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What does fail-safe mean in transmission at electrical synapses?
I'm reading a book named Neuroscience:Exploring the Brain recently. And in the chapter about synaptic transmission, it says "Transmission at electrical synapses is very fast and, if the synapse is large, fail-safe." So what does fail-safe mean? And why is that transmission fail-safe when the synapse is large?
And when is comes to EPSP, it also mentions that "The neuromuscular junction has evolved to be fail-safe; it needs to work every time, and the best way to ensure this is to generate an EPSP of a huge size." I don't understand the meaning of the word and the whole sentence.

To understand what failure means in this context, we need to know a bit about how signals are communicated from one neuron to another.
Types of signals
First of all, it's important to know that synaptic signaling (communication between neurons) comes in two flavors: chemical and electrical.  The signaling is done at the interface between two neurons, known as the synapse.  There are generally dozens to hundreds of synapses between two connected neurons.  At chemical synapses, a chemical (the neurotransmitter) is released into the space between the pre-synaptic site on the axon and the post-synaptic site on the dendrite (or soma).  At electrical synapses, no chemicals are released.  Instead, porous proteins called “gap junction channels” bridge the space between the cell membranes of two neurons and create pores that allow electrical current to pass directly from one neuron to the other.
Signaling is probabilistic
Second, it's important to appreciate that neurotransmission is probabilistic, rather than deterministic.  That just means there’s a chance that signaling from an upstream neuron might fail to evoke a response in a downstream neuron.  There are several reasons why transmission is not 100% efficient, at both the pre-synaptic and post-synaptic ends.
Some of these reasons have to do with spontaneous opening and closing of channels in the membrane.  When researchers examine electrical currents flowing through single ion channel proteins they find that each channel randomly flips between open and closed states.  This is caused by molecular-scale fluctuations in the protein's shape that cause it to either block or allow the passage of electrical current (or ions).
In addition, random fluctuations in how well electrical current is able to be integrated by the downstream neuron add to the variability in signaling that makes responses probabilistic. You probably already know that "response" of a neuron refers to the firing of action potentials. And you probably also know that action potentials are generated when the membrane of a neuron becomes sufficiently depolarized - the result of a process known as synaptic integration.  A simple view of synaptic integration is the summing together of all electrical currents flowing across the membrane from different synapses in a short window of time.  If this current integrates to a total greater than some value (the firing threshold) the neuron fires, otherwise it does not.  What some may not realize, though, is that this process isn't perfect - current can leak out of the cell, other neurons can "siphon off" current, and receptor proteins in the downstream neuron can become inactive and stop contributing to the overall current flux.
All of these factors conspire together to make the signaling process probabilistic. Because there's always less than a 100% probability that signaling from an upstream neuron will sufficiently excite a downstream neuron, there will be occasions where a downstream neuron fails to fire.
So taking these things into account, we can define the following:

SUCCESS = Neuron A fires -> causes Neuron B to fire
FAILURE = Neuron A fires -> Neuron B does not fire

An example
If a synapse has 100 channels, and each channel has a 50% chance of being open at any moment, then we expect that, on average, 50 channels will be open at any given time.  If each channel can allow 1pA of current to pass through, this synapse will transmit on average 50pA of current from Neuron A to Neuron B.  Let's say 25pA is needed to bring Neuron B to threshold and cause it to fire.  Then this synapse will typically transmit more than enough current to evoke a response in Neuron B.
But here's the catch.  Because the inactivation of each channel is spontaneous, sometimes there will be more than 50 channels open, and sometimes less than 50 - just by chance.  On some rare occasions, fewer than 25 channels will be open, and if Neuron A fires at one of these crucial moments, our 100 channel synapse will transmit less than 25pA, and fail to bring Neuron B to threshold.  This is how an electrical synapse "failure" occurs. You can imagine how, evolutionarily, this might be a bad thing if that failure to fire Neuron B occurs at a crucial moment when the muscle under control of Neuron B is needed to jump out of a predator's reach.
This leads us to the question:
Given these definitions, how would we increase the chance of success, and correspondingly decrease the chance of failure?
Scaling up
Well, probability makes things a numbers game, and here's where size comes into play.  One way we could make sure that Neuron A has a really good chance of firing Neuron B is to mitigate the risk from spontaneous channel inactivation.  We could do this by simply scaling up the synapse - making it larger and adding more channels.  If we had 200 synapses, rather than 100, and they all still had a 50% chance of being closed at a given moment, then the chance becomes incredibly remote that, at a given moment, fewer than 25 channels (the number needed to fire Neuron B) are open and able to transmit signal.  This is what's meant by being made fail-safe.
It's easy to see that another means to the same end is to scale up the corresponding response in Neuron B - the EPSP - as observed at the neuromuscular junction.  By scaling up the strength of the response, it becomes less likely that random, uncontrollable influences on the cell (or muscle) would cause a failure to fire.
Hopefully, now you can see how neurons may fail to signal, and why scaling things up can, in general, make a synapse more fail-safe.

It would be great if you can add some references that people can go to if they need to know the details. References are, in general, always appreciated.


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How to grow a spirulina biofilm on a carbon/graphite cylindrical cathode?
I am trying to grow a spirulina biofilm on my cathode for a fuel cell but it doesn't seem to be sticking to the cathode. I have a culture of spirulina  and I've submerged a few cathodes in it to try and develop a biofilm. This is not working. Is there anything I can do to promote spirulina growth on my cathode like coating it in glucose or something?

I keep finding articles that say Spirulina Platensis actually inhibits biofilms. Research is underway to use this property of Spriulina Platensis to disrupt the biofilms that protect pathogenic bacteria from antibiotics.

source: Stack Exchange

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

sort: votes


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Identification of a red arachnida (?) (picture and video)
I found this in a greenhouse in Norway. It is a few millimeters in size, I could fit 5-6 of them on my thumbnail.

It looks a lot like this one from Wikipedia https://en.wikipedia.org/wiki/Trombidiformes
Can someone help me identify it? Is it a parasite or a harmless creature?
Also a video of it moving around
https://1drv.ms/v/s!AlmW2TG6jr_7ga4eTDLz7qzKM4W_8w
Update:
I found a link description which makes me think it is a mite (same as the Wikipedia link).

One of the most common sources of confusion between ticks and mites is color. No known species of naturally occurring red tick exists. But ticks can sometimes appear to be red if they’re in the act of feeding. However, the spider mite, red velvet mite, clover mite and the larvae of the harvest mite—known colloquially as chiggers—all take various shades of red.

It might also be a type of predatory mite -- these are frequently used in organic or IPM agriculture to control spider mites. See for example this wikipedia page. I would talk to someone at the greenhouse and see whether they release predatory mites.

looks like a tick to me

@aminabzz I thought it looked like a tick as well, but I have never heard of red ones or seen a description of one. Going to update the question with a reference regarding that.

it is clover mites here is a video about them: https://www.youtube.com/watch?v=BftGk-S2GyU

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


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Can gene mutations cause Down's syndrome in humans?
I am working on an A levels questions:

Which of the following statements about gene mutation is incorrect?
A. It can occur in both somatic and sex cells
B. It can cause Down's syndrome in humans
C. It can change a dominant allele into a recessive one.
D. It can be brought about by exposure to ionising radiation

The answer at the back of the book says the correct answer is C. Its explanation is

A gene mutation cannot cause a dominant allele to become recessive, but can disallow it from being expressed phenotypically.

But I think that it should be B. From what i understand, Down's syndrome is caused by an extra chromosome (21). And it is not possible to grow an extra chromosome just by gene mutations?
Is the answer from the back of the book wrong, or did i make a mistake? Thank you for helping me with my A levels.

Mutation is a very general term that defines „change of genetic material“ (not just sequence) and can include the loss or acquisition of complete chromosomes. So down syndrome can be caused by mutation. However, I don‘t know why mutations shouldn‘t be able to convert dominant alleles into recessive ones (E.g, a mutation that halfens an enzymes activity?). In general, this page is not meant to help you with your A-level without efforts from your side. If you have googled the issue, please show us which sources you already checked.

"And it is not possible to grow an extra chromosome just by gene mutations?" Did you google this question? What did you find?

C is not impossible. A mutation in Gene A can cause alleles x and y of Gene B to swap dominance. E.g. if gene A encodes a enzyme that changes the substrate of gene B so that it is first recognized by allele x instead of y. The word "can" quite surely includes theoretical possibilities.

Don't feel bad, that question is horribly worded.
Gene mutation is a confusing choice of words, it is not a specific thing.
First, down syndrome IS caused by a mutation, specifically a duplication. Trisomy itself is a mutation, but not caused by a mutation to a single gene, which could be what "gene mutation" is referring to. If so, it is just bad wording and the book answer is wrong. But trisomy itself can be caused by a mutation to a single gene so even then it is iffy.
The question is a "gotcha question" at best or just straight-up wrong at worst. "Which of the following statements about gene mutation is incorrect?" There is no right answer here: a mutation can cause all of these things, since we don't know what exactly is meant with "gene mutation".
At first is seems like all of the answers could be caused by mutations, but there is twisted logic to C being correct.
A mutation can change alleles, thus, it can change a dominate allele into a recessive and vice versa. What it can't do is change a dominate allele into a recessive one... wait that sounds insane, but it is technically true. It is a confusion of language; lets go a little deeper.
A mutation can turn one allele into another different allele...but, if you referring to the allele as in the defined allele and not the gene then a mutation cannot change it. A mutation can never make the blue eye allele as it is defined, recessive, it can however change the gene from blue eyes to brown eyes, thus making gene go from recessive to dominant and thus changing from a recessive allele to a dominate allele. Think of it this way, I can make steel change color by heating it but I can never change the color blue itself. So C could technically be incorrect but from a slightly different angle it is complexly possible, thus the questions is just bad.
Why textbooks often have sucky questions.
You run into this problem with textbooks a lot for two reason.
The people who write/edit textbooks rarely understand the subject and even when they kinda do, they often reuse and shuffle questions often changing key terms without understanding how it changes the question. this is done to create a new "edition" which they can sell again when they drop online support for the old edition.

