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Genetic information storage and the extent to which it controls appearance/structure
So there are often articles about cloning from a small piece of tissue etc.
My question is (two actually) Is the Complete information about entire organism's structure stored (as in duplicated) all over the body? And is everything actually stored/based on DNA information, such as number of hairs you have including their position and texture. That would be a lot of information, I mean just taking hair as an example and its quantity and position, but there are also things about every aspect of structure, from bone composition, to position of organs, veins etc. None of it is random (ignoring mutations aspect) and all of it has to be "programmed" in initially. How can this be possible when the number of specifications is so huge?

The common phrase I've heard is "DNA isn't a blueprint, it's a recipe". More specifically, the nucleotides in DNA correspond to which proteins get made (coding DNA) and when and where (regulatory DNA). Just like a recipe doesn't specify the exact color of a cake or the position of each raisin, but does say "cook the cake for this long" (which will, in interaction with the heat of the oven, determine its color) or "put in this many raisins, at this general point in this general area", DNA doesn't contain the exact information of how you end up looking (hence why identical twins aren't really identical), but it does say how to make you how you are.
It also illustrates how much has to be "programmed" initially; how we are really needs to be understood as an interaction between DNA and the environment through the process of development, just as you can't completely understand a cake just from the recipe, you also need to know how chemistry and physics cause the things in the recipe to have the effects that they do. A lot of what goes on in development is cells growing, changing or dying depending on the chemical environment they're in, which includes what their neighboring cells are. The information in DNA basically consists of affecting that via what proteins get made when and where during development.
As for whether complete information about the entire organism's structure is stored all over the body, yes and no (but mostly yes). Yes, by default every cell in your body inherited its whole genome from the original zygote that started things, and you can indeed in theory clone a whole person from many random cells in the body. However in practice it depends on the cell: some cells lose their nucleus entirely, like red blood cells, so of course they don't contain the body's whole genome. Other cells could theoretically multiply or eliminate certain genes in a similar way as they specialize for the specific task they need to do, meaning they won't end up with the same genes as all the other cells in the body, but this isn't thought to be a common phenomenon especially in humans (cells will vary more in the expression pattern of their genes without necessarily changing the DNA sequence itself). This is also ignoring the ordinary mutation rates in DNA as the cell divides, which will yield differences between different cells of a given body even without that being a deliberate process. Hence cancer !
Some references on the possible variations of DNA in somatic cells (i.e. not ova or sperm)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497787/

It is commonly assumed that all healthy cells that arise from the same zygote possess the same genomic content, with a few known exceptions in the immune system and germ line. However, a growing body of evidence shows that genomic variation exists between differentiated tissues.

Elimination of actual DNA in nematodes and lampreys :
https://www.ncbi.nlm.nih.gov/pubmed/23123092
https://academic.oup.com/mbe/article-abstract/33/9/2337/2579241/Characterization-of-Somatically-Eliminated-Genes?redirectedFrom=fulltext
Quote from the first abstract:

Chromatin diminution is the programmed elimination of specific DNA sequences during development. It occurs in diverse species, but the function(s) of diminution and the specificity of sequence loss remain largely unknown.

I have found no mention of it happening in humans however.

Thank you for definitive answer to my first question, makes it clear now. However regarding the 2nd question (blueprint-related) I'm still not 100% clear (probably because I didn't elaborate enough). Using computer terminology, we can write a detailed Instruction that performs exact task, or we can use/rely on a Library that is "known" to accomplish a particular task. This library being Environment, the instruction would be Environment(Plant Hairs in area X). Two ways -- same result. To create the organism, DNA (or something else) must know how to use the Library. Please explain :)

I'm not sure quite what you mean by "know how to use". The computer analogy is a terrible one, but I'll try and explain as best possible in the frame you're starting from. Do you mean "know how to use" as in "is compatible with" (uses the correct syntax, etc) or as in "is aware of the adequation of the library to the program's ultimate goals" (uses a scipy library for science calculations, etc) ? In the former case, the library is the laws of physics and chemistry, DNA follows those by default because it exists in the world. In the latter case (...)

the "instructions" in DNA (also not a good analogy btw) don't come from an ultimate goal; it just so happens that various proteins being made at various points has an effect on the final organism (because chemistry and physics), and when that effect promotes the final organism's reproductive success the originating DNA pattern spreads through the population, until all organisms have it and it looks like it was put there on purpose to have that effect (which in a way it was for a certain understanding of "purpose": the effect had a causal influence on why that instruction is there now).

