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Why do telomere lengths not predict differences in life spans among species?
We read that ageing is related to cell death when we run out of telomeres at the end of our DNA molecules. Humans live roughly for 70 years - the traditional three-score years and ten. This compares with the great apes, such as chimps and gorillas, which live for about 40 years. So we would expect the great apes to have fewer telomeres than humans. In fact the reverse is the case. Humans have telomeres of about 10 kilobases in length whereas the equivalent length in chimps and other great apes is about 23 kilobases. So what is going on? Why do we live longer?

Great question. However, a few references that contain the numbers would help people answer. +1

I think the problem is that you mix up the ageing of a cell with the ageing (or life span) of an organism. Of course the maximal lifespan in a perfect environment could be based on telomere length, but there are other factors shortening this life span as health care, general safety, behaviour,...

In response to Skymingen's comment, in captivity chimps live on average for 31.7 yrs (m) to 38.7 yrs (f). I suppose 'captivity' is the equivalent of good nutrition and health care in humans, which still leaves a huge 'longevity gap'.  If cells die off in large numbers, isn't that the main cause of ageing?

Just remember the life expectancy of Mice is about 3 years, but they have really long telomeres. http://learn.genetics.utah.edu/content/chromosomes/telomeres/ I think a lot of the claims on here are absurd, but it gives a general overview.

You are incorrect about your figures. Chimpanzees live up to 60 years of age in captivity. The blog you are quoting is wrong. This is detail from the University of Wisconsin's National Primate Research Center (http://pin.primate.wisc.edu/factsheets/entry/chimpanzee).

Besides being wrong about telomeres, you are also forgetting the fact that through the 19th century, where we saw public sanitation for the first time and the advent of modern medicine, human life expectancy was between 35-40 years. Prior to the Renaissance and Industrial Revolutions, it was more like 30. So we had similar life expectancies to our cousins up until the point where we figured out the Germ Theory of Disease.

As a side note: titles starting with Please explain...,  question about... or help for...  are not very helpful. A better title would be Why isn't life expectancy correlated with telomere length?

The answer should be obvious: Telomeres do not determine an organism's longevity.
There's only a vague correlation between telomere length and a species' lifespan.  See Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination for a starting point.  Telomeres are a part of the longevity story, but probably a fairly small part.
The Hayflick limit is generally associated with telomere length. Human telomeres are a little on the long side as species go, but are not extraordinary. Many species of mice, and other rodents, have far longer telomeres than humans, for example, and obviously have much shorter lifespans. There's also such a thing as a "mega-telomere", found in a number of bird species, which can hundreds of times longer than human telomeres.

Absolutely. One of the likely culprits is Mitochondria no longer being able to perform their roles properly. Though to improve upon your answer, you should probably paraphrase and reference the paraphrases to the relevant primary literature on aging.

Please could you provide references in your answer

It's not really necessary to give references, because as I say it's trivially obvious -- as the original question shows -- that telomere length isn't connected with aging.  It would make more sense that the bizarre belief that telomeres are associated with organism aging -- which defies these well known and simple observations -- should support itself.

Telomere length is linked to aging - there's a number of links here: https://www.google.se/search?q=telomere+length+aging&oq=telomere+length+agi&aqs=chrome.1.69i57j0l3.9980j0j4&client=ms-android-samsung&sourceid=chrome-mobile&ie=UTF-8 @iayork

I asked the question because I am an Earth scientist, not a biologist, and I am not familiar with the primary literature. So what is 'trivially obvious' to iayork isn't obvious to me. As I understand it, with each death and replacement of a cell, the telomere shortens. After multiple cell regenerations there are no telomeres left, and the cell dies. The death of millions of cells effectively results in ageing. Maybe I phrased the question badly, but the question still stands: why don't chimps, who have more telomeres, live longer than humans?

@rg255 Most recent research on neurodegeneration point to the formation of amyloid plaques due to misfolded proteins being able to nucleate the misfolding in normally folded forms of those proteins. The plaques accumulate and are toxic to the cell. Many of these diseases are associated with aging and they have nothing to do with the length of telomeres.

@iayork I just think being so dismissive of the link between telomeres and ageing is misleading, while telomere length does not determine ageing entirely that does not mean they are unrelated to ageing - http://www.nature.com/nrg/journal/v6/n8/full/nrg1656.html and http://www.gizmag.com/telomerase-aging-harvard-reverse-process-telomeres/17107/ - besides that discussion, I was only asking for references because that is the normal standards we set on biology SE, which you might not be familiar with as you seem to be fairly new, just trying to be helpful

Perhaps you could modify your answer to say that between-species the telomere length appears to explain little to none of the variance in ageing, while they appear to some of the variance in ageing within-species, I think this would be a more accurate interpretation and answer to the question.

There is not one simple cause of aging, like short telomeres, and the fact is that it hasn't even been settled whether aging is caused by evolution failing to evolve good enough repair mechanisms, or whether it evolved with a purpose, it might be that the genes of an organism are better spread if that organism doesn't live too long for example. For more details on the latter debate see this previous issue of Current Aging Science (all the articles are free).

Updated research seems to be showing it's the rate of shortening, not the initial lengths of telomeres, that affect species life spans.  Here is a 2019 study supporting this view:
https://www.pnas.org/doi/full/10.1073/pnas.1902452116
From the abstract:

We found that the telomere shortening rate, but not the initial telomere length alone, is a powerful predictor of species life span. These results support the notion that critical telomere shortening and the consequent onset of telomeric DNA damage and cellular senescence are a general determinant of species life span.


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Trying to identify a bug that left a blood spot when killed

Hi, this was flying around inside the car in northwestern Maryland, USA, yesterday. When I squished it with a tissue I was surprised to see a red spot that appeared to be blood. Cannot find a picture of this bug online and was hoping someone can identify it. Thanks in advance.

I'm from California and my Husband was bitten or stung by the same bee or fly. He was outside on the hammock and told me something stung his foot. It was the exact same fly and when i squished, It was full of blood. I took a photo because It was very weird that this fly or bee was feeding on blood. I ask several people but no one believes us at all.

it's a harmless hover fly, a flower pollinating wasp mimic that migrates hundreds of miles every year and have quite interesting biology. you can recognize them because they hover in one place a bit like small humming birds.

That looks like a species of syrphid fly (aka. hover fly, flower fly) — not sure about the red fluid, but it probably wasn't blood.  These flies are pollinators and the larvae eat pests such as aphids.
I don't know for sure what species that is, but it appears very similar to Toxomerus politus:

Other sources of information on this group of flies:

http://thingsupclose.com/syrphidae-hoverflies/
http://bugoftheweek.com/blog/2017/10/31/flies-that-mimic-wasps-masquerading-syrphid-fly-ihelophilusi-sp
http://bugoftheweek.com/blog/2016/10/19/a-flower-fly-grows-in-brooklyn-flowers-flies-syrphidae

That hoverfly was probably feeding on red pollen from flowers. Many types of flowers have red pollen:

They were scientifically proven to eat pollen and nectar as early as 1883, when Muller disected the flies up to study their crop and insides.
Entomology Division, Department of Scientific and Industrial Research,
Private Bag, Auckland, New Zealand

Analyses of the pollen contents of the crop and intestine of 11 species of New Zealand Syrphidae .
showed that small, sparsely haired hover-flies with unbranched hairs, short, simple bristles, and a
short proboscis had ingested at least 99% anemophilous pollens, and that larger, more hairy hoverflies with pollen-collecting hairs, long, spirally grooved bristles, and elongate mouthparts had ingested
pollens almost exclusively from nectar-bearing flowers. Pollen-feeding behaviour was studied in
one hairy species, the drone-fly Eristalis tenax, and in one sparsely-haired species, Melanostoma
fasciatum. Using granulated charcoal as a substitute for pollen, it was found that in E. tenax particles
trapped among the body hairs are combed off by the front and hind tibiae and transferred to pollenretaining bristles on the front and hind tarsi respectively. Particles retained among the front tarsal
bristles are ingested directly from the bristles. Those retained by the hind tarsi are transferred in
flight by leg-scraping movements to the front tarsi, from which they are subsequently eaten. E. tenax
also eats pollen directly from anthers. In M. fasciatum apparently all the pollen ingested is taken
directly from anther lobes or stigmas. The few pollen grains that adhere to the body of this species
are combed off by the front and hind tibiae and transferred to the front and hind tarsi, but are not
retained there because the bristles are short and simple.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

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What is the chemical structure of myosin?
What is the chemical structure of myosin? Specfically, what functional groups or monomers are they made of?

What have you already learned in searching?

I just know the functions and the categories of it.:( Based on the research, I know that it is a motor protein and acts with actin to perform muscle contraction. Also that some types of myosin performs other  activities like phagocytosis or transporting vesicles  and that there are powered by ATP hydrolysis. I only have basic knowledge of chem and bio but I assume that since it is a protein it is made of amino methyl or carboxyl groups.

Ok. Why do you want to know the chemical structure? What will it tell you? With proteins, we don't usually talk in terms of chemical structure, but as chains of amino acids. Really you should probably learn more about amino acids first based on your comment.

