text:
Does dairy negatively affect the voice for singing?
Singers and actors are warned not to consume dairy, primarily milk, before a performance. From personal experience, I know that this is a very valid warning. It is commonly assumed that this is due to milk causing either more or thicker phlegm.
Has the mechanism behind this been studied and verified?

As it turns out, dairy products do not produce phlegm in the majority of people (the exception is the tiny group of people who are allergic to casein, the protein in some types of milk). Instead, the high fat content in dairy products thickens the mucous that is already present in a person’s airway, making it seem like there is more phlegm to deal with. Of course, having thicker phlegm can be just as problematic as having more phlegm. Luckily, this thickening sensation can be diminished simply by eating dairy products that have a lower fat content.

(https://www.operapulse.com/refine-your-craft/guide-to-opera-training/the-rules-of-singing-mythbusters-edition/)
Regarding the above quote, there is no medical evidence that states milk consumption causes phlegm production even for casein allergic individuals.
The study cited at the end shows that there is a correlation between milk consumption and thicker phlegm. However correlation is not causation. The authors explain that the allergy-like effects of milk are produced only when tissues are actively inflamed and exorphins (peptides produced when milk is broken down) stimulate mucus production from gut glands. The thicker phlegm effect is shown in only a segment of the studied population. Unless you're one of the few with inflamed tissues, you should be ok with drinking milk before a performance.
(http://www.researchgate.net/profile/Jim_Bartley/publication/40026300_Does_milk_increase_mucus_production/links/0fcfd5138d5212ef80000000.pdf)


text:
Will someone with a double mutation in the allosomes be normal?
Normally a female human has an X allosome from her father and an X allosome form her mother. What if an double mutation happened, which causes that someone has two X allosomes form her mother and no allosomes form her father? Will this person be a normal female?
Note that it is both possible that there are no allosomes form the father or mother (known as Turners syndrome, (45, X)) and that there are two X allosomes form the mother (known as (47, XXX) and (47, XXY) respectively).
Since the Turner syndrome happens for 1 in 5000 births, and the Triple X syndrome happens for 1 in 1000 births, I estimate that this would happen once in 5 million births.

Is your question Can a female (human) be "normal" if her two Xs are exactly the same, that is if she is homozygous at all sites on the allosomes??

@Remi.b I somehow didn't realize that would imply it. Yes that is basically the question, however, I am not sure if there wouldn't be other consequences.

It does not necessarily imply this. If the two Xs come from the mother, then with probability 0.5, she may receive the two different chromosomes (let's assume no recombination for ease). In which case, she wouldn't be any different from her mother for the sex chromosomes. If the two Xs are the exact same then, she will likely suffer from some level of inbreeding depression but she might be fine.

Causality is not causation.  Be careful with 'estimates' like that.

Turner syndrome occurs in about 1 in 2,500 female births.

I agree that there is a theoretical possibility. This post (Chris' answer) should answer this question.

source: Stack Exchange

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

sort: votes


text:
Viruses. Alive or Not?
I saw this fascinating article today about how HIV moves through a mouse host in real time.
http://www.engadget.com/2015/10/02/watch-hiv-spread-through-mouse-in-real-time/#continued
It's common to hear a virus' activity described in the way the article does: with intent.
I have a hard time understanding this. Something is considered alive when it has a metabolism, takes in nutrients and expels waist.  It has to have some kind of respiratory system and it's own reproductive mechanism. Although locomotion is optional, most forms of life have some form of getting around.  Some plants are able to move somehow...
Viruses have no sensing organs and no method of locomotion.  They cannot smell or see or move on their own.  This means they have to be carried inside a cell or if free floating in a host's fluids, rely on random motions to get about.
In order to invade, as far as I understand this; they must essentially wait until they come into physical contact with a compatible target.  At this point, their protrusions (I call them "keys") attach to a host cells "door" and they then inject their DNA.
Most (or all?) cells use Mitochondria for "power" so they can do things - like metabolize and reproduce.  I've never seen a diagram of a virus that shows where it get's it's energy to power the 'injection' part of it's 'life cycle'.
How is this done?
In the mouse video, the HIV virus looks like it has a "plan" and that it knows how to select which initial cells to invade and then how to pick a good method of remaining hidden.  How can this be when they have no sense organs?  How can they "know" of other virus particles are being successfully attacked by the host?
This is incredible and incredibly complex.
I'm not a medical professional. I'm just a fascinated by-stander.

I don't think it's a duplicate, given the specific questions.

The questions posed here are neither answered nor asked in the question which this supposedly duplicates.

So in terms of finding ways to infect a host, a virus is entirely passive?  Like I mentioned before; without sense organs or locomotion of it's own, it would not have any method of seeking targets.  Is this correct?

If you think about the sheer number of viruses that probably enter at once, all they have to do is tumble into a cell for which their binding receptor has something to bind to, and adhere. Then, either the cell senses something and engulfs the virus, or another viral protein makes it favorable for the virus to get into the cell (for example).

You cannot expel your waist, because it is stuck in the middle of your torso.

When we're thinking about cells that get infected with viruses, we have a two of subgroups to consider, often denoted susceptible or permissive. In essence, a cell which a virus is meant to successfully infect must not only possess a receptor to that virus for adhesion, but also the ability to replicate the virus (so it needs the machinery!). So these cells must be susceptible and permissive!
After adhesion you end up with an entry phase, this differs by virus, but you can essentially break it down into endocytosis, membrane fusion, or injection. You can get an idea of injection from something like lambda phage, outlined here. Enveloped viruses can fuse with the host membranes because these envelopes are often derived from ER, golgi network, or another plasma membrane. (Remember, viruses are essentially coding 3 basic sets of genes: for structure, replication and binding. It can't just code for everything it needs, either, so viruses hijack the host cell machinery to replicate.) Naked viruses, those that are just a protein coat and nucleic acid in essence, enter the cell through endocytosis and end up uncoating in a vesicle. And to stress it again, if the cell didn't have a receptor for the virus, it probably didn't get it. Portal of entry does make a difference, but I'm trying to keep it simple for our purposes!
Being said, when we're considering most viruses, membrane fusion and endocytosis aren't really using any energy but the host cell's, right? And then when the virus gets in there, they continue to use the host's resources becauase they really didn't bring a lot of baggage, either!
On the matter of "knowing" what they're doing, viral particles really don't do anything themselves. What I'd argue is that they've evolved methods of becoming particularly good at being viruses, many of which make it seem like they're making conscious choices, but suppose the following: Most of the time, viruses are probably just reproducing in such great numbers that it's just faster to get lucky and produce a strain with a better overall fitness.
Mind you, this whole time your body is attempting to fight off the virus, as in HIV, for example, eukaryotic cells have methods at each stage of attempting to protect themselves,

Source: Cellular Self-Defense: How Cell-Autonomous Immunity Protects Against Pathogens
You also have NK cells and macrophages responding to IFN produced by cells distressed by viruses, and eventually the presentation of viral antigens which result in effector T cells and antibodies unique to the virus in question. Another article here shows some methods by which some inhibitors of HIV infection can be evaded by the virus, as well, and just as likely, you also see that HIV has mechanisms of evading innate/active immunity as well! For example, if your antibodies recognize a viral capsid protein, what do they have to bind to if there's a lipid membrane in the way, as in HIV? What if the receptor composition changes?
In closing, viruses are obligate intracellular parasites. They need you to survive, but their objective is to replicate, so sometimes they do end up killing their host, but they aren't really communicating with each other in a fashion like: "I wonder how those other viruses are doing?" They really don't have a means of responding like that, so the end goal? Just keep moving from host to host and keep replicating, in the most basic sense.

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


text:
Corneal transplant and HLA matching
Is HLA matching/ blood grouping required for corneal transplants ? I think,it shouldn't be, because cornea is avascular.
I tried searching on the net but most of the references are old and controversial. So please provide a reliable and latest reference for your answer.

Just because it's avascular doesn't mean immune cells can't/don't infiltrate. There are plenty of inflammatory eye processes where the cornea and lens can be targeted.

Cornea is considered as an "immune-privileged" site and tissue, neither HLA nor blood grouping is required for allogeneic corneal transplant.
In terms of reference:
This could be one: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2802514/


text:
Why does SDS-PAGE use for protein, and agarose use for nucleic acid?
My question maybe very primary, but after I learned this part, questions always follow me.
SDS-PAGE gel works for detect protein, agarose gel works for detect nucleic acid, so here is my question:
1. Why does SDS-PAGE works for protein, and agarose gel works for nucleic acid? Is it any possible to use SDS-PAGE to detect DNA? Or use agarose to detect protein?

Why does the SDS-PAGE gel always runs vertically, and agarose gel runs horizontally? Are they necessary?
Is any other material could be use in gel electrophoresis?

Mad Scientist explains why you would make different choices regarding size and desired resolution. Polyacrylamide gels can provide a higher degree of resolution for small molecules, you need to realize that proteins are small. A good-sized protein is around 400kDa., where as a 1000bp DNA molecule is 650kDa. Agarose pore structure is larger, so you use it for larger molecules like DNA. Another reason is toxicity. Polyacrylamide is a toxic substance, Agarose is a sugar, so if you can avoid using polyacrylamide, you do; sometimes you can't.

You can use polyacrylamide gels for RNA and DNA, and this is the common way to examine shorter nucleic acids. Agarose gels can be used for larger nucleic acids like plasmids that are a few thousand base pairs long, polyacrylamide gels work better for shorter nucleic acids around a hundred nucleotides long.
You don't need SDS for nucleic acids, they already have a negative charge at the phosphate backbone. Polyacrylamide gels for nucleic acids also don't use a separate stacking gel like in SDS-PAGE, it is just one single gel.

