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What is the exact definition of a "gene"?
(In this question, I'm only considering the molecular-biology notion of a gene, not the older Mendelian notion.)
Wikipedia defines a "gene" as "a sequence of nucleotides in DNA that is transcribed to produce a functional RNA", and an "allele" as "a variation of the same sequence of nucleotides at the same place on a long DNA molecule". Typically, one says that different alleles can be different "versions" of the same gene.
Taken literally, these definitions imply that both a "gene" and an "allele" are fully specified by their base pair sequences. But this contradicts that notion that different alleles can be different "versions" of the same gene - which implies that the notion of a "gene" is more general than that of an allele, since different alleles can correspond to the "same" gene.
The notion of "same place" in Wikipedia's definition of an allele seems to suggest that a gene is characterized by its location within a DNA molecule. I.e. two different alleles correspond to the "same gene" if they occur at the same locus on a chromosome.
So what exactly specifies the boundaries of a single gene, i.e. what specifies which alleles correspond to that gene as opposed to a different gene?
Put another way: what is the minimal amount of information required to fully specify a gene? It can't just be a base pair sequence, because that instead seems to define an allele. Is it a particular genetic locus? Or is it defined functionally, i.e. a set of alleles are instances of the "same" gene if they all code for RNA strands that are functionally similar/equivalent? If it's the latter, then is there a precise way to define "functionally similar/equivalent", or is there there some degree of subjective convention in demarking different genes? (If one allele leads to a healthy organism and another allele leads to a nonviable organism, then those seem very functionally different - so is it meaningful to say that those alleles are variations of the "same" gene?)
Or is the resolution just the empirical fact that the functional purpose of a protein is so well-correlated with the locus of its encoding DNA that we can be imprecise about specifying whether the locus or the function defines the gene?
(I've also seen the notion of a "gene" defined purely phenotypically, as in the older Mendelian framework. But my understanding is that in reality, quite few phenotypic parameters are directly controlled by individual genes - most arise from complicated polygenetic interaction effects. So it seems that in practice, a purely phenotypic characterization can't precisely demarcate individual genes.)
Yet another way to frame this same question: is "allele" or "gene" the more primitive concept?

Too many questions at once. Can you focus a bit?

I'm not following your reasoning. A dog is a dog. A Border Collie is a dog, as is a Poodle. And a Chihuahua, a Mastiff, and a Belgian Tervuren. Does that mean a dog isn't just and fully a dog? Does that mean more is required to define a dog? Does the fact that they are all so different mean that "dog" is an impossibly imprecise definition? If a dog is born with a heart defect causing death, was it really a dog? Or is it our quotidian way of thinking about dogs that allows us to be imprecise about what a dog is? This seems to be your logic. Please forgive me if I've misunderstood.

@alec_djinn There is only a single distinct question here, which I framed in several different ways in order to clarify what I meant to ask. Unfortunately, it doesn't seem to have worked.

@anongoodnurse You have misunderstood. Up to a few nuances, there is a simple characterization of whether two animals are the same species: whether or not they can interbreed. What is the corresponding equivalence relation that determines whether or not two alleles are the same gene?

@tparker And you have made the all-too-common mistake of assumint that, because I posit something contradicting you, that I "don't understand." I understand quite well, thank you. Two alleles are even more alike than two dogs.

@anongoodnurse You literally said "I'm not following your reasoning", thereby admitting yourself that you don't understand my question. This is not a criticism of you or your biology expertise; maybe my question was unclearly posed. But you are incorrect in assuming that I said "You don't understand" because I contradicted you; I said "You don't understand" because you said that you didn't understand, and then confirmed that with your subsequent sentences.

I was being polite. Instead of coming right out and saying, "This is really misunderstanding genetics," (which it is), I was deflecting to allow you to reconsider. My analogy stands.  Just as dogs which are different in appearance are still wholly dogs, genes coding for a specific functional protein but with differing base pairs are still wholly genes. You're reading too much into the whole thing; that's what the analogy shows.

Folks were identifying genes for 75 years before we understood the role of DNA in heredity. Originally genes were defined as the unit of heredity from back when Mendel posited that the mechanism of inheritance was pairs of indivisible particles, each pair acting in combination to control one heritable trait.

In this question, I'm only considering the molecular-biology notion of
a gene, not the older Mendelian notion.

That's where it begins to get confusing. It's not like we discovered DNA and then went back and re-worked all of our thinking about genetics to be in terms of DNA sequences rather than Mendel's abstract gene. People still do a huge amount of classical genetics: looking for interesting traits that breed true. They may eventually start looking for the underlying DNA sequence responsible for the trait, but that can still come very late in the game. That means people still often use the term 'gene' in the purely Mendelian sense: the unit of control for a heritable trait.
Of course the discovery of the role of DNA changed things. At the crudest level the model went from
One gene determines one heritable trait
to
One gene determines one protein
As the model became richer and we became aware of things like alternative splicing and lncRNA that was modified to
One gene determines (at least) one protein or one non-protein-coding RNA that has a structural, regulatory, or catalytic function.
Part of your difficulty may be that you aren't appreciating how subtle and complex simple concepts like "the same" or "similar" are when applied to biology. Two proteins or two DNA sequences may be considered "the same" without being amino acid for amino acid or base for base identical. It usually means "indistinguishable for the context in question". If we talk about a "gene for hair pigmentation", we care that the protein generated by the gene controls the color of the animal's hair, but we don't necessarily care whether the hair comes out as blonde or brunette. At other times that subtle difference is exactly what interests us, and we'll talk about the blonde allele or the brunette allele.
You can find plenty of formal definitions for the gene in references and text-books. However in actual usages people are pretty careless about what they call a gene.
My own take is that a real definition of the 'gene' is multi-level:
A gene is the unit of control of heredity  which is implemented as a    sequence of DNA bases which directs the synthesis of a particular    protein which has a particular biological function. Said sequence is    typically located at one or more specific locations in the host    organism.  In actual usage, people may use the word 'gene' when referring to  a structure at any level of the definition without    regard to the properties of the other levels.

I found a dedicated paper about the definition of what is a gene. Their short definition is:

“a gene is a discrete genomic region whose transcription is regulated
by one or more promoters and distal regulatory elements and which
contains the information for the synthesis of functional proteins or
non-coding RNAs, related by the sharing of a portion of genetic
information at the level of the ultimate products (proteins or RNAs)”

To your individual questions:
Speaking of the human genome, different sequences on the same locus are called alleles. It is thereby the locus that is most important for the definition. The phenotypic definition of genes is outdated. You cannot have different alleles on different loci. It is thought that gene duplication is an important mechanism of evolution; you have the same sequence on different loci so that they can evolve without functional pressure, but those are then considered different genes.
Example of paralogs, genes that are related through duplication

The genes encoding myoglobin and hemoglobin are considered to be
ancient paralogs. Similarly, the four known classes of hemoglobins
(hemoglobin A, hemoglobin A2, hemoglobin B, and hemoglobin F) are
paralogs of each other.

Although similar, paralogs are considered different genes.
Addressing comments:
There were comments asking at which similarity two sequences are considered the same gene and someone implied this is a grey-zone and analyzed with computational tools.
Here topics were mixed up! What is done computationally is the evaluation of the probability that two genes are homologous. Even with 100% sequences identity, two genes of different species or at different loci within the human genome would not be considered to be „the same gene“. These would be called homologos (orthologs or paralogs).

I'm not a geneticist, so that must be taken into account in this comment. Reading from the National Human Genome Research Institute website, the gene seems to be the important thing, the locus is simply like a home address, a place where a gene is located. It would be nice to have input from a geneticist.

Thank you. It makes sense to me that a gene is specified entirely by its locus within the genome. I can't think of any other definition that I can understand.

@anongoodnurse Suppose I gave you two different sequences of base pairs, without specifying their locuses within the chromosome. How would you know whether they are two alleles for the same gene, or alleles for two different genes?

Because they would be far more alike than different, @tparker. And I would take the definition by the National Human Genome Research Institute over a 2007 opinion piece. An address is simply an address. It's who lives there that counts.

@anongoodnurse So your proposed definition of a gene is "a set of alleles that are far more alike than different"?

@tparker - Not at all. You're putting words into my mouth, which is a poor form of rebuttsl, and isn't very educational. Did you read the link I posted?

@anongoodnurse: The word locus means location, nobody is arguing against that and a gene is a functional unit on the DNA. I am not saying, that the words gene and locus are interchangeable in any way, the OP presented conflicts between 3 aspects of the definition of a gene (locus, sequence, phenotype) and my answer was that locus is most important, given paralogs exist.

@tparker It'll be a lot easier to learn biology if you don't constrain yourself to think of definitions as things that can be condensed to a single pithy statement. That's just not how people use terminology in the real world.

"So your proposed definition of a gene is "a set of alleles that are far more alike than different"?" That's actually a decent working definition since it also covers the case where there are multiple copies of a gene occurring in different locations. Definitions in biology are not like mathematical definitions and are frequently highly dependent on context. Sometimes it's the location that's important, sometime the general biological function, sometimes the specific sequence, and sometimes a combination of all the above.

@BryanKrauseisonstrike I certainly understand that terms in biology cannot be defined as precisely as they can in (say) physics. My issue is that I truly don't understand in the slightest how different genes are distinguished or considered identical. By locus? By sequence (I don't think it can be that, because that's "alleles")? By function?

@BryanKrauseisonstrike There are specific databases of genes whose construction requires people to make decisions about which alleles constitute one gene vs. different genes. Are there patterns or rules of thumb for these decisions? Or is each one just a separate accident of history?

@CharlesE.Grant Thank you for constructively responding to my honest request for clarification instead of resorting to ad hominem attacks. Your comment seems to somewhat disagree with answer above, so I suggest making it a separate answer (and I will upvote it).

