text:
Do Traits Have to be Adaptive in Order to Survive?
I'm reading Michael Pollan's book 'How to Change Your Mind', which is largely about psychedelic mushrooms. In discussing the biology of the mushrooms, he writes:
'Even if psilocybin in mushrooms began as 'an accident of a metabolic pathway', the fact that it wasn't discarded during the course of the species' evolution suggests it must have offered some benefit.'
I'm wondering if this is actually true. In general, I'm wondering if it is true that traits that do not confer advantage will eventually be weeded out.
Being ignorant of the finer points of evolution/natural selection, I can make arguments both ways. On the one hand, it seems that the intense competition would make investing any resources at all in a trait that was not beneficial a totally losing proposition. Therefore no traits that weren't positively adaptive would survive. On the other hand, there seem to be all kinds of traits that are 'neutral' in fitness terms but which survive anyway. E.g. coccyx, male nipples, appendix, whale legs, etc.
I am not talking about information encoded in the genome, which can be present but not expressed. I am talking about phenotypes, i.e. traits that get expressed in interactions with the environment, such as the psilocybin chemicals in these mushrooms. (Though I suppose unexpressed genetic info could never be selected for or against by natural selection by definition.)
So to put a very fine point on my question: Is it possible/likely that psilocybin mushrooms produce a chemical that happens to engender hallucinations, not because doing so is adaptive, but just incidentally? So that this property would be something like the redness of blood, i.e. not adaptive in itself but just a matter of happenstance?

Possible duplicate of Why do some bad traits evolve, and good ones don't?

Good question. And good analysis. I have little to add! I'll simply provide my own list of thoughts to complement your ideas, which are not mutually exclusive.

The fact that it wasn't discarded during the course of the species'
  evolution suggests it must have offered some benefit.

This statement is speculative. The key word here is suggests. i can think of several speculative scenarios, of course the list is by no means exhaustive:

Traits that are not adaptive can still exist in the organism as vestigial traits. This can be because the trait was recently useful but no more, over evolutionary time scales, and not enough time has passed for the trait to be lost.
The trait may also be floating, i.e. has not been selected against, and acts as a neutral trait. It therefore remains as a phenotype. Traits are theoretically unlikely to float for very long periods of time, as I will describe later.
Some traits can very indirectly affect other traits. In practice it is often difficult to completely describe or understand which traits are a result, or cause, of other traits.
Many traits can also be byproducts of other useful traits. With nipples it might have something to do with early exposure to hormones; developing a way to bypass male nipple formation could be difficult and costly. With psylocibin, it may be a side-effect of a particularly useful biochemistry to the fungus, perhaps metabolic, that is completely unrelated to its neuroactivity in humans. It may be that a biochemical pathway might form psychoactive intermediates or products that are difficult to remove or metabolize, and find themselves in the mushroom co-incidentally.
The trait may simply be very useful, but we don't understand why it is useful. Humans often overlook this possibility; for instance, I assume you have not considered that psylocibin may have unknown effects on non-human or even non-vertebrate life.
I am not an expert but filamentous fungi sometimes/often have very complicated sexual reproductive strategies. Psylocibin may be maintained through sexual selection, rather than natural selection. This is probably far fetched, but hey- we're speculating about our ignorance.
Lastly, but very importantly, all organisms face pressure to survive and replicate. It is expensive to maintain useless features and traits, or to produce excesses, or to overdevelop or harbor chemistry that is not doing anything. Natural selection is ever-active in limiting in which traits are maintained within a population. This I think is the most convincing argument; the principle of economy. This argument fares well in all discussions on biology; life is difficult, and the costs of survival are very important to consider, always. It is expensive to store or maintain constituent chemicals, even if they are not toxic, nor if they have no use for the survival of fungi. It is more economical, and less costly, to lose such traits; selection will favor fungi that save or spend this energy elsewhere. This is a very important point, and I think it is the most salient to understand the quote you provide.

I think it would also be a good idea to study the number of times psylocibin arose. If it occurred ('was invented') multiple times independently, it must have had some functionality for the organism, like wings, or vision. If it occurred only once, one can ask whether the majority of descendant strains has lost it, or whether they maintain the trait. That could also shed some light on whether it is maintained through positive selection. Lastly, psylocibin may be a chemical that allows to explore a very specialist niche of the ecosystem. If few descendant strains contain it, that can mean it is still selected for, though only by fungi that rely on it as a strategy. This would also mean that psilocybin-less fungi would have found no need to maintain it, and may point to the occurrence of negative selection. Hope that makes sense.
Mandatory reading for you on relaxed selection.
tl;dr yes, psylocibin may be maintained by happenstance, though likelier via positive selection, at least in specialist fungi

Also, a trait may be adaptive in some circumstances, but maladaptive in others.  For instance, the sickle cell anemia gene, which protects against malaria (if there is just one copy) but causes serious health problems with two copies, and/or if you live where malaria is not present: https://www.sciencedaily.com/releases/2011/04/110428123931.htm

S Pr lists a number of reasons that might allow non-adaptive traits to spread. One other that's probably important in some populations is "allelic surfing".
If you imagine a smallish population that suddenly expands (say, starlings in the Americas, or humans in the past few thousand years), the original genes are going to expand no matter what - even useless, or mildly harmful, genes will be carried along on the overall success of the rest of the organism. The most obvious example of this is the founder effect, where populations can carry along irrelevant or harmful effects simply because there were very few founders, and some happened to have red hair or Tay-Sachs Disease; but more subtle effects can be seen whenever populations expand.

Several studies have found strikingly different allele frequencies between continents. This has been mainly interpreted as being due to local adaptation. However, demographic factors can generate similar patterns. Namely, allelic surfing during a population range expansion may increase the frequency of alleles in newly colonised areas. ...  We therefore conclude that most of the observed large allele frequency differences between continents result from demography rather than from positive selection.

--Large Allele Frequency Differences between Human Continental Groups are more Likely to have Occurred by Drift During range Expansions than by Selection

... remember that it isn't actually the gene that has the advantage, it is the person who has that gene. Usually the two are linked but not always. ... The difference is that the genes weren't the advantage, the situation was. The frontier people's genes were just in the right place at the right time and so were spread more widely.

--Gene Surfing: The Surprising Genetic Advantage of Being on the Frontier


text:
What is this plant with yellow large fruit?
Found this in a garden in San Francisco. Can't decide if it's pomelo, capri lemon or something else, ideas?

How large are the fruit? It is definitely citrus.

Also, is it fruiting now?  (Mid April.)  It looks rather like a quince, but that fruits in the fall.

@jamesqf - quince have the opposite shape - pear-like; larger at bottom than top, rather than larger at top, smaller at bottom like these ones. Quince also have obtuse, thin paler green leaves, not glossy dark green ovate leaves. Also note spines on stems - definitely citrus.

@bob1: You're welcome to come look at my quince tree next fall :-)  And I don't see any spines on the stems.

@jamesqf - I am well aware of the shape of quince. Check out the ~horizontal branch just below middle of the pic. Look where the stalk of the leaf joins the branch. Also see the branch passing in front of wall on lower right of pic; see the spikes sticking out...

@bob1: There are a number of varieties of quince.  This is the variety I have: https://onegreenworld.com/product/aromatnaya-2/  As you can see, the fruit is not noticably pear-shaped, and the leaves are dark green and glossy.

@jamesqf: {Doyenne du comice] (https://commons.wikimedia.org/wiki/File:Pyrus_communis_%27Doyenn%C3%A9_du_Comice%27.jpg) pear is similar. Turn the quince leaves over and they will be paler and slightly fuzzy, also on a reddish/brown stalk and brown bark cf. green stalks and green young (1-2 year) branches on citrus. Still note the fruit in the picture is smaller at bottom than top - opposite of quince. Actually most of the fruit in the pic are squashed spheres. All of them lack the bracts you see on the bottom of quince

source: Stack Exchange

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

sort: votes


text:
List of proteins by number of amino acids / chain length
Is there any protein database online where I could obtain a list of proteins ordered by the length of their chains / number of amino acids, starting from the shortest, as well as to see their amino acid sequences?
I'd like to start from the short & simple protein structures to see how their particular sequences of amino acids translate into their folding shape, and what those short chains are capable of doing in organisms. (I heard about the LILs, but they are artificially-generated and consist of just two amino acids, Lysine and Isoleucine, so not much variety to study in there :q )
But I'm quite new to these databases, they present a lot of details, but usually not the one I'm looking for, and one has to know what too look for first to get any meaningful information :q

I like this web quite good :)

@aaaaaa: as I said, I'm quite new to those databases, I'm still trying to figure out how to use them. I know some of them, but they don't seem to have any way to list proteins by chain length, starting from the shortest.

@L.Diago: Yup, this one seems nice, especially the pictures ;) And I see there's an option to search by sequence length. Unfortunately, I can only set the minimum and maximum length, but I don't see any way to order the search results by chain length. There's a "residue count", but I'm not sure if it's the same, since I get some weird resuls :q

Have you reviewed the extensive literature on prediction of protein structure? You wouldn't be trying to reinvent the wheel, by any chance?

You can find the data you need in the Protein Data Bank.

Since 1971, the Protein Data Bank archive (PDB) has served as the
  single repository of information about the 3D structures of proteins,
  nucleic acids, and complex assemblies.
The Worldwide PDB (wwPDB) organization manages the PDB archive and
  ensures that the PDB is freely and publicly available to the global
  community.

Each of the PDB member organisations provides the same data with a different interface:

PDBe,
PDBj,
RCSB.

In general, you either query the database through one of the web interfaces, or you download all the data and search it locally. In this case, the RCSB website has the option you asked about (sorting by the residue count):

Alternatively, you could download:
ftp://ftp.wwpdb.org/pub/pdb/derived_data/pdb_seqres.txt
and parse it and sort it as you wish.
This file has sequences of all chains in the PDB entries.
But since your goal is to find the relationship between the sequence and the folded structure, you should probably start from reading about the protein folding problem and about methods used in protein structure prediction.