You just answered the first question, it makes sense to me, thank you. But could please answer the 2nd and 3rd questions?


text:
How much force can connective tissue withstand?
I have been studying a 3D anatomy model. Based on visual observation,  it doesn't look like the bones would be able to stabilize themselves at all without the connective tissue like ligaments. In the model I have been studying, i've noticed that all the ligaments are clustered around joints or areas where the bones connect and it looks like it they act as a kind of glue to in essence keep the joints intact. However, I don't really understand how much force connected tissue must withstand on a regular basis.
How hard is it to keep bones aligned and confined enough that the bodies overall shape remains pretty constant? Is this the role of connective tissue? if so, how much force does such tissue need to withstand on a regular basis?

Do you have a specific connective tissue in mind? I'm guessing you are thinking of cartilage and ligament (blood is technically a connective tissue). Also in what orientation are the loads you are thinking of? Compression is very different from tension.

Ligaments and cartilage. Isn't that all there is? Is blood actually a significant player as a connective tissue?


text:
Are there examples of animals that adapt to their environment very quickly? The phenomenon is called Phenoptic Plasticity
Evolution and speciation may take millions of years. This made me wonder if there is an animal that adapts itself relatively rapidly to its environment? I don't mean a simple adaptation like a change of a color by chameleons, but a real evolutionary change.
I've heard that some animals can adapt quickly to the environment like snakes (I am not sure they do). When they have a lot of water (e.g., a big river), they grow big, while the same species does not grow as big in a smaller water tank (small body of water). And when you take this animal to a bigger water it starts to grow quickly.  I want to be sure it is a snake or there is some other animals that evolve change like this...

What do you mean? All of them do. Every single one.

I've heard that some animals can adapt quickly to the environment like snakes (I am not sure). When they have a lot of water (big river ie) they grow big and the same species do not grow as big in smaller water tank (small body of water). And when you take this animal to a bigger water it stars to grow.  I want to be sure it is a snake or there is some other animals that evolve change like this...

First of all, that also happens with all animals. If you have enough food, you grow big, if you don't you remain small. Please [edit] your question and clarify.

Given your snake example, I think it is unclear whether you are interested in evolutionary change or phenotypic plasticity.

If phenoptic plasticity means changing the size due to better environment and opposite: not growing or changing (evolving) due to bad ones - I am interested in that. Thanks

@Arcadio Phenotypic plasticity is dealing with phenotypic differences in between individuals in different environments that are not the result of differences in genotype (so that the same genotype can result in completely different phenotypes). The body size differences that you describe are often the result of this. Phenot plasticity does not involve evolution, since the genotype doesn't change. However, also the plastic response (the reaction norm) can be the target of selection and evolve.

@Arcadio You're welcome! You can edit your question to narrow down the answer set (focus on either rapid evolution or plastic responses), so that it is more well-defined and can be reopened.

The snake example you provide is a single animal that adapts itself to its surroundings. Adaptation is similar, yet very different from evolution. Adaptation happens on a short timescale (as little as seconds, to perhaps years, but within a single life time, without substantial changes in DNA other than, perhaps, epigenetic ones), while evolution may occur over the course of millions of years or more, and likely involving gross changes in appearance and hereditary material. I am not entirely sure what you are exactly after.
A striking example of adaptation is the fish Tilapia, an invasive species of fish (Fig. 1) that is capable of sustaining fresh water as well as sea water environments. The transition from one medium to the other is mediated by gross changes in endocrinology. Your specific snake example on size adaptation seems, however, unsupported based on non-scientific websites at least.

Fig. 1. Nile Tilapia. Source: Sea EX
If you are after examples of swift evolution -There is a nice example of the Waterlily Beetle, Galerucella nymphaeae (Fig. 2), that shows striking host-race formation, i.e., the same species of beetle shows clear adaptations (on an evolutional scale) dependent on which plant it has been found. It has been shown that these beetles extracted from different plants (Nymphaeaceae versus Polygonaceae) showed strong morphological and ecological differentiation to their different host plant families. Beetles from Nymphaeaceae were significantly larger and had disproportionally larger mandibles than beetles from Polygonaceae. It is argued that these differences are adaptations (on an evolutional scale) to the tougher leaves of the Nymphaeaceae, which has been linked to genetic differences. In addition, females showed a strong oviposition preference, and all beetles showed distinct feeding preferences for the host family from which they originated. Moreover, these host preferences resulted in clear differences in survival: survival was 2 to 11 times higher on the natal host family than on the alternative host family.

Fig. 2. Waterlily Beetle. Source: Wikipedia.
Exactly how fast these beetles have adapted I am unsure of, but the interesting thing is that these beetle races are not geographically separated by a natural barrier like a sea, a mountain range etc. Instead, they live side-by-side, but have adapted to a specific host plant.
Reference
- Pappers, Evolution in action: Host race formation in Galerucella nymphaeae. PhD thesis (2001), Radboud University, Nijmegen, the Netherlands

Thanks for that answer ! Do you know the name of that snake. Is it Anaconda?


text:
Why are there no known animals with an odd number of legs?
In my 6th grade science book it is said that there are no three legged animals, and that no animal with an odd number of limbs exists. I checked Wikipedia and could confirm this:

There are no known naturally occurring three-legged animals

On yahoo it is said that

When an embryo is developing, it grows by cell division - the first single cell divides into two, then four, then eight etc. It doesnt' divide into odd numbers - each cell divides in half. So, this means that every creature develops the same on each side of it's body - same number of limbs per side.

It seems to be a valid explanation. So is it true that any organ in any living organism is either one in amount or is in even number? And the explanation of yahoo.com is fine?
I am a beginner in Biology. Please explain in simple terms.

related: http://biology.stackexchange.com/questions/19318/list-of-asymmetric-animals

Starfish (sea stars) have radial symmetry and often have five "natural" limbs.

That Yahoo answer thing is rubbish, by the way. Growing by cell division is not sufficient to ensure bilateral symmetry, for example plants grow by cell division. And as others have said, even within animals not all show bilateral symmetry.

Ahh, the trichordates.

Gastropods only have one so-called foot.

What about starfish,which have 5 arms?

Are you really in 6th grade ?! You are asking great questions ! Keep up the good work and don't always believe what the textbooks say :)

@biogirl No I'm not in 6th grade. I am an Engineer who has started to study biology.

@user31782 LOL ! Sorry for the misunderstanding... Have fun studying bio ;)

Sea stars can have odd numbers of arms (such as 5 as mentioned in other comments) but they have many hundreds of legs underneath their arms. There are possibly an odd number of legs but not necessarily the same number of legs per individual from the same species.

@SteveJessop "That Yahoo answer thing is rubbish, by the way." Hence the entire reason for Stack Exchange's existence :-)

related: Why do we have two of some organs, but not all?

Also @SteveJessop was right to say the Yahoo answer is rubbish. Specifically what happens if we have 6 cells, or any other even multiple of an odd number of cells. By that same broken logic we have the potential for odd number of limbs or asymmetric division. That's clearly not why bilateral symmetry occurs.

@GoodGravy I could not understand your comment. "6 cells, or any other even multiple of an odd number of cells" So what 2N will always be even whatever N you choose.

@user31782 Asymmetric expansion can occur due to directional growth from an odd number of nodes (even if the cell count remains even). But here's the kicker of why that argument is broken; it is taking a cellular principle and making a lot of assumptions about it (constant cell cycle period, uniform cell death etc)  and oversimplifying it (for example it ignores inter-cellular communication and genetic control systems), and then applies that watered down concept at a complex multi-tissue organism scale involving not millions, nor billions, but tens of trillions of cells.

Dear all people everywhere: do not believe what you read on Yahoo Answers. Ever. Or anywhere on the internet for that matter, unless there are citations or some form of expert support. Also, Google Scholar is 100% free to the public...

@theforestecologist Although, note the conspicuous lack of primary sources cited in accepted biology.se answers... we could certainly do a better job of this ourselves. I would love to assume any answer on here constitutes "some form of expert support," but that is a precariously specious assumption.

It depends what you mean by 'leg'.
The instinctive way to define a 'leg' is based on its functional use: we use legs to walk on. But if we adopt that definition of 'leg' then there certainly are animals with odd numbers of legs: kangaroos, for instance, have a five-legged gait, functionally using their tail as a fifth leg. There is no developmental process that stops an animal from growing an odd number of appendages, and if one of those appendages happens to be used as a leg, evolution and development will have no problem with that.
However, there is another way to define 'leg', and that is by homology - 'legs' are the appendages derived by evolution from the legs of a common ancestor. Under this definition, (for vertebrates, at least) you're a bit more hard-pressed to find examples of animals with an odd number. This is because those legs are paired appendages, and the developmental pathways for the leg on one side of the body are tied into the developmental pathways for the leg on the other side of the body, so it is hard to evolve an odd number of legs from these appendages.
Hard is not the same as impossible, though. A comparable piece of evolution is the severe reduction in size of fins from one side of the body in flatfishes (flounders, sole, etc). I am struggling to think of terrestrial examples, but it is certainly evolutionarily possible to lose one appendage from a pair but keep the other.

Among terrestrial animals, gastropods have lost one from some paired appendages (although that happened in an aquatic ancestor). And although their "foot" (or perhaps at a stretch for the purposes of this question "leg"?) isn't one of the appendages that became un-paired in this way, they do have an odd number: one.

