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Can elephants really paint?
I saw this youtube video of an elephant painting. (https://www.youtube.com/watch?v=foahTqz7On4&t=301s) There are others as well.
It looks completely real. However, like other people in the comments, I was also skeptical if someone was conditioning the elephant to paint, or if there was some trickery involved.
I'd like to know from a scientific perspective (i.e. via research or from some credible source) if elephants can actually paint things without being conditioned (someone shows them what to paint, then they recreate it) or trickery (someone has lines on the paper the elephant traces which are not visible to the camera).
Specifically, do elephants really have the creativity and mental capacity to paint things like flowers and elephants from their own imagination? Are they really that smart?

Can most  (excluding the possibility of a few genusies) humans paint without being conditioned?  Or is it just that with humans, we call the conditioning "art class"?  FTM I can't paint despite those elementary school art classes :-)

@jamesqf Any parent of a toddler can testify to the sheer enthusiasm of spontaneous artistic creativity that is often expressed by humans. The motor skills aren't great, however, and choice of media may often be disheartening to the adults...

@jakebeal: But how do the productions of toddlers splashing paint on paper (or other materials on any available surface) compare artistically with elephant painting?  (Always recognizing that in the modern world, "artists" can get remarkably high prices for splashing paint :-()

Interesting question! While it doesn't exactly address the topic of your question, I think the paper Is painting by elephants in zoos as enriching as we are led to believe? might have some insight.
I originally found this paper from the animal-made art wikipedia page, which states that:

The elephants draw the same painting each time and have learned to draw it line-for-line.

Although I couldn't find that claim in the paper they cited, it does seem like this is a highly structured activity (as opposed to a more free-form "art"). For example, from the above paper:

Painting involved following instructions from the keeper and performing the task in front of an audience. ... The brush was then handed to the elephant, which it then held with its trunk. Instruction was given by the keeper to the elephant when to start and stop painting, and when to give the brush to the keeper for colour changes. ...  Each session lasted between 2 and 5 min, and was a highly structured event. For example, when the elephant was not holding the paintbrush and awaiting the next instruction it was directed to rest its trunk tip on the ground.

There might be more information in this book, Cerebrum 2009: Emerging ideas in brain science, as it's cited a lot in the introduction, but it doesn't seem to be available online.
Overall, it doesn't seem like the elephants have much agency in what/how they paint. As the authors put it:

[T]he results indicated that elephants gain little enrichment from the activity of painting. Hence, the benefits of this activity appear to be limited to the aesthetic appeal of these paintings to the people viewing them.

Could and elephant paint from its own creativity? maybe but unlikely
Gorilla and chimps can paint creatively. elephants might be able to is allowed although studies on elephants in zoos show elephants do not have much desire to paint. elephants are not as visually oriented as apes, so creative painting may not hold enough attraction to do so, even if they could. But that is not what we are seeing in the video.
Is the elephant in the video painting creatively? No
The painting elephants are trained to paint line for line, stroke for stroke. the elephants in question always paint the same picture every time. the training to paint itself is not abusive, but the training to get the elephant to submit to training generally is abusive. Desmond Morris, a well known ethologist, (animal behavioral scientist) went to observe this personally and up close which requires special permission (link below). He noted that each animals always paints the same picture and the trainer is likely guiding the elephant with taps and tugs on the ear. so this is not a creative exercise but a trained response like a dancing bear or counting horse.
https://www.bbc.co.uk/sounds/play/p049jfky

In 1980 or so an elephant named Ruby exhibited some destructive behavioral problems. She was provided with finger paints and started to spontaneously generate art. It was abstract but once when a fire occurred within sight of her enclosure she created a painting which displayed colors like red and yellow -- it was suggested that the uniforms and color of the truck inspired this.
So the answer is yes - however, I do not think any elephant has yet to do actual drawings as seen by human-guided or memorized paintings -- but the fact that however produced such drawings can be made suggests that perhaps some elephant could independently make representational drawings.
In the wild, elephants have been observed making scratches in the dust and perhaps there is some utility in this -- maybe when a herd of elephants is embarking on a trek to find food or water they are communicating the route, maybe even discussing alternatives. Given that bees communicate via their dance paths to flowers or other food source (and this has been extensive documented) why is it impossible that elephants do something similar?


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Is this some kind of crane fly?
I found this insect inside my house in Austria and it looked like some kind of wasp-moth to me. It is quite large with about 3 cm in lenght (excluding legs).
I looked up various images of crane flies here but couldn't find one that resembled the one I photographed, especially with those antennas and wasp-like imitation of the lower back.
Can someone help me identifying this insect and also tell me if it can bite or sting?

Looks like something in Ctenophora (true crane flies), potentially Ctenophora ornata? They're found in Europe and appear to have similar wing and body coloring, as well as the large antennae:

Image from Wikimedia commons, by Jean-Marc Liotier
I don't believe crane flies sting, but I am not an entomologist, so I defer to the experts on that point (and the species ID as well).

No, they definately cannot sting, since they are flies (i’ve no stinger). Crane flies cannot bite either, so harmless and the coloration is only for show and mimicry.

source: Stack Exchange

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

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Why doesn’t heart have smooth muscle tissues?
Smooth muscle tissues are involuntary. And so is cardiac muscle tissue. So why doesn’t heart have smooth muscle tissues like most organs?
I know that they are visually different (branched vs non-branched, striated vs non-striated) but how does that affect the heart?

Striated muscle contraction is synchronized by the structure at the individual fiber level, this also produces a lot more force. They also have a faster recovery time than smooth muscle. Presumably the heart needs that higher power, synchronization, and/or quick response to pump blood under high pressure. I would put money on synchronization at the individual fiber level being the main factor, but I could find no definitive study, possibly because the effects can't easily be separated.
https://journals.physiology.org/doi/full/10.1152/advan.00152.2018
https://www.ncbi.nlm.nih.gov/books/NBK526125/

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


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Why is it possible to render fat if it's in cells?
To the casual onlooker, fat seems like a mass of yellow-white material, composed of lipids. Biologically speaking however, rather than being a large mass, it's actually divided among countless cells, each of which is composed chiefly of lipids stored in vacuoles, in addition to a few other organelles. In essence, while it looks like a giant mass, akin to a big pile of coconut oil, it's practically more like a big pile of sandwich baggies, each filled with coconut oil, and a small amount of rice for good measure.
Yet when rendered, fat melts as if the cells and structure didn't exist, and many food animals are bred to have fat that melts at slightly above body temperature. These two models, the pile of coconut oil, and the pile of baggies of coconut oil, seem to conflict when it comes to expected behavior. For the latter to act like the former, the cells would have to be broken down, but I wouldn't expect cell membranes to rupture at just above body temperature.
So my mental model is badly predicting reality. Where is it wrong?

"many food animals are bred to have fat that melts at slightly above body temperature" - can you cite this?

Melting point of the fat is not the same as rendering temperature.

@bryankrause Apparently rather than being just above body temperature, it’s below, and now I’m even more confused

Interesting question connecting biology and industrial processes! Re: " it's practically more like a big pile of sandwich baggies, each filled with coconut oil," I think a better analogy would be soap bubbles rather than baggies. The phospholipid membranes (which also contain a lot of lipids) are not physically robust. The general descriptions of the rendering process indicate a main goal is to remove the water; the remaining material is fats and a proteinaceous meal. Without water, the membranes should all go away as you won't be able to maintain the bilayer anymore.

@TheEnvironmentalist I would say Armand's comment just before yours should explain the confusion.


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Is there a name for the natural law that any population of a species will increase until it utilizes all available resources in the area it inhabits?
A squirrel population in a forest will only be as big as the available food source allows, and probably a little smaller after you account for predators, disease, etc. What is the name of the tendency of a species to multiply until it reaches terminal population?
Sort of like how when you drop a tennis ball from a building, gravity will only accelerate its fall so much until wind resistance counteracts it. This results in the ball reaching a constant velocity, known as “terminal velocity” in physics.
Similar to the phrase “evolutionary niche”, but not really involved with evolution.

Malthus is the fellow usually credited with the idea of exponential population growth: that a population unchecked by resource limitations will grow proportional to its own size. He was particularly concerned by the catastrophe that would occur when this growth would lead a population to exceed the ability to support itself.
Later, Verhulst came up with the idea of logistic growth. The logistic function approximates exponential growth when populations are small, but eventually growth slows as it gets closer to some capacity. If you think just in terms of food, this would represent members of a population having more and more trouble finding the limited food supplies as it gets closer to the limits.
I would simply call the scenario you describe "logistic growth". It's a fairly common "null hypothesis" on which other models can be built.
Accounting for predators is a bit more complicated, but you could see the Lotka-Volterra equations as a starting point.

the term closest to "terminal population" is probably "carrying capacity" ( https://en.wikipedia.org/wiki/Carrying_capacity ) though that's a property of a particular environment rather than a species within it.


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Can vaccines drive viruses to evolve? If so, how?
Obviously, destroying vaccine-vulnerable strains of a virus will leave the vaccine-resistant ones to represent an increased fraction of the overall viral population.  I'm asking, though, whether/how vaccination can allow a particular strain of a given virus to reproduce more than it would do without vaccination against another strain of the same virus, or to infect more hosts than it would infect without such vaccination.
If only vaccine-vulnerable strain A exists, might application of an anti-A vaccine somehow directly cause the mutation that creates resistant strain B?  If so, how?  Or are such mutations only random (in which case strain B might randomly arise even if the vaccine it was resistant to was never even invented)?
If strain A and strain B both already exist before any vaccine is developed, and then strain A is perfectly eradicated by a vaccine that strain B happens to perfectly resist, then of course strain B will remain - but will it actually benefit, in the sense of becoming able to increase its own population or its host population beyond what the respective count would have been without the anti-A vaccine?  If so, by what mechanism?

