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Why are there three stop codons but only one start codon?
I was wondering whether there is any specific reason that there are three stop codons but only one start codon in prokaryotic and eukaryotic cytoplasmic mRNAs.

There are more than 1 start codon. E. coli have 3, for example.

Yes, I just saw that. Though in most cases AUG dominates. Thanks

@David: I guess you didn't read all of my answer. I'm waiting for you to dive into the reasons behind the varying translation efficiency of different start codons. I'm not sure the OP really wants that level of detail for a question like this.

@David: and don't forget to downvote the answers on this question: https://biology.stackexchange.com/questions/9990/why-is-aug-the-initiation-codon

@Fizz — Although not really relevant as a comment to this question, I am obliged for your pointing out another which is certain to have poor answers.

Disclaimer
It is important to realize that it is not possible to answer questions of this sort (the evolution of translation)  in anything other than a speculative manner. Please bear this in mind, especially if you find the speculation below persuasive.
Summary
It is suggested that the redundancy of termination codons is largely similar to that for ‘elongation codons’ decoded at the A-site of the ribosome, although protection against suppressor tRNAs may also be a factor. The consideration here is, therefore, mainly focussed on the question why there is only a single codon for methionine (initiation and elongation), and I suggest this may have been a combination of the late appearance and infrequent usage of methionine, together with the particular requirements for an initiation tRNA at the P-site of the ribosome, where standard wobble is apparently not possible.
Disposing of a Red Herring
Although alternative initiation codons are sometimes used, this usage differs in prokaryotes and eukaryotes, is very limited, and is not seen with the use of methionine in elongation. I would therefore consider this does not invalidate the question, but perhaps rephrase it as:

“Why does the genetic code have only one codon assigned to methionine,
  the initiation codon, whereas other amino acids and termination have
  generally more than one?”

Time of appearance of and extent of use of Methionine
It is generally thought that genetic code initially encoded a small number of amino acids, and that this number increased over time. Methionine is one of the most complex (and energetically expensive) to synthesize (see Wikipedia entry), so is likely to have appeared late. One can argue that most of the codons would have been ‘taken’ (assigned) by that time. This argument is consistent with the situation for tryptophan, the other amino acid which has only a single codon, and which is also synthetically complex. Furthermore, these are the two least abundant amino acids so on can argue that their number of codons reflects their relative usage.
Admittedly, there need only be one stop codon per protein, but it is possible that the mechanism of termination evolved before that of methionine-specific initiation. (Initiation might originally have been from the 5′-end of the mRNA.) There is also the question of protection against suppressor tRNAs, but I shall delay discussion of this until the end.
The unique features of the initiator tRNA
Elongation involves several dozen amino acyl-tRNAs being recognized by an elongation factor which binds them to the A-site of the ribosome, at which 3′-codon wobble occurs where the redundancy of the genetic code allows and the anticodon of the tRNA has evolved appropriately.
In contrast initiation involves exclusive recognition of a special tRNA by initiation factors but not elongation factors, and subsequent binding at the P-site The tRNA has unique structural features that allows it to be N-formylated — structural features that are retained in eukaryotic initiator tRNA, even though there is no transformylase in eukaryotes. (see this SE Question]
This uniqueness may explain why there is only one tRNA for initiation. However one might ask why there is a not a group of methionine codons (e.g. AUA as well as AUG) recognized by the same initiator tRNA through wobble. The reason for this would seem to be that the P-site does not allow third position wobble (as I explain in the answer to a related question), so the initiation met-tRNA would be codon-specific.
Loose Ends
Although perhaps straying a little from the question, one might still ask why there are not alternative elongation codons for Met — e.g. AUA, which could have been ‘stolen’ from Ile, which already has AUU and AUC. In fact in mammalian mitochondria this codon reassignment has happened, but unfortunately does not help explain things. In mitochondria there is only one tRNAmet for both these codons, consistent with the simplification of tRNAs for the small mammalian mitochondrial genome. Initiation requires the formylation of the methionine.
I will finish by returning to the question of multiple termination codons, which are not really consistent with my suggestion that the extent of redundancy reflects usage. Although termination codons, like elongation codons, are recognized at the A-site they are recognized by protein release factors rather than tRNAs. This means that they will be affected differently by a mutation in a tRNA that alters the anticodon. For an amino acid codon, an altered non-cognate tRNA would only cause some misreading and an altered cognate tRNA might be neutralized by wobble or by duplicate or redundant tRNA genes. AS termination codons are not normally decoded by tRNAs, a suppressor tRNA would cause read-through at all the suppressed codons. The presence of two alternatives means that termination would be likely to occur within about 30 codons 3′ to the original termination codon. Variation in the length of the N- and C-termini of proteins is common among related species, and thus need not be deleterious to the cell.
Related SE Questions

‘Wobble’ in Initiation and Elongation — I have contributed an answer to this.
Why is AUG the Initiation Codon? — I will respond to this presently.
Redundancy of the Genetic Code — I have contributed an answer to this.
Initiator and Elongator tRNAs in Translation — I have contributed an answer to this.

Since my initial post of an answer I have added a section considering the possible reasons for multiple termination codons.

The simplest answer is that redundancy has evolved into these codons. A cell would not want a mutation at the stop location and have the protein get excessively large before another stop codon is hit.
Here is a better explanation and if you are very interested in the subject, I would recommend Lehningers Principles of Biochemistry.
Lehninger, A. L., Nelson, D. L., & Cox, M. M. (2000). Lehninger principles of biochemistry. New York: Worth Publishers

it would be helpful if you expanded your answer with some of the material from the link, e.g. "In prokaryotes, E. coli is found to use AUG 83%, GUG 14%, and UUG 3% as START codons. "

But it would also not "want" a mutation in the start codon so that no protein at all was made.

Somewhat obvious, there's weaker selection on the stop codons than on the start codons:

The selection affecting stop codons is relatively weak. In particular, comparison of the strength of purifying selection to that on start codons indicates that purifying selection on UAA is slightly lower than that on GUG and UUG start codons and much weaker than purifying selection on AUG, the primary start codon.

The reasons for this difference are a bit more difficult to grasp... but even for stop codons...

UAA is the optimal stop codon based on its higher proportion in highly expressed genes

On the other hand there's drift ("switches") in the stop codons

Fast-evolving genes generally accrue more stop codon switches than slow-evolving genes, suggesting that the higher evolutionary rate involves also the stop codons.

So come back in a few billion years with the same question on the stop codons.
On the other hand it's fairly well-established that

In prokaryotes, the start codon is one of the major translation initiation determinants: replacement of AUG with an alternative start codon, such as GUG, typically leads to a several-fold drop in the translation efficiency

As for the stop codons:

The causes of the observed preference for UAA as the stop codon, particularly in highly expressed, slow-evolving genes remain unknown. One potentially plausible possibility is that UAA is less prone to formation of stable secondary structures in RNA molecules than UAG or UGA which facilitates the release factor access and is likely to be particularly relevant for highly expressed genes. Furthermore, the frequency of readthrough differs for the different stop codons and is the highest for UGA, at least, in E. coli. Because the deleterious effect of readthrough is the greatest for abundant proteins, the difference in readthrough frequencies could, in part, explain the strong preference for UAA in genes encoding such proteins.

So, in summary, the selection reason for the start codon is fairly well understood, but the reason for the observed preference for UAA as an optimal stop codon (in highly expressed genes) is more speculative, which goes hand in hand with its purifying selection not being as strong as that for the AUG start codon.

I didn’t downvote this answer but your first quote is essentially a restatement of the question: It doesn’t in the least provide a rationale for why this is. The rest of your answer is merely describing facts, again not offering reasons why. I actually prefer the answer you’ve just posted on the related question about AUG.


text:
What is this bug
This insect flew into my house in Singapore while it was raining.  Size is around 1.5 inches. What is this?

What we need: https://biology.stackexchange.com/tags/species-identification/info

My own "wish list" would include extreme close-ups (if possible) of the feet; the top photo suggests a "tarsal formula" of 5-5-4 (five segments in the front and middle feet, four segments in the hind), which would place this in the infraorder Cucujiformia (which group includes most of the beetles, so narrowing it that far isn't as much help as it could be).

As a singaporean, I'd say this is a tenebrionid, probably one of the Strongylium sp, possibly Strongylium erythrocephalum. Most of the Strongylium species here tend to only be found in the forest, but this species in particular seems to occasionally be found in urban areas.

Photo courtesy of Len Worthington, CC BY-SA 2.0 https://creativecommons.org/licenses/by-sa/2.0, via Wikimedia Commons

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

Very nice find! Thanks, and added a photo. Hope that's ok.

This is a beetle Coleoptera, possibly from the family of the 'ground beetles' Carabidae
As this family is one of the most speciose animal families, pinpointing an exact species will be difficult, especially in the tropics.
I think your specimen belongs to the genus of Carabus, they look similar as you can see on the picture from  wikipedia commons below:
- Long legs.
- Often a distinct pattern of dots and stripes on the shields.
- Long antenna with many segments
EDIT: As @theforestecologist pointed out, the body shape more resembles the family of Meloidae.   Most Meloidae don't have dots on the shield, but for example lytta does. https://bg.m.wikipedia.org/wiki/Файл:Lytta_aenea.JPG

Body/wing shape doesn't quite match many Carabidae. I was actually thinking the OP's specimen looked more like Meloidae. Lytta sayi which is found in North America is very similar, but I do not known Singapore insects well and thus do not know any relevant relatives -- a quick search didn't pull up any good choices.

