected in MPAs is genetic diversity. In the study, the initial hypothesis was that within these areas there would be greater genetic diversity, but this has not been the case. In fact, we have seen, at a global level, that there are no differences in genetic diversity between inside and outside the MPAs," notes Laura Figuerola-Ferrando, who is doing her doctoral thesis under the supervision of Cristina Linares (UB) and Joaquim Garrabou (ICM-CSIC).
A new pattern of equatorial biodiversity at the poles
The authors have also identified a specific pattern in the distribution of genetic diversity of the marine habitat-forming species that differs from the traditional models known to date. "This is a bimodal latitudinal pattern: it is a complex biogeographic model and it implies that if we model how the genetic diversity of these species varies with latitude, we find two peaks in temperate zones and a small dip in genetic diversity at the equator," notes the ICREA Academia professor Cristina Linares (UB-IRBio), one of the coordinators of the study together with Jean-Baptiste Ledoux (CIIMAR).
This scientific discovery is relevant because until a few decades ago it was considered that the distribution of biodiversity on the planet followed a unimodal pattern, that is, it had maximum values at the equator and decreased towards the poles. "This is not always the case, especially in terms of species diversity in marine ecosystems. For example, in the case of benthic species, this pattern is biomodal rather than unimodal in terms of both species richness and genetic diversity," explains Cristina Linares.
"In our study, the bimodal latitudinal pattern is influenced by taxonomy: in the used model, we found statistically significant differences between animal species (more genetic diversity) and plant species (less genetic diversity). Furthermore, if we explore the latitudinal pattern separating animal and plant species, we can see that a bimodal pattern continues to be observed in animals, but the same cannot be said for plants," adds researcher Jean-Baptiste Ledoux (CIIMAR).
Genetic diversity: improving conservation management plans
The conclusions of the work recall the need to include the genetic diversity of populations in biodiversity management and conservation plans on the planet. "The importance of having genetic diversity in biodiversity management and conservation plans has just been reinforced with the 'Kunming-Montreal Global Biodiversity Framework' within the Convention on Biological Diversity (CBD/COP/15/L25, 2022). In this context, we believe that the baseline on genetic diversity patterns in marine habitat-forming species defined as our work can be very relevant," notes Jean-Baptiste Ledoux.
This study also reveals that the Mediterranean and Atlantic regions are among the most present in the scientific literature used in this work on macrogenetic patterns of deep-sea structural species.
"On the other hand, if we look at the analyzed taxa, we see that the Mediterranean Sea is the marine province where we have studies of more different taxa (octocorals, hexacorals, sponges, marine phanerogams and algae). In the northern Atlantic there is also quite a variety of taxa (mainly algae, marine phanerogams, but also hexacorals, octocorals, bryozoans and sponges). On the other hand, in the southern Atlantic, studies are mainly focused on algae," the researchers conclude.
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Scorpions have a scary reputation, thanks to their alien looks, pincers and stingers. But scorpions are also fascinating critters, as researchers Harper Forbes and Prakrit Jain know. The pair are the lead authors of a paper in ZooKeys describing two previously unknown scorpion species found in California. Also, they were in high school when they made the discoveries.Forbes and Jain, who've since graduated high school, collaborated with arachnologist Lauren Esposito of the California Academy of Sciences on the species descriptions. "Harper and Prakrit went through all the steps to formally describe a species, sampling the populations and comparing them with existing specimens in our collection," said Esposito in a statement on Monday.Harper Forbes (left), Prakrit Jain (right), and Academy Curator of Arachnology Lauren Esposito (center) out on a search for scorpions. Gayle Laird/California Academy of Sciences The species -- Paruroctonus soda and Paruroctonus conclusus -- are called playa scorpions as a reference to their habitat in dry lake beds. The students first spotted them on the iNaturalist app, which people use to upload pictures of fauna and flora to share with a wide community of enthusiasts and scientists. Starting in 2019, Forbes and Jain investigated an unknown species of scorpion found in Koehn Lake in the Mojave Desert. It had gone unidentified on the app for six years. "We weren't entirely sure what we were looking at," Jain said. "Over the next couple years, we studied scorpions in the genus Paruroctonus and learned they frequently evolve to live in alkali playas like Koehn Lake." Two juvenile specimens of P. conclusus. Prakrit Jains/Harper Forbes/Lauren Esposito/ZooKeys The second unknown scorpion popped up on iNaturalist in 2021 after being seen in a spot called Soda Lake in San Luis Obispo County. The students went to work seeking out specimens for both species, which live in extremely small areas. The scorpions' tiny range is a concern. P. soda lives in protected lands within Carrizo Plain National Monument, but P. conclusus is in a more vulnerable position. "The entire species could be wiped out with the construction of a single solar farm, mine, or housing development," said Forbes.The study shows there's still much to be learned about the wildlife of California. The scorpion-finders seem to have also found their passion. They're working with Esposito on a book about scorpions, and both are going on to study biology at different universities. | Biology |
Most birds that flit through dense, leafy forests have a strategy for maneuvering through tight windows in the vegetation -- they bend their wings at the wrist or elbow and barrel through.
But hummingbirds can't bend their wing bones during flight, so how do they transit the gaps between leaves and tangled branches?
A study published today in the Journal of Experimental Biology shows that hummingbirds have evolved their own unique strategies -- two of them, in fact. These strategies have not been reported before, likely because hummers maneuver too quickly for the human eye to see.
For slit-like gaps too narrow to accommodate their wingspan, they scooch sideways through the slit, flapping their wings continually so as not to lose height.
For smaller holes -- or if the birds are already familiar with what awaits them on the other side -- they tuck their wings and coast through, resuming flapping once clear.
"For us, going into the experiments, the tuck and glide would have been the default. How else could they get through?" said Robert Dudley, a professor of integrative biology at the University of California, Berkeley, and senior author of the paper. "This concept of sideways motion with a total mix-up of the wing kinematics is quite amazing -- it's a novel and unexpected method of aperture transit. They're changing the amplitude of the wing beats so that they're not dropping vertically when they do the sideways scooch."
Using the slower sideways scooch technique may allow birds to better assess upcoming obstacles and voids, thereby reducing the likelihood of collisions.
"Learning more about how animals negotiate obstacles and other 'building-blocks' of the environment, such as wind gusts or turbulent regions, can improve our overall understanding of animal locomotion in complex environments," noted first author Marc Badger, who obtained his Ph..D from UC Berkeley in 2016. "We still don't know very much about how flight through clutter might be limited by geometric, aerodynamic, sensory, metabolic or structural processes. Even behavioral limitations could arise from longer-term effects, such as wear and tear on the body, as hinted at by the shift in aperture negotiation technique we observed in our study."
Understanding the strategies that birds use to maneuver through a cluttered environment may eventually help engineers design drones that better navigate complex environments, he noted.
"Current remote control quadrotors can outperform most birds in open space across most metrics of performance. So is there any reason to continue learning from nature?" said Badger. "Yes. I think it's in how animals interact with complex environments. If we put a bird's brain inside a quadrotor, would the cyborg bird or a normal bird be better at flying through a dense forest in the wind? There may be many sensory and physical advantages to flapping wings in turbulent or cluttered environments."
Obstacle course
To discover how hummingbirds -- in this case, four local Anna's hummingbirds (Calypte anna) -- slip through tiny openings, despite being unable to fold their wings, Badger and Dudley teamed up with UC Berkeley students Kathryn McClain, Ashley Smiley and Jessica Ye.
"We set up a two-sided flight arena and wondered how to train birds to fly through a 16-square- centimeter gap in the partition separating the two sides," Badger said, noting that the hummingbirds have a wingspan of about 12 centimeters (4 3/4 inches). "Then, Kathryn had the amazing idea to use alternating rewards."
That is, the team placed flower-shaped feeders containing a sip of sugar solution on both sides of the partition, but only remotely refilled the feeders after the bird had visited the opposite feeder. This encouraged the birds to continually flit between the two feeders through the aperture.
The researchers then varied the shape of the aperture, from oval to circular, ranging in height, width and diameter, from 12 cm to 6 cm, and filmed the birds' maneuvers with high-speed cameras. Badger wrote a computer program to track the position of each bird's bill and wing tips as it approached and passed through the aperture.
They discovered that as the birds approached the aperture, they often hovered briefly to assess it before travelling through sideways, reaching forward with one wing while sweeping the second wing back, fluttering their wings to support their weight as they passed through the aperture. They then swiveled their wings forward to continue on their way.
"The thing is, they have to still maintain weight support, which is derived from both wings, and then control the horizontal thrust, which is pushing it forward. And they're doing this with the right and left wing doing very peculiar things," Dudley said. "Once again, this is just one more example of how, when pushed in some experimental situation, we can elicit control features that we don't see in just a standard hovering hummingbird."
Alternatively, the birds swept their wings back and pinned them to their bodies, shooting through -- beak first, like a bullet -- before sweeping the wings forward and resuming flapping once safely through.
"They seem to do the faster method, the ballistic buzz-through, when they get more acquainted with the system," Dudley said.
Only when approaching the smallest apertures, which were half a wingspan wide, would the birds automatically resort to the tuck and glide, even though they were unfamiliar with the setup.
The team pointed out that only about 8% of the birds clipped their wings as they passed through the partition, although one experienced a major collision. Even then, the bird recovered quickly before successfully reattempting the maneuver and going on its way.
"The ability to pick among several obstacle negotiation strategies can allow animals to reliably squeeze through tight gaps and recover from mistakes," Badger noted.
Dudley hopes to conduct further experiments, perhaps with a sequence of different apertures, to determine how birds navigate multiple obstacles.
The work was funded primarily by a CiBER-IGERT grant from the National Science Foundation (DGE-0903711).
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Scientists at the National Institutes of Health have identified new genetic risk factors for two types of non-Alzheimer's dementia. These findings were published in Cell Genomics and detail how researchers identified large-scale DNA changes, known as structural variants, by analyzing thousands of DNA samples. The team discovered several structural variants that could be risk factors Lewy body dementia (LBD) and frontotemporal dementia (FTD). The project was a collaborative effort between scientists at the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA) at NIH.
Structural variants have been implicated in a variety of neurological disorders. Unlike more commonly studied mutations, which often affect one or a few DNA building blocks called nucleotides, structural variants represent at least 50 but often hundreds, or even thousands, of nucleotides at once, making them more challenging to study.
"If you imagine that our entire genetic code is a book, a structural variant would be a paragraph, page, or even an entire chapter that has been removed, duplicated, or inserted in the wrong place," said Sonja W. Scholz, M.D., Ph.D., investigator in the neurogenetics branch of NINDS and senior author of this study.
By combining cutting-edge computer algorithms capable of mapping structural variations across the whole genome with machine learning, the research team analyzed whole-genome data from thousands of patient samples and several thousand unaffected controls.
A previously unknown variant in the gene TCPN1 was found in samples from patients with LBD, a disease, that like Parkinson's disease, is associated with abnormal deposits of the protein alpha-synuclein in the brain. This variant, in which more than 300 nucleotides are deleted from the gene, is associated with a higher risk for developing LBD. While this finding is new for LBD, TCPN1 is a known risk factor for Alzheimer's disease, which could mean that this structural variant plays a role in the broader dementia population.
"From a genetics standpoint, this is a very exciting finding," said Dr. Scholz. "It provides a point of reference for cell biology and animal model studies and possibly down the road, a target for intervention."
By looking at a group of 50 genes implicated in inherited neurodegenerative diseases, the investigators were able to identify additional rare structural variants, including several that are known to cause disease. The analyses also identified two well-established risk factors for FTD changes in the C9orf72 and MAPT genes. These proof-of-concept findings bolstered the strength of the study's new findings by demonstrating that the algorithms were properly working.
Because reference maps for currently-available structural variants are limited, the researchers generated a catalog based on the data obtained in these analyses. The analysis code and all the raw data are now available to the scientific community for use in their studies. An interactive app also allows investigators to study their genes of interest and ask which variants are present in controls vs. LBD or FTD cases. The authors assert these resources may make complex genetic data more accessible to non-bioinformatics experts, which will accelerate the pace of discovery.
"Research to unravel the intricate genetic architecture of neurodegenerative diseases is resulting in significant advances in scientific understanding," said Bryan J. Traynor, M.D., Ph.D., senior investigator at NIA. "With each discovery, we shed light on the mechanisms behind neuronal cell death or dysfunction, paving the way for precision medicine to combat these debilitating and fatal disorders."
Researchers expect that the dataset will continue to grow as additional data are analyzed.
This work was supported in part by the Intramural Research Program at NINDS and NIA.
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A new gene therapy that "resets" the brain's reward system could help treat alcohol use disorder, a new study in monkeys suggests.
In monkeys who tend to drink heavily when provided lots of alcohol, surgically injecting a gene therapy into the brain increased the production of the so-called feel-good hormone dopamine, the study showed. This, in turn, dramatically reduced the primates' alcohol consumption, the effects of which were sustained over a year.
If safe and effective in humans, the therapy could provide a "one-time" treatment for alcohol use disorder (AUD), a medical condition in which patients can't stop or control their drinking despite it negatively impacting their daily life. Excessive drinking causes 140,000 deaths a year in the U.S., and although AUD is one of the most common psychiatric disorders, only three drugs for it have been approved by the U.S. Food and Drug Administration (FDA).
None directly target the underlying brain changes seen with sustained heavy drinking.
Related: What does alcohol do to the body?
Alcohol boosts the brain's production of dopamine, which leads to feelings of relaxation and improved mood. However, in AUD, the brain adapts by producing less dopamine on its own, meaning people need to drink more to achieve the same positive effects.
That's also true in monkeys that drink heavily, even during periods when they aren't consuming any alcohol, study lead author Kathleen Grant, a professor of behavioral neuroscience at Oregon Health & Science University, told Live Science.
In the new study, published Monday (Aug. 14) in the journal Nature Medicine, Grant's team injected a genetically modified virus into the ventral tegmental area — a region in the brain involved in reward processing — of four monkeys as part of a surgical procedure. Those monkeys had been given access to increasingly higher amounts of ethanol dissolved in water over several months to the point where their consumption levels simulated chronic alcohol binge drinking in humans.
Using a similar approach to what has already been used to treat Parkinson's disease and a rare genetic disorder known as aromatic L-amino acid decarboxylase deficiency, the harmless virus carried a gene that encodes the protein glial cell line-derived neurotrophic factor (GDNF), which helps preserve and regrow neurons. By putting the GDNF gene into cells that make dopamine, the team assumed it would spur them to produce normal levels of the chemical.
The monkeys reduced their alcohol consumption by more than 90% compared with controls, and their dopamine levels were restored to "normal levels" for at least a year after treatment, roughly equivalent to nine to 12 years in human time, Grant said. Because relapse is such an "integral part of the cycle" of AUD, getting back to levels the animals had before they started drinking heavily is crucial, she emphasized.
Andrew Mcquillin, a professor of molecular psychiatry at University College London who was not involved in the research, told Live Science in an email that the long-term side effects of this treatment are still unclear. Although brain surgery is "generally well-tolerated" in humans, he said it "seems a somewhat invasive approach for all but the most severe cases of alcohol use disorder."
Grant also urged caution in over-generalizing the findings. "This is only proof-of-principle that it is possible to reverse this behavior in people with drinking disorders that are resistant to all other treatments," she said. "This would not be your first line of treatment, [it] would be appropriate only for very severe cases of alcohol use disorder."
Mcquillin added that future studies will be needed to test the acceptability of this treatment for substance use disorders. The findings could, however, open doors for other treatment options.
"There is also the possibility that new or existing small molecules that mimic the therapeutic mechanism in this study may represent new treatment targets for substance use disorders," he said.
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Emily is a health news writer based in London, United Kingdom. She holds a bachelor's degree in biology from Durham University and a master's degree in clinical and therapeutic neuroscience from Oxford University. She has worked in science communication, medical writing and as a local news reporter while undertaking journalism training. In 2018, she was named one of MHP Communications' 30 journalists to watch under 30. ([email protected]) | Biology |
The Tara Pacific program and expedition focused on coral reefs across the Pacific Ocean and used a coordinated sampling effort to address questions at multiple scales using a common suite of samples. Here, we highlight some of the Tara Pacific achievements, discussing the benefits of long-duration sea expeditions for investigating a wide array of research questions within a selected ecosystem.
Coral reefs are the most biologically diverse marine ecosystem on the planet, hosting about 5% of the world’s known species and about 35% of known marine species in a surface area of only 0.16% of the ocean1. The Pacific Ocean, including the South Asian Sea, contains about 60% of the world’s coral reefs, hosting many important biodiversity gradients as well as the most biodiverse region in the oceans, the coral triangle including Indonesia, Philippines, and Papua New Guinea.
Based on a 2-year-long continuous scientific expedition at sea, which traversed the coral reefs of the Pacific Ocean and the Asian seas, the Tara vessel covered a journey of more than 100,000 km with about 3000 scuba-dives (Fig. 1). Similar to earlier long expeditions like those of James Cook in the 18th century, Charles Darwin on the Beagle (1831–1836), or James Dana (1838–1842) which helped develop theories on reef formation and reef biodiversity (see2 for a history of reef research), the Tara Pacific expedition aimed to provide a baseline of the ‘omics’ complexity of the coral holobiont (the Cnidarian animal host and its resident microbial assemblage) and its ecosystem across the Pacific Ocean3.
The Tara Pacific program used very high-throughput genetic sequencing and molecular analyses to reveal the entire microbial and chemical diversity of coral holobionts as well as their functional traits at a basin-wide scale. This ambitious project aimed to reveal a new facet of the biodiversity of coral reefs by shedding light on the complex links between genomes, transcriptomes, metabolomes, organisms, and ecosystem function in coral reefs and to provide a reference of the biological state of modern coral reefs in the Anthropocene. During its 2-year voyage, the Tara Pacific expedition sampled coral ecosystems from 32 islands across the Pacific Ocean and ocean surface waters at 249 locations, resulting in the collection of nearly 58,000 samples using various approaches (Table 1, Fig. 2). At each reef site, we systematically sampled two species of scleractinian corals, one hydrocoral, and two species of fish together with water and aerosols and environmental context data obtained from taxonomic registries, gazetteers, almanacs, climatologies, operational biogeochemical models, and satellite observations (Fig. 3)4. Following major advances in the field of marine biology made by the previous Tara expeditions like Tara Oceans5, the Tara Pacific program is now giving new insights into the diversity and plasticity of coral reef ecosystems. Here, we present major aspects of what we have learned from this unique and incomparable experience. We discuss these achievements on behalf of the Tara Pacific consortium and provide recognition of all the participants involved in the Acknowledgements.
Experimental design and organization
The first aspect is related to experimental design and organization. The baseline we developed, which used an efficient sample collection and processing strategy to meet numerous research demands and provide environmental context4, was instrumental in organizing and classifying the 3.8 million environmental data points collected across 74 metadata sources. In parallel, we set up a workflow for multi-omics data generation from sample handling to nucleotide sequence data generation and deposition6. This workflow makes it possible to manage what we think is the largest environmental science sequencing effort ever conducted to date, with approximately 102 Terabytes of metabarcode with different primers, metagenomes, and metatranscriptomes, as well as more than 5000 metabolomic profiles. Metabolomes were described by applying a wide-ranging analytical approach using both liquid chromatography–high-resolution mass spectrometry (for the lipidome) and nuclear magnetic resonance imaging (for the hydrophilic component) analyses to assess and annotate a broad range of the metabolome of three coral holobionts (Reddy et al., in prep.). This unique multidimensional framework also includes a large number of concomitant metadata collected side-by-side, all now publicly available for a larger audience.
High-resolution dataset
The second aspect is linked to the description of the different ‘omics’ data sets. As such, in the framework of the Tara Pacific expedition, we assembled two coral genomes, Porites lobata and Pocillopora meandrina, with vastly improved contiguity that allowed us to study the functional organization of these genomes. We annotated their gene catalog and reported a relatively higher gene number than that found in other public coral genome sequences: 43,000 and 32,000 genes, respectively, which may be explained by a high number of tandemly duplicated genes7. Overall, the metabolomic analysis of the host was significantly distinct at higher taxonomic levels (at the genus level) but not within species (intraspecific). Instead, a large majority of the observed metabolomic variability within the host was explained by differences in biogeography (Reddy et al., in review).
We also demonstrate a very large richness of reef microbiota compared to other environments. If this diversity, highlighted in three Cnidaria and two fish, is applied to the number of fish and Cnidaria in the Pacific Ocean, then this diversity alone is equal to the total prokaryotic diversity currently estimated for the whole of the Earth, which suggests that the world’s microbial biodiversity is largely underestimated8. Microbial communities varied among and within the three animal biomes (coral, fish, and plankton) geographically. These microbiomes were species-specific and differed from those of the planktonic communities. Surprisingly, these microbiomes did not follow the well-known diversity gradients seen for corals8.
Within the coral microbiota, Endozoicomonadaceae, a globally distributed bacterial family, has been identified as a key bacterial symbiont of corals. A specific analysis of this taxon has now shown that the same clades are found across the Pacific Ocean but are host-specific at the species level and may harbor different specific functions9. We also show that within a coral genus, Endozoicomonadaceae biogeography is driven by the host rather than the environment9. Then, a survey of the viral compartment of the coral holobiont found heritable integrations of multiple Dinornavirus (a dinoflagellate-infecting non-retroviral RNA virus) endogenous viral element genes in Symbiodiniaceae scaffolds (especially that of the genus Symbiodinium) from within the cnidarian metagenomes. Such a result suggests widespread and recurrent or ancestral integration and conservation of these endogenous viral elements, which might have a role in reef health, for example, as an antiviral mechanism10.
Unique outcomes
The third aspect is related to the unique outcomes beginning to emerge from analyses combining multi-omics and environmental data. The 32 archipelagos surveyed made for formidable natural laboratories and offered a wide range of environmental conditions in terms of temperature, acidification, and reef health state, making it possible to study the relationships between environmental and genetic parameters at large spatial scales. As an example, we provide evidence of high host–photosymbiont fidelity across environments in Pocillopora corals, with coral and microalgal gene expression profiles responding to different drivers11. Differences in the photosymbiotic association had only weak impacts on host gene expression, which was more strongly correlated with the historical thermal environment. Conversely, photosymbiont gene expression was largely driven by microalgal lineage. Overall, these results reveal a three-tiered strategy of heat resistance in Pocillopora underpinned by host–photosymbiont specificity, host transcriptomic plasticity, and differential photosymbiotic association under extreme warming. Utilizing the same samples, we analyzed the genetic diversity of the three coral genera in relation to climatic and environmental proxies12, showing that the impact of environments on evolutionary trajectories is species-specific. Porites, Pocillopora, and Millepora show different strategies: while the first has a resilient physiology with low biogeographical structuring, the other two corals show a stronger genomic imprint dependent on the environment, suggesting they are adapted to a narrower set of reef niches.
These different adaptative strategies in corals were confirmed by the study of stress markers (Porro et al., in review) and telomere length variation13. Porro et al. (in review) showed that Porites spp. has a stable phenotype within host lineages, while Pocillopora spp. have more diverse phenotypes structured by the geography and the environment, strategies which could be characterized as “the Oak and the Reed strategies”. A similar pattern was observed by measuring the telomere DNA length on 1029 colonies of the three coral genera with the telomere DNA lengths of the short-lived, more stress-sensitive Pocillopora spp. colonies being largely determined by seasonal temperature variation, whereas those of the long-lived, more stress-resistant Porites spp. colonies were insensitive to seasonal patterns but rather influenced by past thermal anomalies13.
Finally, we integrated the analysis of coral skeletal cores, which, like the trunk of a tree, retain the signature of events that prevailed at the time of their deposition (Canesi et al., in review). This property has made it possible to study the impact of different environmental conditions on the control of calcification and, therefore, on coral and reef growth. Throughout the Pacific Ocean, we show that the skeletal properties and calcifying fluid chemistry of Porites are primarily driven by the gradient in temperature. This unique comparative study of the massive coral Porites and Diploastrea at the Pacific Ocean basin scale demonstrated that the biological regulation of calcification parameters in their internal fluids in response to a temperature gradient is taxon-dependent.
Outlook
The Tara Pacific expedition and program are unique and incomparable and will provide several years’ worth of material for large-scale analyses of coral ecosystem diversity. This program is unique in that samples were collected following the same protocol across multiple locations and years, with corals being screened in an identical manner at each site, rendering them fully comparable and linking their physiology to a large set of in situ and historical environmental data. The Tara Pacific expedition and program is not only the largest genotyping study conducted on a marine system, but it also represents a significant and large effort towards structuring and managing ecosystem-scale data to make them ‘open access’ and available to a broader community. By presenting summaries of our preliminary results above, we demonstrate the potential of such datasets for addressing major questions in the field of coral research. Answering these questions will lead to a better understanding of the conservation issues facing this unique ecosystem. It is our hope that the open-access data from the Tara Pacific expedition will provide an avenue for addressing these outstanding questions in coral reef research.
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Acknowledgements
We are keen to thank the commitment of the people and the following institutions for their financial and scientific support that made this singular expedition possible: CNRS, PSL, CSM, EPHE, Genoscope/CEA, Inserm, Université Côte d’Azur, ANR, agnès b., UNESCO-IOC, the Veolia Environment Foundation, Région Bretagne, Billerudkorsnas, Amerisource Bergen Company, Lorient Agglomeration, Smilewave, Oceans by Disney, the Prince Albert II de Monaco Foundation, L’Oréal, Biotherm, France Collectivités, Fonds Français pour l’Environnement Mondial (FFEM), the Ministère des Affaires Européennes et Etrangères, the Museum National d’Histoire Naturelle, Etienne BOURGOIS, the Tara Ocean Foundation’s teams, and crew. Tara Pacific would not exist without the continuous support of the participating institutes. This study has been conducted using E.U. Copernicus Marine Service Information and Mercator Ocean products. We acknowledge funding from the Investissement d’avenir project France Génomique (ANR-10-INBS-09). The Tara Pacific expedition would not have been possible without the participation and commitment of over 200 scientists, sailors, artists, and citizens (see https://zenodo.org/record/3777760#.YfEEsfXMLjB). This publication is number 36 of the Tara Pacific Consortium.
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Planes, S., Allemand, D. Insights and achievements from the Tara Pacific expedition. Nat Commun 14, 3131 (2023). https://doi.org/10.1038/s41467-023-38896-6
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DOI: https://doi.org/10.1038/s41467-023-38896-6 | Biology |
Novel nano-optical technology tracks communications in living cells
Microbes may be among the smallest living things on Earth, but bioimaging to understand the chemistry that fuels these organisms could reveal important clues about the intricacies of gene function and the health of the planet. Because of this, scientists have long sought ways to eavesdrop on conversations between living microbes in their environment.
This has been exceptionally difficult, in part because microbes communicate using molecules instead of words. Deciphering conversations means identifying small, specific, and quickly changing molecules called metabolites, something even the most powerful instruments struggle to attempt. But a team of researchers at Pacific Northwest National Laboratory (PNNL) have spent the last decade continuously developing a next-generation bioimaging instrument that is making progress toward this goal.
The Chemical Dynamics Initiative (CDi), an internal PNNL investment, supported PNNL chemist Patrick El Khoury and his team as they developed the technology to measure phenomena in the quantum realm. Here the team imaged subatomic waves of energy called phonons as they formed, beat, and dissipated in a single trillionth of a second.
"Similar technologies can be used to image phonons and metabolites in real space and real time," said El Khoury. "The fundamental advances required in both areas comprise a challenge worthy of a national laboratory and continued investments."
Now researchers are taking the technologies to the next level as they use bioimaging to map metabolites exchanged by live microbes.
Bioimaging to fish out whispers in a crowd
The bioimager is known as BIGTUNA, short for BioImaginG Technology Using Nano-optical Approach. The keys to BIGTUNA are its multiple optical capabilities, each providing complementary information about the position and composition of molecules in a study sample. Many laser sources focus on the tip of a very sharp nanosized needle. Researchers position the needle's tip in the sample area they want to examine, then use the light focused on the tip of the needle to measure the sample's physical and chemical features. Through this, researchers identify molecules and understand how they interact.
Chemical bioimaging with light has been done for a hundred years, but never at this molecular scale.
"Some methods illuminate a relatively large area, but these far-field approaches are like listening in to a crowd and expecting to understand individual conversations," said PNNL chemist Scott Lea. To overcome this challenge, researchers focused on combining a wide range of near-field techniques to capture and characterize the maximum information in an area as small as a few molecules.
"If we don't have multiple streams of data coming from multiple techniques, we only get partial information," said El Khoury. "And in addition to developing the techniques, we developed our understanding of optical selection rules to maximize the information we get from one sample in one set-up."
In the most recent iteration of this project, the researchers zoomed out to a larger area, although still only a thousandth the thickness of a strand of hair. At this slightly farther distance, they identified the most promising approaches to capture information about the patterns of molecular bonds and the distribution of electrons. These new nano-optical measurements are addressing a much smaller number of molecules; therefore, the researchers must continue developing new theories that describe nanoscopic interactions of light and matter.
Combining these conceptual and technological developments will allow the researchers to move beyond model systems they studied using early incarnations of BIGTUNA. The chemical signals in these model systems were much stronger than chemical signals from the metabolites involved in microbial communications. In addition to having weaker signals, biological samples are also susceptible to damage by light, which is why BIGTUNA's noninvasive approach makes it ideal to develop for bioimaging applications. Including state-of-the art data and computational techniques from PNNL data scientists Sarah Akers and Edo Aprà will help automate where and how the instrument balances exploration with the sensitivity of a living system.
Bioimaging to tune in to talking microbes
As an initial foray into biology, researchers are focusing BIGTUNA's bioimaging power on a community of symbiotic microbes that live in deep ocean sediments. One microbe reduces sulfur, the other oxidizes methane, a powerful greenhouse gas.
Previous approaches to unraveling microbial interactions have mainly focused on identifying influential genes or on examining isolated enzymes and pathways. The approaches often include fixing, freezing, or combining the biological system. But these approaches lose out on time-dependent or space-specific details. And the researchers can't look at the flow of metabolites to get a predictive understanding of how and why microbes interact.
Even so, PNNL collaborator and CalTech geologist Victoria Orphan has theories about how these symbiotic microbes share metabolites. Bioimaging with BIGTUNA could produce the first close-up view of the metabolites in action as the instrument sends light through the sample and measures what gets absorbed or scattered. Researchers use the information to identify metabolites and create a detailed record of microbial intercellular communication pathways. In turn, this knowledge could help researchers understand the degree to which microbes respond to environmental changes.
A new generation of nano-optics
"Possibilities for BIGTUNA extend far beyond the realm of bioimaging," said Peter Sushko, CDi's chief scientist. "Because this highly adaptable instrument can obtain detailed information describing atomic motion and electronic processes, it will be useful in seeking answers to a broad range of questions that are of interest to chemists, physicists, and materials scientists as well."
Potential applications include quantum materials, catalysis, and human health, in addition to the current work in microbial systems. In that realm, planned future developments could incorporate environmental controls to further generalize the approach.
A portion of the blueprint for BIGTUNA was designed under PNNL's CDi, a five-year internal investment in capabilities to better understand and predict the evolution of complex chemical systems in real-world or operational environments.
Provided by Pacific Northwest National Laboratory | Biology |
Cells have a fascinating feature to neatly organize their interior by using tiny protein machines called molecular motors that generate directed movements. Most of them use a common type of fuel, a kind of chemical energy, called ATP to operate. Now researchers from the Max Planck Institute of Molecular Cell Biology and Genetics (MPI-CBG), the Cluster of Excellence Physics of Life (PoL) and the Biotechnology Center (BIOTEC) of the TU Dresden in Dresden, Germany, and the National Centre for Biological Sciences (NCBS) in Bangalore, India, discovered a novel molecular system that uses an alternative chemical energy and employs a novel mechanism to perform mechanical work. By repeatedly contracting and expanding, this molecular motor functions similarly to a classical Stirling engine and helps to distribute cargo to membrane-bound organelles. It is the first motor using two components, two differently sized proteins, Rab5 and EEA1, and is driven by GTP instead of ATP. The results are published in the journal Nature Physics.
Motor proteins are remarkable molecular machines within a cell that convert chemical energy, stored in a molecule called ATP, into mechanical work. The most prominent example is myosin which helps our muscles to move. In contrast, GTPases which are small proteins have not been viewed as molecular force generators. One example is a molecular motor composed of two proteins, EEA1 and Rab5. In 2016, an interdisciplinary team of cell biologists and biophysicists in the groups of MPI-CBG directors Marino Zerial and Stephan Grill and their colleagues, including PoL and BIOTEC research group leader Marcus Jahnel, discovered that the small GTPase protein Rab5 could trigger a contraction in EEA1. These string-shaped tether proteins can recognize the Rab5 protein present in a vesicle membrane and bind to it. The binding of the much smaller Rab5 sends a message along the elongated structure of EEA1, thereby increasing its flexibility, similar to how cooking softens spaghetti. Such flexibility change produces a force that pulls the vesicle towards the target membrane, where docking and fusion occur. However, the team also hypothesized that EEA1 could switch between a flexible and a rigid state, similar to a mechanical motor motion, simply by interacting with Rab5 alone.
This is where the current research sets in, taking shape via the doctoral work of the two first authors of the study. Joan Antoni Soler from Marino Zerial's research group at MPI-CBG and Anupam Singh from the group of Shashi Thutupalli, a biophysicist at the Simons Centre for the Study of Living Machines at the NCBS in Bangalore, set out to experimentally observe this motor in action.
With an experimental design to investigate the dynamics of the EEA1 protein in mind, Anupam Singh spent three months at the MPI-CBG in 2019. "When I met Joan, I explained to him the idea of measuring the protein dynamics of EEA1. But these experiments required specific modifications to the protein that allowed measurement of its flexibility based on its structural changes," says Anupam. Joan Antoni Soler's expertise in protein biochemistry was a perfect fit for this challenging task. "I was delighted to learn that the approach to characterize the EEA1 protein could answer whether EEA1 and Rab5 form a two-component motor, as previously suspected. I realized that the difficulties in obtaining the correct molecules could be solved by modifying the EEA1 protein to allow fluorophores to attach to specific protein regions. This modification would make it easier to characterize the protein structure and the changes that can occur when it interacts with Rab5," explains Joan Antoni.
Armed with the suitable protein molecules and the valuable support of co-author Janelle Lauer, a senior postdoctoral researcher in Marino Zerial's research group, Joan and Anupam were able characterize the dynamics of EEA1 thoroughly using the advanced laser scanning microscopes provided by the light microscopy facilities at the MPI-CBG and the NCBS. Strikingly, they discovered that the EEA1 protein could undergo multiple flexibility transition cycles, from rigid to flexible and back again, driven solely by the chemical energy released by its interaction with the GTPase Rab5. These experiments showed that EEA1 and Rab5 form a GTP-driven two-component motor. To interpret the results, Marcus Jahnel, one of the corresponding authors and research group leader at PoL and BIOTEC, developed a new physical model to describe the coupling between chemical and mechanical steps in the motor cycle. Together with Stephan Grill and Shashi Thutupalli, the biophysicists were also able to calculate the thermodynamic efficiency of the new motor system, which is comparable to that of conventional ATP-driven motor proteins.
"Our results show that the proteins EEA1 and Rab5 work together as a two-component molecular motor system that can transfer chemical energy into mechanical work. As a result, they can play active mechanical roles in membrane trafficking. It is possible that the force-generating molecular motor mechanism may be conserved across other molecules and used by several other cellular compartments," Marino Zerial summarizes the study. Marcus Jahnel adds: "I am delighted that we could finally test the idea of an EEA1-Rab5 motor. It's great to see it confirmed by these new experiments. Most molecular motors use a common type of cellular fuel called ATP. Small GTPases consume another type of fuel, GTP, and have been thought of mainly as signaling molecules. That they can also drive a molecular system to generate forces and move things around puts these abundant molecules in an interesting new light." Stephan Grill is equally excited: "It's a new class of molecular motors! This one doesn't move around like the kinesin motor that transports cargo along microtubules but performs work while staying in place. It's a bit like the tentacles of an octopus."
"The model we used is inspired by that of the classical Stirling engine cycle. While the traditional Stirling engine generates mechanical work by expanding and compressing gas, the two-component motor described uses proteins as the working substrate, with protein flexibility changes resulting in force generation. As a result, this type of mechanism opens up new possibilities for the development of synthetic protein engines," adds Shashi Thutupalli.
Overall, the authors hope that this new interdisciplinary study could open new research avenues in both molecular cell biology and biophysics.
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The Washington Post published a report Monday slamming Discovery Channel’s "Shark Week" programming for featuring too many White males as shark experts and continuing to peddle "negative messages" about sharks.The report highlighted a study done by the Public Library of Science led by Allegheny College biology professor Lisa Whitenack. The project observed that "Discovery’s programming emphasized negative messages about sharks, lacked useful messaging about shark conservation and overwhelmingly featured White men as experts — including several with the same name."Before delving into the study, the Washington Post provided a brief introduction on Whitenack, noting that the biologist "loved sharks as a kid" and watched "Shark Week" every summer. AUSTRALIAN TEENAGER SENT FLYING INTO THE AIR AFTER GREAT WHITE TAKES MASSIVE BITE OUT OF HIS SURF SKI Jupiter, Florida - May 05, 2022: A bull shark gets up close to inspect divers during an eco tourism shark dive off of Jupiter, Florida on May 5, 2022. (Photo by Joseph Prezioso/Anadolu Agency via Getty Images)However, the piece stated, "when the scientists appeared on her TV screen, she rarely saw any women she could look up to." Thinking about that later in life, she lamented, "I don’t come from a family of scientists. I didn’t see very many people that looked like me on television."As an adult, Whitenack decided to explore these "misconceptions" – as the Post characterized them. The piece claimed, "When the pandemic lockdowns came in 2020, she saw an opportunity to study the source of her old misconceptions. Was ‘Shark Week’ feeding audiences the wrong messages about sharks — and who studies them?" This question prompted Whitenack’s study. The report stated, "Whitenack led a team of researchers to examine hundreds of ‘Shark Week’ episodes that aired between 1988 and 2020."In addition to the study revealing the programming’s negative depiction of sharks, it "featured more White experts and commentators named ‘Mike’ than women," noted Arizona State University conservationist David Shiffman, the study’s co-author. CRITICAL RACE THEORY-RELATED IDEAS FOUND IN MANDATORY PROGRAMS AT 58 OF TOP 100 US MEDICAL SCHOOLS: REPORT Tiger shark, Galeocerdo cuvier, Tiger Beach, Bahamas. (Photo by: Andre Seale/VW PICS/Universal Images Group via Getty Images)Shiffman implied that this may be due to discrimination on the part of Discovery Channel. He said, "When there are hundreds of people of color interested who work in this field, [and] when my field is more than half women, maybe it’s not an accident anymore that they’re only featuring White men."The Post noted Discovery has yet to comment on the findings, though they rejected responding to findings from a "preliminary version" of the study in 2021, claiming it "has yet to pass any scientific approvals."According to the study, "the trend persisted throughout almost all of the television event’s history. Over 90 percent of the 229 experts featured in 201 ‘Shark Week’ episodes were White, the study found, and about 78 percent were men." Shark Week’s Alison Towner, a marine biologist based in South Africa, got drone footage of three killer whales hunting a nine-foot great white shark. (Credit: Discovery's Shark Week)CLICK HERE TO GET THE FOX NEWS APPThe piece quoted Minorities in Shark Sciences co-founder and biologist Carlee Bohannon, who praised the study for "putting numbers to her and her colleagues’ long-standing concerns about diversity in both the media and shark science."Bohannon stated, "We all grew up seeing one type of person on TV. ‘Shark Week’ was really the biggest thing, and it was always filled with White men." Gabriel Hays is an associate editor for Fox News Digital. | Biology |
New research can help better predict the health and sustainability of 'grassy' ecosystems
Newly published research from UNC Greensboro's Dr. Kevin Wilcox and colleagues will help scientists better predict how global changes—such as droughts, fires, and heat waves—will impact the health and sustainability of the Earth's grassy ecosystems.