A kangaroo's front legs only touch the ground when it is eating. When standing it uses its tail like the third leg of a tripod. When it is running only its hind legs touch the ground, both together, using its tail for balance with its front legs dangling high off the ground. So when running it's using an either one or two legged gait, depending whether you consider two legs in unison to be one or two. Even when eating it moves its legs in pairs instead of individually. So although it has four limbs and a tail it uses them as two limbs and a tail, but with extra lateral stability.

@CJDennis: It's not true that kangaroos only use their tail as 'the third leg of a tripod'. In the study I linked to, the authors defined the kangaroo's tail as functionally a leg because the tail provided forward propulsion in the animal's five-legged gait. In fact, while walking on five legs, the tail provided as much forward propulsion as both the front legs and hind (should I say middle?) legs combined.

I did say "when standing" not "when walking".

Consider also the case of Hopsorrhinus Aureus

It might be worth mentioning that Hopsorrhinus aureus is fictional. Entertaining, but fictional.
https://en.wikipedia.org/wiki/Rhinogradentia

By "Leg" I mean a specific type of body part(perhaps organ). Leg is different from tail because in leg there are two straight bone connected with a joint(perhaps socket joint) on the other hand in tail there is no joint nor does the end of tail terminate with a hand like structure. There can be one tail, two tails, four etc and one leg, two leg, and four leg etc, everything in even numbers. Just as we have two kidneys, eyes etc in pairs.

@user31782: It sounds like your definition of 'leg' is by structure. I would argue that it is not a useful definition of 'leg' for evolutionary questions. e.g., the hindlegs of horses are not 'two long bones with a hand-like structure at the end', because there are three long bones (the bones that are homologous with the arch of our feet are fused into a third long bone, IIRC). But they are definitely 'legs' in the way most people understand the term! Biologists avoid semantic problems by defining from homology - in which case, see the second part of my answer re: development and asymmetry.

@user31782: if you're defining legs in terms of "bones", then you're talking about vertebrates, not all animals. Which is a fair enough thing to ask about, but this restriction means that straight away, all terrestrial vertebrates are tetrapods, who all (including kangaroos) have inherited a basic body plan with bilateral symmetry from a common (fish) ancestor. The success of this body plan has yet to be challenged by any odd-limbed species, other than those using their tail as a limb. Depending on your view of "arms" and vestigial limbs, they all have 0, 2 or 4 "legs".

I can't think of any example with legs, but lots of land animals have reduction or loss of one half of a pair of organs. E.g. most birds have only one ovary, snakes have only one functional lung.

Short answer
The body plan of terrestrial organisms that feature limbs is typically bilaterally symmetric, and hence these organisms have an even number of appendages.
Background
Terrestrial animals featuring appendices for motility (legs, arms) are typically higher organisms. Typically, the body plan of higher animals such as us mammals is typically bilaterally symmetric (Fig. 1). Lower animals may be radially symmetric (e.g. round worms, jelly fish and star fish). Only the simplest of animlad have an asymmetric body plan, such as sponges. With a symmetrical body plan comes an even number of appendages.

Fig. 1. Different body plans. Source: Estrella Mountain Community College.
The symmetrical body plan is already defined in the blastocyst stage during development. The blastocyst in humans forms in the first two weeks after gestation and contains 10 to 20 cells only (Fig. 2).

Fig. 2. Human blastocyst at day 5. Source: University of NSW
While the blastocyst is not more than a globular clump of cells, it has two well-defined poles and a well-defined axis. In fact, it is thought that the single-celled zygote already has a well-defioned axis as it is has been shown that surviving polar bodies during oogenesis (the formation of egg cells in the ovaria) have well-defined highly non-random positions in the zygote (Fig. 3.). These findings show that the single-celled zygote in bilateral symmetrical animals may already be defined at a single-celled stage (Gardner, 1997).

Fig. 3. Blastocyst bilateral symmetry based on a mouse model. Source: (Gardner, 1997)
Reference
- Gardner, Development (1997); 124(2): 289-301

-1 this does not answer the implicit question why are animals symmetrical.

@QuoraFeans - How about now, see my edit showing embryonic development in bilateral symmetrical animalia

Also it does not explain internal asymmetry. Appendix, heart?  As a rider, I'd ask (and I don't know the answer) whether we have odd numbers of internal appendages where n>1.

@chaslyfromUK - that's a different question altogether - feel free to ask a new question, though.

Leaving aside the extra part, my objection was to your statement, "With a symmetrical body plan comes an even number of appendages."  If that were true then surely it would apply to internal appendages.(?)

@chaslyfromUK - This may be another question entirely. I would think that internal (organ) formation has more to do with hormone secretion and division timing (both of which are intended to trigger the differentiation of specific cells) and external (limb) formation would have more to do with symmetry. Would you agree?

@AliceD - +1 for a great answer.

In your "Background" paragraph, you switch between talking about "animals" and "organisms". Plants can be extremely complex, are defined as organisms, and also have varying types of symmetry, depending on the plant and the portion being studied. I think you need to carefully clarify your language.

@MattDMo - thanks for your critical reading. Done.

The other part of the question has already been amply answered, so I will concentrate on the part of the question which asks about "doesn't divide into odd numbers"
The assumption that organisms must have even numbers of cells merely because cells divide into two each time is false. For example, the nematode Caenorhabditis elegans has either 959 or 1031 cells depending on its sex. Cells can be lost due to apoptosis or natural wear and tear.
Even if that was not the case, cells divide at different rates and times, so it is perfectly plausible for an organism to have an odd number of cells. For example, when one of two cells divide, and the other does not, the final result would be 3 total cells, which is an odd number.

Imagine if the tail of a fish did behave like a leg (imagine a one legged frog). One side, either the left side or the right side, of that tail would naturally dominate and the fish would end up swimming naturally in circles.
Now assuming that being able to go in a straight line over longer distances is a small evolutionary advantage. It would make sense that that a fish tail evolved and grew an internal muscle symmetry that allows it to eventually maintain a straight line.
The same goes if you were to grow a third leg tomorrow. In order for that third leg to be useful to you in evolutionary terms, it would have to be placed in such a way that it doesn't interfere with your balance and your maximum propulsion. Also, its muscle structure would need to be symmetrical between the left and the right side, so as not bias one side over the other.
And of course, such a third leg wouldn't behave like the two other legs because of its forced internal symmetry, so we humans wouldn't call it a leg, we'd most likely call it a tail instead (a cat tail, a kangaroo tail, a snake tail, a fish tail, etc.)
Now let's take a star fish with five "leg-like" appendages (although, that number can vary depending on the kind of star fish). Does my reasoning work with that kind of star fish also? The internal muscle structure of those five appendages are internally symmetrical, just like tails would be, not legs. Also, take a look at how a star fish moves. The propulsion doesn't come from its five appendages. Those five appendages help more with its balance and its positioning. And the propulsion actually comes from its many little tube legs at the bottom of those five appendages. So I'd say "no", a star fish is an interesting example, but it doesn't just have only five legs.

What about the Haggis? http://www.maths.ed.ac.uk/~jcollins/Haggis.pdf

Not all animals are symmetrical. Look at the adult flounder, for example.

I didn't say they were. This is what I said:  "It would make sense that a fish tail evolved and grew an internal muscle symmetry that allows it to eventually maintain a straight line. [...] Also, its muscle structure would need to be symmetrical between the left and the right side, so as not bias one side over the other." The flounder is also a perfect example of this. Its tail has a left-to-right symmetry.

The reason 'there are no known animals with an odd number of legs' - if that is indeed the case, given that stating a negative truth of high probability requires a great deal of examination of facts and records! - could be because it was a stage of development of organisms of a pre-Cambrian period stage of development, or at latest Early Cambrian.
What I am thinking of specifically is the 'Ediacaran' organism/fossil named Charnia.  It shows 'glide reflection' in its development and organization, in which successive branches are opposite to the previous branch and a little further along the body axis.
Charnia was, of course, a frond-like animal, resembling nothing relatively modern so much as a fern (which is a plant of course).  Given that it was an animal not a plant, and a very early animal for certain, it did not have opposite symmetry and thus, if it had evolved directly into a perambulating organism with legs, it might have had an odd number of them.
When thinking of the conformation of animal life, it is as well to keep the Burgess Shale fossils in mind:  animal life that long ago, would appear to have been somewhat 'experimental' still (or, in a phase where all the basic problems were being worked out), and many differing types, some nowadays unrepresented, occurred, outre' in appearance, such as Hallucigenia and Opabinia.
So to sum up, though I cannot point out a known and discovered odd-legged animal (in natural form, as opposed to through amputation or loss of limbs), it is quite possible there was such an animal in Cambrian or pre-Cambrian times, whose fossil remains are as yet undiscovered or not-yet-clearly-interpreted.
Citations:
https://en.wikipedia.org/wiki/Charnia
http://paleobiology.si.edu/burgess/


text:
Bergmann's rule and Allen's rule: endotherms and ectotherms
Surface area to volume ratio (in terms of heat conservation) is not the only mechanism, but it is still an important mechanism for explaining Bergmann's rule and Allen's rule. Given that, I want to know why these rules are primarily applied to endotherms. I know there are some ectotherms that follow the rules, but here I am not asking for examples.

I guess, it is because these rules refer to how animal bodies are evolved to minimize heat loss, which is relevant only for endotherms (who have a different internal homeostatic temperature) and not for ectotherms, whose body temperature is equilibriated with that of the environment, making heat saving mechanisms redundant.


text:
meaning of "initial gene constructions" vs. "under the control of plant promoters" in an article on GM plants
From "Risks from GMOs due to Horizontal Gene Transfer", by Paul Keese:

Antibiotic resistance genes have been introduced to GM plants either as part of the bacterial cloning vectors used for the initial gene constructions or under the control of plant promoters to select for successfully modified cells. The concern is that the presence of antibiotic resistance genes in GM plants could provide a reservoir for the appearance of new drug resistant bacteria through HGT from plants to pathogenic bacteria.