Still not 100% clear. Lets say initially these proteins started out at various positions and now we have a particular organism. Whatever the physics/chemistry may be, in order to survive, DNA needs to accommodate for these things. The closer the match the better success rate. Lets take an eye for example and try to design it in a biological 3D printer (if one existed) We need 1) "blueprint" or some sort of "instruction set" and 2) Something that has the ability to transform/delegate it into "design" stage.  Otherwise, why would cells just stick together forming an organ of such complexity?

@Emil the eye isn't designed in a 3D printer. Organisms are self-assembling. And there isn't a clear division between "blueprint" and "assembly", just like the brain doesn't have a clear division between "software" and "hardware". DNA isn't the passive repository of the information to build something; it is an active part of the functioning of the cell, given it's part of the production of proteins. And cells split and stick together depending on what proteins they're secreting in their membrane, and that's determined on which genes are expressed.

@Emil this is becoming quite the conversation, and I suspect you might be at the point where you'd need to post a new question, but I don't know what it would be. I would be happy to talk more to straighten out exactly what points you don't understand and why, but maybe the chat would be a better place for that: http://chat.stackexchange.com/rooms/1997/the-biosphere


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Is there a name for dominant-intraspecific competition?
Some ecological competition dynamics have particular names (e.g.: scramble competition, contest competition, ...). I wonder if there's such a name for competition dynamics where the interspecific interaction is weaker than the intraspecific one.
By weaker I mean that the non-diagonal elements of the community matrix are lower than the diagonal ones.

source: Stack Exchange

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

sort: votes


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Using catalase-test to determine if Staphylo- or Streptococcus
If the microscope clearly shows bacteria of cocci morphology but it is difficult to determine if they are Staphylo- or Streptococcus, are catalase tests a good way to differentiate between the two since Staphylococcus are positive and Streptococcus are negative? Are there any traps/exceptions?
Thanks!

Generally yes: streptococci are catalase negative while staphylococci are catalase positive.

The catalase test is important in distinguishing streptococci (catalase-negative) [from] staphylococci which are catalase positive.

Unlike Staphylococcus, all streptococci lack the enzyme catalase.

However, there are exceptions to every rule:
Catalase negative Staphylococcus aureus.
Catalase positive Streptococcus sp.

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


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Transcription Factor expression level
Could someone explain me in detail what is meant by "TF expression LEVEL", what does it represent and how is it measured? This is for example used in figure 3 of this paper: A census of human transcription factors: function, expression and evolution.

Where did you find this expression?

@Chris In scientific litterature, I am trying to understand a paper on the topic. Google gives more than 15o.ooo results containing the exact expression "Transcription Factor expression level". Any ideas what it means ?

I understand that. Can you link the paper in quest and probably also say in which section it is? That may make the answer easier.

http://www.nature.com/nrg/journal/v10/n4/full/nrg2538.html see Figure 3, for example

Transcription factors are an important cellular regulatory mechanism to control gene expression. The expression of TF is important for cell function, differentiation and also for responses to environmental signals.
We know quite a number of different TF, but only for a little part of them their exact function (in terms of which in which tissues they are expressed, when and which genes they regulate) and this is where the paper you read comes in.
They test for the expression of roughly 1400 TF in a number of different tissues, to see where they are expressed (figure 3 from the paper):

The group used micro-arrays to analyze the expression levels (in this case how much transcript from the genes is made assuming that this also translated). The quantification was done using the signal strength of the array - the more transcript you have, the stronger the signal is.
The expression of a certain TF in a specific tissues shows its involvement in gene regulation (either direct or indirect) there.