@theforestecologist Meloidae often do not have the dots on the shield, but you might be right about the body shape. Hmm, dunno.

@theforestecologist I did find any good choices either. I've edited my answer to reflect your doubt (and my own). Or should I remove the answer  now?

I'd keep the answer, since our back-and-forth should be enough to inform others that this answer is not definitive. I think if you're actually doubtful as you indicate in your last comment, that you should edit your post further to make that uncertainty more explicit  -- e.g., replace "it is" with "it possibly could be" or something similar...Perhaps someone more familiar with the fauna of Singapore can use this discussion as a jumping off point. Thanks.

source: Stack Exchange

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

sort: votes


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Meaning of PAM matrix values
If PAM-1 matrix refers to time or evolutionary event for 1% change in amino acid sequence of a protein then how come there is PAM250? shouldn't PAM 100 be the highest where the two concerned sequences are 100% different

What attempt have you made to find the answer to this frequently asked question on line? Please read the help on asking good questions. Tell us what pages you have consulted and why you do not understand the explanation. Then we can help.

I used Xiong's and Jhumur Ghosh's bioinformatics books. they both explain how the matrix are made pretty well but my confusion is what I stated in my question. Page 148 Jhumur Ghosh's book states that the PAM 100 matrix corresponds to 100 accepted mutations per 100 residue. So, shouldn't it be the highest available matrix where the entire sequence is different. it clearly states there is 100% change in 100 amino acids after all. but then it also states one residues can also change more than once. how come one single residue can change multiple times when I am comparing two sequences only.

English is not my first language, so, may be a little different set of words might be helpful for me to understand what really is going on. that's all

No. The terminology is difficult even for English native speakers. The key is what an “accepted” mutation is. Try Wikipedia or other sources that explain that. I’m on vacation so can’t actually check. Search for “accepted point mutation” perhaps.

Accepted mutations are those that are accepted by nature, for example a hydrophobic amino acid substituted by another similar hydrophobic aa which does not negatively hamper with the protein structure and thus naturally selected. Any lethal mutations or silent mutations won't be part of accepted mutation.

No. Not in this context. Do as I say and search.

https://en.m.wikipedia.org/wiki/Point_accepted_mutation?wprov=sfla1

Let us continue this discussion in chat.

You misunderstood slightly what PAM1 means; it's actually (from Wikipedia) "1 [PAM] mutation to occur per 100 amino acids". So PAMn makes sense for any n, as in the 100 amino acids may mutate more than once each, on average.
Or if you put it in terms of PAM distance...

Is possible for two sequences to be more than 100 PAM
  apart?
  Yes: One position can mutate multiple times.

An attempted analogy: what does 600% casualty rate (for soldiers) mean? Well it means not only the original guy died, but his 5 replacements got (successively) killed as well.

If I am dealing with multiple sequences it makes sense if one position is getting mutated time and again but if I am comparing only two then how come one position is mutating multiple times?

For example, if the query is MFPIMW and the sequence I am trying to align is MWPIMW then one spot at F is mutated, how can this specific spot mutate twice when I am dealing with only these two sequences.

@Anindya: it can because a PAM is not a simple mutation. Given two randomly chosen amino acids, you may not have a PAM of 1 between them. Look at PAM1 for instance; note that the matrix entries are probabilities multiplied by 10,000 in there, i.e. the actual numbers are less than 1.

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


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What's the difference between releasing hormones and tropic hormones?
I've been reading my textbook and two terms have appeared that, after a bit of looking, I still can't seem to be able to distinguish. Here's what the textbook says (McGraw Hill Bio 12, 2011):

After receiving signals from various sensors in the body, the
  hypothalamus secretes what are referred to as releasing hormones,
  which often travel to the pituitary gland. The releasing hormones
  stimulate the pituitary gland to secrete hormones that act on other
  endocrine glands. Hormones that stimulate endocrine glands to release
  other hormones are called tropic hormones. (pg. 394)

From the work I've done, it all seems to indicate that releasing hormones regulate the secretion of other hormones, and that tropic hormones target and stimulate other endocrine glands (to release hormones). And yet my textbook appears to use the terms separately later on as if they're related rather than identical (e.g.: "the pituitary gland is controlled by the hypothalamus via releasing hormones and it secretes tropic hormones" (pg. 396)). So are they identical? And if not, what distinguishes between them?

The releasing hormones could also be considered tropic hormones, and indeed they fit the definition as you noticed, but aren't usually named as such.
The special thing about the ones your textbook is specifically highlighting as releasing hormones is that they communicate from the hypothalamus to the pituitary through the hypophyseal portal system, vessels that travel directly from the hypothalamus to the anterior pituitary.
Therefore, they aren't really released into the broader circulation (they can get there, but they'd be in too low a concentration). They are easily identified in a list of hormone because they all share a naming convention where they are called "____-releasing hormone" and their primary function is to cause the pituitary to release whatever is in the "_____".
In terms of overall neuroendocrine function, the "releasing" hormones all cause release of tropic hormones, which in turn cause release of hormones that affect other tissues.
Therefore, the sequence is releasing -> tropic -> non-tropic. They could have been named something else, like "primary tropic" and "secondary tropic" but this terminology keeps them separate as "tropic hormones that cause release of other tropic hormones."


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What is the difference between Regulatory Gene and Modifier Gene?
If both controls the expression of another gene by physically or genetically interacting with the target gene, which attributes make "Regulatory gene" different from "Modifier gene" or vice-versa?

Leaving a comment when down voting would help. I upvoted.

Different terms in different fields
I think that the two concepts are very similar but are used in different fields. The term "modifier genes" is often used in quantitative genetics and in evolutionary genetics while the term "regulatory gene" is often used in molecular genetics.
Example of a modifier gene that is not a regulatory gene
The concept of modifier gene can also be used in modelling when considering genes that "modify" the recombination rate (e.g. Otto and Barton, 2007; or other properties of the genome) in a quantitative manner. As such, a modifier gene is not really a regulatory gene (as it does not regulate the expression of another gene). As such I consider definitions like this one from ndsu as being too restrictive.
What I think about when I hear these terms
I would tend to think as a modifier as a more general concept than the concept of regulatory gene. Also, when I think of a regulatory gene, I think of this gene by the mechanism by which it affects other genes while when I think of a modifier gene, I think of the statistical effect of this gene on genetic properties of the organism.

Thnx for ur comment @Remi.b. Can it be that "regulatory gene" does not have any functional phenotype? It just can modify another gene? On the other hand "modifier gene" has its own functional phenotype and at the same time, it can have an epistatic relationship with another gene?

I am not sure I understood your comment but please see edit in my answer.


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Why aren't mammals and reptiles considered amphibians?
We've all heard it: birds descend from dinosaurs, so they're dinosaurs too. But this got me thinking: doesn't this mean that, for instance, all terrestrial vertebrates – including humans – are technically fish? A recent video by MinuteEarth and the Wikipedia article for "Fish" confirmed my shower thought hypothesis.
Interesting. But... all amniotes, i.e. reptiles (and, by extension, birds) and mammals, descend from amphibians, right? If so, then why aren't they considered amphibians too?

It's for logical clarity. Languages aren't perfect and there can be only 1 word when 2-3 words would be useful. Amphi means both and bios is life. It means double life technically it doesn't mean water and air. the combination of AM AN and IBI in the word amphibian make it a word that has stood the test of time.

Mammals and reptiles aren't considered amphibians, because amniotes are not hypothesized to descend from Amphibia. That is to say that Amphibia did not evolve into Amniota. They are sister clades (actually Reptiliomorpha in the Tree of Life tree below).

Ah yes, this makes more sense. I must've misread something and concluded that amphibians are the ancestors of mammals and reptiles. Still though, doesn't Mammalia descend from Reptilia? If so, what about the fact that Mammalia isn't classified within Reptilia?

Follow the Amniota link on the page linked above. You will see sister clades Synapsida and Reptilia. I'm not sure what wikipedia says, but I wouldn't trust it in general.

Some named groups are not monophyletic (see this post for definition if needed). Fishes do not represent a monophyletic group. Groups like "fishes" are completely awful to define but everyone would agree that no, humans are not fish!
Now, it is important to understand for many terms, there might have a scientific and a popular definition of the term. For example, when people talk about reptiles, they talk about turtles, snakes, lizards, squamates but they don't talk about mammals. Hence by "reptile" they don't mean "Reptilia". Have a look at the post If dinosaurs could have feathers, would they still be reptiles?).

Huh. I thought the Scientific Classification of life was 100% cladistic, but since the reptilia and mammalia classes aren't contained within amphibia, I guess middle-school Biology kinda lied to me...

I think my answer was a little unclear. I edited it. Please read it again. I did not mean that in cladistic, we name groups that aren't clades (clade = monophyletic group). I mean that the terms "Reptilia" and the term "reptiles" don't mean the same thing.