The article, published October 10, 2023, in Global Change Biology, provides key steps forward to improving mathematical models that forecast changes to our planet's savannas, prairies, grasslands, and arctic tundras.
"Forest ecosystems tend to get the lion's share of public attention," said Wilcox. "But ecosystems dominated by non-tree vegetation—that is, 'grassy' ecosystems—make up 40 percent of Earth's land surface. So our research is playing important scientific 'catch-up' in these landscapes."
Grassy ecosystems provide many necessary resources and services to humans, including food production, pollinators, and carbon sequestration. They also serve as critical habitat for wildlife, such as elk and bison in North America.
Yet, when one looks deeper into humankind's ability to predict how these ecosystems will persist under forthcoming global changes, the research lags far behind the predictive capacity for forests. Wilcox's research on Earth system models is helping to close this gap.
Scientists use these models to simulate the effects of physical phenomena, such as droughts and heat waves, on landscapes. The mathematical equations that make up these models are strung together to create thousands of lines of computer code that ultimately provide an abstraction of reality. These models represent a wide range of ecological processes, such as rainfall penetrating the soil, insects defoliating a savanna, or heat stress causing plant and animal mortality.
"But if our models don't accurately represent ecological processes, their predictions are meaningless," said Wilcox.
An important facet to get right, Wilcox explains, is the ever-changing nature of these grassy systems.
"We can't just assume that all of the major components of the ecosystem, such as plant communities, will remain unchanged as droughts and heat waves continue to occur."
One of the biggest challenges is how grasses are represented. Currently, many models represent grasses as either miniature trees or as a 'green slime' that exists on the surface of the planet. The authors say this representation may be part of why the models have had trouble matching real-world observations in grassy ecosystems.
"Better collaboration between empiricists and modelers will also be key for improving herbaceous dynamics within ecosystem models," adds Wilcox.
Implementing these changes, the authors say, will be vital in helping guide public policy and management of these important ecosystems in the future, when droughts and deluges are more frequent and extreme, disturbances such as fires are more severe, and human pressures continue.
More information: Kevin R. Wilcox et al, Accounting for herbaceous communities in process‐based models will advance our understanding of "grassy" ecosystems, Global Change Biology (2023). DOI: 10.1111/gcb.16950
Journal information: Global Change Biology
Provided by University of North Carolina at Greensboro | Biology |
New genetic technology developed to halt malaria-spreading mosquitoes
Malaria remains one of the world's deadliest diseases. Each year malaria infections result in hundreds of thousands of deaths, with the majority of fatalities occurring in children under five. The Centers for Disease Control and Prevention recently announced that five cases of mosquito-borne malaria were detected in the United States, the first reported spread in the country in two decades.
Fortunately, scientists are developing safe technologies to stop the transmission of malaria by genetically editing mosquitoes that spread the parasite that causes the disease. Researchers at the University of California San Diego led by Professor Omar Akbari's laboratory have engineered a new way to genetically suppress populations of Anopheles gambiae, the mosquitoes that primarily spread malaria in Africa and contribute to economic poverty in affected regions.
The new system targets and kills females of the A. gambiae population since they bite and spread the disease.
Publishing July 5 in the journal Science Advances, first-author Andrea Smidler, a postdoctoral scholar in the UC San Diego School of Biological Sciences, along with former master's students and co-first authors James Pai and Reema Apte, created a system called Ifegenia, an acronym for "inherited female elimination by genetically encoded nucleases to interrupt alleles." The technique leverages the CRISPR technology to disrupt a gene known as femaleless (fle) that controls sexual development in A. gambiae mosquitoes.
Scientists at UC Berkeley and the California Institute of Technology contributed to the research effort.
Ifegenia works by genetically encoding the two main elements of CRISPR within African mosquitoes. These include a Cas9 nuclease, the molecular "scissors" that make the cuts and a guide RNA that directs the system to the target through a technique developed in these mosquitoes in Akbari's lab. They genetically modified two mosquito families to separately express Cas9 and the fle-targeting guide RNA.
"We crossed them together and in the offspring it killed all the female mosquitoes," said Smidler, "it was extraordinary." Meanwhile, A. gambiae male mosquitoes inherit Ifegenia but the genetic edit doesn't impact their reproduction. They remain reproductively fit to mate and spread Ifegenia.
Parasite spread eventually is halted since females are removed and the population reaches a reproductive dead end. The new system, the authors note, circumvents certain genetic resistance roadblocks and control issues faced by other systems such as gene drives since the Cas9 and guide RNA components are kept separate until the population is ready to be suppressed.
"We show that Ifegenia males remain reproductively viable, and can load both fle mutations and CRISPR machinery to induce fle mutations in subsequent generations, resulting in sustained population suppression," the authors note in the paper. "Through modeling, we demonstrate that iterative releases of non-biting Ifegenia males can act as an effective, confinable, controllable and safe population suppression and elimination system."
Traditional methods to combat malaria spread such as bed nets and insecticides increasingly have been proven ineffective in stopping the disease's spread. Insecticides are still heavily used across the globe, primarily in an effort to stop malaria, which increases health and ecological risks to areas in Africa and Asia.
Smidler, who earned a Ph.D. (biological sciences of public health) from Harvard University before joining UC San Diego in 2019, is applying her expertise in genetic technology development to address the spread of the disease and the economic harm that comes with it. Once she and her colleagues developed Ifegenia, she was surprised by how effective the technology worked as a suppression system.
"This technology has the potential to be the safe, controllable and scalable solution the world urgently needs to eliminate malaria once and for all," said Akbari, a professor in the Department of Cell and Developmental Biology. "Now we need to transition our efforts to seek social acceptance, regulatory use authorizations and funding opportunities to put this system to its ultimate test of suppressing wild malaria-transmitting mosquito populations. We are on the cusp of making a major impact in the world and won't stop until that's achieved."
The researchers note that the technology behind Ifegenia could be adapted to other species that spread deadly diseases, such as mosquitoes known to transmit dengue (break-bone fever), chikungunya and yellow fever viruses.
More information: Andrea L. Smidler et al, A confinable female-lethal population suppression system in the malaria vector, Anopheles gambiae, Science Advances (2023). DOI: 10.1126/sciadv.ade8903
Journal information: Science Advances
Provided by University of California - San Diego | Biology |
Cephalopods like octopuses, squids and cuttlefish are highly intelligent animals with complex nervous systems. In “Science Advances”, a team led by Nikolaus Rajewsky of the Max Delbrück Center has now shown that their evolution is linked to a dramatic expansion of their microRNA repertoire.If we go far enough back in evolutionary history, we encounter the last known common ancestor of humans and cephalopods: a primitive wormlike animal with minimal intelligence and simple eyespots. Later, the animal kingdom can be divided into two groups of organisms – those with backbones and those without. While vertebrates, particularly primates and other mammals, went on to develop large and complex brains with diverse cognitive abilities, invertebrates did not. With one exception: the cephalopods. Scientists have long wondered why such a complex nervous system was only able to develop in these mollusks. Now, an international team led by researchers from the Max Delbrück Center and Dartmouth College in the United States has put forth a possible reason. In a paper published in “Science Advances”, they explain that octopuses possess a massively expanded repertoire of microRNAs (miRNAs) in their neural tissue – reflecting similar developments that occurred in vertebrates. “So, this is what connects us to the octopus!” says Professor Nikolaus Rajewsky, Scientific Director of the Berlin Institute for Medical Systems Biology of the Max Delbrück Center (MDC-BIMSB), head of the Systems Biology of Gene Regulatory Elements Lab, and the paper’s last author. He explains that this finding probably means miRNAs play a fundamental role in the development of complex brains. In 2019, Rajewsky read a publication about genetic analyses conducted on octopuses. Scientists had discovered that a lot of RNA editing occurs in these cephalopods – meaning they make extensive use of certain enzymes that can recode their RNA. “This got me thinking that octopuses may not only be good at editing, but could have other RNA tricks up their sleeve too,” recalls Rajewsky. And so he began a collaboration with the Stazione Zoologica Anton Dohrn marine research station in Naples, which sent him samples of 18 different tissue types from dead octopuses. The results of this analyses were surprising: “There was indeed a lot of RNA editing going on, but not in areas that we believe to be of interest,” says Rajewsky. The most interesting discovery was in fact the dramatic expansion of a well-known group of RNA genes, microRNAs. A total of 42 novel miRNA families were found – specifically in neural tissue and mostly in the brain. Given that these genes were conserved during cephalopod evolution, the team concludes they were clearly beneficial to the animals and are therefore functionally important. Rajewsky has been researching miRNAs for more than 20 years. Instead of being translated into messenger RNAs, which deliver the instructions for protein production in the cell, these genes encode small pieces of RNA that bind to messenger RNA and thus influence protein production. These binding sites were also conserved throughout cephalopod evolution – another indication that these novel miRNAs are of functional importance. New microRNA families “This is the third-largest expansion of microRNA families in the animal world, and the largest outside of vertebrates,” says lead author Grygoriy Zolotarov, MD, a Ukrainian scientist who interned in Rajewsky’s lab at MDC-BIMSB while finishing medical school in Prague, and later. “To give you an idea of the scale, oysters, which are also mollusks, have acquired just five new microRNA families since the last ancestors they shared with octopuses – while the octopuses have acquired 90!” Oysters, adds Zolotarov, aren’t exactly known for their intelligence. Rajewsky’s fascination with octopuses began years ago, during an evening visit to the Monterey Bay Aquarium in California. “I saw this creature sitting on the bottom of the tank and we spent several minutes – so I thought – looking at each other.” He says that looking at an octopus is very different to looking at a fish: “It’s not very scientific, but their eyes do exude a sense of intelligence.” Octopuses have similarly complex “camera” eyes to humans. From an evolutionary perspective, octopuses are unique among invertebrates. They have both a central brain and a peripheral nervous system – one that is capable of acting independently. If an octopus loses a tentacle, the tentacle remains sensitive to touch and can still move. The reason why octopuses are alone in having developed such complex brain functions could lie in the fact that they use their arms very purposefully – as tools to open shells, for instance. Octopuses also show other signs of intelligence: They are very curious and can remember things. They can also recognize people and actually like some more than others. Researchers now believe that they even dream, since they change their color and skin structures while sleeping. Alien-like creatures “They say if you want to meet an alien, go diving and make friends with an octopus,” says Rajewsky. He’s now planning to join forces with other octopus researchers to form a European network that will allow greater exchange between the scientists. Although the community is currently small, Rajewsky says that interest in octopuses is growing worldwide, including among behavioral researchers. He says it’s fascinating to analyze a form of intelligence that developed entirely independently of our own. But it’s not easy: “If you do tests with them using small snacks as rewards, they soon lose interest. At least, that’s what my colleagues tell me,” says Rajewsky. “Since octopuses aren’t typical model organisms, our molecular-biological tools were very limited,” says Zolotarov. “So we don’t yet know exactly which types of cell express the new microRNAs.” Rajewsky’s team are now planning to apply a technique, developed in Rajewsky’s lab, which will make the cells in octopus tissue visible at a molecular level. Text: Catarina Pietschmann Further information The visionary – a portrait of Nikolaus Rajewsky Literature Grygoriy Zolotarov et al. (2022): „MicroRNAs are deeply linked to the emergence of the complex octopus brain“, Science Advances. DOI: 10.1126/sciadv.add9938 Downloads Cephalopods playing with microRNAs (yellow): microRNAs may be linked to the emergence of complex brains in cephalopods. Illustration: Grygoriy Zolotarov Octopuses have both a central brain and a peripheral nervous system – one that is capable of acting independently. Photo: Nir Friedman Octopuses have complex “camera” eyes, as seen here in a juvenile animal. Photo: Nir Friedman Contacts Prof. Nikolaus Rajewsky
Scientific Director, Berlin Institute for Medical Systems Biology
of the Max Delbrück Center (MDC-BIMSB)
+49 30 9406-1585 (office Rajewsky)[email protected] or [email protected] (office Rajewsky) Jana Schlütter
Editor, Communications Department
Max Delbrück Center
+49 30 [email protected] or [email protected] | Biology |
People of normal weight may be able to extend their life span by restricting calories, according to a new study that attempted to measure the pace of aging in people asked to cut their calorie intake by 25% over two years.
“We’ve known for nearly 100 years that calorie restriction can extend healthy life span in a variety of laboratory animals,” said senior author Daniel Belsky, an associate professor of epidemiology at Columbia University Mailman School of Public Health.
“It does this by changing biology in ways consistent with a slowing of the process of aging, although the specific mechanisms of how this occurs are still under investigation,” said Belsky, who studies longevity. “We decided to drill down to the cellular level in people to see if the same is true.”
The study used what are commonly known as “biological clocks” to determine the pace of aging in its participants. Bioclocks are designed to measure how old people are biologically compared with their real ages chronologically.
“Our study found evidence that calorie restriction slowed the pace of aging in humans,” said colead author Calen Ryan, an associate research scientist at the Robert N. Butler Columbia Aging Center at Columbia.
“Our findings are important because they provide evidence from a randomized trial that slowing human aging may be possible,” Ryan said in a statement.
But longevity scientist Dr. Peter Attia dismissed the study results as “noise.”
“I just don’t see any evidence that any of the biologic clocks have meaning,” Attia, who was not involved in the study, said via email. He hosts “The Drive,” a podcast dedicated to explaining and applying longevity research to everyday life.
“The only validation that matters — which to my knowledge has not been done, but hopefully will be — is to see if ‘biologic age’ can predict future life better than chronological age,” he said.
Biological age predictors are controversial, said calorie restriction researcher Pankaj Kapahi, a professor at the Buck Institute for Research on Aging in Novato, California.
“At best, they’re telling you something about a very small aspect of aging,” said Kapahi, who was not involved in the study. “For example, grip strength is also a biological age predictor, how active you are is a predictor, and we all know people who fall apart physically but are cognitively all there, so you also need to test cognitive aging.
“Some researchers are trying to boil it down with bio-aging tests,” he added. “This is a much more complex problem, and I think it’s an overstatement to say the tests really predict biological age.”
The CALERIE study
Decades of research in animals have shown that calorie restriction produces health benefits, even slowing the pace of aging. Would the same be true in people?
A study in the 1950s asked people to reduce 50% of their calories, leading to malnutrition or a lack of key micronutrients in participants. Later research often focused on calorie reduction in people whose body mass index would be considered medically obese.
The first clinical trial of calorie restriction in people at normal weight (a BMI of about 20 to 25) started in 2007. It was called CALERIE, or the Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy.
Because of the malnutrition found in the earlier study that cut calories drastically, CALERIE asked 143 adults between the ages of 21 and 50 to cut 25% of the calories they typically ate for a two-year period. Another group of 75 people maintained their normal diets, serving as a control group.
During the trial, all manner of tests were done at six-month intervals to gather information on weight loss, change in resting metabolic rate, impact on cognitive function and markers of inflammation, cardiovascular health and insulin sensitivity.
The results of CALERIE, published in 2015, found that on average people in the restricted group were able to cut 14% of their calories, or about half of the 25% goal. However, that amount reduced their fat mass by about 10% and decreased their cardiometabolic risk factors with no adverse effects on quality of life, researchers said. There were also reductions in tumor necrosis factor alpha, a protein that promotes insulin resistance and obesity-induced type 2 diabetes.
A number of other studies have used blood samples and other data collected on the CALERIE participants to explore other ways modest calorie restriction might benefit the body. For example, Yale University researchers found restricting calories increased the health of the thymus, an organ that produces immune system T cells — one of the body’s key warriors against invaders.
A difference in findings
The new study, published Thursday in the journal Nature Aging, culled DNA sequences from white blood cells taken at 12-month intervals from participants in CALERIE. Belsky’s team then analyzed methylation marks — signs of epigenetic changes — on the DNA, looking for symptoms of aging.
Epigenes are proteins and chemicals that sit like freckles on each gene, waiting to tell the gene “what to do, where to do it, and when to do it,” according to the National Human Genome Research Institute.
“Increasingly, changes to our cells’ epigenomes, the systems that control which genes in the genome are turned on and off, are being recognized as drivers of the aging process,” said anti-aging expert David Sinclair, a professor of genetics in the Blavatnik Institute at Harvard Medical School and codirector of the Paul F. Glenn Center for Biology of Aging Research.
“Clocks that measure these changes are proving to be indicators of future health and what interventions might slow and even reverse the aging process,” said Sinclair, who was not involved in the study.
In the new study, researchers used two epigenetic clocks — PhenoAge and GrimAge — and a new tool Belsky recently invented in conjunction with Duke University. This third bioclock, called DunedinPACE, attempts to determine the pace of aging from a single blood test, Belsky said.
The PhenoAge and GrimAge bioclocks showed no signs of reduced aging in the blood samples of participants in CALERIE, said Belsky, who is also a scientist with Columbia’s Robert N. Butler Aging Center.
However, DunedinPACE, the clock created by Belsky’s and Duke’s teams, did find a 2% to 3% reduction in the pace of aging, “which in other studies translates to a 10-15 percent reduction in mortality risk, an effect similar to a smoking cessation intervention,” according to a statement from Columbia.
Controversy over bioclocks
Critics of the study, however, were not impressed. The performance of the DunedinPACE test was “mediocre at best,” Attia said, finding only a weak association with biological aging.
The fact that the two other bioclocks found no anti-aging benefits was no surprise, said the Buck Institute’s Kapahi: “These biological age predictors don’t agree with each other and don’t necessarily agree with other biological measures.
“It’s going to confuse the public, and unfortunately people are buying these tests when there’s very little useful information that comes out of them.”
While it’s true epigenetic biomarkers are not yet ready to be used in clinical trials, “many different studies in many different datasets and populations have shown these algorithms are predictive of differences between people in who gets sick and who lives or dies,” Belsky countered.
“This is not a game over moment. It’s more like game on,” Belsky said. “What we have now is a proof of concept — a methylation biomarker that shows faster aging in people we know to be at higher risk for disease, disability and death, and slower aging in people who we know to be at lower risk.”
Does caloric restriction work?
Putting aside the debate over how slower aging is measured, there is a role for caloric restriction in extending life, especially in “overnourished” individuals, Attia said.
“I don’t want a reader to think this intervention (calorie restriction) is of no value, only that (the study) does not ‘prove’ a reduction in the pace of aging,” he said in an email.
Time-restricted eating and dietary restriction of certain foods are two additional ways to curb “overnutrition,” which Attia believes is the biggest driver of insulin resistance, type 2 diabetes and other chronic diseases.
“I am not aware of any evidence that one ‘strategy’ or method is superior. The best one is the one that works for a person, but calorie restriction certainly works for some, and therefore is clearly beneficial,” Attia said. “All of these interventions will lead to a longer and better life, but these aging clocks tell us less than zero about that process.”
There are many other ways to curb aging as well, Kapahi said.
“We’re trying to learn more about aging and we are, but calorie restriction is just one intervention,” he said. “You likely need to do that in combination with exercise, with good sleep, with a positive attitude and good mental health. All these things combined will likely play a much bigger role in slowing aging.” | Biology |
Image: Shutterstock (Shutterstock)The mind-altering effects of a well-known parasite may extend to more species than we thought. In new research this month, Yellowstone scientists are making the case that Toxoplasma gondii infection can influence the behavior of gray wolves in the area. It appears to increase their odds of risk-taking behaviors, such as leaving their packs or becoming pack leaders.OffEnglishToxoplasma gondii is a single-celled protozoan parasite. To complete its complex life cycle and reproduce, it has to eventually infect members of the cat family. In order to accomplish this, T. gondii is thought to shift the behavior of infected rodents—a common intermediate host. T. gondii-infected rodents become less wary of cat urine and less fearful of predators in general, which then makes them more susceptible to getting eaten by a cat.Though T. gondii would probably prefer to end up inside rodents or birds that cats like to munch on, their hardy cysts regularly infect all sorts of warm-blooded species. These infections seem to only rarely cause acute illness, but the cysts themselves often survive in the body for a lifetime. And over the years, some studies have shown, this infection might have subtle behavioral or neurological effects in non-rodent animals. Most of this research has looked at humans, with studies finding that infected humans might have a higher risk of schizophrenia, for instance. But wildlife researchers at Yellowstone National Park wanted to know what factors could affect the prevalence of T. gondii infection in their wolves, and whether this infection can have far-reaching consequences for them as well.The team analyzed over 25 years of data on the park’s gray wolf populations, which included blood tests that could screen for antibodies to T. gondii. They also looked at data on the park’s cougars, since they suspected that wolves living closer to these cats would have a higher risk of infection.As expected, cougars were regularly exposed to T. gondii (about 50% of the sample tested positive). And when wolves lived in areas that overlapped cougar populations, they more often had T. gondii antibodies—likely obtained through direct contact with cat droppings or cysts in the environment, the researchers say. These infected wolves were then more likely to display risky behaviors than non-infected wolves, such as dispersing (leaving their pack and traveling far elsewhere) or becoming the breeding leaders within their pack. Interestingly enough, this influence may then create a sort of feedback loop, the researchers speculate, since bolder infected wolves could be more likely to lead their packs into cougar territory, allowing the parasites to infect more wolves.“This study is a rare demonstration of a parasite infection influencing behavior in a wild mammal population,” the authors wrote in their paper, published this month in Communications Biology. “These two life history behaviors represent some of the most important decisions a wolf can make in its lifetime and may have dramatic impacts on gray wolf fitness, distribution, and vital rates.”The findings, intriguing as they are, should ideally be confirmed by other studies before they’re assumed to be true (even in humans, there is an ongoing debate over how much T. gondii infection really affects us). And it’s not clear exactly how T. gondii could be affecting wolf behavior, though the authors hypothesize that the infection might raise testosterone levels. But this is only the latest piece of research to suggest that T. gondii isn’t just capable of playing puppet master with rodents. A study last year, the authors note, found that infected hyenas were bolder and more likely to be eaten by lions than non-infected hyenas. So, if nothing else, more research is needed to understand and untangle the many ways that T. gondii and similar organisms may be influencing the world around them.“Incorporating the implications of parasite infections into future wildlife research is vital to understanding the impacts of parasites on individuals, groups, populations, and ecosystem processes,” the authors wrote. | Biology |
Image source, Getty ImagesImage caption, Leprosy can damage the nerves, leading to disabilityLeprosy bacteria may hold the secret to safely repairing and regenerating the body, researchers at the University of Edinburgh say. Animal experiments have uncovered the bacteria's remarkable ability to almost double the size of livers by stimulating healthy growth. It is a sneakily selfish act that gives the bacteria more tissue to infect. But working out how they do it could lead to new age-defying therapies, the scientists say.'Biological alchemy' Leprosy causes disability when it infects the nerves, skin and eyes. Throughout history, those infected have been shunned. But the bacterium that causes it, Mycobacterium leprae, has other, unusual properties, including the ability to perform "biological alchemy", converting one type of bodily tissue into another, which are fascinating scientists.So the researchers turned to the only other animals to catch the disease - armadillos. Image source, Getty ImagesImage caption, The armadillo is the only other known host for the leprosy bacteriumThe infection heads to the armoured animals' livers, where, the researchers found, it performed a controlled hijacking of the organ to reprogram it for its own purpose. "It was a totally unexpected," Prof Anura Rambukkana, from the University of Edinburgh's centre for regenerative medicine, told me.The results, published in Cell Reports Medicine, showed the liver nearly doubled in size. You might expect such growth to be defective or even cancerous - but detailed analysis showed it was both healthy and functional, complete with the usual array of blood vessels and bile ducts. "It is kind of mind-blowing," Prof Rambukkana said. "How do they do that? There is no cell therapy that can do that." Rapidly increaseIt appears the leprosy bug is rewinding the developmental clock in the liver. Fully grown liver cells are metabolic powerhouses with hundreds of jobs in the body. But the bacteria are taking them back a stage - like becoming a teenager again - where they can rapidly increase in number before maturing back into adulthood.Interrogating the activity of different parts of the cells' DNA revealed a picture more akin to that of a much younger animal or even a fetus, when the liver is still forming. 'Natural process'But the precise details of how this is all happening remain elusive. Nobel Prize-winning research has shown it is possible to forcibly turn the clock all the way back to the point at which cells regain the ability to become any other type of cell in the body - but this runs the risk of turning them cancerous. "The [leprosy] bugs use alternative pathways," Prof Rambukkana told me. "It's a much safer way and they take a longer time to do that, so this is a natural process." 'Promising results'The hope is the approach can be harnessed for repairing the livers of people waiting for a transplant - or even to reverse some of the damage caused by ageing elsewhere in the body. "The dream is to use the same bacterial strategy, to use the ingenuity of bacteria to generate new medicines for regeneration and repair," Prof Rambukkana said."If you can harness that, you should be able to turn that mechanism into a jab you have every three months or something."All these ideas remain untested, however.Dr Darius Widera, of the University of Reading, said: "Overall, the results could pave the way for new therapeutic approaches to the treatment of liver diseases such as cirrhosis."However, as the research has been done using armadillos as model animals, it is unclear if and how these promising results can translate to the biology of the human liver. "Moreover, as the bacteria used in this study are disease-causing, substantial refinement of the methods would be required prior to clinical translation." | Biology |
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Scientists based in China have created a monkey chimera with two sets of DNA, experimental work they say could ultimately benefit medical research and the conservation of endangered species.
The monkey, which lived for 10 days before being euthanized, was made by combining stem cells from a cynomolgus monkey — also known as a crab-eating or long-tailed macaque, a primate used in biomedical research — with a genetically distinct embryo from the same monkey species. It’s the world’s first live birth of a primate chimera created with stem cells, the researchers said.
A proof-of-concept study detailing the research, which published Thursday in the scientific journal Cell, said it was notable that the monkey was “substantially chimeric,” containing a varying but relatively high ratio of cells that grew out of the stem cells throughout its body.
“It is encouraging that our live birth monkey chimera had a big contribution (of stem cells) to the brain, suggesting that indeed this approach should be valuable for modeling neurodegenerative diseases,” said study coauthor Miguel Esteban, principal investigator at the Guangzhou Institute of Biomedicine and Health, Chinese Academy of Sciences and a researcher with BGI-Research Hangzhou, a nonprofit arm of Chinese genetics firm BGI.
“Monkey chimeras also have potential enormous value for species conservation if they could be achieved between two types of nonhuman primate species, one of which is endangered,” he added. “If there is contribution of the donor cells from the endangered species to the germ line, one could envisage that through breeding animals of these species could be produced.”
History of chimeras in research
The term chimera originated from the monstrous hybrid creatures that populate Greek myths, but chimeric mice were first created in the 1960s and have been commonly used in biomedical research.
Chimeric lab mice allow scientists to track how normal cells interact with genetically altered or mutated cells, which is useful for understanding biological processes and disease. But there are limitations with research on mice that make pursuing efforts with monkeys worthwhile, the scientists said.
“Mice don’t reproduce many aspects of human disease for their physiology being too different from ours. In contrast, human and monkey are close evolutionary, so human diseases can be more faithfully modeled in monkeys,” said senior study author Zhen Liu of the Chinese Academy of Sciences.
More controversial are human-animal chimeras, which contain some human cells, and some cells from other species. Scientists have created mouse embryos that are part human, and in 2021, scientists reported that they had grown human-monkey chimeric embryos.
Scientists hope that part-human chimeras may one day help to fill the demand for organ transplants. In September, researchers reported that they had grown kidneys containing mostly human cells inside pig embryos.
Liu said at a news briefing that it would be crossing an ethical red line to attempt to produce a monkey-human chimera beyond early embryonic stages of development.
Making a monkey chimera
The team cultured nine stem cell lines using cells removed from 7-day-old monkey embryos. The researchers made the cells pluripotent — giving them the ability to organize into all the different cell types needed to create a live animal.
Then they selected a subset of cells to inject into genetically distinct 4- to 5-day-old embryos from the same monkey species. The cells were also infused with a green fluorescent protein so the researchers would be able to determine which tissues had grown out of the stem cells.
The embryos were implanted into female monkeys, resulting in 12 pregnancies and six live births. One of the monkeys that was born and one fetus that was miscarried were “substantially chimeric,” containing cells that grew out of the stem cells throughout their bodies, according to the study.
“This is an important study, but I wouldn’t consider it’s a breakthrough as the chimeras generated are not viable,” said Jun Wu, an associate professor in molecular biology at the University of Texas Southwestern Medical Center.
He added that the team also hadn’t been able to demonstrate that the stem cells used to generate the chimeras were inheritable by offspring — something that would be necessary to generate monkey disease models for medical research. Wu wasn’t involved in the study but has worked on human-animal chimeras.
The percentage of stem cells in the monkey’s tissue ranged from 21% to 92%, with an average of 67% across the 26 different types of tissue that were tested, according to the study. The percentage was notably high in brain tissue.
“It is a very good and important paper,” said Jacob Hanna, a professor of stem cell biology and embryology at the Weizmann Institute of Science in Israel who was not involved with the study.
“This study may contribute to easier and better making of mutant monkeys, just like biologists have been doing for years with mice,” Hanna added. “Of course, work with (nonhuman primates) is slower and much harder but is important.”
The ethics of medical research on monkeys
The use of monkeys in scientific research is a contentious issue because of ethical concerns about animal welfare. The team said it followed Chinese laws and international guidelines governing the use of nonhuman primates in scientific research.
Penny Hawkins, head of animals in science at the Royal Society for the Prevention of Cruelty to Animals, said that she was “deeply concerned about the inherent animal suffering and wastage associated with the application of these technologies to sentient animals.”
She noted that 40 female macaque monkeys had embryos implanted, of which only 12 led to pregnancies. Six of these resulted in live births, but only one had the desired genetic makeup. A vet euthanized it after 10 days due to respiratory failure and hypothermia.
In the United States, research on nonhuman primates made up 0.5% of all animals used in scientific research, according to a report by the panel of the National Academies of Sciences, Engineering and Medicine released in May.
The panel found that research involving monkeys, because of their similarities to people, had been critical to lifesaving medical advances, including the creation of vaccines against Covid-19. The report also concluded that a shortage of nonhuman primates had negatively affected research necessary for both public health and national security. | Biology |
In a changing ecosystem, Yellowstone grizzly bears are resilient
Grizzly bears in the Greater Yellowstone Ecosystem have been able to gain the body fat they need for hibernation even as population densities have increased and as climate change and human impacts have changed the availability of some foods, according to a new study by the U.S. Geological Survey and its partners. The study is published in the journal Global Change Biology.
In recent decades, several high-calorie foods for grizzly bears in the Greater Yellowstone Ecosystem have declined, most notably the cutthroat trout and seeds of the now federally threatened whitebark pine, as well as some elk herds in and near Yellowstone National Park. At the same time, grizzly bear population densities have increased due to concerted interagency conservation efforts following the bear's 1975 listing as threatened under the federal Endangered Species Act. The Greater Yellowstone Ecosystem, a 22-million-acre region encompassing portions of Wyoming, Montana and Idaho, including Yellowstone and Grand Teton National Parks, is home to one of the largest grizzly bear populations in the contiguous United States.
Body composition can serve as an indicator of how grizzly bears have coped with these changes. Using more than 20 years of data, the new study found that lean body mass (total body weight minus body fat) was lower in areas with higher grizzly bear population density. However, body fat levels stayed the same over the study period, regardless of bear population density. These findings suggest that grizzly bears were still able to gain sufficient energy reserves and able to cope with changes in food availability and increased competition by prioritizing body fat storage.
Body fat is vital for grizzly bears because it is an energy source during winter hibernation. Fat is especially important for reproductive-age female bears, who need to have enough energy to support pregnancy, birth and lactation during this time.
"Our analyses indicate grizzly bear population density influenced lean body mass, but fat storage wasn't affected in the same way," said Andrea Corradini, lead author and post-doctoral researcher at Fondazione Edmund Mach, Italy. "The capacity of grizzly bears to shift feeding tactics allowed them to respond to changing conditions and prioritize calorie intake for fat storage during late summer and fall, regardless of bear density."
The study found that the pattern of lower lean body mass was most pronounced in still-growing female bears, but they too were able to gain the high levels of body fat they needed. Even though these bears had lower lean body mass while growing, they reached their typical total body mass as they matured, possibly by delaying reproduction or moving to areas with fewer bears.
When it comes to their diets, grizzly bears are omnivores, meaning they eat many different types of foods, including elk, bison, insects, fish, roots, seeds and berries. They are also opportunistic in their use of those foods. Big, long-lived omnivores like grizzly bears have large home ranges and they can rapidly shift to more readily available food resources to compensate for dwindling ones. This flexible feeding strategy helps grizzly bears respond to changing environmental conditions more easily than animals that depend on a specific food source. The Greater Yellowstone Ecosystem is a large, well-protected landscape, which has facilitated bears' shifting diets and allowed them to expand to new areas, although that increasingly comes at the cost of more human-bear conflicts.
"The study findings demonstrate the resilience of grizzly bears in the face of ecosystem change and enhance our understanding of their life history strategy," explained Frank van Manen, USGS scientist and team leader of the Interagency Grizzly Bear Study Team. "Interagency investment into long-term research data allowed us to disentangle these complex relationships."
Though the grizzly bears of the Greater Yellowstone Ecosystem have been able to maintain fat levels and overall body size as environmental conditions changed over the past two decades, it is not known how they will adapt to more extreme disturbances in the future, such as continued warming, changing wildfire patterns and increasing human development and recreation.
More information: Andrea Corradini et al, Evidence for density‐dependent effects on body composition of a large omnivore in a changing Greater Yellowstone Ecosystem, Global Change Biology (2023). DOI: 10.1111/gcb.16759
Journal information: Global Change Biology
Provided by United States Geological Survey | Biology |
The Yangtze giant softshell turtle (Rafetus swinhoei), the world's largest freshwater turtle and one of the most endangered species on Earth, is now essentially doomed to extinction after the last known remaining female washed up dead in Vietnam.
The female turtle, which was around 5 feet (1.5 meters) long and weighed 205 pounds (93 kilograms), was discovered dead on April 21 on the shores of Dong Mo Lake, in Hanoi's Son Tay district. The turtle likely died several days earlier, but the cause of death is still unknown, Vietnamese news site VNExpress reported (opens in new tab).
This particular female Yangtze giant softshell turtle was just discovered in October 2020. At the time, no other female Yangtze giant softshell turtles were known to exist; the last known female of the species had died after a failed attempt at artificial insemination at Suzhou Zoo in China in April 2019.
When the dead turtle was discovered last month, conservationists had hoped that it belonged to another unknown female, and that the known female might still be alive in the lake. But experts have now confirmed this is not the case..
"It is the same individual that we've been monitoring in recent years," Tim McCormack, director of the Asian Turtle Program for Indo-Myanmar Conservation, told TIME magazine (opens in new tab). "It's a real blow."
There are now just two known R. swinhoei males left in existence: one in Suzhou Zoo and another that still resides in Dong Mo Lake.
Researchers had hoped that the female and male in Dong Mo Lake would eventually mate and produce a clutch of eggs. Based on its size, the female was likely several decades old, meaning it was probably sexually mature.
"It was a large female that obviously has great reproductive capacity," McCormack said. "She could have potentially laid a hundred eggs or more a year." However, the pair never mated, even though researchers built an artificial nesting beach at the lake for the female to lay her eggs if she ever needed it.
Yangtze giant softshell turtles, also known as Hoan Kiem turtles and Swinhoe's softshell turtles, were once abundant throughout the Yangtze River in China and the surrounding freshwater ecosystems, like Dong Mo Lake. However, historically, humans hunted the turtles for their meat, and they have lost most of their natural habitat, according to the Asian Turtle Program (opens in new tab).
There is a chance that other males and females may be found in the future. After all, this female did evade detection for years. But if another female cannot be found in the wild, R. swinhoei will eventually become the latest name on a growing list of species that have been wiped out by humans.
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Harry is a U.K.-based staff writer at Live Science. He studied Marine Biology at the University of Exeter (Penryn campus) and after graduating started his own blog site "Marine Madness," which he continues to run with other ocean enthusiasts. He is also interested in evolution, climate change, robots, space exploration, environmental conservation and anything that's been fossilized. When not at work he can be found watching sci-fi films, playing old Pokemon games or running (probably slower than he'd like). | Biology |
Science & Society Picture Library via Getty Images
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Lice have irked humans for many centuries. In this 1497 woodcut printed in Strasbourg, Germany, a man is de-loused.
Science & Society Picture Library via Getty Images
Lice have irked humans for many centuries. In this 1497 woodcut printed in Strasbourg, Germany, a man is de-loused.
Science & Society Picture Library via Getty Images
Head lice are considered a nuisance — a pest to be evicted from the hair on your head or the head of a loved one with a special comb or shampoo. But there's more to lice than their elimination. These parasites have been stowaways on our heads for so long that they've recorded our history as humans in their DNA.
"We can think of human lice as heirlooms of our past," says Marina Ascunce, an evolutionary geneticist at the U.S. Department of Agriculture in Gainesville, Florida.
Bret Boyd, an entomologist at Virginia Commonwealth University, agrees. "They're really like a little tape recorder that's been following us around throughout our time on this earth," he says.
And Ascunce says lice are particularly helpful in answering questions about human history that we can't resolve using our own DNA or the archaeological record.
In a new study in the journal PLOS One, she and her colleagues present evidence that our head lice seem to have recorded in their DNA the massive human migrations that led to the inhabitation and colonization of the Americas.
That is, where humans went, so did our head lice.
Looking at the DNA of lice
Head lice are the tiniest of hitchhikers, each one about the size of a sesame seed. They grab hold of our locks, glue their eggs to our hair and annoy us for a time by tickling our scalps and making our heads itch — before crawling into the next person's head of hair. We may not need these pesky little insects, but they sure need us.
"These are a parasite that live [on] our head," says Ascunce. "And to survive, they need to take our blood and suck our blood. So they cannot live outside of our head." In biology parlance, they are obligate parasites. To survive, they are obligated to live upon us.
Like gazillions of humans, Ascunce has had head lice. "When I was a kid in Argentina, I remember one time at least that I have for sure," she says. "It wasn't fun. My mom [was] freaking out."
Ascunce's mom's generation battled with lice, too. As did her grandmother's generation. In fact, head lice have been clinging to human hair for as long as there've been humans — and likely even before that to the hair of our hominid ancestors.
"Basically," says Ascunce, "both we humans, which are the host, and the lice, which is the parasite, have evolved through time together."
And so, while still a researcher at the Florida Museum of Natural History in the early 2010s, she set out to see what these parasites and their DNA could tell us about our past.
The first thing she needed was a bunch of lice. So she teamed up with collaborators who collected them from 25 places around the world and sent their corpses to her in Florida.
Ascunce then began her laboratory procedure, which, to anyone who's ever felt tortured by lice, may feel like a kind of karma.
"So first we put them under a microscope, and actually we cut them in half," she says. "And then we put them in another tube to do the DNA extractions."
After she and her colleagues analyzed all that lice DNA, they found further evidence that lice operate as mini recorders of human history. In this case, she says she detected two distinct genetic clusters, which suggest that human head lice arrived in the Americas twice.
"We humans, we migrate and we take the lice with us," she summarizes.
First, some 15,000 to 35,000 years ago, when humans crossed the Bering Land Bridge from Asia into North America, there were likely lice gripping their hair, along for the ride. So it confirms what we knew about humans crossing continents.
"The Native Americans," says Ascunce, "different populations, they went south through the Americas," as did their lice.
Then, 500-some years ago, the Europeans showed up with their own strain of hitchhiking head lice.
In other words, "these lice are mirroring the colonization of the Americas," says Ascunce, "the two migration waves."
Alejandra Perotti, an invertebrate biologist at the University of Reading who wasn't involved in the study, says the approach is solid. But she says the researchers didn't have enough lice from every part of the world to get a complete picture of their diversity — which could lead to a better understanding of broad human movement patterns over the centuries.