Thank you ! What does it mean for a TF to be expressed in a tissue ? Does it mean that it participates in gene transcription in the cells of this tissue ?

Yes, either directly in the expression or indirectly in its regulation. Transcription complexes are often very big.


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Help identifying an insect (I think it was an insect)
While I realize this may be difficult without a photo, I'm hoping someone can say "This is a list of possible species given your location and description" and I can attempt to find a photo that matches from there.
I'm in NE Indiana. I think it was an insect. The species in question looked a bit like a leech, black and shiny but wasn't segmented and it was a bit flattened out (but not entirely), maybe an inch long. It wasn't tapered. Also I don't believe it made any attempt to bite me (or just wasn't around long enough to). Unfortunately it startled me so I smashed it pretty quickly so I didn't get a picture, but I got a good look and couldn't identify any legs, eyes, antennae. It moved fairly quickly, almost in a pulsating motion.
When I smashed it, there was only a bit of white, mealy paste left behind, the body almost seemed to liquefy.
If it hadn't moved so quickly and wasn't so small I'd have thought it was a baby slug. It's possible it could have been some sort of larvae.
I also don't think it was a leech because I found it on my body but I was in my home and can't think where I could have been that would have exposed me to one. I noticed it when after removing my shirt and lying in bed. So it was either inside my shirt for several hours without me noticing, fell out from the covers when I got in bed, or fell from somewhere after I got in bed.

This is not easy to answer without a picture. However, if it was unsegmented, it was definitely not an insect (which have a segmented body plan, both as larvae/nymph and adult). Your description also sounds nothing like an insect. However, the overall description fits fairly well with a flatworm (Phyluym: Plathelminthes), see e.g. Geoplanidae. They can resemble slugs or leeches, but both lack segmentation and antenna. Finding one inside your house sounds a bit strange though, as they generally prefer moist habitats.
Terrestial flatworms are relatively mobile and most are predators or scavengers
Example pictures:

Okay that makes sense. Looking at images, it looked similar to Microplana terrestris or Rhynchodemus sylvaticus But I'm not sure on the range/size of these species or the probability of encountering them in the home.

It was raining outside, is it at all possible it fell onto my clothing from some surface while outside and I just didn't notice until later, or are these likely to be low to the ground?

The terrestial species in Geoplanidae are quite mobile, so you might well have picked it up outside. Most species in Plathelminthes are however marine or parasites.

I would say the bottom picture you provided look almost exactly as I remember it, with the exception of the sliminess. Could it have just been drying out?

@PatrickSchomburg That is definitely possible. I'm not familiar with US flatworms personally though.


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Why are we able to differentiate between colored objects without the presence of light?
Rods help us to see during the dark.
We can see colour of the object when it reflects light.
But in a dark room(room of any color but the light is switched off and it is night),we still can differentiate between colored objects if we open our eyes for sometime.(although not very much clearly)
How the colors are seen when there is no light?
Do we see as the brain remembers their colour?

Any room that is not pitch black still has light in it, what exactly is your definition of a dark room?

@Mesentery if you can see anything at all, then there must be some light.

The premise of your question is wrong. The colors aren't seen when there is no light. In a dark room where you can see things there is light, that's why you can see things in the first place. We don't just need light to see color, we need light to see in the first place ! I'll answer your question though since you seem sincerely confused.

Yes, because there is still light. Coming from the window, any lit electronics, seeping between the door frames, what have you. If you can see, there is light. (the brain can confabulate stuff when it has nothing to work with but unless you're in true mental distress you can usually tell that apart from actually seeing things (usually; it IS easier to mistakenly identify things in the dark)).

@mesentery writing @ the close voter will not work here ;)

To everyone voting to close: http://meta.biology.stackexchange.com/questions/2961/voting-to-close-a-question-as-off-topic-because-it-is-based-on-a-faulty-presuppo

You seem to have many misconceptions about how we see and how that relates to light. I'll address them one sentence at a time:

Why are we able to differentiate between colored objects without the presence of light?