@SasQ Can you please tune down a bit? You have now three comments flagged and deleted for rudeness, which is not something well liked here. All others: If you want to discuss excessively, please move over to the chat and do not do this in the comments. Thank you.

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

It's worth pointing out that many proteins, and especially "short" ones, are going to be human, computational, or experimental error, or will be intentionally trimmed down from the native version to make it easier to crystallize or otherwise handle. That may not be a problem if considering folding, but relying too much on annotations and descriptions may well be misleading.

In the UniProt Knowledgebase, you can have your proteins sorted by protein length, e.g. in this query for all human proteins with a cross-reference to PDB:
https://www.uniprot.org/uniprot/?query=database%3A(type%3Apdb)%20AND%20organism%3A%22Homo%20sapiens%20(Human)%20%5B9606%5D%22&columns=id%2Centry%20name%2Creviewed%2Cprotein%20names%2Cgenes%2Clength&sort=length
Default sorting is by query score, but if you click on the black triangles in the table headings, e.g. for sequence length, you can have them sorted by other criteria.

I think this answer is better than the PDB one for the question as it was asked, i.e. with no requirement for structures. Firstly, you'll get more data. And secondly, you won't just get proteins that are biased by the composition of the PDB.

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


text:
Could an 150 pound human have flown on the back of some species of pterodactyl (assuming they still existed)?
I'm curious if any type of flying animal that ever existed would have been able to carry your average 150 pound man.

Assuming that the heaviest pterosaurs (Quetzalcoatlus, Hategopteryx) probably weighed around 200 kilograms... No. This extra load would have required a huge amount of extra muscles and the forces acting on the wing bones (which are the distal phalanges of the 4th finger) would be too high.
The biggest bird was Teratornis incredibilis with an estimated weight of around 25 kilograms... This should answer your question.

I assume you mean biggest flight capable bird, given modern ostriches typically reach weights of over 150kg (adult males). In any case, the extinct flighted bird Argentavis is estimated to have weighed in excess of 70kg.

Thanks for adding this! I'm no native speaker... So sorry for my confusing English. You are totally right with Argentavis but even this bird wouldn't carry a human


text:
Are there any open phylogenetic projects that don't require coding to make a contribution
I am stay at home learner, not pursuing education formal education and currently doing a part time job. I've however completed masters in biotechnology and I'm studying to pursue PhD in molecular evolution eventually. I'm interested in knowing if there are any online open projects in phylogenetics and computational molecular evolution where I can contribute. Leave the projects involving coding. So are there such open projects that don't require coding? An example of contribution I can think of right now is submitting new phylogenetic trees. Please help, I can't find any information online.


text:
Results of self-administration study about pain in honeybees?
There research on nih.gov about ability of bees feel pain. But I can't understand their conclusion. Could you provide necessary excerpts here from those study so it would be clear what conclusion they've got ?
And that research was granted by This research was funded by ARC Discovery Grant DP140100914. Does it mean that we shouldn't completely trust it ?

The paper shows that honeybees prefer sucrose (sugar) solution to a sucrose+morphine (pain reducing) solution. They find that injuring the bees (i.e., potentially causing pain) does not change the relative preference for sucrose vs. sucrose+morphine, but they do eat more overall when injured.
They indirectly conclude that because the bees do not seek a pain reliever they may not feel pain of the type that, for example, mammals do. This is not the same as the ability to detect noxious stimuli (nociception), which insects definitely have, it's more about the emotional/behavioral impact. They cite some evidence that morphine could potentially have similar pain-relieving effects in insects as it does in mammals due to changes in behavior caused by morphine, but of course the interpretation of their results depend very strongly on whether this is accurate or not.
ARC is the Australian govt's funding mechanism. They don't have any commercial ties to the results of research so there is no reason to have any skepticism particular to the funding source: everything has to be funded by someone.

Thank you very much. I would mark your answer, but I'm not allowed to.


text:
What is the motivation behind fluorinated pharmaceuticals?
From what little research I've done, it appears that a significant portion of modern psychoactive drugs are fluorinated in one way or another (for example, Buproprion, Fluvoxamine, or any number of other antidepressants).
What is the motivation behind the addition of these groups? My initial guess would be that it either increases blood-brain barrier clearance or reduces the drug's metabolism, but I've been unable to find papers supporting either idea (or papers on the subject at all, for that matter). Any books/papers illuminating the subject would be greatly appreciated.

Fluorine has a combination of unique chemical properties, which makes it very useful in drug design :

It is small, such that replacing a C-H with a C-F is often possible, from a sterical point of view. Halogens, which share some of the other desirable properties of fluorine, are much larger.
It is very electronegative: it will attract electrons strongly, which allow polarising, stabilising or destabilising various moieties.
It is not found in natural products (except for trifluoroacetic acid), which means our metabolising apparatus, result of evolution by exposure to such products, can have difficulty dealing with it: thus ut makes drugs more resistant to degradation.

With these properties, you either start with fluorine in mind, to make  molecules that mimics transition state of reactions involving non-fluorinated compounds (thus, enzyme inhibitors), or mimic the peptide bond (but not cleavable as easily); or you add it later to a compound that already work for additional activity, or less clearance.
There are many good books and reviews, but you could start with this one.


text:
Do the centrioles in the centrosome differ in their angle to one another?
The centrioles in the centrosome are often shown at an orthogonal angle, does this arrangement differ between samples, as in, does the daughter centriole show up in different sides of the mother centriole, or on the distal end rather than the proximal end?


text:
What is the relationship between induction of cell differentiation and DNA methylation status?
This may sound like a broad question to ask, but I am working on interpreting a review article for my epigenetics course and I'm having trouble reconciling two seemingly contradictory things this review is saying.
Ehrlich, M., & Lacey, M. (2013). DNA methylation and differentiation: Silencing, upregulation and modulation of gene expression. Epigenomics, 5(5), 553-568. doi:10.2217/epi.13.43
On page 554,

Constantinides
  et al. found that treatment of an embryonic
  fibroblast cell line with 5-azacytidine (5azaCR),
  an inhibitor of DNA methylation, induces the
  formation of [myotubes] [35].

and

Treatment with DNA demethylating agents
  can not only convert non-myogenic progenitor cells to Mt, but also can induce other cell-
  type interconversions in progenitor cells. For
  example, with 5azaCR treatment, the C2C12
  Mb cell line can be induced to express genes for
  key osteogenic transcription factors as well as
  adipocyte markers [40]. The outcome of DNA
  demethylation treatment is dependent upon the
  cell type as well as the treatment and growth
  conditions [41].

and

The conversion of a multipotent adult stem
  cell to dissimilar differentiation products by
  treatment with DNA demethylating agents
  can be explained by the hypothesis that some
  genomic methylation restricts the differentiation
  potential of progenitor cells [40].

These three quotes, all on the same page, seem to indicate that at the very least, induction of differentiation is contingent on demethylation. More specifically, DNA methylation restricts the possible differentiation activity that a progenitor cell can undergo. However, just a little further down,

Terminal
  differentiation predominantly led to increases
  in DNA methylation and both increases and
  decreases in H3K27me3, depending on the
  gene involved.

and

[...] to
  hypothesize that changing the DNA methylation status of pluripotency genes in vivo is critical to their function [43]. DNA methylation is
  considered a more stable repressive mark than
  repression-associated histone modifications [42].
  The association of differentiation and the loss of
  pluripotency with DNA methylation at previously unmethylated sites (de novo methylation)is consistent with the inability of ESCs to differentiate when Dnmt1, the most abundantly
  expressed DNA methyltransferase gene, is
  homozygously knocked out [44].

I'm working on a presentation on DNA methylation and gene silencing, and I want to make an accurate portrayal of the role of DNA methylation in cell differentiation, and this is only a portion of the whole presentation, so I am not including a lot of data on this topic. However, I want whatever I do present to be self-consistent and accurate. How do I reconcile these two phenomena? From what I can tell, there is no explanation in the intervening text between these passages about how these two phenomena are similar but distinct. Am I accurate in determining that this is a difference between induction of differentiation and terminal methylation status? If so, how is it that ESCs can be differentiated with demethylating agents, but also ESCs have trouble differentiating when Dmnt1, which promotes methylation, is knocked out?

This is a good question. I'm not as steeped in this literature as I'd like, but here is my understanding of the process:
Methylation is one of the key methods by which cell fate is restricted. The review you're reading is giving specific examples of cell lines that are at least partially restricted into cells that are of an entirely different type. Thus de-methylation is a method for de-differentiation, which then allows differentiation along a different line.
Your three examples that it sounds like you're interpreting as induction of differentiation, are actually examples of that effect -- de-differentiation that then allows for differentiation to a different fate. Constantinides work, for example, showed the conversion of a non-myoblast precursor into functional striated muscle cells. Not only can fibroblasts be turned into muscle cells, myoblast cell lines can be made to look like bone cells or fat cells. None of these things would happen without re-programming the cell fate by de-differentiating the cell lines to form dis-similar differentiation products.
This is consistent with other findings about de-methylation in vivo. An important example is the global de-methylation of primordial germ cells, as demonstrated in this figure from the linked review, summarizing the methylation state of the germ line in mice. Pay particular attention to the blue line. The pronucleus of the highly differentiated spermatazoon (along with its highly methylated DNA and histones) undergoes global de-methylation. Its products include the primordial germ cells of the developing mouse, the most de-differentiated state, which, in the case that it is a male, then become methylated as they become primed to differentiate, and then differentiate.

Thank you for your help, I actually found a diagram that answered my question but your comment reinforced my understanding.


text:
Finger Millet ( a.k.a Ragi millet ) for house sparrow
I have a sparrow feeder at home, and im wondering whether Finger Millets are good for the little sparrow's tummy .. ? Looking for advice , thanks !