Thanks, but my question remains, though: if – as you've stated yourself – cats are Amphibia, why isn't Felix catus (or any of the other amniotes, for that matter) taxonomically classified within Amphibia?

Amphibia do not contains cats though. Amphibia only contains Anura (the frogs and toads), Urodela (the salamanders), and Apoda (the caecilians) (note I corrected a mistake in my above post). Reptilia do contains cats though but you would never state that a cat is a reptile. I think you have a false belief that mammals are part of Amphibia. Amphibia are a sister lineage to Reptiliomorpha (see here) and cats are part of the Reptiliomorpha

The real - and IMHO only - reason is that some people just think it's "cool" to claim that birds are really dinosaurs.

Whether mammals are reptiles is one of those circular pointless classification arguments you sometimes get in science, that people debate endlessly. It is based on using an archaic classification in a modern system.

@jamesqf birds are dinosaurs, the clade dinosauria is defined using birds. Dinosauria itself is defined as the last common ancestor of Triceratops horridus, Passer domesticus, Diplodocus carnegii, and all of its descendants. Passer domesticus wouldbe the house sparrow.

@John: No, birds EVOLVED FROM dinosaurs (which went on being dinosaurs for many millions of years afterwards).  It is the same sort of logical confusion that would insist on saying that all vertebrates are really just fish :-)  And if your modern classification system insists on such things, perhaps the problem is with the system?

It all depends whether by dinosaurs you mean what most people mean (which exclude birds) or whether you mean Dinosauria. While it somehow makes more sense to state birds are dinosaurs, one must highlight that if you make such statement, you should also say "mammals are reptile" (or that vertebrates are fish) which is not something we would want to say. Personally I am fine with both "birds are dinosaurs" or "birds evolved from dinosaurs".

@jamesqf by that argument human are not mammals, because humans are primates, it doesn't make any sense. Imagine the only surviving mammals were bats, would bats stop being mammals?

@John Following your logic, are humans reptiles? Just accept that in the common language, people can group species in a non-phylogenetic way. I think it is as silly to attack someone that say "birds are dinosaurs" than it is to attack someone that says "birds evolved from dinosaurs".

@Remi.b what makes you think I had a problem with someone saying birds evolved from dinosaurs? I just have a problem with someone saying birds are not dinosaurs, there is no scientific definition of dinosaurs that does not include birds. biological classification is nested, which is why terms like non-avian dinosaurs exists, or non-human animals. I accept that reptiles is a bit weird because the word is so old so the lay term carries a lot of baggage, but even the original use of the word dinosaurs would include birds given what we know now.

reptiles don't work no matter what you do, crocodiles are more closely related to birds than they are snakes. It is hard to say mammals are reptiles because synapsids are likely not in crown reptilia, that is the mammal clade is not in the reptile clade, they are squarely in amniota however. going by lay usage mammoths and ichthyosaurs are dinosaurs, lay usage is generally useless.


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Why are sea dwelling mammals less aggressive than land dwelling mammals?
Many mammals on land seem to be quite dangerous to humans: e.g., tigers, lions, elephants, hypos etc. However, their sea-dwelling counterparts (e.g., orcas, dolphins, sea lions, whales etc.) are relatively friendly to humans (and in contrast to say sharks). Is there a simple reason for this?

Is there an objective way to measure friendliness of wild animals?

There is only one sea mammal specialized in eating seal sized prey and mammals, orcas. Why only one? that's tough, it's the solution to your query. Land based mammals prey substantially on large mammals, bears, big cats, wolves... When mammals size up another animal they think: "what is that animal shape doing? is it a food or a monster?" and "what is that face?" when they look at other animals. When sea mammals sea us they think "that's an alien from another world, he swims like a clown but his face is cool"

More encounters on land
There are more land animals that meet humans walking around than there are sea animals that meet humans swimming around. If fewer attacks happen on humans in the sea environment, it might just be because there are fewer encounters with marine mammals than with land mammals.
Greater species diversity on land
In your list used as example, you cherry-picked a few aggressive(-ish) land mammals but the vast majority of land mammals are not aggressive toward humans. The fact that there are no marine mammal that are aggressive toward humans might just be because there are too few fewer marine mammal species.
Pseudoreplication and phylogenetic signal
I would argue that your sample size is not as large as you might think. There are only four lineages of mammals that evolve to live in the seas. There is therefore a phylogenetic signal and ignoring it would be a problem of pseudo replication.
For example, I could very well think of territorial behaviour (which is where a lot of aggressive behaviour comes from) as having a strong phylogenetic signal.
Why considering only humans?
Your post title talks about aggressiveness in general and the content of your post talks about attacks against humans. It sounds that considering only attacks against humans to be very unfair. Orcas, typically, are fierce and violent predators although no orcas have ever attacked a human in the wild.
Are they really that friendly to humans?
There has been a number of attacks in captivity (well known cases with orcas). Also, there have been a number of whales attacks against boats (according to this BBC article).
In short...
In short, I think your comparison is unfair. I think you are looking for an explanation for a pattern that does not really exist.

I think there are actually 4 lineages of marine mammals: cetaceans (whales & dolphins), pinnipeds (seals & walruses), sirenia (manatees and dugongs), and mustelids (sea otters).  Maybe 5, if you include polar bears - which aren't all that friendly to humans.  Wikipedia has a diagram: https://en.wikipedia.org/wiki/Marine_mammal

@jamesqf Thanks for correcting! I forgot sirenia and the sea otters. I edited the post

Another example of a predatory cetacean would be the sperm whale.  But since they prey mostly on squid that live at depths of 300-800 m or more, you are not in much danger from them.  Unless you are Captain Ahab, of course - and that was pure self-defense on Moby Dick's part :-)  (Yes, I know that's fiction, but it was inspired by actual events, notably the sinking of the Essex: https://en.wikipedia.org/wiki/Essex_(whaleship) )

They actually aren't less aggressive than terrestrial mammals. I've heard a lot of biologists talk about this weird trend in marine mammals (and more or less only marine mammals) where for some strange reason, marine mammals have this weird predilection for sexually assaulting other species. Warning, most of the below links are scientific articles or news sources reporting scientific articles, but they can still be a bit explicit due to the subject matter.

Bottlenose dolphins are well known for having sex with just about everything that moves, including other dolphins (of both genders), humans (there is actually a wealth of literature on this), their own parents, and other sea life, including the females and babies of other dolphin species (and the babies of their own, by the by). Gender, willingness, or even the fact of the other individual being alive need not matter. They've been known to drown baby porpoises due to assaulting them so hard, and then continue to have sex with the body. This isn't unique to bottlenoses but has also been documented to some degree in botos (Inia geoffrensis), dusky dolphins (Lagenorhynchus obscurus), and Hector's dolphins (Cephalorhynchus hectori). It hasn't been documented yet in orcas, though this is probably a tracking issue more than anything else.
There's actually some evidence that dolphins may not be attacking other marine life for any definable survival or directly Darwinian reason, but are doing it for fun (or, from an etho-evolutionary perspective, the play behavior of killing or assaulting other marine life gives dolphins practice for when they commit infanticide on their own kind). Dolphins, at the very least, are some of the few animals aside from great apes that are known to perform non-copulatory reproductive behavior for pleasure.
Sea otters are well known for sexually assaulting and raping female sea otters, and frequently they will do this to baby seals as well. They are so rough about it the females and baby seals often drown, and again like the bottlenoses the otters continue copulating with the body
True seals aren't perpetual victims of this, as grey seals have been observed sexually assaulting seals of other species
Elephant seals also get in on the act, though so far only with their own species.
Fur seals (a relative of sea lions, rather than true seals) have been observed chasing down and forcibly copulating with penguins. They sometimes eat them afterwards.

This is seemingly commonplace among marine mammals, and nobody really knows why. Some of it definitely seems to be purposeful rather than the result of misplaced instincts, at least the way the researchers in the primary literature listed in the articles linked describe it. However, you almost never hear about this among terrestrial mammals. The only thing I've heard close to this is how traumatized young bull African elephants have been known to kill adult rhinoceroses and try to copulate with the dead body, and in that case it's clearly not normal behavior for the species.
So in at least some ways marine mammals are violent in ways that terrestrial mammals rarely are, and at least some of this (in the case of dolphins) is directed at humans.


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Relationship between the ambiguity (wobble) at codon position 3 in elongation and codon position 1 in initiation
In prokaryotes the usual observed start codon frequency is AUG > GUG > UUG.
An explanation for this is that

AUG is the most common initiator codon because it forms the most stable interaction with the CAU anticodon in fMet-tRNA

But does this have anything to do with the more general wobble rules?

Codon-anticodon pairing takes place according
  to the wobble rules (Crick 1966). During translation,
  base-pairing occurs in the usual way (A with U, and
  G with C) between the first and second nucleotides
  and the second and third anticodon nucleotides. The
  wobble rules state that in the pairing between the
  third codon nucleotide and the first anticodon nucleotide,
  there is a certain amount of play, or "wobble."
  This enables G in first anticodon positions to
  pair with U or C in codons, U with A or G, and I
  (inosine) with U, C, or A. In first anticodon positions,
  C pairs only with G, and A (very rare) only
  with U. These rules are fundamental to all discussions
  of codon capture. Table 1 shows anticodons
  in the universal genetic code as predicted by the
  wobble rules (Crick 1966).