I think you've identified the most reasonable unreasonable way to consider option C the correct answer here, though it makes their "explanation" even worse than the question itself.

Honestly, I'm not sure what exactly is meant by "changing a dominant allele to a recessive one".  But if you have a mutation which breaks a gene, that mutation certainly could be recessive as compared to the original, functional allele.
Down syndrome is clearly not a mere "gene mutation", and I think high schoolers are meant to know that.  I think you book is just wrong; maybe there was a typo claiming the answer was C, and someone made up a justification for that that doesn't make a lot of sense.

Duplication is considered a type of mutation. It's a bit weird to describe a whole extra chromosome that way, but it's likely technically correct according to the textbook definitions given in a course. I agree that C doesn't make much sense, though.

I would think that part, if not the whole point of the question is "do you know know the general kind of genetic differences that causes Down Syndrome?  "

Perhaps, but if that was the goal they could have just asked about Down Syndrome. Instead, they may be trying to communicate the scope of changes that are included when someone says "mutation" and that "mutation" when used in evolutionary terms should not be confused with "point mutation"/substitution. E.g. the Wikipedia page on Mutation includes a section "large-scale mutations" that covers chromosome-level changes.

I think that's an area that is especially confused by anti-evolution arguments that fail to consider the importance of duplications of entire genes and larger and instead make silly arguments about the improbability of some combination of point mutations, and I'd think it's an apt target for exams assessing science literacy.

down syndrome is caused by a mutation, trisomy is by definition, a mutation. it is not is a point mutation but it is a mutation.


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Can Coronaviridae mutate into something as dangerous as Flioviridae?
Can coronaviruses mutate to an extent to get as dangerous as fliovirusues such as Marburg viruses, Ravn or Ebola Zaire?

I would say this is rather unlikely. The virus would have to change everything from the cells it infects, probably the way it enter the cells and infects new cells to the mode of action and the genetic material responsible for that.

Please do some research on viruses  (eg read the Wikipedia pages) before posting here. Has the possibility of flu mutating into Ebola virus also been bugging you? Or dogs mutating into wolves?

Corona and filoviruses are far more different than cats and dogs. They are more different than humans and bacteria. If you're concerned about corona mutating into filo, you should worry about your children being single-celled thermophilic archaebacteria. I voted to close this question as lacking in basic research.

@David - Unless the poster edited the post, then the question specifically asked whether Coronavirus could mutate into something 'as dangerous as Fliovirus', not 'into Fliovirus'. This is a perfectly valid question to ask.

@4agalaxy7 — The question is not perfectly valid here because it is ambiguous in this respect and shows no evidence of prior research on virus (molecular) biology. Your literal interpretation is possible, but the lack of response of the poster to my comment suggests otherwise. It is more likely a scare scenario type question demanding reassurance rather than explanation.

SE Biology is concerned with the mechanisms of biological processes, and questions are generally answered by people with biological rather than medical or epidemiological expertise. It is possible, therefore, that some questions about coronaviruses relating to the recent 2019-nCoV outbreak may not receive a satisfactory answer. You may therefore wish to consult this list. of reputable external sources of such information.

As a matter of simple numbers, the current coronavirus is FAR more deadly than the Ebola virus.  At a rough estimate, under 20,000 people have died from Ebola since it was discovered.  So far, almost five times that many have died from Covid-19 in the US alone, and the count is increasing.

Each existing virus can mutate until it becomes ready to affect new species, organisms, cells or whatever.
Coronaviruses too are capable of mutating, so they could become more dangerous.
But can coronaviruses (which cause respiratory tract diseases) mutate into filoviruses (which cause hemorrhagic fevers)?
Of course not.
Filoviridae and coronaviridae are two different families of viruses, like felidae and canidae are two different families of mammals, in the order carnivora.
And you would never ask if cats can mutate in dogs!

'Dangerous' is quite a subjective term, and can be defined in different ways.
Viruses vary in their pathogenicity, which is essentially the ability of the virus to cause a disease in a single individual. This can influence other factors, such as the case fatality rate, which is the proportion of people who die from the disease once they have contracted it. For example, the Ebola virus has a very high case fatality rate of up to 90%.
However, those aren't the only ways in which you could define 'dangerous'. We might also consider the total number of people that the virus can kill. This often isn't a linear relationship with the case fatality rate. Often, viruses with a high case fatality rate 'burn out' before than can inflict a global pandemic, because people die before they can spread the disease on to others. Vice versa, viruses with a relatively low case fatality rate, such as the Spanish Flu (2-3%) can be extremely 'dangerous' and kill millions of people.
But there is no hard and fast rule, as the propensity of a virus to cause a global pandemic is influenced by many, many other factors.
So to answer your question: is it possible for the Covid-19 to mutate into something as dangerous as Ebola? Well, if we are thinking about it's pathogenicity - Influenza A H5N1 (bird flu) had a case fatality rate of about 60%, which is pretty high for a flu virus. For context, the seasonal flu which has a case fatality rate of about 0.1%. I'm not an expert in Virology, so it would be great if someone with more knowledge could confirm this, but it seems very unlikely that the Covid-19 virus could acquire mutations to the degree where it would kill as high as 90% of the people who acquire it, like Ebola does. Ebola is a hemorrhagic virus, which is a totally different mechanism of pathogenicity to the Coronavirus family.
It's plausible that Covid-19 could obtain mutations which allow it to transfer more quickly between humans. For example, we know that the Spanish Flu acquired mutations in hemagglutinin subtype which allowed it to be more transmissible between humans. Generally, Coronaviruses have relatively lower R0 rates than other disease (~2/3 compared to Measles which is 12-18). The total number of people killed by the Ebola outbreak was about 11,000. Covid-19 has already killed ~3000 (although the exact figure is hard to quantify), so it seems like on the global level, Covid-19 will be more dangerous than Ebola, if we consider the total number of people killed.

This does not in any way answer the question.

I don’t think you understand the question.

As I understand it — correct me if I am wrong — your statement that "the Spanish Flu acquired mutations…" means that this strain of flu virus differed from previous or reference strains in containing certain mutations, rather than during the course of the pandemic it underwent mutations that increased its transmissability. i.e Spanish flu differed from the previous year's flu in the way flu does each year. This is important because my reading of the question is that the poster wishes to know whether the currently circulating virus could suddenly become more virulent: now, not next year.


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Winter is getting shorter and warmer. Does this mean deciduous trees can photosynthesise for longer and thus absorb more carbon dioxide?
As springtime is starting earlier this year, I wondered if that would mean deciduous trees had more time to photosynthesise and, therefore, they could absorb more CO2 or have longer periods to grow, etc.
Also, is there any evidence that colder climate deciduous trees would fare better or worse as conditions change for them?

yes, you can see from the growth rings that they vary year upon year based on warmth and water. Deciduous trees fair differently to climate change depending on species, the ones on the far ends of their ranges can get outcompeted by other trees. http://www.euforgen.org/species/ check the ranges. don't know what references to add.

A warmer climate in this regard is beneficial to photosynthesis and plant growth. The thickness of the tree rings are constrained by the length of the growing season according to University Corporation for Atmospheric Research:

In some areas the limiting factor for growth is water availability, in other areas (especially at high latitudes) it is the length of the growing season.

Thanks for the downvote but I do not understand why. If you want me to react you have to write something. Is the question about if buds burst earlier and leaves fall later? Is the cited source not fitting?


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Why aren't leaves black?
I s'pose this is a variant of the age-old question, "Why are leaves green?"  It's fairly easy to ask teh internets and find plenty of answers for that one.
I have a different but related question: why aren't leaves black?  That is, chlorophyll varieties in leaves' cells mostly absorb red and blue wavelengths.  Why isn't there a pigment in photosynthesis that absorbs green?
Instead, the green gets reflected back to the atmosphere.  Its energy is otherwise lost to the plant.  Nature is awfully well optimized to so many niches; why would this band of light be wasted?
There are some plants that do absorb green (and have dark leaves).  These pigments -- such as anthocyanins, betalains, and carotenoids -- don't have any role in photosynthesis, and play other roles (such as protection against extreme temperature, or acting as an anti-oxidant).  Am I missing some pigment in my list that is green-absorbing and participates in photosynthesis?  If there were such a plant with a pigment like that, why wouldn't these plants dominate?  Is there a large cost to producing the green-absorbing pigment that mostly negates the advantage of the extra energy gained?
After a little more searching on SO, I found the top answer to this question.  In slightly different words, it says that light arrives in quanta, the chemistry in photosynthesis is driven by a certain threshold of energy, and any excess energy from a photon goes to waste heat (that tends to denature some of the proteins involved).  The answer points to another answer with similar reasoning.  However, their explanations don't account for the fact that chlorophylls strongly absorb blue in addition to red, where blue photons have nearly twice the energy of red ones.
Moreover, the answer goes on to say:

Of course, this is still no explanation why leaves are not simply black — absorbing all light is surely even more effective, no? I don't know enough about organic chemistry, but my guess would be that there are no organic substances with such a broad absorption spectrum and adding another kind of pigment might not pay off.