Mutations are random.  Also, I think it would help clarify your question if you considered whether you are interested in virus "benefit" as absolute number of virus particles vs. percentage of total virus particles, particles in one individual vs. in a population, and at one point in time vs. dynamic change over time. Finally, "vaccine-vulnerable" is not yes/no, but a dynamic continuum involving many factors and portions of the virus lifecycle.

"absolute number of virus particles vs. percentage" - this should be clear already. "particles in one individual vs. in a population" - in a population (of potential and actual hosts), unless the other option is highly relevant in a way I'm not aware of. "at one point in time vs. dynamic change" - whatever is most relevant. I don't know much about this; that's why I'm asking. "'vaccine-vulnerable' is not yes/no" - in my A-and-B example it is, for the sake of simplicity. In reality: One case in which vulnerability of any sort helped a less-vulnerable mutant would suffice to answer the question.

Antibodies/serum escape mutants are better studied (in-vitro and mice). Usually one escape mutation is not enough, the virus must accumulate 10 of these to be "resistant" and if each of these 10 mutations would have occurred anyway, the combination of the 10 would have been very unlikely without the selective pressure of the serum, making the 1st mutation rapidly fixed, then the 2nd and so on, with the neutralization by the serum decaying a bit each time. Change of selective pressure: some deleterious mutations becomes fit and conversely.

@reuns "the combination of the 10 would have been very unlikely without the selective pressure of the serum," - but why? How is the pressure exerted? If the mutations are random (meaning vaccination doesn't encourage or cause them), then vaccination shouldn't directly make that combo of 10 more or less likely to arise. Does it allow that rare mutant to flourish and become common by vanquishing the competition that would normally have kept the mutant in check? But in that case, HOW do viruses compete? Or is there some mechanism for application of pressure other than competition among viruses?

Isn't it obvious? Mutation 1 is likely to arise without selective pressure but it will likely stay at a very low frequency and eventually disappear, with the selective pressure its frequency rapidly increases which gives a lot of chances for mutation 2 to appear in the background of mutation 1, and so on, the fit mutations accumulate. This process works as soon as the vaccine/serum pressure is not too high, so that the virus doesn't get extinct before finding the good combos of mutations. It's easier to study in lab with antibodies cocktail, decreasing the titer until the virus can proliferate

@reuns "but it will likely stay at a very low frequency and eventually disappear," - why? How?  THAT is my entire question here.  If it can rapidly increase without the unmutated virus around, then why couldn't it do so with that original virus still around?  Would the original virus hold it back?  If so, how? If it does so, then yes, the rest seems obvious.

Because the virus with the mutation replicates better, it evades the Ab a bit. This mutation will often be not fit without the Ab.

In what way does the presence of antibodies it can evade a bit help it to reproduce more than it would without any of those antibodies to have to evade at all?

OK, if you insist on the vaccine vulnerability being yes/no, then you've essentially got a situation where A and B are totally unrelated viruses. Here's a real-world situation:
Let's call A "COVID" and B "RSV". Before we had a COVID vaccine and during the lockdowns, RSV (respiratory syncytial virus), had dropped to very low levels because little kids were not mingling and transmitting it due to the school shut-downs, etc. This allowed the pool of non-RSV-exposed kids to grow and become a larger fraction of the population than normal. Once COVID vaccines began to be administered, society began to re-open and just recently, mid-2021, there have been many RSV outbreaks, with larger numbers of symptomatic individuals than typical, and more serious cases than normal.
In thinking about what you wrote a bit more, it seems like your "benefit to B from a vaccine against A" would require:

Infection with A at least partially protects against later infection with B.
The Anti-A vaccine provides less protection against infection with B than does previous infection with A.
The Anti-A vaccine reduces the number of people who are infected with A before being exposed to B.

Items 1) and 3) together mean that the anti-A vaccine reduces the number of people infected with A, thus reducing the number of people at least partially protected against B because of earlier infection with A. (1) and (3) seem plausible to me.
However, the "benefit" for B would then require (2), that the anti-A vaccine provides less protection against B than does earlier infection with A.  That is, those people who now are not infected by A would have less protection against B even after vaccination.
Although theoretically possible, this seems quite implausible to me, given the real-world data we've seen over the past year. What tests have been done seem to show that the Moderna and Pfizer vaccines provide better protection against variants than does previous infection with another variant.


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Do same DNA sequences lead to the same proteins in all organisms?
I'm not a biologist, but I am curious about a particular question about DNA.
As I understand DNA encodes proteins using special sequences of nucleotides and cells decode these proteins from DNA during cell division. My question is whether all organisms on earth have the same "decoding scheme" for DNA? Meaning that given a particular nucleotide sequence, will all organisms produce the same protein or some organisms evolved a different "decoding apparatus" that will produce some different protein?

The decoding scheme that you refer to is called the Genetic Code. Your question is answered on this list here. Your understanding is incorrect in certain instances. It is mRNA — not DNA — that is decoded, and this occurs all the time, and not particularly at cell division. These latter aspects of your question are very basic, which is why you really need to read the relevant chapters on transcription and translation in a text book.

Aside from the genetic code itself, "post translational modification" can affect protein sequence and structure. Here's a brief overview: https://www.thermofisher.com/us/en/home/life-science/protein-biology/protein-biology-learning-center/protein-biology-resource-library/pierce-protein-methods/overview-post-translational-modification.html


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What is role of centriole in the formation of microtubule during cell divison?
I was learning about the centriole from different sources , and a common misconception I had was that centriole forms spindle fibres but the reality is very different.

Gamma Tubulin protein found in pericentriolar material serves as a
anchor for formation of Microtubule,

So my question is
What is the function of centrioles( two barrel shaped structure perpendicular to each other) in the formation of microtubule? Is it gives support to the pericentriolar material thoughts its appendages? As we can see it is not involved in microtubule formation
photo

What is the function of centrioles( two barrel-shaped structure perpendicular to each other) in the formation of microtubules?
Let's clear your basics first, Centrioles have no function in the formation of microtubules. Why ??
Because, Structurally, centrioles are made up of microtubules.
Even this paper states

At the core of most centrioles is a microtubule scaffold formed from a radial array of nine triplet microtubules.
The triplet microtubules define the cylindrical barrel of centrioles and basal bodies. The triplets are at a small angle off the
circumference giving the centrioles the look of a turbine.

Eukaryotic centrioles consist of 9 triplet microtubules arranged in a particular spatial arrangement. Each microtubule has 3 tubules ie., A-, B- & C-tubules. That's even visible in the image you provided in the question.

Each tubule is a protofilament ie, a chain of 13-16 tubulin subunits. Each subunit is a heterodimer of α-tubulin and β-tubulin molecules. The overall tubulin structure can differ from species to species based on the tubulin genes they encode for. Many species also have γ-, δ-, and ε-tubulin encoding genes.
The same tubulin proteins are also found in structures of cilia, flagella, and basal bodies.

REFERENCES

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4113101/pdf/rstb20130457.pdf
https://www.ncbi.nlm.nih.gov/books/NBK21580/
Molecular Cell Biology (Lodish et.al), Eighth Edition

So centriole is just a scaffold of centrosome nothing more???

Apart from centriole, centrosome also contains pericentrin, ninein and gamma tubulin molecules as pericentriolar material. So I won't say, centriole is just a scaffold of centrosome.


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Can you please help me identifying these parasite (eggs?) on rose?
My aunt today saw the following objects on roses in her garden

and asked what it is but nobody could tell her yet, but it seems to be some kind of parasite or some caterpillar eggs.
As you can see, they differ in size since they appear in larger groups, but each egg (I call it so since I have no better name) has a diameter of about 1 cm. On the outside, there are red spikes.
Loaction is Germany.
Would be great if someone could tell me what this is and whether it should be removed from the roses.
Thanks in advance

Please insert the pictures into your post rather than links.

Looks like galls; growths of the plant in reaction to an irritant. Generally not necessary to remove them.

These are not eggs, they are rose leaf galls caused by the spiny rose gall wasp (Diplolepis bicolor) larva that encases itself inside the gall and then matures and chews a hole in the gall to escape in spring, laying its eggs on a newly emerged leaf bud. The larvae generate the gall in the fresh leaves, perpetuating the cycle.
Remove the galls in late summer or winter if you want to get rid of the larvae. Personally, I like them, so I would leave them. New larvae will generate new galls, but they will usually only be a few each year.


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How does the shape of a protein determine its function?
There is currently much interest in protein folding and the problems in predicting how the sequence of amino acids determines how proteins fold into specific shapes. Accounts of this generally mention in passing that the shape of a protein determines its function.
How, in fact, does the shape of a protein determine its function?
And, looking at the other side of the coin, is it possible to predict how a protein will behave and function merely from its structure? If so, how?

Welcome to SE Biology. Unfortunately your question is very basic and shows no effort of having researched the question yourself as required here. There are whole books written on this topic, but you can find many sources by Googling.

@David Tahnk you. maybe you could give me an example of an article or book which explains HOW the shape of a protein determine its function. I Have been googling for hours. Asking here is my last resort. Also I am using the phone which is a bit limiting or slow. Looking forward for an answer if you have time?