"If you look at the data they gather," she says, "some of the populations have only one louse, including Africa, for example. So there is an issue with the sampling size."
Future work will correct this data gap. And Ascunce and her colleagues plan on looking for signals in our head lice of ancient interactions between our human ancestors and Neanderthals who would have carried their own lice as well. These interactions would have included "any type of close contact from sharing sleeping sites to fights to interbreeding," she says.
You just can't keep a juicy secret from a head louse. | Biology |
New research has uncovered a surprising link between empathy and our health. The study suggests that while empathy is highly valued in our society, it may come at a biological cost for some individuals. The findings have been published in the journal Biological Psychology.
Empathy, the ability to understand and share the feelings of others, is often seen as a noble trait associated with compassion and kindness. Prior research has shown that empathic individuals tend to engage in more altruistic acts, report lower levels of loneliness, and enjoy higher-quality relationships. However, Erika M. Manczak, the author of the study, wanted to delve deeper into the physiological consequences of empathy.
“I’m interested in how our social experiences can ‘get under the skin’ to influence our health,” explained Manczak, an assistant professor at the University of Denver and director of the Biology, Environments & Mood Studies Lab. “As a society, we tend to highly value empathy as a personal trait and yet I have conducted some previous research that found that parents who were high in empathy also had higher levels of markers of chronic inflammation, suggesting that empathy may come at a biological cost.”
“In this study, I used data from a much larger, nationally representative study to look at whether these associations may be true for all individuals, not just parents. Inflammation plays a key role in many chronic diseases (such as heart disease and asthma), so understanding what personal factors can predict inflammation is important for determining who might be at risk for worse health.”
Manczak analyzed data from the National Longitudinal Study of Adolescent to Adult Health (known as ‘Add Health’). This ongoing study has been tracking a representative sample of adolescents since the 1994–1995 school year. In this particular study, data collected when participants were between 24 and 32 years old were used, along with data collected 8 years later when participants were between 32 and 40 years old.
Importantly, the study obtained data regarding three key factors: affective empathy (participants were asked how much they agreed with statements about feeling others’ emotions), depressive symptoms (participants reported their feelings of depression over the past week), and c-reactive protein (a marker of inflammation in the body).
Higher levels of empathy were linked to higher levels of c-reactive protein in the blood but only among individuals with low levels of depressive symptoms. This means that for people without significant depressive symptoms, empathy appeared to contribute to higher inflammation.
“In this study, I found that reporting higher levels of empathy was associated with higher levels of c-reactive protein, a marker of chronic inflammation, eight years later, even after taking into account participants’ levels of inflammation at baseline,” Manczak told PsyPost. “However, this pattern was only true for individuals who did not have high levels of depressive symptoms; for individuals experiencing more depressive symptoms, inflammation was high regardless of their levels of empathy.”
These could findings have significant implications for our physical health. Elevated c-reactive protein levels are commonly associated with conditions like heart disease, stroke, and inflammatory bowel disease. Individual differences in c-reactive protein levels can become more pronounced as individuals age, particularly in early midlife.
But the study has some limitations, such as the use of a single-item measure of empathy and self-reported assessments of depressive symptoms. “Empathy is something that can be tricky to measure in research and in this study, we relied on participants’ responding to a question about how much they typically feel other people’s emotions,” Manczak explained. “It would be great to look at other ways of measuring empathy and see if similar results emerge.”
“An important remaining question is: what are the pathways through which empathy relates to inflammation? For example, is it due to more empathic people feeling more stressed because of the emotions of people around them? Is it because of other intermediary biological processes that increase inflammation?”
The study, “Is there a cost to caring? Dispositional affective empathy interacts with depressive symptoms to predict higher C-reactive protein 8 years later“, was published on May 5, 2023. | Biology |
The Nobel Prize in Physiology or Medicine has been awarded to a pair of scientists who developed the technology that led to the mRNA Covid vaccines.
Professors Katalin Kariko and Drew Weissman will share the prize.
The technology was experimental before the pandemic, but has now been given to millions of people around the world to protect them against serious Covid-19.
The same mRNA technology is now being researched for other diseases, including cancer.
The Nobel Prize committee said: "The laureates contributed to the unprecedented rate of vaccine development during one of the greatest threats to human health in modern times."
Both were told they had won by telephone this morning and were said to be "overwhelmed".
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Vaccines train the immune system to recognise and fight threats such as viruses or bacteria.
Traditional vaccine technology has been based on dead or weakened versions of the original virus or bacterium - or by using fragments of the infectious agent.
In contrast, messenger ribonucleic acid (mRNA) vaccines use a completely differently approach.
During the Covid pandemic, the Moderna and Pfizer/BioNTech vaccines were both based on mRNA technology.
Professor Kariko and Professor Weissman met in the early 1990s when they were working at the University of Pennsylvania, in the United States, when their interest in mRNA was seen as a scientific backwater.
An mRNA Covid vaccine contains the genetic instructions for building one component - a protein - from the coronavirus.
When this is injected into the body, our cells start producing lots of the viral protein.
The immune system recognises these as foreign so it attacks and has learned how to fight the virus, and therefore has a head start when future infections occur.
The big idea behind the technology is that you can rapidly develop a vaccine against almost anything - as long as you know the right genetic instructions to use.
This makes it far faster and more flexible than traditional approaches to vaccine development.
There are even experimental approaches using the technology that are teaching patients' bodies how to fight their own cancers.
Scientists analyse a patient's tumour, look for abnormal proteins being produced by the cancer that are not in healthy tissue and develop a vaccine to target those and inject that into the patient.
Profs Kariko and Weissman made the crucial breakthroughs that made mRNA vaccines happen.
The principle taps into normal human biology. RNA's role in our body is to convert the instructions that are locked away in our genetic code, or DNA, into the proteins that our body is built from.
However, there were challenges. But by refining the technology, the researchers were able to produce large amounts of the intended protein without causing dangerous levels of inflammation that had been seen in animal experiments.
This paved the way for developing the vaccine technology for use in people.
Katalin Kariko is now a professor at Szeged University in Hungary and Drew Weissman is still working as a professor at the University of Pennsylvania.
Previous Nobel winners
- 2022 - Svante Paabo for his work on human evolution.
- 2021 - David Julius and Ardem Patapoutian for their work on how the body senses touch and temperature.
- 2020 - Michael Houghton, Harvey Alter and Charles Rice for the discovery of the virus Hepatitis C.
- 2019 - Sir Peter Ratcliffe, William Kaelin and Gregg Semenza for discovering how cells sense and adapt to oxygen levels
- 2018 - James P Allison and Tasuku Honjo for discovering how to fight cancer using the body's immune system
- 2017- Jeffrey Hall, Michael Rosbash and Michael Young for unravelling how bodies keep a circadian rhythm or body clock
- 2016 - Yoshinori Ohsumi for discovering how cells remain healthy by recycling waste | Biology |
Progress on Self-Cloning Crops
A Q&A with Mary Gehring, plant biologist at MIT’s Whitehead Institute, about synthetic apomixis.
My latest essay, about why it is difficult to genetically engineer rice, was published today in Works in Progress magazine. I hope you’ll read the piece and send me your thoughts. Lots of fun anecdotes didn’t make it into the text, including some notes on “synthetic apomixis,” a scientific quest to make plants that produce clones of themselves. If plant engineers figure this out, it could improve life for millions of the world’s poorest farmers. This Q&A with Mary Gehring, plant biologist at MIT, explains how it works and why it matters.
Keep up with the biological revolution.
A typical farmer in India makes ₹15,000 per month, or about 180 U.S. dollars. They could make more money by growing hybrid crops, which grow faster and larger than anything else on the market. But the seeds are very expensive. They must be purchased from a large company, such as Syngenta, Bayer, or Biostadt India.
Hybrid rice (the staple crop for half of the world’s population) is often 10-20 percent bigger than even the best inbred strains. In the U.S., more than 99 percent of all corn is hybrid. But in low- or middle-income nations, less than half of farmers can afford to plant these special seeds, which are made by painstakingly taking pollen from one crop and using it to fertilize another.
Hybrid seeds are also only good for one year. They cannot be replanted for a second generation or they lose their vigor. A hybrid’s offspring, often, won’t grow as big because all the ‘good’ genes are washed out and lost.
But change is coming. We are now hurtling toward a future in which farmers could possibly buy hybrid seeds once, and then grow them forever, without relying on the big seed companies at all. It’s called synthetic apomixis.
A small number of plant biologists are making genetically engineered plants that produce clonal offspring without any fertilization. The plants don’t have sex. They just…clone themselves. If we figure this out, it would be possible to fix a plant’s traits in perpetuity, without worrying about messy genetics. It would be possible to make a hybrid plant once, and then propagate its traits forever. In the right hands, this could boost global crop yields and uplift millions of the world’s poorest. It would probably be the biggest agricultural breakthrough since the invention of hybrid rice in the 1970s.
Dandelions and hundreds of other plants naturally do apomixis, but none of the nutritional staples — like rice, corn, or soybeans — do. Mary Gehring, associate professor of plant biology at MIT’s Whitehead Institute, is trying to solve that. We recently sat down to talk about synthetic apomixis and the future of agriculture.
This interview has been edited. Additional notes, my own, are included in parentheses.
Niko McCarty: Hey, Dr. Gehring. It’s hard to understand what the impact of synthetic apomixis might be without first understanding how hybrid seeds are currently produced. Can you explain that process?
Mary Gehring: Many of the seeds that you buy from seed companies are hybrids. It’s easy to make hybrid seeds from some plants, but more difficult in others, depending on where the pollen or female parts are located. Soybeans tend to self-fertilize, so it’s relatively difficult to breed hybrid plants. Rice also self-fertilizes, so it’s tricky. They are fairly expensive to make because you need to make sterile males first, and then breed those with the other female parent, to ensure the plants don’t self-pollinate.
Niko: Do the big seed companies keep a portion of their crops each year to breed the next generation? How do they maintain all the parental lines?
Gehring: Yes, inbred lines have to be carefully maintained. You need to prevent cross-pollination, and you must be sure of the genetic purity of your line each time you plant it. Inbred lines are maintained by just crossing the same genotype to itself over and over again. And in some species, this will just happen through self-fertilization. A hybrid is created by crossing two different inbred lines.
Niko: Hybrid seeds produce larger plants because of something called hybrid vigor. But what does that mean?
Gehring: There are many, many inbred lines. These inbreds have no genetic variation; there’s no diversity. The two alleles are the same for every gene, so this genotype can be propagated indefinitely if you keep breeding that plant. And just like in animals, an inbred line is generally less vigorous than a heterozygote. Many, many years ago people realized that if you cross two inbreds, the resulting F1 will be more vigorous than either parent. That is hybrid vigor. Hybrid plants are generally larger, more robust, more resistant to stresses, and will typically have higher yields.
Niko: Got it.
Gehring: But then, if you take that hybrid plant and self-fertilize it, the progeny will lose this vigor. There'll be a segregation of traits, where some plants are vigorous, like the parent, but some will be more like the inbred grandparent, and some will be even worse than that. Uniformity is generally desired for agriculture. But if you take the progeny of a vigorous hybrid, you would just have this diversity of plant phenotypes, many of which would be negative.
Niko: Ahh, I see. So that’s why big agricultural companies keep generating these hybrids and selling the seeds?
Gehring: Exactly.
Niko: Now tell me about synthetic apomixis. How would it change how hybrid plants are made today?
Gehring: Right. The idea is this: If you could engineer seeds so that they reproduce asexually, then you could pass on the vigorous genotype year after year. You could breed a hybrid plant that's really good for a specific region, and then maintain its traits without having to generate that same hybrid over and over again.
Niko: Do seed companies want to stop research on apomixis? Are they concerned that it could slash into their monopoly on seed supplies?
Gehring: No, I mean, I think companies are actually interested in apomixis because it would make breeding programs so much faster. If you can transmit a genotype without recombination, then that is also good for seed companies because it takes so long to breed plants currently.
Niko: What is the current state of synthetic apomixis? What do we still have to figure out?
Gehring: Yeah, I mean, you've probably come across the recent work in rice. (Researchers altered two genes — called MiMe and BABYBOOM1 — in rice to make “hybrid plants that produce more than 95% of clonal seeds across multiple generations.) But there have been a couple of exciting papers over the past couple years.
There are three main components of apomixis that we need to figure out. The first step is to bypass meiosis so that you make a gamete and an egg cell that is diploid (maintains two copies of each chromosome.) It basically is like a mitotic cell rather than a product of meiosis.
Second, you have to get that diploid cell to make an embryo without fertilization, without the addition of sperm. The third component, which is probably the most complicated and where there's the least progress, is to make the embryo’s nutritive tissue, the endosperm, without fertilization.
Niko: Why is the endosperm important?
Gehring: Well, the endosperm is the part of the plant that we eat. And so the properties, the quality of endosperm, is very important. If your hybrid gives you a particular endosperm quality or phenotype, then you wanna be able to maintain that.
Niko: Got it. And so what have recent papers shown, at least for those first two steps?
Gehring: Well, this really exciting paper came out in rice this year. It showed that they could bypass meiosis in rice to make this diploid egg cell, and then they could induce parthenogenesis (develop an embryo from an unfertilized egg cell) in a hybrid plant. They showed that they could transmit that hybrid phenotype. But the third piece was missing. The endosperm was still a product of sexual fertilization.
Niko: The amazing thing about that paper, from what I understand, is that the engineered hybrid plants produced more than 95% clonal seeds, and they did it across three generations. Is that good enough for the seed companies? Do we need synthetic apomixis to be 100% efficient?
Gehring: I think 95% is amazing. It’s certainly farther than anything else, but you’d probably have to ask a seed company. If you buy a seed, and 95% of its offspring are clonal, is that good enough for farmers? I'm not an expert in agricultural economics, so I don’t know.
Niko: And the paper only did this in one specific type of rice, right? There are thousands of different rice cultivars grown around the world, and something like 3,000 species of rice in India alone. If we figure out synthetic apomixis in one plant, will it be possible to transfer it to another?
Gehring: Yeah, that's really important. Obviously the more lines you can do this in, the more impact it will have. But my guess is that, once we figure out the key genes for a particular species, it will probably be transferable to other genotypes within that species. I don't think that what we develop for rice, say, will work for soybean. I don't think there's going to be a single solution.
Niko: Do you think in 10 years we'll have this figured out?
Gehring: We will probably have it figured out in a laboratory context within 10 years or less. Getting it to farmers as a commercially viable product will take longer.
Niko: And what happens then? What impact would this have on poor farmers, who currently buy expensive seeds from agricultural monopolies?
Gehring: What I’d say is that this probably is not a magic bullet. The question is: Who has this technology? Will it be open access, or will it be in the hands of a company? That’s going to impact how this gets distributed throughout the world. In an ideal world, it would help poor farmers, but I don’t know if that will actually happen.
But synthetic apomixis does have the potential, still, to make agriculture require less inputs and be more resistant to climate variability, because of the vigorous nature of hybrids. Right now, hybrid seeds are too expensive to buy in some cases, right? But if poor farmers could get their hands on hybrid seeds with these traits, they could keep propagating them. So this could still help in places with fewer resources.
Thanks to Will Shaw and Alice Boo for helpful discussions.
Disclosure: The views expressed in this blog are entirely my own and do not represent the views of any company or university with which I am affiliated. | Biology |
image: Where bats are excluded, young tree seedlings are munched by three times more caterpillars and other insects, according to new research from the University of Illinois. view more Credit: Elizabeth Bielke, University of Illinois URBANA, Ill. – Bats help keep forests growing. Without bats to hold their populations in check, insects that munch on tree seedlings go wild, doing three to nine times more damage than when bats are on the scene. That’s according to a groundbreaking new study from the University of Illinois. “A lot of folks associate bats with caves. But as it turns out, the habitat you could really associate with almost every bat species in North America is forest. And this is true globally. Forests are just really important to bats,” says Joy O’Keefe, study co-author and assistant professor and wildlife extension specialist in the Department of Natural Resources and Environmental Sciences at Illinois. “We wanted to ask the question: Are bats important to forests? And in this study, we've demonstrated they are.” Other researchers have demonstrated bats’ insect-control services in crop fields and tropical forest systems, but no one has shown their benefits in temperate forests until now. “It's especially important for us to learn how bats affect forests, given that bats are declining due to diseases like white-nose syndrome or collisions with wind turbines. This type of work can reveal the long-term consequences of bat declines,” says Elizabeth Beilke, postdoctoral researcher and lead author on the study. The research team built giant mesh-enclosed structures in an Indiana forest to exclude the eight bat species that frequent the area, including two federally threatened or endangered species. The mesh openings were large enough to allow insects free movement in and out, but not flying bats. Every morning and evening for three summers, Beilke opened and closed the mesh sides and tops of the structures to ensure birds had daytime access to the plots. That way, she could be sure she was isolating the impacts of bats. Beilke then measured the number of insects on oak and hickory seedlings in the forest understory, as well as the amount of defoliation per seedling. Because she erected an equal number of box frames without mesh, Beilke was able to compare insect density and defoliation with and without bats. Overall, the researchers found three times as many insects and five times more defoliation on the seedlings when bats were excluded than in control plots that allowed bats in each night. When analyzed separately, oaks experienced nine times more defoliation and hickories three times more without bats. “We know from other research that oaks and hickories are ecologically important, with acorns and hickory nuts providing food sources for wildlife and the trees acting as hosts to native insects. Bats use both oaks and hickories as roosts, and now we see they may be using them as sources of prey insects, as well. Our data suggest bats and oaks have a mutually beneficial relationship,” Beilke says. While insect pressure was intense in plots without bat predation, the seedlings didn’t succumb to their injuries. But the researchers say long-term bat declines could prove fatal for the baby trees. “We were observing sublethal levels of defoliation, but we know defoliation makes seedlings more vulnerable to death from other factors such as drought or fungal diseases. It would be hard to track the fate of these trees over 90 years, but I think a natural next step is to examine the impact of persistent low levels of defoliation on these seedlings,” Beilke says. “To what extent does repeated defoliation reduce their competitive ability and contribute to oak declines?” The researchers point out that birds, many of which share the same insect diets as bats, are also declining. While they specifically sought to isolate bats’ impact on forest trees, the researchers are confident insect density and defoliation rates would have been higher if they had excluded both birds and bats in their study. In fact, similar exclusion studies focusing on birds failed to account for bats in their study designs, leaving mesh enclosures up all night. “When we were initially working on the proposal for this research, we looked at 37 different bird exclusion studies, across agriculture and forest systems. We found nearly all of them had made this mistake. Most of them had not opened or removed their treatment plots to bats,” Beilke says. In other words, before Beilke’s study, birds were getting at least partial credit for work bats were doing in the shadows. Clearly, both types of winged predators are important for forest health in temperate systems. And, according to O’Keefe, that makes these studies even more critical to inform forest management. “I think it’s important to stress the value of this type of experimental work with bats, to really try to dig into what their ecosystem services are in a deliberate manner. While we can probably extrapolate out and say bats are important in other types of forest, I wouldn't discount the value of doing the same kind of work in other systems, especially if there are questions about certain insect or tree species and how bats affect them. So rather than extrapolating out across the board, let's do the work to try to figure out how bats are benefiting plants,” she says. “And before they're gone, hopefully.” The article, “Bats reduce insect density and defoliation in temperate forests: an exclusion experiment,” is published in Ecology [DOI: 10.1002/ecy.3903]. The research was supported by USDA’s National Institute of Food and Agriculture, the Indiana State Department of Natural Resources, the Indiana Space Grant Consortium, the Department of Biology at Indiana State University, and the Department of Natural Resources and Environmental Sciences at Illinois. The Department of Natural Resources and Environmental Sciences is in the College of Agricultural, Consumer and Environmental Sciences at the University of Illinois Urbana-Champaign. Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system. | Biology |
Detailed map of the heart provides new insights into cardiac health and disease
The study also presents a new tool that uncovers the effects of drugs on heart rate
In a new study, published today (12 July) in Nature, researchers have produced the most detailed and comprehensive human Heart Cell Atlas to date, including the specialised tissue of the cardiac conduction system – where the heartbeat originates.
The multi-centre team is led by the Wellcome Sanger Institute and the National Heart and Lung Institute at Imperial College London, and has also presented a new drug-repurposing computational tool called Drug2cell, which can provide insights into the effects of drugs on heart rate.
This study is part of the international Human Cell Atlas* (HCA) initiative, which is mapping every cell type in the human body, to transform our understanding of health and disease, and will form the foundation for a fully integrated HCA Human Heart Cell Atlas.
Charting eight regions of the human heart, the work describes 75 different cell states including the cells of the cardiac conduction system – the group of cells responsible for the heartbeat – not understood at such a detailed level (1) in humans before. The human cardiac conduction system, the heart’s ‘wiring’, sends electrical impulses from the top to the bottom of the heart and coordinates the heartbeat.
By using spatial transcriptomics, which gives a “map” of where cells sit within a tissue, researchers were also able to understand how these cells communicate with each other for the first time. This map acts as a molecular guidebook, showing what healthy cells look like, and providing a crucial reference to understand what goes wrong in disease. The findings will help understand diseases such as those affecting the heart rhythm.
The assembly of a Human Heart Cell Atlas is key given that cardiovascular diseases are the leading cause of death globally. Around 20,000 electronic pacemakers are implanted each year in the UK for these disorders (2). These can be ineffective and are prone to complications and side-effects (3). Understanding the biology of the cells of the conduction system and how they differ from muscle cells paves the way to therapies to boost cardiac health and develop targeted treatments for arrhythmias.
The team also presents a new computational tool called Drug2cell. The tool can predict drug targets as well as drug side effects. It leverages single-cell profiles and the 19 million drug-target interactions in the EMBL-EBI ChEMBL database.
Unexpectedly, this tool identified that pacemaker cells express the target of certain medications, such as GLP1 drugs, which are used for diabetes and weight loss and are known to increase the heart rate as a side-effect, the mechanism of which was unclear. This study suggests that the increase in heart rate might be partly due to a direct action of these drugs on pacemaker cells, a finding the team also showed in an experimental stem cell model of pacemaker cells.
“The cardiac conduction system is critical for the regular and coordinated beating of our hearts, yet the cells which make it up are poorly understood. This study sheds new light by defining the profiles of these cells, as well as the multicellular niches they inhabit. This deeper understanding opens the door to better, targeted anti-arrhythmic therapies in the future.”
Dr James Cranley, joint first author, a cardiologist specialising in heart rhythm disorders and PhD student at the Wellcome Sanger Institute
“The mechanism of activating and suppressing pacemaker cell genes is not clear, especially in humans. This is important for improving cell therapy to facilitate the production of pacemaker cells or to prevent the excessive spontaneous firing of cells. By understanding these cells at an individual genetic level, we can potentially develop new ways to improve heart treatments.”
Dr Kazumasa Kanemaru, joint first author and Postdoctoral Fellow in the Gene Expression Genomics team at the Wellcome Sanger Institute
The study unearthed an unexpected discovery: a close relationship between conduction system cells and glial cells. Glial cells are part of the nervous system and are traditionally found in the brain. They have been explored very little in the heart. This research suggests that glial cells are in physical contact with conduction system cells and may play an important supporting role: communicating with the pacemaker cells, guiding nerve endings to them, and supporting their release of glutamate, a neurotransmitter.
Another key finding of the study is an immune structure on the heart’s outer surface. This contains plasma cells, which release antibodies into the space around the heart to prevent infection from the nearby lungs. The researchers also identified a cellular niche enriching for a hormone (4) that could be interpreted as an early warning sign of heart failure.
“We often don’t fully know what impact a new treatment will have on the heart and its electrical impulses – this can mean a drug is withdrawn or fails to make it to the market. Our team developed the Drug2cell platform to improve how we evaluate new treatments and how they can affect our hearts, and potentially other tissues too. This could provide us with an invaluable tool to identify new drugs which target specific cells, as well as help to predict any potential side-effects early on in drug development.”
Dr Michela Noseda, senior Lecturer in Cardiac Molecular Pathology at the National Heart and Lung Institute, Imperial College London, a Coordinator of the Human Cell Atlas Heart BioNetwork and a lead author
“Using cutting-edge technologies, this research provides further intricate detail about the cells that make up specialised regions of the human heart and how those cells communicate with each other. The new findings on the heart’s electrical conduction system and its regulation are likely to open up new approaches to preventing and treating rhythm disturbances that can impair the heart’s function and may even become life-threatening.
“International collaboration is key to scientific progress. This impactful study and other discoveries from the broader Human Cell Atlas initiative are excellent examples of what can be achieved when the international research community works together across borders. Our combined efforts can ultimately produce better outcomes for patients worldwide.”
Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation, which part-funded the research with the German Centre for Cardiovascular Research (DZHK)
“This Heart Cell Atlas reveals cardiac microanatomy in unprecedented detail, including the cardiac conduction system that enables each heartbeat, and is a valuable reference for studying heart disease and designing potential therapeutics. An important contribution to the global Human Cell Atlas initiative, which is mapping every cell type in the body to understand health and disease, it will form the foundation for a fully integrated HCA Human Heart Cell Atlas. In addition, our suite of computational methods will help identify possibilities for repurposing existing drugs to treat diseases in other tissues.”
Dr Sarah Teichmann, a senior author of the study from the Wellcome Sanger Institute and co-chair of the Human Cell Atlas Organising Committee
More information
Human Cell Atlas
*This study is part of the international Human Cell Atlas (HCA) consortium, which is aiming to map every cell type in the human body as a basis for both understanding human health and for diagnosing, monitoring, and treating disease. An open, scientist-led consortium, the HCA is a collaborative effort of researchers, institutes, and funders worldwide, with more than 2,900 members from 94 countries across the globe. The HCA is likely to impact every aspect of biology and medicine, propelling translational discoveries and applications and ultimately leading to a new era of precision medicine.
More information can be found at https://www.humancellatlas.org/
1. Single cell sequencing is a technology that provides cell-specific genetic information. Multi-omics is a biological analysis approach which uses several techniques to obtain a large quantity of data. This can include data from genomics, proteomics, epigenomics or metagenomics studies, all combined to give a holistic view.
2. NICOR report
3. Mirza, M., Strunets, A., et al. (2013) Mechanisms of Arrhythmias and Conduction Disorders in Older Adults. Clin Geriatr Med. 2012 Nov; 28(4): 555–573. DOI: 10.1016/j.cger.2012.08.005
4. They found that some cells located in the heart produce a hormone called Brain Natriuretic Peptide (BNP) which is measured clinically as a biomarker to detect heart failure. This work shows that even in healthy hearts, a small population of muscle cells produces this substance. By comparing with publicly available data from failing hearts researchers found that these same cells grow in number in failing hearts. This opens the door to new therapeutic opportunities to prevent disease progression by targeting specific cell types.
The researchers used novel sequencing techniques, such as single-cell sequencing to analyse which genes are activated in single cells, and spatial transcriptomics. The research includes data from the hearts of 25 healthy organ donors ranging from 20 to 75 years old. Hearts were donated from 25 organ donors whose hearts were healthy but not suitable for organ transplantation for a number of reasons. We are grateful to the deceased donors and their families for their invaluable gift.
Publication:
Kanemaru, K., Cranley, J., et al. (2023) Spatially resolved multiomics of human cardiac niches. Nature. DOI: 10.1038/s41586-023-06311-1 https://www.nature.com/articles/s41586-023-06311-1
Funding:
This research was supported by joint funding from Wellcome, the British Heart Foundation (BHF) and the German Centre for Cardiovascular Research (DZHK), the Chan Zuckerberg Foundation, the National Institute for Health and Care Research (NIHR) Blood and Transplant Research Unit in Organ Donation and Transplantation, the NIHR Imperial Biomedical Research Centre, the Leducq Foundation, the ERC-advanced grant under the European Union Horizon 2020 Research and Innovation Program, and the Deutsche Forschungsgemeinschaft.
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A protein hidden in plain sight helps cells time their escape
When a cell is getting ready to divide, it needs to duplicate its DNA, which is divided among its chromosomes, and arrange the chromosomes so that each new cell gets one complete set. If the chromosomes get sorted incorrectly, the resulting cells with the wrong number or set can become dysfunctional, or even cancerous.
Because the risks are so severe, cells have evolved strong controls to ensure that upon division, each of the daughter cells has the correct chromosomes. If a cell's machinery detects errors while the cell is preparing to divide, division is paused until those errors are corrected.
However, if division gets paused for too long, a state called being in arrest, the cell will eventually die. To escape this fate, every type of cell has a different timer for how long it will stay in arrest before escaping. When the timer runs out, cells exit the process of cell division without completing it, and resume life with double the normal number of chromosomes.
Researchers have wondered what mechanisms determine how long a cell will remain in arrest and how they manage to escape it. The question is particularly important in the context of cancer cells, which can use early escapes from arrest to evolve—changing their sets of chromosomes—and resist common cancer drugs.
New research from Whitehead Institute Member Iain Cheeseman and postdoc Mary-Jane Tsang identifies a way in which cells set their timers for arrest. The key player is a previously undiscovered variant of a known protein, CDC20.
What Cheeseman and Tsang discovered, as published in Nature on April 26, is that cells produce both full-length and shortened, alternative versions of CDC20, and that the shifting ratio of these versions determines when cells will escape arrest.
Alternative proteins like these are very hard to find, because cells don't make them in the way that researchers and common analytic tools typically look for, but researchers including Cheeseman are coming to appreciate their prevalence and importance to biology.
"By looking at data in a new way, we were able to discover this alternative protein that turns out to be central to a very important process in cells," Tsang says. "The protein has been there all along, but no one knew to look for it because the cell doesn't make it in the traditional way."
CDC20—the full-length protein, that is—has a well-known role in cell division. If no issues are detected at the checkpoint before chromosomes are pulled apart, then CDC20 binds to and activates a molecular complex called the anaphase-promoting complex (APC/C), which in turn initiates the end stages of cell division. If an issue is detected, then a mechanism called the spindle assembly checkpoint (SAC) inhibits CDC20, arresting cell division.
Tsang discovered that CDC20 plays another important role at this checkpoint, thanks to its previously undetected alternatives. As a protein, CDC20 is assembled according to a genetic sequence contained in messenger RNA. However, Tsang found that sometimes the machinery translating the CDC20 RNA into protein skips the normal starting point, and begins following the instructions from one of two unofficial starting points farther down the RNA sequence, which causes it to create alternative short versions of the molecule. These short versions vary from the full-length protein in one crucial way: they are not inhibited by the SAC. This means that the cell cannot stop them from activating the APC/C, even in the presence of errors that should arrest cell division.
This difference between versions of CDC20 enables cells to set a timer for arrest. Early in cell division, the APC/C is most likely to be bound by full-length CDC20, because cells produce more of the full-length protein than the alternatives. This keeps the cells responsive to the signal to enter arrest.
As cells spend more time in arrest, they continue to produce all versions of CDC20, but they break down full-length CDC20 faster than the shorter versions. The ratio of full-length to short CDC20 shifts in favor of the short versions. Eventually, the ratio shifts enough that the APC/C is most likely to be bound by short CDC20, which means that the SAC can no longer inhibit it. At this point, the timer runs out: the cells activate the APC/C and escape arrest.
A cell's arrest timer is therefore determined by factors that affect its starting levels of full-length and short CDC20 and the speed at which it makes and breaks them down, such as what machinery the cell has active for translating RNA. These factors vary from cell type to cell type, so different cell types have different length timers. Tsang notes that this is likely not a complete picture of how cells set their timers—other molecules than CDC20 may be able to affect timer duration—but the shift in CDC20 ratio is a key regulator of the process.
Understanding how cells set their timers helps to explain why some cancer cells are better at resisting certain cancer drugs. Drugs that work by trapping cancer cells in arrest (to then be killed) are common treatments for breast, ovarian, and other cancers. The researchers found that different cancer cell lines had different ratios of full-length to short CDC20. This correlated with how long the cells would spend in arrest before escaping, and, correspondingly, to how effective arrest-causing drugs were against them.
Additionally, when Tsang added full-length CDC20 to cells that only had the short version, the cells became more sensitive to the drugs. These findings could be useful for predicting whether arrest-causing drugs will be effective for a given patient, and they also suggest a possible strategy for sensitizing resistant cancer cells.
This work has shifted the Cheeseman lab's focus towards searching for other proteins hiding in plain sight. The mechanism that allows cells to make short variants of CDC20 could do the same for many other proteins, and other mechanisms may also create variant proteins.
"The differential turnover of these forms of CDC20 creates an elegant timer for arrest, and we never would have known that if Mary Jane hadn't looked at CDC20 in a way no one else had thought to before," says Cheeseman, who is also the Herman and Margaret Sokol Professor of Biology at the Massachusetts Institute of Technology. "This work demonstrates that there's a world of hidden biology out there waiting to be discovered."
More information: Mary-Jane Tsang et al, Alternative CDC20 translational isoforms tune mitotic arrest duration, Nature (2023). DOI: 10.1038/s41586-023-05943-7
Journal information: Nature
Provided by Whitehead Institute for Biomedical Research | Biology |
It’s the most famous mathematical sequence in biology—the description of a spiral with a particular ratio found in the evolution of plants going back millions of years, and that is seen today in succulents like this aloe, but also in pineapples, sunflowers, and pinecones.
Named for the Italian mathematician that discovered it, the Fibonacci Sequence, or Fibonacci Spiral, is also known as nature’s secret code, as it also predicts the spiral of invertebrate shells like ammonites and snails.
Now though, scientists have just discovered where its spiral ends, and one would have to go back 407 million years ago.
The Early Devonian Period produced a plant known as the clubmoss, which arranged its leaves in a spiral, but which doesn’t follow the Fibonacci Sequence.
“Spirals are common in plants, with Fibonacci spirals making up over 90% of the spirals,” University of Edinburgh paleontologist Alexander Hetherington and colleagues wrote in their paper describing the discovery.
MORE MATHEMATICS IN LIFE: The Mind-Blowing Mathematics of Snowflakes
“Based on their widespread distribution it has long been assumed that Fibonacci spirals were an ancient feature that evolved in the earliest land plants and became highly conserved in plants.”
They characterize the Fibonacci spiral as being found in the arrangement of their organs around their stems. In most existing plant species, organs emerge at 137.5° from the previous organ. This results in continuous spirals of organs, with the number of clockwise and anticlockwise spirals forming consecutive numbers in a Fibonacci sequence.
The Fibonacci Sequence has also been found in spiral galaxies and large hurricanes. Fans of the band Tool probably know that band leader Maynard James Keenan wrote a song with the lyrics and time signature arranged in the numbers of the Fibonacci Sequence.
Asteroxylon mackiei was a clubmoss that featured among the world’s oldest leaf-bearing plants. The exceptionally preserved fossil subjected to 3D imaging for the study was found in the famous fossil site the Rhynie chert near the Aberdeenshire village of Rhynie in Scotland.
MORE MATHEMATICS IN LIFE: The Mind-Blowing Mathematics of Sunflowers …From Scientific American Magazine on Their 175th Birthday
“The clubmoss Asteroxylon mackiei is one of the earliest examples of a plant with leaves in the fossil record,” said Holly Anne-Turner, the study’s first author. “Using these reconstructions we have been able to track individual spirals of leaves around the stems of these 407 million-year-old fossil plants. Our analysis of leaf arrangement in Asteroxylon shows that very early clubmosses developed non-Fibonacci spiral patterns.”
“This transforms our understanding of Fibonacci spirals in land plants,” the researchers said. It indicates that non-Fibonacci spirals were common in ancient clubmosses and that the evolution of leaf spirals diverged into two separate paths.”
SHARE This Break In Mathematical Evolution With Your Friends… | Biology |
(Credit:Photo credit: Eric Bronson, Michigan Photography.) A mounted skeleton of the Buesching mastodon, based on casts of individual bones produced in fiberglass, on public display at the University of Michigan Museum of Natural History in Ann Arbor. The Buesching mastodon is a nearly complete skeleton of an adult male recovered in 1998 from a peat farm near Fort Wayne, Indiana. A new study, led by Joshua Miller of the University of Cincinnati and Daniel Fisher of the University of Michigan, uses oxygen and strontium isotopes from the mastodon's right tusk to reconstruct changing patterns of landscape use during its lifetime. Just as scientists can determine the age of a tree using its tree rings, scientists can also determine the age of a mastodon using its tusks. And thanks to modern technology, scientists can now understand more about this prehistoric mammal. Researchers from the University of Cincinnati, the University of Michigan and the University of Nebraska-Lincoln used a geochemical process to determine the migration patterns of the Buesching mastodon, and published the findings in a recent study. The Buesching mastodon was first discovered near Fort Wayne, Ind. in 1998. Experts believe a rival mastodon tusk punctured the right side of his skull and killed the mastodon. Researchers believe it had migrated to a summer mating territory — nearly 100 miles away from his home territory — and that a potential mate had been the cause of the fight. Now, with the use of Strontium Isotope Geochemistry, researchers may be able to prove that mastodons were indeed migratory animals. "The result that is unique to this study is that for the first time, we've been able to document the annual overland migration of an individual from an extinct species," says Joshua Miller, the study's first author and University of Cincinnati paleoecologist in a press release. "Using new modeling techniques and a powerful geochemical toolkit, we've been able to show that large male mastodons, like Buesching, migrated every year to the mating grounds," says Miller in a press release.A tree ring can determine age and climate conditions during certain years, and now, the mastodon tusk can determine the types of vegetation the animal was eating, along with the chemical elements in their drinking water. Operating under a microscope, researchers drilled half a millimeter into the 13,000-year-old tusk, and collected powdered residue to chemically analyze. They took over 30 samples from the tusk. Some from the early years of the mastodon's life and some from its final years. After chemically analyzing the residue, researchers were able to find that the strontium isotopes levels, found in certain areas, in the tusk acted like a map to pinpoint where the mastodon had been during his life. The oxygen isotopes also found in the tusk were able to determine what time of year the mastodon spent at a certain location. "Every time you get to the warm season, the Buesching mastodon was going to the same place — bam, bam, bam — repeatedly. The clarity of that signal was unexpected and really exciting," says Miller in a press release. Miller and his colleagues then fed the isotope samples into a movement model, determining that the Buesching mastodon most likely called Central Indiana home, but had ventured into Michigan and other surrounding areas. This is something that has never been done before for an extinct species. "The field of strontium isotope geochemistry is a real up-and-coming tool for paleontology, archaeology, historical ecology and even forensic biology. It's flourishing,” says Miller in a press release. "But, really, we have just scratched the surface of what this information can tell us." | Biology |
Researchers describe the first molecular processes in the eye when light hits the retina
Researchers at the Paul Scherrer Institute PSI have deciphered the molecular processes that first occur in the eye when light hits the retina. The processes—which take only a fraction of a trillionth of a second—are essential for human sight. The study has now been published in the scientific journal Nature.
It only involves a microscopic change of a protein in our retina, and this change occurs within an incredibly small time frame: it is the very first step in our light perception and ability to see. It is also the only light-dependent step. PSI researchers have established exactly what happens after the first trillionth of a second in the process of visual perception, with the help of the SwissFEL X-ray free-electron laser of the PSI.
At the heart of the action is our light receptor, the protein rhodopsin. In the human eye it is produced by sensory cells, the rod cells, which specialize in the perception of light. Fixed in the middle of the rhodopsin is a small kinked molecule: retinal, a derivative of vitamin A. When light hits the protein, retinal absorbs part of the energy. With lightning speed, it then changes its three-dimensional form so the switch in the eye is changed from "off" to "on." This triggers a cascade of reactions whose overall effect is the perception of a flash of light.
Tied, yet free
But what happens in detail when retinal transforms from what is known as the 11-cis form into the all-trans form? "We have known about the starting point and the end product of the retinal transformation for some time, but so far no one has been able to observe in real time exactly how the change occurs in the sight pigment rhodopsin," says Valérie Panneels, a scientist with PSI's Biology and Chemistry Research Division.