I'm afraid I don't understand the "either ... or" contrast here. As I understand, antibiotic resistance genes are routinely introduced into GM plants with the sole goal: to check what cells have underwent transformation (got the neccessary foreign genes in their genome) and what have not.
I would be grateful to learn what are "initial gene constructions" here, and how does the method using "the control of plant promoters" differ from the first method. Is the purpose of introducing antibiotic resistance genes similar in both cases - to check what cells have underwent transformation? Sorry if the questions are too stupid. Please direct me to relevant Wikipedia pages or articles.

I think the distinction here is: When you want to introduce a new gene, then you either design a plasmid de novo and transfer it into the cell, or you insert the gene into the genome. But in the latter case you have to put it into a region that is controlled by a promoter (hence under the control of a plant promoter). I am not sure on the  initial gene constructions part, though.

I think initial gene constructions is referring to the construction of the actual vectors i.e. you build the antibiotic resistance marker into the vector. In the latter case they simply edited a resistance marker into a region controlled by a promoter. Pretty straightforward in my opinion.

@Kendall - Did they simply edit the marker into a plant? Before shooting with bio guns? But why use bio guns and vectors at all, if you can simply edit a gene precisely "under the control of a plant promoter" by some other means?

So basically, most plasmids that you buy have an antibiotic resistance marker, I think it's relatively standard, because you want to know which bacteria were transformed, right? Ergo, the initial cloning vectors being used. These markers are under control of a plasmid promoter like T7, for example, not a plant promoter (unless you contsructed it de novo to do this). But your plasmid is going to have a cloning site where you can make a cut, insert more DNA, and ligate it back together.
At least pursuant to the patent by Monsanto here, my assumption is that if you're looking to modify plants, your insert for the cloning site is probably a plant promoter, followed by a structural gene, and then a UTR sequence. I think what the authors are saying is that some groups put an antibiotic resistance gene into the insert as the structural part, and when you use something like an A. tumefaciens system to integrate that vector into the plant genome, you end up with an antibiotic structural gene under the control of a plant promoter. You should keep in mind that the whole plasmid gets integrated, but not all of it is transcribed by the plant, only that within the transcribed region controlled by a promoter the plant can utilize!!*
*I'll add, what they're worrying about in the linked OP article, is that whether or not the plant is actively producing antibiotic proteins, that the sequence for the antibiotic resistance has been introduced at any point in the plant's genome carries the risk that some bacteria will randomly obtain it through horizontal gene transfer.


text:
why haven't other species developed language?
Scientists say there are 15 million insect species, 2 million marine species, more millions of bird and animal species.
Yet, only one- humans - developed language. If evolution is true - that species evolve continually higher and better - why haven't other species developed language?

Welcome to Biology.SE. Your question has several issues. MINOR ISSUES: The title is too broad. "Scientists say" is a horrible way to start a sentence, you should have references for your claim. MAJOR ISSUE: The theory of evolution doesn't say that species evolve higher and better. What make you think that language is a goal, an achievement that all species should tend to? I am voting to close.

If you take some time to learn a little bit about evolutionary biology, you will then be able to ask clear questions. Consider taking a few course on Understanding Evolution (or other good online ressource)

Define a language too, many species communicate with vocal signals and this can contain information just like our speech. Also voting to close, it's a terribly flawed question.

"If evolution is true - that species evolve continually higher and better" That's not what evolution says. Not at all. And yes, many other species have developed their own languages. I can't believe this is news to you.

If evolution is true - that species evolve continually higher and
  better - why haven't other species developed language?

I'll discuss that question first, and then move on to what we know about languages in animals.
"Species evolve continually higher and better" is not what evolution actually postulates; there is no real sense of progress towards ever-smarter ever-better organisms; merely that the frequencies of genes in populations follow dynamics that is dependent on the relationships between the traits they are responsible for and the relationships between traits and the environment which further determine how many offspring a carrier of a given set of traits are likely to have.
Secondly, new traits don't pop out of nowhere; for a trait to appear in a population, let alone spread through a population, mutations that generate those traits must happen in the first place. That species don't evolve along some imagined ladder of progress has nothing to do with the veracity of evolution.
Coming to languages ; there are recorded instances of bonobos using modulations of their calls to communicate information; which is, simply put, language. Whales do it to a limited degree as well; communicating clan identity through ultrasound.

ants did have the advantage of language-type communications. The problem is ant language failed to evolve any further. why?

There are neural structures that regulate language; structures whose development is still regulated by genes, and the origins of novel structures requires mutations to happen first; mutations happening and spreading through populations is a matter of chance (mutations are stochastic processes). Even if hypothetically a trait would give a species a reproductive advantage, the mutations to produce that trait must happen first, and there is no guarantee they will (that is the whole point of evolution being stochastic, not deterministic)

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


text:
Why does supercoiled DNA run faster?
The DNA exists in linear and cirular forms. The latter form has interesting feature called Supercoiling. The more number of writhe makes it more supercoiled because of which it gets more compact. Hence the supercoiled DNA runs faster compared to other forms in a gel electrophoresis experiment.
But why does the circular DNA run slower than linear DNA? Isn't circularity supposed to make it compact?

I thought circular DNA would run slower because it isnt compact? In order to make linear DNA, dont you need to apply some type of chemical to "straighten" it out and get rid of the proteins attached to it, like SDS? So wouldnt the faster one in the gel be the one with less proteins on it, assuming they are both the same length of DNA and so on?

You have different conformations of circular DNA that result in different bands of the same thing: Supercoiled, relaxed and linear. Supercoiled runs very quickly by comparison, and relaxed or linear plasmid run slowly, but you'll find that linear DNA runs faster than the open circular DNA, which is often a result of DNA damage like single-stranded nicks. Remember: Your DNA is moving through a polymer matrix, so the more potential to get "caught" in the pores, the slower net movement.

Doesn't it follow the logic: writhe 2 > writhe 1 > writhe 0. Here '>' means faster. Then writhe 0 means circular dna which has to be slower just compared to writhe 1 dna and linear dna should be the slowest. Isn't it so?

Can you write a title that more closely relates to the question? Reading the title, I thought the question was about snakes.

It's compact so that it can go through faster agarose pores.

To understand this, you have to understand how an agarose gel is able to effect the size separation of DNA in the first place.
The reason agarose gels work to separate DNA based on size is that the electric field produced the electrophoresis machine is imparting force on the DNA. The effect of the increasing charge for DNAs with increasing nucleotides is offset almost exactly by the increasing mass of those larger DNA molecules, so in the absence of the gel, all pieces of DNA would migrate through the apparatus at a constant rate.
The reason they don't is because of the mesh framework of the agarose gel. This is like a dense forest or a large number of sieves with random sized holes. There's small holes (of varying size) and in order for large pieces of DNA to work its way through the gel, it has to weave through these pores. Smaller pieces of DNA can go through smaller pores, so they take a faster, more direct path, while larger pieces have to make detours, and even when they find a pore they can fit through have to spend a bunch of time flopping around before they can stuff themselves through the pore.
So it's not strictly speaking "size" or "compactness" by which the agarose gel separates molecules, but instead it's the ability of the piece of DNA to navigate through the mesh of agarose molecules. While relaxed, circular  DNA is more compact than an extended linear DNA of the same nt length, that doesn't necessarily mean that it has an easier time working its way through the network.
For example, a linear piece of DNA can orient itself so it goes "end first" through the mesh. Once the end of the DNA goes through a pore, it's relatively easy to pull the rest of the DNA through the same pore, as compared to trying to bend the DNA and pull it "sideways" through the pore - you have to remember that on molecular scales, DNA is rather stiff. You can't kink it in half very easily, so a piece of DNA that has to go through the pore "sideways" takes much more space than one that can be threaded through end-wise, even if you bend it as much as possible into a hairpin.
With a relaxed circular DNA, there's no end, so it's always going through the pores "sideways" so it's limited to the larger pores. In addition, it's large and floppy, so it takes quite a while to go through the pores that are there. When you add supercoiling, you don't fix the issue with going through pores "sideways", but you do limit the flopping around it does, so once you do find a pore of a usable size, you get the rest of the DNA through faster. In fact, with enough supercoiling you reduce the time spent flopping around enough that it goes through the agarose even faster than the linear DNA, which - while it can fit through smaller pores - still spends a bunch of time flopping around instead of going through the pore that it's started to go through.


text:
Help in identifying an insect
My cat has been messing with that insects. It looks quite unusual.
Anybody here can help me identify it, so I can make sure it's not dangerous?
Location: Israel

Please provide location information and any possible info about the insect (e.g., where you found it, approx size, observed behavior, etc.). The answer you accepted is wrong, but a correct ID is not possible without more info

Once again, this is a  longhorn beetle (Cerambycidae).
The overall appearance fits well with the subfamily Lamiinae (flat-faced longhorns). I would also guess it's in the Batocerini tribe. Though I don't think this is your species, per se, here is an image of a female Batocera rufomaculata with white stripe for comparison:

Once you provide more information about location I can give you a more precise answer.
Monochamus scutellatus is almost certainly incorrect. Notice the lighter coloration , wider body shape, and presence of a lateral white stripe along the side of the OP's insect vs that of M. scutellatus.