There are two levels of sequence you have to think about: the DNA sequence and the amino acid sequence. Two DNA sequences may differ quite a bit and still produce the same protein, which moves the debate to when are two proteins the same. There are a whole bunch of computational and experimental tools for quantifying how different two DNA sequences or protein configurations are. And people do argue violently over where to draw the line sometimes.

@CharlesE.Grant Thank you, this is very clarifying. So a specific gene is characterized by the protein that it codes for? Two genes are the same if they code for the same protein, and they are different if they code for different proteins? And so the challenge of delineating different genes simply boils down to the challenge of delineating proteins?

@CharlesE.Grant This seems to imply that the exact same (protein-coding) base pair sequence occurring at two completely different loci of the genome would could as the same gene, since they would necessarily code for the same protein.

@tparker I'd expect such a database to have some rules, sure, but those rules don't determine what a gene is for all biology, they are decisions of convenience for that specific database, and yes in some cases the rules applied may be ad hoc or inconsistently applied to respect history and consistency of terminology with the literature.

The topic can always be made more complicated. Even synonymous sequences (coding for the same peptide sequence) can lead to different proteins (by structure). So I would side with Bryan Krause and suggest not to dwell too long on definitions.

I edited my answer.

There are other good answers already, so I'll give an overview of the ways genes are used.

Biology paper gene: string of DNA that encodes for a some unit, often a protein, with some function
High school biology classroom gene: the above definition, but also any monogenic variation which gives rise to a phenotypic change (used as synonymous with allele or SNP)
Laymen gene: any hereditary factor, including overall polygenic predisposition, to some phenotype. This would probably be in "using the word incorrectly" territory.


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Additive property of taste
It might be a dumb question to ask, but I find it confusing.
Is the perception of taste additive?
Or to be more precise, can two tasty food items combine to give a more delicious product?
For me, this sounds logical. I believe that the sense of taste is due to some chemical reactions in our mouths, which in turn fire up our taste receptors to give some specific signals to the brain. So when two tasty foods combine, there would be more signals that are identified as 'Tasty' by the brain. That should give the food combination a stronger taste than its constituents.
But I found some contradicting examples.

I like to drink tea and coffee. But once, when I accidentally mixed a cup of tea with coffee, it wasn't tasty at all.
I have seen some specific 'COMBINATIONS' of foods that taste better than their constituents.

What does this mean? More likely, my understanding of taste perception is flawed.  If it is, then what is the real working mechanism of taste?

What we think we are "tasting" is usually a combination of taste and smell. I assume you are asking about the broader experience which involves both? In that case it's pretty complicated. 1, 2, 3 If you like mixing things and you're asking only about taste by the tongue, then try eating anything citrus with a bit of miracle fruit!

Maybe this would be a good question for https://cooking.stackexchange.com/.

taste is itself a combination of smell and "taste" an apple and an onion taste the same without your sense of smell.

I would classify the neurological phenomenon of "taste" or "tastyness" as an emergent property (1), and therefore synergistic (i.e. not adequately explained simply by additive effects). For example, when something "tastes like chicken" that's a synergistic sensory pattern in your brain involving the specific ratios of the 5 basic tastes(2) on your tongue, along with your sense of smell, and the sensation of the food's texture in your mouth (is it moist, dry, viscus, etc). This helps explain why simply combining two tasty flavors (coffee+tea) does not necessarily yield something twice as tasty, and also why foods which might not be tasty on their own, can be tasty in the right combination (e.g. potatoes+onions+salt+oil+heat makes tasty hashbrowns, but none of those foods are especially tasty on their own).
Taste preference (tastyness) also involves a certain amount of neurological learning, which is partially why often people don't like the taste of something like coffee when they are young, but learn to enjoy it as they find it elicits a response from the reward centers of the brain.
In summary, "tastyness" is most likely an emergent and synergistic property of a system of complex sensory and neurological interactions, and not simply an additive.

Long answer from a non-biologist.
I was dreaming about explaining coffee flavors as an n-dimensional space spanned by the discrete detectable flavors/aromas present in a cup. In this model, a single flavor state is comprised of one distinct association (e.g. "blueberries") and amplitude (e.g. "a lot" or "not at all"), which mechanistically must comprise a certain molecule and chemical state.
In this model, a fictional ground truth exists for a given cup, which would correspond with a delta distribution on the 1D projection of a single flavor. The perceived flavor is convolved with various aberrations: grind size distribution causing over/under extraction (sample-specific, an alteration of underlying chemical states); a smoker whose sensory apparatus are perturbed (detector-specific).
Getting to the point, from a chemical sensing perspective, it seems that you could treat flavor as additive if the discrete molecules comprising it are non-interacting. That's at least two fold: (1) no molecular interactions, e.g. chelation of a salt; and (2) no sensory interactions of chemical constituents underpinning a flavor.
At least one common case in cooking comes immediately to mind: a pinch of salt heightens the perceived sweetness of a recipe, which would invalidate clause 2 above.
Summing up, it seems the answer is non-trivial. Perhaps the underlying molecular/chemical states are additive, but our human sensory apparatus is severely non-linear in its detection scheme.

The last sentence is the correct interpretation. Nerve density is different for different receptors and senses over different parts of our body. I'm not a neruro guy, but I would hazard a guess that we have more receptors for salt and sugar than we do for say bitter as we need salt, but can survive some bitter or short term exposure to a lot of bitter toxins.

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Does adenylate cyclase stimulate or inhibit acid secretion in the stomach?
I am confused about my teacher's notes.
"Acid secretion is stimulated by ACh, gastrin and histamine.
Histamine stimulates adenylate cyclase which increases cAMP production."
When I looked this up apparently gastrin decreases AC (adenylate cyclase) production. If histamine and gastrin both stimulate acid secretion why does one increase and the other decrease AC?
Also in her notes the acid secretion inhibitors are acid, protein, fat as they cause the secretion of CCK and secretin and these stimulate AC. But I thought AC stimulated acid secretion not inhibited it?
Thank you.

Can you share your reference for your reading about gastrin decreasing adenylate cyclase? In parietal cells, gastrin acts through a separate second messenger system, $IP_3$ and $Ca^{++}$, where histamine acts through cAMP.

That makes more sense. Does the CCK only use AC to stimulate acid secretion then? I think CCKb receptor is used to stimulate acid secretion and inhibit it by the CCKa receptor? It says this in my teachers notes: "CCK and secretin both act to stimulate adenylate cyclase (pro-secretory): hence, actions on acid secretion are indirect." but why are CCK and secretin in the inhibitory section of gastric secretion.

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What if the luminosity of Sunlight increased by 10%
If the luminosity of sunlight increased by 10%, would people be able to survive outside? Would such brightness of light be very harmful to them, for exemple as much as the Mercury Vapour Lamp deprived of its protection from UV light? I omit the temperature issue, I mean radiation itself, because I'm curious whether man (or bacteria) could survive if he went outside completely naked?

We don't typically like these sorts of speculative questions here, you might be better off at Worldbuilding.SE. That said, there's quite a bit of additional critical thinking you could do here, such as thinking about how the intensity of sunlight changes seasonally and with latitude. Also omitting the "temperature issue" is a pretty big step, but I think I understand that you mean to just talk about UV. Maybe ask on worldbuilding about a planet that got more UV radiation from its star.

I'm voting to close this question as off-topic because it isn't really on topic for Biology; I'd suggest another stack like Worldbuilding.

People from PhysicStackExchange said it would be better to ask this question here. This is the proof that the users in here complain only about the questions etc. No more questions here, promise! Bye bye.

Well it didn't belong on Physics either - they aren't responsible for determining what is on topic at Biology, they were just trying to help you out.

If not Worldbuilding, then Earth Science.  But since Earth orbits close to the inner edge of the "Goldilocks Zone", I would guess that a 10% increase in solar radiation might be enough to kick the planet into a Venus-like runaway greenhouse.  If that doesn't happen, then sure, humans could survive outside on most of the planet, just as they do in tropical areas today.

From the total luminocity at ground level ~$1000\space W/m^2$ only $3-5\%$ consititute of UV-rays, so UV part is $30-50 W/m^2$. Hence increase of luminocity for $10\%$ means that UV part will increase to $3 - 5\space W/m^2$ so it is quite miniscule increase if we are talking about going naked outdoors. E.g.  tanning beds however have different spectra have stronger UV components than current Sun radiation.


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Does amount of sperm affect fitness of baby?
If there's a 3 day ovulation period in which to have intercourse, would it be better (to create a more fit/healthy baby) to have sex once and ejaculate more sperm than have sex three times with reduced sperm count?
You would think that the more sperm ejaculated at once would result in much more competition to reach the egg, leading to a more fit spermatozoa, and presumably a more fit baby.
If the egg is fertilized during a lower level ejaculation, a less fit spermatozoa can fertilize the egg since there's less competition. Meaning a less fit baby?
Keep in mind I'm NOT asking about the chance of getting pregnant, I'm talking about the fitness/health of the baby. Obviously having sex once instead of three times decreases the chance of getting pregnant.

Expecting competition between spermatozoa to make the child "more competitive" (or "fit") is like expecting that somebody winning a singing competition could be advantaged for winning a Nobel Prize.
The child doesn't use the genetic information which regulates the shape of the spermatozoon or the motion of its tail, hence maybe some future Nobel Laureates could be awful at swimming as spermatozoa.

Sperm actually survives for ~5 days so it really should not matter much.

@The_Vinz This is only partially correct since overall sperm fitness does inversely correlate with complications during early embryonic development, which in turn correlates with later life outcome in a variety of ways.

You are arguing that Usain Bolt is not as good a runner than a child who is the fastest among a mob of her classmates?