I'm no expert, but several things come immediately to mind.   First, as you know, small birds like to eat millet, which must seem like fast-food to them.   However, sparrows are ordinarily urban creatures these days, and while they might have forgotten how nice millet is to eat, they'll probably enjoy it too, in sensible quantities.   You might even want to experiment with various seeds to determine just how much; bearing in mind that just because a creature loves a particular food does not mean that it is not also harmful to them.   (Consider the case of sunflower seeds and cancer in white cockatoos; and pizzas in humans).
It's hard to imagine a creature as tough and versatile as a sparrow having any difficulty with such food though.  Don't worry.


text:
Separate DNA fragments with very different size (oligo and lambda-DNA)
I am running a ligation reaction to one of the sticky ends of lambda-DNA.
The oligo for the ligation is 25 bp (10x excess), whereas lambda-DNA is 48 kbp. I would like to recover the lambda-DNA and discard the unreacted excess oligo.
Given their vastly different molecular weights, they should be easy to separate, but I could not find a standard methodology online.
I do not want to run gel and my total sample volume is 0.5 mL. There are some filtration columns that may work, but the input volume is only 25 uL (I have 20 times that).
I don't have to get rid of all the oligo, having slightly more lambda-DNA than oligo at the end would suffice.
Which simple protocol may work in this case?

A spin column might work for your purposes since you can do multiple rounds of binding if your volume is too large to bind in a single pass, but for DNA of that size a lot will be irreversibly stuck to the column.  See for example the protocol for the Monarch® PCR & DNA Cleanup Kit.
Consequently I would recommend just doing an ethanol precipitation, which favors recovery of longer DNA molecules (see for example this protocol).

Nice answer. The Monarch stuff only seems to work for DNA up to 25 kpb (may not work for my 48 kbp). My lambda-DNA didn't seem to go trough the gel filtration column, I may take a look into that ethanol precipitation.


text:
Scorpion in Ohrid, Macedonia, 5cm long

Hi, can u please help to identify what kind of scorpion is this? A friend of mine found it at home, in urban area in Ohrid, Macedonia. It is aroun 5 cm long.
Thank you.

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


text:
What are some examples of animals who return to their group when threatened?
Based on my (limited) understanding, some types of animals use the power of numbers for protection. I assume, then, some species instinctively respond to threat by immediately seeking out and joining their group/hive/pack, not just to hide or get lost within the group (eg., school of fish), but to also take advantage of the power of the organized group (eg., swarm of bees).
Is this correct? If so, what are some examples?
[Note: It is my understanding that bees don't flee to their hive in response to threat, but rather sting and release a pheromone to draw the other bees to the area and create a swarm.]

The specific description you have made is almost the definition of mobbing behaviour. Some animal species protect each other and especially their offspring by cooperatively attacking and harassing a predator. Individuals can't cope with the predator alone, but by working together they increase the chance of discouraging the predator.
African buffaloes, bison, gulls show mobbing behaviour.
Wikipedia article
The Royal Society for the Protection of Birds article

That's a great lead, although mobbing seems to be more like a bee's behavior, which is initially aggressive. I'm curious if there are animals who retreat to the safety and protection of their group prior to being aggressive.

If you're referring to a behavioral pattern consists of "flight-incorporate into group-organise counterattack", there's not a classification for this. These are different behaviors. A baboon or buffalo flights, joins to its group and joins a counterattack which is mobbing. That kind of high level behaviour which there's an organisation of an attack can be only found in wars between groups of same species; e.g., chimpanzees. But I don't think that it's  interpreted as a behavior triggered by a threat; rather it's interpreted as a part of competition. Humans orga

Humans organize attacks on threats after one of them has been attacked by a predator or else, but this counterattack is a decision, not a certain response.

I should clarify. I don't mean a retreat to produce a coordinated attack, but two different responses to a threat depending on whether the organism is alone or in a group. If alone, the organism would retreat to the safety of the group. If in a group, the group itself responds to threat via a "coordinated" attack like mobbing.
I'm guessing this doesn't exist?


text:
Thousands of Reporters Integrated in Parallel (TRIP) barcodes
Has anyone worked with constructing barcodes for TRIP? How does constructing of barcodes work in general? I don't seem to be able to grasp the basics of constructing these barcodes.

From the paper and user manual it seems that barcodes are random sequences of pre-defined length of 16-20bp ± 1bp. On data analysis step they are combined and all barcodes 2 Hamming distance apart (it means that two words have difference in one letter from each other) will be discarded from the list of genuine barcodes.


text:
What's a good reference for learning about recombinant proteins?
I'm looking for books and articles that can bring me up to speed on the design, expression, and purification of mammalian proteins in recombinant systems, both in E. coli and in more complex systems like CHO or Sf9 cells. I have a weak but functional background in general molecular biology.

Hello and welcome to Bio.SE! Take the tour to learn about the site and earn yourself your first badge. Have a nice stay!


text:
Among primates, is it true that homosexual behavior is extremely unnatural and uncommon?
I was recently reading a book published by some anonymous biologist known as Lynn Saxon, in which she appears to want to refute Christopher Ryan's thesis in Sex at Dawn that prior to the invent of agriculture, humans were presumably far more promiscuous and had sex not just for reproductive purposes.
In order to do this, she then goes on to show how, in the animal world, the great majority of all sexual activity is directed only towards reproduction. Another author, David Barash, says similar things: namely, that "evolution is very much about reproduction—variation in reproductive success is evolution".
However, homosexual behavior is anything but reproductive. Saxon appears to suggest indirectly that all such "non-reproductive" behaviors that are "useless from a evolutionary point of view" are rare and unnatural among primates, who are our closest relatives.
One more biologist, known as Antonio Pardo, says:
"Properly speaking, homosexuality does not exist among animals…. For reasons of survival, the reproductive instinct among animals is always directed towards an individual of the opposite sex. Therefore, an animal can never be homosexual as such."
Is this true? Is homosexuality really uncommon and unnatural among our closest relatives who are primates? Is sex mostly for reproduction?

If you feel like John answered, you can click on the checkmark next to his answer as to classify this question as "answered".

regarding sexuality previous to agriculture, tribal sexual practice and culture varies starkly and heterogeneously per tribe, some tribes are hyper sexual, homo, straight, cannibal, nonviolent, sadistic, spiritual, there is great variety in cultures, just see bhutan vs aztec, hawaiian vs european. ... In human history there is the book of the dead from Babylonian times, the epic of Gilgamesh, the 1001 nights, and the Greek cultural documents, which give a lot of information about early historical orgies and homosexuality. Generally, humans tribes are dominantly heterosexual.

First Antonio Pardo is not a biologist, he is a professor of bioethics and his degrees are in medicine and philosophy.
Second, Clearly he does not know anything about primates, since there is one famous great ape that has sex even more often than humans do, the Bonobo. Bonobo have sex for everything, hello, goodby, conflict resolution, social bonding, ect. Bonobo engage in homosexuality and a hundred other sexual practices, including some things humans can't do, like penis fencing. Bonobos along with chimps are also our closest living relative.
As for other animals there are hundreds of examples of homosexuality in nature. I hate using all these wiki links but this is such general biological knowledge I would need either dozens of links or a link to a textbook.
As for Lynn Saxon, first let me say she does not have a degree in anything, It is possible Lynn Saxon is not even her real name.
Now for her argument, it is true that in nature sex is most often directed towards reproduction (that is why it evolved in the first place* and just consider how many sexual animals have very simple behavior), but as I have pointed out there are notable exceptions one of them our closest relative. And not just homosexuality, masturbation is observed in nature as well. Also consider monogamy is also extremely rare in nature with the exception of birds, arguing humans should behave based on how other animals act will not help their argument. It is also a common fallacy, what is natural and what is ethical are not related, Sanitation, science, religion, medicine and reading are also not natural.
If you want to read more about humans and our relatives I suggest the book (the Third chimpanzee" by Jared Diamond as a t least a good starting book.
"Wild Connection" by Jennifer L. Verdolin is even better, both have actual degrees in biology.
*Of course your legs originally evolved as fins,  so what something starts as is not necessarily what it is used for now.

"As for Lynn Saxon, first let me say she does not have a degree in anything, It is possible Lynn Saxon is not even her real name." How do you know that she doesn't have a degree in anything? And yes, OP said: "book published by some anonymous biologist known as Lynn Saxon", so yes, according to OP she is anonymous and it appears not to be her real name.
As for Bonobos being homosexual. It depends on what you mean by homosexual precisely. See my answer that attempts to clarify this point. Other than, I agree with your answer, and I think the answer is good.

Because she hasn't claimed one, and may not have even be using her real name. Degrees and expertise are not something you get the benefit of the doubt on.

No, degrees are something you either have or you don't. I know many people who don't talk about their degrees despite having one. The fact that they don't mention their degrees doesn't mean they don't have one.

talk about is not the same as publish a book on the subject.Sure it is hypothetically possible she has a degree in something, but the default position and only reasonable way to consider her words has to be she does not unless she demonstrates otherwise.

First, let me say that there are vast amounts of criticism toward the book Sex at Dawn by experts on the topic of the evolution of human sexuality, but generally for reasons other than homosexuality. See here. But that's not what you're really asking about.
I believe there is possibly some miscommunication going on here. Some of the statements in the question, I think, are true and makes sense. Some statements are not totally clear, and the answer depends on how exactly they are interpreted. Others are wrong. Let's see.

In order to do this, she then goes on to show how, in the animal world, the great majority of all sexual activity is directed only towards reproduction.

It is possible that this is true statistically. I'm not sure. However, there is certainly many examples of non-reproductive sexual behavior. See the Wikipedia article: Non-reproductive sexual behavior in animals. One obvious example is the Bonobo.

Another author, David Barash, says similar things: namely, that "evolution is very much about reproduction—variation in reproductive success is evolution".