Panneels compares the process to a cat falling back-first from a tree but somehow landing on its feet unharmed. "The question is: what states does the cat adopt during its fall as it rights itself to land on its feet?"
As the PSI scientists discovered, the "retinal cat" starts off by turning the middle of its body. For Valerie Panneels, the "eureka moment" came when she realized something else that occurs: the protein absorbs part of the light energy to briefly inflate a tiny amount—"like our chest expanding when we breathe in, only to contract again shortly afterwards."
During this "breathing in" stage, the protein temporarily loses most of its contact with the retinal that sits in its middle. "Although the retinal is still connected to the protein at its ends through chemical bonds, it now has room to rotate." At that moment, the molecule resembles a dog on a loose leash that is free to give a jerk.
Shortly afterwards the protein contracts again and has the retinal firmly back in its grasp, except now in a different more elongated form. "In this way the retinal manages to turn itself, unimpaired by the protein in which it is held."
One of the fastest natural processes
The transformation of the retinal from 11-cis kinked form into the all-trans elongated form only takes a picosecond, or one trillionth (10-12) of a second, making it one of the fastest processes in all of nature.
The only way of recording and analyzing such rapid biological processes is with an X-ray free-electron laser like the SwissFEL. "The SwissFEL allows us to study in detail the fundamental processes of the human body, such as vision," says Gebhard Schertler, Head of PSI's Biology and Chemistry Research Division and joint lead author of the study along with Valérie Panneels.
To return to the analogy of the cat, this would be like filming its fall with a high-speed camera, but with one major difference: the filming speed of the SwissFEL camera is a million times faster. Working with large research facilities also involves much more than simply pressing a shutter button. The Ph.D. student Thomas Gruhl, who went on to work as a postdoc researcher at the Institute for Structural and Molecular Biology in London, has spent years developing a method of producing high-quality rhodopsin crystals capable of delivering ultra-high resolution data. Ultimately only these data made it possible to perform the necessary measurements at SwissFEL and—before the SwissFEL was built—at the X-ray free-electron laser SACLA in Japan.
This experiment once again shows SwissFEL's vital role in Swiss research. "It will probably help us come up with many more solutions in future," says Gebhard Schertler. "Amongst other things, we are also developing methods for investigating dynamic processes in proteins that are not normally activated by light." The scientists use artificial means to make such molecules responsive to light: either they make appropriate changes to the binding partners or they mix proteins with binding partners in the crystal so quickly that they can be examined at the SwissFEL. In any case, the procedure involved is definitely much more complicated than simply pointing a camera at a cat falling from a tree.
More information: Valerie Panneels, Ultrafast structural changes direct the first molecular events of vision, Nature (2023). DOI: 10.1038/s41586-023-05863-6. www.nature.com/articles/s41586-023-05863-6
Journal information: Nature
Provided by Paul Scherrer Institute | Biology |
Lung cancer radiotherapy From left to right: xenon-enhanced ventilation CT, showing a right upper lung tumour causing obstruction and non-ventilation; functional lung evaluation; registration with simulation CT; standard plan; functional-lung-avoidance plan. The arrows highlight regions with the most prevalent functional lung sparing. (Courtesy: Int. J. Radiat. Oncol. Biol. Phys. 10.1016/j.ijrobp.2022.07.034) Radiation therapy for patients with lung cancer may be less toxic using a functional lung avoidance treatment plan guided by xenon-enhanced ventilation CT (XeCT). In a clinical study at the National Taiwan University Hospital, only 17% of patients developed radiation pneumonitis, the most severe radiation-induced adverse effect, a significant improvement compared to historic norms.
Chemoradiotherapy is the recommended treatment for inoperable or locally advanced non-small cell lung cancer (NSCLC), but toxicities from this treatment are a significant concern. Approximately 30% of patients develop grade 2 or higher radiation pneumonitis (lung inflammation), which seriously affects their quality-of-life.
Currently, radiotherapy treatment planning is based on anatomic imaging and the premise that all lung tissues are equally important. But for lung cancer patients with chronic pulmonary disease, dose may be more accurately delivered based on functional, rather than anatomical, lung volume – a hypothesis that is now being investigated worldwide.
Principal investigators: Yu-Sen Huang (left) and Yuen-Chung Chang (right) of the National Taiwan University College of Medicine. (Courtesy: Yuen-Chung Chang)
Principal investigators Yu-Sen Huang and Yuen-Chung Chang, also at the National Taiwan University College of Medicine, and colleagues tested this approach in a phase 2 clinical trial of 36 patients with NSCLC. They investigated whether radiotherapy planning guided by XeCT, which has been proven feasible and safe for visualizing lung ventilation, could reduce the rate of grade 2 or higher radiation pneumonitis. The idea is to use the XeCT images to minimize radiation dose to regions of functional lung, while favouring radiation deposition in areas of non-functioning lung.
For the study, patients initially underwent pre-treatment XeCT and pulmonary function tests to determine lung ventilation. Each subject had an unenhanced baseline CT scan of the whole thorax, followed by a five-cycle respiration with a xenon gas rebreathing system (during which they inhaled a mixture of 30% nonradioactive xenon and 70% oxygen) and then a XeCT scan during breath-hold at full inspiration. Finally, patients inhaled 100% oxygen for 1 min, and underwent a post-washout XeCT at full inspiration. The total time for the XeCT exam was 20–25 minutes.
The XeCT images displayed the ventilated areas of lung enhanced by xenon in colour, and areas with poor or no enhancement as black. After subtracting baseline CT images from the xenon wash-in images, the researchers generated xenon-enhanced functional lung volumes and imported them into the treatment planning system for registration with the planning CT.
The researchers created a standard plan without reference to XeCT, and a functional-lung-avoidance plan (fAP) optimized to lower dose to functional lung without compromising target volume coverage and organ-at-risk dose constraints. They treated all patients with fAP, using intensity-modulated radiotherapy or volumetric-modulated arc therapy to deliver 60 Gy of thoracic irradiation in 30 fractions. The patients were followed up with chest CT and clinical examinations at 90-day intervals.
Writing in the International Journal of Radiation Oncology Biology Physics, the researchers report that total functional lung sparing was significantly better in the fAP treatments. The total functional lung volume receiving more than 20 Gy decreased from 23.3% to 20.6% and the mean lung dose from 14.3 to 12.4 Gy. Importantly, the predicted risk of grade 2 or greater radiation pneumonitis reduced from 5.7% to 4.0%, while the predicted risk of developing symptomatic radiation pneumonitis within six months of treatment decreased from 6.3% to 4.4%. Read more Neural network generates lung ventilation images from CT scans Five of the 36 patients developed grade 2 radiation pneumonitis and one developed grade 3 radiation pneumonitis, significantly lower than expected from historical controls. There were no grade 4 or greater toxic effects. The researchers point out, however, that the advantage of providing better sparing of the functional lung was counterbalanced by a higher maximal dose within the targets and less conformal target dose distributions.
Despite its benefits, XeCT is expensive and limited in availability, and requires strong cooperation between the radiology and radiation oncology departments. The researchers also acknowledge that recent technological advances in modern radiotherapy may outweigh the expected benefits of fAP treatments. But they believe that their study provides robust evidence for the benefit of XeCT-guided functional lung avoidance in radiotherapy, and are continuing their research. | Biology |
A massive hammerhead shark that recently washed up dead on a beach in Alabama was carrying 40 unborn pups, a necropsy (animal autopsy) has revealed. But it is unclear what killed the expectant mother.
The female great hammerhead (Sphyrna mokarran), which measured around 14 feet (4.3 meters) long, was discovered April 20 in the shallows near Orange Beach. A group of passersby pulled the lifeless giant onto the beach and contacted the city's coastal resources team, who recovered the corpse, city officials wrote on Facebook (opens in new tab).
The dead shark was in such good condition that officials contacted researchers at Mississippi State University's Marine Fisheries Ecology (MFE) group, who carried out a necropsy on the shark the next day.
The team found that the hammerhead was carrying 40 pups, each around 1.5 feet (0.4 m) long. The brood and the mother were likely already dead before they washed ashore, according to city officials.
"While it was very sad that the shark passed," the team's findings could help vastly improve what we know about this species' reproduction, city officials wrote.
Great hammerheads are listed as critically endangered, according to the International Union for Conservation of Nature (IUCN) Red List of Threatened Species (opens in new tab). There are no clear estimates on how many are left globally, but they are believed to be decreasing year on year.
During the necropsy, the team removed and examined key organs, including the mother shark's heart, liver, esophagus, stomach, spleen, kidneys and pancreas. There were no signs of trauma or disease in any of these body parts, MFE representatives wrote on Facebook (opens in new tab). They also sent of samples from the animal's vertebrae, muscle tissue and fins to be further analyzed in the lab.
The shark's stomach was empty — normally a red flag during a necropsy — but female hammerheads often go without food for several months while pregnant, so this was expected, MFE representatives wrote.
Although MFE researchers could not determine a cause of death, they suspect it may be fishing-related.
"We know that great hammerheads are especially prone to the physiological effects of capture stress, more so than most other shark species," they wrote, adding that pregnancy can compound this physiological stress.
Capture-induced stress was also linked to a failed shark pregnancy last year. In May 2022, a dead juvenile thresher shark (Alopias vulpinus) washed up on a U.K. beach. Experts suggested that the shark, which was not fully developed, had likely been aborted by its mother after she was accidentally caught and released by fishers.
Although the baby hammerhead sharks will never be born, they will have a second life in the education system. The pups will be preserved and donated to local classrooms to help teach children about sharks and reproduction, MFE representatives wrote.
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Harry is a U.K.-based staff writer at Live Science. He studied Marine Biology at the University of Exeter (Penryn campus) and after graduating started his own blog site "Marine Madness," which he continues to run with other ocean enthusiasts. He is also interested in evolution, climate change, robots, space exploration, environmental conservation and anything that's been fossilized. When not at work he can be found watching sci-fi films, playing old Pokemon games or running (probably slower than he'd like). | Biology |
A growing pile of evidence indicates that the tens of trillions of microbes that normally live in our intestines — the so-called gut microbiome — have far-reaching effects on how our bodies function. Members of this microbial community produce vitamins, help us digest food, prevent the overgrowth of harmful bacteria and regulate the immune system, among other benefits. Now, a new study suggests that the gut microbiome also plays a key role in the health of our brains, according to researchers from Washington University School of Medicine in St. Louis. The study, in mice, found that gut bacteria — partly by producing compounds such as short chain fatty acids — affect the behavior of immune cells throughout the body, including ones in the brain that can damage brain tissue and exacerbate neurodegeneration in conditions such as Alzheimer’s disease. The findings, published Jan. 13 in the journal Science, open up the possibility of reshaping the gut microbiome as a way to prevent or treat neurodegeneration. “We gave young mice antibiotics for just a week, and we saw a permanent change in their gut microbiomes, their immune responses, and how much neurodegeneration related to a protein called tau they experienced with age,” said senior author David M. Holtzman, MD, the Barbara Burton and Reuben M. Morriss III Distinguished Professor of Neurology. “What’s exciting is that manipulating the gut microbiome could be a way to have an effect on the brain without putting anything directly into the brain.” Evidence is accumulating that the gut microbiomes in people with Alzheimer’s disease can differ from those of healthy people. But it isn’t clear whether these differences are the cause or the result of the disease — or both — and what effect altering the microbiome might have on the course of the disease. To determine whether the gut microbiome may be playing a causal role, the researchers altered the gut microbiomes of mice predisposed to develop Alzheimer’s-like brain damage and cognitive impairment. The mice were genetically modified to express a mutant form of the human brain protein tau, which builds up and causes damage to neurons and atrophy of their brains by 9 months of age. They also carried a variant of the human APOE gene, a major genetic risk factor for Alzheimer’s. People with one copy of the APOE4 variant are three to four times more likely to develop the disease than people with the more common APOE3variant. Along with Holtzman, the research team included gut microbiome expert and co-author Jeffrey I. Gordon, MD, the Dr. Robert J. Glaser Distinguished University Professor and director of the Edison Family Center for Genome Sciences & Systems Biology; first author Dong-Oh Seo, PhD, an instructor in neurology; and co-author Sangram S. Sisodia, PhD, a professor of neurobiology at the University of Chicago. When such genetically modified mice were raised under sterile conditions from birth, they did not acquire gut microbiomes, and their brains showed much less damage at 40 weeks of age than the brains of mice harboring normal mouse microbiomes. When such mice were raised under normal, nonsterile conditions, they developed normal microbiomes. A course of antibiotics at 2 weeks of age, however, permanently changed the composition of bacteria in their microbiomes. For male mice, it also reduced the amount of brain damage evident at 40 weeks of age. The protective effects of the microbiome shifts were more pronounced in male mice carrying the APOE3 variant than in those with the high-risk APOE4variant, possibly because the deleterious effects of APOE4canceled out some of the protection, the researchers said. Antibiotic treatment had no significant effect on neurodegeneration in female mice. “We already know, from studies of brain tumors, normal brain development and related topics, that immune cells in male and female brains respond very differently to stimuli,” Holtzman said. “So it’s not terribly surprising that when we manipulated the microbiome we saw a sex difference in response, although it is hard to say what exactly this means for men and women living with Alzheimer’s disease and related disorders.” Further experiments linked three specific short-chain fatty acids — compounds produced by certain types of gut bacteria as products of their metabolism — to neurodegeneration. All three of these fatty acids were scarce in mice with gut microbiomes altered by antibiotic treatment, and undetectable in mice without gut microbiomes. These short-chain fatty acids appeared to trigger neurodegeneration by activating immune cells in the bloodstream, which in turn somehow activated immune cells in the brain to damage brain tissue. When middle-aged mice without microbiomes were fed the three short-chain fatty acids, their brain immune cells became more reactive, and their brains showed more signs of tau-linked damage. “This study may offer important insights into how the microbiome influences tau-mediated neurodegeneration, and suggests therapies that alter gut microbes may affect the onset or progression of neurodegenerative disorders,” said Linda McGavern, PhD, program director at the National Institute of Neurological Disorders and Stroke (NINDS), which provided some of the funding for the study. The findings suggest a new approach to preventing and treating neurodegenerative diseases by modifying the gut microbiome with antibiotics, probiotics, specialized diets or other means. “What I want to know is, if you took mice genetically destined to develop neurodegenerative disease, and you manipulated the microbiome just before the animals start showing signs of damage, could you slow or prevent neurodegeneration?” Holtzman asked. “That would be the equivalent of starting treatment in a person in late middle age who is still cognitively normal but on the verge of developing impairments. If we could start a treatment in these types of genetically sensitized adult animal models before neurodegeneration first becomes apparent, and show that it worked, that could be the kind of thing we could test in people.” Method of Research Experimental study Subject of Research Animals Article Title ApoE isoform- and microbiota-dependent progression of neurodegeneration in a mouse model of tauopathy. Article Publication Date 13-Jan-2023 COI Statement D.M.H is a cofounder of C2N Diagnostics, LLC, and is on the scientific advisory board and/or consults for Genentech, Denali, C2N Diagnostics, Cajal Neurosciences, and Alector. D.M.H. is an inventor on a patent licensed by Washington University to C2N Diagnostics on the therapeutic use of anti-tau antibodies and a patent licensed by Washington University to Eli Lilly on a humanized anti-Ab antibody. The Holtzman laboratory receives research grants from the National Institutes of Health, Cure Alzheimer’s Fund, the Rainwater Foundation, the JPB Foundation, Good Ventures, Novartis, Eli Lilly, and NextCure. The authors declare no other competing interests. Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system. | Biology |
Abstract
Genetic liability to substance use disorders can be parsed into loci that confer general or substance-specific addiction risk. We report a multivariate genome-wide association meta-analysis that disaggregates general and substance-specific loci from published summary statistics of problematic alcohol use, problematic tobacco use, cannabis use disorder and opioid use disorder in a sample of 1,025,550 individuals of European descent and 92,630 individuals of African descent. Nineteen independent single-nucleotide polymorphisms were genome-wide significant (P < 5 × 10–8) for the general addiction risk factor (addiction-rf), which showed high polygenicity. Across ancestries, PDE4B was significant (among other genes), suggesting dopamine regulation as a cross-substance vulnerability. An addiction-rf polygenic risk score was associated with substance use disorders, psychopathologies, somatic conditions and environments associated with the onset of addictions. Substance-specific loci (9 for alcohol, 32 for tobacco, 5 for cannabis and 1 for opioids) included metabolic and receptor genes. These findings provide insight into genetic risk loci for substance use disorders that could be leveraged as treatment targets.
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Data availability
The MVP summary statistics were obtained via an approved dbGaP application (phs001672.v4.p1). For details on the MVP, see https://www.research.va.gov/mvp/ and ref. 76. This research is based on data from the MVP, Office of Research and Development, Veterans Health Administration, and was supported by the Veterans Administration Cooperative Studies Program award G002.
The datasets used for the BioVU analyses described were obtained from Vanderbilt University Medical Center’s biorepository, which is supported by numerous sources: institutional funding, private agencies and federal grants. These include the National Institutes of Health-funded Shared Instrumentation grant S10RR025141; and Clinical and Translational Science Awards (CTSA) grants UL1TR002243, UL1TR000445 and UL1RR024975. Genomic data are also supported by investigator-led projects that include U01HG004798, R01NS032830, RC2GM092618, P50GM115305, U01HG006378, U19HL065962 and R01HD074711; and additional funding sources listed at https://victr.vumc.org/biovu-funding/.
Data from Yale–Penn 1 are available through dbGAP accession no phs000425.v1.p1 including 1,889 African American subjects and 1,020 European-American subjects. Yale–Penn 1 data are also available through dbGAP accession no phs000952.v1.p1 including 1,531 African American subjects and 1,339 self-reported European-American subjects. Summary statistics for all Yale–Penn data are available on request to J.G. ([email protected]).
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Acknowledgements
The authors would like to thank Cold Harbor Labroatory for posting a preprint of this work on MedRxiv (https://www.medrxiv.org/). The authors thank Million Veteran Program (MVP) staff, researchers and volunteers, who have contributed to MVP, and especially participants who previously served their country in the military and now generously agreed to enroll in the study. Funding: K01 AA030083 (A.S.H.), T32 DA007261 (A.S.H.), DA54869 (A.A., J.G., H.E.), R01 DA54750 (A.A., R.B.), K02 DA32573 (A.A.), R21 AA027827 (R.B.), U01 DA055367 (R.B.), K01 DA51759 (E.C.J.), K23 MH121792 (N.R.K.), DP1 DA54394 (S.S.-R.), T32 MH014276 (G.A.P.), R01 AA027522 (A.E.), F31 AA029934 (S.E.P.), R01 MH120219 (E.M.T.-D., A.D.G.), RF1 AG073593 (E.M.T.-D., A.D.G.), P30 AG066614 (E.M.T.-D.), P2CHD042849 (E.M.T.-D.), R33 DA047527 (R.P., G.A.P.) and T32 AA028259 (J.D.D.)
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H.R.K. is a member of advisory boards for Dicerna Pharmaceuticals, Sophrosyne Pharmaceuticals and Enthion Pharmaceuticals; a consultant to Sobrera Pharmaceuticals; and a member of the American Society of Clinical Psychopharmacology’s Alcohol Clinical Trials Initiative, which was supported in the last three years by Alkermes, Dicerna, Ethypharm, Lundbeck, Mitsubishi and Otsuka. H.R.K. and J.G. hold US Patent 10900,082: ‘Genotype-guided dosing of opioid agonists’ issued on 26 January 2021. The remaining authors declare no competing interests.
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Hatoum, A.S., Colbert, S.M.C., Johnson, E.C. et al. Multivariate genome-wide association meta-analysis of over 1 million subjects identifies loci underlying multiple substance use disorders. Nat. Mental Health 1, 210–223 (2023). https://doi.org/10.1038/s44220-023-00034-y
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DOI: https://doi.org/10.1038/s44220-023-00034-y | Biology |
High-quality sequencing of nearly the entire kākāpō population, funded through a Genomics Aotearoa project, is helping New Zealand to manage the health of this critically endangered species.
Not only is it already making a difference to kākāpō survival, but establishing sequencing methods to work with populations under threat is also likely to be the foundation for the future of endangered wildlife science in New Zealand and the rest of the world.
The state-of-the-art methods developed by Dr. Joseph Guhlin (University of Otago ) and an international team to study kākāpō has revealed important aspects of kākāpō biology. The methods, reusable code, and pipeline is a blueprint and tool for conservation genomics in other species, especially intensively managed species. This has massive implications.
Dr. Guhlin's work over the last year have two very significant outcomes:
This has given researchers the tools needed to identify specific genetic characteristics that are crucial to survival.
"Using technology created by Google, we have achieved what is likely the highest quality variant dataset for any endangered species in the world. This dataset is made available, through DOC and Ngai Tahu, for future researchers working with kākāpō," Dr Guhlin said.
Department of Conservation's Science Advisor for kākāpō Recovery, Dr. Andrew Digby, believes the genetic tools this study provides will make an immense difference to kākāpō conservation.
"kākāpō suffer from disease and low reproductive output, so by understanding the genetic reasons for these problems, we can now help mitigate them. It gives us the ability to predict things like kākāpō chick growth and susceptibility to disease, which changes our on-the-ground management practices and will help improve survival rates."
While the study marks the beginning of a new era of kākāpō conservation genetics, Dr Digby acknowledges what it means for the future of all threatened species.
"The Kakapo125+ project is a great example of how genetic data can assist population growth. The novel genetic and machine learning tools developed can be applied to improve the productivity and survival of other taonga under conservation management."
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Cellular Atlas of Amygdala Reveals New Treatment Target for Cocaine Addiction
Findings could help address an unmet medical need and shed light on the molecular underpinnings of addiction
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Researchers at University of California San Diego School of Medicine and the Salk Institute for Biological Studies have created a unique, cell-by-cell atlas of the amygdala, a small structure deep within the brain that plays a crucial role in controlling emotional responses to drugs. The findings, published October 5, 2023 in Nature Neuroscience, helped the researchers identify a potential new treatment for cocaine addiction, a disease that is poorly understood at the molecular level and has virtually no approved pharmacological treatments.
“There are some drugs that can help treat other addictions, such as those to opioids or nicotine, but there are currently no safe and effective drugs approved for cocaine addictions,” said co-senior author Francesca Telese, PhD, an associate professor in the Department of Psychiatry at UC San Diego School of Medicine. “These findings help address that problem and could also point to universal molecular mechanisms of addiction that we haven’t understood until now.”
Cocaine is a widely used illicit drug and addiction to cocaine is a major public health concern, associated with a rising number of overdose deaths and a high rate of relapse. Despite the threat cocaine addiction poses, not every person who uses cocaine develops an addiction. According to the National Institute on Drug Abuse, an estimated 4.8 million people used cocaine in 2021, while only 1.4 million people had a cocaine use disorder.
“Some people use cocaine recreationally and never develop an addiction, while others are extremely susceptible to addiction after very little exposure to the drug or may relapse even after years of abstinence,” said Telese “Our long-term goal is to understand why there are these inter-individual differences in drug addiction behavior.”
The researchers studied brain samples from rats that had been allowed to self-administer cocaine for an extended period before being cut off from the drug for a period of abstinence. These samples were obtained from the cocaine brain bank at UC San Diego, established by study co-authors Abraham A. Palmer, PhD, and Olivier George, PhD, both professors in the Department of Psychiatry at UC San Diego School of Medicine.
“The cocaine brain bank is an exceptional resource and was invaluable for this study because it allowed us to study a cohort of rats with a large amount of genetic variety, which mimics the diversity we see in human populations,” said Telese. “Further, using a model of cocaine addiction where rats administered the drug to themselves let us look at the connection between our molecular discoveries and actual addiction behaviors.”
The team used single-cell sequencing to determine what genes were expressed in individual cells from the rats’ amygdala, a part of the brain that is central to processing emotions and is highly active in people with addictions.
"Being able to look at individual amygdala cells from rats with different vulnerabilities to addiction was an asset for our study because we wanted to understand how specific cell populations of the amygdala contribute to addiction development,” Telese added.
To make sense of the large amount of data generated through their sequencing experiments, Telese collaborated closely with bioinformatics expert and co-senior author Graham McVicker, PhD, an associate professor at the Salk Institute of Biological Studies and an assistant adjunct professor in the Department of Cellular & Molecular Medicine at UC San Diego School of Medicine. Jess Zhou, a UC San Diego graduate student working with McVicker, developed the bioinformatics workflow needed to assemble their sequencing data into a molecular atlas of the rat amygdala.
The results revealed never-before-seen connections between addiction behaviors and genes involved in energy metabolism.
“This tells us that energy metabolism may be playing a key role in the activity of neurons in the amygdala and that this effect could be contributing to addiction-like behaviors,” said Telese. “This is a brand-new way of thinking about the molecular biology of cocaine addiction.”
In addition to identifying molecular factors that influence cocaine addiction behaviors, the researchers were able to test a drug in the rats that helped reverse these behaviors by targeting an enzyme involved in both energy metabolism and signaling between neurons.
“The fact that we were able to link our findings at the cellular level to behaviors exhibited in the rats and were even able to modify these behaviors with a drug puts us one step closer to understanding the extremely complex mechanisms in the brain driving addiction and relapse,” added Telese.
The researchers are now working on larger sample-size studies that can help determine how much of the effects they observed were based on preexisting genetics in the rats and how much were based on responses to extensive cocaine usage.
“This research suggests that preexisting genetics may play a much bigger role in addiction than we’ve previously understood,” said Telese. “Unraveling these genetics will be key to improving personalized medicine for addictions. If we don’t understand the risk of relapse in individual people, we can’t fully understand the disease.”
Co-authors of the study include: Giordano de Guglielmo, Marsida Kallupi, Narayan Pokhrel, Apurva S. Chitre, Daniel Munro, Hai-Ri Li and Lieselot LG Carrette at UC San Diego, Aaron J. Ho at the Salk Institute for Biological Studies and Pejman Mohammadi at Scripps Research and University of Washington.
The study was funded, in part, by the National Institutes of Health (grants U01DA050239, F31DA056226, U01DA043799, P50DA037844 and R01GM140287), the Brain and Behavior Research Foundation and the Tobacco Related Disease Research Program (grant T31KT1859 UC).
Disclosures: Abraham A. Palmer holds a patent related to the use of GLO1 inhibitors (US20160038559, active).
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Science & Technology New study tracks cephalopod nervous system development, finds striking similarities to process of vertebrates Four squid embryos in their egg sac. These are the squid species Doryteuthis pealeii. Credit: Kristen Koenig New study tracks cephalopod nervous system development, finds striking similarities to process of vertebrates Cephalopods are capable of some truly impressive behaviors. They can quickly process information to transform shape, color, and even texture, blending in with their surroundings. They can also communicate with one another, show signs of spatial learning, and use tools to solve problems. They are so smart they even get bored and start making mischief.
It’s no secret what makes this all possible: These marine animals, which include octopus, squid, and their cuttlefish cousins, have the most complex brains of any invertebrates on the planet. What remains something of a mystery, however, is how cephalopods developed those big brains in the first place. A Harvard lab that studies the visual systems of these soft-bodied creatures — which is where two-thirds of their central processing tissue are focused — believe they’ve come close to figuring it out.
Researchers from the FAS Center for Systems Biology describe in a new study how they used a new live-imaging technique to watch neurons being created in squid embryos almost in real-time. They were then able to track those cells through the development of the nervous system in the retina.
They were surprised to discover that these neural stem cells behaved very much like those in vertebrates during nervous-system development. The results suggest that while vertebrates and cephalopods diverged from one other 500 million years ago, the process by which both developed big brains was similar. In addition the way the cells act, divide, and are shaped may essentially follow a kind of blueprint required for this kind of nervous system.
“Our conclusions were surprising because a lot of what we know about nervous system development in vertebrates has long been thought to be special to that lineage,” said Kristen Koenig, a John Harvard Distinguished Fellow and senior author of the study. “By observing the fact that the process is very similar, what it suggested to us is that these two independently evolved, very large nervous systems are using the same mechanisms to build them. What that suggests is that those mechanisms — those tools — the animals use during development may be important for building big nervous systems.”
The scientists from the Koenig Lab focused on the retina of a squid called Doryteuthis pealeii, more simply a longfin inshore squid. The squid grow to be about a foot long and are abundant in the northwest Atlantic Ocean. The embryos look like adorable anime characters with big heads and eyes. Late-stage squid embryos in their egg sack. Credit: Kristen Koenig The researchers employed similar techniques to those regularly used to study model organisms, like fruit flies and zebrafish. They created special tools and made use of cutting-edge microscopes that can take high-resolution images every 10 minutes for hours on end to see how individual cells behave. The researchers used florescent dyes to mark the cells so they could map them and track them.
This live-imaging technique allowed the team to observe stem cells called neural progenitor cells and how they are organized. The cells formed a special kind of structure called a pseudostratified epithelium. Its main feature is that the cells are elongated so they can be densely packed. Researchers also saw the nucleus of these structures move up and down before and after dividing. This movement is important for keeping the tissue organized and allowing for continued growth, they said.
This type of structure is universally seen in brain and eye development in vertebrate species. It long has been considered one of the reasons the vertebrate nervous system could grow so large and complex. Scientists have observed examples of this type of neural epithelium in other animals, but the squid tissue was also strikingly similar to that of vertebrates in size, organization, and nucleus movement.
The research was led by Francesca R. Napoli and Christina M. Daly, research assistants in the Koenig Lab.
Next, the lab plans to look at how different cell types in cephalopod brains emerge. Koenig wants to determine whether they’re expressed at different times, how they decide to become one type of neuron versus another, and whether this action is similar across species.
“One of the big takeaways from this type of work is just how valuable it is to study the diversity of life,” Koenig said. “By studying this diversity, you can actually really come back to fundamental ideas about even our own development and our own biomedically relevant questions. You can really speak to those questions.” | Biology |
For the first time ever, researchers have succeeded in cryopreserving and reviving pieces of adult coral—a breakthrough that could eventually help save reefs struggling from the effects of climate change.
Using antifreeze and liquid nitrogen, scientists froze coral fragments in a glasslike state, then thawed and returned them to seawater. For 24 hours after the corals were revived, they consumed oxygen at a rate comparable to corals that had never been cryopreserved, the team reports in a new study published last week in Nature Communications.
This new method could one day preserve other organisms—even human organs—for decades, says marine biologist Mary Hagedorn, a research scientist at the Smithsonian’s National Zoo and Conservation Biology Institute and a co-author of the study. The breakthrough comes at a critical moment for coral reefs, which are facing heightened threats from warming oceans.
“Coral reefs are essential to the baseline health of our oceans, and cryo-conservation of endangered coral species can help to ensure that these invaluable and marvelous organisms do not go extinct,” Matthew Powell-Palm, a mechanical engineer at Texas A&M University and the paper’s lead author, says in a statement.
The new cryopreservation process has been years in the making. Hagedorn and her collaborators previously pioneered the cryopreservation of coral sperm, with techniques similar to those used in human sperm banks.
But while sperm—which are single-celled—are generally easier to freeze than a more complex adult coral, they can be incredibly difficult to collect. Corals often dwell in remote and hard-to-reach areas on the seafloor, and they’ll usually release their sperm on only a few days each year—leaving a narrow window for the researchers to act.
“It can be very, very challenging to get there at the right time,” Hagedorn says. “One year, we missed it by a whole month, because they spawned early because the water was warm.” Another year, the team was hit by a hurricane, and they had to abandon their work.
Corals are extremely sensitive to temperature changes. If it gets too hot, they will expel the algae living in their tissues and turn completely white. This process, known as coral bleaching, stresses the organisms and makes them more susceptible to death and disease.
Climate change, overfishing and pollution have already contributed to the disappearance of half the planet’s coral reefs since 1950. The Earth lost 14 percent of its reefs—an area larger than all the coral currently living in Australia—in just one decade, between 2009 and 2018. And researchers have predicted the crisis will only get worse.
A 2018 report from the Intergovernmental Panel on Climate Change estimated with high confidence that the world’s coral reefs would decline by 70 to 90 percent with 1.5 degrees Celsius of warming over pre-industrial levels. Currently, the planet is projected to reach that threshold between 2030 and 2052, if temperatures continue to rise at the current rate. And if air temperatures rise by 2 degrees Celsius, reefs will decline by 99 percent.
“Coral reefs are simply too valuable to lose,” Joe Pollock, a senior coral reef resilience scientist with the Nature Conservancy’s Hawaii and Palmyra Programs who was not involved in the research, says in an email. “They support over a quarter of marine life, protect our coastlines during storms and contribute an estimated $375 billion to the global economy annually.”
This year, temperatures are hitting historic highs. July 2023 was the hottest ever on record, and seawater temperatures above 100 degrees Fahrenheit in Florida caused mass coral death and bleaching. As the ocean continues to warm, bleaching will become more consistent, Hagedorn says.
With environmental pressure on the reefs rising, the researchers needed a cryopreservation strategy that was more effective than focusing on sperm.
“We felt like we needed to go faster,” Hagedorn says. “We’re going too slow. … It’s important that we get the genetic diversity and biodiversity while it still exists.”
So, in 2019, Hagedorn and her colleagues—including researchers at the University of California, Berkeley, and Texas A&M University—began their work to cryopreserve and revive entire pieces of finger coral (Porites compressa) from Hawaii. Using their new process, called isochoric vitrification, they preserved coral fragments, each consisting of about 20 individual polyps within a calcium carbonate skeleton. These are among the most complex organisms to be cryopreserved and thawed successfully.
“This work progresses the field by expanding cryopreservation of corals beyond sperm and symbionts to include entire coral fragments,” Pollock says. “Barriers still exist to rearing these fragments beyond a day to two post-thaw, but this is certainly a noteworthy advance.”
The process is relatively simple, Hagedorn says. First, researchers find a healthy adult coral and harvest off a thinly sliced chunk about the size of a human thumbnail. They bleach the coral and place the fragment into a small aluminum cylinder filled with an antifreeze solution. While the goal is to freeze the coral piece, the team must avoid ice formation, which would damage the animal’s tissue. Finally, the cylinder is dunked into liquid nitrogen and cooled to nearly minus 321 degrees Fahrenheit, causing the coral to rapidly freeze.
To revive the coral, scientists place the cylinder in a warm water bath for two minutes, then remove the coral fragment and put it back into seawater.
“It’s conceptually complicated because of thermodynamics,” Hagedorn says. “But the actual process itself is really dead easy.”
Simplicity was part of the team’s goal; they wanted a process that could be quick and economical for coral reef managers to use in the field around the world. Smithsonian’s National Zoo and Conservation Biology Institute is participating in the Coral Biobank Alliance, a network of professionals working to preserve coral biodiversity. So far, the global team has banked sperm cells from 50 coral species and live specimens of 200 species. Eventually, Hagedorn hopes to have an “army of people” trained to collect and preserve corals—and the biobank alliance wants to store genetic material from every known coral species by the end of the decade.
“This study represents a very exciting breakthrough for our capacity as coral reef scientists and managers to safeguard coral genetic diversity,” Olivia Williamson, a coral researcher at the University of Miami, says in an email. She was not involved in the new paper but has previously collaborated with Hagedorn and co-author Jonathan Daly of the Taronga Conservation Society Australia on coral sperm cryopreservation.
Williamson says the new technology needs to be tested on more species, but she’s optimistic it will eventually allow for a “dramatic scaling up of coral genetic banking.”
In the new study, the team only tested the coral’s survival for 24 hours after its revival, but Hagedorn says they’re now working on refining some of their processes to allow for survival up to three weeks. Down the line, she predicts the technique could be adapted to preserve human organs, like ovaries, testes and embryonic kidneys and hearts.
“I think it’s going to have an amazing trajectory in terms of doing … more whole pieces of organisms,” she says. “It’s very, very cool technology, and it is the wave of the future.” | Biology |
A Japanese researcher has told a major genetics conference that he has created eggs from the cells of male mice.
The research, still in its early stages, involved turning male XY sex chromosomes into female XX ones.
Prof Katsuhiko Hayashi from Osaka University is working on developing fertility treatments.
The development, which he has submitted for publication in the scientific journal Nature, raises the prospect of male couples having their own children.
Prof George Daley of Harvard Medical School, who is not involved in the research, said that there was still a long way to go before society was faced with such a decision.
''Hayashi's work is unpublished but fascinating. [Doing this on Humans] is harder than the mouse," he said. We still don't understand enough of the unique biology of human gametogenesis (the formation of reproductive cells) to reproduce Hayashi's provocative work in mice''.
Details were presented at the human gene-editing summit at the Crick Institute in London.
Prof Hayashi, a globally respected expert in the field, told delegates at the meeting that the work was at a very early stage. The eggs, he said were of low quality and the technique could not be used safely on humans at this stage.
But he told BBC News that he could see current problems overcome in ten years and he would like to see it available as a fertility treatment for both male and female and same sex couples if it is proven to be safe to use.
"If people want it and if society accepts such a technology then yes, I'm for it".
The technique involves first taking a skin cell from a male mouse and then turning it into a stem cell - a cell that can turn into other types of cell.
The cells are male and therefore have XY chromosomes. Prof Katsuhiko's team then delete the Y chromosome, duplicate the X chromosome and then stick the two X's together. This adjustment allows the stem cell to be programmed to become an egg.
The technique could be used to help infertile couples where women are not able to produce their own eggs. He stressed though that it was a long way off from being available as a fertility treatment.
"Even in mice there are many problems in the quality of the egg. So before we can think of it as a fertility treatment we have to overcome these problems, which could take a long long time," he said.
Prof Hayashi said he would not be in favour of it being used by a man to create a baby using his own sperm and artificially created eggs.
"Technically this is possible. I'm not so sure whether at this stage it is safe or acceptable for society".
Prof Amander Clark, a stem cell scientist from the University of Californa, Los Angeles said that the LBGTQ+ community should have a say in the use of the technology for reproduction.
"The LGBTQ+ community have unique needs when it comes to having a family. It may be possible in the future for same-sex reproduction based upon current research using laboratory models to develop the technology.
"However, today this technology is not available for human use, safety and efficacy has not been proven, and it is unclear how long the technology will take to get to the clinic. There is still much to learn about the human germ line and fundamental knowledge gaps serve as a barrier to translating this research to humans."
Cultural differences
Alta Charo, professor of law at the University of Wisconsin Maddison, said different cultures would have "profoundly different views" on whether to use the technology, if it became available.
"In some societies a genetic contribution to one's children is considered absolutely essential, and for them it's a question of 'is this a step to take?' for those who are not in a heterosexual arrangement.
"For other societies that's not as nearly as important, and child adoption is perfectly acceptable, because for them families are more about the personal relationship and less about the biological connection."
Prof Haoyi Wang, of the Chinese Academy of Science believes there is a very a long way to go before the technology could be considered for use in the clinic.
"Scientists never say never, in principle it has been done in mice so, of course, it may be possible in humans, but I can foresee a lot of challenges and I couldn't predict how many years that would be."