With a photo of this quality and zoom, it really looks creepy! :>

I think that your insect is a White-spotted sawyer. For more information check this: Monochamus scutellatus, commonly known as the white-spotted sawyer or spruce sawyer,is a common wood-boring beetle found throughout North America. Adults are large-bodied and black, with very long antennae; in males, they can be up to twice the body length, but in females they are only slightly longer than body length. Both sexes have a white spot on the base of the wings, and may have white spots covering the wings. Both males and females also have a spine on the side of the prothorax. Most research done on M. scutellatus focuses on their relationship with burned forests and the logging industry,with interest also being shown in their mating behaviours.

This is almost certainly incorrect. Notice the white stripe along the side of the OP's insect, which is absent in M. scutellatus. Also notice that the OP's insect is not black. Further, insect ID answers should always provide references (because of people's propensity to provide incorrect answers)


text:
What are the major steps of follicular B cell development
This is a learning objective in my curriculum, and after having spent two hours trying to answer it for myself using official course resources (many of which are online, but some of which are behind paywalls and so may be inaccessible to other community members), it's clear to me that I need some assistance.
So I would just like to know what is the latest understanding of the major steps of follicular B cell development in mouse and human.

According to Basic Immunology - Functions and Disorders of the Immune System (3rd Ed.) by Abbas and Lichtman (Copyright © 2011 by Saunders), p.133:

A majority of B cells are called follicular B cells because they
  reside in the follicles of lymphoid organs. These follicular B cells
  make the bulk of T-dependent, class-switched, and high-affinity
  antibody responses to protein antigens and give rise to long-lived
  plasma cells.

and in the caption for FIGURE 7-2:

Subsets of B cells. Follicular B cells make T-dependent responses to protein antigens, and marginal zone and B-1 B cells account for
  most of the T-independent antibody responses. In mice it has been
  shown that B-1 B cells arise earlier in development, from progenitors
  in the fetal liver, and follicular and marginal zone B cells arise
  later, from bone marrow precursors. Comparable differences in the
  origins of these subsets have not been defined in humans. Note also
  that the distinctions in the type of response are not
  absolute—follicular B cells can make T-independent responses and
  marginal zone B cells can make some T-dependent responses. Ig,
  immunoglobulin.

(emphasis not in original)
From the sentence I emphasized, it seems to me that as of 02011, there is still a great deal that is not well-understood about the origins (and perhaps also development?) of human follicular B cells.
Interestingly, in the 4th edition of this textbook (Copyright © 2015 by Saunders), the details have changed slightly (as below):

Subsets of B cells. Follicular B cells make T-dependent responses to protein antigens, and marginal-zone and B-1 cells account for most
  of the T-independent antibody responses. In mice, B-1 cells arise
  earlier in development, from progenitors in the fetal liver, and
  follicular and marginal-zone B cells arise later, from bone marrow
  precursors. Note also that the distinctions in the type of response
  are not absolute; follicular B cells can make T-independent responses,
  and marginal-zone B cells can make some T-dependent responses. Ig,
  Immunoglobulin.

Most interesting to me is the removal of the 3ed sentence: "Comparable differences in the origins of these subsets have not been defined in humans." Which leads me to believe that comparable differences in the origins of these subsets have now been defined in humans (in the past 4 years).
So I have a definition and description of follicular B cells, but I am unable to find anything else in either edition of this book on the development of follicular B cells (in either mouse or human).
Another reference in my course resources is Cellular and Molecular Immunology, 8th ed., 2014, by Abbas, Lichtman, and Pillai.
In it (Chapter 12: B cell activation and Antibody Production), I find the following about follicular B cells:

Distinct subsets of B cells respond preferentially to different types of antigens ( Fig. 12-3 ). Follicular B cells in peripheral
  lymphoid organs primarily make antibody responses to protein antigens
  that require collaboration with helper T cells.

Which strikes me as yet another description of follicular B cells, but not a list of steps in their development (which is my learning objective).
The same textbook makes several other mentions of follicular B cells, but does not address their development. Although I should probably already know this (and this may be in some of my lectures but these are not universally searchable and I have precious little time to read), I do not know about either their progenitors or their progeny, and I think this is what is meant by this learning objective: the major steps in their development.
In the same chapter of the same textbook, I also see:

Most mature naive B lymphocytes are follicular B cells (sometimes also
  called recirculating B cells) that constantly recirculate in the blood
  and migrate from one secondary lymphoid organ to the next in search of
  antigen. Follicular B cells enter secondary lymphoid tissues (spleen,
  lymph nodes, mucosal lymphoid tissues) through blood vessels located
  in the T cell zones, and then they migrate into the follicles, the B
  cell zones of these tissues. The movement into lymphoid follicles is
  guided by the chemokine CXCL13 secreted by follicular dendritic cells,
  the major stromal cell type in the follicle, as well as by other
  stromal cells. CXCL13 binds to the CXCR5 chemokine receptor on the
  recirculating naive B cells and attracts these cells into the
  follicles. As we will discuss later, the same chemokine-receptor pair
  is also important during immune responses because it can attract a
  subset of activated T cells to the follicle.

This seems like a great description of the follicular B cell that also delves into its function, but seems to include nothing about its development.
The same chapter of the same textbook also includes:

Naive follicular B cells survive for limited periods until they
  encounter antigen (see Chapter 2 ). Follicular B cell survival depends
  on signals from the BCR as well as on inputs received from a tumor
  necrosis factor (TNF) superfamily cytokine called BAFF (B
  cell–activating factor of the TNF family, also known as BLyS, for B
  lymphocyte stimulator), which provides maturation and survival signals
  through the BAFF receptor. BAFF and a related ligand, APRIL, can
  activate two other receptors, TACI and BCMA, which participate in
  later stages of B cell activation and differentiation (and will be
  discussed later). These cytokines are produced mainly by myeloid cells
  in lymphoid follicles and in the bone marrow.

This paragraph briefly address a little bit of what seems like the development of the follicular B cell ("Follicular B cell survival depends on..."). And in chapter 2 I see that follicular B cells are a class of B lymphocytes (along with Marginal zone B cells), but I interpret this learning objective as about the development of follicular B cells after they become follicular B cells, not before this point in their development.
So this is the best answer I can find on my own after many hours of searching and reading relevant passages in recent textbooks on the subject. Yet this answer also seems incomplete to me. After all this reading, I still have no "steps (per se) of follicular B cell development."
So I could really use a more complete answer.

Try Janeway's Immunobiology 8th edition, Chapter 10 The Humoral Immune Response. It is a bit too long to summarize in an answer here, but it should give you everything that you want to know about B-Cell development, maturation, and differentiation.

Very basically it is, migrate to secondary lymphoid organs, have antigen presented by follicular dendritic cells, migrate to boundary with T-cell area, (for simplicity) get activated by Helper T-cell, proliferate, migrate to red pulp (if the secondary lymphoid organ they were activated in was the spleen) and differentiate (or while differentiating) into a plasmablast, then terminally differentiate into antibody-secreting plasma cells, start pumping out Immunoglobulins and let the opsonization begin.

Thanks @AMR for this very helpful comment. I actually do have Janeway's so I'm looking at Chapter 10 now. But I'm not seeing what you described in your second comment. Do you have a page number or a section number? The caption for Fig. 10-7 talks some about this, but I don't see in Janeway that very comprehensive list of steps in the development of a follicular B cell that you listed. I'm in chat right now if you can spare the time to continue the conversation there. What are all the synonyms for "follicular B cell"? Not obvious to me.

Section 10.5 beginning on 392. It is summarized in Figure 10.7 on page 394. I think that they are called follicular B cells for the simple reason that the area where they migrate to and are activated in secondary lymphoid organs is known as the B-cell Follicle. Biologist are nothing if not unoriginal... Except for fly geneticists...


text:
How long can a plant generate oxygen from its own carbon dioxide, produced during nighttime?
I recently bought one of these miracle fruit plants (Synsepalum dulcificum).  Since they are of tropic origin, they need higher humidity and temperature as we have it here in Austria. So I decided to cover it in a transparent plastic bag, together with a small water basin, in order to maintain better conditions.
Assuming the bag is absolutely gas-tight, allowing no diffusion, my question is:
For how long could the plant generate $\ce{O2}$ from its own $\ce{CO2}$, produced during night? And as a little subquestion: Will the plant eventually run out of oxygen at night?
I know there are no exact answers to this, so an rough approximation is more than enough for me.

Just to give you better notion of my experimental conditions:

enclosed gas volume: ~ 3 L
(onesided) leaf surface area: ~ 0.5 dm$^2$
temperature: ~ 15$-$25 °C

For how long could the plant generate $\ce{O2}$ from its own $\ce{CO2}$, produced during night?
Plants do not generate $\ce{O2}$ from $\ce{CO2}$.
Photosynthesis consists of two general steps, one that requires light and one that does not. The first step occurs in the thylakoid membrane, and splits water into oxygen, hydrogen ions, and energy. The second step is the carbon fixation step, which occurs in the chloroplasts and uses energy to convert the carbon dioxide into carbohydrates.
Step 1: $\ce{2 H2O + light → 2 H+ + O2 + energy}$
Step 2: $\ce{3 CO2 + 6 H+ + energy → C3H6O3-P + 3 H2O}$
The more detailed chemical equations can be found on the Wikipedia Photosynthesis page.
Since the first step which produced oxygen is light-dependent, it occurs mostly during the daytime. To keep growing during the night, the plants break down the carbohydrates they produced and stored during the day. This cellular respiration uses up oxygen and generates carbon dioxide just as animals do.
Will the plant eventually run out of oxygen at night?
As mentioned, plants require oxygen for cellular respiration, which occurs both at day and night. The difference is that during the night, they are not producing oxygen via photosynthesis. Assuming the plant is in sufficient light and temperature conditions during the day, the plant will not run out of oxygen at night. Plants can survive in sealed environments for very long times. A fun example is a reportedly 53 year-old bottle garden. In a bottle garden, which is essentially the system you are creating, the only difference from a plant out in the environment is that the same oxygen, carbon, and hydrogen molecules are constantly being recycled via photosynthesis and cellular respiration.