OK, the problem is that there are detailed chapters in texts on different proteins with various functions from which students gain an appreciation of how composition determines structure and structure determines function. Perhaps I can come up with a brief summary with references to examples, but you need to understand the basic chemical properties of amino acids to get anywhere.

Perhaps review this to start? https://www.khanacademy.org/science/biology/macromolecules/proteins-and-amino-acids/v/introduction-to-amino-acids

@David That sounds great! Looking forward to read it. I am sure it will be beneficial, not only for me but for the community :)

Determining function and predicting function are two separate things. For example, a screwdriver's shape determines its function, but it might be hard to predict that function unless you also see some screws.
There are obviously a zillion different other molecules a protein might interact with, so just from its shape one probably couldn't tell much. However, we normally also have other information about the protein.  To start with, the amino acid sequence gives us information about what other proteins are related by evolution; smaller parts of the sequence may include known functional motifs.
Also, experimental work may indicate other molecules that physically interact with the protein, and we may then be able to identify if a part of the protein "matches up" with part of another known molecule (this is the "lock and key" idea). Genetic analysis may show that changes in the protein tend to affect a certain function, and so forth.

+1 Thanks for your answer!

Scope of this answer
As with any machine or useful artefact, the structures (including shape and surface chemo-electrical properties) of proteins determine their ability to fulfil the functions they perform. This relationship (and the way in which the structure arises from the amino acid composition and sequence) is illustrated in any textbook on biochemistry, which typically devote whole chapters to individual proteins. That, paradoxically, makes it difficult for the naïve student to obtain an overall perspective of the topic before going into more detail. This is the purpose of my answer, which is illustrative rather than exhaustive, and merely provides links to detailed accounts of different proteins. I shall use Berg et al. Biochemistry at NCBI Bookshelf for all my examples.
I shall not deal with prediction of function from structure. That is covered in another answer.
DIFFERENT FUNCTIONS
It seems to me best to start with functions and then indicate the general structural aspects, followed by detailed structural features that can accomplish such functions.
1. Acting as fibres
The spider’s web, the maiden’s flowing locks, the athlete’s muscles all constitute and depend on the properties of fibres which are protein in nature. All share the shape of having an extended chain. Each differs in how the chains are constituted, and with what other proteins it might interact (e.g. to give muscle its contractile properties).
Berg et al. include Fibrinogen as an example of fibre formation.
2. Binding of small molecules in an aqueous environment
Many proteins have a function that involves binding small molecules in an aqueous cellular environment. To do this they need to be folded into a roughly globular shape with a surface that renders them soluble in water, and they need to have a specific binding site for the molecule — an indentation in the surface of the correct shape and electrical charge. Examples of such proteins are those that bind oxygen (e.g. myoglobin and haemoglobin), antigens (immunoglobulins) and steroid hormones (soluble receptors). These proteins differ in which molecules they can bind (the binding site is specific) and differ in what events follow (are triggered or are possible) following binding. These latter are determined in a more or less obvious way by other aspects of the proteins structure. For example in the case of immunoglobulins which have two arms, the possibility of cross-linking to form larger aggregates occurs.
Berg et al. have a short introductory section on myoglobin and extensive treatment of haemoglobin, which shows how its subunit structure allows its function to be fine-tuned.
3. Binding of small molecules at the membrane
This is analogous to 2, above, but here the overall structure is partly hydrophobic, so that part of the protein can interact with and be embedded in the membrane. In this case the binding of a molecule (hormone, agonist) generally causes a change in shape, allowing interactions with other molecules or catalytic function, transmitting a signal across the membrane.
Berg et al. have quite an extensive section on an abundant class of membrane receptors.
4. Transporting molecules across membranes
Cell membranes are impermeable to polar molecules and special channels are needed to allow their passage. For a protein to be able to act as a membrane channel it needs to fold so that it has hydrophobic exterior interacting with the membrane, and (simplistically) a polar ‘hole’ through the middle, tailored to the specific molecule it will transport. The types of channel vary, but there are a set of common designs, some of which (such as porin channels) are more easily recognized visually than others (e.g. calcium ion channels).
Berg et al. consider the system involved in pumping calcium across membranes.
5. Catalysis
The largest category of proteins is enzymes — the proteins that catalyse the chemical reactions that allow life to occur. Although these are generally globular in shape, they have specific binding sites for the reacting molecules (substrates) — like the binding proteins. However, in addition, there are generally strategically positioned specific amino acid side-chains that actually participate in the reaction, often providing a pathway with a lower energy barrier. Families of enzymes exist with such similar reaction mechanisms, but working on different molecules (e.g. the digestive enzymes trypsin and chymotrypsin).
Berg et al. section 9.1 considers structure–function aspects of serine proteases such as trypsin.


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ID request - small green caterpillar
This was eating my mustard spinach (Brassica rapa subsp. nipposinica) plant in Washington state, USA; about 1cm in length.

That's a really beautiful photo! Can I ask how you got it on such a pure white background and yet the hairs show up so nicely?

@uhoh Thanks! I spent quite a lot of time editing the image: used various masks to select non-green and almost white things and make them white.

I don’t know the exact species but he is a type of inchworm.

I was going to say Pieris (cabbage white), but those aren't "inchworms".

I went to images.bing.com and typed Brassica pest lepidoptera, which led immediately to photos of the cabbage looper (Trichoplusia ni)
I thought this image was particularly persuasive.

Nicely done, I don't know how I missed it.

Found it using the terms "inchworm species washington" in google.
It is the Winter Moth (Operophtera brumata). This is a common species of invasive pest in the USA and Canada, introduced from Europe. It is an "inchworm" or "looper" as they are known colloquially. The caterpillars have yellowish rings on the body at the segments and longitudinal white stripes.

I don't think this is Operophtera brumata. The host plant is different, the time of year is different, coloration/marks are different.

@SergiiDymchenko - I agree; see Mike Serfas's answer, looks like the right one.


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Methods of investigating the occurrence of non-standard bases in nucleic acids
Recently the popular scientific press gave considerable publicity to three publications in Science (30th April 2021 — see below) relating to the substitution of the nucleic acid base, 2-amino adenine, for adenine in certain bacterial viruses (bacteriophages). For example Quantum Magazine:

DNA Has Four Bases. Some Viruses Swap in a Fifth.
A few decades ago, researchers found viruses that had swapped one of the four bases in their DNA for a novel fifth one. Now, in a trio of papers published in Science in April, three teams have identified dozens of other viruses that make this substitution, as well as the mechanisms that make it possible. The discoveries raise the thought-provoking possibility that this kind of fundamental genomic change could be much more widespread and important in biology than anyone imagined.

I am interested in (and my question is) how this was established experimentally, and how widespread it is in nature, but find the original papers too technical for the non-specialist. Is it possible to provide a summary explaining this, and in general terms how one would search for nucleic acid analogues in organisms?
Original Science Papers
These are listed below, with an extract from the summary of each, where I have difficulty with the technical terminology.

A third purine biosynthetic pathway encoded by aminoadenine-based viral DNA genomes “We show that S-2L and Vibrio phage PhiVC8 encode a third purine pathway catalyzed by PurZ, a distant paralog of succinoadenylate synthase (PurA), the enzyme condensing aspartate and inosylate in the adenine pathway.”
A widespread pathway for substitution of adenine by diaminopurine in phage genomes “We identified dozens of globally widespread phages harboring such enzymes, and we further verified the Z genome in one of these phages, Acinetobacter phage SH-Ab 15497, by using liquid chromatography with ultraviolet and mass spectrometry.”
Noncanonical DNA polymerization by aminoadenine-based siphoviruses “Congruent phylogenetic clustering of the polymerases and biosynthesis enzymes suggests that aminoadenine has propagated in DNA alongside adenine since archaic stages of evolution.”

If posted an answer now. It's not short, but I've tried to make it intelligible and to address the points in the question. However I have not attempted to explain the sentences word by word. The language is technical and I thought it better to indicate what each paper claimed to have achieved and the evidence for the claims.

General approach to identifying non-standard bases in organisms

Purify from source material with standard separation methods
Identify using chemical methods and comparison with known compounds
Establish the biochemical pathway for synthesis etc. — the specific reaction(s) required to produce (and handle) the compound and the enzymes responsible for catalysing these reactions.
Identify the genes for any new enzymes identified
Search the Genbank nucleic acid database for similar groups of genes in other organisms.

Notes
1 and 2. Modern methods can detect molecules in small quantities in impure mixtures
3 and 4. Often done in concert. Genes in a small viral genomes may suggest possibilities.
5. If one wishes to work on a different organism, it is then necessary to establish that the genes do encode enzymes that catalyse the synthesis of the base.
In general, a knowledge of chemistry is much more important than biology in being able to carry out this sort of work.
SPECIFIC EXAMPLE FOR BACTERIOPHAGES SUBSTITUTING 2-AMINOADENINE FOR ADENINE
1. Purification
In this case purification is relatively easy. One can physically separate the phage particles on the basis of size etc., and then extract the DNA from the protein using standard chemical separations and break it up (hydrolyse) into individual components including bases. This was first reported in 1977 in Nature by Kirnos et al..

Cyanophage S-2L was isolated from water samples taken in the outskirts
of Leningrad. It can lyse blue-green algae Synechococcus sp. 698 and
S. eloniatus strains 58 and 6907 … The phage was grown on S. sp. 698
and concentrated by chromatography on DEAE-cellulose (Whatman DE-32)
and purified by centrifugation in CsCl gradient.