I can see where you're coming from, and keep in mind I am no expert in the area, but have you considered that there may be many, perhaps important factors at play than if the sperm had many competition or few? Take the parents genetic and epigenetic profile for instance, meaning not only what the mother and father could each pass on, but whether or not what they pass on will be active or not. And to use your own example, the fittest sperm, who outperformed the larger group; say it required more energy and thus produced more ROS, with which to damage to it's DNA, than the winner in the smaller group - which would be weaker and which stronger? Say the health of the sperm which fertilises the egg could not be influenced by you in any practical way, which method would you choose then?


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What kind of species is this?
Does anyone know what this is? It is seen in France. It looks like it has eight legs and is about 8-10 cm long.

It is a longhorn beetle, family Cerambycidae. Two of the "eight legs" are antennae. It looks a lot like the one pictured here: https://hiveminer.com/Tags/cerambycidae%2Cfrance


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Are there any pairs of animal species that regularly prey on other?
I don't mean cannibalism within a single species - I mean, are they are any pairs of species A and B such that members of species A regularly prey on members of species B, and also members of species B regularly prey on members of species A? I'm considering adults preying on other adults of the other species, not on individuals early in their life cycle.

Caiman and Anacondas - though each hunts the other at a stage of development when the hunter is larger.1 2
Occasionally this occurs with Orcas and Sharks.3
Some species of shark3
Spiders and mantids4
Alligators and catfish (catfish prey on infant alligators)
Many species of predatory fish
Some species of constrictor and venomous snake.
Some frogs and Epomis circumscriptus / Epomis dejeani5
Some amphipods6
In Antiquity, hominids and lions7 8
Big cats preying on eachother, among other large predators:

Carnivores eat a variety of vertebrates: e.g. desert coyotes eat … carnivores (roadrunners, reptiles, and mammals)… Carnivorous mammals often overlap substantially in diet (30). Many “readily prey on other carnivores” (125), e.g. tigers prey on bears (black, brown, and sloth bears), dogs, wolves, lynx, and badgers (125): leopards prey on lions, cheetahs, wild dogs, and spotted hyenas (also raptors, crocodiles, and pythons; …
Leopards are mutual predators with lions, spotted hyenas, tigers, large raptorial birds, crocodiles, and pythons…

The Ecology and Evolution of Intraguild Predation: Potential Competitors That Eat Each Other

A python will eat an alligator:

Source:  http://www.miamibeach411.com/news/python-snakes
and an alligator will eat a python:

Source:  https://www.palmbeachpost.com/news/gator-chows-down-python-florida-golf-course/9HUGKYz7j3qF1BGJwc2RUL/


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What is the distribution of gene polymorphism levels across human genes?
Of the approximately 19,000 human genes, about how many have one allele that occurs with appreciable frequency in the current human population, how many have two alleles, and so on? (By "appreciable frequency", I mean, say, is found in at least 1% of the population, which seems to be the rule of thumb for classifying a gene as polymorphic in the population.)
I'm not looking for an exact breakdown for every single number of allele variants - I'm just curious, does the typical human gene have only one (frequently found) allele? Or two, as is often implied in elementary genetics texts? Or five, or 10, or 100? What does the approximate distribution look like?
According to the Wikipedia article linked above, the most polymorphic genes known are those coding for the Major Histocompatibility Complex (MHC), with the HLA-B HLA-DRB1 loci having 200 significant alleles, so I guess 200 is the upper end of the spectrum. (Although I don't know whether "the HLA-B HLA-DRB1 loci" refers to a single gene or several, so maybe 200 alleles is higher than any single gene has.)

Also, when Wikipedia says that the MHC genes are "the most polymorphic genes known", do they mean the most polymorphic human genes, or the most polymotphic genes across all species? I would assume that e.g. bacteria display a much higher level of gene polymorphism than humans, because they have a much higher rate of mutations per base pair.

Ah, I might have misunderstood what you are after. Are you interested in 1) the distribution of the number of alleles per locus or in 2) the distribution of frequencies per allele. The second one is the SFS. You can totally consider a SFS for loci that have more than one allele. Although, most often SFS are drawn from SNP data, as such there is rarely more than two alleles at a given SNP.

@Remi.b I'm after distribution (1).

Ok, I've removed most of my comments, then!


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Are mosquitoes actually louder than similar flying insects, or have we evolved to hear them?
I've come across many flying insects smaller than the common housefly, but (anecdotally) the only such species that I can hear from an appreciable distance away is the mosquito, with its distinctive buzzing whine. It may just be luck that the loudest small flying insect (in my everyday experience), and therefore the easiest to detect and avoid, is also by far the most annoying. On the other hand, mosquitoes are the single deadliest animal for humans and were probably common on the African savannah in which we evolved, so maybe this apparent loudness is actually an auditory illusion, and similar-sized insects are equally loud but at frequences that we haven't evolved to hear or focus on. Are mosquitoes objectively louder than similar-sized flying insects, or might we have evolved to be particularly sensitive to their emitted frequencies?
(This question is the flip side of this one, which focuses on the mosquito's evolution rather than the human's.)


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Can you convert smells to variables?
Is there a way to map smells to numerical values of different variables?
I.e. With RGB colours, each colour is made up of numerical values from 0-255. For example, red is (255,0,0), and yellow is (255,255,0). Is there a way to do this with smells. I.e, the smell of Candy is (140,70,255), and the smell of grass is (255,34,27)? How many different sets of numbers (like red, green and blue) would you need, and what would they represent?

Given that the human genome has genes for about 700-800 different smell receptors (very ballpark from the top of my head), you'd probably need around that many numbers to encode smells into numbers


text:
Why don't macaws get selenium poisoning from brazil nuts
Google research has indicated macaws love or eat a lot of Brazil nut. These are highly toxic to humans in somewhat small quantities due to their selenium content.
Given the mass difference between a human and macaw, lets say 80kg and 2kg, if toxicity for humans 'starts' around 900micrograms or ~9 nuts, maths would indicate toxicity for a macaw might be around 20% of a nut?
These figures are all based on google and the margin of error I expect is quite large, nonetheless it seems quite disparate if a macaw could consume even a single nut a day on average, without consequence?

I know that macaws congregate around mud banks and eat mud (maybe clay?) I wonder if this might have something to do with it.

@KarlKjer Not according to this, though I don’t know how trustworthy it is.

this is good article but about amazona parrrots. The clay is really good call. But it detoxicate only quinidine by 60%.

Interesting question. You should consider, though, that the excretory system in birds is quite different from mammals. For example, they have two different types of nephrons. You've assumed the toxic dose is proportional to mass. It's not. You have to account for differences in kidney function, even in humans.

One explaination is that macaws (Ara sp.) eat clay and other food item which absorb the toxins. Here is the full answer from Wikipedia:

Like all macaws and most parrots seeds and fruit are the major part of the diet of the genus Ara. The particular species and range of diet varies from species to species. Unlike many birds macaws are seed predators not seed dispersers, and use their immensely strong beaks to open even the hardest shells. Their diet overlaps with that of some monkey species; in one study of green-winged macaws in Venezuela they shared many of the same trees as bearded sakis, although in some cases they ate the seeds at an earlier stage of ripeness than the sakis, when they contained more poison. Macaws, like other parrots, may consume clay to absorb toxic compounds produced by some poison...but with further research we now at last know it is just to eat life saving sodium that is missing. As well, the toxic compounds of some foods may be neutralized by compounds, such as tannins, found in other foods consumed at the same time...but we have found that it is untrue and really just to gain access to sodium missing otherwise in their diet because of the area they live in.

Source: Wikipedia - Ara (genus)

Your premise Is bad. Selen Is not ONLY toxin And  your answer actually doesnt answer thé question. However with that clay Is actually quite good call but i didnt find any information on selen but other chemicals such as quinidine.


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How do I efficiently grow bioluminescent algae?
I have 6 vials of Pyrocystis lunula that I would like to grow. What would be a more suitable container, a tank or a clear jar? Also, I would like to know what kind of nutrient solution to use. Is it possible to get them to reproduce at a rate that eventually there can be a whole tank full of them?

What sort of research have you done to try and answer your own question?

I have no experience with that particular species but dinoflagellates are often slow growing, very tricky to get to high densities and hard to maintain for a long time without proper experience and lab conditions.
If you still want to have a go I would recommend the following. Growth conditions are rather similar for most dinoflagellates: use a rotary shaker (gentle rotation) in a 12:12 day night regime, don't dilute to hard when subculturing and use standard F2 medium (see link for recipe). If you cannot get hold of seawater you can use saltwater aquarium salts such as Instant Ocean.
Most hate temperature changes so best to keep them at 18-21C

So I can just go to the beach and get some sea water from their?

You will have to sterilise it first (autoclave) and add nutrients such as iron, nitrate and phosphate. See the F2 recipe on the link provided

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What is the source of the fat in adipose tissue?
I have heard the opinion that all of it comes from de novo lipogenesis of carbohydrates, but I'm skeptical. Is there evidence either way - either that dietary fat definitely gets stored in the adipose tissue, or that it never does, and all of it is from carbohydrate transmutation?

The proximal source of adipocyte lipids is mainly fatty acids from circulating lipoproteins (1) after hydrolysis by lipoprotein lipase (LPL).
LPL is activated by ApoC-II, which is present in hepatic-originating VLDL and IDL lipoprotein, but also chylomicron of direct dietary source. Insulin, secreted after meals, stimulates LPL production by adipocytes.
Thus the ultimate source of these lipids is both hepatic lipogenesis (from other substrates like glucids) and dietary fats.
Lipid transport in blood, for reference purpose (Michal G. Schomburg D., Biochemical Pathways, 2012)


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Apolipoprotein B48 and fat storage
Can chylomicrons formed in the intestine, with apolipoprotein B48, transport lipids to adipose cells for storage?

Fatty acids originating from  chylomicron  triacylglycerol  are delivered mainly  to  adipose  tissue,  heart, and muscle (80%), while ~20% goes to  the liver. - source: Harper's illustrated biochemistry.