Nice clear answer, good reminder that the oxygen comes from water splitting. Wish I could +1 again for the 1960's bottle garden!

I've re-used a bit of your explanation in this question.


text:
Heteromaternal Superfecundation - Any known cases?
Superfecundation in mammals (fertilization of two or more ova from the same cycle by sperm from separate acts of sexual intercourse) -- Is possible in nature from different fathers (Heteropaternal) as after the first zygote is formed, a second act of intercourse within a certain time span has the potential (of another ovum is present) to form a second zygote.
Has there been any cases where a naturally pregnant mammal was implanted (IVF) with a second zygote from a different set of parents?  Heteromaternal/paternal Superfecundation?

This would be termed superfetation rather than superfecundation. While this extremely rarely happens in humans, superfetation does occur naturally in some mammalian species. These pregnancies occur when the mother ovulates after she is pregnant.
Superfetation consisting of a natural pregnancy and implanted embryo has been done in cattle. In this case, 7-day embryos were successfully transferred to 14-day pregnant cows to produce superfetation. See Joel Carter's dissertation Superfetation in Beef Cattle (2002).
There have also been successful cases of superfetation in cows that were first implanted with a 7-day embryo, and then followed by natural service. See WH Hall, Bovine superfetation by natural conception secondary to an embryo transfer pregnancy, Cornell Vet. 1987 Jul;77(3):282-3.
An excellent summary of the existing literature on superfetation in many species is K Roellig et al., The concept of superfetation: a critical review on a ‘myth’ in mammalian reproduction, Biol Rev Camb Philos Soc. 2011 Feb;86(1):77-95.

I don't think that's what the OP is asking about. If I'm understanding the OP correctly, by "heteromaternal superfecundation" they mean that the implanted zygote's genomic mother is not the same individual as the mother in whose womb the zygote has been implanted. This is emphasized by the later clarification "different set of parents".


text:
Effect of a doubling of the start codon in a gene
I am learning about frameshift mutations. Frameshifts can occur due to a nucleotide deletion. Suppose that due to a frameshift, because of a deletion somewhere upstream from the original start codon, two additional start codons are generated, just before the stop codon in the new reading frame. What would happen in terms of translation?
AUG-GCC-AUA-AUG--------UAA
Start       Start then stop

If one of these answers solved your issue, please take a moment and accept it by clicking on the check mark to the left. That will mark the question as answered and is the way thanks are expressed on the Stack Exchange sites.

This is an old question, but it should say, or the answers should say, whether they are referring to eukaryotic or prokaryotic systems. All the answers appear to assume eukaryotic systems.

There is a basic misconception in the question you have asked, which @biogirl has explained. There is only one start Codon in any mRNA and it defines the open reading frame.
All other AUGs in the open reading frame are simply codons that encode for the Amino Acid Methionine and have no function in the start of translation. There are factors other than AUG that determine the start of translation.
So a frame shift that gives you an additional AUG only means that you will have a different Amino Acid encoded for in the resulting polypeptide. A frame shift will generally completely alter the protein product of the gene. If however the frameshift does disrupt the start codon, then it is unlikely that you will have any translation what-so-ever, as the other elements necessary for determining the start of translation will likely not be present in other areas of the coding sequence. In prokaryotes, you need a Shine-Delgarno sequence to initiate translation, and in Eukaryotes, though all of the factors for translation start are not well understood many genes carry a Kozak sequence that indicates to the ribosome the start of the open reading frame.
The more important codons to look for are introductions of stop codons. These three codons, UAA, UAG, and UGA do not have tRNAs with complementary anticodons (for the most part, as tRNA genes can also sustain mutations that change their anticodon) and therefore all result in the termination of translation if the shifted frame results in the ribosome reading one of the three stop codons in frame.

Very good answer and +1. Just a nitpick: strictly speaking, there are actually tRNAs that recognize STOP codons. Such nonsense tRNAs can be the product of a specific mutation but also, as is the case for tRNASec, wild type sequences that insert a specific amino acid.

@terdon, Learn something new (or old as this was discovered in the 80's) every day. I had a hard time finding references, but Molecular Biology of the Cell 6th Edition mentions selenocysteine and it does indeed have an ACU anti-codon. It looked like there needs to be a secondary stem-loop structure in the mRNA for it to be incorporated instead of having a release factor bind and terminate transcription, but it definitely shows the remarkable flexibility and diversity of the genetic code. Thanks!

mRNAs can include multiple start codons (and thus multiple ORFs). Upstream AUGs and their effect on translational regulation are an active area of research. They are also sensitive to neighboring mutations. http://science.sciencemag.org/content/352/6292/1413

AUG functions as a start codon only when it is at the 1st position of the open reading frame.  Whenever AUG is present in between, it codes for methionine amino acid. Go through the basics of translation from a good book.

The start codon is not sufficient to start translation. A ribosomal binding site is also required. It's likely that translation would initiate at its normal location and then simply proceed through any additional start codons in the new ORF until it reaches the first stop codon.

That is half the story as it is only in Prokaryotes that the ribosome binds to the Shine-Delgarno sequence and the starting AUG. In Eukaryote small ribosomal subunits bind near the 5' cap and scan through the 5' UTR until the Start codon. In many mRNAs that is near the Kozak sequence, but not all Eukaryotic mRNAs have a Kozak sequence.

@AMR Nowhere in my answer did I make the claims you say I did. The ribosomal binding site is self explanatory, be it the SD sequence or 5' cap.

It is because you are answering a questionabout two AUGs, and you are saying that there needs to be a ribosomal binding site, which is correct, but when taken with the question implies that the ribosome is choosing between one or the other AUG based on where it binds, and that would only be relevant in the case of prokaryotes as it would bind to the AUG in the SD sequence. Eukaryotes would scan to the start site. AUG is simply the codon for methionine so even saying additional start codons as you have in your edit obfuscates the situation.

@AMR I really don't understand your point. The start codon is chosen based on where the ribosome binds. What is the controversy?

In Eukaryotes you can have an AUG or multiple AUGs in the 5'UTR, so your last comment doesn't hold, and your answer is not complete and is confusing. Eukaryotic translation does not necessarily begin with the first AUG encountered. And as I pointed out before, there is one start codon, which defines the open reading frame; any other AUGs are methionine codons or are in the UTRs and are untranslated, so no additional AUG is called a start codon.


text:
Is there nutrient absorption in the large intestine of hindgut fermenters?
In hindgut fermenters, plants are digested in the caecum by microbes. I want to know whether hindgut fermenters can absorb the nutrients obtained from the digestion in the large intestine because the absorption of digested materials is not the main function of the large intestine in other animals. I know some hindgut fermenters reingest the materials created in the caecum, but I think not all hindgut fermenters perform this behavior. I want to know the main site of absorption after the caecum.

There is quite a difference between a horse and a rabbit - for example, the colon is enormous in the horse compared to the rest of the GI tract, much less so in the rabbit. it would help if you could specify what hindgut fermenter your question pertains to.

Maybe I want to know different kinds. Is it that the ones that cannot absorb nutrients in the large intestine will reingest (e.g., coprophagy)? And others that can absorb nutrients in the large intestine will not reingest?

I have divided this answer into a section on horse and rabbit. While there are many other hindgut fermenters, these species are good illustrations of  different ways hindgut fermenters can digest and absorb nutrients from their food.
Horse
As you know, absorption of "nutrients" occurs along the intestines, but at varying degrees at different sites. Most compounds are primary absorbed in the small intestine of the horse. This includes protein, glucose (soluble carbohydrates), fats, calcium, and magnesium.
Any carbohydrates that are not absorbed in the small intestine reach the hind gut. Here they are fermented by bacteria to short-chain volatile fatty acids  (VFAs) and lactic acid. Horses can use the VFAs (propionate, butyrate, and acetate) as an energy source, but a diet too high in grain can also lead to excessive lactic acid production in the hindgut, and as a result the horse may experience colic.  As your question pertains to the hind gut, a nutrient of main concern is therefore volatile fatty acids.
The hindgut of the horse is very long and developed. To review with the anatomy of the horse hindgut, it consists of the caecum, ventral colon, dorsal colon, transverse colon, descending colon (or small colon), and rectum.

In a study in 1974, RA Argenzio et al. determined that among the parts of the horse hindgut, most VFAs were produced and absorbed in the ventral colon, 8-12 hours after feeding. This is depicted by the graph below, which shows a large negative net production of VFAs after 8-12 hours (i.e. more VFAs absorbed than produced). Note that the caecum and dorsal colon are also important sites of VFA production and absorption.

The hindgut is also an important site for phosphorus absorption in the horse, unlike many other species that primarily absorb phosphorus in the small intestine. This is thought to be because most of the dietary phosphorus in the horse in phytin phosphate, which must be exposed to the enzyme phytase produced by the microbial flora in order to be absorbed. Studies such as Schryver et al. (1972) and T. Matsui et al. (1999) have shown that most phosphorus is excreted by the small intestine and caecum, and most is absorbed in the dorsal colon and small colon. The figure below from Schryver shows the net absorption of phosphorus on the various experimental diets. Note that this is oriented opposite to the VFA figure above; absorption is positive rather than negative on this graph.