Are there nothing other than educated guesses at an answer?  And why not use a combination of pigments, instead of a single, broad-spectrum absorbing pigment?  For example, some metabolic pathways use parallel processes.  Quoth the Wackypedia:

Sometimes more than one enzyme can catalyze the same reaction in parallel; this can allow more complex regulation: with, for example, a low constant activity provided by one enzyme but an inducible high activity from a second enzyme.

It appears bacteriorhodopsin has a somewhat complementary absorption spectrum to that of chlorophylls: https://biology.stackexchange.com/q/58572/48437

Does this answer your question? Why do plants have green leaves and not red?

Evolutionary answer: I like to go one step before green plants and consider the humble alga. Algae were historically classified as green, red, and brown, based on the wavelengths that their characteristic pigments absorbed. It is believed that land plants evolved from a common ancestor of algae, so you might wonder why we don't have similar broad categories of green, red, and brown plants.
Our best guess is that the organisms we call "plants" came from a single evolutionary event and share a common ancestor with green algae, rather than a different group. These green plant-like beings were probably the first big land organisms to try photosynthesis and happened to do well enough to out-compete any other plant-like being that might arise in their environment. Being green was "good enough" to for photosynthesis, allowing these organisms to survive and thrive.
Meta-answer: "Why" questions in biology often have probabilistic (and intuitively unsatisfying) answers. It's very hard to collect data that can "prove" why certain things evolved the way they did. Plus, evolution is not an engineering or design process. It leaves dead ends and doesn't always find the right solution. Founder effects can be very strong. But organisms which last long enough for us to study tend to be "good enough" at what they do. Here, the most parsimonious explanation for why leaves aren't black is that land plants came from green algae and didn't need to produce more of other pigments to take over the world.
Biochemical side-note: Plants can suffer from photooxidative stress when exposed to intense light due to the generation of reactive oxygen species, which disrupt metabolism. Therefore, some non-green pigments, like xanthophylls, are actually responsible for quenching chlorophyll and dissipating energy away from light-harvesting complexes. More energy is not always a good thing.

Thanks!  If I can restate in my own words, it's two things.  (1) Absorbing only red and blue light is good enough to dominate; why bother expending extra effort that isn't necessary (or if it ain't broke, don't fix it).  And (2) green light is used for other purposes such as quenching chlorophyll (regulation) and fueling anti-oxidants.  Neat!  TIL carotenoids play both roles.  The xanthophylls you mention assist quenching.  Carotenes absorb shorter wavelength light, scatter longer wavelengths, and transmit what they do absorb to chlorophyll (to provide extra energy to the photosystem).

Another intriguing hypothesis is that the first successful photosynthesizer was purple (absorbed abundant green and reflected red and blue).  The green algae then exploited a niche by doing the reverse (reflecting green and absorbing red and blue).  Eventually the second comers out-competed the first movers, and began to dominate.  There was never a need to re-adapt once dominant and absorb green.  See this answer: https://biology.stackexchange.com/a/45335

Circling back to this a loooong time later, here's another piece of the puzzle: it's hypothesized that eukaryotes engulfed cyanobacteria -- becoming chloroplasts -- and this event only happened once in all of evolution.  (That is, no convergent evolution at play among all plants and algae.)  All descendants of that common ancestor all have the same green appearance.

In addition to the points mentioned in the other answer, there is also this paper highlighting the importance of a steady energy flow compared to simply optimising energy capture. See this article in Quanta Magazine for a summary.
From the Quanta article:

Gabor and his team developed a model for the light-harvesting systems of plants and applied it to the solar spectrum measured below a canopy of leaves. Their work made it clear why what works for nanotube solar cells doesn’t work for plants: It might be highly efficient to specialize in collecting just the peak energy in green light, but that would be detrimental for plants because, when the sunlight flickered, the noise from the input signal would fluctuate too wildly for the complex to regulate the energy flow.
Instead, for a safe, steady energy output, the pigments of the photosystem had to be very finely tuned in a certain way. The pigments needed to absorb light at similar wavelengths to reduce the internal noise. But they also needed to absorb light at different rates to buffer against the external noise caused by swings in light intensity. The best light for the pigments to absorb, then, was in the steepest parts of the intensity curve for the solar spectrum — the red and blue parts of the spectrum.

Thanks for the addition. We ask that answers not simply link to outside info in case such links later die. Leave the links but either quote or summarize the main points in your post please. Thanks!

Leaves are usually dark green meaning they actually do absorb some green light and convert it to useful energy, they just reflect more green light than any of the other wavelengths that we can see, thus giving them a green color.
Also, not all plants have green leaves, cactuses for example, have more like green stems with no leaves at all.  And in fact, many desert plants have a very strong white tinge to them because of all the white light they reflect in an effort to not overheat and kill themselves by absorbing such absurd amounts of light.  Many have evolved reflective wax coatings or tiny hairs that provide shade.  The conclusion from this seems to be that the limiting factor for many plants growth is not how much radiation they can absorb per area of leaf, and therefore, there isn't an evolutionary pressure to increase their energy absorption by evolving black pigments.
Note: I disagree with the other answer stating that it is the result of all plants being descendant from a common ancestor that used green pigments.  While it is true that all plants are descendant from a common ancestor, I haven't seen compelling evidence that black plants have never evolved or never had the opportunity to evolve.  Far more likely in my mind is that they are perfectly possible and don't evolve simply because there is no advantage to doing so.  Which I think is incredible; and very surprising.  But, I think that's the answer with the most evidence.

Hmm.  I'm not buying the excess heat thing.  Cacti are the exception, not the rule, when it comes to leaf shape.  Most leaves are thin: the have an extraordinary amount of surface area relative to volume.  Heat transfer to the surrounding fluid seems more than adequate.  I say "fluid" because some plants live in air, but others in water.  Which brings me to: they evolved in water, and water provides an enormous heat sink.  How could heat be a concern for those first-evolvers?

yeah, you're right i think.  I don't have much evidence, so this is mostly conjecture.  To conjecture, I'd say that forestecol provides a compelling overview of what selection pressures the "first-evolvers" were dealing with.  However, to change my answer from above, the most intense limiting factor with the "heat" is probably at the molecule level and substructure level, so it doesn't matter how much water the leaf is, because the clustered pigments and proteins will heat up faster than they can transfer their energy to the surrounding water.


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Can you identify this snake?
On a walk through I’ON Swamp/Natural Forest in Mt. Pleasant, SC, we came upon this snake. We did not get too close for fear it may be poisonous.
It had a very dark brown/taupe exterior with almost a diamond shaped head. It had a reddish, orange belly. It was ~3-4’ in length and fairly large girth.

Welcome to Biology.SE! Identifications questions must include one or more clear closeup photos of the organism (photos from multiple angles if possible) — photos must be uploaded (not links). Also note that personal medical questions (e.g. were we in danger) are not appropriate for this site. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

there is a Yellow Belly Water snake here in TX that the book says is the same as a Red Belly Water snake in the east. Looks like a good possibility.

How do I upload a photo?

When you are making (or editing) a post there is a picture icon (looks like white mountains on a black background) in the tool bar at the top of the editing field that you click on.

Hard to tell without a clearer picture, but the size and color pattern seem to match the description for the Plain-bellied Watersnake.
See for example the following picture from the Virginia Herpetological Society:

I assume from the location being in something called a swamp that the habitat (in and near slow moving bodies of water) also fits.

That’s it! That’s the same snake we saw on the trail. Thank you!

Great, glad I could help!


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Why do coliform bacteria smell so bad?
I have done multiple cultures of E. coli bacteria and related species over the course of my education. Almost every time, they had this revolting smell. However, other organisms used for genetics experiments (eg. Saccharomyces cerevisiae) rarely have a bad scent, if a scent whatsoever. My question is, what is it about the coliform metabolism that produces such a pungent and revolting odor? Any and all answers are appreciated.

I'll note that "revolting" is a characteristic of the owner of the nose, not the producer of the scent chemicals; perhaps the nose owning organism evolved an aversion to those chemicals for some reason.

xD Well I guess it is, isn't it?

E. coli and other bacteria metabolize tryptophan into odoriferous skatole and other indole compounds.
If you're culturing these organisms in medium that contains tryptophan, that may be what you're smelling.

Ah, Skatole! That makes sense. Thank you for your answer!


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Range for which the Verhulst-Pearl model is a good approximate
The Verhulst-Pearl model describes the growth of a population using the differential equation,
$$\frac{dN}{dt}=rN \left(\frac{K-N}{K} \right)$$
where N is the population (no. of organisms), r, the intrinsic growth factor and K the carrying capacity of Nature for that species.
Solving the differential equation, we can obtain a relation between time and instantaneous population, given as,
$$\frac{N}{K-N}=\frac{N_o}{K-N_o}e^{\frac{rt}{K}}$$
Where $N_o$ is the initial population.