Thank you for the reply. I'm  doing a project related to macromolecules, and for me it is myosin.  The thing that concerns me is that there is one part asking about the chemical structure (functional groups ,monomer, and polar regions). I researched and read some article for hours. I understand how it functions and impacts the body but I could't really grasp  how it is chemically made and I feel like I'm lost:(  This sounds like a stupid question but would you mind recommending me how to approach this kind of research, like what concepts I could know for better understanding?

Probably the Wikipedia pages on proteins and amino acids would help you - you probably also have a textbook with similarly helpful descriptions. You kind of need to understand those basics before trying to understand the structure of a particular protein.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Differentiating Antaresia (Children's Complex) Pythons using something other than color pattern
I have a standard wild-type Children's python (Antaresia childreni) that I'm planning on breeding in the next few years and was just sold a male "Children's python" that I think might actually be a spotted python (Antaresia maculosa). Unfortunately, he's of some kind of reduced pattern morph (granite, I think) that has completely blown out his natural patterning, so my main method of identification is useless.
I know that along with the Stimson's python (Antaresia stimsoni) all of these snakes have been identified as "Children's pythons" at some point in the not-too-distant past, but someone saw fit to distinguish between them and I can't seem to find any basis for doing so that isn't based on range and pattern, both of which are meaningless for a captive-bred snake of a morph that makes its natural pattern indiscernible.
Is there some reliable way to tell the difference between these snakes other than coloration and range? Perhaps some difference in number or placement of certain scales or details about the eyes?
I've included a picture in case anyone can comment and tell me what this little guy actually is on the basis of the modified pattern - but I'd still like a better way if anyone can provide a real answer.

I finally got frustrated enough to dig up A Revision of the Liasis childreni species-group (Serpentes: Boidae) L.A. Smith, 1985 - the original paper that split up this species complex, and when even Smith made primary determinations off of pattern and color alone, I took matters into my own hands and dug into the his raw data.
I have compiled the mean scale counts for each species into a table, and truncated any rows that showed no useful degrees of deviation for any species, resulting in the following:
             A. Childreni  A. Maculosa  A. Stimsoni  A. Stimsoni Orientalis  A. Perthensis
Ventrals     272.8        263.5         279.5        263.8                   232
Subcaudals   47.3         42.1          46.2         42.8                    38.7
Midbody      41.3         38.3          43.4         40.3                    32.7
Loreals      7.9          4.7           12.2         7.9                     7.3
Postoculars  3.6          3.1           4.2          3.8                     3.4
Pits         4.5          4             5.6          4.8                     3.1

I am including this table in its entirety to assist future identification efforts within the complex, as the original paper did a poor job of presenting this data.
The most useful difference for my purposes - distinguishing between A. maculosa and A. childreni - appears to be loreal scale count. The loreal scales sit between the eye and nostril of the snake, and do not include scales which belong to the orbital and nasal structures (The region marked "l" in the diagram below).

Following up on this, I examined a number of close-up photos of known examples of both species, and very quickly identified a distinctive difference in not just the count but also the pattern of loreal scales. Once you're looking in the right place, the difference is obvious.
A. Childreni showing its distinctive granularly-clustered loreal scales:

A. Maculosa showing its smaller number of tightly structured loreal scales:


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Virus cannot survive on surface after certain time period, but why and how?
I'm not a biology student at all, but I'm trying to get a clearer picture on what is meant by "virus cannot survive after a certain period".
To my understanding, a virus cannot be killed it can only be inactivated (for example, by means of heat and lowered pH).
So I really don't understand how can virus get inactivated by just being on a certain surface for an extended period.
I've come across numerous articles which told me virus won't survive on a surface. They usually focus on comparing the survival time between different types of surfaces but never touch on how the virus gets inactivated.
Can someone help me understand the "how"?

Related: 2019 Novel Coronavirus (nCoV) lifetime outside an organism

"To my understanding, virus cannot be killed" This is just because they're generally deemed not to be alive in the first place.

It does depend on the surface, and the virus, different ones are destroyed in different ways. A virus survives in the same way an antique car survives, as in it still exists in good enough shape to function.

I am thinking virus can be degraded by lots of extracellular enzymes (e.g. proteases) which microorganisms are constantly secreting. That's how elements locked up in "biomass" cycle again. And that explain why virus survive more poorly in moist and hot environment where microbial activity is the highest. I could be wrong but just saying.

Many important viruses are coated with a lipid envelope and rely on this to enter the host cell. This envelope is fragile - it's similar to a soap bubble - and it can be disrupted in many ways. Lipids will oxidize in air over time and this will degrade their ability to maintain an envelope. Surfactants such as soap or solvents such as alcohol will disrupt an envelope quickly. Even if the genome inside survives, if the envelope is disrupted the virus won't be able to infect cells.
The exact mechanism of inactivation likely varies a lot from virus to virus, and hasn't been studied extensively.
This paper found that Hepatitis C virus RNA survived alcohol treatment, but lost infectivity, presumably due to envelope disruption. In contrast, heat treatment (80°C) destroyed both the envelope and the RNA.
Another paper found enveloped viruses survived being dried out a shorter time than non-enveloped viruses. (5 days vs. weeks)
Speaking generally, the environment outside a body is hostile! If you were taken out of your home and dropped somewhere in the wilderness, there's many different ways you could die, and it's more remarkable if you survive. A similar situation arises for viruses.

+1 To be fair I don't think the last paragraph is a good comparison, as a virus is just a bunch of molecules and not a living thing. And I think it's from this understanding that the original OP asked his question. If you put a table outside on a surface it won't get destroyed either. Obviously the answer is "viruses are relatively fragile, because evolutionary the advantages of surviving away from organisms that could replicate them was fairly pointless" . Does make me wonder whether with the increased population density of human organisms there will be a point where it's worth surviving.

The point I was trying to make is that viruses are complex systems that have many potential points of failure. In that regard, they are closer to a living thing than a table, which can take a lot of damage and still function as a table. Maybe a better comparison would have been to some electronic device like a PC that you'd expect to stop working if its left outside. But, I expect rain would destroy it before anything else 99% of the time so it doesn't work the same way.

@DavidMulder: To give a better analogy, a virus is like a car that functions well in the city but will break down gradually if left into the wilderness, rapidly if it is thrown into a pond or the sea. Similarly, viruses 'survive' well in their hosts, but will gradually break down if left outside, and rapidly so in certain environments.

@DavidMulder Even with the table, leaving it outside under the sun / rain / snow etc. versus leaving it in your home over a long period of time means different rates of degradation.

@DavidMulder I would argue that there's a fine line between a "bunch of molecules" and a "living thing". The death of a "living thing" is just what happens when a sufficient number of internal systems of the thing (which are themselves "bunches of molecules") are placed in hostile scenarios for a sufficient time for them to cease function. I would think the comparison of a virus on a surface to a human in a desert is apt (if incredibly simplified) - the concept of "death" might be different from a micro to a macro scale, but the ultimate result is the same for the subject.

thanks for the response, it helps me to better understand how Virus break down in the wild.
I can understand how solvents and heat can disrupt or destroy the envelope or even some structure within the virus.
The point about oxidization seems to explain mildly.
So if a virus is being filtered by a mask, and then if I put a mask inside my home for extended period, oxidization will gradually disrupt the stability of the virus envelope, does my understanding correct?

yes, oxidation will eventually degrade viruses stuck in a mask, and speed up inactivation by other processes like drying out.

Ultraviolet (UV) light emitted from the sun has enough energy to break chemical bonds in DNA and RNA.
Some frequencies of UV light can cause damage in the DNA in skin cells that can lead to replication and expression errors, which lead to cancer (melanoma).
Similarly, UV can break up and inactivate the genomic payload of a virus:

Sunlight or, more specifically, solar UV radiation (UV) acts as the principal natural virucide in the environment. UV radiation kills viruses by chemically modifying their genetic material, DNA and RNA. The most effective wavelength for inactivation, 260 nm (55), falls in the UVC range, so-named to differentiate it from near-UV found in ground-level sunlight, i.e., the UVB and UVA portions of the spectrum, 290 to 320 nm and 320 to 380 nm, respectively (51). Nucleic acids are damaged also by UVB and UVA but with lower efficiency than by UVC radiation (64).

Surfaces exposed to sunlight would see partial to complete inactivation of virus particles over time.
There is a paper here that discusses using a safer frequency of UVC radiation as a biocide:

The biophysical reason is that, due to its strong absorbance in biological materials, far-UVC light does not have sufficient range to penetrate through even the outer layer (stratum corneum) on the surface of human skin, nor the outer tear layer on the outer surface of the eye, neither of which contain living cells; however, because bacteria and viruses are typically of micron or smaller dimensions, far-UVC light can still efficiently traverse and inactivate them13,14,15.

So your saying natural sun light is enough to kill viruses. though it can take days/ hours dpending on the surface? Also that it only kills the viruses that are on the surface, and not behind something/ embedded deep inside? So a moist though thin hankie, would take longer to disinfect than a similar dry one?

You'd need to measure how different UV frequencies get through layers of fabric, but people wear clothes and hats to protect against sunburn. This should perhaps give an intuitive sense to what extent a hankie can be sanitized.