Follow Pallab on Twitter | Biology |
Sign up for CNN’s Wonder Theory science newsletter. Explore the universe with news on fascinating discoveries, scientific advancements and more. CNN — Around the world, a parasitic fungus transforms ants into “zombies.” The fungus is like something out of a horror movie: The organism hijacks the body and brain of its ant host, mind-controlling it into abandoning its nest and climbing a nearby tree. There, the infected ant clamps its jaws around a leaf, dangling above the forest floor, and dies in a matter of days as the fungus digests it. Bursting through its host’s body, the fungus then sends down a shower of spores to infect the next generation of ant prey. Scientifically categorized in the genus Ophiocordyceps, the more than two dozen species of zombie ant fungus populate the globe, including Florida, Brazil and Japan; scientists suspect that each of the dozens of ant species affected has its own specialized Ophiocordyceps strain. So far, scientists have figured out the molecular mechanism of the parasitic interaction between fungus and ant that forms the basis of the behavioral manipulation, according to a 2020 study. How exactly these parasites systematically operate, however, is poorly understood. Now, scientists have revealed that the ant-attacking fungus is infected with fungal parasites of its own, which could be helping to keep ant zombification in check, according to a new study. Dr. João Araújo, an assistant curator of mycology at the New York Botanical Garden, has been trekking through tropical forests in search of zombie ants for more than a decade. Over the years, he kept noticing something strange: a fuzzy white fungus growing on top of the zombie ant fungus. Other scientists have noted the mystery fungus for decades, but Araújo and his colleagues decided to become the first scientists to systematically dig into the matter, zeroing in on a strain of zombie ants from Florida. The researchers described the physical structure of the fungi growing on top of the zombie ant fungus and sequenced their DNA in a study published November 9 in the journal Persoonia. In doing so, the team discovered two new genera of fungus previously unknown to science. “We realized that there were two different lineages of fungi, novel lineages of fungi, infecting one species of zombie ant fungus in Florida,” said Araújo, the study’s lead author. Each of the two newly discovered fungi belongs to its own genus. One of the new fungi, Niveomyces coronatus, is responsible for the fuzzy white coating on the zombie ant fungus — a component of its name (“niveo”) comes from the Latin for “snowy.” The second new fungus, Torrubiellomyces zombiae, is harder to spot: The little black blobs “look like fleas,” according to Araújo. The fungi attacking the zombie ant fungus don’t, in turn, zombify their host, but they do feed on its tissues and appear to cause it harm. “Every time we see these new genera we described growing on the fungus, the fungus looks pretty beaten up, really consumed by this other fungus,” Araújo said. “In some cases, it castrates Ophiocordyceps (the zombie-making fungus) first, so it cannot shoot the spores anymore, and then it grows and then consumes the whole fungus.” Since Niveomyces and Torrubiellomyces are so new to science, it’s not yet clear how much of an effect they have on zombie ant fungi populations overall. These new genera are the first parasites officially described as infecting the zombie ant fungus, but the researchers suspect there could be others out there. “I think it’s more common than we think. Parasitism is a super lucrative sort of lifestyle,” said senior study author Dr. Charissa de Bekker, an assistant professor at Utrecht University in the Netherlands. “It might be the most dominant lifestyle on the planet.” What’s more, she said, parasites in general and parasitic fungi in particular are poorly studied. “The fact that we had to invoke two new genera tells you how little we know about this part of the fungal tree of life,” de Bekker said. By deepening our understanding of the zombie ant fungus, the new research could have applications that go beyond the study of fungi, said Dr. Carolyn Elya, a postdoctoral fellow in organismic and evolutionary biology at Harvard University. She was not involved with the study. “Ophiocordyceps has basically over evolutionary time become an expert neuroscientist. It knows exactly what buttons to push and how to get the ant to do what it wants,” she said. “By studying how it’s figured out how to solve this problem, we can have insight into our more general goal of trying to understand how brains work or produce behavior.” Kate Golembiewski is a freelance science writer based in Chicago who geeks out about zoology, thermodynamics and death. She hosts the comedy talk show “A Scientist Walks Into a Bar.” | Biology |
The Tyrannosaurus rex, and other members of the tyrannosaurus family, are not the only carnivorous dinosaur to have tiny arms, according to a study recently published in Current Biology. Researchers from Ernesto Bachmann Paleontological Museum in Neuquén, Argentina, discovered fossilized remains of the Meraxes gigas, a large carnivore — like the T. rex — that also had disproportionate arms. These findings indicated that the T. rex and M. gigas evolved independent of each other and the use of these shorter arms. “The fossil of M. gigas shows never seen before, complete regions of the skeleton, like the arms and legs that helped us to understand some evolutionary trends and the anatomy of Carcharodontosaurids — the group that M. gigas belongs to,” says Juan Canale, lead author of the study, in a press release. The study suggests that these two carnivore families evolved independently from each other and that they each happened to develop small arms. M. gigas went extinct nearly 20 million years before T. rex became a species and according to Canale, the two dinosaurs are far apart on the evolutionary tree. “There is no direct relationship between both,” says Canale in a press release, though the author believes that shorter arms gave both the M. gigas and the T. rex some sort of survival advantage.“I’m convinced that those proportionally tiny arms had some sort of function,” Canale says. “The skeleton shows large muscle insertions and fully developed pectoral girdles, so the arm had strong muscles.” These large muscles suggest that the arms did not shrink due to atrophy — or lack of use. Prior research has established that for dinosaurs — like the M. gigas and the T. rex — the larger the head, the smaller the arms. “I’m inclined to think their arms were used in other kinds of activities,” says Canale in a press release. Adding, “they may have used the arms for reproductive behavior such as holding the female during mating or support themselves to stand back up after a break or a fall.” The fossil is in great shape and contains new evidence that can help researchers better understand this species of dinosaur. The skull has crests and small hornets. Canale believes that M. gigas developed these features later in life and used them to attract a mate. “Sexual selection is a powerful evolutionary force. But given that we cannot directly observe their behavior, it is impossible to be certain about this,” says Canale in a press release.From the fossils, the research team could piece together the life of this M. gigas before it died. The dinosaur was around 45 years old and made its home in northern Patagonia in Argentina. It was about 36 feet (11 meters) long and weighed around four tons. Research also suggests it was part of a large, thriving family before it went extinct. | Biology |
As we intensify our plans to explore the moons of Jupiter and Saturn and colonize mars, some may argue that we stand at the beginning of the epoch of space exploration. In an effort to outline the hazards of intensifying space exploration, an international team of invasion biologists wrote a paper in the Oxford Academic journal BioScience about a particular risk that hasn't yet been talked about a lot, namely biological invasion.Not the type of invasion with flying saucers and other sci-fi tropes one might think of by reading the word invasion in correlation with space exploration, but the potential risk of extraterrestrial microbiological contamination of our planet (and the other way around). If extraterrestrial microbes exist, the risk may not be as far-fetched as you might think. Terrestrial microbes living on other celestial bodies in the solar systemEven though space organizations adhere to strict rules regarding microbes, the risk of contamination may be greater than predicted in the past. Numerous spacecraft have been sent out into space. Some have landed on the Moon and Mars; others are flying towards distant asteroids. There is already a chance that terrestrial microbes dwell on these celestial bodies. According to the researchers, bacterial strains have been found in NASA's clean rooms used to construct spacecraft. Moreover, these strains have displayed exceptional resistance to disinfectants and ionizing radiation. It is therefore not inconceivable that some organisms have been deposited on the red planet, for example. It is also conceivable – though unlikely – that some of them survived. So should astrobiologists discover life on Mars, they need to be able to distinguish organisms native to Mars from those accidentally traveled on previous space missions.Taking extraterrestrial microbes back to EarthOur efforts to explore space will only intensify in the future. Not only do we have manned space travel on the horizon, NASA, among others, plans to visit many more celestial bodies in our solar system. What we will encounter on these exotic worlds is unknown, and we may unintentionally take alien microbes with us back to Earth. According to Professor / Anthony Ricaarde, invasive species biologist at McGill University and lead author of the paper, biological invasions are a global biosecurity threat. An incident of this nature would demand stringent international cooperation. To tackle potential incidents, the team has outlined an approach to deal with this subject matter. The developing field of invasion science will investigate the causes and impact of the introduction of organisms outside their evolved ranges.Ricciardi and his partners stated that the field has already formed valuable insights on rapid evolution, the relationship between population stability and biodiversity, accelerated evolution, and the dynamics of parasite-host and predator-prey interactions that may prove to be helpful. Preparing for extraterrestrial microbiological contamination of EarthAccording to the team, it is possible to modify existing protocols such as hazard evaluation and containment processes currently used for invasive species on Earth to suit possible extraterrestrial microbial contaminants.In their paper, the researchers empathize that several understandings derived from the field of invasion biology could be used to mitigate or better understand extraterrestrial biosecurity problems. Examples of this are the understanding that isolated systems like lakes and islands are more susceptible to invasion threats and the insight that a microbial hazard must be detected early if we want to be able to manage it. Ricciardi and colleagues advise that portable real-time DNA sequencing technologies joined with databases of known organismal contaminants could allow for a fast response.Why biosecurity should be a consideration in space mission planningNotwithstanding their potential value for biosecurity, the researchers assert that invasion biologists have yet to be involved in Committee on Space Research planning. This should change soon, they argue, because "greater collaboration between invasion biologists and astrobiologists would enhance existing international protocols for planetary biosecurity—both for Earth and for extraterrestrial bodies that could contain life."The team outlined their case for improved biosecurity more extensively in their paper published in the science journal BioScience. We listed it below for those that are interested in the subject.Sources and further reading:Planetary Biosecurity: Applying Invasion Science to Prevent Biological Contamination from Space Travel (Oxford Academic / BioScience)Effects of rapid evolution on species coexistence (PNAS) | Biology |
An antiviral drug used to treat COVID-19 may be driving the virus that causes the disease to evolve, a new study suggests.
But is this concerning, or particularly surprising? Not at this point, and not really, experts told Live Science.
Scientists analyzed more than 15 million SARS-CoV-2 genomes — genetic material from the virus that causes COVID-19 — and found that molnupiravir induces a "mutational signature" that, if the virus isn't completely obliterated by a course of the drug, can be transmitted to other people. Molnupirivar works by causing mutations in the SARS-CoV-2 genome that prevent the virus from replicating.
"Previously people had raised the mutagenic effect of molnupiravir on viruses as a theoretical risk," study lead author Theo Sanderson, a researcher at the Francis Crick Institute in London, told Live Science in an email. "Our work makes this more concrete because we have found that molnupiravir can give rise to extensively-mutated viruses that remain transmissible," he said. What's more, some of the mutations that cropped up repeatedly seem to be ones that could help the virus evade the immune system, he added.
The authors of the study, published Monday (Sept. 25) in the journal Nature, found that after molnupiravir's rollout, this mutational signature was common in countries that widely used the drug, such as the U.S. and U.K. However, countries where molnupiravir is not licensed, such as Canada, had fewer examples of these signatures.
The findings could help regulators to assess the risks and benefits of using the drug, but experts told Live Science that many questions remain unanswered.
"We should not be concerned with mutations themselves, but rather whether they allow the virus to adapt to infect or transmit better," said Vaughn Cooper, a professor of microbiology and molecular genetics at the University of Pittsburgh who was not involved in the research. "In this case, we see relatively little evidence that molnupiravir is fueling more adaptations to escape prior immunity or alter infectiousness," Cooper told Live Science in an email.
Indeed, Sanderson said from this data alone, it is difficult to quantify how common it is for molnupiravir-derived lineages of SARS-CoV-2 to spread between people. That's because, if a single sample of the virus with this molnupiravir signature shows up in a database but doesn't have any close relatives, scientists can't easily tell if it came from someone treated with the drug or another person infected further down the line.
The study also didn't address the potential risks and benefits of using molnupiravir for individual patients, Sanderson said. This will be important to understand, especially for those with weakened immune systems, he said. These patients have a higher risk of prolonged COVID-19 infections that give the virus more opportunities to pick up lots of mutations.
Future modeling studies could help predict whether the drug could influence the risk of new variants of concern emerging — another question that the current study didn't explore, Sanderson added.
"We have yet to see evidence of more fit sequences arising from molnupiravir" — meaning viruses that can more easily spread and multiply — "but this work certainly provides pause for thought and should weigh heavily in considerations around future use of the drug, necessitating at the very least mitigations of the risks of this effect, alongside real world data on the effectiveness of the drug," Aris Katzourakis, a professor of evolution and genomics at the University of Oxford who was not involved in the research, told Live Science in an email.
Mitigation strategies could include selective prescribing and monitoring chronically infected patients for evidence of viral evolution, but these safeguards would need to be balanced against patients' clinical needs and the availability of alternative treatments, he said.
This article is for informational purposes only and is not meant to offer medical advice.
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Emily is a health news writer based in London, United Kingdom. She holds a bachelor's degree in biology from Durham University and a master's degree in clinical and therapeutic neuroscience from Oxford University. She has worked in science communication, medical writing and as a local news reporter while undertaking journalism training. In 2018, she was named one of MHP Communications' 30 journalists to watch under 30. ([email protected]) | Biology |
COVID-19 may continue to dominate headlines, but this year’s biomedical advances weren’t all about “the Rona.” 2022 saw fruitful and seemingly fantastical research that could one day mean good news for patients. Growing synthetic embryos Two reports this year revealed how to fabricate the early stages of mammalian life. With a bit of laboratory wizardry, scientists mingled mouse stem cells, which self-assembled to spawn what appears to be a kind of fledgling embryo — no egg or sperm required. As they grow, these stem cell–derived synthetic embryos can form proto hearts, brains and guts. But the similarity to natural mouse embryos fades quickly. The synthetic and natural versions match up for only about eight days of development. Still, studying similar clusters of human stem cells might one day offer a way to probe the development of human embryos without relying on the real thing. Science News headlines, in your inbox Headlines and summaries of the latest Science News articles, delivered to your email inbox every Friday. Next-level organ transplants Organ transplants have started mirroring science fiction. In January, an ailing 57-year-old man received a heart from a genetically engineered pig and survived for two months with the transplanted organ (SN: 3/12/22, p. 26). Other surgeries plugged pig hearts into the bodies of brain-dead patients, a step that prepares researchers for future clinical trials (SN Online: 7/12/22). And a high-tech system hooked up to pigs’ bodies an hour after death helped keep organs functioning. The technology, which might one day preserve human organs slated for surgery, pumps a mix of real and artificial blood through the animals (SN: 9/10/22, p. 12). In July, a surgical team at NYU Langone Health transplanted a pig heart into a brain-dead patient, part of a larger effort to evaluate the potential of using animal organs for transplantation.JOE CARROTTA FOR NYU LANGONE HEALTH Epstein-Barr’s link to MS Scientists dropped an Epstein-Barr bombshell early this year when they suggested that the virus is the main cause of the neurodegenerative disease multiple sclerosis. Infection with the virus greatly upped the odds of later developing MS, an analysis of millions of U.S. military recruits found. The link between the virus and MS, which scientists had suspected but never outlined so clearly, might guide the way to potential MS treatments — or even, one day, vaccines to prevent the disease (SN: 8/13/22, p. 14). Epstein-Barr viruses (red) emerge from an immune system B cell in this colorized electron micrograph.STEVE GSCHMEISSNER/SCIENCE SOURCE A complete human genome, finally Researchers announced back in 2003 that they had read all the genetic info packed into strands of human DNA — the first sequence of the human genome. But that genome was not quite complete; some tangled-up lengths of DNA remained difficult to decipher. This year, a team tied up the loose ends. In March, the researchers reported a new and improved human genome — this time, complete from end to end (SN: 4/23/22, p. 6). New technologies have helped researchers decipher the final, challenging stretches of DNA bases in the human genome.ERNESTO DEL AGUILA III/NHGRI AI predicts protein structures Artificial intelligence has taken structural biology to warp speed. A deep-learning program called AlphaFold has now predicted the 3-D shapes of more than 200 million proteins (SN: 9/24/22, p. 16). Though the shapes are not lab-verified structures, the massive dataset could help researchers studying health and disease in all sorts of organisms, from humans to honeybees. Now, looking up a protein’s predicted structure is almost as easy as typing it into Google, according to the cofounder of the AI company that created AlphaFold. Alphafold predicted this structure (blue is highest confidence, red is lowest) for a honeybee protein called vitellogenin that helps protect against bacterial infections.Deep Mind | Biology |
Researchers use genomes of 241 species to redefine mammalian tree of life
Research led by a team of scientists from the Texas A&M School of Veterinary Medicine and Biomedical Sciences puts to bed the heated scientific debate regarding the history of mammal diversification as it relates to the extinction of the non-avian dinosaurs. Their work provides a definitive answer to the evolutionary timeline of mammals throughout the last 100 million years.
The study, published in Science, is part of a series of articles released by the Zoonomia Project, a consortium of scientists from around the globe that is using the largest mammalian genomic dataset in history to determine the evolutionary history of the human genome in the context of mammalian evolutionary history. Their ultimate goal is to better identify the genetic basis for traits and diseases in people and other species.
The Texas A&M University research—led by Dr. William J. Murphy, a professor in the Department of Veterinary Integrative Biosciences, and Dr. Nicole Foley, an associate research scientist in Murphy's lab—is rooted in phylogeny, a branch of biology that deals with the evolutionary relationships and diversification of living and extinct organisms.
"The central argument is about whether placental mammals (mammals that develop within placentas) diverged before or after the Cretaceous-Paleogene (or K-Pg) extinction event that wiped out the non-avian dinosaurs," Foley shared. "By performing new types of analyses only possible because of Zoonomia's massive scope, we answer the question of where and when mammals diversified and evolved in relation to the K-Pg mass extinction."
The research—which was conducted with collaborators at the University of California, Davis; University of California, Riverside; and the American Museum of Natural History—concludes that mammals began diversifying before the K-Pg extinction as the result of continental drifting, which caused the Earth's land masses to drift apart and come back together over millions of years. Another pulse of diversification occurred immediately following the K-Pg extinction of the dinosaurs, when mammals had more room, resources and stability.
This accelerated rate of diversification led to the rich diversity of mammal lineages—such as carnivores, primates and hoofed animals—that share the Earth today.
Murphy and Foley's research was funded by the National Science Foundation and is one part of the Zoonomia Project led by Elinor Karlsson and Kerstin Lindblad-Toh, of the Broad Institute, which also compares mammal genomes to understand the basis of remarkable phenotypes—the expression of certain genes such as brown vs. blue eyes—and the origins of disease.
Foley pointed out that the diversity among placental mammals is exhibited both in their physical traits and in their extraordinary abilities.
"Mammals today represent enormous evolutionary diversity—from the whizzing flight of the tiny bumblebee bat to the languid glide of the enormous Blue Whale as it swims through Earth's vast oceans. Multiple species have evolved to echolocate, some produce venom, while others have evolved cancer resistance and viral tolerance," she said.
"Being able to look at shared differences and similarities across the mammalian species at a genetic level can help us figure out the parts of the genome that are critical to regulate the expression of genes," she continued. "Tweaking this genomic machinery in different species has led to the diversity of traits that we see across today's living mammals."
Murphy shared that Foley's resolved phylogeny of mammals is crucial to the goals of the Zoonomia Project, which aims to harness the power of comparative genomics as a tool for human medicine and biodiversity conservation.
"The Zoonomia Project is really impactful because it's the first analysis to align 241 diverse mammalian genomes at one time and use that information to better understand the human genome," he explained. "The major impetus for putting together this big data set was to be able to compare all of these genomes to the human genome and then determine which parts of the human genome have changed over the course of mammalian evolutionary history."
Determining which parts of genes can be manipulated and which parts cannot be changed without causing harm to the gene's function is important for human medicine. A recent study in Science Translational Medicine led by one of Murphy and Foley's colleagues, Texas A&M geneticist Dr. Scott Dindot, used the comparative genomics approach to develop a molecular therapy for Angelman syndrome, a devastating, rare neurogenetic disorder that is triggered by the loss of function of the maternal UBE3A gene in the brain.
Dindot's team took advantage of the same measures of evolutionary constraint identified by the Zoonomia Project and applied them to identify a crucial but previously unknown genetic target that can be used to rescue the expression of UBE3A in human neurons.
Murphy said expanding the ability to compare mammalian genomes by using the largest dataset in history will help develop more cures and treatments for other species' ailments rooted in genetics, including cats and dogs.
"For example, cats have physiological adaptations rooted in unique mutations that allow them to consume an exclusively high-fat, high-protein diet that is extremely unhealthy for humans," Murphy explained. "One of the beautiful aspects of Zoonomia's 241-species alignment is that we can pick any species (not just human) as the reference and determine which parts of that species' genome are free to change and which ones cannot tolerate change. In the case of cats, for example, we may be able to help identify genetic adaptations in those species that could lead to therapeutic targets for cardiovascular disease in people."
Murphy and Foley's phylogeny also played an instrumental role in many of the subsequent papers that are part of the project.
"It's trickle-down genomics," Foley explained. "One of the most gratifying things for me in working as part of the wider project was seeing how many different research projects were enhanced by including our phylogeny in their analyses. This includes studies on conservation genomics of endangered species to those that looked at the evolution of different complex human traits."
Foley said it was both meaningful and rewarding to definitively answer the heavily debated question about the timing of mammal origins and to produce an expanded phylogeny that lays the foundation for the next several generations of researchers.
"Going forward, this massive genome alignment and its historical record of mammalian genome evolution will be the basis of everything that everyone's going to do when they're asking comparative questions in mammals," she said. "That is pretty cool."
More information: Nicole M. Foley et al, A genomic timescale for placental mammal evolution, Science (2023). DOI: 10.1126/science.abl8189
Provided by Texas A&M University | Biology |
Certain physical traits of flowers affect the health of bumblebees by enabling the transmission of a harmful pathogen, research at the University of Massachusetts Amherst has shown. The scientific experiment masterminded by Jenny Van Wyk – who is a postdoctoral researcher and the study’s lead author – confirms that the length of a flower’s corolla seriously influences how a bumblebee parasite called Crithidia bombi gets transferred between the insects. Shorter corollas mean that fewer faeces wind up inside the flower itself and in the path of the bees in search of nectar, according to Ms Van Wyk. The bumblebee has been under threat by the excessive usage of pesticides and a continuing reduction of habitats. However, parasites have seriously endangered the insect – which is an important pollinator – as well. Ms Van Wyk explained: “We are trying to gather information on how floral traits impact pollinator health so that we can think beyond species-specific information. “Flowers with shorter petals may transmit fewer pathogens than flowers of the same species with longer petals. Bees crawl deep into flowers in their search for nectar. When the petals are long, a bee might wiggle its entire body inside. UMass Amherst research assistant Fiona MacNeill trimming one of the 105,000 flowers in undated photo. Certain physical traits of flowers affect the health of bumblebees by enabling the transmission of a harmful pathogen, research at the University of Massachusetts Amherst has shown. (Ben Barnhart, NewsX/Bee) “When that bee defecates, its faeces remain inside the flower, and the next bee to come through in search of nectar and pollen will wind up smeared in another bee’s poop. If that poop happened to contain Crithidia bombi, then the second bee would be at high risk for infection.” The researcher underlined: “However, in shorter-petalled flowers, bees’ butts hang out and their faeces fall harmlessly to the ground.” To reach this conclusion, the biology department experts planted patches of native wildflowers before enclosing them in tents. They then put bumblebees into these tents. Half of them were healthy while the other half were inoculated with Crithidia bombi. The healthy insects were painted blue for identification reasons. The physical traits of the flowers in each tent were altered to test which trait had the most impact on the insects’ condition. The researchers and a group of students they asked for support used small scissors to trim more than 105,000 flowers to determine the impact of corolla length. They also tested if the amount and the distribution of nectar played a role in the health of the insects by inserting a tiny nectar-filled pipette into more than 6,500 flowers and by squirting more of the sweet substance. The team of researchers furthermore compared the activity at tightly and loosely bunched flower plantings. To track which bees’ excrements landed where, Van Wyk and her colleagues fed the bees fluorescent paint. They then used a black light to locate the faeces. The experiment revealed that pathogen transmission was reduced when the corolla lips were trimmed, when nectar was distributed evenly within a group of flowers or when the flowers were planted more widely apart. Higher levels of larvae production were registered at trimmed corollas and plant patches where the nectar was more evenly distributed. Lynn Adler is a professor of biology at the University of Massachusetts Amherst and the study’s senior author. Picture shows one of the countless bumblebees painted blue to track bee health, undated. Certain physical traits of flowers affect the health of bumblebees by enabling the transmission of a harmful pathogen, research at the University of Massachusetts Amherst has shown. (Ben Barnhart, NewsX/Bee) Prof Adler said: “This work is really exciting and novel because there’s only a handful of studies that have compared how flowers from different species can transmit bee diseases – and only a single study, published more than 25 years ago, that manipulated a floral trait to establish its causal role in disease spread. Our work demonstrates that a wide range of traits may be important.” Ms Van Wyk added: “The number one question I get when I give public talks is: ‘What should I plant for bees?’ Our research opens the door to further efforts to understand how specific physical flower characteristics support bee health, which can inform management practices.” The University of Massachusetts Amherst researchers’ study entitled “The Manipulation of multiple floral traits demonstrates role in pollinator disease transmission” has been published in the journal Ecology. The University of Massachusetts Amherst is a public higher education and research institution in Amherst in the US State of Massachusetts. It was founded as an agricultural college in 1863. | Biology |
A team of scientists in Israel say they’ve accomplished an incredible feat of biology: The creation of a completely human-like embryo model without the need for a sperm or egg. The synthetic embryos were grown using stem cells instead and appeared to have the same structures and components of a typical human embryo up through 14 days of development. The team believes their work will help us better understand the earliest stages of pregnancy and could even one day pave the way for breakthroughs in organ transplantation and other fields of medicine.
The research was led by scientists from the Weizmann Institute of Science. The group is one of several teams around the world that’s working on growing more complex synthetic embryos. Last summer, they published a study showing their creation of mice embryos derived entirely from mouse stem cells—mere weeks before another team from the UK published findings on their own mice model. Now, they seem to have done the same with human stem cells.
Stem cells are often considered the building block of life since they mature into other types of cells. However, not all stem cells have the same potential. Pluripotent stem cells, for instance, are known for their ability to turn into many, but not every type of cell. These cells play a large role relatively early on in helping the human body develop. Scientists have known for a while how to convert adult stem cells into their pluripotent state. But the Weizmann group has gone further, learning how to convert these cells into their earliest “naïve” state, cells that theoretically can become every other cell in the body. And it’s these naïve cells that are at the forefront of the team’s project.
To create their lab-made embryos, the team mixed together three groups of stem cells. One group was allowed to grow unperturbed, serving as the embryo itself. The two other groups were chemically prodded into becoming the parts of the structure that are meant to support the embryo, such as the placenta and yolk sac. The team’s experiments produced many clumps of stem cells, most of which failed to develop. But about one percent of these clumps kept growing and organizing themselves into something that could truly be considered an embryo, the researchers say.
These stem cell-based embryo-like structures, or SEMS, were purportedly able to grow in the lab for about 8 days. By that point, the SEMS seemed to have all the necessary components of a typical embryo that has reached 14 days of growth in the womb, the stage right before the embryo begins to develop what will eventually become organs. The researchers even performed pregnancy tests on their SEMS, since these tests rely on detecting a hormone produced by the embryo, and the tests came back positive.
The team’s findings were published Wednesday in Nature.
Scientists today can develop already created embryos in the lab to a certain extent, as well as produce artificial but simplistic models of embryos or individual organs. But these models still don’t allow us to closely look at the earliest stages of human development. And the authors say their work can do just that.
“The drama is in the first month, the remaining eight months of pregnancy are mainly lots of growth,” said study author and research leader Jacob Hanna in a statement from the Weizmann Institute. “But that first month is still largely a black box. Our stem cell-derived human embryo model offers an ethical and accessible way of peering into this box. It closely mimics the development of a real human embryo, particularly the emergence of its exquisitely fine architecture.”
One of the initial hopes of this research is that we can learn more about why miscarriages occur, which most commonly happen in the first trimester. These models could also make it easier for scientists to study how drugs or other exposures can potentially affect a fetus. Eventually, these advances might even enable us to create fully working organs in the lab that can be used for transplantation. | Biology |
To conserve precious and fragile biodiversity hotspots, a crucial step is knowing how the fruit eaters are doing. To assist in that, scientists and students at Michigan State University (MSU) have supersized a database to keep track of such animals and birds.
In this month's open-access journal Global Ecology and Biogeography, the group introduces for the first time a hulking list of more than 45,000 traits for creatures that eat fruit. Frugivoria, named for the species called frugivores who survive mainly on fruit, supersizes existing databases by providing researchers and conservationists with one-stop listings of both critters and birds in the forests of Central and South America. Frugivoria's data and workflow are open and accessible to all to help facilitate its use for addressing the biodiversity crisis.
In a time of rapid climate change, it's crucial to understand how the fruit eaters are doing in specific ways.
"With climate change, seed dispersion is really important," said Beth Gerstner, a PhD candidate in the MSU Department of Fisheries and Wildlife who led the development. "Fruit eaters maintain forest composition and health by pooping -- which spreads seeds. Frugivoria is an important contribution because researchers can use this to understand the diversity of their roles in the ecosystem."
Knowing what is doing the fruit eating and pooping, as well as their distribution and life traits -- their life expectancies, breeding habits, habitat preferences -- is critical to tracking changes that climate change may bring. Yet current databases were fragmented or incomplete.
Starting in 2018 at MSU, 12 undergraduate students were tasked with sleuthing through of mounds of scientific publications to flesh out existing records of fruit eaters, adding birds for a more holistic understanding of the forests. Most exciting, Gerstner said, was entering 44 new species, like the olinguito.
That's a member of the same family as racoons that lives in the cloud forests of the northern Andes, and one that Gerstner studies. The olinguito had been mistaken for the larger olingo, but upon being discovered in 2013 has been found to indeed be genetically different.
"Natural history is entering the age of big data," said Phoebe Zarnetske, associate professor in integrative biology and director, Institute for Biodiversity, Ecology, Evolution, and Macrosystems (IBEEM). "Through Frugivoria, we are contributing to increasing the accessibility of natural history information traditionally found in museums and collections. This project provided a unique opportunity to engage numerous undergraduates in research with data science and functional ecology.
Zarnetske said Frugivoria can help with both basic and applied questions about species' functions in their environment. It can be used by community scientists to learn more about species' natural history, and it can aid in species conservation assessments
"As a result," she said, "Frugivoria is part of something bigger -- we can leverage the power of its big data to help solve the biodiversity crises."
Getting Frugivoria out where it's needed is Gerstner's goal. "My hope," she said, "is for the database to be used by the International Union for the Conservation of Nature and people doing on-the-ground conservation."
Both Gerstner and Zarnetske are members of MSU's Ecology, Evolution, and Behavior Program and Spatial and Community Ecology (SpaCE) Lab
The work behind "Frugivoria: A trait database for birds and mammals exhibiting frugivory across contiguous Neotropical moist forests" was supported by a NASA Future Investigators in NASA Earth and Space Science and Technology, a National Science Foundation Campus Cyberinfrastructure program and computational resources and services provided by the Institute for Cyber-Enabled Research of which co-author Patrick Bills is a member. In addition to the open access paper in Global Ecology and Biogeography, the database itself is published open access with the Environmental Data Initiative.
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Scientists record first-ever brain waves from freely moving octopuses
Scientists have successfully recorded brain activity from freely moving octopuses, a feat made possible by implanting electrodes and a data logger directly into the creatures.
The study, published online in Current Biology on February 23, is a critical step forward in determining how octopus' brains control their behavior, and could provide clues to the common principles needed for intelligence and cognition to occur.
"If we want to understand how the brain works, octopuses are the perfect animal to study as a comparison to mammals. They have a large brain, an amazingly unique body, and advanced cognitive abilities that have developed completely differently from those of vertebrates," said Dr. Tamar Gutnick, first author and former postdoctoral researcher in the Physics and Biology Unit at the Okinawa Institute of Science and Technology (OIST).
But measuring the brainwaves of octopuses has proven a real technical challenge. Unlike vertebrates, octopuses are soft bodied, so they have no skull to anchor the recording equipment onto, to prevent it being removed.
"Octopuses have eight powerful and ultra-flexible arms, which can reach absolutely anywhere on their body," said Dr. Gutnick. "If we tried to attach wires to them, they would immediately rip if off, so we needed a way of getting the equipment completely out of their reach, by placing it under their skin."
The researchers settled on small and lightweight data loggers as the solution, which were originally designed to track the brain activity of birds during flight. The team adapted the devices to make them waterproof, but still small enough to easily fit inside the octopuses. The batteries, which needed to work in a low-air environment, allowed up to 12 hours of continuous recording.
The researchers chose Octopus cyanea, more commonly known as the day octopus, as their model animal, due to its larger size. They anesthetized three octopuses and implanted a logger into a cavity in the muscle wall of the mantle. The scientists then implanted the electrodes into an area of the octopus' brain called the vertical lobe and median superior frontal lobe, which is the most accessible area. This brain region is also believed to be important for visual learning and memory, which are brain processes that Dr. Gutnick is particularly interested in understanding.
Once the surgery was complete, the octopuses were returned to their home tank and monitored by video. After five minutes, the octopuses had recovered and spent the following 12 hours sleeping, eating and moving around their tank, as their brain activity was recorded. The logger and electrodes were then removed from the octopuses, and the data was synchronized to the video.
The researchers identified several distinct patterns of brain activity, some of which were similar in size and shape to those seen in mammals, while others were very long lasting, slow oscillations that have not been described before.
The researchers were not yet able to link these brain activity patterns to specific behaviors from the videos. However, this is not completely surprising, Dr. Gutnick explained, as they didn't require the animals to do specific learning tasks.
"This is an area that's associated with learning and memory, so in order to explore this circuit, we really need to do repetitive, memory tasks with the octopuses. That's something we're hoping to do very soon."
The researchers also believe that this method of recording brain activity from freely moving octopuses can be used in other octopus species and could help solve questions in many other areas of octopus cognition, including how they learn, socialize and control the movement of their body and arms.
"This is a really pivotal study, but it's just the first step," said Prof. Michael Kuba, who led the project at the OIST Physics and Biology Unit and now continues at the University of Naples Federico II. "Octopus are so clever, but right now, we know so little about how their brains work. This technique means we now have the ability to peer into their brain while they are doing specific tasks. That's really exciting and powerful."
The study involved an international collaboration between researchers in Japan, Italy, Germany, Ukraine, and Switzerland.
More information: Tamar Gutnick et al, Recording electrical activity from the brain of behaving octopus, Current Biology (2023). DOI: 10.1016/j.cub.2023.02.006. www.cell.com/current-biology/f … 0960-9822(23)00145-8 | Biology |
Credit: CC0 Public Domain Scientists from Trinity College Dublin believe our brains could use quantum computation. Their discovery comes after they adapted an idea developed to prove the existence of quantum gravity to explore the human brain and its workings. The brain functions measured were also correlated to short-term memory performance and conscious awareness, suggesting quantum processes are also part of cognitive and conscious brain functions. If the team's results can be confirmed—likely requiring advanced multidisciplinary approaches—they would enhance our general understanding of how the brain works and potentially how it can be maintained or even healed. They may also help find innovative technologies and build even more advanced quantum computers.
Dr. Christian Kerskens, lead physicist at the Trinity College Institute of Neuroscience (TCIN), is the co-author of the research article that has just been published in the Journal of Physics Communications. He said, "We adapted an idea, developed for experiments to prove the existence of quantum gravity, whereby you take known quantum systems, which interact with an unknown system. If the known systems entangle, then the unknown must be a quantum system, too. It circumvents the difficulties to find measuring devices for something we know nothing about.
"For our experiments we used proton spins of 'brain water' as the known system. 'Brain water' builds up naturally as fluid in our brains and the proton spins can be measured using MRI (Magnetic Resonance Imaging). Then, by using a specific MRI design to seek entangled spins, we found MRI signals that resemble heartbeat evoked potentials, a form of EEG signals. EEGs measure electrical brain currents, which some people may recognize from personal experience or simply from watching hospital dramas on TV."
Electrophysiological potentials like the heartbeat evoked potentials are normally not detectable with MRI and the scientists believe they could only observe them because the nuclear proton spins in the brain were entangled. Dr. Kerskens added, "If entanglement is the only possible explanation here then that would mean that brain processes must have interacted with the nuclear spins, mediating the entanglement between the nuclear spins. As a result, we can deduce that those brain functions must be quantum. "Because these brain functions were also correlated to short-term memory performance and conscious awareness, it is likely that those quantum processes are an important part of our cognitive and conscious brain functions. "Quantum brain processes could explain why we can still outperform supercomputers when it comes to unforeseen circumstances, decision making, or learning something new. Our experiments, performed only 50 meters away from the lecture theater where Schrödinger presented his famous thoughts about life, may shed light on the mysteries of biology, and on consciousness which scientifically is even harder to grasp." More information: Christian Matthias Kerskens et al, Experimental indications of non-classical brain functions, Journal of Physics Communications (2022). DOI: 10.1088/2399-6528/ac94be Citation: New research suggests our brains use quantum computation (2022, October 19) retrieved 20 October 2022 from https://phys.org/news/2022-10-brains-quantum.html This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only. | Biology |
Enzyme ATE1 plays role in cellular stress response, opening door to new therapeutic targets
A new paper in Nature Communications illuminates how a previously poorly understood enzyme works in the cell. Many diseases are tied to chronic cellular stress, and UMBC's Aaron T. Smith and colleagues discovered that this enzyme plays an important role in the cellular stress response. Better understanding how this enzyme functions and is controlled could lead to the discovery of new therapeutic targets for these diseases.
The enzyme is named ATE1, and it belongs to a family of enzymes called arginyl-tRNA transferases. These enzymes add arginine (an amino acid) to proteins, which often flags the proteins for destruction in the cell. Destroying proteins that are misfolded, often as a result of cellular stress, is important to prevent those proteins from wreaking havoc with cellular function. An accumulation of malfunctioning proteins can cause serious problems in the body, leading to diseases like Alzheimer's or cancer, so being able to get rid of these proteins efficiently is key to long-term health.
Tantalizing implications
The new paper demonstrates that ATE1 binds to clusters of iron and sulfur ions, and that the enzyme's activity increases two- to three-fold when it is bound to one of these iron-sulfur clusters. What's more, when the researchers blocked cells' ability to produce the clusters, ATE1 activity decreased dramatically. They also found that ATE1 is highly sensitive to oxygen, which they believe relates to its role in moderating the cell's stress response through a process known as oxidative stress.
"We were very excited about that, because it has lots of very tantalizing downstream implications," particularly related to the enzyme's role in disease, says Smith, associate professor of chemistry and biochemistry.
Smith's lab works initially with the yeast protein but also showed that the mouse version of ATE1 behaves similarly. That's important, Smith explains. "Since the yeast protein and the mouse protein behave the same way," he says, "there's reason to believe, that because the human protein is quite similar to the mouse protein, it likely behaves the same way as well."
A new approach
Before they made their breakthrough discovery, Smith and then-graduate student Verna Van, Ph.D. '22, biochemistry and molecular biology, had been attempting for quite some time to induce ATE1 to bind with heme, a compound that contains iron and is necessary to bind oxygen in blood, to confirm another group's results. It wasn't working, and they were getting frustrated, Smith admits. But one day, as Smith was preparing a lecture on proteins that bind with clusters of metal and sulfur atoms, he realized the proteins he was about to cover with his students looked similar to ATE1.
After that realization, Smith and Van took a new approach. In the lab, they added the raw materials for creating iron-sulfur clusters to a solution with ATE1, and the results showed that ATE1 did indeed bind the clusters. "This looks promising," Smith remembers thinking. "We were super excited about it."
The fact that the enzyme binds the clusters at all was interesting and new, "but then we also asked if that's affecting the enzyme's ability to do what it does," Smith says. The answer, after more than a year of additional experiments, was a resounding yes. In the process, Smith's group also determined the structure of ATE1 in yeast (without the cluster bound to it), which they published in the Journal of Molecular Biology in November 2022.
Subtle but significant
Around the same time, another group also published a slightly different ATE1 structure. The other group's structure had a zinc ion (another metal) bound in place of the iron-sulfur cluster. With the zinc in place, one key amino acid is rotated about 60 degrees. It might seem inconsequential, but Smith believes that rotation, which he presumes is similar with the cluster, is the key to the cluster's role in ATE1's function.
The rotated amino acid is directly adjacent to where a protein would interact with ATE1 to be modified, ultimately flagging it for degradation. Changing the angle of that amino acid changes the shape of the location the protein would bind "very subtly," but changes its activity "more than subtly," Smith says.