For a general value of $N_o$, the logistic growth model can predict the the population fairly accurately. But I don't think the graph would be entirely correct if we have very low or very high values of initial population (nearing saturation).
So, What is the range of initial population where the logistic model works as a good approximate?

"I don't think the graph would be entirely correct if we have very low or very high values of initial population." Why?

@AdhishSethi For very low populations, I guess external factors play a much pronounced role, and fluctuations are fairly high. For the very high values (still less than K), I think the graph would exceed the carrying capacity and later come down to the value of K (not in the way the graph shows).


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Why is PCR possible to amplify DNA template before Sanger Sequencing for unknown DNA sequences?
Most of the informations show that both PCR and cloning can be used before Sanger Sequencing to amplify the DNA template. But how is it possible for us to design the primers if we don't know the DNA sequence yet? So, in my opinion, only cloning is possible to amplify the sequences. Can anyone tell me how PCR can work in this way? Thank you!

Can you link these informations?

Some comments in this question. There are different aspects which confuses me. https://biology.stackexchange.com/questions/40988/in-sanger-sequencing-why-do-we-resort-to-cloning-why-doesnt-pcr-suffice

PCR is used to amplify a sequence included inside two known regions. So, if you're able to clone (for example with recombination) two sequence forward and backward to your sequence, by using PCR you'll amplify also the sequence included.
This image in example will clarify my statement.

There are several tricks that can be used to PCR amplify an "unknown" sequence.
1) If the protein sequence is known, than it is possible to guess the entire range of DNA coding possibilities for a small region of that protein. Making the complementary primers for two regions is thus possible.
2) If you know several homologous of that gene several species, you can attempt to identify highly conserved regions within the gene. ie parts of that genes that does not change between species.
3) If the genome is small and your lab is well to do, you can just sequence the whole genome. Then you will have the DNA sequence and can thus design primers at your leisure.
4) If you have isolated the gene (via BAC cloning) but do not know the sequence, you may still PCR amplify it using primer that bind to the vector containing the gene of interest.
5) You may ligate dsDNA oligos to the unknown DNA sequence. Then use primers complementary to the oligos


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Why can't we always create a vaccine against a virus when an ELISA test to detect it is possible?
Before precising my question, here are some facts that I presume to be true:

A vaccine works by injecting the antigens of a virus into the body to train the immune system to recognize the virus and to be prepared to fight it if it shows up.
The ELISA test indirectly recognize the presence of a virus into a blood sample by testing the presence of the antigens of the virus and the antibodies that fight against it.
One of the reasons there are still no vaccine against HIV is because this virus has a very high mutation rate.
The ELISA test is used to detect the presence of HIV.

I have the feeling these facts contradict themselves and I would like to know where I am misleading.
Indeed, if we have an ELISA test for HIV, we should be able to create a vaccine because we know the antigens of the virus and we can inject a harmless version of them into our body, right?
Apparently, the answer to this question is no because the HIV virus has a high mutation rate and the antibodies produced thanks to the vaccine won't be able to fight every mutation of the virus (that's the answer that gave me my former biology teacher in high school). But if the HIV has a high mutation rate, how can we be able to produce an ELISA test for it?

I found the question quite interesting and will to provide a concept and a speculation although I could not answer the question to my own satisfaction (edits to this regard are welcome)
Currently (2020), the advanced form of ELISA tests for HIV are designed to simultaneously detect both the HIV P24 antigen (produced by the virus) and anti-HIV igG and igM antibodies (produced by the body in response to the virus). Refs (CDC: What kinds of tests are available, and how do they work?)(HIV Diagnostic Testing: 30 Years of Evolution)
While it is easy to detect known viral antigens like the p24 capsid protein in a diagnostic, it is not straightforward to use the same antigen as a vaccine and expect the host to mount an immune response that neutralizes the viral infection, although attempts have been ongoing. Possible scenarios could be that the binding strength of the antibody to P24 might be good enough for detection, but not enough for immunity or that recognizing and binding to P24 does not inhibit the infection. Coming to the evolution/mutation question, since both the p24 antigen and a few antibodies are being detected, it is unlikely the virus would mutate so as to evade the ELISA for all the targets.
The first point in Charlie's answer might be getting at this but it did not come through clearly.

Yes. What you said was absolute right. It's a complicated question. Here are some key points:

To begin with, it very very important to understand that ELISA is a well-established experimental set-up, it does not make any sense to make strong correlations between ELISA results and human vaccination outcomes. This is applicable to any research: We cannot try to make direct link between lab work and real-world problems.
To answer your question 'But if the HIV has a high mutation rate, how can we be able to produce an ELISA test for it?'. We now know that there is a type of antibodies called broadly-neutralizing antibodies (short name: bnAbs) that can fight against a wide variety of mutated viruses. About 20% of HIV patients have bnAbs, and it would take them months even years to have bnAbs. What we do in ELISA is detecting HIV with bnAbs that we found from HIV-infected individuals. But that does not mean we can induce bnAbs with vaccines easily. So these are two completely different process: ELISA takes bnAbs we found to detect HIV, we have those antibodies made and we use it in experiments. Vaccine try to elicit bnAbs in all patients, we know some of the patients can produce bnABs, most of them don't, scientists are working on why that's the case and how we can tackle that.

I'm not sure to understand your second point. If only 20% of HIV patients have bnAbs and ELISA only detects HIV with bnAbs, the test should produce a lot of false negatives, right?

@Pierre He is saying HIV has a few conserved epitopes, when your antibodies target them you won't develop AIDS, and once sucessfully isolated + hydroma stuffs such antibodies provide a good way to detect HIV-antigens independently of its immune-escape intra-host acquired mutations. What is strange to me is that since the virus stays for a while into the body shouldn't our B-cells pools eventually always find those conserved epitopes ?

@reuns It's very difficult to find epitopes on HIV. One of the main reasons is that the virus is covered in glycan (sugars). And these glycans are produced by infected human cells-that is to say, we the virus is covered in glycan, it looks like us. Our immune system do not want to attack ourselves. Even if B cell find these epitopes, not every antibody is effective. In many cases, antibodies against conserved epitopes are not very effective.


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What is the biochemistry of love?
How is love induced between humans? Say, between mother and child, couples, etc.
Does the phenomenon of love exist in other mammals, too?

"Love" is a subjective phenomenon that can't really be applied to non-human animals because we can't ask them about their subjective experiences. However there is some clear evidence, especially in more social mammals, of caring behavior and social bonds for other conspecifics.
As far as biological basis, I suppose you could consider it biochemistry, the peptide hormone oxytocin is correlated with formation of social bonds between animals of many species (although Wikipedia isn't the greatest source, you will find this particular page is saturated with links to scientific literature). I would caution against the popular press treatment of oxytocin as "the love hormone" and caution against simplifying a complex set of behaviors to the action of one peptide, but certainly the evolutionary conservation and broad applicability suggest that this is indeed an important hormone in social relationships.

Till now, I only knew oxytocin as a birth hormone and milk let down hormone.Never heard about this love hormone concept.

@San If you search for something like "oxytocin love hormone" you will get a broad mix of crazy hyped pseudoscience as well as some fairly nice popular science press articles that are much more nuanced. There is good evidence that oxytocin can (moderately) change human behavior in certain situations, but it definitely isn't nearly as simple as put two people together, add oxytocin, stir 5 minutes, love! More like, "there is a modest statistically significant difference in trusting behavior versus controls."

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


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Why don't we have vaccination against all diseases caused by microbes?
People can be vaccinated against certain diseases. Principle of vaccination is to use live attenuated load or inactivated. My question is - why we dont have vaccination against all diseases which are caused by microbes?

We do. It says I'm due for my penumonia vaccine in some thirty years.

Imagine the stress on your immune system when you're up for a booster with 10,000 different antigens.

Mainly cost/benefit analysis. Using vaccines has a cost, both in dollars and in risk. That cost may be very low (cheap safe vaccines, like measles vaccine), or may be relatively high (smallpox vaccine is relatively risky, with around a 1 in 300,000 chance of moderate to severe side effects); but there is always some cost.
Vaccines may not have any significant benefit. I live in the urban USA; it's unlikely that an Ebola vaccine would offer me any benefit (as of the current situation in 2019). Very few people in 2019 have a significant chance of being exposed to smallpox, since it's extinct in the wild; the benefit of universal smallpox vaccine would be small.
So if the risk of a vaccine is greater than the benefit, delivering the vaccine would be more harmful than good. This calculation is done as a routine, and the vaccines people receive are known to be ones that confer more benefit than risk.
In fact, with vaccines, the benefit needs to be much higher than the risk, because with vaccines the benefit is invisible (nothing happens - you don't die of measles) while the risk is something that happens. Typically, vaccine benefit/cost ratios are very high, for that reason.
Monetary cost is also a factor. It may seem harsh to think that saving a child's life with a vaccine is given a price, but at some point the finite supply of money can be used more effectively elsewhere. If it costs a billion dollars to give a particular vaccine, and it ends up saving one life, is that the best use of money? Could it be better spent on nutrition, sanitation, etc?
This applies to quite a few diseases. There are, in academic labs and in the freezers of pharmaceutical companies, vaccines against a lot of pathogens that are not being used, because the cost is too great for the benefit. That's an equation that changes all the time; it applied to the Ebola vaccines at one point, but in the face of an Ebola outbreak those vaccines -- in those areas -- are now cost-effective.
Finally, there are a handful of pathogens for which a reasonably-priced good vaccine would certainly be cost-effective (HIV, malaria, tuberculosis, for example) but for which reasonably-priced good vaccines don't exist, because vaccines are sometimes really hard to make.