Answer: the premise of the question is wrong: we aren't able to differentiate between colors without the presence of light, because we aren't able to see without the presence of light. Light is what allows us to see. "Seeing" is the act of detecting the light coming from the environment and using it to derive what the environment is like.

Rods help us to see during the dark.

It sounds a bit like you think rods help us to see during the dark... without light ? This is not the case: BOTH rods and cones absorb light and thus allow us to see. Rods help us see in low light because they are more sensitive (to light !) than cones. Nothing can help us see with no light.

We can see colour of the object when it reflects light.

It depends on how much light it reflects ! The correct form of that sentence is "We can see the object when it reflects light". (even more correct would be "when it reflects enough light to trigger the light receptors in our eyes, i.e. rods and cones). Whether we can see its colour depends on whether it reflects enough light to trigger the cones specifically.

But in a dark room(room of any color but the light is switched off and it is night),we still can differentiate between colored objects if we open our eyes for sometime.(although not very much clearly)

Indeed; this is because no room is completely dark. Even more so in our artificially lit world, but even in a moonless cloudy night you may have a few errant photons coming from the stars and Sun (via diffusion in the atmosphere), fireflies, what have you; to be fair in our artificially lit world I haven't experienced it. As far as I know you can get true pitch darkness in things like underground caves (once you're far enough from an exit of course).
Basically, if you can see anything then there is some light. (well, short of your optical cortex confabulating stuff, which in fairness it will do).

How the colors are seen when there is no light?

As I hope you understand now, they aren't.

Do we see as the brain remembers their colour?

I think that may actually be one reason we perceive colour in low-light environments. I'm sure some of it is that there's enough light to trigger the cones a little bit, but I wouldn't underestimate our brain's ability to show us the world as it knows it is as opposed to as whatever information it's receiving right this second says it looks like.
EDIT
Some references :
The state of seeing things in such low light that we only use the rods is called "scotopic vision" :
https://en.wikipedia.org/wiki/Scotopic_vision
Some sources for how "dark" environments still contain low amounts of light (one word for "amount of light" being "illuminance", measured in Lux) :
http://www.engineeringtoolbox.com/light-level-rooms-d_708.html
https://en.wikipedia.org/wiki/Aphotic_zone (thank you to @Johnny for that one)
HOPEFULLY LAST EDIT
On reflection I thought I'd say some more about scotopic vision since it's very relevant to the question. It turns out "scotopic" vision is opposed to "photopic" vision (the vision we have in full lighting, where the cones do the work because the rods are saturated), and in between there is an intermediate range called "mesopic" vision, which is likely the kind of vision we experience when it's dark but we still see color (this is ignoring our brain filling in colors, which could also be a factor and in that case could also happen with scotopic vision - but I didn't find any sources on that).
Mesopic vision is used under lighting conditions that seem to range from low indoor lighting or streetlights to starlight; scotopic vision is used with luminances darker than that. This page is all about it and includes a very nice drawing, sadly it's a pdf so I can't show it in the answer:
http://www.visual-3d.com/Education/LightingLessons/Documents/PhotopicScotopiclumens_4%20_2_.pdf

@Mesentery : that was harder to look up than I expected, but this looks good: http://www.engineeringtoolbox.com/light-level-rooms-d_708.html  it shows a table with the illumination in different environments. As you can see the lowest number it shows, for an overcast night, is not zero. It doesn't give numbers for a dark room though. Another reference I found to the concept: https://en.wikipedia.org/wiki/Scotopic_vision (turns out "seeing under low light" is called "scotopic vision", this gives specific illuminances as well).

@Mesentery I support Rozenn Keribin's answer that it is next to impossible to find a room that is aphotic (free of light) on the surface of the earth. Perhaps, the way we define the aphotic zone in Oceans (less than 1% of light) suffices as a reference? See article: https://en.wikipedia.org/wiki/Aphotic_zone

@Mesentery Done, and you're welcome !