Well I have used a hat and a hankie. A hat worked well. But a hankie made me feel hot very soon. I'm bald. I don't trust my intuition here. Was curious to know your knowledge or best guess? :-)

I don't know the answer, but I suspect keeping a handkerchief in your pocket will allow it to accumulate a lot of bacteria and viruses. You could put your handkerchief on a clothesline to expose it to the sun, but then there are pollen and mold spores in the air, which are allergens for some people. I hope you find an answer.

okay thank you. hopefully multiple researchers will do a bunch of studies and answer these question in the coming months

Like other forms of life, viruses are composed of fragile molecules susceptible to damage from the environment.  They may oxidize in the air, suffer mechanically stresses, be hit by UV light, etc.  Metabolism in cellular life combats this effect by actively making repairs and by forming and maintaining protective barriers.
Viruses don't do that.  Outside of a cell, they don't do anything.  They don't have a metabolism.  They can't make repairs.  The damage accumulates until they can't work anymore.

Welcome to Biology.SE! Your point about viruses not be able to make repairs is a good one, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!

Virus as complex ordered system, without actively maintaning the order, the order will lose after time and finally lose the ability to infect the host.
Even the virus in a host body that is not destroyed by the immune system will "die" (means not functioning any more). It doesn't matter a single virus live or die, the important thing is the pupulation - if virus get replicated is more than that is dead in a period, the population will increase in the host body.
Infection is also about statistics, you need enough virus to get into the host body for them to successfully start the pupulation increasing process before they all become dead (killed by immune system or degraded in other ways)
We are not sure whether the virus particales outside host are all dead or not, only sure about the chance they infect the host after a time is low.
So another reason (besides detailed mechanisms) is that they are not replicating to sustain the population that is dense enough to easily infect the host.

For the record, I would like to place here a response that was received for How do viruses die outside of host cells?, which was deemed to be a duplicate of this post and closed.

This isn't very professional, but there are the basics. Viruses are obligate parasites, which means they can't live outside a host (in this case, a cell) for long. Viruses get damaged as everything else, the damage taking many forms, such as hydrolysis, photolysis, free radical damage, reaction with other molecules (like detergent), conformation changes, dehydration, maillard reactions, and changes induced by heat of labile molecules (like decomposition). All types of damaging processes happen at an increased reaction rate with increasing light and heat. Viruses have rudimentary repair mechanisms if any, so it's a matter of time before they become inactivated. A damaged virus entering the body wouldn't be able to do much harm if any, as their genetic information would be damaged beyond repair, and so, not able to be replicated to make more viruses. Their proteins and genetic bits would still trigger an immune reaction and immunize against intact and not very damaged viruses (which is why damaged viruses are used in vaccines). Those damaged viruses that remained outside just become microbe food.


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Action potential attenuation in unmyelinated axons vs demyelinated axons
I learnt that action potentials travel much faster along myelinated axons, and when these axons are demyelinated the action potentials travel much slower and sometimes die out. Why do action potentials die midway in unmyelinated axons?

In unmyelinated axons, there are voltage-gated ion channels along the entire length of the axon. Depolarization in one segment depolarizes and opens ion channels in the adjacent segment, which further depolarizes the next segment, etc.
Myelinated axons are built differently. They have stretches of myelinated axon which are (mostly) free of voltage-gated channels, interrupted by nodes of Ranvier that lack myelin but have dense voltage-gated channels. The depolarization at one node has to be sufficient to reach the next node for the signal to propagate.
Normally this is no problem. Thanks to insulating myelin, the signal propagates unattenuated for a long distance. However, if you start to lose myelin then some of the signal is lost along the way (specifically, the current goes to charge the membrane capacitance, which is reduced by myelin) and it may not be enough to open voltage-gated channels at the next node of Ranvier.

Myelinated axons have schwann cells around them, electrically insulating the neuron axons except for gaps in the sheath which are called the Nodes of Ranvier. The insulation increases the speed of transmission of action potentials.

Without myelination conduction signals along the nerve can be impaired or lost.
There are some diseases E.g. Acute disseminated encephalomyelitis where myelination is lost.


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What are cells not affected by hormones called?
Cells that are affected by hormones are called target cells which have their own receptors that listen to signals. I'm unsure of the actual name of cells that are not affected by hormones, I tried searching around on pages relating to target cells and the endocrine system, but no one seems to actually give a name to these cells that don't have receptors.

How about non-target cells? I found several examples of that usage including:

A book section titled: 9.3 How are steroid hormone target cells differentiated from non-target cells?1
Containing the following line:

Thus, estrogen will stimulate mRNA and protein synthesis in a target cell, but not in a non-target cell.

A book chapter titled: Target or non-target: Hormonal signal perception and response in the determination of cell performance2

References
1: Brown, R., Brown, R. E., & Brown, R. E. (1994). An introduction to neuroendocrinology. Cambridge University Press., p. 149.
2: Osborne, D. J., & Thompson, D. S. (1992). Target or non-target: hormonal signal perception and response in the determination of cell performance. In Progress in Plant Growth Regulation (pp. 237-247). Springer, Dordrecht.


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Large caterpillar with prominent eye-spots and a Morse-code pattern
I would appreciate any help in identifying this caterpillar.

Location: Goa, India. Tropical climate
Currently rainy season. Seen in the morning
Length: about 5cm, Diameter: about 1cm

Can you describe what’s happening in that video? Is the caterpillar being flipped around by a push of air, or is it moving on its own accord (in reaction to a visual stimulus?)?

@KonradRudolph The caterpillar was flipping on its own, most certainly reacting to the movement of the dog's paws (seen in the corner). The dog spotted it first and was  freaking out and barking at it, though keeping a safe distance.

This is really cool! Thanks for posting. :)

This appears to be an oleander hawk-moth caterpillar (Daphnis nerii) shortly before pupating. Otherwise the caterpillar would be bright green in colour:

Newly hatched oleander hawk-moth larvae are three to four millimeters in length, bright yellow, and have a black, elongated "horn" on the rear of the body. … As they get older, the larvae become green to brown with a large blue-and-white eyespot near the head and a yellow "horn" on the rear. […] Just before it pupates, the oleander hawk-moth larva becomes browner in colour.


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What bug has similar legs to a prawn?
This is a bug that I observe in Melbourne.
This bug is living in wet places and jumping a few centimeters while its length is 8.5mm.
It does not have insect legs. It's legs are more similar to prawn.
Sorry my camera cannot capture a better picture as the bug is too small.

https://en.wikipedia.org/wiki/Springtail

It is "Lawn Shrimp", an Australian indigenous creature. It is harmless.

Hello ar, welcome to Biology. This answer is very brief and adds little beyond what another answer has already stated except an additional nickname of the species and a great (but redundant) picture. Please refer to our [help] for guidance on how to answer questions. Enjoy the site.

@ARogueAnt., I wonder why you call this answer redundant when the previous answer does not specify the type of the creature. It only refers to the family of it. I see no "lawn shrimp" in the answer above.

Whilst the picture you've supplied appears to belong to the same family as the other answer, lawn shrimp usually refers to Arcitalitrus sylvaticus which is quite a bit smaller than the size specified in the question (and a different colour, but that may not matter). --Unless I've misread or misunderstood the descriptions.

@ARogueAnt., I have no better photo. I removed it.

This is a "sand hopper" (Talitridae), also known as "land hoppers" or "sand fleas". The Talitridae are a cosmopolitan family of arthropods, known for their hopping behaviour when disturbed.
Which of the genera it is from would be impossible to determine without detailed close-up pictures and a bit of expert knowledge which is well outside my expertise.


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Identify bug found eating wood table
This bug came out of a hole in a wood table.
I'm in south-west France but since we bought that table one year ago, it was most probably in the table when we bought it so it could be from anywhere.
I'd like to know what it is.

More context and pictures in https://diy.stackexchange.com/questions/232607/holes-in-wood-furniture-identifying-the-cause.

I'm not an entomologist at all, or even in Europe, so take my answer with a grain of salt.
I think this is a beetle of the long-horn beetles, which are all beetles that have a larval stage that borrow in wood. In particular I think this is in the genus Clytus and may be Clytus arietis, which is quite common in Europe and North America. There are other species in the genus that look pretty similar too (e.g. C. rhamni, so I can't be sure).
C. arietis is pretty small - about 10-18 mm, which looks about right for your hole size, and it has very similar patterns on its elytra. It is also hairy, as yours is. Apparently it is called the "wasp beetle" as it is a Batesian mimic, and may even make a buzzing noise when disturbed.

Thanks. The Clytus aeietis is much more yellow but the patterns totally match, so I believe it is definitely from the same family.


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Can the SAME histone tail have both H3K4me3 and H3K27me3?
I'm studying bivalent promoters and enhancers. I understand that the same region of genome can have both H3K4me3 and H3K27me3.
But can they occur on the same histone tail?
Please provide me with a reference to support your answer.

This paper suggests that people have tested if two proteins can bind on a histone tail that contains both epigenetic marks. This implies that indeed both markings can be on the same tail.
"Next, we investigated if a histone tail bearing both H3K4me3 and H3K27me3 marks can be combinatorially recognized by SHL."


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Doubts about what is growing in my bacteriological cultivation
Foreword: I don't belong to the field at all, I am a high school student with a passion for science so I apologise in advance if I formulate the question incorrectly or make some mistakes.
Out of personal curiosity, I tried growing a colony of bacteria.
I was amazed today when I opened the culture and found a kind of white spider's web with a few black dots hanging from it. Can anyone tell me what this is? I assume it is mould, but I am not sure.