Cost-benefit also needs to look into alternative treatment options.  For example, if a bacterial infection can be treated quickly, cheaply, and with few effects by antibiotics, it needs to be extremely common for vaccination to be worthwhile.

I feel like your answer would be better if you included a disclaimer at the top in bold about how incredible small the risks of vaccines are. Currently some people may misinterpret it.

@iayork Why it is hard to make in the cases you mentioned? Using the same principles as used in other vaccinations, why we cannot make vaccine for TB, malaria, hiv etc

@AmitMaurya The problem is that a vaccine is essentially a "substance" that tricks your immune system into mounting the same response it would have to the pathogen that causes the disease. The trick is to find something similar enough to the live pathogen to represent a threat, but different enough to not cause the disease in the first place.

@AmitMaurya:  There actually are vaccinations for TB.  They aren't used in the US because they weren't effective enough (too many strains to have to cover.)  My older sister was innoculated against TB.  I'm two years younger, and by that time the TB innoculation program had stopped. I was then later exposed to TB, and have some slight damage to my lungs as a result.  It is not certain that an innoculation would have helped me.  What is certain is that innoculation interferes with the simple "tine test" for TB.  TB can be cured with antibiotics.  Detection is more important than prevention.

@Amit TB immunisation is standard practice in the UK (I had my BCG at school along with all my peers); an HIV vaccine is in the works but is non-trivial to make.

Others noted that there are vaccines for TB (old, but not extremely effective) and HIV (highly experimental, so far not very effective at all). There's also a vaccine against malaria in clinical trials. All these are good examples of my point: They are not highly effective vaccines, but the diseases are so prevalent (in certain areas) and so severe that the cost/benefit analysis might become positive even with relatively ineffective vaccines. The question of why some vaccines are hard to make at all is a separate one (which I think may be answered on this site already)

@Nathan: If the reader is too lazy to note that iayork is characterizing a 1 in 300,000 chance as "risky," then they either already believe in the anti-vax nonsense, or they were probably going to be fooled by it eventually anyway.

@Kevin I completely understand where you're coming from. But I do strongly feel that in this case, it may be better to spell it out. Some people may not understand how minuscule 1 in 300,000 is.

@akm In the case of viruses like HIV it's due to evolution - they evolve faster than we can make vaccines for them. We have lots of vaccines for AIDS and they do work but they don't work against the current generation of the virus.

@slebetman that's not correct, but it's off topic here and needs more room than is in the comments.

I would suspect that it's because not every disease caused by microbes can be treated by vaccines. For example vaccines are not as effective on microbes that cause skin infections because the antibodies generated by being vaccinated travel in the blood and some microbes damage the skin and nearby tissues without going into the circulatory system to be detected by the immune system through antibodies.
Furthermore, when bacteria reach the blood circulatory system they cause septic shock as the body responds with an inflammatory response to both the microbe and the toxins it produces, which can be fatal. But the amount of microbes that can cause sepsis is extremely diverse: bacteria (Gram negative and positive), fungi, viruses, and parasites; sometimes it happens in combination of microbes [1]. It seems impractical and inefficient to design vaccines against every microbe that cause disease because it seems that anything that can proliferate in the blood will cause disease. Microbes can even cause sepsis without going in the blood [1].
Reference:
[1] Sepsis and Septic Shock: Current Treatment Strategies and New Approaches. Gizem Polat, Rustem Anil Ugan, [...], and Zekai Halici. Eurasian J Med. 2017

Another factor that can limit the effectiveness of vaccines is antigenic variability in the pathogen — influenza viruses being a classic example, but also seen in many bacteria.

@tyersome That's a good point you can edit that in if you'd like.

@tyersome: Yeah; as I'm sure you realize, that's the same reason that people can get the flu over and over again. Another example is the malaria protozoan (Plasmodium).

Even more extreme than the flu is the common cold.  I found some research from 2016 that achieved success in animal trials, but they had to include dozens of strains in one vaccine.  And I expect that, even if this comes to humans in everyday life, it would be like the flu vaccine: a shot each year with the best guess of which strains to include that year.  https://www.nature.com/articles/ncomms12838


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Do we know of any "species ending bugs"?
Are we aware of a "bug" (virus, bacterium, prion, ...) that has completely exterminated an entire species? Either through direct observation or maybe some form of archeological evidence? If not, are there realistic scenarios where this could happen?
I am primarily interested in cases where the disease was the driving factor of extinction of an otherwise well established and healthy population, but examples of species that were in bad shape to begin with are welcome as well.
My understanding is that this is unlikely, since very deadly infections tend to burn out or evolve towards being less deadly. Killing your host is not conducive to your survival. But maybe it would be possible to reduce the number of individuals so much that reproduction became problematic. I imagine a species confined to an island or something might be susceptible.
I'm asking this because in an interview I saw, an epidemiologist said that his usual research interest are "bugs with species ending potential". The interview was on COVID-19 so he didn't elaborate on what he meant by that or give any examples.
For the special case of humans, I was able to find this article that claims such an event to be unlikely, but I suppose we are the best equipped species that has ever existed on this planet to deal with such a threat.

Can you provide a link to the interview and the name of the epidemiologist? Have you tried looking at some of his papers or his website (many academics have one devoted to their research)? Those would seem like good ways to find out what kind of microbe(s) he might have in mind ...

@tyersome Have been looking for that since I asked the question. Had watched so many interviews that it took a while. It was actually the interviewer (Sam Harris) introducing the interviewee Amesh Adalja: https://youtu.be/E9vIUtXa9ug?t=150 . He mentions a bird flu with a 60% case fatality rate becoming highly infectious for people but no details.

Not a species, but the Gros Michel was almost driven to extinction by a fungus. Apparently the now-dominant variety of bananas is also being attacked by fungus and isn’t doing so well. The other noteworthy thing here is that these bananas are sterile and must be asexually reproduced by humans (creating clones of no genetic diversity).

From the vantage point of other species, humans might be considered "bugs" in the sense that we are organisms that are causal in the ongoing extinction of numerous species. We're doing a pretty good job of it, so far:

The included extinctions span numerous families of plants[4] and animals, including mammals, birds, amphibians, reptiles and arthropods. With widespread degradation of highly biodiverse habitats such as coral reefs and rainforests, as well as other areas, the vast majority of these extinctions are thought to be undocumented, as the species are undiscovered at the time of their extinction, or no one has yet discovered their extinction.   The current rate of extinction of species is estimated at 100 to 1,000 times higher than natural background rates.

Well, maybe you can interpret the question like this, but it is not what I meant at least :-). I mean none of the species we exterminated could be classified as hosting us.

@user1136 That's an interesting theory and it would definitely be an answer to the question.


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Has a bird ever been seen stalling?
Note: I am not sure this is the right site, but I believe birds are off-topic on Aviation SE.

Has a bird of any species ever been seen experiencing an aerodynamic stall by increasing the angle of attack (AoA) over its wings or flying at too low of an airspeed?

I suppose you could technically call a dive a "stall". Watch a predatory bird stalking prey sometime. Once they're ready to attack, some species will just fold in their wings and let gravity do its thing for a time.

@MattDMo so when they do that they have no lift because their wings are folded in?

For a while, yes. They're in full control of the dive, so they can change direction using their tail if necessary, and can unfurl their wings to adjust speed whenever they want. It's not uncontrolled, just unpowered. On the other hand, there are birds that do power dives - flapping while diving. Here is an eagle doing just that.

And here is a blue-footed booby diving with wings folded.

Where have you looked for an answer to this question? Because basically stall is the mechanism by which many birds land on a perch.

Somewhat related

@kmm searching for "bird aerodynamic stall" just brought up things about the aerodynamics of birds (not stalling), aerodynamic stalls in airplanes, and explanations of why birds don't usually stall.

Yes.
Kereru (Hemiphaga novaeseelandiae) from New Zealand do a type of display flying where they deliberately induce a stall by flying on an upwards curve and allowing momentum loss to decrease air-speed such that they stall.
A video of this can be found linked through iNaturalist on Youtube.

Kereru were my first thought too. Nice work finding a video, they often fly to a decent height before stalling. So great to watch them on a windy day.


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Are mutation rates normally distributed? If not, what are they?
On average, there are  64 mutations per generation in the human genome. Is this constant, or can we expect variation in the number of mutations?

You have posed a different question in your title and in the main text which is a bit confusing. As a short hint: Quantities that are bounded (i.e. mutation rate can only be a positive number) cannot be normally distributed. But they can be, for example, distributed by the log-normal distribution.

this depends a lot on the mutation, different types of mutations have different probabilities. Its all based on the laws of chemistry.