I'm confused because that seems the exact opposite of what happens in the start codons' case, i.e. the "play" is in the first (not third) codon nucleotide in the start codon case. And the table in this last paper only gives CAU Met as the only pairing for CAU, so no wobble.
Am I interpreting this correctly and there's no "Crick" wobble in the AUG > GUG > UUG start codon, but rather another wobble-like mechanism that explains the start codons' first nucleotide wobble-like behavior?

I have changed the title, retaining the sense while not prejudging the nature of any "rules".

Summary
The difference in the nature of codon–anticodon ambiguity seen between bacterial initiation and elongation lies not only in the position of the codon at which it occurs (5′ v 3′, respectively), but in the partial or absolute nature of the interactions (only some AUG and GUG etc. codons initiate and insert fMet, whereas all AUU and AUC codons will recognize the Phe-tRNA with anticodon, 3′-UAG-5′. It can be accounted for by the quite different molecular interactions occurring at the ribosomal P-site (for initiation) and the A-site (for elongation) and the importance of the base-pairing between the Shine & Dalgarno (RBS) region of the mRNA for initiation.
Wobble in context
Wobble was the term applied by Crick in 1966 to the non-standard base-pairing between the 3′ position of mRNA codons and the 5′ position of anticodons of certain tRNAs. To avoid violating the genetic code Crick assumed strict base pairing at the first two codon positions and asked the question “If one sRNA [old term for tRNA] codes both XYU and XYC [because of experimental evidence that this might be the case for Phe codons], how is it done?”. And then, given the many ways bases might be paired added the constraint “How many base pairs are there in which glycosidic bonds occur in a position close to the standard one?”.
On the basis of geometry Crick predicted that anticodon 5′-U might be able to pair with a codon 3′-G (in addition to the standard A), and anticodon 5′-G with codon 3′-U (in addition to the standard C). He — unwisely in my opinion — referred to these predictions (and his prediction for inosine, I) as ‘rules’. The predictions are summarized below, together with the actual pattern that has since emerged.

It should be noted that although the two predictions involving G=U base pairs would appear reciprocal, that involving an anticodon 5′-U does not occur except in mitochondria, were it is incorrect in that the interactions are not restricted to Crick’s ‘rules’.
The subsequent elucidation of the structure of phe-tRNA by Quigley and Rich in 1976 suggested why the wobble occurred at the 5′ position of the anticodon. This position (G34 in my modification of their figure, below) lacks the base-stacking that would be expected to constrain the interactions at the other two positions of the anticodon, and which was aided by a modified base (yW37) 3′ to the anticodon.

As the amino acid, methionine, has only a single codon (AUG) in the genetic code, one would expect it to have a tRNA that does not allow wobble at the 5′-codon position. This turns out to be the case:

Both the tRNAmet for elongation and initiation have
  the anticodon 3′-UAC-5′.

In summary: 5′-codon wobble allows mRNA to be decoded accurately by fewer than the 61 amino acid codons, and one can speculate that its emergence involved evolution of both the structures of tRNAs and the ribosomal A-site.
Initiation and decoding ambiguity
In bacteria (eubacteria) there are two main differences in codon recognition during translation from that in elongation.

There is a single specific tRNA species involved which, uniquely, can interact with initiation factors and be bound to the P-site of the ribosome.
Interaction is required between the 16S rRNA of the 30S ribosomal subunit and a polypurine sequence 5′ of the initiation codon (the Shine & Dalgarno sequence or ribosome-binding site) in addition to the codon–anticodon interaction.

To adopt an extreme position, the situation in initiation may almost be thought of as one in which the fMet-tRNA is bound at the P-site of the small ribosomal subunit waiting for mRNA to bind, in contrast to elongator Met-tRNA binding to an A-site with the elongation codon AUG. The energy provided by the Shine–Dalgarno interactions may thus be enough to allow initiation if one of the initiation codon bases is incorrect. This raises at least two questions:

What advantage would allowing such ambiguous recognition have?
Why is the ambiguity in the first codon position and how does it operate in molecular terms?

I have no answer to the first question. Perhaps it has none, but is tolerated because it has no disadvantages either. The second question is the crux of the poster’s concerns.
First, ambiguity at the 3′-position of the codon would not be expected on grounds of structure or precedent: the table above shows anticodon 5′-C only base-pairs with codon 3′-G.
Second, the anticodon loop of initiator tRNAmet differs from that of elongator tRNAmet in having an internal-facing rather than an external-facing disposition (Woo et al., 1980). Furthermore it lacks a modified base 3′ to the anticodon.
Third, the interactions between initiator and elongator tRNAs with the rRNA at the A- and P-sites, respectively are quite different (Berk et al. 2006), conceivably allowing more flexibility at the 3′-anticodon position.
Despite the fact that the predicted anticodon-U/codon-G wobble never occurs at the A-site, it is reasonable to suppose that structural differences allow it at the P-site, explaining the second bacterial initiation codon, GUG. As regards UUG, U=U base-pairs were considered by Crick but regarded as “rather close together”. Presumably in certain contexts this is not too energetically unfavourable to be prevented.
Finally…
The poster asked:

Am I interpreting this correctly and there's no "Crick" wobble in the AUG > GUG > UUG start codon, but rather another wobble-like mechanism that explains the start codons' first nucleotide wobble-like behavior?

To which I would reply that:

There is not and cannot be any wobble at the 3′-position of either initiation or elongation AUG codons of bacteria because it would involve non-standard base-pairing of the anticodon C. To the extent that the ambiguity at the 5′-position of the alternative initiation codons used (GUG>UUG) follows a pattern consistent with the most likely non-standard base-pairing predicted by Crick, it would seem to involve base-pairing achieved by movement (wobble) of the 3′-anticodon residue U of initiator fMet-tRNA.

Also, did look at a paper comparing the initiation and elongator myself (has nice diagrams on both eukaryotes and prokaryotes (Rassmusen et al.), but  they didn't hint to anything about function with respect to wobble-like behavior from the structural difference. So I do wonder how speculative the mechanisms are.


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Why do genetic testing companies (FTDNA,AncestryDNA,23andme) express DNA shared in centimorgans (cM) instead of in number of base pairs or in percent?
Expressing DNA shared in number of base pairs or in percent of total genome would be so much simpler and easier to understand for the customers.
.

What kind of data / reports are you referring to? Also not that these comapies do not perform DNA sequencing, they do DNAchip based SNP characterisation; therefore any actual basepair positions they could give would come from a refernece genome, which has to have a specific version and is not easy to use/understand for customers.

@Nicolai You could probably make an answer out of your comment.


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Repopullation after a mass extinction
Is it possible to restart the whole human species with less than 10 individual.
let say that the whole human species was wipe out of the surface of the earth by a catastrophe only 8 different couple survive the catastrophe could they restart the human species?

The estimate is probably going to depend on the source, but it's generally at least an order of magnitude more than that.

Back in 2002, John Moore, an anthropologist at the University of Florida, calculated that a starship could leave Earth with 150 passengers on a 2000-year pilgrimage to another solar system, and upon arrival, the descendants of the original crew could colonize a new world there—as long as everyone was careful not to inbreed along the way. [...]
A starting population of 40,000 people maintains 100 percent of its variation, while the 10,000-person scenario stays relatively stable too. So, Smith concludes that a number between 10,000 and 40,000 is a pretty safe bet when it comes to preserving genetic variation.

For the general concept see minimum viable population.


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Why don't mitochondria have plasmids?
According to the endosymbiotic theory, mitochondria are descended from specialised bacteria (probably purple nonsulfur bacteria) that somehow survived endocytosis by another species of prokaryote or some other cell type, and became incorporated into the cytoplasm [ref].
And plasmids naturally exist in bacterial cells, and they also occur in some eukaryotes [ref].
I was however taught that mitochondria have no plasmid and only have circular DNA. If the endosymbiotic theory is true, then how come mitochondria have no plasmid?

The mitochondrial genome is highly reduced; many mitochondrial genes have been transferred to the nuclear genome (see endosymbiotic gene transfer) and therefore the mitochondria are fully dependent on the nucleus to function.
Bacteria need not necessarily have a plasmid. Usually, all the important genes are present in the chromosomal DNA. Since the mitochondria have lost most of their genes and retain only a few genes that are highly essential for their function, the likelihood of retention of any plasmid DNA is very low. However, there are some reports of plasmid-like DNA in mitochondria (mostly in plants).

Handa (2008): in Brassica
Robison et al., (2005): in carrots
Collins et al., (1981): in Neurospora (a fungus)

Likewise, chloroplasts also harbour plasmid-like DNA (google-scholar hits).