Lipoprotein lipase which is present in wall of blood capillaries anchored to endothelium by negatively charged proteoglycan chains of heparin sulfate requires phospholipids and apoC2 for its activity to take place.
Hydrolysis takes place while the lipoproteins are attached to  the enzyme on  the endothelium. Triacylglycerol  is hydrolyzed progressively through a diacylglycerol  to  a monoacylglycerol  and finally to  FFA plus glycerol with the help of lipoprotein lipase.  Some of the released free fatty acid return to general circulation bound to albumin but the bulk is transferred to peripheral tissues like adipose tissue, muscles of heart etc.
Fate of chylomicron
The lipase activity results in loss of 70%-90% of triacylglycerols and apoC2.(source: Harper's illustrated biochemistry) The remnant chylomicron is then taken up by liver by receptor mediated endocytosis. Here cholesteryl esters (present in concentrated form after loss of most of triacylglycerol) and remaining triacylglycerols are hydrolysed and metabolised.

Do you know what proportion of the fats in chilomicrons of dietary-origin get transported to what kind of tissue? I mean the parts that don't go to the liver - "adipose tissue, heart, and muscle (80%)". How much of that goes to adipocytes?

@Abu Dhabi It depends on surface area of distribution (by blood vessels ), need for utilisation of fatty acid and many other factors.

Do the "20% to the liver" refer to  "... after loss of most of triacylglycerol) and remaining triacylglycerols are hydrolysed and metabolised"?  In other words: 20% of triglycerides in chylomicrones go to the liver? Any other easy reference on that?


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Delta G and Temperature
I'm now designing primers for PCR. I use Oligo analyzer to check the primer secondary structures.
Ex: Delta G:  -4.16 kcal/mole  Base Pairs: 4
5'        GCCGTCTAGCAGCACATAATG
            :  ||||  :
3' GTAATACACGACGATCTGCCG

So my question is with delta G = -4.16, how do I know how much temperature degree can break these bonds?


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During what phase is the cell polyploid?
During what phase is the cell polyploid? Why is it polyploid at this point--what has happened to create this state and why is it important to the process?

I assume that you mean phase of cell division. First off all i will write down a definition of word polyploid. Polyploid is cell which has two or more pairs of homologus chromozoms. There are two basic types of cell division are meiosis and mitosis

Technicly you can say that in reduction meiosis when chromozomes go from diploity to haploid state (which is first anaphase in this process), but ussually polyplidy occure when something goes wrong in cell division.

The major cause of polyploidy is found to the non disjunction of sister chromatids during the meiotic recombination events. Prior to meiosis chromosome numver doubles followed by chromosome separation during gamete formation (anaphase).
Artificial generation of polyploidy have been found to be useful both in research as well as economic purposes. Colchicine, the chemical which inhibits formation of spidle apparatus is widely used.

Unfortunately colchicine is only used in mitosis. Result of this process is new cultivars of plant specious.


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Why are the cells the smallest unit of life?
Please Tell me why the cells are called the smallest unit of life. According to me I know that they are called so because they are smallest entity which is alive that is they show the properties of life on their own but if we divide them then the life will be destroyed. If that's the case so why they need to stay in a body why they can't be alone. I want to ask that if we separate a human cell from its body then can the cell be alive. If there is any better explanation that can explain why are the cells called the smallest unit of life please tell

Lots of cells exist that don't need to be in a body.  Bacteria, protozoa, single-celled algae, and many others.


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Delay of sleeping on cortisol cycle
I was told that cortisol has to be measured at 9am or 4pm, because those where its peak level. But I wonder if changes on sleep patters affect the cortisol cycle.
I mean, if I usually go to sleep around 11pm, but certain day I go to sleep at 4am.
My cortisol cycle would vary according to my change in sleeping?
Probably the same question can be done using other hormones as example.


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What function will survive evolution?
I wrote the following phrase in my scientific text:
X is ubiquitous in life of Y. On some occasions X might be detrimental, resulting, for example, in so so phenomena. But is it plausible that a function that takes 50% of organism resources would have only negative effects? The answer is likely "no" because such a function would have likely not survived the evolution.
But I was suggested that there a bug in my logic because if an adaptation is neutral and has no effect on reproductive fitness, it can be preserved. Would you agree with this critique? If so, how should I rephrase so that it become more correct?
Many thanks

is it plausible that a function that takes 50% of organism resources would have only negative effects? It sounds highly unlikely that an organism would invest half of its ressources into doing something that will reduce its own fitness (I should say "inclusive fitness" to be safer here). A mutation that would lead to such trait would be highly deleterious and should not raise in too high frequency in the population (unless eventually if the population size is really really small). That being said a recent and sudden environmental change could eventually lead to this type of 'maladaptation'.

On some occasions X might be detrimental, resulting, for example, in so so phenomena. Many traits can have environment dependent fitness effects and environmental heterogeneity can lead to strong variation in the trait's contribution to the individual fitness. Is this what you are referring to?

"would have only neutral and negative effects" would partly cover the critique, as it appears to me the argument hinges on the "50% of organism resources" which must have been previously firmly established.  It would be helpful to add language emphasizing that such an enormous drain on an organism cannot plausibly survive long in a species since that drain, itself, is a huge negative effect on individual fitness and hence on reproductive fitness.

Can you please let know whether my comment seem to answer your question. I am unsure I really understand your question and your feedback would help.

detrimental to what? Many adaptations are detrimental to an organisms but beneficial to their genes. Just look at social insects, or even your own somatic cells.

Detrimental for behavior. For example, sleep at night wastes our time. So, it should have some benefits.

Ia m sorry for the late reply (time zones differences). Thank you very much for the answers. So, the bottom line: do you think my phrase sounds?

@student a behavior cannot be detrimental to behavior, biologically speaking that makes no sense, it has to be detrimental to the organism, cells, or genes.


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History of plasmid maps
To create a small history of visual representations in biology, I am seeking the earliest published papers or books that have used plasmid maps as figures ; or strategies to effectively search for these publications.
I have examples like this one (from the 1977 publication presenting pBR322), but as it seems quite modern looking, it may be that earlier examples exist.

I spent an hour trying to follow this one up, without much sucess. My feeling is that, although there must be earlier figures, you are unlikely to find anything for plasmids before 1970, because the advent of restriction enzymes was an important tool in mapping them, because the idea of plasmids emerged only slowly, and because the plasmids from which pBR322 was derived were much larger and more complex. Sorry not to be more constructive.

Thanks for your insight. I think I will follow the restriction enzyme lead, maybe show early restriction maps, then skip to "modern" plasmids.

I imagine you have already considered this, but the switch from genetic maps to physical maps might be worth looking at. There were clearly quite detailed (if incomplete) genetic maps of E. coli, and  I remember in the early 70s that there were genetic maps of E.coli ribosomal RNA genes, that were partly physical, because the sizes of the precursors and mature species could be estimated by sucrose density gradient. The problem with the wild plasmids is that although you could say they contained, e.g. a drug-resistance gene, you couldn't easily map its position with respect to anything else.


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How to distinguish the Ct of the target gene from the Ct of the housekeeping gene? (very basic qPCR question)
I will do a qPCR experiment for the first time, and I have a bottom-level question to ask. I know that for normalizing the quantity of your target gene you have to add an endogenous control, like a housekeeping gene, in your qPCR sample, and then you subtract the Ct of the housekeeping gene from the Ct of your target gene. However, since the same SYBR green fluorophore is used to quantify both the target gene and the housekeeping gene in the same sample, how do you know which Ct is from the target gene and which one is from the housekeeping gene?

You do not take readings from the same reaction, you split the sample. You would run each primer pair in their own reaction. You also want to run each reaction in triplicate so you can get some idea of the error.
So, a general plate set up might look something like this:
A1: Control sample, housekeeping primers; A2: Control sample, target gene primers
B1: Control sample, housekeeping primers; B2: Control sample, target gene primers
C1: Control sample, housekeeping primers; C2: Control sample, target gene primers

D1: Treatment sample, housekeeping primers; D2: Treatment sample, target gene primers
E1: Treatment sample, housekeeping primers; E2: Treatment sample, target gene primers
F1: Treatment sample, housekeeping primers; F2: Treatment sample, target gene primers

So in this scenario, the delta-delta Ct value comes from the following:
delta-delta Ct = ( Ct(treatment, target) - Ct(treatment, housekeeping) ) - ( (Ct(ctrl, target) - Ct(ctrl, housekeeping) )

If the PCR machine does not offer to do the delta-delta Ct analysis for you I recommend this blog which both explains it well and provides and excel spreadsheet so you can just drop you Ct values in.
HTH.

That makes more sense, I got that information wrong. Thanks for the clarification.

No problem. As much as possible, make master mixes and decant them in down in to the single reactions to keep things as homogeneous as possible. Good luck.


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does being battered build muscle?
My crude understanding of how people normally go about building muscle is something like this following 2 step process:
1) a person can lift weights (for example), which tears muscle and stimulates the nervous system.
2) They can then eat protein and get sleep, which build the muscle back up stronger than it was before, as the nervous system tells the body that more muscle is needed to handle the type of stimulation its been getting.
Now to my question: exotic training techniques like EMS exist which do the same in principle as lifting weights.  What about something as simple as the muscles taking a beating (as in kickboxing)?  If a muscle is battered in a systematic way, will it be built up stronger as per the muscle building process?  If so, what type of muscle would this be (Fast twitch/slow)?  Would it transfer well to overall strength?


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Interesting examples of models
I am studying the general use of models in biology in terms of methodology, applications, usefulness etc, and I would really appreciate any recommendations of some specific examples of models from any area in biology. Some examples are the logistic growth model or the Lotka-Volterra prey predator model.
It would be nice if you could shortly explain what the model is used for and why do you think it's an interesting case, and give a reference for further study.
Also any recommendation of books on model development and other meta-model questions in biology is very welcome. Thank you.