Welcome to Biology.SE. Please tell us what sort of media you are using — that may be of some help in narrowing down an identification. However, note that fungi are notoriously difficult to identify based on appearance. That being said, the white threads with black spots does resemble common bread mold (Rhizopus stolonifer).

If black dots seem to be swimming then it might be a yeast infection.

Almost certainly a mold (the black dots being some sort of fruiting structure with spores). As far as which mold, it's difficult to say. The typical way to ID a mold is to look at spore morphology under phase-contrast microscopy, but even then it can be difficult (sometimes impossible) to distinguish between common genera by microscopy alone.


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Is the response to a vaccine correlated with the reaction to the disease?
I was wondering if the response to a vaccine correlates with the reaction to the disease.
For example, if someone had a strong reaction to a vaccine, this person would also have had a severe course of the disease.
It is clear that it is hard to test a hypothesis in this case, but maybe someone could answer this question based on the biological mechanisms at work (receiving a vaccine vs. getting infected).
A similar question was already asked in Medical Sciences SE (for Covid vaccines), but was closed without an answer.

I see some theoretical potential that the general virulence of a bug (virus, bacterium..) to the human host could be (negatively) correlated to the immune-response caused by diverse vaccination methods against same bug.
While the ability of a bug to evade the hosts immune system e.g. by minimizing easily recognizable epitopes could establish a logical connection to the hosts immune reaction against vaccines presenting same epitopes, vaccine adjuvants diminish the correlation.
However, practically the bugs evolution against antibody recognition aims at preventing neutralization, while the prevention of immune-system activation is achieved via other mechanisms:
A common bacterial strategy, which is entirely uncorrelated to vaccination responses, is to produce proteins (virulence factors) that bind host antibodies to inhibit the host's immune system defenses. Another example that indicates poor correlation is  production of virus-induced anti-inflammatory cytokines that may suppress T cell outgrowth.
Such suppressed cytokines include: Interleukin 10 (IL-10) or transforming growth factor β (TGF-β), or reduced production of inflammatory cytokines, such as IL-12 (Marshall, Urban, Welsh; 2011).
However, you seem to approach this question from a different standpoint:

For example, if someone had a strong reaction to a vaccine, this
person would also have had a severe course of the disease.

Here, you you seem to define the correlation as a function of different people as opposed to different bugs, while assuming constant vaccines and other factors.
Also, you define the "reaction to a disease" as the severity of the course of the disease. In contrast, the vaccination response quite unambiguously must be interpreted as the immune response.
As a persons good immune response against a vaccine should be correlated with a good immune response against the bug itself (independent events; no temporal order) and a good immune response against a bug (necessarily) has to negatively correlate with severity of caused diseases (as you passively define all other factors to be constant), the severity of disease should theoretically be negatively correlated with immune response to the vaccine. This also assumes that the recognized epitope(s) of the vaccine, that define the "vaccination response" are the same that define the immune response against the bug. Also, please mind that existence of a negative correlation per se does not state degree of variance coverage (compared to other factors).

I appreciate the answer! But I still can't deduce whether having stronger side-effects (fever, fatigue vs. say pain at injection) to the vaccine (say, mRNA covid?) would imply a stronger reaction to infection (death vs fever). You said "vaccination response ..must be interpreted as the immune response.", but I do not know if immune response (number of antibodies?) is proportional to "symptoms". I also do not know how much of a role the absence of adjuvant would play when infected. If I had strong / weak side-effects to vaccination, would I be more likely to die from / survive an infection?


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How are Moluccan cockatoos so loud?
They say a Moluccan cockatoo's screech has a decibel level of around 129 or even more (e.g., 135). That is almost as loud as a jet engine (140 dB at 100 feet).
How are they able to emit a screech that loud? Don't they hurt themselves?

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I was able to find a reference to the book Good Parrotkeeping by Robin Deutsch (©2009) from a forum post which purports to list several species' call loudness level (sorted by dB):

Nanday conure, 155 dB
Moluccan cockatoo, 135 dB
Mealy amazon, 124 dB
Quaker parrot, 113 dB
Mustached parakeet, 111 dB
Macaw, 105 dB
Mitred conure, 100 dB

I don't have a copy of the book so was not able to check the author's sources. However, I can answer a more general question about how birds are able to make loud noises in general.
Birds have a syrinx instead of a larynx as in mammals. This is situated at the bottom of the trachea, instead of at the top. Given this, birds can take advantage of acoustic resonance, which can allow for some extremely loud calls.
In a 21 Oct 2019 article in the New York Times titled "The Loudest Bird in the World Has a Song Like a Pile Driver" (paywall), the South American white bellbird is said to be the loudest bird in the world at 125 dB. (With the screaming piha now in second place). The study, "Extremely loud mating songs at close range in white bellbirds" was conducted by Dr. Jeffrey Podos and Dr. Mario Cohn-Haft in 2018. Unfortunately, it does not seem to cover the biological mechanics that produce such loud calls, but rather focuses on the evolutionary and sexual pressures that have led to such outliers in avian acoustics.
Edit:
Note that decibels are a measure of acoustic sound pressure, and vary greatly depending on the distance from the source they are measured. In order to be scientifically sound, the loudness of something should be measured from a fixed distance under controlled conditions. Note that the table of examples of sound pressure levels contains a "distance" column, which is extremely important for comparison purposes between sounds. I have no idea whether the parrot measurements were conducted using the same criteria as the white bellbird study (very likely not). Therefore, the higher dB values listed there may be due to measurements with much smaller distances.

It seems like you might be a valuable member of a proposed Bioacoustics Stack Exchange. Please consider committing to the page so we can get closer to making it to the Beta stage. Cheers!
https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680


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Identification of odd jellyfish-like creature in the Mediterranean
My parents encountered this unknown creature on a beach in Karpathos, Greece.
None of the locals have seen it before, it may be a species that has moved further north due to ocean warming.
Any ideas what it is?

@tyersome - Thank you for migrating to the proper page.

It seems to be a "Hula skirt siphonophore" - Physophora hydrostatica

Physophora hydrostatica, also known as hula skirt siphonophore, is a
species of siphonophores in the family Physophoridae.1

https://en.wikipedia.org/wiki/Physophora_hydrostatica

Nicely done. Distribution is in the Mediterranean and much of the Atlantic, so that fits. There are some nice photos of it here


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How can I confirm that this pedigree is of a pseudodominant trait?

This is an example of an autosomal recessive trait masquerading as autosomal dominant.  I carried out genetic analysis for each generation as if the trait was either recessive or dominant, and both modes of inheritance seem to fit the pattern observed. Does the pedigree have any defining features that might indicate that it is indeed autosomal recessive? Or would we simply have to carry out further analysis with other pedigrees?
Thanks to anyone that can help

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What type of bug is this?
Found two larva/eggs in a suitcase. The egg/larva were around same size or maybe little bigger than a grain of rice. When I put them on counter top to better examine, one hatched and a SINGLE insect popped out! It was fast moving when hatched and kept cleaning its legs. It was maybe the size of a grain of rice. I personally was thinking cockroach but it was a single insect from egg/larva!?!? Is it a bed bug or something else??? (We reside in Alabama.)
https://share.icloud.com/photos/0mQiO0JfeRwR3z7duvPSthrZw

If you have the photo on your device, use the mountain symbol to put the photo directly in your question

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — photos must be uploaded (not links); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information; and 4) an estimate of the size of the organism. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

In addition, there is an excellent post with information about bed bugs already on this site. If that is your primary concern please search on this site for "bed bug" and then delete this duplicate post if that answers your question.

I edited post as instructed. And also searched “bed bug” as instructed  Still left with question... Any advice on bug type? Comments? Please help...

From the evidence at hand, we can say Order Diptera (two-winged flies) with certainty; the suborder Brachycera seems more likely (the antennae of the adult in closeup are very short; Nematoceran flies usually would have antennae at least as long as the head is wide [those that don't bear NO resemblance to the OP photo]); beyond that, there are too many good possibilities (members of the family Drosophilidae [the geneticist's "fruit fly"] being just one of many possible groups).


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Neisseria meningitidis transformation into a pathogen
I read the wikipedia article about Neisseria meningitidis, and it says that

N. meningitidis is a part of the normal nonpathogenic flora in the nasopharynx of up to 5–15% of adults

In some cases however, it infects the bloodstream, creating a Meningococcemia disease which is highly lethal. It may also create a meningococcal meningitis.
The article also says that this disease is somewhat infectious. Not as infectious as common cold, but it is known to cause epidemics in Africa and Asia.
My question is: How can it be so abundant in its non-pathogenic form (up to 15% of adults) yet cause epidemics? It seems that it's transmitted from nose to nose somehow and doesn't cause a disease, yet when it does cause a disease it also causes a disease upon transmission.
It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people. Because then it wouldn't cause epidemics, since the majority of the population is immune to it as evidenced by the fact that it's part of their microbiota.
Does N. meningitidis mutate to become pathogenic? Do the nasal strain and the pathogenic strain have different genotypes?
I tried searching for an answer but didn't find any.
Thank you very much.

Welcome to Biology.SE! This seems like an interesting question, but I would note that 5-15% is not "the majority of the population" ...  ——— You may benefit from taking the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

If you can come up with a well supported (referenced) answer to your question I encourage you to post it as an answer here. ——— The wikipedia article on epidemics may be of interest. You also might want to read up on epidemiology and opportunistic pathogens — many "infections" by disease causing organisms can be asymptomatic (e.g. typhoid).