Mutations in this context are being treated as discrete count data (there either happen or they don't). So the number of mutations per person in a given generation should form a discrete probability distribution. Because they are a single count variable bounded at zero (can't have negative counts) and finite (genomes don't go on forever), a Poisson distribution(pwɑːsɒn/) is probably the expected best fit. A Poisson distribution can sometimes be approximated by a normal distribution when the Poisson count mean (λ) is large (some say λ>20, some say λ>100).

Note: there are 60ish substitutions per generation, on average. There are probably many times that number including all mutations (e.g. microsatellites, centromeric satellite repeats, etc). There is almost by definition a telomeric mutation on every chromosome end at every cell division, which alone is comparable to substitution number per generation.
Figure 1d of this paper suggests that the distribution of substitutions alone is log-normal in cancer, as suggested by the commenter.
I am not aware of a reference for distribution of other mutations.

What does log normal mean

@ShannonT The lognormal is a distribution that looks normal after a logarithmic transformation of the underlying data. For more info I'd suggest googling it.


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Is double-stranded DNA denatured to single-stranded DNA in retorted canned tuna?
A PCR reaction has a cycle of about 55°C annealing, 72°C extension and 95°C denaturing with short time spans. Retorting canned tuna heats the tuna to 115°C to 121°C for 30 minutes to 2 hours depending on steam temperature and can size. So, much of the DNA is degraded into short segments of less than 150 to 200 bp long.
Has the DNA at that temperature been degraded to single-stranded DNA as well, or is is just short segments of double-stranded DNA?

Citations for heating causing shorter DNA fragments in processed meats:

Ebbehøj, K. F., and P. D. Thomsen. 1991. Species differentiation of heated meat products by DNA hybridization. Meat Science, 30(3), 221-234.

Şakalar, E., M. F. Abasiyanik, E. Bektik, and A. Tayyrov. 2012. Effect of heat processing on DNA quantification of meat species. J Food Sci. 77(9): N40-N44.

Retorting fragments mtDNA in any meat product. More than 3 dozen papers on retorted tuna DNA alone.

Welcome to Biology.SE. Your second paragraph sounds like a conclusion, but isn't obviously based on the preceding paragraph. Are you claiming that 'retorting' fragments the DNA? If so, can you provide a citation or other reference that supports that? ——— It would also be helpful if you could say why you want to know this seemingly random factoid. ——— Please take the [tour] and consult the [help] starting with [ask] for details about site usage and expectations.

Ebbehøj, K. F., and P. D. Thomsen. 1991. Species differentiation of heated meat products by DNA hybridization. Meat Science, 30(3), 221-234.  https://doi.org/10.1016/0309-1740(91)90068-2

Şakalar, E., M. F. Abasiyanik, E. Bektik, and A. Tayyrov. 2012. Effect of heat processing on DNA quantification of meat species. J Food Sci. 77(9): N40-N44.  https://doi.org/10.1111/j.1750-841.2012.02853.x

Retorting fragments mtDNA.  in any meat product.  More than 3 dozen papers on retorted tuna DNA alone.

Great, please [edit] those into your post — comments on this site are ephemeral and often overlooked, so they should only be used to discuss the post not to amend it. ——— You may be best placed to answer this question. In a typical molecular biology context I would hazard an answer, but I'm not sure how relevant what I do know will be for a complex, non-aqueous material like tuna. In solution, DNA that has 'melted' (strands are separated) will reanneal, but the rate of that reannealing depends on the complexity of the sequence — see: Cot curves.

Thank you sir.  the Cot curves site is very helpful.  My question has not practical significance for us, except it is very helpful to exactly how things are working, in the PCR reaction.  Again, thanks very much for your help.

What does the word “retorted” mean in this context? The only definition I can deduce is from the chemical apparatus, retort. Please clarify by editing your question.

It is ssDNA. At retort temperatures (110C - 135C) the hydrogen bonds are broken and the DNA is single stranded. From what you wrote the size of the DNA fragments also changes based on temperature. If however you let the DNA sit for some time and cool after exposure to these temperatures some fragment can reanneal.


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Does the string "...CATCAT..." appear in the DNA of Felis catus?
In Hofstadter's Gödel, Escher, Bach: An Eternal Golden Braid (GEB), the following claim appears:

...in the species Felis catus, deep probing has revealed that it is indeed possible to read the phenotype directly off the genotype. The reader will perhaps better appreciate this remarkable fact after directly examining the following typical section of the DNA of Felis catus:
...CATCATCATCATCATCATCAT...(OP note: truncated because, you get it)

Is this true? A cursory search for the DNA of Felis catus gives me this 1996 paper by Lopez, Cevario, and O'Brien and the given sequence does not appear – there are some instances of "CAT" but not repeated enough to make it as remarkable as claimed in GEB.
I don't know enough Biology to judge the veracity of this claim. Some points I am considering are:

GEB is full of wordplays. However, the tone of this part of the text does not sound like one to me.
GEB was written/published around 1978. The paper I linked to – which was cited by some 236 others according to Google – was published in 1996, way after GEB's time. If my impression that Lopez et al.'s work is significant because it is the first time Felis catus has been sequenced, then there is no way Hofstadter could've known of it when he wrote GEB. Then again, I don't know enough Biology that there might be some nuance to Lopez et al.'s paper that I'm missing (i.e., the results of the paper might not be mutually exclusive to the claim made in GEB).
GEB has reference notes and bibliography and there is no reference cited to back this claim. However, GEB does not attempt to be a rigorous academic thesis and the references is only called upon more when Hofstadter quotes other works directly while the bibliography is a list of readings which the reader may want to check out, regarding the main thesis of the book.

So are cats recursions with no base cases?

Welcome to BiologySE! You came with a bang! ;)

Does Lady Gaga's DNA have GAGAGA?

While I don't know the cat genome, I'm pretty sure the dog genome doesn't contain DOG.

I'm voting to close this question as off-topic because, amusing though it may be, but the relationship between the Englsih word cat and the abbreviations used for molecules can in no respect be regarded as being about biology. Perhaps it has something to do with statistics or English literature.

I’m voting to close this question because this is trivial and stupid.

I’m voting to close this question because as @David has pointed out in the past this question is trivial and has no biological relevance.

@tyersome Yet, it has been upvoted at least 92 times and favorited 22 times.

I’m voting to close this question because it is of no scientific interest whatsoever.

Interesting. I now see both @tyrsome and I voted to close this previously   Why were our close votes removed?

@David Bcoz no one else supported and your votes aged away. They age away after 14 days.

@user237650 — Thanks for the info. Well, at least the comments don't.

The Felis catus genome has been published, annotated, and updated quite a bit since 1996, including spans of so-called intergenic regions, which are basically scaffolding and other structures, along with perhaps some unidentified genes, pseudogenes, regulatory sequences, etc. Basically, pretty much the entire DNA sequence is available now, not just the gene sequence of the mitochondrial genome, which was what was published in the 1996 paper you referenced. Mitochondria are the power plants of the cell, but are just an organelle that happens to contain its own DNA; they are separate from the chromosomal DNA in the nucleus. All of this is available for free (if you know where to look) at the National Center for Biotechnology Information (NCBI), part of the National Library of Medicine (NLM) at the National Institutes of Health (NIH) in the United States. Other sites are also available, such as Ensembl, a joint project between the European Bioinformatics Institute (EMBL-EBI), part of the European Molecular Biology Laboratory (EMBL), and the Wellcome Trust Sanger Institute (WTSI). Both institutes are located on the Wellcome Trust Genome Campus in the United Kingdom.
So, to the genome. Genomic sequences can be searched in a couple of different ways, depending on what you're looking for, but the most common way is to use BLAST, the Basic Local Alignment and Search Tool. As the name implies, it takes sequences as input and searches one against the other, aligning the results as best as possible using certain algorithms that the user can define and tweak. The BLAST web interface to the cat genome is here. You don't need to worry about any of the other options here except the "Enter Query Sequence" box. FASTA format is just using the single-letter abbreviations for nucleotides (AGCT), all strung together.
The genome we're searching is of an Abyssinian cat named Cinnamon:

Cinnamon, the cat which was chosen to be the definitive genetic model for all cats in the feline genome project. Image courtesy of the College of Veterinary Medicine at the University of Missouri.
To start with, I typed in CATCATCATCAT and to my surprise got back over 200 hits, covering every chromosome the cat has. So, I doubled the length of the input to 8 CATs, and got back the same result set. Unfortunately, 12 CATs was too many (and really, it is too many), so I worked backwards.
The final results are here (sorry, link expires 10/13/16. To regenerate, go to BLAST link above and enter CATCATCATCATCATCATCATCATCATCAT). Apparently, popular wisdom is incorrect, and Felis catus chromosomes really contain 10 CATs each, one more than is needed for their 9 lives. No word yet as to why this may be, but scientists are presumably working on it.

The irony might be taken seriously, I don't think it is a good place for joking.

@har-wradim what is ironic here? The last sentence? No harm there as I'm not interested in deep research on cats, per se. I find the answer well-detailed and, limited as my biology knowledge is, Matt's explanation adds up, reproducible and verifiable. Well, NCBI Blast's UI isn't Apple-quality but it holds up as far as I can interpret it.

My question is, is felis catus the only species for which this is true? I would suppose otherwise.

@Jan: I would say it's highly unlikely. This is just pattern matching with an astronomical input set.