2. Identification
Classically a chemist would analyse the atomic constituents and their ratio in an unknown molecule, perform partial degradation to produce known constituents, deduce a possible structure and attempt to synthesize to confirm this. The ease of identifying unknown molecules has increased over the years as the number of already identified compounds with which one can compare has increased (there had been much work done on minor bases found in transfer RNA) and the methods available have grown and become more discriminating. It is interesting that the cyanophage work was done in the former Soviet Union, where biological sciences were low in prestige and funding. Standard equipment for examining the spectral properties of compounds (the light or other electromagnetic radiation emitted or absorbed on excitation of particular chemical bonds) would be available, however. The conclusion that an unknown base was present in the DNA of this phage was almost certainly serendipitous, resulting from standard analysis of the purity of the DNA by simple spectrophotometry. (Protein contamination results in absorption at 260nm.)
There were unusual features in the spectrophotometric properties, and even more marked changes when analysis was performed by the method of circular dichroism. As 2-aminoadenine was among the base analogues that had already been described and characterized, establishing that this was the base in the phage DNA that was present instead of adenine was possible by comparison of their physical chemical behaviour.
I find it ironic, in the context of the recent publicity, that this report (which was accompanied by a more extensive paper in the journal, Virology) received little attention in the subsequent 43 years.
3. and 4. Biochemical Pathway and Genes
The first of the triplet of recent Science papers established the pathway for the synthesis of the dZTP (where Z is 2-aminoadenine) that is the precursor for DNA synthesis, the DNA polymerase enzyme that was needed to handle this modified base, and an enzyme dATPase that removed the normal DNA precursor, dATP.

It also established that four of the genes that encoded these proteins are encoded by the phage genome. The strategy by which this was accomplished is worth presenting as it has been used in other circumstances to identify the genes for particular reactions. The general logic is:

Enzymes to perform reactions not carried out by the host are likely
to be coded by the phage.
We expect a new phage enzyme to arise from the acquisition of a host
enzyme that performs the required reaction, but on a different
substrate (reacting molecule) which we know can quite easily mutate
to bind a different molecule and hence give a different product.
(Change its substrate specificity.)
Families of enzymes that catalyse the same reaction share
recognizable structural features, so we can identify candidates in
the phage genome for the reaction of interest by conceptual
translation into protein.
We can then attempt to test our putative candidate by expression and
biochemical assay and by observing the effects of deletion or other
genetic manipulation.

The summary sentence for the first paper indicates that in this case they found a gene in the phage related in this way to host gene purA. The host gene catalysed a reaction of the same chemical type as the one required, but reacted with normal purines (hence the Pur) in standard pathway, and they were subsequently able to establish that the product of the phage gene  (which they named purZ) catalysed the reaction in the pathway above. A comparison of the chemistry is shown below.

5. Identification in other organisms
One could, of course, search for 2-aminoadenine by purifying DNA from other phages (in 1977 this would have been the only option) and the authors of the recent paper did this in one case (the summary of their second paper) but they also employed the much faster
general strategy of searching the phage genome sequences deposited in Genbank for genes similar to purZ (and the other three mentioned). This is aided by the grouping (clustering) of the genes of interest — an additional indication that they work together. This clustering is not always the same, but the diagram below shows the similarities between several phages and how this gives one confidence of the presence of the pathway in phages other than S-2L.

How ancient is this evolutionarily?
The last paper is concerned with the question of when this base change occurred in evolutionary time. The general strategy is to consider a phylogenetic tree of phages — which is generally assumed to reflect the phylogeny of their host bacteria. The diagram shows an imaginary simplified phylogenetic relationship. 1. Indicates the current species at the right, with their divergence from each other at various periods in the past on the left. 2. Represents the identification of phages in which the base changes are currently found by red balls, so that in 3. by colouring the branches in red we can deduce at what point in the past the enzyme system for producing and using the modified base arose.

The third paper, in effect does this sort of thing and finds that this indicates that the 2-aminoadenine:

…has been used as an information carrier among siphoviruses since the
evolutionary divergence of actinobacteria, cyanobacteria, and
proteobacteria ~3.5 billion years ago.

Does this occur in bacteria?
This cluster of genes has not been reported in any bacteria (and you can be sure that the authors of the three Science papers looked), although one cannot exclude that this change has happened in some unstudied bacteria. However it is unlikely to be occur in known bacteria because of the rationale for its existence in phages. Bacteria have a system to combat phages called the restriction/modification system. They encode specific restriction endonucleases that cleave at specific sites in the DNA (generally 4-6 base pseudo-palindromes) and protect their own DNA by methylating bases in these sites. It was established in the 1980s that the substitution of 2-aminoadenine for adenine in phage S-2L renders its DNA resistant to many restriction endonucleases — i.e. this is a viral response to the bacterial defence system.

+1 I am relieved to see that I will (with some effort) be able to understand this thorough answer. Thanks!

I know comments aren't meant for this kind of thing, but thank you David for yet another fantastic and informative answer


text:
Should fat calories' numerical values be increased to better reflect the new scientific findings?
According to a study discussed on this website, people lose more weight on a calorie restricted fat reduced diet than on a similar calorie restricted carb reduced diet.

Is this study a fair dinkum, non-bogus study?
If so, shouldn't fat calories' numerical values be increased to better reflect the new scientific findings?
And if so, how should this be done?

Because the calories of food are not estimated with a dice but with a calorimeter.

@Chris. That is the present way of doing it. In light of new scientific evidences, isn't it time for an overhaul of the method? Or are you saying that this study is false?

I am not saying the study is false, but a certain amount of food has a measurable amount of calories. This will not change because a social construct demands changing it.

I’m voting to close this question because it is about the articulation of dietary advice, rather than a problem in biology.

@David. A calorie is “the amount of heat needed to raise the temperature of 1 kilogram of water from 0 to 1 degree Celsius”. There seems to be contention between chemistry and biology here. Maybe it is time to distinguish between dietary calories and calories in general.

That single definition is fine as heat is a form of energy. The digestion of food involves oxidation of molecules but the energy released by this is not only in the form of heat but also chemical energy that can be used to build new large molecules including, but not exclusively, fat, or mechanical energy to do muscle work. The new molecules synthesised will depend to some extent on the constitution of the food — what small units it is broken down to. So although calorific value may be a general indicator of whether a foodstuff will make you put on weight it cannot be an exact measure.

It should be pointed out that the study doesn't conclude that "people lose more weight on a calorie restricted fat reduced diet than on a similar calorie restricted carb reduced diet." More like, some people in study lost more weight. But a study sample size of 19 without a non-intervention control group isn't nearly enough evidence to make inferences about the human population as a whole.

@MikeyC It is also an extremely short study of what is supposed to be a long-term effect (to be of any practical relevance).

Calories is a unit of energy, which cannot be changed. The efficiency of using the energy coming in different forms is however different. The original article in which the study was reported points out that indeed the matter at stake is the balance between the fat consumed and the fat burned:

The most sensitive method for detecting the rate of body fat change requires calculating daily fat balance as the difference between fat intake and net fat oxidation (i.e., fat oxidation minus de novo lipogenesis) measured by indirect calorimetry while residing in a metabolic chamber. At the end of the diet periods, our study had a minimum detectable difference in daily fat balance of 220 kcal/day (or 23 g/day) and the cumulative fat loss had a minimum detectable difference of 110 g. The observed differences in fat balance and cumulative body fat loss between RC and RF diets were substantially larger than these values and were statistically significant. While the fat balance method does not determine the anatomical location of lost fat, decreased adipose tissue triglyceride likely makes up the majority. Any additional loss of ectopic fat from liver or skeletal muscle would likely be even more beneficial.

What makes me personally skeptical is comparing the fat intake with net fat oxidation, since the former does not really replace the latter. It is better to say that carbohydrates are used more efficiently, i.e., they satisfy energetic needs of the organism better than the fatty foods, and hence the energy shortage that needs to be replenished at the expense of burning the fat stocked in the body is lower, and the weight loss os lower.
This could be modeled by the simplest energy balance equation:
$$
\frac{d M(t)}{dt} = \alpha E - \beta M^{3/4},
$$
where $M(t)$ is the body mass measured in the energy units, $E$ is the energy intake (in calories), $\alpha$ is the efficiency of energy extraction, and the last term describes the energy expenditure due to metabolism, according to the Kleiber's law.
The equilibrium solution of this equation is
$$
M=\left(\frac{\alpha E}{\beta}\right)^{\frac{4}{3}}
$$
Now, if we assume that $\alpha_{fat} < \alpha_{carb}$, the fatty foods should result in lower body mass, provided the same energy intake $E$.
In principle, one could label foods by the effective caloric content relative to that of pure fat, that is by value $\alpha_{food}E/\alpha_{fat}$.
Remark:

since the argument in the comments is about the meaning of calories, let me also point out that calories defined as "the amount of heat needed to raise the temperature of 1 kilogram of water from 0 to 1 degree Celsius" are actually kilo-calories - a rather common misuse of this word.
I also agree with the comments pointing out the shortcomings of the study in question: the small sample size and its short duration.


text:
difference between biotic and living?
how  can we differentiate between biotic and living things,is  there any difference? and same for abiotic and non-living?
I think it is that biotic is like biomass and living should carry out life processes.