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Why do polyneuropathies affect the extremities first?
Polyneuropathy is an anatomic pattern of nerve damage most commonly seen in Diabetes mellitus.
To quote Robbin's Pathology,

In most polyneuropathies, axons are affected in a length dependent fashions leading to deficits that start in the feet and ascend with disease progression. The hands often start to show involvement by the time deficits extend to the level of the knee, resulting in a characteristic 'stocking and glove' distribution of sensory deficits

What is the reason behind longer neurons being preferentially affected?

Polyneuropathy is actually not a very specific term, so the reasons will no doubt vary depending on which specific class you are talking about.
That said, here are two reasons that longer neurons are preferentially affected:

Some polyneuropathies involve conduction problems that include "failures" where action potentials aren't propagated down the full length. It doesn't matter where along an axon the failure occurs, and longer axons therefore have more "chances" to fail.
Axons are somewhat isolated from the soma where most proteins are created, and it is common in certain neuropathies for degradation to begin furthest from the soma, presumably because the neuron has less capability to deal with problems or repair damage in those areas far from the soma. Neurons with longer axons by definition will have some part of their axons that are further from the soma than neurons with shorter axons. This is the answer that is most relevant to your question, see for example this source that reviews the causes of diabetic neuropathy.

References:
Yagihashi, S., Mizukami, H., & Sugimoto, K. (2011). Mechanism of diabetic neuropathy: where are we now and where to go?. Journal of diabetes investigation, 2(1), 18-32.

Thanks. Id like to add some more. Further reading the same chapter I came across another line. It says neuronopathies (which attack the soma of the neuron eg zoster and platinum) unlike axonopathies (which polyneuropathies mostly are) are equally likely to affect both proximal and distal parts of the body since here it's the cell body and not the axon to be damaged. So, this helps as a differentiating point bet the two

@Polisetty I don't think it is accurate to think of neuronopathies and polyneuropathies as independent groups; there is definitely a Venn diagram-like association: it is just as possible for a neuronopathy to be a polyneuropathy as not (zoster would be a good example of a neuronopathy that is not a polyneuropathy).

Yup one is an anatomical classification while the other is a functional one...


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Which DNA elements belong to the definition of a gene?
I see a lot of different DNA elements mentioned as part of a gene (talking about eukaryotes):

The length of DNA following the promoter is a gene and it contains the
  recipe for a protein. (video)

This implies that the promotor is not part of the gene.

This actually defines a gene without enhancers/silencers

 (source)

Here the gene also includes the enhancers/silencers
Question
Is there an accepted gene definition regarding the DNA elements? Thus which sequences like promotors, enhancers, silencers etc. are considered part of the gene?

Do you have a use case or that definition, something specific that requires you to have definition, i.e. "if A is gene why B is not"? Also, if I say "gene is X", how will you know if it is good or bad?

Usually a promoter is not considered a part of the gene. Distal regulatory elements qualify even lower for being considered a part of a gene because they can regulate many genes simultaneously.
Basically, a geneic region starts from the transcription start site (TSS) and ends at the terminator (or polyadenylation/cleavage site in eukaryotes). If a gene gives rise to multiple transcripts, those which have similar products (no frameshifts) but different TSS/terminators, we should consider the geneic region as a union of all the primary transcripts produced from that site.
There is a relatively old article on this topic: What is a gene, pose ENCODE? History and updated definition. It summarizes that:

There are three aspects to the definition that we will list below,
  before providing the succinct definition:

A gene is a genomic sequence (DNA or RNA) directly encoding
  functional product molecules, either RNA or protein.
In the case that there are several functional products sharing
  overlapping regions, one takes the union of all overlapping genomic
  sequences coding for them.
This union must be coherent—i.e., done separately for final protein
  and RNA products—but does not require that all products necessarily
  share a common subsequence.

This can be concisely summarized as:
The gene is a union of genomic sequences encoding a coherent set of potentially overlapping functional products.

.

My summary is that a gene, if it codes for a protein, would be a union of all primary transcripts that produce identical proteins (originating from transcripts with different TSS/terminators) or splice variants.
Ideally, all the different transcripts produced from the locus would have the same promoter.
Overall, it appears that a common promoter is imperative for considering the different products under the same gene because if two products are produced from different promoters then we consider them as products of overlapping genes.
Whether we should consider the promoter as a part of a gene is an open debate.