This statement I think is far more reasonable. It is true, in the ultimate sense, that the main purpose of sex is reproduction. And behavior that increases the probability of reproduction is going to be selected for. (Technically, it would be more true to say that natural/sexual selection is about variation in reproductive success. Evolution contains more than selection, for example drift).
However, homosexual behavior can easily arise naturally in the animal kingdom, especially as a side-effect. One way this can happen is the following: feeling pleasure through sexual stimulation is adaptive, because this increases the probability that individuals engage in sexual behavior, which ultimately leads to more offspring. However, as a side-effect of sex being pleasureable, this means that animals may engage in sexual behavior that is non-reproductive (e.g. homosexuality or masturbation).
As long as non-reproductive sexual behavior is not done to the exclusion of reproductive sexual behavior, there is no reason to suspect that the non-reproductive sexual behavior negatively affects reproductive success (and hence, non-reproductive sexual behavior can perfectly well exist).
Despite the original ultimate reason for sexual behavior is to facilitate procreation, sexual behavior may even possibly become adaptive for reasons other than procreation. For example, it may start facilitating social bonding.
This naturally leads to the following problem, when looking at the following quote:

"Properly speaking, homosexuality does not exist among animals…. For reasons of survival, the reproductive instinct among animals is always directed towards an individual of the opposite sex. Therefore, an animal can never be homosexual as such."

When asking whether homosexuality is common in nature, we need to define precisely what we mean by homosexuality. If a human man says that they're homosexual, that can mean several things. It may be that they are attracted to mostly men, or both men and women, or only men. If they are attracted to only men, they are, what I would call, strictly homosexual. If given free choice they would in a majority of situations prefer to have sex with another man, I would call them primarily homosexual. In this sense, our Bonobo male friends are typically neither strictly homosexual or even primarily homosexual, because a male that engages in homosexual behavior is also willing to engage in heterosexual behavior. Strict homosexuality or primary homosexuality does appear to be quite rare in nature (although there are some examples known. For example, in rams a few percent seem to prefer same-sex even when given the choice). In the quote, when they say 'properly speaking' they may be talking about what I have denoted strict homosexuality. The quote is a bit hard to interpret. If they simply mean homosexual behavior, then no, that is not particularly rare.

Is this true? Is homosexuality really uncommon and unnatural among our closest relatives who are primates?

Strict or primary homosexuality is uncommon, homosexual behavior is fairly common (and therefore clearly not extremely unnatural).

Is sex mostly for reproduction?

In the ultimate sense, the original and most important purpose of sex is reproduction. But as I've detailed out, non-reproductive sex can still easily arise without it negatively affecting fitness. It may even possibly become adaptive (if it is not done to the exclusion of reproductive sexual behavior).

I would hesitate to claim what the most common form homosexuality humans engage in without evidence. research shows such forms of homosexuality are actually very rare, https://www.tandfonline.com/doi/abs/10.1080/15299716.2014.929553?scroll=top&needAccess=true&journalCode=wjbi20 and https://yougov.co.uk/news/2015/08/16/half-young-not-heterosexual/

@John I think you misunderstand what I meant. Perhaps I didn't communicate myself properly. I am not saying that the most common non-heterosexual orientation is strict homosexuality. I am saying that when people say that they're homosexual, they tend to prefer only or mostly their own sex. Otherwise, they tend to use another term ("bisexual", "queer", etc). I completely agree that strict homosexuality is not the most common form of non-heterosexual orientation.

@John Nevertheless, it is also not important for my answer whether which type of homosexuality is the most common. My only reason for making the term 'strict homosexuality' is to make the answer more clear, and to adress the fact that some types of non-reproductive sexual behavior exists and are more common than other types. I have edited my answer to remove emphasis of which type is more common (because it is not necessary for my answer).

And again studies show otherwise people do not identify in those ways consistently or reliably, it is a bad assumption to make.  Additionally strict homosexuality is  mostly irrelevant since it is the quoted authors are not defining homosexuality that way.

@John No, what is irrelevant is how common strict homosexuality is. It still is worthy of clarification. If the authors don't define homosexuality that way, then even better that I clarify exactly what I mean with each term. You don't have to go to strict homosexuality, but just preferred sex. If a man in more than 50% of occasions will prefer to have sex with another man rather than a woman given free choice, you could call him 'primarily homosexual.' Primary homosexuality is also not common in the animal kingdom, although as I discussed there is some evidence for it (in rams, in particular).

To make your life easier you could use the kinsey scale. It is a bit oversimplified but it is also heavily used.


text:
Waggle dance in the dark
Karl von Frisch discovered waggle dance [1] as communication system when bees talk about feed resources;
Long story short, using a polar coordinate system, bees dance to reveal flowers to sisters.
My question is simple: how can this be possible since bees are in hives, which are dark?
That is, how can a bee sees its sister dancing in a dark hive?

[1] https://en.wikipedia.org/wiki/Waggle_dance

You may want to look into the evolution of the dance, many of the different stages in its progression still exist, the most primitive form is done in the sunlight. https://www.nature.com/articles/43372

In bees that dance in the dark (not all do, some dance in the light) they don't watch the dance, they participate. The follow the dancer using their antenna and sound to keep track of them.

Beehives are often dark, so instead of watching the scout dance, the recruit bees follow the dancer using their antenna and the sounds produced during the dance to determine the directions to the food source.

https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/waggle-dance#:~:text=The%20dance%20conveys%20information%20about,directions%20to%20the%20food%20source.

I've never caught this detail in many books I read; just another side of this fascinating insect


text:
Where is catalase produced?
I am doing a research project on the peroxisomes, and in it I referenced the enzyme catalase, which breaks down hydrogen peroxide into water and oxygen. However, the assignment asks me to specify the production location of all enzymes, and I cannot find any useful information about where the enzyme is created. I think it is created in the peroxisome itself, but am not so sure of that. Where is catalase produced?

According to this source https://www.ncbi.nlm.nih.gov/books/NBK26858/ , peroxisomes don't have ribosomes. Thus the source of catalase isn't the peroxisome.

According to this source all peroxisomal proteins are synthesized on free ribosomes in the cytosol.


text:
Can Huntington's Disease be homozygous dominant?
Can Huntington's Disease be homozygous dominant? I am not sure whether the individual who is homozygous dominant for Huntington's Disease will survive into adulthood, or die when they are infants or fetuses. I cannot find any good information on that topic.

It's a one gene defect AFAIK.

We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, a quick look at the "Related" links automatically generated next to your post will show you that many Huntington's patients reach adulthood before they show symptoms. For example: this. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site . Thanks!

Yes, but it's relatively rare.
The disease progresses more rapidly in homozygotes than in heterozygotes.1
Reference
1: Ferdinando Squitieri, Cinzia Gellera, Milena Cannella, Caterina Mariotti, Giuliana Cislaghi, David C. Rubinsztein, Elisabeth W. Almqvist, David Turner, Anne‐Catherine Bachoud‐Lévi, Sheila A. Simpson, Martin Delatycki, Vittorio Maglione, Michael R. Hayden, Stefano Di Donato, Homozygosity for CAG mutation in Huntington disease is associated with a more severe clinical course, Brain, Volume 126, Issue 4, April 2003, Pages 946–955, https://doi.org/10.1093/brain/awg077
Sourse: Homozygosity for CAG mutation in Huntington disease is associated with a more severe clinical course; Ferdinando Squitieri et.al. Brain, Volume 126, Issue 4, April 2003, Pages 946–955, https://doi.org/10.1093/brain/awg077

Welcome to Biology.SE! Good job on providing a supporting reference, but in the future please include the complete reference information since links can break. Also, do you have a reference to support the rarity of homozygotes and what that means? Are they less common that would expected for the prevalence of heterozygotes in the population? Underrepresented in the children of two heterozygotes? Thanks!


text:
The average of Ct values in real-time PCR
The Ct value is the number of cycles when the "PCR amplification curve with the horizontal axis as the number of cycles" and the "predetermined threshold" intersect, and is not necessarily an integer value.
Real-time PCR was performed on n series of samples under the same conditions, and the Ct values, ${Ct_1},{Ct_2},\cdots {Ct_n}$, were obtained for each. Then, in many instructions, the average of these Ct values is determined as follows;
$$\bar{Ct}:=\frac{{Ct_1}+{Ct_2}+\cdots +{Ct_n}}{n}\tag{1}$$

My question:
What is the meaning of such an average? How do I justify taking such an average?

The amplification curves are ideally considered to consist of the following when the initial template quantities are ${N}_{1}(0), {N}_{2}(0), \cdots N_{n}(0)$, respectively;
$${N}_{i}(k)={N}_{i}(0){a}^{k}\tag{2}$$
It is my understanding that the Ct value is for calculating ${N}_{i}(0)$ backwards.
Let the threshold value be X, then, for all $i=1,2,\cdots n$,
$$X={N}_{i}(0){a}^{{Ct}_{i}} \tag{3}$$
therefore, for all $i=1,2,\cdots n$,
$$X{a}^{-{Ct}_{i}}={N}_{i}(0) \tag{4}$$
therefore,
$$\bar{{N}(0)}
:=\frac{{N}_{1}(0)+ {N}_{2}(0)+ \cdots + N_{n}(0)}{n}
=X\frac{{a}^{-{Ct}_{1}}+ \cdots + {a}^{-{Ct}_{n}}}{n} \tag{5}$$
therefore, a better Ct average , $Ct_{avg}$ shall satisfy
$$X=\bar{{N}(0)}{a}^{Ct_{avg}} \tag{6}$$
therfore ,
$$X{a}^{-{Ct}_{avg}}=X\frac{{a}^{-{Ct}_{1}}+ \cdots + {a}^{-{Ct}_{n}}}{n} \tag{7}$$
$${a}^{-{Ct}_{avg}}=\frac{{a}^{-{Ct}_{1}}+ \cdots + {a}^{-{Ct}_{n}}}{n} \tag{8}$$
Based on the above discussion, wouldn't it be more natural to use the following?
$$Ct_{avg}=-{log}_{a}(\frac{{a}^{-{Ct}_{1}}+ \cdots + {a}^{-{Ct}_{n}}}{n}) \tag{9}$$

I believe 'a' may vary depending on template, primers and reaction conditions.