Looking ahead and looking back
Smith would also like to explore how other metals, beyond zinc and the iron-sulfur cluster, may affect the enzyme's activity. Additionally, his lab is working to determine the structure of ATE1 in an organism other than yeast and to confirm the ATE1 structure with an iron-sulfur cluster bound.
All these steps will build up a clearer picture of how ATE1 functions and is regulated in the cell. Smith also says he believes proteins that so far have not been shown to bind iron-sulfur clusters may indeed rely on them.
This new paper actually harkens back to Smith's first days at UMBC. He has always been interested in protein modifications, and adding arginine is a more unusual one. "It's always something that I had filed back in my mind, and thought, 'Oh, it would be really interesting to get a better understanding of how that works,'" he says.
Several years later, his group is now on the leading edge of discovering how arginine modifications influence cellular function and disease.
More information: Verna Van et al, Iron-sulfur clusters are involved in post-translational arginylation, Nature Communications (2023). DOI: 10.1038/s41467-023-36158-z
Provided by University of Maryland Baltimore County | Biology |
Every year from the age of 20 my mother, Jean Combes, who has died aged 96, recorded the time of year that four tree species – oak, ash, horse chestnut and lime – came into leaf. What started in 1947 as a personal project, driven by a simple love of nature, turned out to demonstrate with textbook clarity that the long-term trend in Britain has been for spring to start much earlier than it used to. Her 76-year dataset has been used by scientists in climate change modelling, and earned her national recognition in 2008 with appointment as an OBE for services to phenology, the study of periodic events in biological life cycles.
Jean’s data first came to the attention of scientists in 1995, when she read about the work of the Coventry University climate expert Tim Sparks, and contacted him about what she had been doing. Tim later described her records as “probably unique in phenological recording and, as far as we know, the longest recording by a single person anywhere in the world”.
Born in south London to Ernest Laney, an insurance salesman, and Dorothy (nee Martin), a seamstress, Jean acquired her interest in the natural world when she was evacuated to the countryside with her sister, Pauline, at the start of the second world war. First they lived in Hertfordshire and then in Sussex.
After being educated at Chichester girls grammar school she went on to work as a housing manager at various local authorities in the London area. While at Merton council she met Reg Combes, a payroll clerk, and they married in 1951.
After raising three daughters as a full-time mother, Jean completed a three-year field biology qualification at London University in 1977. This was the springboard for 25 years of teaching natural history adult education classes, first for the WEA in Surrey, then at Surrey University in Guildford and for the Field Studies Council.
Jean also undertook survey work, including 20 years of the common bird census on Ashtead common in Surrey, and was commissioned by the Local Agenda 21 Committee for Surrey to carry out a study of a proposed oil pipeline route through Surrey and Sussex, which got the go-ahead only on the basis that hundreds of rare wild daffodils identified by her were first transplanted to safety.
She was involved with a number of wildlife bodies, including on the committees of the Surrey Wildlife Trust and of the City of London body that manages Ashtead Common. After the award of her OBE there was considerable media interest in her exploits, and she appeared on The One Show in 2009 and Springwatch in 2010.
Her fine pencil drawings of tree buds, catkins and leaves were exhibited annually for 10 years at the Botanical Society of Britain and Ireland. She also had a love for Scottish landscapes, literature, poetry and art, and remained interested in politics and the state of the world.
Reg died in 2006. She is survived by her daughters, Sue and me, and four grandchildren, Alex, Lewis, Joe and Jenna. Another daughter, Jenny, died in 2018. | Biology |
PISCATAWAY, N.J. — No invention signifies humanity’s ingenuity and intelligence quite like the computer. A miracle of the modern age, countless works of science fiction have predicted an inevitable confrontation in the not-so-distant future: man versus machine. Now, according to researchers at Rutgers University, it appears machines have already bested humanity when it comes to at least one scientific subject.
Professor Vikas Nanda of Rutgers University has spent over two decades meticulously studying the intricate nature of proteins, the highly complex substances present in all living organisms. He has dedicated his professional life to contemplating and understanding the unique patterns of amino acids that make up proteins and determine if they become hemoglobin, collagen, etc. Additionally, Prof. Nanda is an expert on the mysterious step of self-assembly, in which certain proteins clump together to form even more complex substances.
So, when study authors set out to conduct an experiment pitting a human – someone with a deep, intuitive understanding of protein design and self-assembly – against the predictive abilities of an AI computer program, Prof. Nanda made for a perfect participant.
Study authors wanted to see who, or what, could do a better job at predicting which protein sequences would combine most successfully — Prof. Nanda and several other humans, or the computer. The published results indicate the intellectual battle is close, but the AI program beat out the humans by a small margin.
What can scientists use protein self-assembly for?
Modern medicine is heavily invested in protein self-assembly because many scientists believe that fully grasping the process may lead to numerous revolutionary products for medical and industrial uses, such as artificial human tissue for wounds or catalysts for new chemical products.
“Despite our extensive expertise, the AI did as good or better on several data sets, showing the tremendous potential of machine learning to overcome human bias,” says Nanda, a professor in the Department of Biochemistry and Molecular Biology at Rutgers Robert Wood Johnson Medical School, in a university release.
Proteins consist of large amounts of amino acids, joined together end to end. These amino acid chains fold up to form three-dimensional molecules with complex shapes. The exact shape is important; the precise shape of each protein, as well as the specific amino acids it contains, determines what it does. Some scientists, including Prof. Nanda, regularly engage in an activity called “protein design,” which entails creating sequences that produce new proteins.
Most recently, Prof. Nanda and a team of researchers designed a synthetic protein capable of quickly detecting the dangerous nerve agent known as VX. This protein may lead to the development of new biosensors and treatments.
For reasons still unknown to modern science, proteins self-assemble with other proteins to form superstructures important in biology. Sometimes it appears the proteins are following a design, such as when they self-assemble into a protective outer shell of a virus (capsid). In other cases, however, proteins will self-assemble seemingly in response to something going wrong, ultimately forming deadly biological structures associated with diseases ranging from Alzheimer’s to sickle cell.
“Understanding protein self-assembly is fundamental to making advances in many fields, including medicine and industry,” Prof. Nanda adds.
How did the AI program perform?
During the test, Prof. Nanda and five other colleagues received a list of proteins and had to predict which ones were likely to self-assemble. The computer program made the same predictions, and then researchers compared responses from man and machine.
The human participants made their predictions based on their prior experimental protein observations, such as patterns of electrical charges and degree of aversion to water. The humans ended up predicting 11 proteins would self-assemble. The computer program, meanwhile, via an advanced machine-learning system, chose nine proteins.
The human experts were correct regarding six out of the 11 proteins they chose. The computer program earned a higher accuracy percentage, with six out of the nine proteins it picked out indeed able to self-assemble.
Study authors explain the human participants tended to “favor” certain amino acids over others, which led to incorrect predictions. The AI program also correctly identified some proteins that weren’t “obvious choices” for self-assembly, opening the door for more research. Prof. Nanda admits that he was once a doubter of machine learning for protein assembly investigations, but now he is much more open to the technique.
“We’re working to get a fundamental understanding of the chemical nature of interactions that lead to self-assembly, so I worried that using these programs would prevent important insights,” he concludes. “But what I’m beginning to really understand is that machine learning is just another tool, like any other.”
The study is published in the journal Nature Chemistry. | Biology |
In spring 1858, the German scientist Rudolf Virchow published an unorthodox vision of the nature of living organisms. In his book, Cellular Pathology, he argued that the human body was simply “a cell state in which every cell is a citizen”. From a single originator, all other cells are derived, he argued, and when their function is disturbed, disease will often ensue.The origins of Virchow’s arguments are intriguing. A reclusive, progressive, soft-spoken physician who had eschewed a career in the church because he thought his voice too weak for preaching, he championed the cause of public health and promoted free thinking. His views led to frequent clashes with German authorities. He became particularly incensed over their failures to tackle outbreaks of typhus and denounced them in print. For his pains, Virchow was forced to resign from his hospital post in Berlin.Exiled to suburban Würzburg, Virchow began work on his book. It was time well spent for the young physician who produced a work that would “detonate through the world of medicine”, as Siddhartha Mukherjee puts it. By comparing the human body to the perfect citizen state – a cause he firmly endorsed – and by showing the cell is the locus for all disease, Virchow provided a new vision of human physiology. In doing so, he unleashed a phalanx of scientists who followed up his insights to reveal the crucial roles of cells in determining the human condition. These included John Snow’s work on cholera in London and the bacterial breakthroughs of Louis Pasteur in Paris.Later, in the 20th century, researchers probed more closely and began to peer inside cells – with greater and greater precision. Virchow had been the first to propose that cancers are caused by cells dividing uncontrollably. A century later, scientists were pinpointing the precise pathways involved in this wayward urge, work that has continued to this day. Tumour treatments have been transformed, surgical procedures improved, and a host of diseases, from sickle cell anaemia to heart defects, are being tackled with increased success. And for this we can thank Virchow’s idea of the citizen cell. Or as Mukherjee describes his vision: “We are built of unitary blocks – extraordinarily diverse in shape, size and function, but unitary nonetheless.”Yet mysteries remain, as Mukherjee acknowledges. As an example, he points to the liver and spleen. These are broadly similar collections of cells; they are the same size; they are anatomical neighbours; and they possess virtually the same flux of blood – yet one, the liver, is among the most frequent sites of cancer while the other, the spleen, rarely has any. What subtle distinction separates these two collections of cells and explains the extreme difference in their behaviours?The problem is that we “can name cells… but we are yet to learn the songs of cell biology”, says Mukherjee, a US-based oncologist already hailed for his prizewinning books on genetics and cancer. In other words, we understand the structure of these basic building blocks of life but still do not fully know how they relate to one another, how they interact – how they sing to each other. And the quicker we learn that music, then the more speedy will be our unravelling of the diseases that still afflict us and our ability to treat them, he adds.It is a fascinating vision of illness and Mukherjee supports it well, presenting a wide variety of characters who have each played their roles in unravelling the song of the cell while peppering his narrative with case studies and cryptic pen portraits of his protagonists. Robert Edwards and Patrick Steptoe, pioneers of in vitro fertilisation – perhaps the ultimate medical act in cellular intervention – are described as “mavericks but careful mavericks”, while Nobel prize-winner Paul Nurse, one of the UK’s most senior scientists, is likened to an “elderly, wizened version of Bilbo Baggins”. A Nobel winner as a hobbit – it is an interesting notion, if nothing else.An assured book, The Song of the Cell is free of overly complex detail that would submerge the reader. The result is a confident, timely – and most importantly, biologically precise – exploration of what it means to be human. | Biology |
This graphic depicts how scientists believe water interacts with rock at the bottom of Enceladus’ ocean to create hydrothermal vent systems. These same chimney-like vents are found along tectonic plate borders in Earth’s oceans, approximately 7000 feet below the surface. Credit: NASA/JPL-Caltech/Southwest Research Institute Surrounded by a vast ocean underneath a thick ice shell, Enceladus is a hot candidate for potentially harboring alien life. A team of researchers led by the University of Arizona concluded that a future mission could provide answers even without landing on the tiny world. The mystery of whether microbial alien life might inhabit Enceladus, one of Saturn's 83 moons, could be solved by an orbiting space probe, according to a new study led by University of Arizona researchers. In a paper published in The Planetary Science Journal, the researchers map out how a hypothetical space mission could provide definite answers. When Enceladus was initially surveyed in 1980 by NASA's Voyager 1 spacecraft, it looked like a small, not overly exciting "snowball" in the sky. Later, between 2005 to 2017, NASA's Cassini probe zipped around the Saturnian System and studied Saturn's complex rings and moons in unprecedented detail. Scientists were stunned when Cassini discovered that Enceladus' thick layer of ice hides a vast, warm saltwater ocean outgassing methane, a gas that typically originates from microbial life on Earth. The methane, along with other organic molecules that build the foundations of life, were detected when Cassini flew through giant water plumes erupting from the surface of Enceladus. As the tiny moon orbits the ringed gas giant, it is being squeezed and tugged by Saturn's immense gravitational field, heating up its interior due to friction. As a result, spectacular plumes of water jet from cracks and crevices on Enceladus' icy surface into space. Last year, a team of scientists at UArizona and Université Paris Sciences et Lettres in Paris calculated that if life could have emerged on Enceladus, there is a high likelihood that its presence could explain why the moon is burping up methane. "To know if that is the case, we must go back to Enceladus and look," said Régis Ferrière, senior author of the new paper and associate professor in the UArizona Department of Ecology and Evolutionary Biology. In their latest paper, Ferrière and his collaborators report that while the hypothetical total mass of living microbes in Enceladus' ocean would be small, a visit from an orbiting spacecraft is all that would be needed to know for sure whether Earthlike microbes populate Enceladus' ocean underneath its shell. "Clearly, sending a robot crawling through ice cracks and deep-diving down to the seafloor would not be easy," Ferrière said, explaining that more realistic missions have been designed that would use upgraded instruments to sample the plumes like Cassini did, or even land on the moon's surface. "By simulating the data that a more prepared and advanced orbiting spacecraft would gather from just the plumes alone, our team has now shown that this approach would be enough to confidently determine whether or not there is life within Enceladus' ocean without actually having to probe the depths of the moon," he said. "This is a thrilling perspective." Located about 800 million miles from Earth, Enceladus completes an orbit around Saturn every 33 hours. While the moon isn't even as wide as the state of Arizona, it visually stands out because of its surface; like a frozen pond glinting in the sun, the moon reflects light like no other object in the solar system. Along the moon's south pole, at least 100 giant water plumes erupt through cracks in the icy landscape much like lava from a violent volcano. Scientists believe that water vapor and ice particles ejected by these geyser-like features contribute to one of Saturn's iconic rings. This ejected mixture, which brings up gases and other particles from deep inside Enceladus' ocean, was sampled by the Cassini spacecraft. The excess methane Cassini detected in the plumes conjures images of extraordinary ecosystems found in the lightless depths of Earth's oceans: hydrothermal vents. Here, at the edges of two adjacent tectonic plates, hot magma below the seafloor heats the ocean water in porous bedrock, creating "white smokers," vents spewing scorching hot, mineral-saturated seawater. With no access to sunlight, organisms depend on energy stored in chemical compounds released by the white smokers to make a living. "On our planet, hydrothermal vents teem with life, big and small, in spite of darkness and insane pressure," Ferrière said. "The simplest living creatures there are microbes called methanogens that power themselves even in the absence of sunlight." Methanogens convert dihydrogen and carbon dioxide to gain energy, releasing methane as a byproduct. Ferrière's research group modeled its calculations based on the hypothesis that Enceladus has methanogens that inhabit oceanic hydrothermal vents resembling the ones found on Earth. In this way, the researchers calculated what the total mass of methanogens on Enceladus would be, as well as the likelihood that their cells and other organic molecules could be ejected through the plumes. "We were surprised to find that the hypothetical abundance of cells would only amount to the biomass of one single whale in Enceladus' global ocean," said the paper's first author, Antonin Affholder, a postdoctoral research associate at UArizona who was at Paris Sciences & Lettres when doing this research. "Enceladus' biosphere may be very sparse. And yet our models indicate that it would be productive enough to feed the plumes with just enough organic molecules or cells to be picked up by instruments onboard a future spacecraft." Enceladus has garnered recent attention as a location to someday be revisited and more thoroughly scrutinized. One proposal, the "Enceladus Orbilander," designed by Johns Hopkins Applied Physics Laboratory, envisions a mission that would collect extensive data about Enceladus by landing on and orbiting this celestial body beginning in the 2050s. "Our research shows that if a biosphere is present in Enceladus' ocean, signs of its existence could be picked up in plume material without the need to land or drill," said Affholder, "but such a mission would require an orbiter to fly through the plume multiple times to collect lots of oceanic material." The paper includes recommendations about the minimum amount of material that must be collected from the plumes to confidently search for both microbial cells and certain organic molecules. Observable cells would show direct evidence of life. "The possibility that actual cells could be found might be slim," Affholder said, "because they would have to survive the outgassing process carrying them through the plumes from the deep ocean to the vacuum of space—quite a journey for a tiny cell." Instead, the authors suggest that detected organic molecules, such as particular amino acids, would serve as indirect evidence for or against an environment abounding with life. "Considering that according to the calculations, any life present on Enceladus would be extremely sparse, there still is a good chance that we'll never find enough organic molecules in the plumes to unambiguously conclude that it is there," Ferrière said. "So, rather than focusing on the question of how much is enough to prove that life is there, we asked, 'What is the maximum amount of organic material that could be present in the absence of life?'" If all measurements were to come back above a certain threshold, it could signal that life is a serious possibility, according to the authors. "The definitive evidence of living cells caught on an alien world may remain elusive for generations," Affholder said. "Until then, the fact that we can't rule out life's existence on Enceladus is probably the best we can do." More information: Antonin Affholder et al, Putative Methanogenic Biosphere in Enceladus's Deep Ocean: Biomass, Productivity, and Implications for Detection, The Planetary Science Journal (2022). DOI: 10.3847/PSJ/aca275 Citation: What it would take to discover life on Saturn's icy moon Enceladus (2022, December 21) retrieved 21 December 2022 from https://phys.org/news/2022-12-life-saturn-icy-moon-enceladus.html This document is subject to copyright. Apart from any fair dealing for the purpose of private study or research, no part may be reproduced without the written permission. The content is provided for information purposes only. | Biology |
New insights into an old drug: Scientists discover why aspirin works so well
New research has revealed important information about how aspirin works. Even though this drug has been available commercially since the late 1800s, scientists have not yet fully elucidated its detailed mechanism of action and cellular targets. The new findings could pave the way to safer aspirin alternatives and might also have implications for improving cancer immunotherapies.
Aspirin, which is a nonsteroidal anti-inflammatory drug, is one of the most widely used medications in the world. It is used to treat pain, fever and inflammation, and an estimated 29 million people in the U.S. take it daily to reduce the risk of cardiovascular diseases.
Scientists know that aspirin inhibits the cyclooxygenase enzyme, or COX, which creates messenger molecules that are crucial in the inflammatory response. Researchers led by Subhrangsu Mandal, a professor of chemistry and biochemistry at the University of Texas at Arlington, have discovered more about this process.
Prarthana Guha, a graduate student in Mandal's lab, will present the team's findings at Discover BMB, the annual meeting of the American Society for Biochemistry and Molecular Biology, March 25–28 in Seattle. Avisankar Chini also made significant contributions to the study.
"Aspirin is a magic drug, but long-term use of it can cause detrimental side effects such as internal bleeding and organ damage," Mandal said. "It's important that we understand how it works so we can develop safer drugs with fewer side effects."
The team found that aspirin controls transcription factors required for cytokine expression during inflammation while also influencing many other inflammatory proteins and noncoding RNAs that are critically linked to inflammation and immune response. Mandal said this work has required a unique interdisciplinary team with expertise in inflammation signaling biology and organic chemistry.
They also showed that aspirin slows the breakdown of the amino acid tryptophan into its metabolite kynurenine by inhibiting associated enzymes called indoleamine dioxygenases, or IDOs. Tryptophan metabolism plays a central role in the inflammation and immune response.
"We found that aspirin downregulates IDO1 expression and associated kynurenine production during inflammation," Mandal said. "Since aspirin is a COX inhibitor, this suggests potential interplay between COX and IDO1 during inflammation."
IDO1 is an important target for immunotherapy, a type of cancer treatment that helps the body's immune system seek out and destroy cancer cells. Because COX inhibitors modulate the COX–IDO1 axis during inflammation, the researchers predict that COX inhibitors might also be useful as drugs for immunotherapy.
Mandal and his team are now creating a series of small molecules that modulate COX–IDO1 and will explore their potential use as anti-inflammatory drugs and immunotherapeutic agents.
More information: Prarthana Guha will present this research from 4 to 5:30 p.m. PDT on Tuesday, March 28, in Exhibit Hall 4AB of the Seattle Convention Center (Poster Board No. 185) | Biology |
A better understanding of gas exchange between the atmosphere and ocean can improve global climate models
The injection of bubbles from waves breaking in turbulent and cold high-latitude regions of the high seas is an underappreciated way in which atmospheric gases are transported into the interior ocean. An improved mechanistic understanding of gas exchange in high latitudes is important for several reasons, including to better constrain climate models that are used to predict changes in the ocean inventory of key gases like oxygen and carbon dioxide.
A new WHOI-led study, "Dissolved gases in the deep North Atlantic track ocean ventilation processes", published this week in Proceedings of the National Academy of Sciences, combines new geochemical tracers and ocean circulation models to investigate the physics by which atmospheric gases get into the deep ocean.
The study uses a new technique to precisely measure noble gas isotopes dissolved in samples of seawater collected from as deep as 4.5 kilometers in the North Atlantic. Noble gases—the elements on the far right-hand side of the periodic table—are unreactive and unused by biology, making them useful tracers of physics.
Noble gases are neither added nor removed from water after the exchange with the atmosphere at the sea-surface. As a result, measuring dissolved noble gases in the deep North Atlantic off the coast of Bermuda tells scientists about the physics of gas exchange that happened in special regions like the Irminger Sea, where the surface ocean becomes dense enough under stormy wintertime conditions to sink and form deep water that slowly flows south.
Alan Seltzer, lead author of the paper, said these new findings suggest that the dissolution of bubbles in the high-latitude ocean "may be the dominant pathway by which all of the noble gases, oxygen, and nitrogen get into the deep ocean." This study is a step forward toward understanding the basic physics by which gases get into the ocean, said Seltzer, an assistant scientist in the Marine Chemistry and Geochemistry Department at the Woods Hole Oceanographic Institution (WHOI).
"Anything we can do to improve the accuracy of the way models represent our world is helpful, especially when it has to do with gases," he said. "We care about oxygen for global ecosystems, and we care about CO2 because the ocean is a huge player in taking up our emissions. So if we can improve the way models represent physical processes such as gas exchange, we can have more confidence in future simulations with models as a way of predicting how things will change in a warmer world with more CO2."
"Understanding how the ocean takes up and releases gases to the atmosphere is a challenging but critically important step toward predicting their response to climate change. Being chemically and biologically inert, noble gases are powerful tools for probing the physical processes involved," said journal article co-author William Jenkins, an emeritus research scholar in WHOI's Marine Chemistry and Geochemistry Department.
"The Seltzer et al. paper is an important step forward in this journey in that it combines new high-precision noble gas concentration and isotope ratio measurements that are key to unlocking an understanding of these vital processes. Their results also shed light on the oceanic nitrogen cycle, which is both important for climate change issues, but also our fundamental understanding of how ocean food web is supported."
Measurements for the study come from the Bermuda Atlantic Time Series (BATS) site (31°40 N, 64°10 W), where repeat cruises have surveyed the ocean from top to bottom nearly monthly since 1988. The BATS site is an ideal place to collect samples, because it is located downstream of deep-water formation regions.
Deep-ocean noble gas concentrations at the BATS site allow scientists to study gas exchange during wintertime events where the deep ocean is formed as surface waters cool and become more dense. Under these harsh conditions, direct observations are challenging and scarce, which is why measurements from the deep ocean in warmer, more southern locations are so valuable.
Seltzer said a way to understand why bubbles play such a huge role in transporting noble gases, oxygen, and nitrogen into the deep ocean is to realize that "every time a wave breaks, that massively increases the available surface area for the exchange of gases between the atmosphere and the ocean."
"The exchange of carbon dioxide and other greenhouse gases between the deep ocean—approximately 75% of the total ocean volume—and the atmosphere occurs at high latitudes during winter, particularly during storm events. Measurements of inert noble gas concentrations in the deep North Atlantic Ocean documented the importance of large bubbles that form during windy storm events, significantly increasing our understanding of the gas exchange rate for the deep water," said co-author William Smethie, special research scientist and retired research professor at the Lamont-Doherty Earth Observatory of Columbia University.
"This improves our ability to quantify the exchange of carbon dioxide and greenhouse gases between the ocean and atmosphere and predict how their atmospheric concentrations will impact the earth's climate, which is critical for developing policies to mitigate global warming."
More information: Alan M. Seltzer et al, Dissolved gases in the deep North Atlantic track ocean ventilation processes, Proceedings of the National Academy of Sciences (2023). DOI: 10.1073/pnas.2217946120
Journal information: Proceedings of the National Academy of Sciences
Provided by Woods Hole Oceanographic Institution | Biology |
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Salesforce’s ProGen designed sequences based on the “sentences” of biological proteins.
Scientists are investigating whether the AI could identify treatment for disorders like rheumatoid arthritis and multiple sclerosis.
Artificial intelligence is a master of imitation. Every time scientists design an AI—whether to mimic human language or master a game like chess—it either matches or far exceeds the capabilities of its biological creators. Now, AI has proven that it can even master the art of biology itself.
Researchers at the University of California-San Francisco, the University of California-Berkeley, and Salesforce Research, a science arm of the SF-based software company, developed an AI capable of copying evolution itself. This doesn’t mean the AI created some sort of evolutionary superior superhuman (yet), but instead, the AI designed sequences of 20 amino acids that make up proteins. When compared to nature’s handiwork, some of the sequences worked just as well as ones generated over millions of years of evolution. The researchers published their findings in the journal Nature Biotechnology.
Interestingly, scientists didn’t design an AI from scratch, but rather, repurposed one from an unlikely field: a language model. Researchers used Salesforce’s ProGen natural language-processing abilities and focused on the “sentences” of biological proteins—essentially a language of amino acids.
“In the same way that words are strung together one-by-one to form text sentences, amino acids are strung together one-by-one to make proteins,” Nikhil Naik, the Director of AI Research at Salesforce Research, told Motherboard. “Building on this insight, we apply neural language modeling to proteins for generating realistic, yet novel protein sequences.”
After training ProGen on 280 million proteins, the AI was “iteratively optimized by learning to predict the probability of the next amino acid given the past amino acids in a raw sequence,” according to the paper. The team eventually focused on five specific artificial proteins and compared them to an enzyme found in chicken eggs called “hen egg white lysozyme”—two of the AI-generated proteins compared favorably.
Overall, Salesforce estimates that 73 percent of ProGen’s proteins could function, compared to 59% of natural proteins, and found that the AI was also able to detect evolutionary patterns (though it wasn’t specifically designed to). AI has designed human proteins before, but this is the first time a language model AI was able to pull off the feat.
But the team isn’t interested in just answering the question of whether language model AIs can design proteins. Because proteins lie at the foundations of many illnesses, The Salesforce AI Research team is already investigating how ProGen could identify treatment for disorders like rheumatoid arthritis and multiple sclerosis.
So while some AIs are trained to beat humans at their own game (literally), language models like ProGen could one day put one over on evolution itself and help humans combat some of the world’s most debilitating health problems.
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Between 6.4 and 5.8 million years ago, most of the land bridge that connects North and South America had already emerged and the channels connecting both Pacific and Atlantic oceans were shallow. Recent fossil discoveries in the northern Panama Canal area suggest that marine species interchange persisted across these shallow waters during the final stages of formation of the isthmus.
In 2017 and 2019, Aldo Benites-Palomino was studying fossils collected in Caribbean Panama, when he came across some unexpected specimens. He was a biology student in Perú, where his training had been very classical. As an intern and later a fellow at the Smithsonian Tropical Research Institute (STRI), his mindset shifted. His mentor, STRI staff scientist and paleobiologist Carlos Jaramillo, encouraged his students to change their focus when looking at fossils: instead of thinking about specimens or methods, to think about the questions that the fossils could help answer.
"I wanted to go to STRI because it is the most important tropical biology center in the world," said Benites-Palomino. "There I was able to learn a lot about the way biology and ecology is done in the modern world."
The fossil remains belonged to small-sized cetaceans, a group of aquatic mammals that includes whales and dolphins, and the specimens were new for the region. Most of them had been collected by Carlos de Gracia from STRI and Jorge Velez Juarbe from the Los Angeles Museum of Natural History, both co-authors in a new paper published in Biology Letters. In the article, Benites-Palomino and his colleagues go beyond describing the specimens, they also unearth the story they reveal about the isthmus' deep past.
The fossils belonged to the Late Miocene, around 6.4 to 5.8 million years ago, when the final stages of formation of the isthmus had already started. This event affected oceanic waters and marine currents across the globe and triggered speciation events, where species separated by the land bridge developed their own unique characteristics on either ocean.
However, these cetaceans found in Caribbean Panama shared similarities with other Late Miocene species from the North and South Pacific Ocean, particularly the Pisco Formation in Peru, suggesting that some organisms were still able to disperse via the shallowing seaway at a time when deep water interchange between both oceans was no longer occurring.
The lack of fossil marine mammals from the western Caribbean has thus far hampered understanding of the region's deep past, so these new findings help strengthen current knowledge regarding the connectivity between the Pacific and Caribbean marine faunas during the final phases of formation of the isthmus.
"The marine vertebrate fossil record of Panama has been barely explored," said Carlos Jaramillo, STRI staff scientist and co-author of the study. "There are still many specimens that need to be studied and many more still in the rocks waiting to be found."
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Forest growing season in eastern US has increased by a month, finds study
The growing period of hardwood forests in eastern North America has increased by an average of one month over the past century as temperatures have steadily risen, a new study has found.
The study compared present-day observations of the time span from budburst to peak leaf coloration in seven tree species to similar documentation that was collected by an Ohio farmer at the turn of the 20th century.
An analysis of changes in those leaf patterns along with decades of temperature data for northwest Ohio showed a clear connection between increased warming during winter and spring and an extended period of tree growth.
The implications of the longer growing period—both positive and negative—remain unknown. But the simple fact that leaves stay on trees about 15% longer than they did 100 years ago is an "obvious indicator that temperatures are changing and shows that things are not the way they used to be—they are profoundly different," said lead author Kellen Calinger-Yoak, assistant professor of evolution, ecology and organismal biology at The Ohio State University.
"An entire month of growing season extension is huge when we're talking about a pretty short period of time for those changes to be expressed," she said.
Calinger-Yoak completed the research with Peter Curtis, professor emeritus of evolution, ecology and organismal biology at Ohio State. The study was published recently in the journal PLOS ONE.
Wauseon, Ohio, farmer Thomas Mikesell recorded temperatures, precipitation and observations of seasonal changes to trees and other plants from 1883 to 1912—creating what may be the only comprehensive dataset of pre-warming tree growing patterns in all of North America, Calinger-Yoak said.
For this study, Calinger-Yoak traveled to Wauseon multiples times per week in the spring and fall between 2010 and 2014 to make her own observations of seven species: American elm, black walnut, white oak, black oak, eastern cottonwood, staghorn sumac and sassafras trees, all of which are hardy species that grow well across most of the United States. The researchers also used monthly temperature and precipitation data from the U.S. Historical Climatology Network's Wauseon station to calculate long-term trends.
Though species did not respond to changing temperatures in exactly the same way—some budded early and most kept their leaf color longer into the fall—Calinger-Yoak said two patterns stood out in the analysis: Average mid-winter and spring temperatures in the region have increased by up to 5 degrees Fahrenheit since 1892, with six of the 10 warmest years in November and December occurring since 1990, and leaves' longer life spans into autumn indicated when most of the growing season extension took place—because foliage coloration was delayed.
Calinger-Yoak used the dates of peak coloration, rather than when leaves fell to the ground, to determine the end point of the growing season to tie in with each tree's peak period for photosynthesis. As leaf colors fade, trees become much less efficient at taking in carbon dioxide and water to obtain the sugars that sustain them.
While extended growing likely increases trees' absorption of carbon dioxide from the atmosphere, the mix of overall warming and extreme temperature fluctuations can stress trees in ways this research couldn't detect. Overall, though, there was quite a bit of variety in the species' responses to changing temperatures—which is a red flag for a biologist.
"If you're exposing organisms to the exact same environmental pressures and you see radically different responses, chances are that one of those responses is going to be better in the long term than the other," Calinger-Yoak said. "Time will tell who the long-term winners and losers will be, and what that means for how different forests will end up looking if some species are consistently underperforming because they can't handle the extremes we've introduced to the system."
These findings point to the need for even more species-specific research to improve models designed to predict how forests, and their valuable carbon-absorption service, will respond as the climate continues to change, she said.
"We are invested in making the bad effects of global warming less horrible, and are wondering how much benefit we can get from trees we already have and from potentially planting more trees—that's really important," she said. "When we're thinking about a relatively low-cost mitigation strategy, planting a whole bunch of trees that suck CO2 out of the air is a really good strategy, but to promote those activities you also have to have evidence of the level of benefit you'd derive from it."
More information: Kellen Calinger et al, A century of climate warming results in growing season extension: Delayed autumn leaf phenology in north central North America, PLOS ONE (2023). DOI: 10.1371/journal.pone.0282635
Journal information: PLoS ONE
Provided by The Ohio State University | Biology |
Image source, Katherine HawkesImage caption, The sunfish was found deceased on a beach at Great YarmouthThe discovery of a dead sunfish on a Norfolk beach is "incredibly important" to scientists studying the biggest bony fish in the world and potential climate change links, an expert said.The juvenile fish, measuring about 1.5m (5ft), appeared on North Beach in Great Yarmouth last weekend.Adults can grow to 4m (13ft) and weigh up to two tonnes.Dr Ben Garrod, from the University of East Anglia, said four had washed up in a year but the reason was unknown."Sunfish are one of the most weird but iconic fish in the sea," the professor of evolutionary biology and BBC science presenter said.The species - Mola mola - is the largest bony fish and generally lives in temperate and tropical waters.Katherine Hawkes photographed the sunfish on the Norfolk beach on New Year's Day and said at first she did not know what she was looking at."Then I realised I'd once seen a sunfish swimming but they are rare at this time of the year," she said.Sunfish (Mola mola)Image source, Getty ImagesThe ocean sunfish is the world's largest bony fishThe fish swim down to depths of between 50 and 200m (164ft and 656ft) They feed mainly on jellyfishTheir name refers to their habit of lying at the sea surface on their side as if sunbathing(Source: Marine Conservation Society)At about 1.5m from the top to bottom fin, Dr Garrod said this was "the largest we've seen... in the last few years"."But it's still a baby compared to the size of the adults," he added.This is the fourth he had been told had washed up on Norfolk's beaches in the past 12 months, three of which have been examined at the UEA."We don't know why they died and this is an ongoing research project, but it's incredibly important as we know so little about them," he said."I know they have washed up on the Norfolk coast - maybe once every 10 years - but to have four in the last 12 months is really interesting."We don't have the evidence to say it's related to climate change but no-one's denying the oceans are changing."Image source, Getty ImagesImage caption, Sunfish are listed as vulnerable on the IUCN Red ListProf Heather Koldewey, senior marine technical advisor at the Zoological Society of London, agreed."A single observation of one fish makes it hard to jump to a big conclusion around climate change, especially as occasionally dead sunfish have been recorded in previous winters off the UK coast," she said."However, as sea temperatures change, we are seeing the distributions of many marine species change. "There have been more sightings of sunfish in the summer in the southwest of the UK, for example, which may be more indicative of climate-driven changes."'A lost migrant'A spokesperson from the Norfolk Wildlife Trust said: "Sunfish are such a unique species to see here in Norfolk. It's unusual for them to be found on our coastline, as they tend to thrive in much warmer waters. "Despite this, a number of sunfish have been found along the Norfolk coast [recently]."The fish are likely to have been following jellyfish - their preferred food source - and found themselves in difficulties in the much colder waters of the North Sea. "Seeing unusual species such as sunfish here in Norfolk appears to be becoming more common, and could be linked to climate change and warming seas."Joint marine recorder for Norfolk, Rob Spray, said: "We do look for trends, and as the climate changes we look for species that are increasing - and the North Sea is a pocket within reach, but a lost migrant like this one has come to the end of what it can survive in."Dr Garrod added: "While it's sad to see that any animal dies, having sunfish here is unusual, exciting, and very interesting." Find BBC News: East of England on Facebook, Instagram and Twitter. If you have a story suggestion email [email protected] Internet LinksThe BBC is not responsible for the content of external sites. | Biology |
New study challenges our understanding of the immune system
Researchers have created a radical new view of how immune cells recognise threats such as viruses. The discovery could be used to design better vaccines and to gain a deeper insight into autoimmune diseases and allergies.
Method
- The researchers applied an interdisciplinary approach, which encompassed, amongst other things, a ground-breaking super-resolution microscopy technique called DNA PAINT, as well as a unique nanoscaffold made of modified nucleic acids and two sophisticated, genetically modified mouse DNA strains.
A recently published study from Aarhus University may mean a textbook chapter on the immune system will have to be rewritten.
In the study, published in the journal Nature Communications, the researchers reveal crucial new knowledge about B cells, which form a vital element in the body’s defence system. B cells are the cells that generate protective antibodies when we are vaccinated or have an infection – and it is also the B cells that produce harmful antibodies in connection with allergies or autoimmune diseases.
The researchers have examined the earliest step in activating the B cells, namely the activation mechanism that is triggered when the cells recognise a specific target or ‘enemy’ – an antigen.
“Previously, it was believed that the antigens from, for example, viruses or vaccines would have to cross-bind a B-cell’s receptors on the cell surface (see illustration). That’s what it says in all the textbooks. But now we have shown that even antigens that can only bind one receptor at a time are able to activate the B cells,” says Søren Degn, associate professor at Department of Biomedicine, who is the senior author of the article.
The discovery is important on several levels, he explains.
“The result is significant because it represents a breakthrough in our understanding of how these important immune cells ‘recognise’ their enemies. Once we understand what is going on, we can imitate it in the design of new vaccines, to ensure maximum effect. One might say that our findings can make us better at mimicking the pathogenic microorganisms, and thus better at provoking or ‘cheating’ the immune system into generating a good immune response when we vaccinate.”
(The article continues under the illustration)
A hotly debated topic in the field
The discovery is interesting for both the immunological field and for cell biology in general, because the researchers have shed new light on the foundation for how receptors on the surface of cells send signals into the cells – a key biological process.
“The study enables us to better understand the background for one of the most important processes in the immune system, and one of the most important processes in cell biology. But it is clear that, in the long term, this could also have important application-oriented aspects,” says Søren Degn.
The researchers have begun preclinical vaccine trials with the aim of translating the findings into clinically relevant vaccine design. They are also attempting to use the same tools in reverse, to target and turn off harmful immune system responses such as allergic reactions and autoimmune diseases.
“When we understand how the B cells are activated, we can create better vaccines. In the slightly longer term, we may also be able to switch off B-cell activation in cases where it is harmful. We are studying both of these in the CellPAT basic research centre at Aarhus University,” says Søren Degn.
For many years, the activation of B cells has been the object of a great deal of discussion among researchers, because the predominant model for how immune recognition takes place could not explain all of the observations.
In the new study, the researchers at the Department of Biomedicine and iNANO in Aarhus, in a cross-disciplinary collaboration with the Max Planck Institute in Munich, have created new tools that make it possible to puncture the predominant model and thereby bury the decades-old paradigm.
“We have shown that the way in which the activation of B cells has been explained over the past thirty or forty years is wrong. This is an important finding, because it opens the door to better vaccines and better treatment of a large group of diseases,” says Søren Degn.
Behind the research results
- The study consists of ex vivo cell experiments, i.e., in vitro studies of cells from mouse models, nanotechnology and super-resolution microscopy (advanced microscopy).
- The study is the result of a collaboration between several groups in the Department of Biomedicine at Aarhus University (Degn, Thiel and Vorup-Jensen), iNANO (Kjems) and the Max Planck Institute in Munich (Jungmann). The work stems from the basic research centre CellPAT, the Centre for Cellular Signal Patterns.