Rabbit
To begin with the rabbit anatomy, you will note that the colon of the rabbit is much less developed than that of the horse. However, both are hindgut fermenters, and what they do have in common is a very large caecum.

As in the horse, much of the digestion and absorption of nutrients occurs in the small intestine. This includes protein, fats, and simple carbohydrates (glucose), as well as some vitamins.
Also like the horse, the digestable material not absorbed by the small intestine passes to the caecum, where it undergoes fermentation by the microbial flora. The large fibrous material passes directly to the colon, where water is absorbed and forms hard faecal pellets, while the small digestible material passes through reverse peristalsis into the caecum. What is different in a rabbit to a horse, however, is that the about 8 hours after feeding, the caecal material is packaged into a small pellet called a caecotrophe. As or shortly after the caecotrophe is excreted, the rabbit re-ingests the caecotrophe. As this food has been digested once already, the small intestine is better able to absorb nutrients from it.
As an example, important nutrients that are able to be absorbed due to caecotrophy in the rabbit are the B vitamins such as niacin, riboflavin, folate, and cobalamin (vitamin B12). One of the early studies on this topic is Kulwich et al. (1953).
Summary
The reason for the difference between the horse and rabbit is fundamentally an anatomical difference. Both species have a large caecum which enables fermentation of plant matter. However, the horse has a long, voluminous colon in which it can absorb many nutrients, but they will lose protein and other nutrients in this process because the colon is less adapted to absorb them. In coprophagic (rat) or caecotrophic species (rabbit), they do not have as long a colon, but can absorb vitamins and proteins lost in the faeces during the second pass through the gastrointestinal tract.
An excellent and very detailed review of the gastrointestinal tracts and nutrient absorption in a variety of species is this freely accesible paper by Stevens and Hume, "Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients."
References
Argenzio, R.A., Southworth, M., and Stevens, C.E. (1974) Sites of organic acid production and absorption in the equine gastrointestinal tract. Am. J. Physiol. 226:1043-1050.
Bugaut, M. (1987) Occurence, absorption and metabolism of short chain fatty acids in the digestive tract of mammals. Comp. Biochem. Physiol. 86B(3):439-472.
Hornincke H., and Bjornhag, G. (1980) Coprophagy and related strategies for digesta utilization. In Digestive Physiology and Metabolism in Ruminants, 707-730. Avi Publishing, Westport, CT.
Kulwich, R., Struglia, L. and Pearson, P.B. (1953) The effect of coprophagy on the excretion of B vitamins by the rabbit. J. Nutr. 49:639-645.
Matsui, T., Murakami, Y., Yano, H., et al. (1999) Phytate and phosphorus movements in the digestive tract of horses. Equine Vet. J. Suppl. 30:505-7.
Schryver, H.F., Hintz, H.F., Craig, P.H., Hougue, D.E. and Lowe, J.E. (1972) Site of phosphorus absorption from the intestine of the horse. J. Nutr. 102: 143-148.
Stevens, C.E., and Hume, I.D. (1998) Contributions of Microbes in Vertebrate Gastrointestinal Tract to Production and Conservation of Nutrients. Physiological Reviews, 78(2):393-427.


text:
Meaning of "pure" in "pure plant DNA" (horizontally transferred to bacteria in soil conditions)
The abstract of Transformation of Acinetobacter baylyi in non-sterile soil using recombinant plant nuclear DNA, by Simpson et al., 2007:

To provide estimates of horizontal gene transfer from transgenic crops to indigenous soil bacteria, transformation frequencies were obtained for naturally transformable Acinetobacter baylyi BD413 using a chromosomally integrated plant transgene. The transgene comprised sequences for two phenotypic markers: kanamycin resistance (npt II) and green fluorescent protein (gfp), expressed from their own bacterial promoters. Recipient bacteria carried a copy of these two genes, with deletions in their 3'-termini abolishing the marker activity, these genes were integrated into a 16S rRNA gene in the bacterial chromosomal genome or carried on a broad host range plasmid. Successful recombination between the plant transgene and the bacterial genome resulted in restoration of the markers, allowing detection through antibiotic selection and fluorescence. Transformation parameters of increasing complexity, without any enrichment steps, were used to approach the field conditions, while still obtaining measurable transformation frequencies. In pure culture filter experiments, transformation was detected using ground, chopped and whole leaves, as well as whole sterile seedlings, and ground roots. In sterile soil microcosms, transformation was detected using pure plant DNA (3.6 × 10-8 transformants per recipient) and ground leaves (2.5 × 10-11). Transformation was also detected for the first time in non-sterile soil using pure plant DNA (5.5 × 10-11). Since the same constructs were used throughout, these data allow predictions of even more complex environmental systems where measurable frequencies are not easily obtainable.

What is the meaning of pure plant DNA? That the transferred DNA was in the form of purified DNA solution dripped onto soil, as opposed to some ground leaves whose cells included donor DNA (and some of these cells were crushed while being grounded and thus shed some DNA material onto soil)?
Was it done in order to promote transformation?


text:
No genes' ID in peak annotations during ChiP-Seq with ChIPpeakAnno R package
I am trying to perfom Chip-Seq Analysis which is greatly described in that conversation: introduction to Chip Seq . The same as autor of mentioned question I am a student of Applied Mathematics and I am doing my best to enter bioinformatics fields.
I am basically at the moment where I would like to annotate peaks with genes' IDs. To do this I am using ChIPpeakAnno R package from Bioconductor. I used below  code to annotate my reads (outputs from MACS) with genes' ID's
> library(ChIPpeakAnno)
> # data(package = "ChIPpeakAnno")$results[,3]
> macsOutput <- toGRanges(data="example_peaks.bed",
+                                               format = "MACS")

> data(TSS.human.GRCh37)
> macs.anno <- annotatePeakInBatch(macsOutput,
+                                                                AnnotationData=TSS.human.GRCh37,
+                                                                output="overlapping", maxgap=5000L)
> library(org.Hs.eg.db)
> macs.anno <- addGeneIDs(annotatedPeak=macs.anno,
+                                               orgAnn="org.Hs.eg.db",
+                                               IDs2Add="symbol")
>
> # no annotations for some genes
> as.character(head(as.data.frame(macs.anno)$symbol))
[1] "PTCHD2" "PTCHD2" "PTGER3" NA       "HFM1"   NA

but there occures that there are no genes' annotations for some peaks. Can anyone tell me why this might happen? And how to avoid this? Does this refer to the maxgap=5000L parameter? When creating output from MACS I set a parameter for length to be 10 000.

I had the same problem.
This how I solved it, I found the solution somewhere here, I don't remember where, and it worked for me.
macs.anno <- annotatePeakInBatch(gr_broadPeak, AnnotationData=TSS.human.GRCh38,
                                     output="both", maxgap=5000L)
 macs.annoL=addGeneIDs(macs.anno,"org.Hs.eg.db",c("symbol", "genename","entrez_id"))
 macs.annoDF=as.data.frame(macs.annoL)
   result=macs.annoDF[which(macs.annoDF$symbol!="NA"),]

I'm on vacations.

I'll check your solution soon and then, if it will work, I accept it :)


text:
What do the numbers in Photosystem I P700 and Photosystem II P680 stand for? Is it the optimum wavelenght? The maximum wavelenght?
I am a bit confused about this because my teacher and english Wikipedia say it's the wavelenght the Photosystem is most reactive to; my textbook and the german Wikipedia say that it is the maximum wavelenght the Photosystem can absorb :-/

It's the absorption maximum of the photosystem.

I'd first like to briefly mention what the P700 and P680 refers to. These are the reactions centers of the photosystems. The Photosystems are where the light is absrobed and converted to the form of electrons. The light is absorbed by the chlorophyll molecules and the energy is transferred to the reaction center which transfers that energy into an electron from a water molecule. Tha elecron is transport tmake ATP and NADPH, which is important for carbon fixation.
The numbers specify the wavelength of light that the reaction center are most reactive to, and therefore, the wavelength where they absorb the most light. That's what's meant by the maximum absorption. So everybody is right, your teacher, the textbook and Wikipedia. They just say it differently.


text:
Explaining the simpson's diversity index
In my biology class, we were trying to compare the biodiversity of two site. In doing so, we were instructed to use the Simpson's Diversity index as follows:
$$ \frac{\sum_i n_i (n_i - 1)}{N (N - 1)}$$
Where $n_i$ is the total number of organisms of a particular species; and, $N$ is the total number of organisms of all species.
We were given a method to calculate the index in a class that required almost naught mathematical understanding for the purposes of the experiment. From what I have read, the Index calculates the probability that any 2 randomly selected organisms belong to the same species, and it is thought that the closer the result is to zero, the more diverse the region is.
What I can't understand, is the math behind the index; for example: why is it multiplying n by n-1? And how is this better than dividing the sum of all the organisms by the number of species?
I'm in Pre-Cal, so when explaining, please do so with minimum emphasis on "advanced" math terms.

Welcome to Biology.SE. Wiki might help a bit.