@JanDvorak can you come up with an animal spelled with A, T, C, and G?

THE MOAR YOU KNOW: Rumor has it that some well known pop singer has lots of "GAGA" in her DNA. In other news: every other carbon-based lifeform does too.

I heard that the entire cast of Gattaca had GATTACA sequences in their DNA.  Most of the crew did to.  I smell a conspiracy.  I think they even passed a law about large numbers to cover it up.

My background is in mathematics; I joined the Biology StackExchange in order to leave this comment. The cat genome, like our own, is about 3 billion base pairs long. The probability of matching a sequence of n base pairs starting at any given position is 1 in 4^n (since there are 4 possible base pairs), which for n=12 is about 1 in 16 million. That means you'd expect to find around 200 matches for CATCATCATCAT if all short sequences were equally likely. This won't be perfectly true, but as March points out the widespread existence of tandem repeats makes matches like this still more likely.

Reading many of the comments on this page, I get the feeling that while some of us here are having fun, others, less informed, are completely confused. My vote goes to @March Ho.

@har-wradim what exactly does that mean?

@har-wradim never mind, I see. Some people have completely missed the joke, and are taking this way too seriously.

@skytreader "NCBI Blast's UI isn't Apple-quality but ..." meaning that it cannot search apples' genomes? or.. ?

@DaniloRamirez Apple as in where Macbooks come from. A lot of scientific tools, heck even industry products, have UIs that aren't Apple-quality but are nonetheless useful and powerful.

I very much appreciate the humor at the end there :)

@skytreader Oh that Apple.... please don't...  :) the pun was intended from the initial comment, but thanks for keeping it very explanatory

@MattDMo So do I understand it correctly, could there be some other cat different from Cinnamon that can have more CATCATCAT... than her? Because we only analysed one genotype and those of other organisms of the same species can differ, right?

@nuoritoveri Yes, that is possible.

I think this is the longest one https://www.ncbi.nlm.nih.gov/nuccore/NC_018733.3?report=fasta&from=72130713&to=72130839   $(CAT)_{41}$ (reverse complemented) perphaps you forgot to uncheck 'mask low complexity regions' ?

While Matt's answer is perfectly correct, it is important to note that the sequence $(CAT)_n$ in DNA is not restricted to cats, and you would expect to find it anywhere.
For example, searching the human genome for the same 3-tandem repeat CAT sequence results in many hits as well.
This is because you are essentially searching for short tandem repeats on the DNA strand. These repeats can occur in any organism, and therefore while finding CAT substrings in the DNA of the cat may be amusing, they aren't special to cats (or any other animal) and are only the result of an artifact of naming of the bases coincidentally matching with the name of the animal.

The bases are not just 'named', they represent the four nitrogenous bases: adenine, cytosine, guanine and thymine.

@SummerEla While you are right, I don't see how it's inaccurate to call that "naming".

Well, it's more like an acronym than a naming system: those three nucleotides together (called a codon) ultimately work together in strings of codons to code for a specific protein.

@immibis what?
My point was that the bases are not named arbitrarily, they actually stand for nucleotides that comprise amino acids, which when combined make up proteins.

But the naming of the nucleotides themselves is ultimately arbitrary. According to http://etymonline.com, adenine is "so called because it was derived from the pancreas of an ox", while guanine is named "from guano, from which the chemical first was isolated" and thymine "from thymic acid, from which it was isolated" (cytosine comes from cyto- meaning "cell"). Had the discoveries occurred differently, those chemicals would have very different names.

HAHAHA (no, not a remapped/renamed nucleotide sequence--really laughing). For some reason, this makes the GEB claim funnier. Thanks for the clarification!

So as per Matt's answer (that there is a 10x sequence), can that 10x sequence be found in any other organisms?

To augment the other answers, let's compute the probability of CATCATCATCAT occurring in random DNA sequence.
Cat DNA length is 2.7 gigabases (source), and there are 4 possible bases.
For 1 CAT there are 3 bases, giving expected number of occurrences in 2.7 Gb as $\frac{2.7 \cdot 10^9}{4^3} \approx 42\,188\,000$
Repeating the calculation for longer sequences gives:

1 CAT: 42 188 000 occurrences
2 CAT:      659 180 occurrences
3 CAT:        10 300 occurrences
4 CAT:             160 occurrences
5 CAT:                2 occurrences
6 CAT:
               0 occurrences

So, indeed, there are many more CATs in cats than could be expected by pure chance alone.

DNA is not such a simple random sequence and, in particular, repeats occur above likelyhood. This is therefore not a good approach.

@JackAidley In my opinion, this is a good approach to demonstrate exactly that repeats occur more often than they would in a random sequence.

@jba: It does. But there's nothing special about the sequence 'CAT' in the cat genome. It's a general property of repeats. Perhaps you could edit your answer to make it clear the point you're making, and why?

Interpreting the expected number of occurrences as a Poisson parameter, you can interpret the occurrences of 6 CATs as a probability (through the transform $\lambda\mapsto1-\exp(-\lambda)$) of about 4% that you would have that many in a random sequence. As jpa points out, this is a good argument that STRs like CATCAT... are more likely than chance alone would suggest.

Rather, it is an argument that DNA sequences aren't random in the way this calculation supposes.

@reinierpost it's random from the CAT point of view.  The meaning we attribute to CAT is arbitrary to DNA. It's as random as the index into the number Pi that you've have to start at to find a cat video.

@CandiedOrange: That is not what this answer means by 'random'. It assumes the C, A, T and G elements are completely random in the sense that the probability of one of them appearing at a specific spot in the sequence is completely independent of what the surrounding elements in the sequence are - and that isn't the case.

@reinierpost those two ideas of random are the same idea of random is my point.

So, there are a few great answers here already, but it seems nobody addressed an interesting part of your question: GEB was published in 1978 and the genome of Felis catus was not sequenced until many years later... so how did he know?
jpa's answer shows that you'd expect to get only about five CATs - not ten, and the chance of getting ten is astronomically low. I expanded his table to show the depressingly low chance of getting ten by perfect randomness:
5 CAT: 2.5 expected per Felis catus genome
6 CAT: 0.04 expected
7 CAT: 0.00061
8 CAT: 9.54 e-6
9 CAT: 1.49 e-7
10 CAT: 2.32 e-9

That means you'd expect to find 10 CATs about 0.00000000232 times per random genome. So how on earth did the Felis catus genome end up with ten CATs in it? And how did Hofstadter know that there would be this many CATs?
As it turns out, this repeated sequence of a few base pairs is called a "short tandem repeat", or "microsatellite". This is when a 2-5 base pair sequence is repeated several times, usually between 5 to 50 times.
So at this point, to recap: we know the chance of getting this 10 CAT sequence is slightly more probable, but since we're restricted to just the Felix catus genome we definitely aren't guaranteed a 10xCAT sequence. So how did Hofstadter state it as if it was a fact?
As it turns out, one critical property of STRs, or short tandem repeats, is that mutations in these areas are far more common, and they represent a large amount of the genetic variation between individual members of a species. This discovery was made with the advent of DNA sequencing, which began only a few years before the book was published. Therefore, given a large population of nonidentical cats (which we have), we can confidently say that there is an extremely high chance for a 10xCAT sequence.
Hofstadter's genius perfectly combined math (only 2.32e-9 expected sequences per genome) with biology (microsatellites increase the chance of finding this sequence) with forensic genetics (in a population of the same species, individuals are likely to have many STR-related differences.) All of this put together gave Hofstadter what he needed to confidently say: yes, CATCATCATCATCATCATCATCATCATCAT almost certainly exists in the Felis catus DNA. Little things like this are why Godel, Escher, Bach is my favorite book of all time.


text:
Why is the null hypothesis of trait evolution Brownian motion?
Many models of continuous trait evolution assume that traits evolve according to Brownian motion. What is the biological or physical basis for this choice?
I realize there are models that do not assume Brownian motion, but what I am interested in asking is why the null model is so often chosen to be Brownian motion.

What else would you choose?

Please define "Brownian motion".

Brownian motion models the random motion of particles suspended in a medium. In biology it is often used to model situations where change in some system occurs via a random walk.

I asked because some people use "Brownian motion" as a synonym for Wiener process. I conclude you are not one of those people.

@RodrigodeAzevedo Thanks for pointing that out. I had believed the Wiener process was one and the same with Brownian motion. Reading the wiki page, it certainly does have the same mathematical properties. What other conception of Brownian motion did you have in mind?

Lévy flight.

I think that the simple answer to this question is that the present comparative methodology was largely established by Felsenstein 1985, American Naturalist. For mathematical convenience, he suggested Brownian motion as a null hypothesis, because "...the variance of the distribution of change of a branch is proportional to the length of time of the branch...", and then "...it is easy to see that the differences between pairs of tips... must be independent." Also: "...after one unit of time, the contrast [between a pair of tips] has expectation 0 and [easily defined] variance..."
He explicitly discusses whether Brownian motion is a reasonable model in the section "What if we lack an acceptable statistical model of character change?"
I would suggest reading that paper in more detail if you are interested in the details of Brownian motion applied to phylogenies.
A recent historical perspective on this influential paper can be found here.
For a more extensive bibliography/more details you can see here.

thank you very much for the papers! Yes, this is exactly what I was looking for. Felsenstein's a giant - I should have guessed he had something to do with it...