While your post is detailed, I'm a fifth year PhD student in genetics and I barely follow it.

@Artem  Possibly, you can ask for specific clarification instead of downvoting.

@WSIWYG. I don't think it's wrong for a textbook answer, I just think it's unclear. What about subsets of non-coding RNA? How much and what kind of non-coding overlap determines a common gene? Or if two non-coding transcripts with the same first exon and different second exons with distinct functions?

@Artem Unfortunately, even the scientific community and the genome consortia have not clearly defined these categories and hence they are unclear. How to differentiate between overlapping genes and a single gene with multiple isoforms? There is no definition out there yet. Usually splice variants are considered under the same gene. If we accept this then it appears that if many transcripts share a common promoter they are considered the product of the same gene.

@ WYIWSYG What happens if in case #2 and #3 the two genes share just a single amino acid or a single helix? The 'Coding Sequence' would be technically be in the first exon and thus it's the same case as 'A-B' 'A-C' which are the same gene.

@Artem Yes the situation is dicey. As per current norms splice variants are considered isoforms of the same gene. However, there can be situations in which independently transcribed products can also end up with the similar kind of products. In the case you pointed out classifying them as two genes because of different CDS is not consistent with A-B-C case. #1 and #2 should be considered splice isoforms. There is a need for a more rigourous definition.

Let us continue this discussion in chat.

My point is that no more rigorous definition using exon boundaries makes any sense, this is simply a convenience for us humans to discuss genic regions of the genome. A gene is first and foremost a unit of heredity.

It depends. There are two broad definitions which work.
The more common definition of a gene is the transcribed portions of DNA, a gene begins at the transcription start site and ends at the Poly-A site. This is common when discussing mRNA, lncRNA, tRNA. It's what most scientists refer to when they say the ACTB gene or IRF5 gene or something.
If you want to explicitly include all introns you say 'Gene Body', if you want to exclude introns you simply say ' ACTB Exons'.
An older and arguably better definition of the gene from Thomas Morgan is a unit of heredity, that when mutated results in a phenotype.
The second definition doesn't say anything about transcription and would be inclusive of things like promoter/enhancer mutations. From a molecular biology stand-point is more difficult to define. It's more useful for genetics because you're interested in how a phenotype is inherited and it's etiology, not how an a species of RNA functions.
98% of the time when people discuss genes they mean the former definition, but this is still an actively debated issue and as we learn more about genetics it will change.


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Is this a bedbug?
Does anyone know if this is a bedbug? Or maybe a cockroach? I am located in Quebec, Canada.
If you need a clearer picture I'll try to take one without the glass in the way so my camera can focus better. Hopefully it doesn't escape.

where are you? country/state?

This is a woodlouse (often called a "pill bug" or "rolly polly"). See this answer for an example of an actual bed bug.

I think I can see 5 extremities sticking out under the shield on one side in your image. Hence I think it has a total of 10 extremities. A bedbug, belonging to the class of insects, should have just 6.
I'm pretty sure it's a pill bug (Fig. 1), a family of woodlice (Armadillidiidae), belonging to the isopoda, an order of crustaceans. Crustaceans include the lobsters, crabs and crayfish, to name a few.

Fig. 1. A Pill bug species. source: Natural History of Orange County, CA
A bed bug is an insect and has six extremities (Fig. 2).

Fig. 2. A bed bug species. source: Terminix
So long story short, your species here is not an insect, and hence not a bed bug.
From the limited amount of information you've provided a specific species determination is difficult; there are many pill bugs.

Thank you! After going through some pictures of the different species of pill bugs, I have found a match.

Do you any special reason to say pill bug? From the unclear picture I find that hard so say. It's clearly a woodlouse though.

No, it looks like a woodlouse. They are perfectly harmless to humans, and feed on decaying plant matter. They are also called isopods, roly-polies, or pill bugs.
Woodlouse on Wikipedia


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Do bisexuals have any evolutionary advantage over straights and gays?
Do bisexuals have  any evolutionary advantage over straights and gays? Bonobos exhibit bisexuality extensively. Why so?