Biology is a large field of knowledge! As you give examples drawn from population biology (logistic population growth and Lotka-Voltera models), I will assume you are mainly interested in ecology and evolution.
For analytical models used in ecology and evolution, I highly recommend the book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto and Day. The book assumes a relatively low level of knowledge in mathematics from the reader and walk the reader through most of the most iconic models in ecology and evolution, their analysis and interpretation. The mathematical tools used in this book include linear algebra, equilibrium analysis, analysis of cyclic behaviour, Markov chain and esp. birth-death processes, diffusion equations, probability theory and stochastic models, approximation theory, class structure models (Leslie matrix and more) and, separation of time scales among others.
For books, mainly theoretical, in population genetics, please have a look at the post Books on population or evolutionary genetics?.
As you talk about the Lotka-Voltera model, you will find an intro to this model in the post What prevents predator overpopulation?.

One nice model to use as a example the Hodgking-Huxley model that describe the current through a nerve fiber given a certain membrane voltage. This model describes the sodium and potassium currents that are the basis of the action potential.
Some characteristics of this model are:
This model explains the membrane currents through the activation of "charged particles" in the membrane that allow the passage of ions (K+ and Na+). It was latter discovered that in the membrane there are Na+ and K+ channels that carry these currents (in the original model there was no evidence of the molecular components of theses channels).
The model can reproduce the action potential of neurons.
The model predicts the existence of "charged particles" in the membrane that must move before the channel open, named gating charges. Since this particle move from one side of the membrane to the other, they generate a small transient current ("gating currents"). These where actually measured 20 years after the proposition of this model.
This is a great model because it described mathematically and physically the behavior of neurons and also predicted several properties that where later fond.
You can read more here:
HH model


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What is the difference between pseudorumination and coprophily?
Can someone please explain me difference between these two terms. any help is appreciated.

Ruminants (e.g. cows) is a classification of animals based on its digestive tract, so these are the animals having four-chambered stomacks. Pseudoruminant (e.g. hippopotamus) have three-chambered stomacks in comparison with ruminants. Coprophilous usually applied for different types of fungi that grow on animal dung.


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Low-tech or low-cost technique for quantitative estimation in enzymology
If an accurate measurement of enzymologic quantities is needed, then following established methods in the field is necessary.
However, it is sometime of great usefulness to ballpark a value before committing to taking the necessary time for protein purification, or buying the necessary equipment/reagents.
For such purpose a little "hack" can go a long way. This often involve using an available equipment
to substitute for another (e.g. maybe I have a FACS readily availably, however no HPLC).
I am seeking examples of "unconventional" use of lab technique that
can be used to determine enzymologic quantities ($K_d$, $V_{max}$, $K_i$ ...) as a first estimate -- whether you have partaked in such heresies, or have merely seen them used, possibly even in a non-formal/DIY environment.

With bacteria, we often use selective or differential media to determine presence or absence of certain enzymatic reactions. Would that sort of think be useful? Probably wouldn't be able to estimate an enzyme kinetics that way though.

If there is a way to:

Make the replication of a common culture organism (e.g. E. coli) dependent
upon the inhibitor or substrate of interest, possibly with a restrictive media.
Express the enzyme of interest in a relatively controlled manner in such organism (e.g. well caracterized promoter in plasmid with well characterized copy number),

Then you can get good mileage out of some serial dilutions and a OD600 meter. Even better with a plate reader.
Exact protocol will depend on the quantity under consideration, but mostly will amount to substituting around in the enzyme kinetics equations until the quantity of interest is a function of the concentration, and devise a scheme to cancel out the other unknown quantities (often substrate concentration ramp + starting OD ramp + curve fitting)


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From DNA to final traits of microorganisms?
From the answer of this topic, could someone indicate me a book or article about how DNA set the phenotype of microorganisms? For example, showing how DNA changes the shape of such a cell or how DNA sets the concentration of a such mineral inside the cytoplasm.

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


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How two genomes adopt when cell goes to recipient's body from donor's body?
We often give blood to another following the blood giving compatibility chart. Heart transplant and similar transplants also brings one's cell to another's body.
My curiosity is, when a cell goes to the recipient's body from the donor's body, what actually happens with respect to the genome?
If the genomes do not merge to one, then how to identify one identically? How does DNA fingerprints, parent detection etc. work correctly? More generally, how does it maintain consistency?
Remarks:
My assumption was : "All the cells of one particular person's body carry the same genome or DNA information. And every individual has a distinct genome or DNA information". But after some study and some comments, I found that the statement is actually wrong.
However,  this article led me to break my wrong notion.

The genomes don't merge. Red blood cells (the vast majority of cells in blood) do not contain a nucleus, and therefore no DNA. White blood cells do contain DNA, but they remain as independent cells and don't "merge" with anything. The same situation applies with the microbes in your gut - they are separate organisms, and don't "merge" with the epithelial cells in our intestines to form some sort of bacteria-human hybrid.

@MattDMo Interesting. That means when one gets blood from another's body, then his blood cells contain two types of information. And if I get blood from several persons, then I would have several types of information in my blood cells. Does not it create any problem when it sees genome in body cells are not identical with genome in blood cells?

I've tried to determine what you are concerned about, place it in a more appropriate context, and answer a reformulated question. Could you please see if this does, in fact, address your concerns. If so, the whole question (and my answer) could be rephrased.

@David Thanks for your cooperation. I have tried my best to rephrase it. Have a look on it. Thanks once again.

@manetsus Fine. Have modified my answer accordingly.

Have you considered the term "alloantigen" which is not a very common one, to be found in the context of MHC. I nteresting to me that there are two alleles  of each gene in one body, and the antigens they both express seem to be identical. I haven't heard of "iso-antigens" - except for MHC.

My previous answer was to the original question which focused on red blood cells which do not contain DNA. Now the question has been revised to focus on tissue transplantation, where the cells do contain foreign DNA, my amended answer deals with a couple of the points raised, but only briefly with the question of identification.
Incorporation of foreign DNA into the human genome
It is extremely unlikely that any of the DNA from the tissue of the donor would be incorporated into the DNA of the cells of the recipient. The donor cells would have to be broken (i.e. die) to release the DNA, which is most likely to be degraded in the process. Even if it survived it would then have to be taken up by the host cells, which is unlikely as there is no specific mechanism to allow this. However if foreign DNA somehow got to the nucleus it would need specific machinery to be incorporated into the host DNA. This involves enzymes making staggered cuts in the foreign and host DNA to allow annealing and enzymes to ligate the two together. We know about this sort of thing because retroviruses and viruses that can exist in the genome in a latent state have specific mechanisms for doing this. It is unlikely to happen just by chance.
Even if foreign DNA did get incorporated, it still has to be in an environment that allows it to be expressed (appropriate promoters). A more likely possibility is insertion in a position that affects a host gene. This can result in uncontrolled division of cells, i.e. they become cancerous, and is a problem that has been encountered using viruses of the type mentioned to insert genes into genomes in gene therapy.
Do the differences in the DNA of transplanted tissue matter?
Obviously differences in the DNA of different individuals has an effect on the individual. It is genetic differences that cause people to differ in size, shape, features, hair colour etc. Oh, and some are girls and some are boys. But when the tissues and organs have finished developing it probably doesn't matter if a piece of transplanted liver is from a male or female donor. The genetic programme that causes sexual differentiation and function isn't the one being expressed in the adult liver. The genes that are being expressed are those for the enzymes the liver needs to play its metabolic role (too numerous to list), and if they work, they work, even if the proteins differ in amino acid sequence by the odd amino acid that doesn’t impair its function.
The problem of identification by DNA
I would have thought that this would not really be a problem. After all, if you want to take a DNA sample from a person you can do it with hair roots, white blood cells or scrapings from mouth skin. You wouldn't need to resort to liver biopsies and the like.
Doctor of Philosophy
Finally, I can see there is a general philosophical concern over who one is if one has tissue or organs from another donor, but until we have brain transplantation I’m not going to worry about that. (And when that comes, I won’t be answering questions on the subject.)


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how to find full mitochondrial genome of plants in GenBank?
I am searching for full mitochondrial genome of a species of Malvaceae family.
To be more specific, I need the genus Corchorus. But I could not find the location where it is in gene bank. After searching in google, I found this, but here I did not found anything for plant.
Can you help me to locate its actual location?
Scientific classification from Wikipedia:
Kingdom:    Plantae
(unranked): Angiosperms
(unranked): Eudicots
(unranked): Rosids
Order:  Malvales
Family: Malvaceae
Subfamily:  Grewioideae
Genus:  Corchorus
L.

Related post: http://biology.stackexchange.com/a/16168/3340

I think, manetsus wants sequence , not definitions. Plus link given in that post is for Human Mitochondria database not plant. The species he/she looking for is not available on NCBI (at least I couldn't find it).

When you search a genome for Corchorus on Genbank you will only find genomes of a virus related to it. There is not a lot of plant genomes available and for the ones you can find it is quite often the case that there is only the chloroplast assembled.
So unfortunately the most plausible answer to your question is: It is not yet available for this plant. There are only very few hits for Malvales at all, and none of them seems to have the mitochondrium assembled.
There might be chances that there is a specific project/database for Malvales or mitochondria, where you could search, but I am not aware of one.

Is this one? http://www.ncbi.nlm.nih.gov/genome/38606?genome_assembly_id=233326
What I did was Google: "search mitochondria genome BLAST"
and clicked the first page for me "Organelle Genome Resources". I then selected
"Browse by Organism" on the lefthand side, which took me to a new page.
I then entered in the top left text box the phrase "Malvaceae" and up came a scroll down list from the text box of choices for the text field.
I chose the first "Malvaceae (taxid:3629)" and upon clicking that, 26 entries came up for organelles. Two of which were from Mitochondria under the "Type" column.
The other entry being: http://www.ncbi.nlm.nih.gov/genome/10704?genome_assembly_id=233221
Sorry if I  was totally off base, I am just a undergrad.