It's not like a strain of E. coli that may cause disease in immunosuppressed individuals yet is a part of normal microbiota for other people.

Well, actually, it is kind of like that.
The answer is complicated, but can be boiled down to, virulent serotypes of Neisseria meningitidis infect susceptible populations. For the short answer, just read between the highlighted boxes.

Invasive meningococcal disease results from the interplay of: (1) microbial factors influencing the virulence of the organism, (2) environmental conditions facilitating exposure and acquisition, and (3) host susceptibility factors favoring bacterial acquisition, colonization, invasion, and survival.

Virulent serotypes have capsules that help them evade detection and destruction; they have an outer envelope that helps them invade and infect susceptable individuals.

The virulence (14) of N. meningitidis is influenced by multiple factors: capsule polysaccharide expression, expression of surface adhesive proteins (outer membrane proteins including pili, porins PorA and B, adhesion molecules Opa and Opc), iron sequestration mechanisms, and endotoxin (lipooligosaccharide, LOS). N. meningitidis also has evolved genetic mechanisms resulting in a horizontal genetic exchange, high frequency phase, antigenic variation, and molecular mimicry, allowing the organism to successfully adapt at mucosal surfaces and invade the host.

The most susceptible populations are infants/babies (most frequently), young children and unvaccinated young adults (during outbreaks). These are the populations most likely to have no to low antibodies against the bacteria.

The meningococcus remains a common cause of bacterial meningitis in children and young adults in the USA (132), now mostly affecting children less than 2 years of age (102, 133). Two-thirds of meningococcal disease in the first year of life in the US occurs in infants less than 6 months of age (134). Worldwide, the rates of meningococcal disease are also highest for young children due to waning protective maternal antibody, but in epidemic outbreaks, older children and adolescents can have high rates of disease. Fifty percent of cases in infants in the US are due to serogroup B; serogroup C is mostly seen in adolescents and serogroups B and Y in older adults. Even though peak incidence occurs among infants and adolescents; one-third to one-half of sporadic cases are seen in adults older than 18 years.

Carrier state isn't lifelong or even year long, in fact, it can last as little as a few weeks.

When approximately 10% of individuals from the general population at any time were carrying N. meningitidis in the nasopharynx (Cartwright et al., 1987), the carriage rate was shown to be <3% in children younger than 4 years and increased to 24–37% in the age-group 15–24 years... Then carriage rates decrease to less than 10% in older age-groups.

and

Meningococcal carriage increases rapidly among university students in the first month of the academic year and much of this increase probably occurred during the first week (Neal et al., 2000). The study, performed at the University of Nottingham, UK, showed the carriage rate increased in the first week of term from 6.9 % on day 1, to 11.2 % on day 2, to 19.0 % on day 3 and to 23.1 % on day 4. High social mixing probably caused this increase.

Carrier state is influenced by protective antibodies, local mucosal factors, and lower virulence of the bacteria in carriers. Smokers, for example, are more likely to be carriers than non-smokers. The type of N. meningitidis  also influences carrier vs. infected individuals.

In Norway, approximately 9% of the carriage isolates belonged to two of the known hypervirulent clonal complexes...

That is, of 100 carriers, less than 10% carry a very virulent type. Non-virulence or low-virulence is the norm.
A non-virulent strain can become virulent to others by sharing of DNA.

Because of mixed colonization with other bacteria and because of its duration, the carrier state is an ideal condition for horizontal gene transfer between different strains of meningococci, and between meningococci and other commensal bacterial species. The human nasopharynx may harbour diverse pathogenic bacteria, like N. meningitidis, H. influenzae, S. pneumoniae, as well as non-pathogenic bacteria, such as N. lactamica and the moraxellae.

Again, carriers ave protective antibodies.

Immunity to invasive meningococcal disease is dependent upon the presence of serum immunoglobulin G (IgG) which elicits bactericidal activity toward the infecting organism. Infants may be protected from meningococcal disease by the presence of maternal IgG which is obtained passively during gestation and lactation. Maternal immunity will be replaced by acquired immunity. Exposure to non-pathogenic Neisseria and other cross-reacting species in the nasopharynx increases the level of specific antibodies during childhood (Sanchez et al., 2001, 2002; Troncoso et al., 2000).

And

Carriage of commensal Neisseria, especially N. lactamica, is associated with a high titre of antibodies against N. meningitidis. Highly homologous structures are present in N. lactamica and N. meningitidis (Troncoso et al., 2000, 2001). Sera from mice immunized with N. lactamica and boosted with N. meningitidis have been shown to kill meningococci.
...Mucosal immunity is not able to prevent the colonization of the nasopharynx by meningococci, but it plays an important role in preventing the invasion of epithelial cell (Griffiss, 1995).

If that answers your question, that's what I hoped for, because the rest is a mystery  to me. But remember, you aren't a lifelong carrier. You might be a weekslong carrier, and every exposure to a non-virulent serotype increases your immunity.
Neisseria meningitidis: Biology, Microbiology, and Epidemiology
Neisseria meningitidis: an overview of the carriage state

Thank you for your answer. I'll have to reread it a few more times and also explore the sources your referenced before accepting though. Thank you very much for such a detailed answer.


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Is there any alternative to peptone and beef or yeast extract?
I am trying to start a small microbiology project and I need a growth culture for bacteria. I do not want to use the costly nutrient agars you can buy online. I would like to create my own nutrient agar using the recipe below, but I do not have peptone. I found a paper that seems to be using extruded beans instead of peptone and beef or yeast extract.
Is possible to edit the recipe below and use extruded beans instead of peptone and beef or yeast extract?
This is the article about beans:
Batista, K. A., Bataus, L. A. M., Campos, I. T., & Fernandes, K. F. (2013). Development of culture medium using extruded bean as a nitrogen source for yeast growth. Journal of microbiological methods, 92(3), 310-315.
The exact recipe I would like to edit.

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There is an article about using cheap substitutes for peptone, one of the main ingredients of culture medium as a nitrogen-source. The authors used coconut cake (meal), ground-nut or gingelly cake which worked just as fine as the peptone.
The article is: An indigenous substitute for peptone as the
ingredient of culture media. by Raghavendra Rao et al. 2020 (ISSN: 2456-1045).


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Insect with long neck—what is it?
I found this insect in Fish Haven, Idaho (right next to Bear Lake) in June and think it’s absolutely fascinating:

If you can’t tell from the picture, it’s a few centimeters in length—very thin with a pair of transparent wings that extend straight backwards past the end of the abdomen. The thorax is brown, and past the point where the wings connect it is long and neck-like, leading to a black head with two long antennae. Can anyone identify this insect?

That appears to be a species of snakefly and the lack of a long needle-like ovipositor indicates that this specimen is a male.
The "kite" rather than rectangular head shape suggests it is in the Raphidiidae.
From the location I think it could be in the genus Agulla and might be the Idaho Snakefly (Agulla adnixa), but I don't know if that is the only species from this group in that area.
Reference image (Copyright © 2007 by Hartmut Wisch) from BugGuide.net:

To identify a snakefly: Texas has the prettiest cicada, green with dark shiny eyes. The first time I saw a snakefly it was like a horror movie. It's as of nature added a neck and head on a cicada's face! Eeeek! (Nature is amazing, sometimes downright astounding.)


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my way of solving the biology question
Pure-breeding tall and pure-breeding short pea plants in the P generation were crossed as shown below. Based on the diagram below, one can assume that
a)short plant height is the dominant trait.
b)the F₂ generation will all be tall in height.
c)the alleles for plant height do not segregate during meiosis.
d)tall plant height is the dominant trait.
My answer: The answer is D becasue tall plant is the dominant trait because  A dominant trait is an inherited characteristic that appears in an offspring if it is contributed from a parent through a dominant allele

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can you help me if your good in biology,if my answer is correct ?@tyersome

and thanyou for the welcoming message,im glad to  join :)


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What is the role of the tissue surrounding neurons in decision making and taking control of impulses?
How does the fatty tissue surrounding neurons supports and enhances the speed of electrical impulses? How does it stabilize connections that take control of impulses and decision-making? The cells surrounding the neurons in this case being either glial cells (neuroglia) which provide support and protection for neurons in the central nervous system and peripheral nervous system, or myelin an insulating sheath around many of the nerve fibers consisting of proteins and phospholipids.

This is a broad question. There are different types of cells that surround the neurons and they have critical roles in ensuring proper function of the nervous system. Each of these cell types have a unique function. Please edit your question to add some details or else this question would be closed.

I hope you aren't confusing "impulse" with action potential (sometimes called nerve impulse).

@Memming Apologies if was not specific/clear enough, I mean impulse as in the relaying of a coded signal that travels along a nerve membrane to an effector, such as muscle or other nerve cells

Possible duplicate of http://biology.stackexchange.com/q/14249/3340

Short answer
This question is pretty broad as it basically translates to "what purpose serves neuroglia in neuronal communication"? In short: next to everything.
Background
In the adult brain there are three types of glia: oligodendrocytes, astrocytes, and microglial cells (Purves, 2001). A few notable examples of their functions:

Oligodendrocytes (peripherally called Schwann cells) generate myelin sheaths around neurons, which increases conduction speeds (saltatory nerve conduction) and increases the metabolic efficiency of neural communication.
Astrocytes are a highly heterogeneic group of supportive cells. To put the impact of glia in perspective: this class of cells is considered to contain as many cell types as there are types of neurons in the brain. They are thought to mediate transfer of nutrients from blood capillaries to neurons, and they also assist in removal of neurotransmitters from the synaptic cleft and thereby speed up the recovery from synaptic activity and hence they increase the speed of information transfer (Tsacopoulos & Magistretti, 1996).
Microglia are the brain's immune cells, and are similar to peripheral macrophages. They act as the major inflammatory cell type in the brain, and respond to pathogens and injury.