I only just noticed that biology.SE supports LaTeX. Finally.

I’m voting to close this question because this isn't a biology question. It might be appropriate for a statistics site, but there is nothing about a biological process or mechanism.

I'm only used to seeing technical replicates averaged in the way you describe at the beginning (arithmetic mean), and I think it makes sense in that case (I could be wrong), because you're measuring technical variation in the measurements, not variation in the amount of starting material in your sample. If you're talking about averaging Ct values across multiple samples from a statistical population, then you are correct that an arithmetic mean is rarely the appropriate measure of center. But I'm not convinced this approach is either.


text:
Can we see the cell cycle of the cells administered using IVIS-like device?
My question;

Can we measure the cell cycle of the administered cells from outside the body, while the recipient is still alive ?　Preferably, by using a device such as IVIS that can read fluorescent labelling in the body non-invasively.

In this paper, cells incorporating a reporter called Fucci are transplanted into mice in which a skin-flap window was created. The mice were observed in CLSM while alive through the skin-flap window. As a result, the cells were individually imaged at very high resolution.

Fucci-explessing cells change colour as the cell cycle progresses, so the researchers were able to visualise which stage of the cell cycle each transplanted cell was in.
However, this method is invasive. So we need a simpler method. The required resolution should  give what proportion of cells are in which stage of the cell cycle.　We don't need the single cell resolution.


text:
What is this insect or worm?
I found it on the cedar siding of my home in Houston, Texas.
It was quite small, I'd estimate 1cm in length. I did not observe it move up or down the side of the house, but when I touched it gently and it did bend over.

Some species of Eupithecia perhaps. A type of moth, the larvae tend to resemble twigs. According to this relatively old text, Eupithecia miserulata is the most commonly distributed species in Texas, but I'm sure identifications stem largely from expertise and adult specimens, both of which I lack. The larvae for E. miserulata don't seem to visually match what you have, there.
In essence, though, it's a caterpillar that will turn into a moth.

I looked up some images and it definitely looks similar, thank you. Quite a strange looking caterpillar


text:
possibly unusual spider behavior?
In Cambridge UK there is this spider:

I know not what species but it is common - I think they look good.
But look at this behavior. What are they doing? I thought malting but do spiders do that? Why would they congregate like this?

Those appear to be Daddy Longleg spiders, and they are known for forming spider clusters, which is considered as gregarious behavior. Quoting Wikipedia:

Many species of harvestmen easily tolerate members of their own species, with aggregations of many individuals often found at protected sites near water. These aggregations may number 200 individuals in the Laniatores, and more than 70,000 in certain Eupnoi. Gregarious behavior is likely a strategy against climatic odds, but also against predators, combining the effect of scent secretions, and reducing the probability of any particular individual being eaten.

Thank you, very interesting. After looking it up it appears to be leiobunum rotundum common in the British Isles. It is very hot at the moment in Cambridge and they're under a window maybe some dew forms at night and yes they all appear to move when I came near them to take the photo as suggested in the wikipedia article.


text:
What are these bugs ?

There are a lot of these little bugs in my backyard. The floor, walls, the bbq island.
Are they hurtful to my dogs ?
What are these ?

Could you please edit your question and add the size of the insects as well as your geographical location and the season(s) when you see those them? That could help to identify them.


text:
Is this a Kestrel?
Apologies for the poor pictures, they are a crop of a tiny part of a picture taken with max zoom.

A nature reserve in Bulgaria, I often see those birds while I hike there. They let people come quite close, but they always care to stay between your eyes and the sun. Only this time I managed to see their back in full daylight, but it happened because they were very far. I searched some information online and I understood that the most commons birds of prey in the area are the Kestrel and the Buzzard, I think the one in the pictures is a Kestrel. But when I tried to search online to confirm the identification I could not find a picture of the back, it seems I am not the only one who can only see them against the sun.

Is there any other information you can give us? An estimate of the size would be very helpful (hard to do by eye, but maybe you've seen it near another bird you can identify). Behavioral information would also be very helpful. How did it fly? Soaring vs. frequent flapping? Level direct flight vs. spiraling vs. a rising and falling  pattern or something else? Did it interact with any other birds? Calls?

@tyersome I am not very good at estimating the size. I could say that it was a bit smaller than a urban crow. As for the behaviour what I usually notice is when they stand still mid air or flap the wings without moving for several minutes and then suddenly dive. But actually the moment I took the picture it was just flying  in a saddle between two peaks.

Well, it does have the characteristic pointy wings of a falcon, so that narrows the choices.  I wouldn't worry about the back - most birds have a fair amount of variability in plumage as it is, and with young birds flying around this time of year, that adds to the fun.  I'd focus on the tail, which is likely to be far more useful.
That black band at the end of the tail seems to be a good fieldmark for Kestrel, but I'm not sure about the white border.  Perhaps it's a young bird and the white border will wear off (as so often happens with young birds' plumage).  Or perhaps it's simply an artifact of the photograph/enlargement process.
Edited To Add:
In the attached links, the various illustrations show both the black terminal band and the white border to that band, as well as the brownish back as we can see from your photo.  I'd lean toward the Eurasian Kestrel rather than Least Kestrel, but I'm not experienced with European birds, so you might want to take that for what it's worth.
https://identify.whatbird.com/obj/469/_/eurasian_kestrel.aspx
https://ebird.org/species/eurkes

Thank you. In the second link, the picture labelled "Immature" seems a good match, at least for the wing and tail tips.


text:
What is a section in botany based upon?
I am a bioinformatician working with plant data. Therefore my formation on plant biology and botany is "ok" but not very strong.
When people talk about sections, I know that they talk about a phylogenetic rank that is lower than the genus but higher than the species. It groups subsets of species belonging to a genus together.
What is the thing that puts them together? Morphology, origin, geography, metabolism, genome identity, ...?

It depends. Sometimes people use it because there is monophyletic group within the genus which share a particular character, but which they don't want to (or can't) segregate into its own genus. Usually you will find sections in large genera which contain quite a lot of morphological diversity.

For more discussion on what makes a "good" name, see comments on this answer: https://biology.stackexchange.com/a/77519/42697

Taxonomic rankings above the species level are arbitrary—that is, they are created just to be a useful handle, much the way one might call the plants in one’s study “my study plants” and the plants in one’s kitchen “my kitchen plants” in order to convey information about them more easily. What makes a handle like “section” or “genus” useful is up to the botanist creating the handle, and, yes, he or she would likely consider many or all the things you mention (metabolism, origin, geography, etc.) while doing such creating. There are some rules, however—-such as respecting taxonomic hierarchy, giving such names only to clades, prioritizing earlier valid names for the same taxon, etc.

Nice answer. I could be improved by references if you can find a suitable one.


text:
What confuses me about "homologous gene"
When I first encountered homologous genes I thought those genes are identical because the text book said so, and "homologous" meant the same knowledge.
But as I studied along, it comes out that diploid is a two sets of haploid, each from mom and dad.
This means they are not identical, doesn't it? How could they be "identical" since they are from mom and dad seperately?
If they were identical, crossing over during meiosis loses a point(mixing chromatids is meaningless if they are "same").
Then, when the text book says homologous genes are identical, what identical trait is the text book referring to?

I wonder which textbook would say that homologous genes are identical. They are not. Homology has to do with common ancestry.

Can you please directly cite your textbook. Either your textbook is wrong or you massively misinterpret it.
The concept of homology refers to the concept of shared ancestry. From wikipedia

In biology, homology is the existence of shared ancestry between a pair of structures, or genes, in different taxa. A common example of homologous structures is the forelimbs of vertebrates, where the wings of bats, the arms of primates, the front flippers of whales and the forelegs of dogs and horses are all derived from the same ancestral tetrapod structure.

I would add that a common counter example are bats wings and bird wings (which is an analogy).
Two genes are homologous if they both derive from the same ancestral gene. Of course, as ultimately, all genes are related, the concept only make sense by comparison to other structures that are more distantly related or relative to a time point in time.
For more information, just have a look at any good introductory course or textbook to evolutionary biology (for example evo101 > homology)

The question asks about "homologous genes" but the question body mentions meiosis and chromatids.  The latter suggests you are really referring to the concept of "homologous chromosomes". These two terms are used in different contexts in biology to refer to somewhat different concepts (despite the fact that chromosomes contain genes).
Homologous chromosomes are two chromosomes which, although not identical, are highly similar so that they pair up during meiosis and participate in crossing over.  If the textbook says they are identical, that is incorrect; they are mostly, but not entirely, identical.

I also believe that the OP was referring to homologous chromosomes and not genes since he talks about haploid and diploid.


text:
Is it theoretically possible to safely eliminate most viruses in the atmosphere, hence preemptively cure all the viral diseases?
Could we create a genetically modified virus or bacteria (with inability to mutate into something dangerous for animals) that would quickly spread all over the planet and selectively kill most of the viruses that we train it against?
Are there any other potential methods we could use to do it safely (without any danger to living creatures)?
Is that something we could actually do with a few billions of dollars?

No (or a bit more scientifically: very very unlikely)
There a couple of reasons why your idea would not work:
Viruses are not alive, so you can't really kill them. The only ways to get rid of all airborne viruses at once would be to either:

A) UV-sterilize the whole atmosphere (bad idea, good xkcd what-if question though) or
B) fill the whole atmosphere with something that replicates itself and consumes very small particles of biological material (oops, we released grey goo).

It's also not possible to create bacteria or viruses that can both spread quickly (which means it need to be able to grow / self-replicate) and is physically unable to mutate.
Mutations arise from errors in DNA replication, and DNA replication is never 100% accurate, you can reduce the error rate, but it will never reach 0, so mutations will always be possible. It's also impossible to predict the 'direction' of mutations so you can't exclude that they will be dangerous for humans either.
As other comments have already mentioned there are even more problems with the idea itself:

not all viruses are airborne, many reside in animal hosts, so getting rid of the airborne ones will not do much
many viruses are not pathogenic for humans but ecologically important, you will get an unknown amount of ecological impact

@Nicolai A baseball thrown near the speed of light should do it.