No. This is wrong species.

To be more specific, I need the genus Corchorus, you can see the scientific classification there.


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Does increasing the value of k in k-fold coverage requires more memory?
Study:
Here is what is k-fold coverage which is know as sequence coverage.
According to this, 2-fold coverage means the whole DNA is sequenced more twice in average.
Question:
If I have a genome sequence of length x with 30-fold coverage, then which of the following is correct?

I have to occupy 30x memory for the genome sequence, it means I would be given the genome sequence of length 30x.
It means I would be given the genome sequence of length x, but the sequence is more purified according to the calculation.

By memory you mean RAM or disk storage?

@EliKorvigo Mainly disk storage, you information about RAM is appreciated.

I guess it might increase RAM consumption, but that would not be a 30-fold increase, though that would depend on the genome assembler you use.

In Next Generation Sequencing (or better called 2nd generation sequencing) you are sequencing many many small genome fragments cut from many DNA molecules. Multiplying molecules, cutting them into fragments and amplifying them is known as library preparation (library of fragments to be read). During that process (of which PCR is important procedure) different errors or biases could be introduced.
What you get from a sequencer is many many short reads in form of FASTQ files that you need to assemble into genome sequence (by de novo assembly or more commonly by alignment to reference genome). It is important to know how sure are we for each nucleotide in assembled genome, which depends on how many times (and with what quality score) sequencer read each nucleotide (see image below).

(source: davidson.edu)
Coverage could mean average coverage across whole genome or coverage of some smaller portion of it (different coverage across genome is usually because of mentioned biases introduced in library prep).
To answer question: In final representation you get one whole genome assembled, if all you need is final representation (so answer 2). If you also store reads, then more coverage means more memory, but final genome is of same length.
NOTE: Coverage is even more ambiguous term that I just described, so you should look at this thread for possible different meanings (for example: which portion of whole genome is covered by sequencing).


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How can one create images like those in the PDB ‘Molecule of the month’?
I am impressed by the illustrations for the Protein Data Bank ‘Molecule of the month’, e.g. the gorgeous image of DNA Helicase below. Does anyone know how they were made or how one might create something similar?

(source: rcsb.org)

While I don't know what is used, David Goodsell should know it, as he is responsible for this, as far as I can see. Write him a friendly email, my best guess is that he will tell you. And please tell us (you can answer your own questions), I am curious, too.

Me also don't find it cool or impressive, However, Chimera has a visualization preset that makes this image style, just a click of buttons. In the presets menue click on publication 1 and BOOOM here you go the image will look similar like this

Those (really cool) pictures are created by David Goodsell using custom-written software.
From an interview to the artist:

PDB: How do you create the illustrations?
Goodsell: Most of the pictures are created with a computer program that I developed back when I was doing postdoctoral work with Dr. Art Olson here at The Scripps Research Institute. I've been using this style of illustration--with flat colors and black outlines--for about 10 years now. I like the way that this style simplifies the molecule, giving a feeling for the overall shape and form of the molecule, but at the same time you can still see all the individual atoms. On the last page of each Molecule of the Month--"Exploring the Structure"--I always use RasMol, to give visitors an idea of the kinds of pictures that they can create themselves with off-the-shelf software.

There are good tools around if you want to replicate that look. Although it may take a bit of tweaking (and possibly programming) I would surely give PyMOL and Bioblender a try.

I found QuteMol got me closest to Goodsell's look :)

@nornagon: nice, I did not know about QueteMol!

"I always use RasMol, to give visitors an idea of the kinds of pictures that they can create". Oh no they can't! Rasmol does not run on Mac OS X. But you can use Jmol instead, which has a command for saving high res png files that you can actually drag back into the application and modify further.

@David there are Mac OS X binaries for RasMol, although I have never tried them. http://www.rasmol.org/software/RasMol_2.7.3.MAC/index.html

@nico — Not quite. They are Unix binaries that will run under an X-windowing environment. It requires you to set up Unix directories and move stuff there. I tried it years ago and it was a real pain compared with the Mac OS9 version. Now a user would have to install XQuartz before they started. For practical purposes it's dead. One feature of JSmol is that it supports all RasMol console commands, so if you are used to RasMol...

@nico — Just tested the 32bit version on a Mac running 10.9.5 (itself old), although the version on the site is for 10.3.9. When I tried to run it I got "Bad CPU type in executable". No great surprise. Presumably a PPC version that doesn't run on Intel.

I don’t actually consider these pictures either “gorgeous” or “cool” — they are not to my taste — and I’m not really sure that the question is about biology, but when it resurfaced after almost 5 years I thought I’d give an answer which explained how one might create something similar, rather than how they were actually made.
The original 3D-graphics program used was RasMol, but as that only runs on Windows, hasn’t been updated for years, and has no viable web version, I would suggest using JMol/JSMol instead. This is free, and you can either download the application and work with it as described in my answer to a previous question. Alternatively you can just find a web page with a JSMol window (such as a page used in my own teaching material) and use that with the Console available from the JSMol logo. So what I do is:

Get the PDB file I want to work with from the Protein Data Bank.
Drag the file into the JMol window, which causes the protein to load in wireframe mode, as in (A), below.
Give a series of commands such as the following to get a spacefilling image (B) in colours other than CPK (you can specify the colours of the chains if you wish) and without the shiny light patches, which are fine for standard images, but will cause problems. One useful feature of JMol is that it allows you to generate high resolution images:

    restrict protein
    wireframe off
    select protein
    spacefill on
    colour chains
    set specular off
    write pngj 2000 2000 "my.png"

You can subsequently drag these back into a JMol window and make further adjustments, as long they haven’t been edited. (So do graphic work on a copy.)

Next you need access to decent bitmap graphics application. If you are in a University someone will have a copy of Photoshop (old versions are fine), but otherwise you will have to make do with what you can find — GIMP is a free cross-platform altenative. I am almost certain that the original artist would have developed the style he uses with Photoshop. He says he wrote a program himself to automate it, but he could just have well used a Photoshop script (Action) in my opinion. Anyway, for occasional use, you can just do it interactively.

The first thing is to get the outlines on the spheres and make the colours flat. The former is done with a filter that finds the edges, and the latter by posterizing (reducing the number of colours in the image). I used a filter called ‘Poster Edges’ to produce frame C. There are sliders that allow you to change the intensity of the edges and degree of posterizing.

Finally to reproduce the rather washed out feel of the colours I used the ‘Exposure’ tool (Image > Adjustments > Exposure), but I could have used curves (Image > Adjustments > Curves) or, no doubt, other options.

And there you have the final image shown in D. It doesn't have quite the same posterization as the DNA Helicase illustrated in the question, but if you really wanted that you could probably achieve it after a little experimentation.

Four years on, and when this question came up again I discovered some typos and missing links. I've remedied them now. Please flag me if you find anything else wrong.


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Can humans eat green leaves to get necessary daily energy intake?
Green leaves make carbohydrates by photosynthesis. This means that green leaves are abundant source of energy. Can humans eat enough green leaves off the trees and get necessary daily energy intake?

Welcome to the site! You may know this already, but early-season leaves of many common trees are edible, including hawthorn and beech (apparently also linden, birch and spruce, but I haven't tried those). Later in the season they accumulate tannins and other secondary metabolites that can be toxic. Unfortunately, I can't find much about their calorie content (although I'm sure it's low), so I can't post a full answer, but I'll leave this here for anyone else who's planning to. My gut feeling is it would be very difficult; assuming similar calories to lettuce, you'd need to eat 13-14kg per day.

Do you mean exclusively the leaves of trees?  If not, there are a number of common foods that are leaves: lettuce, spinach, cabbage, green onions...  Offhand I can't think of any tree leaves commonly used as food, but bay leaves are a common seasoning for soups and stews.  And I like to nibble the new green leaves of spruce when out hiking...

Something can be called a food when it is edible, and most tree leaves are not.
Carbohydrates or other nutrients can be a source of energy when they are digestible, but cellulose and (most) other carbs in leaves are not (Elmhurst.edu).
Finally, to get "necessary daily energy," you need to consume, for example, 2,000 Kcal. So, even if you find edible tree leaves with digestible carbs, they will still not likely provide enough calories. Think of lettuce: 360 grams of lettuce = 54 Kcal.


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Control of gene expression
Eukaryotes have many genes, so how does RNA polymerase recognize a gene needed to be transcripted?

Could you please add information regarding what you know about the question and how you tried to seek information about it?

I.ve just read that RNA polymerase can  slip along the DNA molecule until it finds the gene that needs to be expressed, or this enzyme bind to the promoter after the Transcript factors bind.

Are these two ways right and enough? Is there any other mechanism?

Genes typically have promoter regions attached to them that scan for the presence of certain conditions. When a promoter's condition is met, it changes shape, encouraging RNA polymerase to bind and start making an RNA transcript of the DNA piece.
In other cases, genes can have suppressor regions where a certain condition actively blocks the attachment of RNA polymerase.
(updated for improved explanation)
Think of the (protein-coding) genome as a giant library full of books (genes). Each book tells the reader how to build 1 product (protein). In practice, a gene can code for multiple proteins via introns, but we will ignore that for simplicity here. The overall concept remains the same.
Now think of RNA polymerase enzymes as a population of simple-minded workers wandering around the library who instinctively attempt to reach for and open books on shelves that they bump into. If a worker is able to access a book and read it, the book's product will be produced. If a book happens to be excessively difficult to access or open, the worker will give up on it and resume wandering. Some workers may be more persistent than others.
Varying accessibility per book title dictates overall rate of production. The library shelves are specially designed such that books detailing construction of products in demand are "easy" to pick up (bookshelf is open and unobstructed), while products that are clearly out-of-demand are "hard" to pick up and read (book is locked down, tied to a 10-pound weight, and there's a plastic blocking piece over the front). If a book is hard to access, only the most persistent workers will read it and build the product it describes (low or completely blocked transcription). If a book is easy to access, most workers have ready to access it, causing the book's described product to proliferate.