Have you tried googling dictionary definition of biotic/abiotic?

biotic: relating to or resulting from living things, especially in their ecological relations (Oxford)

While there may be a field-specific connotation that I'm not aware of, I've never heard "biotic" as a category of "things" before. I am most familiar with it's use in the context of ecology, e.g. a parasite might be a biotic factor in the survival of a population of animals in a particular ecosystem.
To get to the heart of your question, I don't think there is a difference, but rather a relation: biotic factors refer to currently or formerly living things (and abiotic refers to things that are or were not alive).

But don't you think that a dead animalis non-living but still biotic facor.

Fair point, I edited my answer to make it hopefully clearer. The main point is that "biotic" and "living" are not two categories to compare; but that "biotic" refers to factors relating to or originating from "living things".


text:
Interpreting replicator dynamic for simplest population model
Suppose the simplest population model where we track the size $y$ of a population:
$$\frac{dy}{dt} = ry$$
for a positive constant $r$ and some $y$ such that $y(0) > 0$.
For this population model there is a corresponding "replicator dynamic" model defined by
$$x_0 := \frac{1}{1+y}$$
$$x_1 := \frac{y}{1+y}$$
These are supposed to model "frequencies" of different variants in a population,
QUESTION
except its not clear to me what the different variants here. There is only a single species here so of course it is 100% of its own population or 100% of all populations being modeled here, so I feel that I must be misunderstanding what the "frequencies" of the replicator dynamic are. Can someone clarify what $x_0$ and $x_1$ correspond to here? Thank you!

The transformation carried here is a particular type of the more general one. As the linked text notes:

The continuous replicator equation on n types is equivalent to the Generalized Lotka–Volterra equation in n − 1 dimensions.

In the case described in the OP the number of types is $n=2$, although "Lotka-Volterra" is a bit too generous a term for the simple model in case.
So indeed an extra species is being added here with a zero growth rate. The advantage is that one can now talk about the relative fitness and otherwise use the rich theory developed for the fixed-size populations, since $x_0+x_1=1$ whereas $y$ may grow without limit. E.g., a lot of such intuition comes from the familiarity with Wright-Fisher and Moran models.

Thank you! Why is that needed for the replicator dynamic? I'm interested in using the replicator dynamic to prove ESS (obviously not in this model, instead suppose there are two populations $y_1$ and $y_1$ with growth rates $r_1$ and $r_2$ respectively, suppose $r_1 > r_2 > 0$ and I want to prove $y_1$ is an ESS), does the dummy population help for that somehow?

@John_Krampf one wants the total population to normalize to $1$. If one has two populations, $y_1$ and $y_2$, one could construct $x_1=y_1/(y_1+y_2)$ and $x_2=y_2/(y_1+y_2)$, but this would behave bad when both populations vanish. So $1$ is a kind of pseudocount here. But I must warn, that I am not a game theorist.


text:
What is this Japanese study of the Pfizer vaccine measuring?
https://www.pmda.go.jp/drugs/2021/P20210212001/672212000_30300AMX00231_I100_1.pdf
If you put it into google translate, the abstract contains the following:

"In the biodistribution test, luciferase RNA-encapsulated LNP was intramuscularly administered to BALB / c mice. theAs a result, the expression of luciferase was observed at the administration site, and the expression level was lower than that in the liver.Was also recognized. Expression at the administration site of luciferase was observed from 6 hours after administration, and 9 days after administration.Disappeared. Expression in the liver was also observed 6 hours after administration and disappeared by 48 hours after administration. Also,Intramuscular administration of radiolabeled LNP encapsulating luciferase RNA to rats to quantify biodistributionUpon evaluation, the radioactivity concentration was the highest at the administration site. Liver is highest except at the administration siteIt was good (up to 18% of the dose)."

Another translation (via DeepL) of the first part of the same paragraph:

In the biodistribution study, luciferase RNA-encapsulated LNP was administered intramuscularly to BALB/c mice, and the expression of luciferase was observed at the site of administration, and also in the liver, although at a lower level.
The expression of luciferase at the site of administration was observed from 6 hours post-dose and disappeared by 9 days post-dose.
The luciferase was also observed in the liver at 6 hours post-dose and disappeared by 48 hours post-dose.

Does this mean that they tracked the actual distribution of the vaccine in the body of the rats, or was it just a study of the lipid byproducts?

Since they are using luciferase, which emits light I would guess direct observation.

Would this study be a reliable measure of the distribution of the spike protein throughout the body? Or no?

Note the DeepL translation says expression was lower in liver while GoogTrans says the opposite.  The length of expression, though, they agree was shorter in the liver.

There are at least three types of studies being described.  In a paragraph before the quoted one, they talk about testing for the PEGylated lipids ALC-0315 and ALC-0159 in plasma, liver, urine, and feces. The lipids rapidly moved from the blood to the liver, and were found in the feces; none were detected in the urine.
The other two kinds of studies are described in the quoted paragraph.  One studied the protein product produced by the animal's cells from the administered mRNA coding for luciferase.  The cell product is detected by the light it emits.  The luciferase was detected both at the site of injection and in the liver, and continued being detected at the injection site for much longer.
The last study was of the same kind of mRNA nanoparticles, except that these were radioactively labeled.  The radioactivity from them was detected at the injection site and in the liver.  This indicates there were nanoparticles (or the radioactive components of them) present in both places.
So they tracked the lipids, and either the whole vaccine nanoparticles or some other component of them, but also, and most significantly, they tracked the animal's cellular product of the vaccine's mRNA (luciferase, standing in for the true vaccine's spike protein).

Thanks. When we see the data from Radiolabeled [Cholesteryl-1,2-3H(N)]-Cholesteryl Hexadecyl Ether, are we tracking just the nano-particles, and the luciferase is tracking where the spike protein would have expressed? Are the two correlated or not? This is a major sticking point as to what was being measured.

Since it's a lipid envelope component that was radiolabeled, that test tracks that part of the envelope, whether or not the nanoparticle remains intact. The luciferase measures a quite a different thing, a protein constructed by the animal following instructions of the mRNA. They would be correlated only in that both lipid and mRNA entered as parts of the nanoparticles.  They go their separate ways.

It looks like they're using the luciferase RNA as a substitute for the actual mRNA used in the vaccine because, since luciferase emits light when exposed to its substrate, it's easy to measure the expression and it's commonly used as a reporter for gene expression in many contexts. As far as I can tell, they seem to be using the same LNP formulation as the real vaccine, the only difference is the luciferase RNA substituted for the spike one. Unless there's a difference in how luciferase protein is expressed compared with spike (this seems unlikely to me), this experiment probably accurately reflects where spike is expressed after vaccination.
[disclaimer: I do not speak Japanese, and am answering with a great deal of assistance from Google Translate]

I have people telling me with absolute conviction that this study is only a study of where the lipid byproducts end up -- you're saying it is NOT that and is a genuine bio-distribution study of where the vaccine is delivered?

@sakurashinken As far as I can tell there is only luciferase RNA included, no luciferase protein. So, the only way they'd get luciferase activity would be if the thing they are injecting is getting RNA into cells that are then translating it into protein. So it's a measure of "if we deliver mRNA this way, where are the cells that end up translating that mRNA". It's a different mRNA than that which produces the viral spikes, but the presumption they make is that the delivery vehicle is what matters for distribution, not the identity of the transcript.

Thank you for the clarification.


text:
Kansas Spider Identification
I live in Kansas (Pottawatomie County), and I found a spider crawling on a wall inside my bedroom:

I'm inclined to keep the spider in my house, but I just want to double check to see if it is venomous or dangerous.
The spider is approximately 3~4 cm long in size, and seemed to be in dark (possibly brownish) color. I saw it crawling on the walls once in the afternoon. And this time I saw it crawling at 10pm.
It doesn't appear to be a widow spider so I was a bit relieved. But could you please tell me what is the name of this spider species? And would it be dangerous to keep this creature in my house?
Thank you very much for your help!

That...looks like a brown recluse spider. The picture is a bit dark so I'm not 100% sure, but they can be identified by a violin-shaped marking on their back. Apparently they are very common in homes Kansas.

Illinois Department of Public Health
They are nocturnal:

Brown recluse spiders are mostly nocturnal, coming out at night to hunt for their insect prey. - TAMU

Assuming my ID is correct, they are venomous. Here are links to three government agency or university pages (hopefully reliable sources) on brown recluse spider control:

Illinois Department of Public Health
Kansas State University
Texas A&M

Thank you so much for your help!

I agree with Luigi - that is a Brown Recluse Spider (if you lighten the image, you can clearly see the diagnostic violin marking; that, plus the Recluse shape, size, legs and habits make me certain that this is what you have, even without seeing the eyes clearly).  By the way, this is an adult male, which is why you noticed it - right now, these guys are wandering around looking for love instead of hiding in some quiet, undisturbed area snacking on cockroaches and other delicious insects.
While these spiders are generally inoffensive, the venom is unpleasant in effect, and may rarely cause significant health effects.  In this case, I would consider calling in a pest control service, although you're in an area where Recluses are pretty common. You might also want to get used to taking some precautions like shaking out your shoes in the morning, laying down sticky traps around the bedroom walls and under the bed frame legs, etc.  I know that many people live their lives in close proximity to Recluses without problems, but once in a while unfortunate things can happen.


text:
Middle European Spider Identification
Yesterday I've encountered the pictured spider in my home in Austria, Europe. The colors are pretty accurate in the picture, the head was striped brown/beige and black, the legs were multicolored with a subtle pattern and the back relatively black.