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What is the role of lactic acid bacteria (such as L. acidophilus and L. bulgaricus) in glycolysis during yogurt fermentation?
I am trying to prove that an increase in monosaccharides (glucose, fructose, galactose) that have been added to milk during fermentation will result in a decreased pH. My current argument is:
"The increase in the concentration of Phoenix Dactylifera is representative of an increase in the disaccharide, sucrose, and the monosaccharides, glucose and fructose — the primary sugars in date palm. This source of sugars adds to the natural sugar content already found in low-fat milk, which are lactose molecules composed of glucose and galactose. As such, more energy from these carbohydrates are available in the process of glycolysis, where LAB facilitate the conversion of six-carbon sugars like glucose, fructose, and galactose into pyruvate. This creates a greater frequency of glycolysis reactions, resulting in a greater overall yield of pyruvate molecules which can be converted into lactic acid. Hence, the increase in overall production of lactic acid increases acidity in the yoghurt and, thus, the pH."
What can I fix with my answer?


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TBX3 Protein structure and function
Is it possible for an anti-cancer monoclonal antibody to target the two repressor domains in the N and C terminal of the TBX3 protein ?

It is very unlikely that an antibody binds to two domains of a protein at the same time. If the two domains have a high structural similarity it might be possible that one TBX3 protein binds two identical antibodies. You could align the two domains and see if they have a common sequence stretch. If that's the case you could check if the stretch is unique, i.e. otherwise the antibody would bind to more than just RBX3.

Hypothetical questions have been asked here and we consider them on-topic if sufficient background and rationale is provided. Can you please elaborate your question? As it stands, it looks like a primarily opinion-based question and is likely to be put on-hold. Moreover, because of the lack of background, your question is also a bit unclear.


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Is it possible to identify this microscopic particle?
So I was playing amateur scientist with my 11 year old.
This photograph is from rainwater in a bird-feeding bowl in south England, at 300x.
It looks biological, but I have no idea what this is. Is it possible to know, beyond speculation, what this item is?

@theforestecologist  It was not moving, that I could tell.

This is an plain old ice crystal. Welcome to the microscopic world! When water evaporates, high-energy molecules escape, leaving low-energy molecules of water. The droplets cool this way, and they freeze - the dirt or debris in the crystallizing droplets make curious patterns. Here are some in my samples I made last week, for comparison:

How about a close-up?

Here's one I made by accident, this time featuring a fluorescent dye.

Notice how cooling droplets never freeze the same way twice. You'll never find two identical crystallized droplets!
If you want to avoid these, prevent evaporation by putting nail polish or glycerol around and between your coverslip and slide, so that water cannot escape.
OFFTOPIC: You should also encourage your kid to try make some of his/her own crystals. You can use food dyes to make beautifully patterned art. Good moment to teach your kid about nucleation; why water doesn't freeze at 0° C, but rather at temperatures that tend to decrease as the volume of the water decreases and as the water impurity increases. And maybe sneak in a funfact about how the freezing of small water droplets into ice is an important process in cloud formation.


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Why does 4-thiouracil labelling to map RNA-binding proteins cause a T-C change?
I am now reading a paper about the purification and identification of mRNAs and its RNA binding proteins by using UV crosslinking and immunoprecipitation. I came upon this sentence which puzzled me

Up to 28% of all uridines present in 3' UTRs showed diagnostic T-C
  changes in the protein occupancy profiling sequence reads. This number
  is reasonably high, considering observations that typically only one
  of a few uridines in RNA binding sites when substituted by 4SU,
  crosslinks to proteins.

What I do not understand is why does 4-thiouracil (4SU) labelling in the cell show T-C changes. Would the uracil-adenine base pairing not be affected?
How does the 4SU labelling really work?

The technique used in that paper is called PAR-CLIP (Photoactivatable Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation; see Ascano et al., 2012 and Spitzer et al, 2014). This technique involves substituting uridine (U) with 4-thiouridine (4SU) or substituting guanosine (G) with 6-thioguanosine (6SG). The rationale behind using these modified bases is that they improve the efficiency of RNA-protein crosslinking. Moreover, PAR-CLIP uses 365nm UV instead of the 254nm UV used in the conventional crosslinking. However, the crosslinking process causes the loss of the sulphur atom causing the U to be read as C during reverse transcription. Likewise, 6SG gets read as A.

Ascano et al., 2012


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Clarification of method notation in yeast cultivation method
I'm reading a paper about yeast culture and in the methods, it says:

Then $5$ ml of sterile $M/15\ KH_2PO_4$, was added to the slant,

What is the meaning of $M/15$?

Can you add the paper itself? or a screenshot of the relevant section?

The only interpretation I can think of is a concentration of (1/15) M, i.e. 67 mM. But I've never seen anyone write it this way.

@VictorChubukov That's what I thought, thanks

@VictorChubukov. That's what it is. I just verified. I don't know much about the history of that though but it is an old notation that is no longer used. Can you please post an answer?


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What part of the skin is damaged under sun exposure?
How exactly does extensive sun exposure lead to skin damage and increase cancer risk. In which part of the skin is the sun doing the most damage. Is it in the epidermis or beneath ? I would like to know if UV-protective tattoos would be possible.

Hi Roy; welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal, Roy, is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail and it will likely be received more positively by out community. Thanks!

Roy, @theforestecologist is completely correct. Long story short, though, tattoos are a kind of skin damage, and may cause cancer.

https://www.youtube.com/watch?v=GRD-xvlhGMc - https://www.youtube.com/watch?v=V9K6gjR07Po


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If a bacterium had a protein on its surface that humans also have, would it cause an autoimmune disease?
Suppose that a bacterium happened to have a protein on its surface. This protein can also be found in the human body. If this bacterium were to then infect a human with an otherwise normal immune system, would his/her immune system attack the person's body, in addition to the bacterium?
The reason I'm asking this is because I have read a book about how, supposedly, the Soviet Union created a bacterium that did just that: they modified Yersinia Pestis to produce myelin which, supposedly, caused multiple sclerosis. The book's author claims that this really happened, but I am skeptical of that claim.

It's believed that many autoimmune cases are triggered by what you describe - pathogens or opportunist bacteria and viruses that contain proteins similar to human proteins.For example:

Autoimmunity to hypocretin and molecular mimicry to flu in type 1 narcolepsy
Translocation of a gut pathobiont drives autoimmunity in mice and humans
Autoantigen cross-reactive environmental antigen can trigger multiple sclerosis-like disease

However, it's important to understand that although these cross-reacting proteins may be required in the process of autoimmunity, they aren't sufficient to cause autoimmunity alone (or else everyone would have autoimmunity all the time). Autoimmunity needs to have a whole bunch of steps, including several pieces of genetic susceptibility and environmental conditions, before the specific trigger will cause a problem (and it's likely that once the many other conditions are satisfied, there are multiple potential triggers that can set up the final cascade).


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Does a severed limb/finger experience pain after its separated?
If a person ends up with a severed finger will that finger, after falling off, experience any pain and start writhing? Can a limb kind of have a mind of its own for a few more seconds after separating from the body like for instance the tail of a lizard?

haha, that's hilarious though, but no, your severed finger will not have/gain own mind nor will "feel" the pain :) however, it may twitch on its own for few seconds/minutes

@cell0 So why will it twitch for a few seconds/minutes? It should lay still right after getting seperated from the body because the connection with brain is lost....am trying to know how it's able to twitch in the absence of life force

Twitching does not require contact from brain. The muscles can respond to local triggers. Anyway, that should be a new question altogether.

@user221238 its due to muscle contraction and fyi human body can twitch even days after being dead. guys from morgue could tell stories...

@cell0 am aware of muscle contractions occurring hours after death as rigor mortis sets in....I was curious wondering if limbs have their own local sensation mechanism, much like the tail of the lizard

@user221238 Just any sensation is different from pain sensation. Pain is not merely a sensation but an "emotional" response. Of course, severed body parts can contain neurons that continue to fire. However, these signals are not reaching spinal cord or the brain and hence there won't be any response.

@WYSIWYG thanks. That's just what I was looking to confirm.

Pain is a signal emitted from a nervous pain receptor cell (called a nociceptor) to the central nervous system (CNS, i.e. the brain). If I hurt myself causing a small cut in my finger, nociceptors around the cut will send the pain signal to the CNS, which in turn processes it and causes the physical feeling of pain in that region.
If a finger is severed, nociceptors just above the cut will be extremely active, interacting with the CNS and causing a lot of pain. On the other hand, nociceptors in the finger itself have nowhere to "push" the pain signal to, so in this sense they cannot measure any pain - there's not a CNS connected to the finger anymore that is able to process the signal emitted by any nociceptors in the finger.


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What are the issues with excessive tandem repeats in replication?
Why is it that tandem repeats like CAGCAGCAG cause primer-template misalignment and diseases like Huntingtons disease? By my understanding, too many such repeats can cause strands to form hairpins and loops that fail to be replicated in the template strand, causing deletions. Is this correct?

What research (see Help) have you done to try to find the answer to this question yourself? You should be able to find it very easily on the internet.

Moreover, your question is unclear. Are you asking how these repeats increase or how they cause disease?