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How does body fat leave your body?
So I know that it’s not from tears or sweat because they are composed of mainly water and sodium, it’s not from going poo or pee as poo and pee are made of the parts of food that supply your body with no nutrients and your body also doesn’t “burn body fat” because there is a theory that no matter is ever destroyed so it’s none of those but another thing is it’s not your hair, ear wax, finger nails or anything of that sort because people can lose over 17 pounds in 3 months but you can’t build up that amount of hair , ear wax or whatever else in three months so how does body fat leave your body

there is a theory that no matter is ever destroyed - what theory is that? Do you have a reference?

@Nathan welcome to Biology SE.  I see that you are new contributor, so i highly recomend you to take a tour in help center. There you can find what we expect from an question. For now your question is full of oppinion based claims, with unclear poin of what you exacly want to know. Please feel free to edit your answer or according to rules of Biology SE it can be close.

Where does wood (or gasoline &c) go when you burn it?

Many of the statements in your question are false, including your ideas about waste products.
Ultimately, fats, just like carbohydrates, end up as water and carbon dioxide if they are used in cellular respiration for energy. The reaction path is different, but the ultimate reaction products are the same as you would get from burning fat in a fire: reaction with atmospheric oxygen oxidizes the reactants to carbon dioxide and water.
This is the reverse process of photosynthesis, where carbon dioxide and water react to form sugars, with oxygen as a byproduct.
The mass leaves the body as exhaled carbon dioxide and as metabolic water through the urine, vapor in exhaled air, etc.


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Semantics Question: epigenetic mark on a person's DNA?
In an article on biomarkers of child abuse, the author referred to an "epigenetic mark on a person's DNA". It's a popular science article, so the language may reflect a combination of the journalist's scientific competency and his or her desire to communicate complex topics efficiently to a lay audience. Is that an example of such language?
My understanding was that anything in the realm of "epigenetics" is happening to something other than DNA. Is it technically correct to refer to an "epigenetic mark on a person's DNA"? Correct enough? Only potentially misleading? I'm trying to wrap my head around the whole epigenetics concept.

This link is totally unhelpful.  You have to link to the actual paper in question.  https://www.nature.com/articles/s41398-018-0252-1

We may restrict your definition of epigenetics as heritable changes in an organism's phenotype that occur without a change in the sequence of DNA bases. That is, changes to the DNA molecule itself is permitted, as long as the sequence of ATCGs are not affected.
In this sense, it would not be wrong to refer to an "epigenetic mark on a person's DNA". For example, a mechanism of epigenetics that does directly change the DNA molecule would be something like DNA methylation.

Then the article is incorrect, because it does not establish that the chemical modification to the DNA has been inherited or will be inherited, regardless of whether it has any function, which clearly has not been established.

@David I don't see any part of this answer that demonstrates that the article is incorrect, again given the interpretation for "inheritance" in epigenetics, which does not necessarily refer to inherited by the offspring (per our comment conversation on your answer and the final paragraph of your answer).

@BryanKrause — It would seems that an extensive answer — considering and distinguishing the different definitions or interpretations of the term is needed on SEBiology to deal with epigenetics. I'm not sure this is the best question to use, as ultimately the poster's concern seems to be more at the level of base methylation v. histone modification as epigenetic.

It all depends on your definition of epigenetic. The one assumed by @ning, that appears to fit the case, is that cited in the Wikipedia article on the topic is:

“Epigenetics is the study of heritable phenotype changes that do not
  involve alterations in the DNA sequence”

Methylation is a change in DNA that does not involve altertion in the DNA sequence. For observations of such marks to be epigenetic it needs to be proved that they also:

Have a phenotype. In this case the association of the methylation with behavioural changes resulting from child abuse is not asserted or demonstrated.
Be heritable. This is also not asserted or demonstrated in the article.

I am unaware of any circumstance in humans in which these three conditions have been satisfied.
Epigenetics without inheritance
I think the confusion and pseudo-science associated with this topic arises from the fact that DNA methylation can play a role in differentiation of cells during the lifetime of higher organisms, which has also been termed epigentic. This has been confabulated with experiments on inheritance of methylation patterns in bacteria. A resulting epiphenomenon has been a revival of credence in the criminal fraud of Trofim Lysenko.

In literature on epigenetics it is common to take the "heritable phenotype" in your first definition to include inheritance within cell lines in an individual, rather than the more common use of the term to mean across generations, though clearly the article in the OP was referring to generational changes. I'd say this is especially true in 'epigenetic' research into cancer where the term really just means "long-lasting changes in gene expression that are carried to daughter cells."

@BryanKrause — Agreed, as I hope my rider made clear. But the abuse of the real science by gutter journalists and people with a political agenda really annoys me.

Understood, and I know you have been an opponent of (intergenerational) epigenetic studies on previous questions here. I have to say though, although imperfect, I thought this article was actually a very fair assessment for a more pop science article, have you actually read it? It makes the controversy pretty clear and identifies accurately the current state of research: someone is reporting some methylation changes in sperm and are uncertain at this point if those make it through to offspring.

I'm not sure you mean confabulate. Autocorrect?

The word suddenly came to mind, so I checked with Merriam Webster who give one definition as "to fill in gaps in memory by fabrication". Seemed quite a good fit.


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How is the timing of gene expression controlled in developing embryo?
I understand how cell differentiation works in general (gradients of homeobox proteins etc), but how is timing controlled? Why do some genes switch on at a very specific moment of development and then switch off.
I imagine that the timing could be enabled by the same homeobox proteins (genes are switched on as soon as the proteins diffuse far enough, and switched off as soon as the homeobox is used up), but perhaps there's some special mechanism of gene expression timing?

I feel like answering this question would require more than one textbook on  developmental biology. Maybe you could narrow it down to a particular event?

It's controlled by the expression of other genes, the environment and/or maternal effect. You might be interested in this answer.

@BryanKrause, well, I am mostly interested in how it's generally possible rather than particular cases.
Say, a cluster of undifferentiated cells initiates differentiation. Half of the cells assume the fate A, and the rest assume fate B: they undergo very different steps of differentiation and transcribe entirely different proteins. And yet, in 24 hours, they all end up differentiated and forming a functional structure. How are the two completely different pathways could be synchronized so perfectly that they finish at around the same time despite having nothing in common?

@Anton Did you check out the answer that canadianer linked? I think something like that is going to be about all someone can say. I also think your conception about them "finishing at around the same time" is a bit off, there's no reason that cells have to be "done differentiating" at the same time in terms of all the maturation that goes on. Often the first steps are separating different types of stem cells which go on to differentiate in potentially multiple other separate paths, and for many tissues this never stops during the lifetime.

How can gene expression timing affect the formation of a developing embryo?
We should know that genetic imprinting is passed down. The formation of an embryo is not. Some takes on form when provoked, it is much like when oocytes are stimulated with a prod duplication
Happens automatically. The embryo is affected by the proximity of cells. Clusters, spread out, far apart. All make the cells behave automatically. But it's the first ignition of development that sets off growth. The cells have been through many phases and timing is not controlled by either proteins or genes.

Does this not answer your question?


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How exactly do microfillaments change the cell membrane's shape?
I understand that they are concentrated under cell membrane and can contract, but the details aren't very clear. How do they attach to membrane, and in what direction do they pull? Do they draw two points of cell membrane together or what?
Also, actin in muscles doesn't just contract itself but anchors to myosin and "crawls" along it: it's not actin that contracts, but the entire actin-myosin complex. Does something similar happen in microfillaments?


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How does axon guidance system precisely targets specific axons?
Axons find their way to the terminus by responding to axon guidance molecules (AGMs) that attract and repel growth cones or make them stir. This I understand.
Through a very specific combination of AGMs, a precise path can be layed out that an axon cone will follow even across half the brain. This I also understand.
What I don't understand is that in developing brain, there are millions of axons moving to their termini at the same time, and millions of AGMs released all over the brain. When an axon departs on a journey to reach an AGM at the opposite end of the brain, it will probably pass by thousands of other AGMs and yet ignore them all.
When an AGM is released, there are like thousands of neurons nearby, and yet they all will ignore it but some single neuron across the brain will reach for it.
I can think of two possible explanations:

There are unique AGMs for every neuron that no other neurons will
follow (but it doesn't seem to be the case).
There are somehow very specific instructions wired into EACH neuron aka ignore five netrins, then follow the sixth, then ignore two more, and then follow the ninth one till you reach it (but how is it possible to program every neuron in the brain like that?).

So, how does it work in reality?

In a nutshell, I would say neurons do have "specific instructions."  However, it isn't so much "ignore netrin X amount then stop."  It's more like "express receptors 1, 30, 48, and 62" which as a unique combination gets the growth cone where its going and prevents it from forming an erroneous connection along the way.  I've provided more context below that might help this make more sense.
A number of factors come into play with proper axon pathfinding and guidance, but I think the two below are sufficient for this:

There are different receptors present or absent on the cell surface depending on what cell type it is, which allows different cell types to respond only to specific cues. However, most developing axons express multiple types of receptors, so they can respond to multiple guidance cues (or respond to a cocktail of different cues).
There are non-diffusible signals present along the path in which the axon is growing.  You can read about one type here: https://www.nature.com/articles/nn.2231.  The main point about non-diffusible cues is that they can either stabilize the growth cone (which might promote growth or initiate the formation of a synapse) or they can repel the growth cone.  Therefore, they play an important role in informing the growth cone what is and is not the proper target.