References
- Purves  et al (eds). Neuroscience, 2nd edition. Sunderland (MA): Sinauer Associates (2001)
- Tsacopoulos & Magistretti, J Neurosci (1996); 76(3): 877-85

Microglia are also involved in synaptic pruning thereby regulating the development of the neural network and reducing noisy impulses (http://www.ncbi.nlm.nih.gov/pubmed/21778362).

@WYSIWYG - there are really a myriad of functions. I mentioned a few notable examples above, as explicitly mentioned in my answer.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Is there a proton gradient across the cell membrane, just like for the mitochondrial membrane?
Mitochondria have a proton gradient, is there also a proton gradient between cells and the extracellular medium?

Welcome to Biology.SE! Please provide more detail — are you only interested in proton gradients or also other electrochemical gradients? In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, since it appears you can easily answer this using reliable sources online this question seems to fit this sites criteria for "homework". (Note this can apply to questions not assigned as homework.) Thanks!

Cell has potassium and sodium gradients obviously. I am not asking about chemical gradients in general. The question is on if there are proton gradients between cells and extracellular fluid.

That's not answered on your link there. So, you can edit your comment and remove that part.

Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Comments are ephemeral and often unread. ———— I recommend that you delete "similar gradient" from your post or otherwise make clear in the body that you only care about proton gradients. In addition, if you aren't interested in the somewhat trivial answer that many (maybe all?) bacteria (e.g. the ancestors of mitochondria) create a proton gradient you will want to specify what types of cells you do care about.

And your name is Mitchell! (At least that’s my hypothesis.) So ask yourself (or research) how the proton gradient is produced, and why. And then consider whether what you propose would be likely

@tyersome Yes, bacteria have proton gradients. Question on eukaryotic cells mainly, could have specified that but it's in some way implied since it compares "the cell" to mitochondria.


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Will a Kozak sequence within a coding sequence interfere with eukaryotic expression?
I want to make a DNA vaccine for fish by using plasmid pcDNA3.1(+) with a bacterial antigen. Unfortunately, there is a Kozak sequence in the middle of my target gene.
I am concerned that this Kozak sequence will interfere with translation inside fish cells.
Can I still use this gene of interest to make a DNA vaccine?
Is there any way to deal with this unwanted Kozak sequence?

You could always try codon editing to interrupt the Kozak sequence, yet still have the same protein sequence.

Thank you so much @MattDMo, such a good idea to try :))

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What causes people to smell one persistent smell during Covid-19 infection?
Some of the people I know got COVID and they lost their sense of smell. They told me that they perceive one persistent smell, everywhere (like onion). Is this frequent for people with loss of smell? How this is possible?

Does this answer your question? https://biology.stackexchange.com/questions/97914/loss-of-taste-and-smell-during-a-covid-infection

I already saw this but it'doesn't answer my question: I do know why people loss the smell but I want to knwo why for some people the smell of things is replaced by one particular smell

I could guess it's similar to tinnitus (which doctors still cannot explain well): You "hear" a tone that isn't there. Or even worse: You cannot hear the tone (e.g. 12kHz) that tinnitus makes you hear occasionally.

Note that there some "smells" that are not perceived through the olfactory system but through the trigeminal system, see, e.g., F. Viana, Chemosensory Properties of the Trigeminal System, ACS Chem Neurosci. 2011 Jan 19; 2(1): 38–50. The pungent smell of onions belongs, among some other chemical sensations, to this group.
Thus, when the olfactory system is blocked, there are still "smells" left and one perceives them more prominently than usual.

Very interesting ! Thank you for your answer !

At this time any hypothesis regarding the parosmia seems to be untested.  Speculative sentences in lay and technical sources point toward the olfactory bulb.  (I have seen indications regarding the cilia of the olfactory neurons, the bulb itself, and the blood supply, but this seems to stray from our topic)
When we look in more detail, the olfactory bulb consists largely of glomeruli (balls of neuropil about 0.1-0.2 mm in size), which receive input from specific kinds of olfactory neurons that receive from specific odorant receptors (ORs).  See this figure for the situation in mice.  The dorsal region of the olfactory bulb is mostly one type of these, Class I ORs, and the ventral part is all Class II. (more)  If you are following this research you might want to try to figure out if the odors people report are mostly Class I (more hydrophilic) or Class II (more hydrophobic), which might allow you to hypothesize something about the relative strengths of signals from these regions in the model you develop.  Reading anecdotes is scientifically useless, but fascinating - this man describes citrus as tasting "extremely oxidized", which certainly fuels a speculation along that line.
Answering the question in any good way would seem to demand good human olfactory tissue from people who catch Covid, suffer ongoing parosmia, die from something else, and then donate their brains to science.  I'm not sure we're going to see a definitive answer that way soon.  It would be worth keeping an eye out for fMRI data.  I suspect that well-focused high-frequency terahertz might be used to image or even stimulate olfactory glomeruli (phones with 'smell-o-vision') but for now that's science fiction.

France have a law that make you donate limb by default, so we better keep an eye on it !


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Identification of moth in Pandemis heparana trap
While monitoring Pandemis heparana in an apple orchard in South Tyrol (middle of August), I frequently observed huge moths accumulating within the trap. The trap itself is working with pheromones for Pandemis heparana.
The moth is 4 cm long and at least 1.5 cm in diameter. It is quite solid and has upper wings which are brownish and lower wings which are bright orange with a distinct black part at the end of the wing.

Can you help me to identify this moth?
Edit: The moth was dead when i touched it.

There's a group of moths known as the "Underwing moths" for their brilliant coloured hindwings. I think these are used to startle predators when they get too close. They have the brilliant red/orange with a black border. If you could open the wings fully, it would help with ID significantly.
The genus is Catocala, which translates to "beautiful lowerone"
For some moths of Austria, you can browse images here, which is how I found the genus name.


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What type of spider is this please?
Can anyone identify this spider please. Found in Herefordshire UK

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It looks to me like a young Steatoda of some sort, but that's really just a guess based on the shape and posture of the brown banded legs and the shape and relative sizes of the cephalothorax and abdomen.  The photo is good, but it would help to have some sort of size comparison like a coin, plus perhaps a bit more flash to expose any patterns on the top surface of the body.


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How do precordial leads measure electrical changes in the heart?
In precordial leads the electrodes from limbs are connected to a common point via resistors. What is the potential at the common point?

For those who post without using spelling checks I would suggest a change of heart.

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Can you predict what the metabolites of pipradrol would be? Are they similar to those of methylphenidate?
As these drugs are structurally very similar, I am curious about how the body would handle them. Ritalinic acid is a major metabolite of methylphenidate, but that's about all I know.
Thanks

Methylphenidate:
https://en.wikipedia.org/wiki/Methylphenidate#/media/File:Methylphenidate-2D-skeletal.svg
Pipradrol:
https://en.wikipedia.org/wiki/Pipradrol#/media/File:Pipradrol.svg
Ritalinic acid:
https://en.wikipedia.org/wiki/Ritalinic_acid#/media/File:Ritalinic_acid-2D-skeletal.svg


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What is the name of this tree?
I noticed this plant growing on the Azores islands. It has a surprisingly perfect distribution of branches, which gives it the appearance of a fake decorative plant. Does anybody know what type of tree this is?

I apologise for the image, I could not find any better ones.
Edit: here is another image I found:

Looks like a Norfolk Island pine to me.

I agree - https://en.wikipedia.org/wiki/Araucaria_heterophylla#/media/File:AraucariaHfoliage.jpg looks very similar to the first image

Answered probably here http://biology.stackexchange.com/questions/35653/what-is-the-scientific-name-of-this-evergreen-plant/35676#35676

I would guess that the symmetrical distribution of branches is because it was trimmed to look like that, it's probably doesn't look like that in nature.

@CactusWoman I think that you are correct, although I did see some very symmetric trees growing in wild habitats.

It's worth taking a look at the tree over Autum and Winter. You will see how dramatically its branches adapt to Winter. The conical shape of these trees has a direct relationship towards their native climate.

"Coniferous trees are very well adapted to the climatic conditions. Their slender, conical shape minimizes snow accumulation on the branches, allowing the trees to generally withstand the weight of the snow for the entire winter without breaking (Radford University 2008). The narrowness and small surface area of the needles, together with a waxy coating, allows the tree to resist the drying effect of strong, cold winds.