@BryanKrause A baseball thrown near the speed of light would flash-vaporize and burn up in the atmosphere, thoroughly obliterating anything in its path for its arguably short existence.

@user1258361 That's the joke; Nicolai was talking about sterilizing the atmosphere and referred to XKCD's "what-if" series; the first in that series was titled "relativistic baseball" https://what-if.xkcd.com/1/


text:
How does the bear mother ensure her cubs don't escape during hibernation?
I have some questions relating to bears- more specifically, the brown bears we have in Scandinavia.
When they go into hibernation, do they fall asleep as we know falling asleep? If a bear mother brings her cubs into the den, how can she keep track of them? How can she make sure they don't wake up, leave the den and get lost in the snow?

Are you aware that brown bear cubs are born during hibernation? Or are you thinking about subsequent years when they remain with their mother?

Yes Bryan Krause - I'm thinking of the next year, when they go to sleep in the den together.

She probably can't, but a bear that wanders out of the den away from it's mother probably won't be doing much reproduction.  Infant wanderlust will be strongly selected against.

Can you afd sources to back up your answer? It looks like a comment.


text:
Is there a difference between splice-site mutations, and non-stop mutations
I'm working on a bioinformatics project where a lot of the biology I've had to learn from scratch. From my current understanding, a non-stop mutation alters a stop codon such that the transcription continues, and a splice site mutation alters the region between introns and exons - where the sequence may include introns, or remove part of the exons from cancer.gov. I'm inferring therefore that these could be the same mutation type.
Is this understanding correct?

No, those kinds of mutations are quite distinct.  Also, you misstate the nature of a nonstop mutation; the change of a stop codon affects termination of translation, not transcription.  This is quite different from a splice-site mutation, which affects splicing, a form of mRNA processing that occurs between transcription and translation.

Great thanks for clearing that up


text:
Slicing cell cultures frozen in vitrified ice with a laser for CryoEM
Could a cell culture frozen in vitrified ice for CryoEM be effectively sliced into thin planes and resolved images produced? I was thinking if this could be done to get images from inside a cell.

Maybe I should take this over to physics. But this is something I'm interested in and not sure were to start.

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


text:
How are Stem Cells Produced for Stem Cell Based Therapies?
I was doing an initial search on google but couldn't come up with anything I'm looking for. I know were stem cells come from and a bit about their levels of differentiation. For example, embryonic stem still becoming mesenchymal stem cells and what not. I also understand that epithelial tissue cells can be converted to a pluripotent stem cell state but at very low efficiency. So, all that aside how are stem cells obtained in the volumes necessary for stem cell based therapies without causing them to start differentiating during production?

Can you give a reference to a particular therapy you're interested in? Different treatments use different protocols.

I've heard of therapies, than in my opinion sound silly, were cancer patients are given a dose of stem cells intravenously. I would assume these would be made from an embryonic stem cell lines. If I'm correct, how are these lines maintained and generated? Is there a specific culture medium that can maintain the pluripotent state while still undergoing continuous growth?

Basically you culture them in a medium that inhibits cell differentiation. ES cells derived from Blastocysts are immortal (like cancer cells) as they express telomerase. Give the correct signaling molecules in the medium, they will continue to divide in an undifferentiated state, for all intents and purposes, indefinitely.

I didn't get your question exactly. If you wanna ask how to maintain the potential of stem cells, yes, there are several compound that could keep stem cells, such as Leukemia Inhibitory Factor (LIF). As far I know, the using of pluripotent stem cell, such as ES, iPS, still has the problem of formatting teratoma in vivo studying. It means totally differentiating pluripotent stem cell still need to be work out.

If you could explain what LIF is, then I think you have answered this question.

@AliceD LIF - Leukemia Inhibitory Factor. It is added to ES Medium to keep them from differentiating.

With LIF alone you also need to use feeders. Labs are starting to switch to 2i so that you only need to plate the ES cells. It makes DNA and RNA analysis much easier, because you do not need to try and remove feeders after the fact so you do not have the fibroblasts confounding your data.

@AMR - thanks for the explanation, and thanks for that edit too. +1

But I think there should be other compounds other than LIF. As far I know, some lab prefer culture human iPS cell without MEF (feeder layer), LIF and even serum. If you have an interest, there are lots well-known protocol in internet and papers. And also, lots of commercial mediums for raising stem cells, such as https://goo.gl/ImF1I8 .Following these compounds in mediums, you will know what can keep stem cell's potential.

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


text:
Phospholipid movement in cell membranes
What causes phospholipids to flow so quickly in cell membranes? In Biology by Cambell et al. they state that a phospholipids can travel up to 2 micrometers per second. Is that a random movement or has anyone found that phospholipids have a current?

There must be charge considerations in the movement of molecules in the lipid membrane. There is also a consideration that some species of phospholipids will migrate to portions of the membrane with sharper or smoother curvature.
Waves of electrical potential can propagate along a lipid bilayer as well, which is very important to nerve axons and extended structures like that.
In general though the membrane is held together by vanDerWaals forces like other non-polar solvents.  As such, the movements of lipids and proteins and other amphipathic molecules in the membrane are still largely Brownian (random) in the 2D surface of the membrane.


text:
Local BLAST Copy Number per Hit
I generated a series of local BLAST databases using makeblastdb of metagenomic data and am searching for the presence of a particular gene. While I can do the normal BLAST analysis looking at e-values, % identity, etc. I haven't been able to figure out how to determine how many times a given sequence exists in the database.
So: given a BLAST database of metagenomic data where a particular gene may exist multiple times, how do I determine the copy number of a given BLAST hit?
Thanks in advance.

That depends on how you define a hit. Are we talking about homologous genes from different species? Multiple, slightly different copies of the same gene in a single genome? Multiple, identical copies of a single gene which is repeated in the database?

I'm defining a hit based on the BLAST results -- I blasted seq1 against the database and it returned seq2...seqn. Depending on what cutoffs I use for bit scores / identity scores, etc. I might have three "hits" - seq2, seq3, and seq4. I want to know how many times seq2 showed up in the metagenomic data.

Define a "Hit" (based on some cutoff- evalue, score etc)
Get output in the tabular format
Count number of hits per query — it is usually given in the header; if you want to look for some selected hits (based on some cutoff, then you can parse the file and find out)

Example file (header):
# BLASTN 2.2.27+
# Query: TCONS_00036712 gene=XLOC_017996
# Database: ../nt_db/nt
# Fields: query id, subject id, % identity, alignment length, mismatches, gap opens, q. start, q. end, s. start, s. end, evalue, bit score
# 1014 hits found

If you want to parse the header to look for number of hits then you can run this command in the terminal (if you have awk — there by default in linux and other unix based systems. For windows install gnuwin32).
awk -v OFS="\t" '/^# Query/{q=$3 FS $4} /^# .* hits found/{h[q]=$2} END{for(i in h){print i,h[i]}}' blastoutput.txt

To get the number of hits for a given criterion (for e.g. I just defined bitscore [12th column] to be >400)
awk -F "\t" '!/^#/ && $12>400{a[$1]++} END{for(i in a){print i,a[i]}}' blastoutput.txt

Great, but I have that already -- I know how many "hits" i.e. unique sequences there are. What I want to know is how many times that given hit's sequence is present in my assembled metagenomic dataset.

@user2030378 Do you want to look for redundant sequences ?

BLAST is not the correct program to use in metagenomics analyses for determining the number of reads that map to a certain region of the genome, as it is optimised for single hits instead of a large number of different hits.
The sheer number of hits within a metagenomics database (which contains a large amount of redundant data) is likely to cause inefficient scaling and high memory usage when the detection of all possible hits is required.
If the number of hits required is low, it is possible to have it return those hits, but if you are looking at >1000 hits, it is probably recommended to use a mapper program such as BWA or Bowtie. They are designed for the express purpose of mapping reads (such as from an RNASeq experiment) onto genomes.


text:
What is an "end-to-end fusion" in the context of telomerase?
Telomerase is said to prevent "end-to-end fusion" of chromosomes.
My question is threefold:

What is an "end-to-end fusion"?
How does Telomerase prevent end-to-end fusions?
Why do end-to-end fusions cause problems in cells?

An end-to-end fusion is the result of two chromosome ends fused together. This happens when telomeres (repeated sequences at the ends of chromosomes) lose their protective telomere-binding proteins. In mammalian cells, loss of TRF2 (telomere repeat-binding factor 2) leads to chromosome fusions.
Here is an example of how it looks with metaphasic chromosomes (the DNA is stained in blue and the telomeres are stained in pink; picture from Rai et al, 2016). The left panel shows normal chromosomes, the right panel shows end fusions upon depletion of TRF2.

What causes chromosome fusions in such situations is the DNA double-strand break (DSB) repair machinery, which is normally repressed by telomere proteins (mainly by TRF2; see van Steensel et al, 1998). In mammalian cells, telomere-binding proteins are collectively called the shelterin complex (they literally shelter chromosome ends; see de Lange, 2005).
Telomerase doesn't repress the DSB repair machinery directly. Because of the structure of telomeres (a single-stranded 3' overhang) and of the way replication is primed, linear chromosomes cannot be fully replicated and will gradually shorten at each replication. When telomeres become critically short, they don't recruit enough telomere-binding proteins and therefore fail to repress the DSB repair machinery. Telomerase, when expressed and activated, maintains the length of telomeres in replicating cells at each replication (by adding repeated sequences complementary of the RNA template that is a component of the telomerase holoenzyme), providing binding sites for telomere-binding proteins, and thus indirectly contributes to the repression of the DSB repair machinery.
End-to-end fusions cause problems in cells in part because fused chromosomes will likely not segregate properly during mitosis and meiosis. The resulting daughter cells end up with altered ploidies that can be severe enough to prevent cell viability.

de Lange T (2005) Shelterin: the protein complex that shapes and safeguards human telomeres. Genes Dev. 19: 2100–2110 https://doi.org/10.1101/gad.1346005
Rai R, Chen Y, Lei M & Chang S (2016) TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions. Nat Commun 7: 10881 https://doi.org/10.1038/ncomms10881
van Steensel B, Smogorzewska A & de Lange T (1998) TRF2 protects human telomeres from end-to-end fusions. Cell 92: 401–413 https://doi.org/10.1016/S0092-8674(00)80932-0

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

Thank you for the suggestion. I just upvoted the question.