The body had a length of around 2.5 cm, with legs extended the spider occupied an area roughly the same as a circle with a diameter of 5 cm.
After catching it with a glass it repeatedly lifted its front legs and whole body, but after some time calmed down, pulled the legs towards the body and lowered the body to the ground, kind of like as it was lying down.
My inital research led me to the conclusion that it might be a Tegenaria atrica. Is this correct?

I wouldn't think Tegenaria; this looks like a Wolf Spider.  Unfortunately, I'm not a European Wolf Spider guy, so here are a couple of sites that might help you get an ID:  https://ednieuw.home.xs4all.nl/Spiders/spidhome.htm  http://www.jorgenlissner.dk/default.aspx

@JohnRobinson: Thanks for the excellent links, I am also inclined to think it might be some genera of wolf spider after consulting the pages.

This is a wolf spider.
It is not Tegenaria because you would see long spinnerets at the back end of the abdomen, and the legs would not have splotchy black marks, but instead have bands of dark annulations throughout the length of the legs.
Zooming in, you can see the lycosidae eyes that are diagnostic of wolf spiders. These are the two eyes that are on top of the head.
The two dark bands down the carapace are common in a number of genera of wolf spiders, but the faint radial lines that can be seen within the dark bands and the dark eye-shaped mark in the centre of the abdomen is reminiscent of the Hogna genus (although it can be found in other Wolf spider genera as well).
Here is a gallery of Hogna for you to compare:
https://bugguide.net/node/view/3381/bgimage?from=72
Unfortunately, distributions of the Lycosidae genera are hard to describe in Europe because the jurisdictional countries are relatively small geographic areas. But we can use iNaturalist to look at the user-submitted photos (and community-decided Identifications) of Wolf spiders in Austria here: https://inaturalist.ca/observations?place_id=8057&subview=map&taxon_id=47416&view=species
and it shows that the most common wolf spiders seen and identified there is Hogna radiata.
And here is a gallery of user-submitted photos of Hogna radiata observed in Austria:
https://inaturalist.ca/observations?place_id=8057&taxon_id=326871

Wow, thanks for the extensive information and the links!


text:
If a small population left one continent and sailed to another, would the genes of the population that left show relation to the original population?
This question has a specific context, a religious one, and so I'm not sure this is the right place to ask, but I can't think of a better place. I would like as objective and unbiased an answer as possible. I hope the religious context doesn't make this an unsuitable question. I'll explain the religious context:
There is a religion that believes that a small number of Jews left Israel circa 600BC and sailed to the Americas, where they multiplied and built their own new civilization(s). This religious organization also has a history of teaching Native Americans that they are the descendants of this population, so therefore that their ancestors are Jews from 600BC.
But we're quite lucky in the modern age that we can do genetic testing! And they have done, and of course they've found no signs of a genetic relationship between any Native American tribes and any known Israeli or Jewish populations. The organizations response to this is that, after 2600 years, you wouldn't expect any genetic similarities between the two populations - if they've been physically separated for so long, all genetic markers of a relationship would have disappeared.
Is that correct? Would 2600 years be enough time to erase all genetic evidence that this population originated from Israel Jewish people?

Related: isolation by distance

You may be interested in recent research about migration between Polynesia and South America 800 years ago that left a genetic signal. It's only a fraction of your time span but still. The New York Times had reported about it.

Related: Genetic history of indigenous peoples of the Americas and Haplogroup

If we assume a population of 100 individuals migrated from the Middle East to Central America 2600 years ago and, even if they underwent admixture from the local population, then there would be extremely clear genetic signal that those individuals were from the Middle East and not 'native' to Central America. Native Americans and individuals from the Middle East are sufficiently diverged that they are easily distinguished from one another.
For example, you could plot all the populations on a Principle Component Analysis and the migrants from the Middle East would cluster with other Middle East populations and not Native Americans. The fact that 2600 years had passed since the migration event doesn't change this. In the context of distinguishing between populations, that amount of time doesn't erase genetic differences.
A very similar event to what you mention has been shown to have occured when migrants from Persia moved to India with their Zoroastrian religion, forming the Parsee community in India. Clearly Middle East and Native Americans are much less genetically similar to one another than Indians and Iranians, so it would be similarly much easier to disinguish them genetically.

That's a fascinating example about Zoroastrians! Thank you.

I've marked this as the answer, but I want to note that the answer of @RogerVadim below  also gives reasons to be skeptical of the idea that any genetic tests of Native Americans would necessarily conclusively prove that they are not Jewish (or at least Middle Eastern) of origin.

I think it would be more accurate to say “migrants from Persia moved to India with their Zoroastrian religion, forming the Parsee community in India“ rather than “… forming the Zoroastrian religion [in India]”. The Zoroastrian religion originated before this migration, probably in Persia.

@KrazyGlew thanks - edited.

@TKoL I’m afraid that your takeaway from the other answer isn’t correct: the evidence is, in fact, pretty damning. I think both you and I may have misunderstood the other answer; alternatively, the other answer is flat out wrong. Either way, it’s pretty misleading.

@TKoL KonradRudolph is correct. Comparing the genome of the religious group to i) Native Americans and ii) Middle Easterners (either ancient or modern DNA) would conclusively and unambiguously show whether the individuals were local or not.

@user438383 I'm curious what you make of this article then: Nearly one-third of Native American genes come from west Eurasian people linked to the Middle East and Europe, rather than entirely from East Asians as previously thought, according to a newly sequenced genome.

That article does show a genetic link to the Middle East, however it potentially still contradicts the LDS story, since the path to the Americas was via Siberia and presumably the Bering Strait. I'm not sure if that makes this evidence for or against the LDS origin story...

@Tkol Native Americans may derive ancestry from those sources, but they are still entirely distinguishable from the sources based on their unique combination of alleles.

@user438383 derive ancestry from those sources would be sufficient for LDS purposes. They've remained (deliberately) unclear if they believe ALL native americans are exclusively descended from from this group of Israelites, or if there may have been other Natives in the Americas prior to the events in the LDS holy book.

@KonradRudolph I don't see the contradiction between the two answers. On the one hand, the genetic signal would be unambiguous in such conditions, as this answer states. On the other hand, genetic signal is not sufficient for proving the point in the OP, since we do not have many genomes directly available form the 2600 ago, and comparison will be indirect, likely relying on non-genetic evidence. It is a problem of scientific study design.

@RogerVadim You don’t need a genome from 2600 years ago to perform comparative genetics. Phylogenies are routinely established based on comparison of leaf genomes, without the presence of ancient genomes.

@RogerVadim we do have ancient DNA from Caanites - only a single sample would really be necessary to show whether the Native Americans were/weren't related to it.

'@KonradRudolph interesting. How do you add geographic metainformation to your phylogeny? What do you use for time labeling? I suggest that we take a context more familiar to you - ancient British island population from 2600 years ago, instead of Israelites.

@user438383 Canaanites is one of many ethnic/cultural groups that populated the region - I doubt that comparison with Canaanite genome proves much. Note that Jews even in those times included such ethnically diverse groups as Ethiopians and Yemeni, from Sabaean kingdom.

From the point of view of genome comparison the signature would be unmistakable, as @user438383 has pointed out in their answer. There may be however other methodological issues undermining this study:

Scientific - one need an attested representative of a Jewish genome from 2600 ago or their attested ancestors
Political/religious - genetic testing is not recognized as a valid proof of Jewishness/non-Jewishness by Jewish communities (see, e.g., here)

While the scientific issue that I mention might not seem as much of a problem, the experinece shows otherwise. E.g., the highly controversial hypothesis of the Khazar ancestry of the Ashkenazi Jews has been a subject of much debate, with many studies both proving and disproving it. Khazars were a people and an Empire to the South of (modern) Russia that were an important political power throughout a few centuries. They are known to have converted to Judaism (or at least their elites). However, as this culture had vanished about fifteen hundred years ago, one cannot attest which people are descendants of Khazars and what genetic signal is an evidence of such a descent. Affirming or disproving this hypothesis is thus dependent on what is taken as a Khazar genome, and arbitrariness of such a choice produces equally arbitrary results.

Update
This is to bring precision regarding some of the remarks made in comments.

Firstly, to quote the OP:

Would 2600 years be enough time to erase all genetic evidence that this population originated from Israel Jewish people?

To summarize my answer in more plain terms:

[..] comparing two genomes proves nothing, if one cannot attest their origin. Jewishness issue was mentioned in passing, as a kind of things that a scientist needs to take into account, when posing an answerable research question.

In more expanded terms, as requested by the author of the OP themselves:

This would not prove that they are Jewish, since there were many other peoples present in the region at the time. 2) Over the two-and-a-half thousand years the region has been subject to many mass migrations (note that this is a land bridge between Europe, Asia and Africa), so it would be likely controversial and dependent more on historical than genetic evidence. Each can have his/her own point of view, but proving something beyond any doubt is next to impossible.

Finally, discussing "what/who is Jewish" would take us far away from biology, since it involves intertwined religious, ethnic, cultural, and historical aspects. The only reason to mention this in this context, is that a scientific question should avoid such complex and ambiguous notions, since they may render it unanswerable.