There are now two things from your question should bring it all together.  First, you state that the precise path comes from a "specific combination of AGMs."  Exactly! The key word here is "combination."  Because there are so many AGMs that can affect the growth cone in so many ways, the combination of receptors (and intracellular secondary messengers) expressed on the growth cone and how they work in concert is what's critical.  Second, you state that growth cones will "ignore" potential targets as they pass them by.  That might sort of be the case (i.e., if a growth cone doesn't have a receptor for something the target is expressing, it won't "grab onto" or respond much to its presence).  However, it may also be that these potential targets express some non-diffusible cue that repels the growth cone, and it doesn't recognize that spot as a its final destination.
This article can also help provide more insight on the nuances of axon guidance:  https://dev.biologists.org/content/145/10/dev151415.long


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How does Genetic drift and selection affect fixation of an allele?
I want to know how does genetic drift, and selection coefficient (s) together affect the fixation of an allele? For example, if there is a neutral allele (s=0), will only genetic drift cause the fixation or loss of an allele? Similarly, if an allele is beneficial which means that s > 0. In that case, how do genetic drift and selection coefficient together determine the fixation and loss of an allele? And what happens when s < 0 that is an allele is deleterious. Lastly, how do genetic drift and selection coefficient gets affected by the population size? I am reading about population genetics, and I am totally confused by this point. I would appreciate if someone can clear this to me.

It would take a lot of writing to fully answer your question. Below I give an answer without spending too much time on the underlying math assuming you are confortable with probability theory and Taylor series. If you really want to understand more of all of that you would just need to consider reading a book in population genetics (see end of the post for recommendation).
Probability of fixation under drift only
In absence of selection, mutation and migration, drift only may yield an allele to eventually reach fixation (or loss). The probability of an allele to get fixed is then just equal to its frequency $P_{fix}=p$. When the neutral mutation has just arisen, this probability is therefore $P_{fix}=p=\frac{1}{2N}$ for a diploid population of size $N$.
See this post for more information.
Drift and population size - Intuition
For some intuition about the effect of population size on drift you might want to have a look at Why is the strength of genetic drift inversely proportional to the population size?.
Drift and population size - Effective population size
To go a little further than the linked post, note that the the strength of genetic drift is defined by what we call the effective population size $Ne$. But before talking about that let's talk about the variance in possible allele frequencies in the next generation (which we'll call $var(p')$).
The number of alleles $A$ in the next generation follows a binomial distribution (if we follow Wright-Fisher model). The variance of this binomial distribution is $2 p N (1-p)$, where $p$ is the frequency of the allele $A$ in the previous generation. Dividing this variance by $(2N)^2$ (the square is caused by the fact that $var(k X) = k^2 var(X)$, where $X$ is a random variable), to get the variance in allele frequency in the next generation
$$var(p') = \frac{p(1-p)}{2N}$$
We define the strength of genetic drift as $var(p')$ and for intuition, we usually refers to it as the value of $N$ that corresponds and to avoid confusion with the actual population size we call this new measure $Ne$. Therefore,
$$var(p') = \frac{p(1-p)}{2Ne}$$
Solving for $Ne$ yields to
$$Ne = \frac{p(1-p)}{2var(p')}$$
and this effective population size $Ne$ is what we use to talk about strength of genetic drift.
Probability of not reproducing
As I will refer to this statistic later, I will introduce it here. What is the probability of a given individual to not reproduce? Let's call this quantity $P(k=0)$ as the probability that the number of offspring $k$ is $0$.
Imagine you sample $2N$ haplotypes (with replacement) to form the next generation and each of them has a probability $1-\frac{1}{2N}$ to be chosen, the the probability of not reproducing is $p(k=0) = \left(1-\frac{1}{2N}\right)^{2N}$. Taking the Taylor series of this expression for large values of $N$ yield to the approximation $p(k=0) = \left(1-\frac{1}{2N}\right)^{2N} ≈ e^{-1} ≈ 0.37$. So, any individual has a probability greater than a third to leave any offspring in the following generation.
Probability of fixation under both drift and selection
If an allele if beneficial, then its probability of fixation is greater than its frequency $p$ (and vice-versa if deleterious).
Approximation
There are a number of ways to derive such probability and they all end up with some complicated form. An easy approximation (which I am not going to make any demonstration) for this probability is
$$P_{fix}≈\frac{1-e^{-4Ns} }{1-e^{-4Nsp}}$$
Just to give you some intuition about the form of the above approximation (but without doing a full demonstration that would be quite long), consider that the number of offspring an individual have follows a Poisson distribution with fitness as the rate. The fitness of the mutant individual is $1+s$, and therefore the probability of this individual of having $k$ offspring is
$$P(k) = \frac{(1+s)^k e^{-1-s}}{k!}$$
Think of the generation where the mutation just arised and only one individual has this mutation. The probability of this mutation to disappear immediately is therefore
$$P(0) = e^{-1-s}$$
, which for reasonable values of $s$ is not very different from the probability of not reproducing when $s=0$ and the probability become $e^{-1}$ (as already shown above via an other mean).
A less accurate approximation (but with a very easy form) for the probability of fixation is
$$P_{fix} = 2Ns$$
Some more calculations about the interplay of drift and selection can be found in this post.
Source of information
The post Book recommendation on population/evolutionary genetics? will give you great sources of information to learn more on the subject. It will also re-explain what I just said with a lower pace. I particularly recommend Population Genetics: A Concise Guide


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Can you identify this species?

It is similar to a kinkajou but it isn't for sure. I would include it into carnivora, and then maybe canifornia but I really don't have a clue.

With Chrome, if you have a picture, you can do a right click on it and do a google image search. Doing so with the image you provided finds, amongst others, the wikipedia page for the Common spotted cuscus


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Explanation for hyenas asymmetric legs length
Hyenas seem to have disproportionately short hind legs. It may be the opposite, maybe the front ones lengthened to raise their heads even higher than their already long necks do. In any case, this trait is not seen in any other cursorial animal (that I know), asymmetry is not a good Ally in the long run. So why?

This website along others claim (without reference) that it is to allow to see further (like gorillas if I am not mistaken). Do you not believe this could be a sufficient reason?

First most animals have limbs of different lengths. consider a house cat at full extension its hind limbs are much longer than the forelimbs.
The relative length of the limbs means almost nothing functionally, it is the relative length of the gait, or the distance the limbs can swing that is important, a longer less flexible limb may swing the same distance as a shorter but more flexible limb. Source
When the limbs have very different gaits you end up with hoppers or so called pendulum runners like rabbits and kangaroo or they do not fully utilize the possible arc of one limb like gorilla this second one pops up when ground travel is not the primary means of locomotion. Hyena do fall in either category their limbs are close enough for a normal gait.
Hyena limbs are not as different in length as many people think, the massive neck and shoulder muscles make the front limbs look taller than they are in many photographs, but yes they are longer. The heavy musculature plus the longer forelimbs are all adaptation to make the animal stronger with more leverage, better able to rip apart a carcass and crush bones. They do not need the massive hind limbs of the large cats becasue they do not "pounce", you see the same adaptation in the so called "Fanged Cats" or saber tooth cats they have massive forelimbs. More importantly the massive muscles on the shoulder and neck make the forelimbs less flexible so to get the same arc swing out of the limb, it has to be longer.

Thank you very much. I found very interesting that of the pendulum runners. I had already realiced that ther lococmotion is very different and a "pendulum" absolutely matches. Your explanation of the different limb lenght to compensate lack of flexibility is perfdect.


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Since frogs are ectotherms and supposed to have low metabolic rate, why do they grow so fast and eat so much?
It's always emphasized in literature that endothermy enables high growth rates but requires more food.
But look at frogs, for example: bullfrogs, toads, pacman frogs etc. They would readily eat a quarter their weight a day, and they grow real fast (I used to keep pet frogs: pacmans, for example, become more that twice as big in one season). And all of that despite being ectotherms. How is that possible?

Rather than saying ectotherms can't grow fast (which is obviously false), it's probably better to think about it as a two-part argument:

Ectotherms and endotherms can grow rapidly at an optimum temperature
Ectotherms can't maintain themselves at their optimum growth temperature

If you keep ectotherms at their optimum temperature, then they can reach optimum growth. In the wild, they might not find that optimum temperature for more than a few hours per day, though in your aquarium they might be at it all day long.
There are several publications supporting this such as

Effects of temperature and volume of water on the growth and development of tadpoles of Pleurodema diplolister and Rhinella granulosa (Amphibia: Anura)
Effects of Temperature on Growth, Development and Survival in Larvae of Pelophylax ridibundus (Pallas, 1771) (Amphibia: Anura): Linking Global Warming to Amphibian Development
Thermal tolerance limits and effects of temperature on the growth and development of the green toad, Bufotes viridis

I don't see a specific reference for this but will add that ectotherm probably have greater growth potential than endotherms if they're at their optimum temperature, because endotherms have to waste energy on a whole suite of molecular machinery that's designed to maintain their body temperature.  All that extra energy can be diverted into growth by ectotherms.

Well, they don't grow slow in wild either; besides, amphibians in general prefer much lower temperatures (they don't bask like reptiles, and prefer something from 18 to 24 C). So basically, their metabolism just works differently?
"Ectotherms and endotherms can grow rapidly at an optimum temperature"
Well, the way I thought it is, in endotherms, their cells conduct reactions faster, which allows them to grow faster - and consequently, faster reactions produce more heat (basicelly, ectoterms grow faster and hence they are warmer, not the other way around).
Thanks for references!

Frogs don't bask like reptiles?  But it's common to see them out of the water, sitting on rocks & logs.

Well, some of them may have such a habit. But many don't, and many are nocturnal in the first place.