Merci bien, Guillaume! :)


text:
What is the difference between a cytokine, a hormone and a protein hormone?
I'm trying to figure out the difference between hormone, cytokine and protein hormone. It's clear to me that all three are biological messengers, but there seems to some ambiguity and overlap between terms and I'm trying to understand the nuances.
In brief:

What do each of these three terms mean and how are they different?
Do any of the three terms represent a superset of the others? e.g are all cytokines, hormones? Are protein hormones just a subset of hormones?
Are the terms context specific at all? For example, cytokines are referenced in the context of immunology below, but are they actually fundamentally different from hormones?

If there is context-dependence, under which contexts should each word be used?
Are there any canonical examples of each? e.g Prolactin is given as an example of a protein hormone below, how about for cytokines and ordinary hormones?

In June 1905, Ernest Starling, a professor of physiology at University College London, UK, first used the word 'hormone' in one of four Croonian Lectures—'On the chemical correlation of the functions of the body'—delivered at the Royal College of Physicians in London. Starling defined the word, derived from the Greek meaning 'to arouse or excite', as “the chemical messengers which speeding from cell to cell along the blood stream, may coordinate the activities and growth of different parts of the body” [1]
Cytokines and chemoattractant cytokines known as chemokines are highly localized soluble signaling proteins produced by many cells of the immune system (neutrophils, monocytes, macrophages, B-cells, and T-cells) to regulate immune responses [2]
A great deal of evidence has accumulated and confirmed that hormones secreted by the neuroendocrine system play an important role in communication and regulation of the cells of the immune system. Among protein hormones, this has been most clearly documented for prolactin (PRL), growth hormone (GH), and insulin-like growth factor-1 (IGF-I), but significant influences on immunity by thyroid stimulating hormone (TSH) have also been demonstrated. [3]

References
[1]: Tata JR. One hundred years of hormones. EMBO Reports. 2005;6(6):490-496. doi:10.1038/sj.embor.7400444.
[2]: Stenken JA, Poschenrieder AJ. Bioanalytical Chemistry of Cytokines-A Review. Analytica chimica acta. 2015;853:95-115. doi:10.1016/j.aca.2014.10.009.
[3]: Kelley KW, Weigent DA, Kooijman R. Protein Hormones and Immunity. Brain, behavior, and immunity. 2007;21(4):384-392. doi:10.1016/j.bbi.2006.11.010.

Some hormones are also considered cytokines (e.g. GH and prolactin) since they target cytokine class of receptors.

Parts of the answer are in the text that you provide yourself. But I shall try to add where i can.
What do each of these three terms [hormone, cytokine and protein hormone] mean  and how are they different?
Both cytokines and hormones are a class of signalling molecules that are secreted by cells.
Cytokines are a group of small protein that  have a fundamental role in the immune system. They are typically short lived and typically have local effects and are specific cytokines are often produced by multiple cell types.
For example they cause local cells to generate heat and cause blood vessels to become wider and more permeable to blood cells. parham (2015) Some cytokines can act over longer distances, IL-6 for example cause local inflammation and regulates fever by targeting the  hypothalamus causing it to increase body temperature overall. For more information check this link.
Hormones are secreted into the blood by dedicated endocrine cells so the can regulate other cells across the body.(alberts, 2008)
Do any of the three terms represent a superset of the others?
Protein hormones are a subset of hormones. An other important subset are steroid hormones.
It can be argued that cytokines function as hormones in some situations. For example: in the case of an infection high concentrations of cytokines can regulate body temperature causing fever. IL-1α, IL-1β and IL-6 are good examples here
Are the terms context specific at all?
In some situations it can be argued that cytokines act as hormones. But the feature that groups them is that the are an actor in the immune response. This wiki discusses some differences.
Classical hormones are produced by a gland and excreted in the blood. This is not context depended.
Are cytokines actually fundamentally different from hormones?
All Cytokines are proteins and don't act fundamentally different from protein hormones. Both have to act through membrane bound receptors since proteins can not pass the cell membrane on their own. Steroid Hormones can pass the membrane and typically have intracellular receptors.
Are there any canonical examples of each?
Interferons and Interleukins are a large classes of cytokines. IFN-γ and IL-6 a well known examples.
Androgens are steroid Hormones . Testosterone is one of them.

"The difference is that cytokines act locally" - as you point out elsewhere in your answer, some cytokines act systemically rather than locally. "are produced by many cell types" - this isn't really much of a difference with hormones, since hormones are also produced by a variety of cell types.

You are right. I could have formulated that both sentence more precise. By  "are produced by many cell types" I meant that specific cytokines are typically secreted by multiple different cell types. For example: IFNγ is secreted by T helper cells , cytotoxic T cells , macrophages, mucosal epithelial cells and natural killer cells. Different hormones are indeed secreted by different cells, but most hormones are secreted  by one cell type. for example: insulin is onl secreted by Beta cells. I will rewrite my answer to be more precise tomorrow.


text:
Which is the correct term haploid daughter cells or haploid parent cells?
Meiosis 2 begins with 2 haploid parent cells and ends with 4 haploid daughter cells (gametes). Gametes from the opposite sex can now merge together and fertilize.
If I were to refer to a specific haploid daughter cell merging with another to produce a zygote; are these daughter cells from Meiosis 2 still called 'daughter' cells or are they now called parent cells?

"Parent" and "daughter" terminology is indeed relative. Any parent cell has been a daughter at some point. However, in the case of the zygote there is no "parent" strictly speaking since it is the result of a fusion between two cells, that you may call "daughter cells" only if you are referring to the previous meiosis event.
In this particular case, there is no cell division, so no "daughter" is formed, so no point in calling the haploid cells from M2 "parents" either.

Hello! This question was deemed worth of an answer, so why not upvote it? Vote early, vote often to encourage new users and keep the community alive!

@LinuxBlanket Don't ask me. I did upvote it. Someone else downvoted back, resulting in 0 votes so far.

Ok! I don't have enough reputation yet to see the vote imbalance, I see only the result. So thank you for voting early and often!


text:
Correlation brain size and muscle volume
I have 3 dogs that weigh ≈ 5 kg, ≈ 20 kg and ≈ 45 kg. The smallest dogs whole head would fit in the mouth of the biggest dog. Although I haven't measured it exactly but by just looking at the dogs I would expect the weight of their brain to approximately correspond to their body weight, that is the 20 kg dog's brain is 4 times heavier than the smallest dog and the 45 kg dog's brain is 10 times heavier.
Meanwhile, all three dogs seem to have similar intelligence.
What is all the extra weight of the brain of the bigger dogs used for?
You can expand this question and note that an average mouse brain weigh 0,5 g while an elephant weighs around 5 kg. Elephants might be smarter than a mouse but not 10 000 smarter. Besides, the brain of a human is much lighter than an elephant and we obviously are much smarter.
Why do bigger animals need bigger brains than smaller animals to accomplish approximately the same intelligence? Is it something along the lines that they have more muscle fibres and every single musle fibre needs a few neurons to control it?

No real expertise in neurobiology, but I know that there are factors to consider other than just mass.  For example, the proportion of the brain that is cerebral cortex varies considerably.  Also, the density of synapses (connections between neurons) is also not constant.  You may find this article helpful: https://mosaicscience.com/extra/does-brain-size-matter/

You may be interested in this question: https://biology.stackexchange.com/questions/61476 and the links therein.

Possible duplicate of Do smaller intelligent animals have a higher neuron density to account for their seeming intelligence? Otherwise, what?

Sorry to get philosophical, but if we do not understand consciousness, then how can we define 'intelligence' and 'smartness' in objective, measurable ways? Furthermore, we can assume abstract ideas like intelligence are physically real, albeit this does not mean we are necessarily correct.

I like the muscle_fiber/more_neuronal_mass theory. It makes a lot of sense having a better networked neural structure if you have more efferent processes to look at (in the form of more muscle fiber to actually move). After a quick search, it doesn't seem like this is a very thoroughly researched field. This review from 2014 states that:

there seems to be a positive relationship between whole brain volume and white matter volume and muscle size
grey matter (GM) volume had no direct relationship with muscle size, yet some areas of the GM were linked to muscle size (more specifically the right temporal pole and the bilateral ventromedial prefrontal cortex)
no relationship exists associating grip strength and whole brain volume
gait speed is positively linked to whole brain volume

The relationships between regional areas of the brain and their functions seem to be something dynamically non-linear enough to prove quite complex to classify properly.
The "extra weight", represented by a larger cerebral cortex, is where the neural integration happens and a study (and possibly others) confirms that cortical thickness is correlated with general intelligence in both hemispheres (samples = [children, adolescents, young_adults]).

References:
Kilgour AH, Todd OM, Starr JM. A systematic review of the evidence that brain structure is related to muscle structure and their relationship to brain and muscle function in humans over the lifecourse. BMC Geriatr. 2014 Jul 10;14:85. doi: 10.1186/1471-2318-14-85. PMID: 25011478; PMCID: PMC4105796.
Menary K, Collins PF, Porter JN, Muetzel R, Olson EA, Kumar V, Steinbach M, Lim KO, Luciana M. Associations between cortical thickness and general intelligence in children, adolescents and young adults. Intelligence. 2013 Sep;41(5):597-606. doi: 10.1016/j.intell.2013.07.010. PMID: 24744452; PMCID: PMC3985090.