Update 2
Seeing the number of up- and down-votes to my answer, as well as the comments, I would like to add a bit more rigorous discussion regarding the difficulties involved in such a study. There are three points that one needs to address:

Do genomes of relatives separated by 2600 years still resemble each other?
What are the genomes that one needs to compare?
What does the positive/negative results of such a comparison proves

Point 1. is easiest to answer: yes. One could do a back-of-the-envelope calculation that 2600 years is about 100 generations, which means about the same number of new mutations in a 3 billion nucleotides long human genome. Recombination poses a greater challenge, but we still expect to be able to compare chunks of genome of tens or even hundred thousand nucleotides long. This perhaps already answers the OP, and this is why they accepted the answer by @user438383
Point 2 can be addressed in (at least) two ways:

Proxy genome @user438383 pointed out that a Canaanite genome is available. If we do find the similarities between this genome and those of our target group, this counts as a result. But if we don't, it again proves nothing, since the ancestors in question could be from a very different ethnic group. Note that we are talking here about a land bridge between Africa and Eurasia, through which the ancestors of most of the non-African human populations passed at least once.
Phylogenetic reconstruction @KonradRudolph mentioned phylogenetic reconstruction, but didn't elaborate. To implement such an approach we will need to

sample genomes from the populations that we believe to descend from the Middle East

build a time-labeled phylogenetic tree, to prove that the most recent common ancestor is located somewhere around 600 BC.

Prove that this common ancestor actually comes from the Middle East

Point 3
A correctly posed scientific question of this type should not make any reference about Jews and should not draw any conclusions about them. Doing so is just bad science. Indeed, Jews is a complex term that may refer to

certain ethnic groups (more than one) - vision widespread due to some sad historical events
religion - anyone can become a Jew by converting to Judaism, and such conversions are known to have happened on a large scale - e.g., the Sabaean kingdom, occupying a part of Arabian peninsula (modern Yemen) and parts of modern Ethiopia is known to have practiced Judaism, and some of their descendants in the region are continuing to do so till these days.
Cultural, political, and other attributions (e.g., Soviet Jews had it written in their passport, even if being non-religious and having rather remote Jewish ancestry.)

It also has a more direct bearing on our question, since it doe snot allow us to attest the ethnicity of the founders of the community in question, nor do the members of thsi community need to be descendants of its founders.

Comments are not for extended discussion; this conversation has been moved to chat.

A good answer, but wouldn't it be sufficient to prove that no admixture has occurred to the Native American gene pool of any group from the larger group of Middle Eastern populations? Jews, however they are defined, were part of that larger group, after all.

@j4nd3r53n One cannot say reliably that one has sampled all the groups. One could prove the converse, that the population in question has common ancestors with some populations that are attested to have lived in the Middle East. I see several possible study designs here, but I don't want to be more specific than the OP. Jews is that the word has multiple meanings: ethnic, religious, cultural, historical - e.g., one can become a Jew by converting to Judaism, but oen can also be a Jew by birth while being non-religious. This word shouldn't be a part of the research question in my opinion.

Molecular Phylogenetics
You may have seen a "tree of life" image like this:

While this particular image only shows amphibians, such trees have been constructed for more or less every known species, using the morphological and genetic information available to us.  The field responsible for studying and constructing such trees is called molecular phylogenetics, and it is predicated on the idea that such a tree may be uniquely constructed with nothing more than the genome of each species.
Although we certainly do not have genomes for every species in history (or even every extant species), it is believed that the "tree of life" is a single tree.  That is, there are no "disconnected" subtrees which have no relation to the rest of the tree.  The notion of a group of organisms which descended from some ancestor, and then became so isolated as to "erase all genetic evidence" of their relationship would imply that some subtree exists which cannot be connected to an ancestor node on the full tree.
It's Possible
Now, we need to be careful here.  It is possible for two groups to only appear genetically related by a common ancestor which is older than their real common ancestor.  For instance, suppose we have that group A begets group B begets group C.  We want to know if C is really descended from B.  It may be the case that, based on the molecular record, we can only say that B and C are both descended from A, because B is only modestly different from A, and C has changed all those differences, even though it was actually descended from B.  So, I would say that it is theoretically possible.
Reality
However, there are a large number of "ancestry-informative markers" (AIMs) which allow us to determine from which continent a person's ancestors most likely originate.  For a given individual genome, we can say with decent confidence whether their ancestors came from Europe/Asia or the Americas.  Note that there are no concerns about populations which might have "bred out" all of their AIMs to confound a determination of their "ancestral continent(s)".  Perhaps that's because some AIMs have 100+ markers which would need to disappear in just a few hundred generations (the most extreme example would be a 13-year generation, which would give 200 generations over 2600 years).  AIMs are far too stable to simply disappear at a rate of nearly 1 per generation (if they did, then we couldn't reliably use them to determine ancestry in the first place).
Now, if we look at the specific example of a central Asian population seeding the Amerindian population, we have the problem that Amerindians are most closely related to northeast Asians (Siberians, in particular).  If Amerindians were really established by Jews, why don't they have strong matches to the Middle Eastern markers common among Jews?  So this claim fails in both directions: First Nations peoples are not genetically similar to any recognized/acknowledged Jewish population, but are similar to the north/east Asian population which almost certainly crossed the Bering land bridge after the end of the last ice age.  So much for Atlantic canoes... (or did the Jews take the long way around, travelling through Asia and Siberia to the Americas?)


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Has anyone tried the petri dish experiment with and without mask but at the side?
There are quite a few videos and experiments online that show the benefits of wearing a mask by holding a petri dish in front of their face while talking, singing, coughing etc., once with a mask and once without a mask. However, I have realised that while wearing a mask, despite the mask doing a good job blocking water droplets in the front, a lot of my breath (i.e. water droplets) goes to the sides of the mask.
Given that authorities are saying that the virus is airborne, I would think that the water droplets that come out of the side of the mask matter as well, especially in an enclosed room where many people would be spending their day. Has there been anyone who has put the petri dish at the side and did the same test as mentioned earlier? I can't seem to find any, but then again, my researching skills are not the best.

I’m voting to close this question because it is not about a problem in biology but appears to be an attempt to start a discussion.

@David Where would you suggest I ask this question then? I'm not looking to start a discussion. I'm asking if it had been tried before. I'm curious, in what way is this question attempting to start a discussion?

I have no idea where you should post your question. All I can say is that this is a Question and Answer site about problems in Biology as made very clear in the [Tour] and Help on asking questions. This is the SE model and what makes SE distinct and valuable.

A properly-fitting mask should not have any breath/droplets leaking out the sides of the mask.

@Armand While that is true, what percentage of the population would/is actually wear/wearing a properly fitting mask? (rhetorical qn) A large number of people either wear surgical masks, which have huge gaps at the sides or cloth masks, which don't fit the face exactly.

Properly-sized surgical masks seem to have huge gaps at the sides, but are intended to seal against the cheek inboard of those gaps, not at the side edges of the mask. I added another paper in the comments of Luigi's answer.

While I'm not sure about the petri dish experiment, I will answer the main question I think you're asking: how important is the air that escapes out of the sides/top of the mask?
This question is answered with really cool visuals in this paper: Visualizing the effectiveness of face masks in obstructing respiratory jets. While the main point of the paper aims to test the effectiveness of different masks in blocking coughs, you can see the trajectory of all the air (including the air coming out of the side). This example here shows a labelled diagram of air moving through and around through a folded handkerchief mask:

Fig 3b
Looking at both the homestitched (top) and commercial masks (bottom) below, you can see that there isn't much leakage around the mask, and the leakage that does happen out of the top of the mask appears to stay close to the cougher:

My interpretation is that the leakage around the mask is likely much less of a risk, since it probably is not moving as rapidly as air expelled directly out of the mouth--since the leaking air has already bounced off the mask, it does not get as far away from the person breathing/coughing. So, while stuff may escape out of the side/top, it doesn't get very far (hence the synergy of social distancing plus masking).

Here's another recent article on mask leakage effects: Cappa, C.D., Asadi, S., Barreda, S. et al. Expiratory aerosol particle escape from surgical masks due to imperfect sealing. Sci Rep 11, 12110 (2021). https://doi.org/10.1038/s41598-021-91487-7


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Meaning of ‘motif’ in molecular biology
I would like to understand the meaning of the term motif as used in molecular biology.
In an article in Nature Biotechnology, Patrik D’haeseleer states:

Sequence motifs are short, recurring patterns in DNA that are presumed to have a biological function. Often they indicate sequence-specific binding sites for proteins such as nucleases and transcription factors (TF).

Does this mean that in the DNA sequence of a gene there are recurring patterns/subsequences of DNA which are presumed to have a biological function? If so, can such motifs be found simply by using a software that detects recurrent substring in a string?
In relation to the biological function of such motifs, I would like clarification of this extract from
a paper by Williams et al.:

P. furiosus ORF PF1193 displayed up to 12-fold increase in mRNA level at 20 min following irradiation (Table S1). PF1193 contains a ferritin-like di-iron motif found in ferritin- and Dps-like proteins and bacterioferritins and was found to belong to a new subclass of ferritin-like di-iron carboxylate superfamily (Ramsay et al. 2006; Tatur et al. 2005).

By “motif”, do the authors mean that the gene PF1193 has a subsequence which is found many times in the DNA sequence of the gene that encodes ferritin- and Dps-like proteins, and that this may indicate that they (genes and the related proteins encoded) have similar characteristics/properties?
How does this relate to the sentence in the extract from the Nature Biotechnology paper?

Often they indicate sequence-specific binding sites for proteins such as nucleases and transcription factors (TF).

They certainly mean a not too bad alignment, you should blast (the AA of) your protein or some parts of it to see how good it is.