Keeping the needles throughout the winter allows the tree to photosynthesize on the occasional sunny, warm winter day, and to begin photosynthesizing in spring as soon as temperatures permit (Lakehead University 2007)." Extremely interesting :)

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Can we cure cancer with CRISPR dead Cas?
Here's a silly idea I had this morning:

Sequence a bunch of normal patient cells.
Sequence a bunch of tumor cells from a biopsy.
Find a DNA sequence that we're reasonably certain exists in the cancer cells but doesn't exist in normal cells.
Create a guide DNA that matches the sequence identified in (3).
Send in a nuclease dead cas9 which stops cell replication through an AAV to all the cells anywhere in the vicinity of the tumour. It specifically binds only to the DNA in the cancer cells, and therefore disables DNA replication only for those cells. Then, target the now-stagnant tumour using conventional chemotherapy.
Alternatively, send in a CRISPR dead cas that induces apoptosis upon binding to the target strand, though this seems harder to pull off.

Would something like this work? If so, has this been attempted? If not, what specific step is impossible?

Related: https://www.frontiersin.org/articles/10.3389/fonc.2020.604948/full

“Fools rush in where angels fear to tread” Pope. And this is a question and answer site about problems in biology.

@David, I'm sure I don't know what you mean by that. If one of these steps is impossible, you can just tell me in an answer instead of quoting aphorisms.

The negative response you have received is probably because this is an opinion-based question since it is asking about a hypothetical situation. From the [help/dont-ask], avoid asking subjective questions where … you are asking an open-ended, hypothetical question: “What if ______ happened?” We expect answers to be based on verifiable facts and references, along with subject-related expertise. This also seems under researched (demonstration of prior research is expected). Please see the [tour] and consult the [help] starting with [ask] for details on what is appropriate for this site.

why would the crispr dead cas inhibit DNA replication? is there some work demonstrating that cas does this rather alarming thing, as opposed to being kicked off by the highly efficient replication machinery?

There are a lot of assumptions implicit in the system you describe, all of which need to be addressed prior to any serious discussion of your method's feasibility.

Sequence a bunch of normal patient cells.
Sequence a bunch of tumor cells from a biopsy.
Find a DNA sequence that we're reasonably certain exists in the cancer cells but doesn't exist in normal cells.

Depending on the tumor stage, its constituent cells may have a great amount of genomic heterogeneity.1,2 How do you know your biopsy will capture all the distinguishing variation?

Create a guide DNA that matches the sequence identified in (3).
Send in a nuclease dead cas9 which stops cell replication through an AAV to all the cells anywhere in the vicinity of the tumour. It specifically binds only to the DNA in the cancer cells, and therefore disables DNA replication only for those cells. Then, target the now-stagnant tumour using conventional chemotherapy.

What proportion of distinguishing mutations do you expect to have a structure that can be differentially targeted by a dCas9 effector? Are SNPs easily distinguished without off-target effects in healthy cells? Is the purpose of using dCas9 to mitigate off-target effects, as opposed to Cas9, for which off-target effects would be more severe (binding vs. cutting)? Can you provide a citation describing the process by which dCas9 binding prevents replication? Is it trivial to design and deliver a pool of AAV vectors that express a guide for each of your targets? Considering the cost (time and money) of your proposed treatment, can you provide a citation asserting that tumor growth stagnation prior to chemotherapy has an added benefit over chemotherapy alone?

Alternatively, send in a CRISPR dead cas that induces apoptosis upon binding to the target strand, though this seems harder to pull off.

Again, please provide a citation describing the mechanism by which dCas9 association induces apoptosis.

References

Turajlic S, Sottoriva A, Graham T, Swanton C. Resolving genetic heterogeneity in cancer. Nat Rev Genet. 2019 Jul;20(7):404-416.
Navin N, Krasnitz A, Rodgers L, Cook K, Meth J, Kendall J, Riggs M, Eberling Y, Troge J, Grubor V, Levy D, Lundin P, Månér S, Zetterberg A, Hicks J, Wigler M. Inferring tumor progression from genomic heterogeneity. Genome Res. 2010 Jan;20(1):68-80.


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Which species of bee or wasp are in this photo?

Please tell me what do you think :)
The photo is from Santander, Colombia. I didn’t take any closeups photos , but these were little bees, like 5 x 1 mm. The tube didn’t seem man-made, it was indoors and the owner of the house said that they are stingless, since no one has been stung.

Quick question, did you notice the bees entering and exiting the "tube", as well as entering and exiting the wall? It is common for some Halictidae species to have two entrances, one "royal" entrance, and a "worker" entrance below it. And I do find it interesting that they built a nest in a wall instead of in the ground.

If these bees are definitely stingless, they're members of the Meliponini tribe, which discounts those Halictid IDs. I'm only familiar with Nearctic Halictidae, but practically every species I'm aware of is a ground nester. The rare exceptions prefer hollow twigs, so I'm fairly confident it's not in Halictidae.
The nest entrance does appear to be consistent with a few Meliponine genera, especially Tetragonisca. Discoverlife only lists T. angustulata as appearing in Colombia, but notes that the name is applied to several undescribed congeners. A quick look at this species' nests makes me fairly confident that the bees in this photo are a Tetragonisca species.
Sadly neotropic bees like Meloponini are extremely under-researched. I'm  personally very unfamiliar with the tribe, luckily this genus in particular seems relatively well-known.

Looks like the family Halictidae to me. Known as a sweat bee. Maybe Lasioglossum zephyrus?

Could you elaborate on your what characteristics make you think of that family and why you suggested Lasioglossum zephyrus?  That species does not appear to be reported in Columbia ...


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What does microglia process length tell us?
I'm reading a study investigating traumatic brain injury and alcohol consumption and the researchers measured microglia process length as an indicator of brain damage. I was wondering what that would indicate and how does it an imply brain damage?

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Part of this question is due to the function of microglia in the healthy brain (as we currently understand it).  The general idea is that microglia in a healthy brain are in "surveillance mode," and have long, thin processes that extend of the cell body to monitor the environment.  It would be like beat cops splitting up and walking the streets when no crime is reported, they're just monitoring one large area by spreading everyone out.  However, when some insult occurs and microglia are activated (which just means they get into a mode responsive to some insult or injury), which results in them having shorter processes and enlarged cell bodies to focus on the damage done in their immediate vicinity.  This would be like one of the beat cops seeing a crime, then calling for back-up.  Now the focus is on the scene of the crime or site of damage.  Therefore, if your microglia have long, thin processes, everything is pretty much normal because these microglia are not activated.  However, having a lot of microglia with short, thick processes indicates that they are activated in response to some injury or insult.  This is why a common practice is to use microglial process length as an indicator of microglial activation and, in turn, some form of damage to the brain.
In shorter terms:

Long, thin processes = lack of microglial activation and little to no brain injury
Short, thick processes = microglial activation, indicative of brain injury

My source is just my experience in neuroscience and reading these types of papers, but there's more information on microglial activation here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5431479/ which includes some discussion of process length and morphology.

This answer is almost certainly correct. Probably the only better reference would be if OP had shared a citation of the paper they are reading, which almost certainly explains this in brief as well.


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Why does hexokinase bond phosphate to the hydroxyl group on carbon-6 of glucose in glycolysis?
When glucose enters the cell, it is phosphorylated by the enzyme hexokinase.
Why is this phosphorylation done at carbon-6? Why not at C-1 or C-2?
In other words, why is glucose-6-phosphate being produced rather than a different isomer of phosphorylated glucose?

To be sure: You want to know, why glucose is phosphorylated at the carbon 6? Or do you want to know, why it is called carbon 6?

I want to this question? why glucose is phosphorylated at the carbon 6?

This is biochemically an interesting question, answer soon.

Weclome to Biology.SE! While you wait for @Chris to answer, you may want to check out the proteopedia article on hexokinase and the associated links. At very least that will make sure you have the background to understand an answer. ——— You may also wish to check out the [tour] and go through the help pages starting with [Ask] questions effectively on this site. Thanks!

What do you mean by “why”? Do you mean “what purpose does this serve”, or do you mean “how is this specificity accomplished”? At present you do not make this clear. I can answer either questions, but it is your job to formulate your question clearly. Please do so.

First of all some nitpicking, but the actual phosphorylation happens not to the Carbon-6 but to the hydroxyl group bound to this carbon atom. The mechanism is a nucleophilic attack of the hydroxyl group on the terminal phosphoryl group of ATP. Schematically, this looks like this (image from here):

The main question, why the reaction happens on this carbon atom can be answered rather simple (although the explanation is a bit longer): Because only this is openly available for a chemical reaction and the others are inside the hexokinase and thus shielded.
Hexokinase exists in two forms: One relaxed, open when no substrate is bound and one closed with a changed morphology when the enzyme has bound its substrate. This mechanism is called "induced fit" and a quite common motif in enzyme catalyzed reactions and brings together the active center of the enzyme, possible co-factors and the substrate and excludes interfering other actions.
In the example of the hexokinase, glucose is brought into close proximity to the terminal phosphoryl group of enzyme-bound ATP to enable the chemical reaction. Because all other potential hydroxy groups are shielded by the enzyme, only the group at the carbon-6 can be chemically active. For more details, see the references.
Schematically, this looks like this, with the open form to the left (the arrow indicates the binding site for glucose) and the closed form right (image from here):

References

The Structure and Mechanism of Hexokinase
Mechanism of liver glucokinase.

I think this answer is much more revealing, chris. Really thank you.As far as I understand, this is related to the way glucose binds to the enzyme.In other words, other hydroxyl groups are closed by the enzyme, so only the carboxyl group is exposed.I got it right, right?