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How do biologists discover information from fossils?
I have a query about the study of fossils (palaeontology). Let me know about the study of fossils. How do biologist discover "DNA" information from dead and old fossils such as a dinosaur?  (answer this question in a paragraph or two)

Your question appears very broad; you can find entire books/reviews dedicated to this topic. Please narrow your question down and add sufficient details such that it is restricted to a specific issue and can be answered in a few paragraphs.

You can give me selected knowledge

This sounds like a homework question...Please review our homework policy. We ask that all question posters here attempt to search for an answer to their own question & explicitly indicate the research they've done, what they learned, and what is still confusing to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail and it will likely be received more positively by our community. Thanks!

@cell0 FYI, I rejected your proposed edit because it makes small style and grammar edits to a generally poor closed question, bumping it and adding it to the reopen queue without any improvement in substance.

How biologist discover "DNA" informations from dead and oldest fossils
  such as dinosaur.

They don't. In general fossils contain very little organic material. It's all been replaced by stone (silicates). On top of that DNA degrades over time.
There have been a handful of cases where researchers have claimed to recover small fragments of DNA from dinosaur fossils, but these are disputed, and are generally thought to be the result of contamination with human or other modern DNA.
DNA has been recovered from some more recent fossils like Neanderthal. For such a general question a better starting place would be to read the Wikipedia article on Ancient DNA.


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Frequency of nucleotide sequences of specific length in DNA

How frequently would you find the nucleotide sequence GGATATCCGC (5' to 3' direction) by chance in a DNA molecule?
On average, how many times do you expect to find a specific 20 nucleotide sequence in a genome with a total size of 4 x 109 base pairs?

Since that probability of finding each base pair in its given position is 1 in 4, thus the total probability of finding that particular sequence would be $0.25^{10}$
But how do I approach the second problem?
TIA

While the 'background' of this question is biology, it's actually a pure combinatorics & statistics question. I'd recommend asking this on a different SE site.

Apply the frequency you calculated in the first part (reworked for a 20mer) to an actual length. May be easier if you work it as 1 in x, then all you have to do divide the genome length l by x. Try my teaching site: https://www.mvls.gla.ac.uk/Teaching/SLS-GMC/ren.html.


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Are there toxins that cause heart attack and/or stroke in multiple individuals in short time frames?
Are there any known environmental factors that would cause more than one person to have a heart attack or stroke within a short period of time (e.g. 2-3 months) of one another? I'm particularly looking for causes that are likely to be found around the home (e.g., chronic low-dose CO poisoning), as opposed to industrial sites.

Could you give us some more details or narrow down your question? I'm afraid right now it reads to me like a request for an entire section of a toxicology text. Many, many substances could lead to a heart attack or stroke. It sounds like you have something specific in mind. What's the context here?

Candidly, I'm not certain how to be more clear, but maybe that's because I lack expertise in this area. I'm looking for a toxic substance that could reasonably be expected to be found in a house, and that could make the house's occupants likely to have a heart attack or stroke over the course of several weeks or months of exposure. I'd be inclined to exclude things like smoking, as the exposure needed in that case is on the order of years or decades. Does that help?


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Transformation of a multicellular organism
I was reading about using RNA-interference as a method of introducing pest-resistance in plants. In tobacco plants, using Agrobacterium vectors, genes specific to the nematode Meloidegyne incognitia were introduced. This was done in such a way that it produced both sense and anti-sense RNA in the host cell, forming dsRNA and ultimately silencing specific mRNA of the nematodes.
My question is, how can every single cell, or a proportion of cells sufficiently large so as to confer pest-resistance, of an already mature plant be transformed? Are a large number of vectors introduced, and as the infection gradually progresses, the immunity spreads throughout? Sorry if it's a stupid question, I've been out of touch with biology for a while.

Your inference is basically correct. The Agrobacterium acts as a vector for a plasmid containing the genetic construct one wishes to introduce into the plant genome. A medium containing a large number of bacterial cells transformed with this plasmid is injected into plant tissue, and the plasmids enter plant cells where parts of their DNA are integrated into the host genome. The overall effect of this is that there is localized integration in the areas where the Agrobacterium was introduced. A nice visual illustration of this comes from a paper from our lab where my colleagues introduced the genes for betalain biosynthesis into the tissue of Nicotiana benthamiana: in Figure 3 you will see only a localized area of cells around the injection site gain the ability to produce betalains.
You can find a nice review of the whole process of transformation with Agrobacterium here.


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How can we smell odor direction if we breathe through one nostril at a time?
It's known that humans breathe mostly through one nostril at a time. How can we then perceive the direction the smell is coming from? Some articles claim similarity between olfactory and auditory directional perception:

The direction of a sound source can be determined binaurally by using
  the time difference and the loudness difference of the sound waves
  arriving at the two ears. Similarly, the direction of an olfactory
  source can be determined by using the time difference and the
  difference in sensation magnitude of the olfactory stimuli between the
  two nostrils as the air surrounding the odorous object is inhaled.
  Time differences of the order of 0.1 msec can be recognized—a value
  similar to that found in hearing.

However, that explanation runs afoul of breathing mostly through only one nostril at a time because at least the difference in sensation magnitude of the olfactory stimuli should depend heavily on which nostril is 85% shut and which one is wide open.

HI Michael. I think your question can be solved by re-reading the source you interpreted to mean humans only "use" one nostril at a time.

@DeNovo, if you barely breeze through the 85% closed nostril you are unlikely to smell through it with the same intensity as through the open one. That makes it unlikely that you can use at least the difference in sensation magnitude of the olfactory stimuli between the two nostrils as the air surrounding the odorous object is inhaled part of the suggested mechanism of directional olfactory sense.

I believe both the low flow and high flow nostril are used to detect smells in a given cycle. I think your question could be improved by changing "use one nostril at a time" to "breathe from one nostril at a time", since you're saying "Its known..." It is not known that humans only detect smells from one nostril at a time.

Good edit, and I think this is a very interesting question. I just edited myself to change breeze to "breathe", which I think is what you meant. Feel free to roll back if i misunderstood. I don't have electronic access to the physiology study from the 60s you referenced, but I am very curious as to whether they took this into consideration.

my guess is that it requires detecting differences in concentration by turning your head.

A more recent (and complete) article: https://www.nature.com/articles/srep05796


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What soft tissue separates bones of toes?
I need to know a little about the "knuckles" of toes; specifically the 4 areas that separate the 5 proximal/metatarsal joins.
I'd like to know the terms for areas that might be damaged if the width of the foot were to be repeatedly compressed there. Is there even a name for just the general "knuckle area"?
Thanks

This question might have a better fit in Biology.SE.

Could you add a picture pointing to the joint(s) you are talking about? It's hard to tell if you are describing the joints between tarsals and metatarsals or between metatarsals and proximal phalanges.


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How much energy can one muscle contraction deliver?
How much energy is available in a single muscle contraction?  I'm guessing the correct units are J/kg, but I'm open to more correct units.  I'm looking for work done, not total energy dissipated (not interested in heat)
The goal of such a number is to figure out an upper bound on how much work a human body can do if it is never permitted to reset a muscle by moving the limb in the opposite direction (If the bicep does work for this test, the triceps isn't permitted to contract to return the curled arm back to its initial straight position)

This question needs substantially editing to make it at all answerable ~ different muscles in a body are different sizes ~ the same muscle in different people are different sizes ~ the size of a muscle necessarily impacts on how much energy it can exert ~ so "one muscle" means almost anything in that sense.

@Pelinore That's why I said I believe the correct units will be J/kg, which resolves that issue.  However, I'm open to other units which are more correct for making such measurements.

Ah, fair enough.


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What are these tiny creatures swimming around my aquarium?
I was checking out my aquarium today, and decided to scoop out a water sample and take a look at it more closely. What I discovered were numerous, very, very tiny white worms (?) swimming around in the water.
The worms hover around 1 mm or smaller, almost invisible to the naked eye, with some exceptional specimens reaching nearly 2 mm in length. They swim very fluently, not by wiggling or waving their bodies around, but simply, effortlessly gliding through the water.
I checked them out under a microscope, and recorded some videos. I apologize in advance for the lackluster quality, as I'm not working with expensive equipment here. It took me hours to locate the worms under the microscope, made no easier by how surprisingly fast they are.
Here's a picture:

When I first saw this, I wasn't sure I was looking at the right thing. As you can see in this video, it appears to stay rooted at the tail, while wiggling its head (?) around in various directions. Its most notable characteristic is the two ball-like structures on the front of its body. I have a feeling that those structures will be key here.
This next part was very poorly recorded, but boy did it surprise me when I saw it. Eventually, the worm stretched forward, its head seemingly morphing into three parts (video):

Finally, here's one more clip showing off how fast they can be when they want to (I swear it's not even sped up!). I wasn't able to get it back under the microscope at this point.
Does anyone know what these are, or at least what kinds of worms they might be related to (with respect to the ball-like structures on its head)?
For a little extra background, I found these in my native tank sourced with creatures caught in southern Alberta. The tank contains some longnose dace, which have been a source of concern due to heavy flashing (scratching) ever since I caught them. It makes me wonder if these worms are related, such as some kind of parasite. I'm happy to have them if they're some harmless detritus worm-- any members of the cleanup crew are welcome-- but if they're something to be worried about, I'd prefer to know.

this time I can help you ID these :). I'm now reminded, though, that I never figured out your fluke question. I'll have to go back and take a look...