For the following answer, assume we have two communities of size 4. Community 1 has two organisms of species A and two organisms of species B. Community 2 has three organisms of species A and one organism of species B.
The probability that two randomly selected organisms belong to the same species
In this example, for either community, the probability that two randomly selected organisms belong to the same species is the sum of the probability of selected two organisms of species A and two organisms of species B. In other words:
P(selecting two of the same species) = sum(P(selecting two of species X))

Where we sum over all species present (in this case, species A and species B)
The probability of selecting two organisms of species X is the probability that the first organism is species X times the probability that the second organism is species X.
The probability that the first organism is species X is simply:
P(first organism is species X) = nX/N

Where nX is the total number of organisms of species X and N is the total number of organisms in the community.
The probability that the second organism is of species X is:
P(second organism is species X) = (nX-1)/(N-1)

Because we are sampling without replacement, we subtract one from each value as we are now sampling from a community that is missing one individual (the one we first sampled).
The probability that two randomly selected organisms belong to species X, is then the sum of the previous two probabilities:
P(Selecting two of species X) = nX/N * (nX-1)/(N-1)

or
P(Selecting two of species X) = nX(nX-1)/N(N-1)

Then, to get the probability that two randomly selected organisms belong to the same species, we sum the above equation for all species. Summing over all species will give us your first equation.
In this case, for both communities we sum over species A and species B.
P(Selected two of same species) = [nA(nA-1)/N(N-1)] + [nB(nB-1)/N(N-1)]

P(Selected two of same species) = [nA(nA-1) + nB(nB-1)]/N(N-1)

For community 1, this comes out to 0.333. For community 2, it comes out to 0.5, accurately representing that community 1 is more diverse.
Why can't you take the total number of organisms and divide it by the total number of species?
The point of the Simpson's biodiversity index is not just to represent the total number of species in a community, but to portray how spread-out organisms are among the species; a community in which one species dominates and the rest are rare is considered less diverse than a community with the same number of species that has a roughly even number of individuals per species.
In the case of our two communities, the total number of organisms divided by the total number of species will give us the same number (4/2), not accurately representing that the communities do not have the same diversity (they have a different spread of organisms)

While this answer resolves the question of what Simpson's biodiversity is, it does not answer why it reflects diversity. Particularly, it is better to demonstrate the index is minimum when all species have equal number of organisms and the index reaches maximum when all organisms belong to only one species.

That's an estimator for Simpson index,
$$ \sum_i p_i^2 $$
where $p_i$ is the probability that $i$-th species is sampled.
This is sum of the probability that two independent samples are from the same species.
There are multiple ways of estimating this quantity from observations $n_i$.
When $n_i$ is small,
$$\hat{p} = \frac{n_i}{N}$$
is unbiased but has high variance, and plugging it in $\hat{p}$ to the definition would also have high variance. (Note that this is equivalent to sampling with replacement.)
If one uses sampling without replacement formula,
$$\hat{p^2} = \frac{n_i}{N} \cdot \frac{n_i-1}{N-1}$$
then, the resulting estimator is
$$ \sum_i  \frac{n_i \cdot (n_i - 1)}{N \cdot (N - 1)}$$
Note that both estimators converge to Simpson index for $N \to \infty$.
But of course, there aren't infinite number of samples, usually.


text:
Electrically facilitated active transport across a membrane
I'm trying to go back to school to do a PhD in control theory, specifically concerned with control of glucose. The glucose system can be controlled using two chemicals: insulin and glucagon. I was wondering if there was any precedent for controlling the active transport of a chemical across a membrane using a tiny electric current. Has this ever been done?
The reason I ask is that I want to avoid relying on mechanical systems that are prone to being bogged down by attacks from the native immune system.
Any knowledge on the subject/recommendations for attacking this problem/alternative subreddits or websites would be greatly welcomed.

Welcome to Biology. Electroporation is an example where DNA is injected into a cell using a (high?) current. But I think it works only with charged particles. Glucose is uncharged.

Thanks for the info. The glucose wouldn't need to be injected anywhere per se, just "let go" from a reservoir into the blood stream.

You may want to take a look at some of the research behind insulin pumps. I don't know the specifics, but I know they use a lot of closed-loop control, and are a fairly active area of research (but potentially difficult to get into--some people have been working on control problems related to glucose since at least the 80's).


text:
What causes goose bumps?
What is the actual process and reflexes that cause the goose bumps? Why is it an evolutionary advantage to have goose bumps in the first place?

Even wikipedia has all details you required for mechanism.

We get goose bumps because of the flight or fight response or because of cool temperature. The process is that whenever our body experiences such stimuli, the arrector muscles contract and thus the hair follicles straight out. As per the evolutionary point of view, mammals possessed this feature to portray the enemy our response ( in fight). Given photo will tell you the arrector muscle's position so that u can understand how the follicles straight up.
And the thing about cool temperature, the goose bumps appear so that they can form an insulation sort of thing to prevent us from losing our body heat to the surroundings.

Where is this pic from?

Working kindersley publication- ultimate visual dictionary

Goose bumps are the hair follicles raising up to increase the surfaces area of your skin. This is flight or fight response as it increases ability of the skin to transfer body heat.


text:
Are there any non-mammalian species known that lactate?
Are there any non-mammalian animals that produce milk to feed their young, or are mammals the only milk-producing animals?

The classical definition of a mammal includes production of milk (hence the name). Your question is a bit circular unless you specify your definition of a mammal.

@Superbest: in which case, equivalently, "are mammals a clade?", to which we can reply, "no, because not all common ancestors of pigeons and humans produce milk", or reply "yes, by a No True Scotsman argument" ;-)

Related question: Do any birds beside the family Columbidae (or any reptile or mammal) feed their young "Crop Milk"

one can find pretty detailed examples and a possible explanation in this article

Short answer
Technically, only mammals lactate. To lactate means to produce milk from the mammaries to feed a baby or young animal. Milk, in turn, is defined as the secretions from mammary glands. However, there are animals other than mammals that produce milk-like substances to feed their young.
Background
Both male and female pigeons (Columba livia) possess the ability to produce a nutrient substance, termed pigeon ‘milk’, to feed their young. A similar substance is produced by flamingos and male emperor penguins. The normal function of a crop is a food storage area located between the oesophagus and proventriculus where food is moistened before further break-down and digestion through the gastrointestinal tract (Fig. 1).

Fig. 1. Schematic of the location of the 'milk'-producing crop in a pigeon (left) and a pigeon feeding its chick from its crop (right). Sources: ZME Science and Bird Ecology Study Group
During the process of pigeon ‘lactation’, a curd-like substance is regurgitated from the crop to the chick. The dry-substance of pigeon ‘milk’ is 60% protein, 32-36% fat, 1-3% carbohydrate and some minerals, including calcium. It has been shown that pigeon ‘milk’ contains IgA antibodies, which provides evidence suggestive that it is more than a nutrients alone. The physiological mechanisms governing pigeon ‘milk’ production and delivery are unknown. It is well documented that the pigeon crop is responsive to the lactogenic hormone prolactin. However, the pigeon crop tissue during ‘lactation’ is structurally unrelated to the mammary glands in mammalians, because it is not glandular and secretory processes do not seem to be involved (Gillespie et al, 2011).
The similarity between this process and lactation in mammals is striking, but is a case of convergent evolution, where unrelated species independently evolve similar traits. 'Milk' production is also recorded in some fishes, where it is fed to their young in the form of a mucous secretion on the skin (Buckley, 2010). Certain amphibians shed skin cells that are fed to the young. But the 'milk' of pigeons and doves is thought to be the most highly specialized of any non-mammalian 'milk' (Australian Geographic, September 2011).
References
- Buckley et al., J Exp Biol; 213: 3787-95
- Gillespie et al., BMC Genomics (2011); 12: 452

'Milk'-producing fishes are something I really would not have expected. Cool.
(extra details at http://jeb.biologists.org/content/213/22/i.1.full.pdf+html?sid=82269227-a55f-4c15-982a-9b5f6f5fa6b0 )

Producing milk, per se, is a strictly mammalian phenomenon. There are functionally similar processes in non-mammals (e.g., 'crop milk', produced by some birds), but because these processes evolved independently from the evolution of mammalian milk, they are not considered to truly be milk.


text:
Why is an A-U bond less stable than an A-T bond?
I have encountered the following fact many times, but have not yet encountered a possible explanation for it. Will you please help me understand the molecular mechanism by which the bond between Adenine and Thymine is more stable than the bond between Adenine and Uracil?
Thanks in advance

Can you add details? Please indicate where you encountered this fact. AU and AT bond comparison in what: Are both DNA, or RNA?

Also have a look at this http://www.ncbi.nlm.nih.gov/pubmed/15977281

check khan acadamy, it explains everything. Also pls tell if you are talking about DNA or RNA

I was not previously aware of this assertion, but on doing a little searching found it discussed in the following paper (I'm not sure whether it is open access or not).

Kamya PR and Muchall HM  (2011) "Revisiting the effects of sequence and structure on the hydrogen bonding and π-stacking interactions in nucleic acids" J Phys Chem A. vol 115 pp. 12800-8

From this it emerges that the claim relates to the effect of substituting U for T in DNA, and the paper references previous claims for a stronger AT hydrogen bond. It also references other studies which did not find any difference, so the question was/is contentious. All studies were made on particular stretches of DNA duplex, and the authors' own studies were on a wider range of duplex structures from the protein data bank and (apparently) used more sophisticated analysis. To quote, they concluded:

"H-bonding in AT can be stronger or weaker than that in AU base pairs, depending on the particular choice of nucleic acids used for comparison"

They explain this in terms of the influence of neighbouring bases in the duplex on base stacking, which, depending on the bases (i.e. the sequence), can be enhanced by interactions with the methyl group of T. (There may also be other effects caused by distortion of the base-pairs from planarity in particular cases.) So it would appear that AT base-pairs are not intrinsically stronger than AU base-pairs, but can be stronger in certain three-dimensional contexts.
As a generalization, the premise of the question would therefore appear to be false.