@SpartanTroy No, only the hydroxyl group on C6 is available.

but if other hydroxyl groups are protected, why is it not protected on c6. Is this related to the enzyme's association with the substrat?

https://www.youtube.com/watch?v=2gZDHMQcgtQ. If this video is as shown; So that's about the enzyme's binding site to glucose and atp. Am I wrong?

I'll look into the video later today.

I'm sorry. I think you are knowledgeable. I'm asking because I don't fully understand.

Hey, be careful. I have no time right now to watch a video to see, what is said in there. And before I watched it, I am not going to say anything about the video. Answering here is voluntary, so if you want to piss me off, you will not get any answer.

Let us continue this discussion in chat.

@SpartanTroy There is nothing to discuss here right now. I have to work and will watch the video later. And then I will answer your question about it.

@SpartanTroy I'm not familiar with the particular biochemistry here, but just take a look at the diagram in Chris's answer: see the ring? There are 6 carbons, but only 5 of them are involved in the ring (an oxygen makes up the 6th ring element). The 6th is that "-CH2-" hanging off with an "-OH" attached to it. The other -OHs are directly attached on the ring: the geometry is different, so it seems obvious that an enzyme would be specific for a particular location.

@bryanKrause yes I have it see. Actually my question is a biochemistry question. But I want to understand.I think I should learn the enzyme and substrate relationship.

In yeast, galactose is phosphorylated at the C1 position and isomerized into glucose-1-phosphate, which is then converted to glucose-6-phosphate to go into glycolysis. Given that it's possible to phosphorylate the C1 position in galactose, which has similar steric considerations, your answer doesn't really answer why it's at C6 in glycolysis. I guess it impressed the questioner at least.


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Selection marker for a cytoplasmic vector that works at low expression levels?
I need to express a selection marker on a plasmid in human cells (e.g. HEK293). However, I am using a cytoplasmic vector derived from a non-human virus with its own mechanism for transcriptional initiation. This means that the expression level of any protein marker will suck: low copy number, very weak promoter, unstable transcripts - these are things that I cannot change in this precise biological context.
Most selection markers (for instance KanMX) come with their own black-box promoter and so I do not know whether they rely on a high number of proteins being produced.
What would be a marker most likely to be selectable despite a very low expression level? I could not find any resource comparing the protein copy numbers of classic markers.
I need to be sure that the cells that cannot survive the selective pressure died because they did not have the marker, and not because the marker was too weakly expressed to protect  cells that have the marker. The standard approach would be to use a regular antibiotic selection and just work with lower concentrations of antibiotics but the number of false positives would most likely be too high.
I can manipulate the host cell to some extent, so I can use antibiotic selection but I can also complement a conditional deletion of an essential gene (auxotrophic marker or non-metabolic genes).

Are you trying to select for the plasmid or for expression of a gene from that plasmid (e.g. by a translational fusion of the gene with a marker)? Can you provide more information about the "technical constraints"?

@tyersome I would be just selecting for the presence of the plasmid after N divisions. Ultimately I would express other things (e.g. luciferase) from the same plasmid but before optimizing that aspect I need to know that the plasmid can stay there for a while. By technical constraints I mean that the plasmid comes with a pre-defined origin of replication and mechanism of transcription initiation, but is derived from a non-human mammalian virus, so it will most likely not "work" as well as in the original host (in which expression levels are already low)

@Mowgli If your plasmid does not have a strong promoter then how are you planning to use it for your later experiments with luciferase etc? Regarding whether the plasmid will stay: for how long would you be doing your experiment (HEK293 divides slowly)?

@WYSYWIG designing and testing better promoters on this platform is part of the ultimate goals. I expect luminescence (or other techniques based on signal integration) to be sensitive enough to detect even the very small expression level of the original construct. I am expecting the plasmid to be maintained for over a week - in theory it will stay "forever" like a genomically integrated lentiviral vector, if it has a replication mechanism (already built in) and a selection system (this question)

Based on your reply it doesn't seem clear why you can't use a standard promoter to drive your selectable marker. Why do you feel constrained to use a "very weak promoter"? Why do you think the transcripts for the marker will be unstable?

@tyersome this DNA does not go to the nucleus (something a bit similar to the HCV life cycle) so I cannot rely on validated host polymerase-driven promoters...

Oh, that makes a huge difference! I think this information would be very helpful to include in the body (if not the title) of your question — I'll make some edits, but feel free to change if you don't think they help. Can you also provide some links for information on this vector — I think that will increase the chance of getting an answer that helps you.

Flow cytometry looking for your plasmid.
These folks labeled their plasmid with a proprietary fluorescent marker, then used flow cytometry to detect cells which had taken up the plasmid.
A novel rapid and reproducible flow cytometric method for optimization of transfection efficiency in cells

An alternative and more direct method to using fluorescent reporter
  genes is to directly label nucleic acids with fluorescent dyes to
  track their intracellular delivery [16]...
  Using the non-enzymatic Label IT® Tracker TM Kits, any plasmid can be
  custom labeled in a simple one-step chemical reaction before
  introduction into mammalian cells [18]. Thus, both subcellular
  localization of the labeled DNA and expression reporter transgene can
  be monitored simultaneously following introduction of the labeled
  plasmid into mammalian cells [16, 18]...
Herein, we demonstrate the development of a flow-cytometric assay to
  determine transfection efficiency by labeling a reporter plasmid with
  Label IT® TrackerTM. This method does not depend on co-transfection of
  two different plasmids and simultaneously quantifies cell death,
  uptake of the labeled plasmid during transient transfection, and
  expression of the target protein.

Even if only a small fraction of your cells take up your glowy plasmid, you will sort those out from the rest with flow.

While the technique is interesting, it does not create a constant selective pressure like an antibiotic cassette or an auxotrophy marker, which means that I would have to sort the cells every few days to maintain a positive population... Additionally, chemical labelling prior to transfection cannot detect replication products.


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What would happen if there were no SOX9 in an XY human?
Would testes be produced? If SRY is functional, can it produce other proteins that can direct the production of testes, which may or may not be sterile?

Quoting the abstract of this paper verbatim:

Sox9 is an Sry-box-containing gene that encodes a transcriptional
  activator. During mouse gonadogenesis, Sox9 is detected in the male
  gonad at 11.5 days postcoitus (dpc). At 12.5 dpc, testicular cords
  form, morphologically distinguishing the male gonad from the ovary.
  From this stage onwards, Sox9 expression is restricted to the Sertoli
  cell lineage and persists in the adult. Humans with heterozygous
  mutations in SOX9 develop a skeletal syndrome known as campomelic
  dysplasia. Furthermore, most XY SOX9 heterozygotes show variable
  male-to-female sex reversal, implicating SOX9 in testis development.
  Sox9 heterozygous knockout mice die at birth with a syndrome similar
  to that of human campomelic dysplasia. In contrast to humans, XY
  Sox9+/- mice form normal appearing testes. Germ-line knockout of Sox9
  using a conditional null allele provides a tool for generating Sox9-/-
  mice by simple genetic crosses. However, Sox9-/- mice die soon after
  11.5 dpc because of cardiovascular defects. In vitro culture of the urogenital ridges of XY Sox9-/- results in gonads lacking testicular
  cords and Sertoli cell marker expression, but with the expression of
  ovarian-specific markers. Therefore, Sox9 is essential for diverting
  an intrinsically ovarian program of organogenesis toward testis
  formation.

From MGI page on Sox9:

Null mutant heterozygotes and conditional knockout mutants display
  perinatal lethality with cleft palate, hypoplasia and distortion of
  numerous cartilage-derived skeletal structures, and premature
  mineralization in many bones. Specific conditional knockout mutations
  are sex-reversed.

SOX9 is indeed the factor which is important for the developent of the sexual organs and not only for men, but also for women. Expression of SOX9 regulates the expression of the anti-Müllerian Hormone, which inhibits the formation of the female reproduction system. See reference 1 for more details.
Mutations in or around (in regulatory regions) of the SOX9 gene lead to severe developmental changes and to the genetic disorder "Campomelic dysplasia". The disorder leads to changes in the bones and also in the sex determination, it is often lethal in the neonatal period due to respiratory problems. Have a look into reference 2 for more details.
In mice, the complete loss of SOX9 is embryonical lethal, have a look at reference 3 for details. Although there are no data available for humans (for obvious ethical reasons) I assume that the effect is the same.
Development of testis starts by the activation of SOX9 by the testis determination factor. SOX9 in turn activates a number of other transcription factors (have a look into references 4 and 5 for details) which finally lead to the development of the testis.
Mutations in SOX9 in men (with XY chromosomes) also lead to the reversal of the sex, meaning these individuals will develop female reproduction organs (see reference 4). It has also been shown that female mice will develop testis when SOX9 is induced in these animals (see reference 6). You can also have a look into the OMIM database for an extensive review.

References:

Direct interaction of SRY-related protein SOX9 and steroidogenic
factor 1 regulates transcription of the human anti-Müllerian hormone
gene.
A clinical and genetic study of campomelic dysplasia.
Sex determination: a tale of two Sox genes
The PGD2 pathway, independently of FGF9, amplifies SOX9 activity in
Sertoli cells during male sexual differentiation.
Fgf9 and Wnt4 act as antagonistic signals to regulate mammalian sex
determination.
Sox9 induces testis development in XX transgenic mice