- External funding (main funders only): The Danish National Research Foundation and the Carlsberg Foundation
- Learn more: Antigen footprint governs activation of the B cell receptor | Nature Communications | Biology |
A new gadget takes advantage of sharks’ sixth sense to send the fish scurrying away from deadly hooks. Sharks, rays and their relatives can detect tiny electric fields, thanks to bulbous organs concentrated near their heads called ampullae of Lorenzini. So researchers developed SharkGuard, a cylindrical device that attaches to fishing lines just above the hook and emits a pulsing, short-range electric field. The device successfully deters sharks and rays, probably by temporarily overwhelming their sensory system, the scientists report November 21 in Current Biology. While many people are afraid of sharks, the fear makes more sense the other way around; numerous shark species are at risk of extinction, largely due to human activities (SN: 11/10/22). One major problem facing sharks and rays is bycatch, where the creatures get accidentally snagged by fishermen targeting other fish like tuna, says David Shiffman, a marine biologist and faculty research associate at Arizona State University in Tempe. Whether sharks and rays would be repelled or attracted by the electric fields generated by SharkGuard devices was an open question. The animals use their extra sense when hunting to detect the small electrical fields given off by prey. So marine biologist Rob Enever of Fishtek Marine, a conservation engineering company in Dartington, England, and his colleagues sent out two fishing vessels in the summer of 2021 — both outfitted with some normal hooks and some hooks with SharkGuard — and had them fish for tuna. In short, the sharks wanted nothing to do with the SharkGuard gadgets. Video reveals blue sharks approaching a hook with SharkGuard and veering away with no apparent harm. When encountering an unadorned hook, sharks took the bait, becoming bycatch. Sharks and their relatives can detect electric fields using organs in the skin called ampullae of Lorenzini. So researchers tested whether attaching a SharkGuard device, which emits a pulse of electricity every two seconds, to a fishing line just above the hook could deter a shark. The results, showing a shark taking the bait of a normal hook but other sharks veering away from hooks with the device, could hold promise for preventing millions of sharks from becoming bycatch. Hooks with the electric repellant reduced catch rates of blue sharks (Prionace glauca) by 91 percent compared with standard hooks, dropping from an average of 6.1 blue sharks caught per 1,000 hooks to 0.5 sharks. And 71 percent fewer pelagic stingrays (Pteroplatytrygon violacea) were caught using SharkGuard hooks, going from seven captured rays per 1,000 hooks on average to two rays. A typical fishing boat like those used in the study has approximately 10,000 hooks. So a boat whose entire set of hooks were outfitted with SharkGuard would go from catching about 61 blue sharks to 5, and 70 pelagic rays to 20. When you scale those numbers up to the millions of sharks and rays that are accidentally caught in longline fisheries every year, Enever says, “you’re going to have massive recovery of these pelagic shark populations.” “It’s definitely a notable and significant effect,” says Shiffman, who was not involved with the study. “If [the devices] went into effect across the fishing fleet that interacts with blue sharks, it would certainly be good news for [them].” But that doesn’t mean that SharkGuard is ready to be rolled out. Tuna catch rates were unseasonably low across the board in this study, which made it impossible to determine yet whether tuna are also bothered by the device. If they are, it wouldn’t make sense for fishermen to use the device in its current form. The team is also working to make SharkGuard smaller, cheaper and as easy to manage as possible, so that fishermen can “fit and forget” it. For example, the current battery, which needs to be changed every couple of weeks, will be swapped for one that can be induction charged while the fishing line is not in use, “like a toothbrush, basically,” Enever says. Shiffman would like to see SharkGuard tested in different environments and on other types of sharks. “There are a lot of shark species that are caught as bycatch on these longlines,” he says. And while this invention seems effective so far, no technology will serve as a silver bullet for shark conservation. “Fixing this problem of bycatch is going to require a lot of different solutions working in concert,” Shiffman says. The need for solutions is urgent. “We’re at a situation now where many of our pelagic species are either critically endangered, endangered or vulnerable,” Enever says. But the new findings are “a real story of ocean optimism,” he says. They show that “there’s people out there … trying to resolve these things. There’s hope for the future.” | Biology |
Scalloped hammerhead sharks hold their breath to keep their bodies warm during deep dives into cold water where they hunt prey such as deep sea squids. This discovery, published today in Science by University of Hawai'i at Manoa researchers, provides important new insights into the physiology and ecology of a species that serves as an important link between the deep and shallow water habitats.
"This was a complete surprise!" said Mark Royer, lead author and researcher with the Shark Research Group at the Hawai'i Institute of Marine Biology (HIMB) in the UH Manoa School of Ocean and Earth Science and Technology. "It was unexpected for sharks to hold their breath to hunt like a diving marine mammal. It is an extraordinary behavior from an incredible animal."
Shark gills are natural radiators that would rapidly cool the blood, muscles, and organs if scalloped hammerhead sharks did not close their gill slits during deep dives into cold water. These sharks are warm water animals but feed at depths where seawater temperatures are similar to those found in Kodiak Alaska (around 5ºC/ 40ºF), yet they need to keep their bodies warm in order to hunt effectively.
"Although it is obvious that air-breathing marine mammals hold their breath while diving, we did not expect to see sharks exhibiting similar behavior," said Royer. "This previously unobserved behavior reveals that scalloped hammerhead sharks have feeding strategies that are broadly similar to those of some marine mammals, like pilot whales. Both have evolved to exploit deep dwelling prey and do so by holding their breath to access these physically challenging environments for short periods."
The research team discovered this unexpected phenomenon by equipping deep-diving scalloped hammerhead sharks with devices that simultaneously measured their muscle temperature, depth, body orientation, and activity levels. They saw that their muscles stayed warm throughout their dive into deep cold water but suddenly cooled as the sharks approached the surface toward the end of each dive. Computer modeling suggested that hammerhead sharks must be preventing heat loss from their gills to keep their bodies warm during these deep-dives into cold water.
Additionally, video of a scalloped hammerhead shark swimming along the seabed at a depth of 1,044 meters (more than 3,400 feet) showed its gill slits tightly closed, whereas similar images from surface waters show these sharks swimming with their gill slits wide open. A sudden cooling in muscle temperature as scalloped hammerhead sharks approach the surface at the end of each dive suggests that they opened their gill slits to resume breathing while still in relatively cool water.
"Holding their breath keeps scalloped hammerhead sharks warm but also shuts off their oxygen supply," said Royer. "So, although these sharks hold their breath for an average of 17 minutes, they only spend an average of four minutes at the bottom of their dives at extreme depths before quickly returning to warmer, well-oxygenated surface waters where breathing resumes."
"This discovery fundamentally advances our understanding of how scalloped hammerhead sharks are able to dive to great depths and withstand frigid temperatures in order to capture prey," said Royer. "It also demonstrates the delicate physiological balance that scalloped hammerhead sharks must strike in order to forage successfully."
Scalloped hammerhead sharks are not listed as threatened in Hawaii but are regionally endangered in other parts of the world due to overfishing, bycatch, and nursery habitat loss.
"This new and detailed understanding of scalloped hammerhead physiology and ecology enhances our ability to effectively manage and conserve this iconic species by revealing potential vulnerabilities associated with changing ocean conditions or future human exploitation of these deep foraging habitats, such as deep-sea mining or large-scale fishing in the mesopelagic "twilight zone," both of which might make it harder or more dangerous for these sharks to hunt their natural prey," said Royer. "This extraordinary physiological feat that allows scalloped hammerhead sharks to expand their ecological niche into the deep sea could very well make them vulnerable to additional human impacts."
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Last November, Northeastern University student Andre Neto Caetano watched the live, late-night launch of NASA’s Artemis 1 from Kennedy Space Center in Florida on a cellphone placed on top of a piano in the lobby of the hotel where he was staying in California.
“I had, not a flashback, but a flash-forward of seeing maybe Artemis 4 or something, and COBRA, as part of the payload, and it is on the moon doing what it was meant to do,” Caetano told VOA during a recent Skype interview.
Artemis 1 launched the night before Caetano and his team of scholars presented their Crater Observing Bio-inspired Rolling Articulator (COBRA) rover project at NASA’s Breakthrough, Innovative, and Game Changing (BIG) Idea Challenge. The team hoped to impress judges assembled in the remote California desert.
“They were skeptical that the mobility solutions that we were proposing would actually work,” he said.
That skepticism, said Caetano, came from the simplicity of their design.
“It’s a robot that moves like a snake, and then the head and the tail connect, and then it rolls,” he said.
NASA’s BIG Idea Challenge prompted teams of college students to compete to develop solutions for the agency’s ambitious goals in the upcoming Artemis missions to the moon, which Caetano explains are “extreme lunar terrain mobility.”
Northeastern’s COBRA is designed to move through the fine dust, or regolith, of the lunar surface to probe the landscape for interesting features, including ice and water, hidden in the shadows of deep craters.
“They never could … deploy a robot or a ground vehicle that can sort of negotiate the environment and get to the bottom of these craters and look for ice water content,” said professor Alireza Ramezani, who advises the COBRA team and has worked with robotic designs that mimic the movements of real organisms, something Caetano said formed a baseline for their research.
“With him building a robot dog and robot bat, we knew we wanted to have some ‘bioinspiration’ in our project,” Caetano said.
Using biology as the driving force behind COBRA’s design was also something Ramezani hoped would win over judges in NASA’s competition.
“Our robot sort of tumbled 80 to 90 feet (24-27 meters) down this hill and that … impressed the judges,” he told VOA. “We did this with minimum energy consumption and within, like, 10 or 15 seconds.”
Caetano said COBRA weighs about 7 kilograms, “so the fact that COBRA is super light brings a benefit to it, as well.”
Ramezani added that COBRA is also cost-effective.
“If you want to have a space-worthy platform, it’s going to be in the order of $100,000 to $200,000. You can have many of these systems tumbling down these craters,” he said.
The Northeastern team’s successful COBRA test put to rest any lingering skepticism, sending them to the top of NASA’s 2022 BIG Idea competition and hopefully — in the not-too-distant future — to the top of NASA’s Space Launch System on its way to the moon.
“I’m not saying this, our judges said this. It’s potentially going to transform the way future space exploration systems look like,” said Ramezani. “They are even talking to some of our partners to see if we can increase technology readiness of the system, make it space worthy, and deploy it to the moon.”
Which is why, despite his impending graduation later this year, Caetano plans to continue developing COBRA alongside his teammates.
“Because we brought it to life together, the idea of just fully abandoning it at graduation probably doesn’t appeal to most of us,” Caetano said. “In some way or another, we still want to be involved in the project, in making sure that … we are still the ones who put it on the moon at some point.”
That could happen as soon as 2025, the year NASA hopes to return astronauts to the lunar surface in the Artemis program. | Biology |
Call them plant motors. Or plant muscles. Tiny bulges of specialized cells in a mimosa plant can fold its feathery leaflets together in seconds, then relax — and do it again.
A new look at these bulges on the Mimosa pudica plant has revealed more details of how a leaf manages its unusually fast folding, says biomechanist David Sleboda of the University of California, Irvine. “I think that these particular organs are really cool because their motion is reversible,” he says. “[W]hen people see plant motion that is reversible, it feels much more similar to animal motion.”
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Scientists have already worked out the basic chemistry that drives a little mimosa motor, or pulvinus, he and colleagues write in a paper slated for the Feb. 6 Current Biology. When a deer hoof or something else scary jostles a leaf, potassium and some other ions shift from one part of a pulvinus toward another. Water follows the swoosh of ions. Cells that lose water deflate and sag while those on the other side bloat. Distortions in multiple pulvini make the halves of a feathery leaf fold toward each other, like an invisible hand gently closing a book.
Instead of studying chemistry, Sleboda and colleagues looked at microscopic structural details in pulvinus cells that help create such useful distortions, he reported January 7 at the annual meeting of the Society for Integrative and Comparative Biology in Austin, Texas. One feature that makes plant-muscle cells bloat more efficiently is reinforcement with microscopic fibrils. They work like corsets, keeping cells from bulging out in all directions. Instead, the corset directs much of the swelling along the axis that will fold up the leaf halves.
Also, pulvinus cells that need to bulge fast have what look like wrinkles of easily expandable tissue for inrushing water, plus special highly porous zones called pit fields. The pits look as if water could sluice through easily in a tickled-leaf emergency. Cell arrangement itself looks specialized for expanding and shrinking. A pulvinus cross section reveals a pattern “like the bellows of a concertina,” Sleboda said.
The widespread M. pudica, or sensitive plant, is one of the better-known leaf flexors. Yet clusters of other plants in the same family, the legumes, also move their leaves, says botanist Thainara Policarpo Mendes of Universidade Estadual Paulista in Botucatu, Brazil. Some relatives close fast like M. pudica, but many are slower. What she also thinks about, though, is why leaves close at all. People have proposed a variety of advantages: discouraging animals from grazing on a plant that suddenly looks more sticklike, or even helping a plant lose less heat on very cold nights.
Sleboda too can reel off proposed hypotheses but remains skeptical of all of them. “There’s not a ton of research,” he says. That, however, is fine with him. “My favorite thing about sensitive plants’ leaf closing,” he says, “is that we don’t know why they do it.” | Biology |
Animals cover themselves in all kinds of unsavory fluids to keep cool. Humans sweat, kangaroos spit and some birds will urinate on themselves to survive hot days. It turns out that echidnas do something much cuter — though perhaps just as sticky (and slightly icky) — to beat the heat. The spiny insectivores stay cool by blowing snot bubbles, researchers report January 18 in Biology Letters. The bubbles pop, keeping the critters’ noses moist. As it evaporates, this moisture draws heat away from a blood-filled sinus in the echidna’s beak, helping to cool the animal’s blood. Science News headlines, in your inbox Headlines and summaries of the latest Science News articles, delivered to your email inbox every Thursday. Short-beaked echidnas (Tachyglossus aculeatus) look a bit like hedgehogs but are really monotremes — egg-laying mammals unique to Australia and New Guinea (SN: 11/18/16). Previous lab studies showed that temperatures above 35° Celsius (95° Fahrenheit) should kill echidnas. But echidnas don’t seem to have gotten the memo. They live everywhere from tropical rainforests to deserts to snow-capped peaks, leaving scientists with a physiological puzzle. Mammals evaporate water to keep cool when temperatures climb above their body temperatures, says environmental physiologist Christine Cooper of Curtin University in Perth, Australia. “Lots of mammals do that by either licking, sweating or panting,” she says. “Echidnas weren’t believed to be able to do that.” But it’s known that the critters blow snot bubbles when it gets hot. So, armed with a heat-vision camera and a telephoto lens, Cooper and environmental physiologist Philip Withers of the University of Western Australia in Perth drove through nature reserves in Western Australia once a month for a year to film echidnas. In infrared, the warmest parts of the echidnas’ spiny bodies glowed in oranges, yellows and whites. But the video revealed that the tips of their noses were dark purple blobs, kept cool as moisture from their snot bubbles evaporated. Echidnas might also lose heat through their bellies and legs, the researchers report, while their spikes could act as an insulator. An echidna looks like a hot spiky ball of yellow, orange and white in this heat-vision video — except for its chilly nose, which shows up as a purple and black blob. That’s because these Australian mammals blow snot bubbles to keep their noses wet, which cools the critters down as the moisture evaporates, a new study concludes. “Finding a way of doing this work in the field is pretty exciting,” says physiological ecologist Stewart Nicol of the University of Tasmania in Hobart, Australia, who was not involved in the study. “You can understand animals and see how they’re responding to their normal environment.” The next step, he says, is to quantify how much heat echidnas really lose through their noses and other body parts. Monotremes parted evolutionary ways with other mammals between 250 million and 160 million years ago as the supercontinent Pangaea broke apart (SN: 3/8/15). So “they have a whole lot of traits that are considered to be primitive,” Cooper says. “Understanding how they might thermoregulate can give us some ideas about how thermal regulation … might have evolved in mammals.” More Stories from Science News on Animals From the Nature Index Paid Content | Biology |
Neanderthals have long been portrayed as our dim-witted, thuggish cousins. Now groundbreaking research has – while not confirmed the stereotype – revealed striking differences in the brain development of modern humans and Neanderthals.The study involved inserting a Neanderthal brain gene into mice, ferrets and “mini brain” structures called organoids, grown in the lab from human stem cells. The experiments revealed that the Neanderthal version of the gene was linked to slower creation of neurons in the brain’s cortex during development, which scientists said could explain superior cognitive abilities in modern humans.“Making more neurons sets the basis for higher cognitive function,” said Wieland Huttner, who led the work at the Max-Planck-Institute of Molecular Cell Biology and Genetics. “We think this is the first compelling evidence that modern humans were cognitively better than Neanderthals.”Modern humans and Neanderthals split into separate lineages about 400,000 years ago, with our ancestors remaining in Africa and the Neanderthals moving north into Europe. About 60,000 years ago, a mass migration of modern humans out of Africa brought the two species face-to-face once more and they interbred – modern humans of non-African heritage carry 1-4% of Neanderthal DNA. By 30,000 years ago, though, our ancient cousins had vanished as a distinct species and the question of how we out-competed Neanderthals has remained a mystery.“One concrete fact is that wherever homo sapiens went they would basically out-compete other species there. It’s a bit weird,” said Prof Laurent Nguyen, of the University of Liège, who was not involved in the latest research. “These guys [Neanderthals] were in Europe a long time before us and would have been adapted to their environment including pathogens. The big question is why we would be able to out-compete them.”Some argue that our ancestors had an intellectual edge, but until recently there has been no way to scientifically test the hypothesis. This changed in the last decade when scientists successfully sequenced Neanderthal DNA from a fossilised finger found in a Siberian cave, paving the way for new insights into how Neanderthal biology differed from our own.The latest experiments focus on a gene, called TKTL1, involved in neuronal production in the developing brain. The Neanderthal version of the gene differs by one letter from the human version. When inserted into mice, scientists found that the Neanderthal variant led to the production of fewer neurons, particularly in the frontal lobe of the brain, where most cognitive functions reside. The scientists also tested the influence of the gene in ferrets and blobs of lab-grown tissue, called organoids, that replicate the basic structures of the developing brain.“This shows us that even though we do not know how many neurons the Neanderthal brain had, we can assume that modern humans have more neurons in the frontal lobe of the brain, where [the gene’s] activity is highest, than Neanderthals,” said Anneline Pinson, first author of the study.Chris Stringer, head of human origins research at the Natural History Museum in London, described the work as “pioneering”, saying that it started to address one of the central puzzles of human evolution - why, with all the past diversity of humans, we are now the only ones left.“Ideas have come and gone – better tools, better weapons, proper language, art and symbolism, better brains,” Stringer said. “At last, this provides a clue as to why our brains might have outperformed those of Neanderthals.”More neurons does not automatically equate to a smarter type of human, although it does dictate the brain’s basic computing capacity. Human brains contain about twice the number of neurons as the brains of chimpanzees and bonobos.Nguyen said the latest work is far from definitive proof of modern humans’ superior intellect, but demonstrates that Neanderthals had meaningful differences in brain development. “This is an exciting story,” he added. | Biology |
New Michigan State University research published in the journal Proceedings of the National Academy of Sciences shows that plants such as oak and poplar trees will emit more of a compound called isoprene as global temperatures climb. Isoprene from plants represents the highest flux of hydrocarbons to the atmosphere behind methane. Although isoprene isn't inherently bad -- it actually helps plants better tolerate insect pests and high temperatures -- it can worsen air pollution by reacting with nitrogen oxides from automobiles and coal-fired power plants.
The new publication can help us better understand, predict and potentially mitigate the effects of increased isoprene emission as the planet warms.
It's a simple question that sounds a little like a modest proposal.
"Should we cut down all the oak trees?" asked Tom Sharkey, a University Distinguished Professor in the Plant Resilience Institute at Michigan State University.
Sharkey also works at the MSU-Department of Energy Plant Research Laboratory and in the Department of Biochemistry and Molecular Biology.
To be clear, Sharkey wasn't sincerely suggesting that we should cut down all the oaks. Still, his question was an earnest one, prompted by his team's latest research, which was published in the scientific journal Proceedings of the National Academy of Sciences.
The team discovered that, on a warming planet, plants like oaks and poplars will emit more of a compound that exacerbates poor air quality, contributing to problematic particulate matter and low-atmosphere ozone.
The rub is that the same compound, called isoprene, can also improve the quality of clean air while making plants more resistant to stressors including insects and high temperatures.
"Do we want plants to make more isoprene so they're more resilient, or do we want them making less so it's not making air pollution worse? What's the right balance?" Sharkey asked. "Those are really the fundamental questions driving this work. The more we understand, the more effectively we can answer them."
Spotlight on isoprene
Sharkey has been studying isoprene and how plants produce it since the 1970s, when he was a doctoral student at Michigan State.
Isoprene from plants is the second-highest emitted hydrocarbon on Earth, only behind methane emissions from human activity. Yet most people have never heard of it, Sharkey said.
"It's been behind the scenes for a long time, but it's incredibly important," Sharkey said.
It gained a little notoriety in the 1980s, when then-president Ronald Reagan falsely claimed trees were producing more air pollution than automobiles. Yet there was a kernel of truth in that assertion.
Isoprene interacts with nitrogen oxide compounds found in air pollution produced by coal-fired power plants and internal combustion engines in vehicles. These reactions create ozone, aerosols and other byproducts that are unhealthy for both humans and plants.
"There's this interesting phenomenon where you have air moving across a city landscape, picking up nitrogen oxides, then moving over a forest to give you this toxic brew," Sharkey said. "The air quality downwind of a city is often worse than the air quality in the city itself."
Now, with support from the National Science Foundation, Sharkey and his team are working to better understand the biomolecular processes plants use to make isoprene. The researchers are particularly interested in how those processes are affected by the environment, especially in the face of climate change.
Prior to the team's new publication, researchers understood that certain plants produce isoprene as they carry out photosynthesis. They also knew the changes that the planet is facing were having competing effects on isoprene production.
That is, increasing carbon dioxide in the atmosphere drives the rate down, while increasing temperatures accelerate the rate. One of the questions behind the MSU team's new publication was essentially which one of these effects will win out.
"We were looking for a regulation point in the isoprene's biosynthesis pathway under high carbon dioxide," said Abira Sahu, the lead author of the new report and a postdoctoral research associate in Sharkey's research group.
"Scientists have been trying to find this for a long time," Sahu said. "And, finally, we have the answer."
"For the biologists out there, the crux of the paper is that we identified the specific reaction slowed by carbon dioxide, CO2," Sharkey said.
"With that, we can say the temperature effect trumps the CO2 effect," he said. "By the time you're at 95 degrees Fahrenheit -- 35 degrees Celsius -- there's basically no CO2 suppression. Isoprene is pouring out like crazy."
In their experiments, which used poplar plants, the team also found that when a leaf experienced warming of 10 degrees Celsius, its isoprene emission increased more than tenfold, Sahu said.
"Working with Tom, you realize plants really do emit a lot of isoprene," said Mohammad Mostofa, an assistant professor who works in Sharkey's lab and was another author of the new report.
The discovery will help researchers better anticipate how much isoprene plants will emit in the future and better prepare for the impacts of that. But the researchers also hope it can help inform the choices people and communities make in the meantime.
"We could be doing a better job," Mostofa said.
At a place like MSU, which is home to more than 20,000 trees, that could mean planting fewer oaks in the future to limit isoprene emissions.
As for what we do about the trees already emitting isoprene, Sharkey does have an idea that doesn't involve cutting them down.
"My suggestion is that we should do a better job controlling nitrogen oxide pollution," Sharkey said.
Sarathi Weraduwage, a former postdoctoral researcher in Sharkey's lab who is now an assistant professor at Bishop's University in Quebec, also contributed to the research.
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Salinity changes threatening marine ecosystems, new study shows
A groundbreaking study published today reveals the critical yet severely understudied factor of salinity changes in ocean and coastlines caused by climate change. The study was co-authored by an international team of researchers, including Dr. Cliff Ross, University of North Florida biology chair/professor, and Dr. Stacey Trevathan-Tackett, UNF biology graduate program alum and research faculty member at Deakin University in Australia.
Changes in salinity, or salt content, due to climate change and land use can have potentially devastating impacts on vital coastal and estuarine ecosystems, yet this has rarely been studied until now. This new research provides valuable insights into the threats posed by anthropogenic salinity changes to marine and coastal ecosystems and outlines consequences for the health and economy of local communities in oftentimes densely populated regions.
The research team looked at how climate change-related variations in rainfall as well as local man-made impacts can lead to extreme flood and drought events, affecting freshwater availability and impacting salinity in sensitive ecosystems. As sea-levels rise, saltwater inflows in coastal and low-lying areas can also cause devastating impacts. Certain groups such as microorganisms, plankton, coral, mangroves, tidal marshes, macroalgae and seagrass are most at risk and can quickly face ecosystem collapse.
The researchers warn that salinity changes are predicted to intensify alongside ocean warming, and they stress the urgency of immediately addressing these salinity challenges to safeguard marine and coastal ecosystems and biodiversity.
"Human-induced salinity changes impact marine organisms and ecosystems" is published in Global Change Biology.
More information: Till Röthig et al, Human‐induced salinity changes impact marine organisms and ecosystems, Global Change Biology (2023). DOI: 10.1111/gcb.16859
Journal information: Global Change Biology
Provided by University of North Florida | Biology |
Oct 07 According to a new study published in the peer-reviewed journal The American Biology Teacher, non-animal teacher methods are at least as effective as animal dissections and may be more effective.
As noted by the study’s abstract, animal dissection is practiced to varying degrees around the world and is particularly prevalent in North America throughout all levels of education. However, “a growing number of studies suggest that non-animal teaching methods (NAMs) (e.g., virtual anatomy tools and three-dimensional models) are better for achieving learning goals compared to dissection.”
With this in mind, researchers for this new study “conducted a systematic review of studies published between 2005 and 2020 that evaluated the pedagogical value of NAMs versus animal dissection.” Their results from 20 published studies “show that in 95% of the studies (19/20) students at all education levels (secondary, postsecondary, and medical school) performed at least as well—and in most of those studies better (14/19)—when they used NAMs compared to animal dissection.” The study states that “These results provide compelling evidence in support of the 3Rs’ principle of replacement. Given that NAMs have been demonstrated as effective for science education, steps should be taken by educational institutions to phase out animal dissection.”
Click here for more information on this study.
The full abstract is below: Animal dissection is practiced to varying degrees around the world and is particularly prevalent in North America throughout all levels of education. However, a growing number of studies suggest that non-animal teaching methods (NAMs) (e.g., virtual anatomy tools and three-dimensional models) are better for achieving learning goals compared to dissection. We conducted a systematic review of studies published between 2005 and 2020 that evaluated the pedagogical value of NAMs versus animal dissection. Our results from 20 published studies show that in 95% of the studies (19/20) students at all education levels (secondary, postsecondary, and medical school) performed at least as well—and in most of those studies better (14/19)—when they used NAMs compared to animal dissection. These results provide compelling evidence in support of the 3Rs’ principle of replacement. Given that NAMs have been demonstrated as effective for science education, steps should be taken by educational institutions to phase out animal dissection. Anthony Martinelli Anthony Martinelli is the Founder and Editor-in-Chief of The Vegan Herald, which launched in 2015 as a daily vegan news and information website. | Biology |
Newly sequenced hornet genomes could help explain invasion success
The genomes of two hornet species, the European hornet and the Asian hornet (or yellow-legged hornet) have been sequenced for the first time by a team led by UCL (University College London) scientists.
By comparing these decoded genomes with that of the giant northern hornet, which has recently been sequenced by another team, the researchers have revealed clues suggesting why hornets have been so successful as invasive species across the globe. Their work is published in Scientific Reports.
Hornets are the largest of the social wasps; they play important ecological roles as top predators of other insects. In their native regions, they are natural pest controllers, helping regulate the populations of insects such as flies, beetles, caterpillars and other types of wasps. These services are critical for healthy, functional ecosystems, as well as for agriculture.
But hornets also tend to be very successful as invasive species. They can become established in areas to which they they are not native, and cause potentially huge ecological and economic damage by hunting important pollinators, such as honey bees, wild bees and hoverflies.
To better understand how these species have so successfully expanded their ranges, the international team of scientists investigated the genomes of three types of hornets.
A genome sequence is the set of instructions—a genetic code—that makes a species. Comparing the genomes of different species can give insights into their biology: their behavior, evolution, and how they interact with the environment.
The researchers have newly sequenced the genomes of the native European hornet, Vespa crabro—an important top predator, which is protected in parts of Europe—and the invasive yellow-legged Asian hornet Vespa velutina, which has become established through much of Europe over the last 20 years threatening native ecosystems, and has occasionally been sighted in the UK. The research team compared these with the genome of the giant northern hornet, Vespa mandarinia—a species known for its role as pest controller, pollinator and food provider in its native Asian range. It is a recent arrival in North America, where it may threaten native fauna.
By analyzing differences among the three related species, the researchers were able to identify genes that have been rapidly evolving since the species differentiated themselves from other wasps and from one another, and found some noteworthy genes that are rapidly evolving, particularly relating to communication and olfaction (smell).
The study's first author, Dr. Emeline Favreau (UCL Centre for Biodiversity & Environment), said, "We were excited to find evidence of rapid genome evolution in these hornet genomes, compared to other social insects. Lots of genes have been duplicated or mutated; these included genes that are likely to be involved in communication and in sensing the environment."
Genome evolution allows organisms to adapt to their environment and make the most of their surroundings by developing new behaviors and physiology.
Co-author Dr. Alessandro Cini, who began the work at UCL before moving to the University of Pisa, said, "These findings are exciting, as they may help explain why hornets have been so successful in establishing new populations in non-native regions.
"Hornets are carried to different parts of the world accidentally by humans. All that is needed is a small number of mated queens to be transported, hidden in cargo perhaps. The genomes suggest that hornets have lots of genes involved in detecting and responding to chemical cues—these may make them especially good at adapting to hunt different types of prey in non-native regions."
Senior author Professor Seirian Sumner (UCL Centre for Biodiversity & Environment) said, "These hornet genomes are just the beginning. The genomes of more than 3,000 insect species have now been sequenced by efforts around the world, but wasps are under-represented among these.
"Genomes tell us about aspects of the ecology and evolution that other methods cannot. Evolution has equipped these insects with an incredible genetic toolbox with which to exploit their environment and hunt their prey."
Armed with these new genomes, the scientists hope to help improve the management of hornet populations, both for their ecosystem services as pest controllers in native zones, and as ecological threats in regions where they are invasive.
More information: Emeline Favreau et al, Putting hornets on the genomic map, Scientific Reports (2023). DOI: 10.1038/s41598-023-31932-x
Journal information: Scientific Reports
Provided by University College London | Biology |
The tiny blobs of lab-grown human brain tissue were just specks, each measuring a few millimeters in diameter. Researchers at Stanford University made them by cultivating human stem cells into three-dimensional clumps of tissue. Called brain organoids, these simplified structures contain some of the cells and properties of a real human brain, offering insight into development and neurological conditions.But they’re not nearly as complex as the real thing, so to boost their realism, researchers elsewhere have tried transplanting human organoids into the brains of rodents. In past experiments, those cells failed to integrate into the animals’ brains. This time, it worked: The organoids formed connections with the animals’ own brain circuits, a sign that these bundles of cells can develop more sophisticated features.The Stanford team transplanted these clusters of human cells into the somatosensory cortices of newborn rats—the area that processes sensory information, such as touch, from across the body. Over several months, the organoids grew to occupy about one-third of the hemisphere of the rat brains. The research was published today in the journal Nature. “This definitely pushes forward what organoids can do in terms of their functional integration into the brain,” says H. Isaac Chen, assistant professor of neurosurgery at the University of Pennsylvania, who wasn’t involved in the study.Chen and others had previously tried similar experiments in adult rodents, but those transplanted organoids didn’t successfully mature. In the latest attempt, the Stanford scientists transplanted the organoids early in development, when the young rats’ neuronal circuits weren’t fully formed. The adult brain is much less plastic, meaning it’s not able to change and form new connections as easily. “The nervous system has a way of shutting down development,” said Sergiu Pasca, professor of psychiatry and behavioral sciences at Stanford and the corresponding author on the study, in a press briefing ahead of the paper’s publication. “We went in and we transplanted before the ability for cells to form connections had stopped.”In a departure from previous studies, Pasca and his colleagues found that the transplanted human neurons grew nerve fibers that extended into the rat brain tissue and formed junctions called synapses between rat neurons. These connections don’t exist in brain organoids grown in a dish, a major limitation that has driven scientists to transplant orgaonids into living animals.“We know that the brain develops and works by receiving activity, either from endogenous networks or from the outside world through sensory stimulation of the tissue,” says Paola Arlotta, a professor of stem cell and regenerative biology at Harvard University, who wasn’t involved in the Stanford research. In a real brain, sensory stimulation is vital to forming neural pathways and promoting normal development.Not only did the organoids grow and integrate with the tissue, but they also revealed characteristics not previously seen in organoids grown in a dish. The Stanford researchers grew some of their organoids from cells taken from patients with Timothy syndrome, a severe genetic disease that often causes the same kind of neurodevelopmental delays seen in autism. When transplanted into rats, the organoids developed abnormal dendrites—the treelike branches that extend from neurons and allow them to communicate with other cells. These defects hadn’t been seen in earlier organoid experiments without animals.The authors also wanted to determine whether the organoids could influence a rat’s behavior. They genetically engineered some of the transplanted neurons to be sensitive to stimulation with light, a technique called optogenetics. The researchers then trained the mice to lick a spout for a reward (a drink of water) every time they delivered bursts of blue light to these neurons. Bursts of red light, used as a control, had no effect on their behavior. This showed that the transplanted human organoids in the rats’ brains were functional and that they engaged with the rats’ reward-seeking brain circuits.Though they mimic some brain structures and activity, brain organoids are still only a rough approximation of an actual human brain. For one, they’re tiny—no bigger than a pea. They also lack some key cell types and the layered structure seen in the human cortex. But as organoids get more advanced, such animal experiments present an ethical conundrum about the blurring of humans and other species.One concern is whether adding human brain tissue affects the well-being of the animals. The Stanford researchers attempted to address this by running a battery of tests to compare the memory and anxiety level of animals that received the human brain organoids versus regular lab rats. They also looked for evidence of seizures and found no differences between the two groups.A 2021 report by the US National Academies of Science, Engineering and Medicine raised other hypotheticals, including the possibility that human brain organoids could enhance animals’ cognitive abilities or cause either the organoids or animals to develop humanlike self-awareness and consciousness. The committee concluded that such experiments don’t yet necessitate special oversight but that new regulations may be needed if brain organoids become significantly more complex. Since researchers don’t know where consciousness arises in the brain, there’s no way to know if the integration of human tissue into an animal brain is a step in that direction.Pasca says he would draw a line at implanting human brain organoids into monkeys because of their similarity to humans. Rats are less similar, he says, because their cortices develop much faster than people’s do. For now, he thinks there’s a lot that researchers can glean from transplanting these organoids into rodents. One application would be to study neurodegenerative disorders that have an early onset in childhood—when the brain is still developing. “That's the motivation for us to try to move some of these three-dimensional cultures and integrate them into living systems,” Pasca says.Transplanted organoids could also be used to test drugs that could be used to treat neuropsychiatric diseases, or to see how genetic defects in organoids alter the behavior of animals. Another avenue of research would be to implant healthy organoids into rodents with brain injuries to see if the tissue is able to integrate with the damaged brain and possibly repair it, Chen says.Arlotta says organoids are still very primitive compared to actual human brain tissue. But the ones created in the Stanford study will allow researchers to study more complex properties of human cell circuits, neurons, and neural functions involved in neuropsychiatric diseases. “If we want to really get to the bottom of what these diseases are, and how they are caused by specific genetics, then we have to be able to look at more than just the cells. We need to be able to look at circuit-level properties,” she says. “There is so much to be gained here in understanding disease pathology and mechanisms, and that value must be considered in any sort of ethical consideration about the work.” | Biology |
Sign up for CNN’s Wonder Theory science newsletter. Explore the universe with news on fascinating discoveries, scientific advancements and more. CNN — A giant sunfish believed to be the world’s heaviest bony fish has been discovered in the Azores archipelago, Portugal, weighing a whopping 2,744 kilograms (3 tons). Researchers said the animal was found dead, floating near Faial Island in the central North Atlantic in December. Although found last year, details of the discovery have only recently been published in the Journal of Fish Biology. Studied by researchers from the Atlantic Naturalist Association and the Azores University for biometrical and morphological data, both in Portugal, the fish was pulled to shore where the animal was weighed, measured and tissue sampled for DNA testing. There are around 29,000 species of bony fish, which have a skeletal bone structure, making them the majority of the world’s fish species. The carcass is more than 400 kilograms (882 pounds) heavier than the previous world record holder for heaviest bony fish – a 2,300-kilogram (5,070-pound) female giant sunfish caught off Kamogawa in Japan in 1996. The sunfish was weighed with a crane scale dynamometer – a device designed to weigh loads typically hoisted by a crane – after being raised above ground using a forklift truck. The animal was 3.25 meters (10.67 feet) long and had a height of 3.59 meters (11.78 feet). Measured around its center (mid-body), it had a maximum width of 86 centimeters (2.82 feet), researchers said. The sex has not been determined. José Nuno Gomes-Pereira, lead author of the paper and postdoctoral researcher from the Atlantic Naturalist Association, told CNN Tuesday that it was saddening “to see the animal in this situation as it must have been a king of open ocean.” The “tremendously big” sunfish has been buried in the Natural Park of Faial Island, he added. Gomes-Pereira said that the finding was a “sign that the oceans are still healthy enough to sustain the heaviest species existing, but a warning for more conservation in terms of pollution and boat traffic near oceanic islands.” Giant sunfish (Mola alexandrini) were first recognized as their own species in 2018 and are known to weigh twice as much as the second heaviest fish species, the ocean sunfish (Mola mola), according to a news release from the Atlantic Naturalist Association last Thursday. Gomes-Pereira said the dead sunfish had a “contusion” – a bruise – on its front, which may have caused the animal’s death. However, it is unknown if the impact was pre- or post-mortem. The wound was embedded with a red paint normally used to coat the keels of boats, the journal article added. With little data available on large specimens such as the sunfish, the researchers believe further study is required to understand their physiology and marine ecosystems in general. The world’s heaviest fish species is the whale shark (Rhincodon typus), according to Guinness World Records, with the heaviest found in Pakistan in 1949, weighing 21.5 metric tons. | Biology |
Newly discovered probiotic could protect Caribbean corals threatened by deadly, devastating disease
Researchers with the Smithsonian's National Museum of Natural History have discovered the first effective bacterial probiotic for treating and preventing stony coral tissue loss disease (SCTLD), a mysterious ailment that has devastated Florida's coral reefs since 2014 and is rapidly spreading throughout the Caribbean.
The probiotic treatment, described in a paper published today in Communications Biology, provides an alternative to the use of the broad-spectrum antibiotic amoxicillin, which has so far been the only proven treatment for the disease, but which runs the risk of promoting antibiotic-resistant bacteria.
SCTLD afflicts at least two dozen species of so-called hard corals, which provide essential habitat for innumerable fishes and marine animals of economic and intrinsic value while also helping to defend coastlines from storm damage. Since its discovery in Florida in 2014, cases of SCTLD have been confirmed in at least 20 countries. The precise cause of the malady remains unknown but once a coral is infected, its colony of polyps can die within weeks.
"It just eats the coral tissue away," said Valerie Paul, head scientist at the Smithsonian Marine Station at Fort Pierce, Florida, and senior author of the study. "The living tissue sloughs off and what is left behind is just a white calcium carbonate skeleton."
Paul has been studying coral reefs for decades, but she said she decided to go "all in" on SCTLD in 2017 because it was so deadly, so poorly understood and spreading so fast.
While probing how the disease is spread, Paul and a team including researchers from the University of Florida discovered that some fragments of great star coral (Montastraea cavernosa) swiftly developed SCTLD's characteristic lesions and died, but other pieces never got sick at all.
Though the precise cause of SCTLD is unknown, the efficacy of antibiotics as a treatment suggested pathogenic bacteria were somehow involved in the progression of the disease.