In the excerpt from your linked paper, "motif" is referring to a protein sequence pattern as opposed to a DNA sequence pattern.

@reuns does AA stand for Amino Acids? I have "Blasted" the protein and I have found some similarities with the Ferritin-like protein of Pleurocapsa (and other DNA protection protein of other bacteria). Then I aligned the DNA sequence of the PF1193 gene and the DNA sequence of the gene that encodes Ferritin-like protein of Pleurocapsa and found similarities also there...

I have edited your question so that it conforms to English scientific style. I have changed biology to molecular biology as ornithologists would understand something quite different by motif.  I simplified the very last part because I could not understand what you were trying to say. You will see how the question is now more compact and readable.  Please note that in referring to published papers, the statements therein should be attributed to the authors and not to the journal. Only attribute opinions to journals when they appear in editorials.

@David thank you .

@David thank you very much ! I would really like to fully understand the questions of my post that you have italicized .

Meaning of Motif in Molecular Biology
In English the word, motif (borrowed from the French), has a variety of meanings in different areas. The one that is borrowed in molecular biology is that of pattern together with a hint, perhaps, of emblem or badge.
The word pattern indicates both repetition and a master mould from which copies are made. In molecular biology this indicates that this is not unique, it occurs repeatedly. The word emblem suggests a means of identifying the group to which something belongs. In molecular biology it is associated with a shared function for members of the group.
Types of Motif in Molecular Biology
Here the word motif is applied mainly to the three related macromolecules, DNA, RNA and protein. All of these are linear chains of restricted varieties of defined components (four nucleotides, 20 amino acids) arranged in defined ways which we refer to the sequence of the macromolecule. Within the overall sequence there can be sub-sequences, which, if they repeat represent patterns, and which may have functional significance. We refer to such patterns as:

DNA sequence motifs
RNA sequence motifs
Protein (or amino acid)sequence motifs

The first of these is what D’haeseleer is referring to. It should be noted that these sequence motifs can be absolute, or consist of consensus sequences, such as the one for the ROX 1-binding site in the article cited:

However the nucleotides or amino acids are not the only components of macromolecules the arrangement of which can produce a pattern. Motifs in molecular biology can be composed of structural components. This is expressed in the following definition of protein motif:

Protein motifs are small regions of protein three-dimensional
structure or amino acid sequence shared among different proteins. They
are recognizable regions of protein structure that may (or may not) be
defined by a unique chemical or biological function.

And a similar definition that considers only structural motifs in proteins adds: “An example… is a helix-turn-helix motif.” This is a motif in certain proteins that bind DNA.
Identifying Sequence Motifs by Computer
The limit of the approach suggested is that statistically one would expect any small sequence pattern to recur in DNA, and the problem is how to tell which recurring patterns have biological significance. It should be realized that is not the sequence motif alone that makes it functional, but the context in which it is found. Thus, a TATA box or other DNA motifs that act as binding sites for transcription factors were discovered (and are differentiated from other random or non-functional occurrences in the genome) by their proximity to the positions where transcription is initiated. Their function was confirmed experimentally, e.g. by binding RNA polymerase to the DNA. (This, I hope, answers the last query about the function of motifs as protein-binding sites.)
So, in general, no. Although I admit that I have personally use computational approaches to discover new small hydrogen-bonded protein motifs (a somewhat specialized area).
The ferritin-like di-iron motif
This is not a DNA sequence motif. It is not even a protein sequence motif, but a structural protein motif. The definition can be found on InterPro:

This entry represents a group of proteins, containing ferritin-like
domain, which is an about 145-residue domain made of a four-helix
bundle surrounding a non-heme, non-sulphur, oxo-bridged diiron site.
The diiron site is contained within a twisted, left-handed four-
helix-bundle constituted of two anti-parallel helix pairs connected
through a left-handed crossover connection.

It is shown here with the helices coloured yellow and the iron atoms red spheres:

[From deMare et al. (1996)]
Footnotes

The helix–turn–helix is also referred to as a domain. The distinction between motif and domain is one of size (note the small in the definition of protein motif). However InterPro does refer to the ferritin-like di-iron pattern as a motif, so this can be regarded as acceptable usage.

One might argue that as the sequence and structure of proteins are specified in the DNA, the motif should also be in the DNA. This is a fallacy. The information is there, but in a cryptic form. The redundancy of the genetic code means that protein sequences are far more conserved than the corresponding DNA sequences, and the three-dimensional structural patterns are not evident from inspecting amino acid sequences.

Thank you very much @David . The situation is more complicated than I thought. But are there some softwares that discover motifs ? Like if I give as input the DNA sequence of the gene and gives me them... I read about "SSR" locator in this forum https://biology.stackexchange.com/questions/38913/how-to-interpret-the-simple-sequence-repeat-ssr-on-the-coding-sequence-but-no

Some software that has implemented the biological context that you need and the experimental evidences (so that it is a sort of "database" of motifs).

Finally, Just to definitely clarify this important point: when you say The word emblem suggests a means of identifying the group to which something belongs. In molecular biology it is associated with a shared function for members of the group. Does it mean that if two genes have in common DNA sequence motif, they share the biological function relative to this motif ?

@Manuella DNA sequence motifs generally relate to recognition by proteins — for binding and perhaps cleavage or chemical modification. We don’t generally talk about the function of the biological function of a DNA motif, and, as I tried to imply, such motifs may be necessary, but not sufficient to initiate transcription. This topic is covered in many reviews of transcription, some of which, no doubt, will have tables of motifs.

@Manuella The prediction angle is more to the fore in proteins, where specific sequence motifs might suggest a protein is tagged for transport to a particular organelle. Thus, sites like SwissProt have databases of particular protein motifs, and allow you to enter a protein sequence to find out what motifs it contains. 3D structure is somewhat different. There have been a number of projects determining the structure of unknown proteins. A putative function is often based on the structural motifs revealed, generally using expertise, although 3D structure comparison software exists.

Ok thank you very much. So DNA sequence motifs generally relate to recognition by proteins... thus I think my initial idea was completely wrong. So a very last question @David to officially confirm that my assumptions were unfortunately nonsense.

By biological function I simply meant that if two genes have a DNA sequence motif in common, maybe their encoded proteins could have some "functional" properties in common... for instance if I consider the gene that encode the Ferritin protein, I know that the Ferritin protein has the capability to avoid the production of free hydroxyl radicals, that can catalyze the oxidative damage of biomolecules, because they can store Iron and avoid Fenton reaction.

So if I consider an other gene that has a subsequence in its DNA gene sequence that is a motif for the gene that encode ferritin protein, can I say that this last gene could encode a protein that has the same nice property of Ferritin protein of storing Iron and avoiding free hydroxyl radicals production ?

One point that I did not emphasize in my answer (which I may include in a later revision) — most DNA sequence motifs fall outside the region of a gene that specifies the amino acid sequence. So if two genes have such a motif in common it implies some sort of similarity in the control of their expression rather than their protein products. I am not a transcription expert, but for example many genes are transcribed in response to interferon and these share motifs — interferon sensitive response elements. However the genes encode many different types of proteins that are needed to fight viruses.

Ok ! @David That was the point that I wanted in really few words... if these motifs are found in the CDS (whose sequence determines the sequence of amino acids in a protein) what happens. Are the encoded proteins similar in their functions ? This discussion made it clear to me that I want to know this.

@Manuela — See Footnote 2. Then it is better to look at the amino acid sequences. Sequence motifs in proteins can indicate function, as in the protein kinases, but can also be transport tags. SwissProt will generally tell you.

Re:

When they say "motif", do they mean that the gene PF1193 has a
subsequence which is found many times in the DNA sequence of the gene
that encodes ferritin- and Dps-like proteins ? And this may involve
that they have similar characteristics/properties ?

Yes, although motif sequences may not be exactly identical, as what really matters is the 3-dimensional structure produced and thus its function (whether binding, enzymatic, or whatever). You can think of them as recognizable functional units, often but not always self-sufficient. For example, a promoter sequence in DNA would be considered a motif, as would be a zinc finger in a protein, as would be a poly-A tail on an mRNA.
A problem in using motif sequences to identify genes of related function is that during evolution, sequences may have changed even as 3-D structure (and function) remain similar. Here's a paper working on that problem from about a decade ago:
J Biol Chem. 2012 Jun 8; 287(24): 20565–20575.
Published online 2012 Apr 25. doi: 10.1074/jbc.M112.367458
PMCID: PMC3370241
PMID: 22535960
"Use of Structural Phylogenetic Networks for Classification of the Ferritin-like Superfamily"

Blast the protein and see if the 1st results are ferritin-like!

Thank you @Armand ! Yes I also read in ncbi that motifs are used as base of proteins classification. But so, since you have confirmed what I wrote (the extract that you reported) at least conceptually , as rough estimate can I find motifs with a Python code that finds recurrent substrings in a string ? (where the string is the DNA sequence of the gene)

This answer is incorrect regarding the ferritin-like di-iron motif cited in the question. This is a protein structure motif, not a DNA motif. Identification of gene families from DNA sequences  is, of course, important, but it is done on the basis of overall sequence similarity, not usually on the basis of particular motifs, and I don't think this is what the poster was asking about in terms of computer analysis. I interpret her question as using computers to discover motifs, rather than identify them in DNA sequences.

@David actually I was particularly interested in identifying motifs in DNA sequences... but yes the answer was lacking of some things .