A fast rummage through the web tells me (alot) that:
The most intelligent dog is a medium dog breed, the border collie.
Big dogs are generally more intelligent than small dogs, only 1/20 of the most intelligent dog breeds are small dogs.
bigger dogs have better short-term memory, able to focus better and have better self control, coordination end executive functioning.
They also have:
More surface area with nerves and skin cells
more muscle fibers.
Primate studies suggest that bigger brains have better executive functioning and not other types of intelligence.

I don't think the causality goes in that direction. Working dogs are smarter than other dogs, especially working dogs that need to interact with humans. Medium size is a good size for working dogs that should be handled by humans, while their size still makes them efficient in their function.

poodles are rated in the top 20 most intelligent breeds, and bulldogs are towards the less intel, I don't know about wolves and foxes, that's tricky to test for.

What is your point?

papillons and poodles are not related to working dogs and are higher on the intelligence tests than most workdogs. it's an just an oddity. https://en.wikipedia.org/wiki/The_Intelligence_of_Dogs

Poodles are working dogs. Papillons aren't exactly working dogs but have been bread to learn tricks that amuses humans so that is basically a working dog, although their works is play.


text:
Why do birds that walk on the ground walk so "bumpy"?
Why do birds that walk on the ground walk so "bumpy"? Most other animals walk quite smooth, doesn't matter if they are mammals, reptiles or insects or walk on two, four or more legs. Birds seem to be an exception and there is no difference between flying or non-flying birds.

Related to this: https://biology.stackexchange.com/q/21200/331

If you mean the head bobbing displayed by many birds when walking: it is believed to help with visual stabilization.

The term head-bobbing, used for the apparent back and forth movement
  of the head of some birds while walking on the ground (think pigeons),
  is a bit of a misnomer. These birds don't actually bob their heads
  back and forth – instead, they move their body forward, leaving the
  head behind, then thrust their head forward past their body (hold,
  high-speed thrust!). This innate behaviour is believed to help several
  key aspects of vision during locomotion and foraging. While the head
  is still, images are stabilized on the retina and moving objects
  become clear against the background, and during the thrust phase,
  depth perception becomes more accurate.

https://jeb.biologists.org/content/jexbio/217/11/1836.1.full.pdf
In this article you can find an stroboscopic photography that shows the particular bumpy walk.

Why is it useful to birds, but no other animals, with this improved vision?

Our human eyes move a lot constantly to track movement, in the case of many birds neck mobility is probably better than eyeball mobility. Not all birds bob their heads as they walk, though.


text:
Why are children so violent, compared to other adolescent animals, when they play?
When children play it is frequent that someone starts crying, suffers minor injuries and that they are intentionally mean towards each other (e.g., bite, pull hair, throws sand, pushes someone so they fall, wrestles so hard that the weaker part struggles with breathing and so on). On the other hand, when my puppies (or even adult dogs) play you never see anything like that. They tumble around and takes turns for who's on top. The only "negative" I have ever seen is when puppies with "flappy" ears play and someone gets hold of an ear with their sharp teeth - then the "victim" might scream, but when this happens the other dog immediately let go of its grip.
Children that play need parental supervision. Young animals that play manage fine without their parents.
Why are humans so cruel when they play compared to other animals?
(I'm not sure if this belongs biology, pets, psychology - if I picked the wrong site, please move the question to where it belongs)

I personally have seen dogs run whimpering and bloody back to their owner after play with another dog at a dog park went off the rails. I suspect your observation is just your observation, not a hard rule of animal behavior.

@CharlesE.Grant Dogs can get into fights but that is not playing. Cats frequently fight, which most cat owners that let their cats out are aware of.

I’m sure it doesn’t belong here. Can you envisage a definitive objective answer?

@David Yes, something with the evolution.

So somebody says "things evolved that way because…" and that is regarded as a definitive objective answer. If I see amino acid sequences I can see evidence for evolutionary propositions. When I read incantations of the former sort — always presuposing the answer — it reminds me of when people would invoke  God in replies.

@David If it can be falsified in line with Popper's ideas about critical rationalism it is an acceptable answer.

I am skeptical of every part of this -- that human play is necessarily violent or that animal play is different. Certainly in my own kids and their cohorts, "wrestles so hard that the weaker part struggles with breathing" would be appalling and highly unusual. Dogs are tamed animals; is play among young wolves non-violent? What about chimpanzees or baboons?

@RaghuParthasarathy Do your kids never form "a pile" with someone at the bottom having a bunch of kids on top making it hard to breathe? Maybe it requires a school class or something but with enough people around, the kid at the bottom might struggle.

I believe wolf puppies play friendly yes. They might fight over food but when playing I have never heard reports of wolf puppies injuring each other while playing. But feel free to prove me wrong.

A litter of puppies start hurting each other (and me) as soon as they develop trazor-sharp teeth and nails, and do it over and over again. A good mom will only take so much before she distracts them, but as they get older, it gets worse, and God help them if they don't get split up before it really gets rough! (I used to breed Border Collies, the best dogs in the world but not the most aggressive by far.) Some babies kill each other (one bird will push it's nest mate out of the nest to secure all its food.) What's worse than murder? Rose colored glasses you have on, I think.

Come to think of it, they try to hurt their parents, too, but the parents put them in their place damn quickly; those are the loudest squeals. It's not all-violence-all-the-time, but there are whimpers galore. If they could use words, I'm sure they would sound just like kids. As to letting go right away, I have a puppy now that grabs onto my other dog by the tail and won't let go unless she scares him (which sometimes results in a scar). I used to have a farm; we had to dehorn the baby goats so that they couldn't impale each other later. And yes, I am an earthling.

@anongoodnurse Pushing a sibling out of the nest is not playing. If you have breed dogs, you should be aware that they never hurt each other when tumbling around. Their fur protects them from their puppy-teeth. Please, this question is about playing, not about fighting for survival.

@d-b - "If you have breed dogs, you should be aware..." I have bred dogs, do you doubt it? I don't know where you got your information from. I've observed and cared for litter after litter - six to be exact. I speak from experience.

@anongoodnurse And what is your experience? Have you ever needed to visit a vet after the puppies have played?

@d-b - It's been a month since you were downvoted (5 times). Why are you being so persistent now? You're not interested in what I think. I'm done here.

That's not answering my question. I have "worked" with two litters of puppies (terriers and spitz) and none of them come close to need a visit to the vet after playing (of course, other accidents happened: they ate things they shouldn't or stepped on broken glass and so on).

This is not a complete answer, but I couldn't fit all of that in a comment. I also don't have any expertise in neither biology nor anthropology, so you should probably take this answer with a grain of salt.
As many others here, I'm not sure that adolescent animals are really less violent than children. I used to keep rabbits and although young bunnies tend to be less aggressive, sometimes there are exceptions. If not stopped, they can mutilate each other pretty horribly.
Still, there are lot of differences between humans and other animals that affect both human behavior and your perception of it.
Prolonged childhood
Compared to other animals, human growth to adulthood is very slow. Most other mammals progress from the short period of infant dependency (toddlerdhood) directly to juvenescence. (1). Humans have 10 years of childhood.  Children are not yet fully developed, but they are already fully operational: can walk, fight and use tools. This stage is long and unusual. Other animals usually don't have a lot of time to play and be violent to each other.
Free time
Children have a lot of time to play and to fight with each other. Wild animals don't have this luxury, they have to hide from predators and provide for themselves. Less time in general means less time for play and fighting.
Pain tolerance
Children are not trained to withstand pain and tend to cry often and they do it loudly. Crying with tears coming out of the eyes is unique to humans and children cry in response to minor physical and emotional discomfort (minor falls, verbal insults). Crying child is likely to get noticed by everybody in its vicinity.
Wild animals have their own reasons to not get noticed and have to keep quite all the time, even after severe injuries. Even domestic animals have a higher sensitivity threshold and are less likely to vocalize in response to pain. Violent games between animals are less likely to be perceived as such because animals tend not to react "negatively" to them. Kittens playfully scratch and bite each other. Calves head butt one another with no mercy during play.
Society
Bear cub is expected to play with at most a couple of siblings during childhood. Young wolf grows in a pack of 5-15 other wolves, most of them adults. Herd animals live in bigger groups, but they are mostly herbivores and less likely to hurt each other during play.
Children, on the other hand, are routinely locked in small areas with hundreds and thousands other children with little to no adult supervision. That gives a lot of opportunities to pick up a fight.
To make it worse, children have human intelligence and their social interactions are extremely complex compared to juvenile animals. This provides a lot of reasons to fight and to hate each other. Lion cubs can't speak and, thus, can't insult each others intelligence and physical shape. Young dolphins are unlikely to mock each others heritage, social background, religious beliefs, political affiliation or sexual preferences. Wombat joey probably won't steal other joey's bike, etc.
The previous paragraph applies equally well to adult humans. Human interactions are uniquely complex. Animals, young and grown, can be violent to each other, but our concepts of hatred and cruelty can't be easily applied to other animals.

I suppose you're right for the best part of it, however it comes to question the generality of your statement. Dogs do become violent while playing, as are other animals. Humans are animals too, what sets them aside are community ethics. Toddlers, on the other hand, are a raw product if I do say so myself, and are animals not yet accustomed to the norms of social law. Indeed, we are a learning species, we evolve as we grow.

Dogs (and other animals) are physical when they play but that doesn't equal violent. When I was a kid, as part of a game, I threw a stone at a friend. It hit him in head and he got a concussion. I aimed for the head so it was no accident that it hit him there. I have never heard of that type of accident among playing animals.

@ d-b - Thank God dogs don't have opposable thumbs, or they'd be hitting each other with sticks as young pups.I don't know what you have been protected from, but your experience is not a universal truth.

@anongoodnurse What do you mean "protected from"? Dogs have sharp teeth and they (most of them) don´t hesitate to use them. Most animals have some kind of pretty good weapons, teeth, horns, claws you name it.