For this reason, the researchers collected samples of the naturally occurring, non-pathogenic bacteria present on a pair of disease-resistant great star coral fragments for further testing. With these samples, the research team aimed to identify which, if any, naturally occurring microorganisms were protecting some great star corals from SCTLD.
First, the team tested the 222 bacterial strains from the disease-resistant corals for antibacterial properties using three strains of harmful bacteria previously isolated from corals infected with SCTLD. Paul and Blake Ushijima, lead author of the study and an assistant professor at the University of North Carolina Wilmington who was formerly a George Burch Fellow at Smithsonian Marine Station, found 83 strains with some antimicrobial activity, but one in particular, McH1-7, stood out.
The team then conducted chemical and genetic analyses to discover the compounds behind McH1-7's antibiotic properties and the genes behind those compounds' production. Finally, the researchers tested McH1-7 with live pieces of great star coral. These lab trials provided the final bit of decisive proof: McH1-7 stopped or slowed the progression of the disease in 68.2% of 22 infected coral fragments and even more notably prevented the sickness from spreading in all 12 transmission experiments, something antibiotics are unable to do.
Going forward, Paul said there is a need to work on improved delivery mechanisms if this probiotic is going to be used at scale in the field. Currently, the primary method of applying this coral probiotic is to essentially wrap the coral in a plastic bag to create a mini aquarium and then inject the helpful bacteria. Perhaps even more importantly, Paul said it remains to be seen whether the bacterial strain isolated from the great star coral will have the same curative and prophylactic effects for other species of coral.
The potential of this newly identified probiotic to help Florida's embattled corals without the danger of inadvertently spawning antibiotic resistant bacteria represents some urgently needed good news, Paul said.
More information: Chemical and genomic characterization of a potential probiotic treatment for stony coral tissue loss disease, Communications Biology (2023). DOI: 10.1038/s42003-023-04590-y
Journal information: Communications Biology
Provided by Smithsonian | Biology |
Scientists believe gonorrhoea might deserve the credit for why humans are one of the few species who look after their grandchildren.The evolution of all life is driven by a single imperative, reproduction, and the biology of most animal species is optimised for that purpose at the cost of longer lifespans.
Humans are one of the only species known to live past menopause. According to the "grandmother hypothesis" this is because older women provide evolutionary important support in raising children.Researchers at the University of California's San Diego School of Medicine had previously discovered a set of human gene mutations that contribute towards this longevity by protecting older adults against cognitive decline.And now in a new study published in the journal Molecular Biology and Evolution they trace the evolution of one of these mutated genes through the human genome and find that its emergence was likely supported by selective pressure from infectious pathogens like gonorrhoea. The key to this investigation is a comparison of human and chimpanzee genomes, which unearthed how humans have a unique version of the gene for CD33, a receptor in immune cells.
In its standard format, this receptor binds to a type of sugar called sialic acid that all human cells are coated with - when the immune cell senses the sialic acid via CD33 it "recognises" the other cell and does not attack. More from Science & Tech Russian cyber spies targeting NATO countries in new hacking campaign Amazon files lawsuit against 10,000 Facebook groups designed to create fake reviews The vitamin supplement that can reduce feelings of depression and anxiety But the CD33 receptor is also expressed in brain immune cells called microglia, where it helps control neuroinflammation - and microglia have an important role in clearing away damaged brain cells and amyloid plaques associated with Alzheimer's disease.Regular CD33 receptors actually suppress this important microglial function and increase the risk of dementia by binding to the sialic acids on these cells and plaques."This is where the new gene variant comes in," the study authors said."Somewhere along the evolutionary line, humans picked up an additional mutated form of CD33 that is missing the sugar-binding site."The mutated receptor no longer reacts to sialic acids on damaged cells and plaques, allowing the microglia to break them down."Indeed, higher levels of this CD33 variant were independently found to be protective against late-onset Alzheimer's," they added.What does this have to do with gonorrhoea?The researchers note that gonorrhoea bacteria coat themselves in the same sugars that CD33 receptors bind to."Like a wolf in sheep's clothing, the bacteria are able to trick human immune cells to not identify them as outside invaders," they said.Altogether their paper proposes that humans initially inherited the mutated form of CD33 because it served to protect our reproductive abilities.However the gene variant was later co-opted by the brain for its benefits against cognitive decline, empowering families of several generations to grow together."It is possible that CD33 is one of many genes selected for their survival advantages against infectious pathogens early in life, but that are then secondarily selected for their protective effects against dementia and other ageing-related diseases," the researchers said. | Biology |
November 16, 2022• Physics 15, s158Physicists have shown that a mathematical transformation called a conformal map can be used to predict how leaves grow. A. Dai and M. Ben Amar [1] In his 1917 book, On Growth and Form, D’Arcy Thompson pioneered the use of mathematics in biology. Now physicists Anna Dai and Martine Ben Amar of the École Normale Supérieure in Paris have taken a page from the century-old book. Noticing that many of Thompson’s diagrams showing plant and animal growth look like conformal maps—angle-preserving transformations—Dai and Ben Amar applied the mathematics of conformal maps to the problem of leaf growth [1]. They prove that the mathematical technique is well motivated by the physical principle of energy minimization.
Many growth processes in biology reflect the fact that, like all physical systems, organisms want to minimize their energy. For growing organisms, that means minimizing internal elastic stresses. But this energy-minimization picture of growth is seemingly unrelated to the mathematical one that Dai and Ben Amar observed in Thompson’s book. Imagine drawing a grid on a baby leaf and watching the grid distort as the leaf grows. If the leaf grows conformally, the lines will stretch and curve, while the angles at which gridlines intersect remain unchanged. At first glance, this simple mathematical transformation doesn’t seem to tell us anything about the physical forces involved in leaf growth.
Nevertheless, Dai and Ben Amar found that it encapsulates the salient features of the complex physics at play. Focusing on leaves from the Monstera deliciosa (or “Swiss cheese”) plant, they showed that conformal maps reproduce leaf growth while minimizing elastic stress, making the mathematical transformation physically well motivated. So far, the researchers have performed their analysis in 2D; next, they plan to explore whether conformal maps can be used to describe the growth of 3D leaves.–Katie McCormickKatie McCormick is a science writer based in Sacramento, California.ReferencesA. Dai and M. Ben Amar, “Minimizing the elastic energy of growing leaves by conformal mapping,” Phys. Rev. Lett. 129, 218101 (2022).Subject AreasRelated ArticlesMaterials ScienceThe Gap-Free Helices of Sea SnailsOctober 17, 2022The shells of some mollusk species have compact helical structures that researchers propose develop from the self-assembly of a liquid-crystalline material. Read More » More Articles | Biology |
Scientists have genetically engineered a hummingbird bobtail squid to remove its pigment, creating an almost completely transparent animal with only its three hearts and brain showing when light hits it at the right angle. According to NPR, "The see-through squid are offering scientists a new way to study the biology of a creature that is intact and moving freely." From the report: The see-through version is made possible by a gene editing technology called CRISPR, which became popular nearly a decade ago. [Scientists Caroline Albertin and Joshua Rosenthal at the Marine Biological Laboratory in Woods Hole, Mass.] thought they might be able to use CRISPR to create a special squid for research. They focused on the hummingbird bobtail squid because it is small, a prodigious breeder, and thrives in lab aquariums, including one at the lab in Woods Hole. Albertin and Rosenthal wanted to use CRISPR to create a bobtail squid without any pigment, an albino. And they knew that in other squid, pigment depends on the presence of a gene called TDO.
"So we tried to knock out TDO," Albertin says, "and nothing happened." It turned out that bobtail squid have a second gene that also affects pigment. "When we targeted that gene, lo and behold we were able to get albinos," Albertin says. Because even unaltered squid have clear blood, thin skin, and no bones, the albinos are all but transparent unless light hits them at just the right angle. Early on, Albertin and Rosenthal realized these animals would be of interest to brain scientists. So they contacted Ivan Soltesz at Stanford and Cristopher Niell at the University of Oregon. "We said, 'Hey, you guys, we have this incredible animal, want to look at its brain," Rosenthal says. "They jumped on it."
Soltesz and Niell inserted a fluorescent dye into an area of the brain that processes visual information. The dye glows when it's near brain cells that are active. Then the scientists projected images onto a screen in front of the squid. And the brain areas involved in vision began to glow, something that would have been impossible to see in a squid with pigment. Because it suggests that her see-through squid will help scientists understand not only cephalopods, but all living creatures. The findings have been published in the journal Current Biology.
"So we tried to knock out TDO," Albertin says, "and nothing happened." It turned out that bobtail squid have a second gene that also affects pigment. "When we targeted that gene, lo and behold we were able to get albinos," Albertin says. Because even unaltered squid have clear blood, thin skin, and no bones, the albinos are all but transparent unless light hits them at just the right angle. Early on, Albertin and Rosenthal realized these animals would be of interest to brain scientists. So they contacted Ivan Soltesz at Stanford and Cristopher Niell at the University of Oregon. "We said, 'Hey, you guys, we have this incredible animal, want to look at its brain," Rosenthal says. "They jumped on it."
Soltesz and Niell inserted a fluorescent dye into an area of the brain that processes visual information. The dye glows when it's near brain cells that are active. Then the scientists projected images onto a screen in front of the squid. And the brain areas involved in vision began to glow, something that would have been impossible to see in a squid with pigment. Because it suggests that her see-through squid will help scientists understand not only cephalopods, but all living creatures. The findings have been published in the journal Current Biology. | Biology |
In India, children under 16 returning to school this month at the start of the school year will no longer be taught about evolution, the periodic table of elements, or sources of energy.
The news that evolution would be cut from the curriculum for students aged 15–16 was widely reported last month, when thousands of people signed a petition in protest. But official guidance has revealed that a chapter on the periodic table will be cut, too, along with other foundational topics such as sources of energy and environmental sustainability. Younger learners will no longer be taught certain pollution- and climate-related topics, and there are cuts to biology, chemistry, geography, mathematics and physics subjects for older school students.
Overall, the changes affect some 134 million 11–18-year-olds in India’s schools. The extent of what has changed became clearer last month when the National Council of Educational Research and Training (NCERT) — the public body that develops the Indian school curriculum and textbooks — released textbooks for the new academic year that started in May.
Researchers, including those who study science education, are shocked. “Anybody who’s trying to teach biology without dealing with evolution is not teaching biology as we currently understand it,” says Jonathan Osborne, a science-education researcher at Stanford University in California. “It’s that fundamental to biology.” The periodic table explains how life’s building blocks combine to generate substances with vastly different properties, he adds, and “is one of the great intellectual achievements of chemists”.
Mythili Ramchand, a science-teacher trainer at the Tata Institute of Social Sciences in Mumbai, India, says that “everything related to water, air pollution, resource management has been removed. “I don’t see how conservation of water, and air [pollution], is not relevant for us. It’s all the more so currently,” she adds. A chapter on different sources of energy — from fossil fuels to renewables — has also been removed. “That’s a bit strange, quite honestly, given the relevance in today’s world,” says Osborne.
More than 4,500 scientists, teachers and science communicators have signed an appeal organized by Breakthrough Science Society, a campaign group based in Kolkata, India, to reinstate the axed content on evolution.
NCERT has not responded to the appeal. And although it relied on expert committees to oversee the changes, it has not yet engaged with parents and teachers to explain its rationale for making them. NCERT also did not reply to Nature’s request for comment.
Chapters closed
A chapter on the periodic table of elements has been removed from the syllabus for class-10 students, who are typically 15–16 years old. Whole chapters on sources of energy and the sustainable management of natural resources have also been removed.
A small section on Michael Faraday’s contributions to the understanding of electricity and magnetism in the nineteenth century has also been stripped from the class-10 syllabus. In non-science content, chapters on democracy and diversity; political parties; and challenges to democracy have been scrapped. And a chapter on the industrial revolution has been removed for older students.
In explaining its changes, NCERT states on its website that it considered whether content overlapped with similar content covered elsewhere, the difficulty of the content, and whether the content was irrelevant. It also aims to provide opportunities for experiential learning and creativity.
NCERT announced the cuts last year, saying that they would ease pressures on students studying online during the COVID-19 pandemic. Amitabh Joshi, an evolutionary biologist at Jawaharlal Nehru Centre for Advanced Scientific Research in Bengaluru, India, says that science teachers and researchers expected that the content would be reinstated once students returned to classrooms. Instead, the NCERT shocked everyone by printing textbooks for the new academic year with a statement that the changes will remain for the next two academic years, in line with India’s revised education policy approved by government in July 2020.
“The idea [behind the new policy] is that you make students ask questions,” says Anindita Bhadra, an evolutionary biologist at the Indian Institute of Science Education and Research in Kolkata. But she says that removing fundamental concepts is likely to stifle curiosity, rather than encourage it. “The way this is being done, by saying ‘drop content and teach less’”, she says, “that’s not the way you do it”.
Evolution axed
Science educators are particularly concerned about the removal of evolution. A chapter on diversity in living organisms and one called ‘Why do we fall ill’ has been removed from the syllabus for class-9 students, who are typically 14–15 years old. Darwin’s contributions to evolution, how fossils form and human evolution have all been removed from the chapter on heredity and evolution for class-10 pupils. That chapter is now called just ‘Heredity’. Evolution, says Joshi, is essential to understanding human diversity and “our place in the world”.
In India, class 10 is the last year in which science is taught to every student. Only students who elect to study biology in the final two years of education (before university) will learn about the topic.
Joshi says that the curriculum revision process has lacked transparency. But in the case of evolution, “more religious groups in India are beginning to take anti-evolution stances”, he says. Some members of the public also think that evolution lacks relevance outside academic institutions.
Aditya Mukherjee, a historian at Jawaharlal Nehru University in New Dehli, says that changes to the curriculum are being driven by Rashtriya Swayamsevak Sangh (RSS), a mass-membership volunteer organization that has close ties to India’s governing Bharatiya Janata Party. The RSS feels that Hinduism is under threat from India’s other religions and cultures.
“There is a movement away from rational thinking, against the enlightenment and Western ideas” in India, adds Sucheta Mahajan, a historian at Jawaharlal Nehru University who collaborates with Mukherjee on studies of RSS influence on school texts. Evolution conflicts with creation stories, adds Mukherjee. History is the main target, but “science is one of the victims”, she adds. | Biology |
Toward a Better World
The successful transfer of a gene that produces HMW-HA paves the way for improving the health and lifespan of humans, too.
In a groundbreaking endeavor, researchers at the University of Rochester have successfully transferred a longevity gene from naked mole rats to mice, resulting in improved health and an extension of the mouse’s lifespan.
Naked mole rats, known for their long lifespans and exceptional resistance to age-related diseases, have long captured the attention of the scientific community. By introducing a specific gene responsible for enhanced cellular repair and protection into mice, the Rochester researchers have opened exciting possibilities for unlocking the secrets of aging and extending human lifespan.
“Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals,” says Vera Gorbunova, the Doris Johns Cherry Professor of biology and medicine at Rochester. Gorbunova, along with Andrei Seluanov, a professor of biology, and their colleagues, report in a study published in Nature that they successfully transferred a gene responsible for making high molecular weight hyaluronic acid (HMW-HA) from a naked mole rat to mice. This led to improved health and an approximate 4.4 percent increase in median lifespan for the mice.
A unique mechanism for cancer resistance
Naked mole rats are mouse-sized rodents that have exceptional longevity for rodents of their size; they can live up to 41 years, nearly ten times as long as similar-size rodents. Unlike many other species, naked mole rats do not often contract diseases—including neurodegeneration, cardiovascular disease, arthritis, and cancer—as they age. Gorbunova and Seluanov have devoted decades of research to understanding the unique mechanisms that naked mole rats use to protect themselves against aging and diseases.
The researchers previously discovered that HMW-HA is one mechanism responsible for naked mole rats’ unusual resistance to cancer. Compared to mice and humans, naked mole rats have about ten times more HMW-HA in their bodies. When the researchers removed HMW-HA from naked mole rat cells, the cells were more likely to form tumors.
Gorbunova, Seluanov, and their colleagues wanted to see if the positive effects of HMW-HA could also be reproduced in other animals.
Transferring a gene that produces HMW-HA
The team genetically modified a mouse model to produce the naked mole rat version of the hyaluronan synthase 2 gene, which is the gene responsible for making a protein that produces HMW-HA. While all mammals have the hyaluronan synthase 2 gene, the naked mole rat version seems to be enhanced to drive stronger gene expression.
The researchers found that the mice that had the naked mole rat version of the gene had better protection against both spontaneous tumors and chemically induced skin cancer. The mice also had improved overall health and lived longer compared to regular mice. As the mice with the naked mole rat version of the gene aged, they had less inflammation in different parts of their bodies—inflammation being a hallmark of aging—and maintained a healthier gut.
While more research is needed on exactly why HMW-HA has such beneficial effects, the researchers believe it is due to HMW-HA’s ability to directly regulate the immune system.
A fountain of youth for humans?
The findings open new possibilities for exploring how HMW-HA could also be used to improve lifespan and reduce inflammation-related diseases in humans.
“It took us 10 years from the discovery of HMW-HA in the naked mole rat to showing that HMW-HA improves health in mice,” Gorbunova says. “Our next goal is to transfer this benefit to humans.”
They believe they can accomplish this through two routes: either by slowing down degradation of HMW-HA or by enhancing HMW-HA synthesis.
“We already have identified molecules that slow down hyaluronan degradation and are testing them in pre-clinical trials,” Seluanov says. “We hope that our findings will provide the first, but not the last, example of how longevity adaptations from a long-lived species can be adapted to benefit human longevity and health.”
Read more
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Category: Featured | Biology |
For many locusts, life in a swarm is a picnic. Crowded conditions create a locust-eat-locust world. But it turns out some migrating insects deploy a “don’t-eat-me” pheromone that can deter their cannibalistic companions.
When jammed together, juvenile migratory locusts (Locusta migratoria) emit a volatile compound known as phenylacetonitrile, or PAN, researchers report in the May 5 Science. Locusts engineered to not give off the pheromone were eaten more often, the study found. And those unable to detect PAN were more likely to eat others producing it. The results suggest the compound has a role in suppressing cannibalism.
The level of cannibalism in a swarm “will be a constant balance,” says Bill Hansson, a neuroethologist at the Max Planck Institute for Chemical Ecology in Jena, Germany. “How hungry are your friends behind you, and how badly do you smell?”
Cannibalism is pretty common in the animal kingdom. It’s typically a convenient way for animals to supplement their diet when food is scarce. For L. migratoria, the behavior kicks in when the insects switch lifestyles.
As solitary insects, the locusts spend time apart and don’t eat each other. When group density increases — around a dwindling food source, say — locusts go “gregarious” (SN: 8/12/20). They become more attracted to each other and increasingly active, migrating and engaging in cannibalism. That allows groups to survive longer while searching for more nutrients. Some research suggests cannibalism may actually underpin locust swarming behavior, as individuals move en masse to avoid being attacked from the rear.
It was known that L. migratoria produce hundreds of chemical compounds, some of which repel their own species. Hansson and colleagues wanted to see if any of these compounds specifically deterred cannibalistic attacks.
First the team screened for compounds given off only during the gregarious phase. One of these, PAN, piqued the researchers’ interest as it breaks down to form hydrogen cyanide and had previously been shown to repel bird attacks against L. migratoria.
Once the locusts start smelling of the compound, they become a dangerous meal, Hansson says. “The higher the PAN, the more toxic they are.”
Initial experiments showed that locusts produced PAN when things started getting crowded, and the amount increased as more locusts joined the group. Next, the team zeroed in on one gene — LmOR70a — in the locust olfactory system with the strongest response to the chemical compound. Using gene editing, the team created some locusts unable to smell PAN, and others unable to produce it.
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The researchers put groups of locusts into crowded cages of 100 individuals. Rates of cannibalism were less than 5 percent among wild-type locusts, but jumped to around 30 percent among those unable to produce PAN. And when placed in cages with 50 starved yet otherwise normal locusts, non-PAN-producing individuals were attacked and eaten significantly more than locusts smelling of PAN. Locusts engineered to not detect PAN showed no preference for eating those producing the pheromone or those who did not.
Cannibalism is more of a threat to juvenile locusts as they don’t have wings yet, so this compound may be more useful to them. “They have to keep walking and being pushed, so cannibalism becomes a real threat,” Hansson says. “When they are adults, they can fly away.”
The work is “an exciting advancement for locust biology and chemical signaling,” says ecologist Arianne Cease, who heads the Global Locust Initiative at Arizona State University in Tempe. The use of this pheromone explains how highly crowded migratory locusts can gain the benefits of group living without incurring the cost of cannibalism, she says.
L. migratoria is the most widespread species of locust, found across Africa, Eurasia and down to Australia and New Zealand. Plagues have been reported as far back as 200 B.C. in China, and it is currently a major agricultural pest in Russia. Swarms can grow to densities of over 10,000 per square meter.
Blocking locusts’ ability to produce or detect PAN could help control swarms, says Greg Sword, an entomologist at Texas A&M University in College Station. As PAN deters birds too, “blocking the locusts’ ability to produce it should make them simultaneously more vulnerable to both their predators and cannibalistic neighbors,” he says.
“We don’t want to eradicate any species,” Hansson says. “But the cool thing would be if you could diminish the size of the swarms.” | Biology |
Researchers at the Francis Crick Institute and Heidelberg University in Germany have shown that sex differences in animals vary dramatically across species, organs and developmental stages, and evolve quickly at the gene level but slowly at the cell type level.
Mammals have different traits depending on sex, like antlers in male deer. These are known as 'sexually dimorphic' traits, and include differences which aren't visible, such as in internal organs. However, researchers didn't know when and where sex differences emerge, and which genes and cells are responsible for them.
In this study, published today in Science, the researchers analysed the activity of genes in males and females over time in humans and four species (mice, rats, rabbits, opossums and chickens), covering the development of five organs (brain, cerebellum, heart, kidney and liver), into adulthood in the animals and up to birth in humans1.
The researchers discovered that the organs which are different between the sexes vary across species. For example, the liver and the kidney were the most sexually dimorphic in rats and mice, whereas in rabbits, the heart was the most sexually dimorphic and liver and kidney not at all.
The researchers also found that, in all animals and humans, few sex differences occurred while organs were developing. Instead, they increased sharply around sexual maturity.
The researchers then investigated the genes responsible for sex differences, finding that different genes are 'sex-biased' (expressed differently depending on sex) across species. Only a very small number of sex-biased genes were shared across species, suggesting that sex differences have evolved quickly. The few genes that were shared were usually located on the sex (X and Y) chromosomes.
Although sex-biased genes differed between species, the study showed that the types of cells that are sexually dimorphic are the same across species. For example, in mice and rats, different genes were sex biased in the liver, but, in both cases, the sex-biased genes were active in the hepatocytes, the main type of cell in the liver. This may explain why there are sex differences in drug processing in the liver.
Leticia Rodríguez-Montes, PhD student at Heidelberg University, and first author, said: "It was interesting to see that despite the fast evolution of sex differences, a few genes located on the X and Y sex chromosomes showed differences between the sexes in all mammalian species. These probably serve as basic genetic triggers for the development of traits specific to each sex in all mammals."
Margarida Cardoso Moreira, Group Leader of the Evolutionary Developmental Biology Laboratory at the Crick, and co-leader of the study with Henrik Kaessmann at Heidelberg University, said: "By taking an evolutionary approach, we've observed that sex differences evolve fast at the gene level but slowly at the cell level. This has implications for how we use animal models to understand sex differences in humans, as it's helpful to know that a particular cell type is sexually dimorphic across species, even if there are other differences.
"It was also surprising to us that there are so few sex differences until sexual maturity. We were expecting most differences to occur in adults because this is when sex differences are most visible, but we also expected to see a gradual increase in sex differences during organ development, instead of an abrupt rise around sexual maturity. This research is another piece in the puzzle of understanding why we are sexually dimorphic and how this impacts us."
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Scientists have developed a new device inspired by octopus suckers that can deliver drugs without requiring needles or pills. They've already tested it in humans in a small, short trial.
The 0.4 by 0.2 inch (1.1 by 0.6 centimeters) patch can stick to the inner lining of the cheek, stretch across it and increase the absorption of an attached drug.
When used in dogs for three hours, the patch efficiently delivered two drugs — desmopressin, which is used to treat excessive thirst and the urge to pee often, and semaglutide, the active ingredient in Ozempic and Wegovy, drugs that are respectively used to treat diabetes and obesity. A version of the patch without a drug attached was also safely used by 40 human volunteers for 30 minutes while they were able to talk, move around and rinse their mouths with water.
Further development is needed. However, the patch could represent a less invasive and more comfortable approach to drug delivery, especially for larger drugs that are poorly absorbed by the digestive system so can normally only be injected using needles.
"This is an interesting and well-designed series of studies expanding the range of drug delivery systems inspired by nature," Adrian Williams, a professor of pharmaceutics at the University of Reading in the U.K., who was not involved in the research, told Live Science in an email. "Stretching is known to increase the permeability of mucosal membranes [the protective layer that lines your organs and cavities like the mouth], and is particularly promising for large biological drugs, such as peptides and proteins, which tend to be poorly absorbed and so are usually given by injection."
"Compared to nasal delivery systems, we would offer something which is much more straightforward to use because you have the drug dose contained in the suction patch, you apply it on your mucosa and then you press. That's it," Jean-Christophe Leroux, senior study author and professor of drug formulation and delivery at ETH Zurich, told Live Science. "If you compare it to microneedles, it is less invasive," he said.
The authors only tested the patch for a short time so would need to find out what would happen if it was used repeatedly. They'd also need to determine which drugs would work with the technology: the target is large molecules, such as those used to treat obesity or osteoporosis, but they can't be too large to fit in the cup, Leroux said.
Chris McConville, an associate professor in pharmaceutics, drug formulation and delivery at the University of Birmingham in the U.K. who was not involved in the research, told Live Science in an email that although the device is interesting, it may not be very practical. The authors tried to mitigate the risk of accidental swallowing of the patch by using dental floss to link it to the volunteer's shirts, for example, but this needs to be further explored.
The authors also used a compound that increases the absorption of drugs called a permeation enhancer with the patch, which could mask any benefits of using it.
"I am not sure what the device offers over buccal tablets [drugs that stick to the inside of the mouth and dissolve] as it seems that it is the permeation enhancers that increase absorption," McConville said.
The findings were published Wednesday (Sept. 27) in the journal Science Translational Medicine.
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Emily is a health news writer based in London, United Kingdom. She holds a bachelor's degree in biology from Durham University and a master's degree in clinical and therapeutic neuroscience from Oxford University. She has worked in science communication, medical writing and as a local news reporter while undertaking journalism training. In 2018, she was named one of MHP Communications' 30 journalists to watch under 30. ([email protected]) | Biology |
It wasn't until 1957 when scientists earned special access to the molecular realm. After 22 years of grueling experimentation, John Kendrew of Cambridge University finally uncovered the 3D structure of a protein. It was a twisted blueprint of myoglobin, the stringy chain of 154 amino acids that helps infuse our muscles with oxygen. As revolutionary as this discovery was, Kendrew didn't quite open up the protein architecture floodgates — during the next decade, fewer than a dozen more would be identified. Fast-forward to today, 64 years since that Nobel Prize-winning breakthrough. On Thursday, Google's sister company, DeepMind, announced it has successfully used artificial intelligence to predict the 3D structures of nearly every catalogued protein known to science. That's over 200 million proteins found in plants, bacteria, animals, humans — almost anything you can imagine."Essentially, you can think of it as covering the entire protein universe," Demis Hassabis, founder and CEO of DeepMind, said in a press conference Tuesday. It's thanks to AlphaFold, DeepMind's groundbreaking AI system, which has an open-source database so scientists worldwide can involve it in their research at will, and for free. Since AlphaFold's official launch in July of last year — when it had only pinpointed some 350,000 3D proteins — the program has made a noticeable dent in the landscape of research. "More than 500,000 researchers and biologists have used the database to view over 2 million structures," Hassabis said. "And these predictive structures have helped scientists make brilliant new discoveries."In April, for instance, Yale University scientists called on AlphaFold's database to aid in their goal of developing a new, highly effective Malaria vaccine. And in July of last year, University of Portsmouth scientists used the system to engineer enzymes that will fight against single-use plastic pollution. "This moved us a year ahead of where we were, if not two," John McGeehan, director of Portsmouth's Center for Enzyme Innovation and a researcher behind the latter study, told the New York Times.The 3D structure of vitellogenin, which makes up egg yolk. DeepMind These endeavors are just a small sample of AlphaFold's ultimate reach."In the past year alone, there have been over a thousand scientific articles on a broad range of research topics which use AlphaFold structures; I have never seen anything like it," Sameer Velankar, DeepMind collaborator and team leader at the European Molecular Biology Laboratory's Protein Data Bank, said in a press release. Others who've used the database, according to Hassabis, include those trying to improve our understanding of Parkinson's disease, people hoping to protect the health of honeybees and even some looking to gain valuable insight into human evolution."AlphaFold is already changing the way we think about the survival of molecules in the fossil record, and I can see it will soon become a fundamental tool for researchers working not only in evolutionary biology but also in archaeology and other palaeo-sciences," Beatrice Demarchi, an associate professor at the University of Turin, who recently used the system in a study on an ancient egg controversy. In the coming years, DeepMind also intends to partner with teams at the Drugs For Neglected Diseases Initiative and the World Health Organization, with the goal of finding cures for little-studied, yet pervasive, tropical diseases such as Chagas disease and Leishmaniasis."It will make many researchers around the world think about what experiments they could do," Ewan Birney, DeepMind collaborator and deputy director of the EMBL, said in the conference. "And think about what is going on in the organisms and the systems that they study."Locks and keysSo, why do so many scientific advancements depend on this treasure chest of 3D protein modeling? Let's explain.Suppose you're trying to make a key that fits perfectly into a lock. But you have no way of viewing the structure of that lock. All you know is this lock exists, some data about its materials, and maybe numerical information on how big each ridge is and sort of where those ridges ought to be. Developing this key wouldn't be impossible, maybe, but it'd be quite difficult. Keys have to be precise, otherwise they don't work. So, before you get started, you'd probably try your best to model a few different mock locks with whatever info you do have so you can make your key. In this analogy, the lock is a protein and the key is a small molecule that binds to this protein. For scientists, whether they're doctors trying to craft novel medications or botanists dissecting plant anatomy to make fertilizers, interplay between certain molecules and proteins is crucial. With medications, for instance, the specific way a molecule in a drug binds to a protein could be the breaking point for whether it works. This interaction gets complicated because even though proteins are just strings of amino acids, they're not straight or flat. They inevitably fold, bend and sometimes tangle around themselves, like headphone wires in your pocket. In fact, a protein's unique folds dictate how it functions — and even the slightest of folding mistakes in the human body can lead to disease.
But returning to small molecule medications, sometimes pieces of a folded protein are blocked from binding a drug. They might happen to be folded in a strange way that makes them inaccessible, for instance. This is important information for scientists trying to get their drug molecule to stick. "I think it's true that almost every drug that has come to market over the past few years has been, in part, designed through knowledge of protein structures," Janet Thompson, a research scientist at DeepMind, said in the conference. Researchers normally spend an incredible amount of time to decode the folded, 3D structure of a protein they're working with in the way you'd begin your key-making journey by piecing together the lock's mould. It becomes a lot easier to tell where and how a molecule would attach to a given protein, as well as how that attachment might affect the protein's folds in response, if you know the exact structure.But this effort isn't simple. Or cheap."The cost of solving a new, unique structure is on the order of $100,000," Steve Darnell, a structural and computational biologist from the University of Wisconsin and researcher at bioinformatics company DNAStar, said in a statement.That's because the solution typically comes from super complicated laboratory experiments. Kendrew, for example, tapped into a technique called X-ray crystallography back in the day. Basically, this method requires you to take solid crystals of the protein you're interested in, place them in an X-ray beam, and watch to see what pattern the beam makes. That pattern is pretty much the position of thousands of atoms within the crystal. Only then can you use the pattern to uncover a protein's structure. There's also the more recent technique known as cryo-electron microscopy. This one's similar to X-ray crystallography, except the protein sample gets straight-up blasted with electrons instead of an X-ray beam. And even though it's considered much higher in resolution than the other technique, it can't exactly penetrate everything. Further, in the realm of technology, some have attempted to digitally create protein folding structures. But early tries, like a few attempts in the '80s and '90s were not great. As you can imagine, laboratory methods are also tedious — and difficult. Over the years, such barriers have given rise to what's called the "protein folding problem." The issue is that scientists don't know how proteins fold, and have faced significant hurdles to get past that problem. AlphaFold's AI could be a game changer. A diagram provided by DeepMind of the explosive growth of the AlphaFold database, by species. DeepMind Solving the 'folding problem'In short, AlphaFold was trained by DeepMind engineers to predict protein structures without requiring laboratory presence. No crystals, no electron firing, no $100,000 experiments.To get AlphaFold to where it is today, first, according to the company's website, the system was exposed to 100,000 known protein folding structures. Then, as time passed, it started to learn how to decode the rest. It's really as straightforward as that. (Well, apart from the talent that went into coding the AI.)"It takes, I don't know, a minimum of $20,000 and a large amount of time to crystallize a protein," Birney said. "That means experimentalists have to make choices about what they do – AlphaFold hasn't had to make choices yet." This feature of AlphaFold's thoroughness is quite fascinating. What this means is scientists have more liberty to guess and check, follow an inkling or gut instinct and cast a wide net in their research when it comes to protein structures. They won't need to worry about cost or timelines."The models come with a prediction error as well," Jan Kosinski, DeepMind collaborator and structural modeler at the EMBL in Hamburg, Germany said. "And usually — actually in many cases — the error is really tiny. So we call that a near-atomic precision." Further, the DeepMind team also says it conducted a wide variety of risk assessments to make sure using AlphaFold is safe and ethical. DeepMind team members also suggested that AI, in general, might carry biosecurity risks we hadn't thought to assess before — especially as such technology continues to permeate the medical space. But as the future unfolds, the DeepMind crew says AlphaFold will fluidly adapt and address such worries on a case-by-case basis. For now, it seems to be working — with an entire universe of protein models built on a legacy initiated by a modest portrait of myoglobin."Only two years ago," Birney said, "we just simply did not realize that this was feasible." | Biology |
A well-preserved skull of a European great ape which could be among the earliest ancestors of the human race has been reconstructed by scientists using CT scans.
The researchers say their results are consistent with the idea that this species represents one of the earliest members of the human and great ape family.
The species, Pierolapithecus catalaunicus, was one of a group of now-extinct ape species that lived in Europe between 15 and seven million years ago.
The researchers hoped to learn more about human evolution from the remains, because they found both a cranium and partial skeleton from the same individual, which is rare.
Ashley Hammond, associate curator and chair of the American Museum of Natural History's Division of Anthropology, said: 'One of the persistent issues in studies of ape and human evolution is that the fossil record is fragmentary, and many specimens are incompletely preserved and distorted.'
'This makes it difficult to reach a consensus on the evolutionary relationships of key fossil apes that are essential to understanding ape and human evolution.'
The remains were first unearthed in Catalonia, Spain, in 2002 and first reported in the journal Science in 2004.
Scientists unearthed parts of the skull, along with other bones such as vertebrae, ribs and parts of the hands and pelvis.
Lead author Kelsey Pugh, a research associate at the American Museum of Natural History said, 'Features of the skull and teeth are extremely important in resolving the evolutionary relationships of fossil species.
'When we find this material in association with bones of the rest of the skeleton, it gives us the opportunity to not only accurately place the species on the hominid family tree, but also to learn more about the biology of the animal in terms of, for example, how it was moving around its environment.'
Previous research on the species suggest it had an upright body, and adaptations which meant it could hang from tree branches and move from tree to tree.
But scientists have been divided on where the ape fitted on the evolutionary tree, due to damage to the cranium.
The researchers used CT scans to virtually reconstruct the cranium of Pierolapithecus, and compare it to other primate species.
The researchers found that Pierolapithecus shares similarities in overall face shape and size with both fossilized and living great apes.
The species also has distinct facial features not found in other apes from the same period.
Co-author Sergio Almécija, a senior research scientist in the Museum's Division of Anthropology said, 'An interesting output of the evolutionary modeling in the study is that that the cranium of Pierolapithecus is closer in shape and size to the ancestor from which living great apes and humans evolved.
The research was published in the journal Proceedings of the National Academy of Sciences. | Biology |
An imbalance of fungi in the gut could contribute to excessive inflammation in people with severe COVID-19 or long COVID. A study found that individuals with severe disease had elevated levels of a fungus that can activate the immune system and induce long-lasting changes.
The work, published on 23 October in Nature Immunology1, raises the possibility that antifungal treatment could provide some relief to people who are critically ill with COVID-19.
“We know inflammation is driving severe disease,” says Martin Hönigl, a clinical mycology researcher at the Medical University of Graz in Austria, who was not involved in the study. This work, he says, provides a potential mechanism of disease-causing inflammation that might have been overlooked.
Inflammation insights
Trillions of microorganisms live in and on our bodies, helping us to digest food, protecting us from harmful pathogens and more. Although much of the microbiome consists of bacteria, past research has shown that the fungal portion — the mycobiota — interacts with the immune system, too2.
Previous studies have shown that many people with COVID-19 have guts with altered microbial make-ups and disrupted protective barriers, which could allow pathogens to enter the blood3,4. And some individuals critically ill with COVID-19 have contracted dangerous fungal infections in their lungs5.
Immunologist Iliyan Iliev at Weill Cornell Medicine in New York City and his colleagues wanted to further investigate the link between the mycobiota and COVID-19. The researchers examined blood from 91 people hospitalized with the disease in 2020. Almost three-quarters of these people had severe COVID-19, who received more than six litres of supplementary oxygen a minute or invasive mechanical ventilation, whereas the rest had moderate or mild disease.
Compared with 36 individuals who had never tested positive for SARS-CoV-2, people with severe COVID-19 produced about four times as many antibodies against three fungal species commonly found in the gut, including the yeast Candida albicans. A high prevalence of antibodies suggests that these people had elevated amounts of those fungi. Faecal samples collected in early 2021 from 10 people with COVID-19 also showed that they had higher overall levels of gut fungi, especially of Candida species, relative to 10 healthy individuals. For these people, the abundance of Candida was positively correlated with disease severity. The presence of some fungal species, C. albicans in particular, has been shown to activate the immune system6.
In a subset of people with severe COVID-19, the number of antibodies against C. albicans in their blood was linked to the number of immune cells called neutrophils, which can trigger inflammation.
When the researchers infected mice with C. albicans extracted from people with severe COVID-19, and then infected them with SARS-CoV-2, they observed that more neutrophils invaded the animals’ lungs and activated an inflammatory response than in mice with SARS-CoV-2 alone. If they gave these mice an antifungal drug, it lowered the number and activity of neutrophils.
Long-COVID theories
The study also found that people with severe COVID-19 continued to have raised levels of antibodies against C. albicans and neutrophil precursors primed to counter fungi long after they had recovered from the disease — up to one year later in some people. These factors hint that mycobiota changes during a SARS-CoV-2 infection could contribute to inflammation associated with long COVID.
“There’s a number of theories of what might trigger persistent symptoms after COVID,” says Aran Singanayagam, a respiratory immunologist at Imperial College London. “Microbial dysbiosis, either of the gut or the lungs, is one major theory that people are proposing, so I think this adds weight to that theory.”
Researchers agree that more work is needed to probe the link between gut fungi and COVID-19. It remains unclear whether the observed changes to the mycobiota in people with COVID-19 resulted from the disease or preceded it and made people more susceptible, says Singanayagam.
If future studies reveal more about the mechanisms involved, existing antifungal treatments could be repurposed to help people with COVID-19. Iliev hopes that this work will “make people start thinking about those common types of biology that we see in very different diseases and how we can leverage that”. | Biology |
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