Hard to tell because of the poor picture/video quality, but almost immediately the body shape, distinct "face", size and behavior made me think of a small invertebrate animal called a rotifer (Phylum Rotifera).

 Rotifer eating protists. Photo Credit: Jacqueline Ronson, 2016
There are about 2000 species occurring worldwide within this primarily freshwater phylum, each of which is fairly simple anatomically. Their name (which means "wheel bearer") comes from the two crowns of quick-moving cilia they possess on their heads:

 Source: Gifer
These cilia attempt to push food posteriorly toward the rotifer's back-set "mouth" (which is actually a modified pharynx called a mastax:

 Photo Credit: Jean-Marie Cavanihac
Rotifers are small (always < 2 mm) and so eat small planktonic and protist prey. From UC Berkeley:

As rotifers are microscopic animals, their diet must consist of matter small enough to fit through their tiny mouths during filter feeding. Rotifers are primarily omnivorous, but some species have been known to be cannibalistic. The diet of rotifers most commonly consists of dead or decomposing organic materials, as well as unicellular algae and other phytoplankton that are primary producers in aquatic communities.

As for body shape:
Although all Rotifer species are bilateral animals, they vary quite a bit in body shape. Box-like shaped rotifers are referred to as being loricate, while more flexible worm-shaped species are considered to be illoricate.

 Photo Credit: Juan Carlos Fonseca Mata
Regarding sometimes staying "rooted at the tail" as the OP observed:
Some rotifers are found usually free-swimming, while others "glue" down their posterior "toes" to anchor themselves to some substrate or debris. Again from UC Berkeley:

The final region of the rotifer body is the foot; this foot ends in a "toe" containing a cement gland with which the rotifer may attach itself to objects in the water and sift food at its leisure.

 Source: Starr et al. 2013 (Cengage Learning)
See here for further "fun facts!"

The "crowns of quick-moving cilia" convinced me beyond a doubt that you are correct; they appeared to be moving exactly as depicted in that GIF. I'm relieved to read that they're harmless, and even beneficial.

@560812508, rotifers may be harmless, but that many of them in your aquarium indicate lots of even smaller organisms are present for them to eat. You might want to consider changing the water more often or adding a biofilter.


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How did the molecular machinery for recombination originate?
I'm wondering about the origins of genetic recombination. During crossover new chromosomes are created. They have different allele combinations from the original two chromosomes. This process allows the combinatorial explosion needed for biological diversity. I am puzzled by the accuracy of this very complicated process of generating new genetic information.
Starting from single cell, When did the first genetic recombination appear? How did it come to existence? In my understanding, it could not have been the result of evolutionary process since genetic recombination must be done right at the first attempt.

"In my understanding, it could not have been the result of evolutionary process since genetic recombination must be done right at the first attempt" is patently false, but the rest of your question is a good question. As far as I know a definitive answer is unknown but it is an area of active research.

If only we knew when the fundamental processes in cells arose! What kind of smoking gun did you expect for this one?

https://en.wikipedia.org/wiki/Chromosomal_crossover#Origins


text:
Why do BRAF mutations appear more in skin cutaneous melanoma?
When looking at the tissue expression of the BRAF protein it seems that BRAF is regularly expressed in almost all of the tissues. There is elevated expression in tissues like the Testis and the Parathyroid gland, but the expression in the Skin is about average. So how does it make sense that for example in tumor samples of skin cutaneous melanoma (TCGA-SKCM) the BRAF mutations are so dominant (about 50% of the cases contain a BRAF mutation)? And on the other hand, it occurs less frequently in other cancer types?

This is a good question - I will try to answer it later.

Chris, if you know why, I will like to hear it please. Even if you only have an assumption about it.


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Have there been any efforts to release opossums as a biological control against ticks?
There's plenty of examples of people recognizing opossums as a great ally in controlling tick populations (here's one example). However, I can't find any examples of opossums being intentionally released or supported in areas specifically to control ticks.
Have there been any efforts documented that deliberately increase opossum populations to reduce tick infestations? If no, are there specific reasons why this has not been done? For the latter, there are of course examples of biological control gone wrong (e.g. cane toads released in Australia), but that doesn't seem to deter all biological pest controls (e.g. nematodes to control fungus gnats).

I think you have given the answer yourself. Opossums can be agressive predators, intentional release in new area's is simply an extremely bad idea from a ecological point of view.

@RHA that's certainly a reason why no one would try this. I wanted to check if anyone has tried it or there's been any serious consideration of it. Maybe it's simply too crazy and no agency has given it serious thought.


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What is the reason behind the subphylum name "Urochordata" for tunicates?
There are two major invertebrate subphyla of the chordates (phylum Chordata):

Cephalochordata (the lancelets)
Urochordata, aka Tunicata (the tunicates)

My understanding is that the cephalochordates are named as such (meaning “head chords”) because the notochord reaches into the head. From Wiktionary:

Any of the primitive fishlike creatures, of the subphylum Cephalochordata, including the lancelets, that lack a true spine but have a notochord which, in the case of cephalochordates, reaches into the head, contrary to the Urochordata.

Urochordata, by contrast, means "tail chord", though I cannot find a reputable source (or any, really) that describes or details why this is the case.
I can surmise it's simply because the notochord doesn't reach the head of a tunicate embryo -- as is corroborated by an image from Lemaire 20111 copied below.

 Image D' shows notochord in red. Credit: Lemaire 2011
However, I would prefer a quotable, reputable source that indicates explicitly that the Urochordates are in fact named as such due to their notochord not reaching their head.
If this is not the case, then my question more broadly stands at: Why are the Urochordates named the way they are?

 1: Lemaire, P., 2011. Evolutionary crossroads in developmental biology: the tunicates. Development, 138(11), pp.2143-2152.

In 1877, Lankester proposed in "Notes on the Embryology and Classification of the
Animal Kingdom" division of the group we now call Chordata into three parts:

Urochorda
Cephalochorda
Craniata

which is more or less the accepted division today, with Urochorda being called Urochordata now.
In this essay, Lankester says:

The evidence of degeneration is admitted as conclusive in the case of the parasitic Crustacea and Cirrhipedes. It is equally incontestable in that very large and varied group of non-parasitic organisms, the Tunicata (Urochordate Vertebrata).2

(in the above 'Vertebrata' is what we call 'Chordata').  He adds this footnote:

2The whole argument as to the Tunicates of course rests on the view- supported by many arguments, that the larval urochord, which many of
  them possess, is not a larval organ acquired by larval adaptation, but is hereditary and transmitted from adult ancestors.

The term 'urochord' seems to be established and used without comment there, and probably is taken as simple neo-Latin for 'tail chord', although that may be somewhat loose, perhaps meaning the notochord is present but does not extend into the head.  A 1913 Webster's Dictionary defines urochord as:

(Zool.) The central axis or cord in the tail of larval ascidians and of certain adult tunicates.

In 1882, Lankester futher discussed the anatomy of the tunicates in the context of the division of the chordata in a paper called "The Vertebration of the Tail of Appendiculariæ".  This paper includes an illustration of a larval tunicate with the "notochord (urochord)" indicated.


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Risks of latent viruses that reside in ancient genomes under research?
Some interesting research in reactivating mammoth genetic material (https://www.nature.com/articles/s41598-019-40546-1) made me wonder what risks are inherent (or are not inherent) in reviving older genomes that may have integrated latent viral code?
Are there potential biohazards in this line of research, where dormant viruses that have otherwise gone extinct (along with the extinct host) and which now may have the potential to be reactivated? Not just in terms of zoonoses that infect across species, but also viruses that infect modern animals that are more closely related or have relatively common ancestry (e.g., from mammoth to elephant).
Could a disease be brought back via this kind of research? Or are the conditions for waking latent viruses from starting material of this kind just not possible to recreate in a lab setting?
Edit: To clarify what I mean by potential biohazard in relation to this question: Experimental conditions result in a latent virus going into lytic phase. The virus is a communicable pathogen; it spreads outside the laboratory environment; it causes sickness or death to living organisms to the extent that it creates a public health, ecological, or other crisis of significance. For background, please also see: Cambridge, The Free Dictionary, and Wikipedia.

I'm sure the extent to which this might constitute and answer, but scientists have in fact resurrected (to some extent) viruses that were otherwise extinct, including an influenza virus and an endogenous retrovirus.

First, I don't understand why you are more worried about viruses of extinct species, instead of ancient viruses of species that haven't gone extinct. Clearly the infectious potential of the latter is greater for the current species. I haven't heard a peep in published literature about the dangers of resurrecting mammoth viruses, but surely recreating (in 2005) the 1918 influenza
did stir some fairly substantial safety debates.
In general, working with ancient DNA (aDNA) does require some safety precautions, but mainly because of the risk of contaminating the aDNA (with modern DNA)-.
Furthermore, I'm not aware of any research having resurrected an ancient virus from an extinct species aDNA (your specific scenario), but one ~5-million y.o. retrovirus (dubbed Phoenix) was assembled from current human DNA (in 2006); the authors were a little worried as to its infectious potential, so they engineered it so it couldn't replicate more than once.
More commonly, the genome of less ancient virus strains is being fairly routinely reassembled from e.g. from mummies, skeletons, or even packrat middens in order to study the evolution of common viral diseases. Most of this goes on without any safety controversies, as far as I can tell. Less commonly, ancient viruses of various species are found fairly intact in permafrost which does also stir some safety discussions (regarding the handling of permafrost).
So is your scenario possible in theory? Yes. Are experts worried about it? Not that I've heard...