@jmah i feel like my main contribution to this website is as a felsenstein stan

Just came across a chapter by Felsenstein on phylogenetic inference with quantitative characters. In it, he states this biological justification for using Brownian motion:

A quantitative trait that has genetic variation controlled by a single locus will change as the gene frequencies at the locus undergo genetic drift...  Brownian motion is a reasonable approximation to change of a quantitative character by genetic drift, provided that ... [additive genetic variance] ... remains approximately constant.

Felsenstein also mentions that Cavalli-Sforza and Edwards (1967) consider that varying selection at a locus can be approximated by Brownian motion.
So I suppose that's another slant on why Brownian motion is used.


text:
Killing enveloped viruses with soap

Unlike non-enveloped viruses, enveloped viruses can be killed with soap, alcohol, etc. Why?

Why does just having an envelope make it susceptible to soap and alcohol?

(+1) Re: "Why does just having an envelope makes it susceptible to soap and alcohol?": We often describe humans as "two-legged" and cats as "four-legged", but in the parallel universe where humans are "handed" and cats are "non-handed", someone is asking why "just having hands" makes humans so much more susceptible to loss of balance.

different but related: How exactly does alcohol solution kill or neutralize viruses?

@Alex Reynolds do you know how soap and alcohol affect other viruses and or bacteria? does it make sense to only use soap or is a good alcoholic desinfectant still better?

If the CDC can still be trusted any longer, it indicates that washing your hands with soap and water is a good way to stay healthy and avoid a number of bugs, and that it does better at that job than alcohol-based hand sanitizer: https://www.cdc.gov/handwashing/show-me-the-science-hand-sanitizer.html

Soap molecules are amphiphilic. This means those molecules have parts which are hydrophilic (water-loving, or "polar") and parts which are hydrophobic (water-avoiding, or "non-polar").
Fat molecules are non-polar. They avoid water. This is why a mixture of oil and water will separate into layers. In this mix, oil molecules prefer to hang around other oil molecules, and water molecules prefer to hang around other water molecules. Soap "likes" both oil and water, so it can be used for cleaning, by helping dissolve this mixture. (For a similar reason, this is why vinegar is used to dissolve or emulsify oil in salad dressings. Vinegar — acetic acid — is amphiphilic and likes both water and oil.)
The coat of an enveloped virus is made up of layer of phospholipid molecules and proteins. Phospholipid molecules are similar to detergents, made up of polar and non-polar ends. These lipids arrange themselves into a two-layered sandwich called a "bilayer". The polar ends of this sandwich are the "bread", while the fatty non-polar ends are the "filling".
Detergents can help disturb this by pulling or dissolving out phospholipids from the virus coat to form micelles, tiny bubbles of fat and soap that can be washed away. This puts holes in the virus coat and helps dissolve it.
The insides of the enveloped virus particle cannot infect directly and must rely on its envelope to get into and infect a cell, so breaking down the coat inactivates (or "kills") the virus.
Alcohols are also amphiphilic. There are many different alcohols, but they all have a hydroxy group at one end, which is polar, and a saturated or partially-saturated carbon chain on the other end, which is non-polar. Like detergents, this amphiphilic property allows an alcohol — at a sufficient concentration — to disturb and break down the virus envelope phospholipid bilayer, inactivating it.
Non-enveloped viruses lack this phospholipid bilayer coating and are instead protected by a protein capsid. The proteins in a capsid will not dissolve with detergents, but they can be attacked with other disinfectants that chemically denature the proteins. Examples of such disinfectants are chlorine (bleach), iodine, peroxides, etc.
Just as soap can put holes into the phospholipid coating around enveloped viruses, destabilizing them, denaturing agents change the structure of proteins that protect non-enveloped viruses, also destabilizing the capsid. If the capsid proteins are damaged sufficiently, the virus particle is not able to infect a cell and so is deactivated.

Great answer, but a minor organic chemistry quibble - alcohols are defined by having a hydroxy group attached to a saturated $\alpha$-carbon, but further down the chain, any existing carbons don't necessarily need to be completely saturated.

Small correction: enveloped viruses also have a capsid.

Feel free to add a better answer to How exactly does alcohol solution kill or neutralize viruses? or we can consider closing that as duplicate of this question. I find this answer much more informative, and you've covered alcohol here to some extent.

I don't mind; whatever you prefer.


text:
At what point in the day do plants start to absorb light for photosynthesis?
My plants sit on a small table in my only window, facing Northwest. They are thriving. They are obviously getting enough indirect light to survive year round. Maybe they have adapted?  They have never really been in direct sunlight.

At what point in the day do they start absorbing this light?
Also, if the sun has risen behind my apartment building on a dull January morning and the sky is light are they reaping any benefits yet?

My plants are:

an asparagus fern with a small grapefruit tree in a tall open terrarium
an African violet
an aloe vera plant
2 sprouting avocado seeds
a small house palm.

I live in Alberta, Canada near the 49th parallel. This is a very sunny part of the province. Your ponderances will be welcome.

You may want to post also at https://gardening.stackexchange.com

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


text:
Where can I find a compendium of microorganisms?
I recently bought a microscope hoping to learn more about algae and bacteria and stuff. I've collected a few samples of pond water and found tons of algae and stuff, but I have no idea what to call the things I have found. I am wondering if there is a list of every known algae with a picture and some characteristics that would help me identify what I am looking at. I've looked around on the internet and haven't found much. Thanks

So you're looking for maybe a book or list with some common microorganisms that you would find in water so that you know what it is?

that is exactly what i'm looking for

It sounds like what you need is an identification key. The most common form of a biological identification key is a dichotomous key. In such a key the sequence and structure of identification steps is fixed by the author. At each point in the decision process, multiple alternatives are offered, each leading to a result or a further choice.
Key can be very region-specific so I suggest to search for a key that focusses on the group of animals you wish to identify and the region/country you live in.

Where are you from? I've got a good suggestion, but apparently it has not been translated in English...

This website will probably provide you with more information than you need at this stage of your investigations but is it one of the most complete and free resources for microbes of various kinds. http://microbe-canvas.com/

I do not know how complex of a key you want, but this one is a good identification guide for beginners. It contains a lot of common freshwater pond algae, what they look like, and some basic characteristics. From here, you can identify your specimen and then be able to look them up further. Hope this helps!


text:
Why are (some) male humans sexually attracted to the breasts of female humans?
Many male humans are sexually attracted to the breasts of female humans. Is there an evolutionary reason for this?

They aren't so much if they are not hidden, i.e. rainforest and old african tribes.

breasts are a signal of fecundity, puberty, age, fitness... plus, if you look at chimp and oprang breasts, they are pretty similar when breastfeeding.

This question is quite misinformed and problematic. 1. It doesn't mean anything to be sexually attracted to a non-reproductive part (like secondary chars. described below). 2. Attraction (perhaps 'mate preference' is better) is not reductionistic, as implied, where the opposite sex is reduced into parts. 3. Sexual selection worked differently across human populations. 4. There is definitely no basis in evolution for the question. As written below, there are evolutionary reasons for breasts and hypotheses as to why they unique in humans, but this is very different than what was asked here.

@Chris Moore How could this question be reworded to make sense? Being outside the field of evolutionary biology, I don't understand your critique. I think this comment could be usefully expanded into a great answer while still addressing the general question being asked even if it is misinformed.

Short answer, we don't know.
There are several competing hypotheses but they are all nearly impossible to test.  Behavior often suffers the same problem as testing, we can come up with a hypothetical reason but since we are the only organism that does it, we have no good testing options. We can't put people in controlled conditions for generations and see if their preferences change. Secondary sexual characteristics in general have problems with testing. Because there is no good way to differentiate reasons for a behavior. We still don't have a great consensus on why secondary sexual characteristics in humans exist, likely because many explanations can be true at the same time, humans have very complex behavior even in out instinctual behavior.  It could just be a quirk of neurochemistry caused X to be attractive, followed by run away selection, and that by itself would create a selective advantage. It can be really hard to test why a preference would arise unless the advantage is obvious because the different hypotheses all behave the same way in practice.
Possible answers include:
-lifting the nipple away from the body to make suckling easier for flat-faced human babies with protruding noses.
-runaway sexual selection (which is also a component of many others as well).
-cryptic signalling of ovulation and/or pregnancy.
-all of the above
Paper reviewing all the different hypotheses

@kmm how is that.

This is a hypothesis that I found in Desmond Morris book, The naked ape.
Basically, humans transit from a rear-penetration position to a frontal-penetration position. In this transition, the sexual clue performs by buttocks was perform now by breast.
In short, according to Morris: breasts are sexual clues because they look like buttocks.

Please, if downvote, explain in a comment why. I understand that this could be a controversial hypothesis, as such, in need to be discussed.

https://www.theguardian.com/science/2017/sep/24/the-naked-ape-at-50-desmond-morris-four-experts-assess-impact

Very good analysis of Morris book. It makes clear that it is loaded of misogynists views. Whit respect for the subject in the discussion, we read: Did boobs replace bums as a sexual signal when we became upright? I don’t know, but the point is that no one does. According to this,  there is no scientific evidence for the hypothesis (nor to confirm or denied it).