About your leading sentence "...I don't understand why you are more worried..." There's no evidence of that being the case in the question whatsoever; it seems personal, gratuitous, and unnecessary. But nonetheless, +1 for the "...the authors were a little worried..." example.

If you would like to edit your answer to include just what is relevant to my question, I'll be happy to mark your answer as "accepted". Thanks again for answering!

@AlexReynolds: and what would that be? There's no research or even an opinion (except mine) directly on your question. It's circumstantial evidence (on related issues) basically supporting my opinion.

Are there potential biohazards in this line of research, where dormant
  viruses that have otherwise gone extinct (along with the extinct host)
  and which now may have the potential to be reactivated?

There are always potential biohazards. If you dig into the unknown, you can't tell in advance what you can find. Said that I would like to point the attention to the fact that we don't know all the viruses already in existence, nor the ones that evolve every day.
You get in contact with new viruses during your everyday life anyway. How much more hazard would come from ancient viruses? I would say, not much but I can't point to any specific supporting experiment, so, it's just my opinion.

Could a disease be brought back via this kind of research?

Hardly. Lot's of parameters (an overview here)  must be just right to have a virus spreading and cause disease. Viruses are usually very attuned to cells metabolism and environmental factors. Current parameters are probably very different from the original ones so, even if an ancient virus can be "revived", its ability to infect and spread would definitely be hindered.

Or are the conditions for waking latent viruses from starting material of this
  kind just not possible to recreate in a lab setting?

There are no standard conditions to awaken a dormant virus, or in general to produce viruses. Each virus is different and it will require specific conditions (here some examples on Lentivirus and Adenovirus). In theory, if all the required viral proteins can be expressed in a compatible cell host, then viable viral particles can be produced (Negev virus, Rhopalosiphum padi virus, Black queen-cell virus). "Reviving" an ancient virus is definitely possible with enough effort, but again, the rate of success will differ from virus to virus.


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Which cells are prefered by the HIV virus to establish an infection?
We always read that HIV infects CD4 cells, macrophages, and dendritic cells. However, is it a common event for HIV to infect non-immune cells within a host? If not, why?
And also if not, why are immune cells the main target of HIV? I could not find information on Google or Google Scholar on this topic. I imagine it doesn't have to do solely with the presence of the expression of co-receptors such as CD4, CCR5, CXCR-4, DC-SIGN etc that attract the virus only to immune cells.
I would like a more complete explanation than this obvious one. For instance, what advantages are provided for the virus to prefer infecting immune cells over non-immune cells?

I guess that by infecting immune cells the virus is further improving its chances of survival.

I find it fascinating that HIV spreads during the latency period (aprox. 8-10 years) within lymph nodes, killing more than 1 billion immune cells per day. It is ironic that one would expect that lymph nodes are one of the most secure places within the body as they are patrolled by immune cells. However, it turns out that HIV is safe there. I find this fascinating. It's like the Trojan Horse story, except at a microscopic level and in real life.


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How to check if a population density obeys replicator dynamics
Say we have a probability vector or population density $p = (p_1,...,p_n)$ with $p_i \geq 0$ and $\sum_i p_i =1$. Also assume we know the functions $g=(g_1,...,g_n)$ such that:
$$p_i(t+1) = g_i(p(t))$$
where $t$ is a discrete time index. Is there a way to check whether $g$ implements a discrete time replicator equation? I.e. whether there is a function $f=(f_1,...,f_n)$, called the fitness landscape, such that:
$$p_i(t+1)= \frac{f_i(p(t))}{\langle f \rangle_{p(t)}} p_i(t).$$
where $\langle f \rangle_{p(t)}:=\sum_j p_j(t) f_j(p(t))$ is the average fitness of the population density.
Pluggin in $g_i(p(t))$ gives an equation that we could try to solve for $f$ but I don't know how:
$$g_i(p(t)) = \frac{f_i(p(t))}{\langle f \rangle_{p(t)}} p_i(t)$$
or equivalently:
$$\frac{g_i(p(t))}{p_i(t)} = \frac{f_i(p(t))}{\langle f \rangle_{p(t)}}.$$
We can of course also drop the time dependency and write:
$$\frac{g_i(p)}{p_i} = \frac{f_i(p)}{\langle f \rangle_{p}}.$$
Is there a (in the best case necessary and sufficient) criterion that has to be satisfied for this equation to have a solution?
I am also grateful for tips how to tackle this problem in a principled way, including numerically.

For discrete time replicator dynamics, fitness is defined only up to a multiplicative factor. I.e. if you pick some number $k$ then $(f_1, ..., f_n)$ defines the same fitness function as $\hat{f} = (f_1/k, ..., f_n/k)$. In particular, this mean for any $p$ you can always pick a $k$ such that $\langle \hat{f} \rangle_p$ = 1.
So using your final equation, just let $\hat{f}_i(p) = g_i(p)/p_i$.
Note that the resulting landscape $\hat{f}$ will be a relative fitness landscape and not an absolute fitness landscape. But there is no way to recover an absolute fitness landscape from the data you have. You would need information on how the population size, not just frequencies evolved for that.
As a final note: if you're trying to match this to experimental data, the discrete time approach might not always be necessary. In that case, you can try the method that I describe in this post or depending on your experimental system, you might be able to just do the game assay as we defined in this paper.


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What's a "constitutionally small penis"?
I'm reading some urology papers and came across one involving penis growth (Kim & Song, 2008); here's an intro passage that I'm confused about:

A total of 58 patients with constitutionally small penises, without chromosomal anomalies and gene-associated syndromes, intersex, and hypospadias, were included in this study. The average patient age at their first visits was 10 years and the average follow-up period was 2.2 years.

What's a "constitutionally small penis"?
Edit:
I've read the paper in detail and I don't see where the authors distinguish between a small penis and a "constitutionally small" penis.
Would a "constitutionally small penis" be the same thing as a "micro-penis"?  If not, then where do we draw the line?
References
Kim, K. S., & Song, G. G. (2008). Penile Growth After Puberty in Patients with a Constitutionally Small Penis. Journal of Pediatric Urology, 4, S63. doi: 10.1016/j.jpurol.2008.01.174

"Constitutional" refers to the physical state of the concerned individual (Merriam-Webster).
In biology, it most probably means a trait that is not pathological or environment induced.
This is in the context of size of babies:

Small for gestational age (SGA) can occur following a pathological
  process or may represent constitutionally small fetuses.
From: Ananth & Vintzileos (2009)

Between18-22% of infants SGA by population
  standards are reclassified as normally grown by customized standards
  and as the perinatal mortality of these reclassified babies is similar
  to those who are normally grown they can be considered to be
  "constitutionally  small.".
From: McCowan et al. (2018)

In most cases, it is difficult to differentiate between
  constitutionally small head size vs pathologic microcephaly, and
  available data regarding prenatal diagnosis of microcephaly are based
  on small numbers of cases of varying etiologies.
From: Ultrasound screening for fetal microcephaly following Zika virus exposure.
   American Journal of Obstetrics & Gynecology, Volume 214, Issue 6, B2 - B4

Regarding constitutionally small penis: Since the article you mentioned is the only source (scientific or otherwise) of this term, I would believe that it is based on the population average (of possibly South Korea from where the authors are). Moreover, since it is not defined rigorously, it is most likely an arbitrary classification.


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Is homocysteine converted to glutathione during oxidative stress?
From the paper titled "The basis for folinic acid treatment in neuro-psychiatric disorders" by Ramaekers et al., 2016:

On the left side of the figure, the purine metabolite GTP serves as the substrate for the GTP-cyclohydrolase I enzyme (GTPCH) to produce tetrahydrobiopterin (BH4), which is the co- factor for enzymes producing dopamine, serotonin and NO.
  At the upper right of the figure the trans-sulfuration pathway is shown.
  It converts accumulated homocysteine to the anti-oxidant glutathione during oxidative stress.

Is this so? Is it true that this pathway is only active when the cell is under oxidative stress conditions?
Or maybe the authors meant to say that the pathway converts homocysteine to glutathione, which is later used to counteract oxidative stress?
Here's the figure from the paper:

Is English your first language? The statement "It converts accumulated homocysteine to the anti-oxidant glutathione during oxidative stress" has no qualification such as "only" that would restrict the conversion to oxidative stress. It does not preclude that this is the general pathway for synthesis of glutathione for use in any situation where its reducing power is required. And you will find that almost certainly to be the case if you research the pathways of glutathione synthesis, e.g. here.

I'm voting to close this question as off-topic because it is based on a misunderstanding of a sentence in a paper and thus has no general value for SE Biology.