Welcome to Biology.SE. You should have a look at Is homosexuality an adaptation in humans? and How can homosexuality evolve despite natural selection?. If insights from these posts don't answer your question, can you please elaborate on why they don't.

those questions are about homosexuality vs heterosexuality, mine is bisexuality vs homosexuality/heterosexuality.

@AmitMaurya Can you point out what elements of the answers of those questions do not apply to your question?

@BryanKrause you tell me which element is applicable? is it established that bisexuality and homosexuality caused by same gene(s)?

The genetic basis of either is not well established. The research cited also doesn't look at all at particular genes, it looks at reproductive rates among relatives. It also doesn't look at purely binary genders or sexual preferences and actually groups people into "heterosexuals" and "non-heterosexuals", the latter clearly including bisexuality. Please at least make an effort to read the answers and citations, like this one.

Also bonobo sexuality is interesting but I would be careful to overly anthropomorphize bonobos, despite their similarities to humans. It isn't right to consider bonobos bisexual without considering all of bonobo sexuality. Actions that humans interpret as sexual in bonobos are a major way that they interact with each other: you might as well ask why bonobos socialize with both sexes rather than why they interact sexually with both sexes.

so  are  you saying the behaviours observed in bonobos and interpreted as sexual by us may not be sexual at all for bonobos?

Like many things, whether bisexuality is advantageous for an individual's reproductive success or not depends on the environment. The fact that a wide variety of sexual systems and behavior exists in the animal kingdom suggests that. Also, "advantageous for an individual's reproductive success" doesn't necessarily imply "will spread via the processes of evolution"; for a trait to spread via natural selection+random mutation you need the trait to promote the individual's reproductive success, and for it to be reliably passed down to its offspring. And as the causes of sexual orientation in humans aren't well understood there is always the possibility it isn't strongly or genetically inherited.
As far as bonobos go, I am given to understand they use sex as a social tool, much more so than we do. In that context it does seem like bisexuality would be advantageous; it's silly to only be able to use your most powerful tool for conflict-resolution and social bonding on half of your community. This particular advantage won't be true, or will be much reduced, in species that don't use sex in the same way, i.e. all or most other species that we know of.

are you saying bonobos' bisexuality is because of social learning rather than being genetically determined which is naturally selected?

"Like many things, whether bisexuality is advantageous for an individual's reproductive success or not depends on the environment"  so what environmental characteristics  make bisexuality advantageous in bonobos but not other animals?

@AmitMaurya I'm not saying that no; I don't know why Bonobos are bisexual. I certainly think it's plausible that bisexuality is subject to natural selection, and that it was naturally selected in Bonobos because of their social use of sex, but I don't know whether those things are true or not and I don't think research has demonstrated anything on the subject.

@AmitMaurya "so what environmental characteristics make bisexuality advantageous in bonobos but not other animals?" I described them in my answer; things like "other organisms of the species", "the social structure of a social species", etc are part of the environment.


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How can I determine the mRNA sequence from a given template DNA strand?
Can I determine the sequence of nucleotides of the mRNA strand transcribed from a template DNA strand that goes from (5' to 3')?
I know that RNA-Polymerase enzyme cannot work but on the (3' to 5') direction of the template DNA strand. So, for instance, if the question was to:
Determine sequence of nucleotides in the transcribed mRNA from the DNA strand
5'...A-T-T-C-G-T-T-A-C....3'
Which direction should I start with?

If that is the template strand, and you know RNAP travels along the template from 3' -> 5', you are able to determine the answer.

And remember that the direction has to be complementary to the template strand. Or, identical to the coding strand.

@canadianer  The problem is that when I got a bit confused and referred to an answer to the question, the answer was to use the complementary strand to this as a template and transcribe the mRNA strand so I just got more confused not sure if this was the right thing to do..

Is the sequence you wrote the template or coding strand?

@canadianer the question was exactly to determine the sequence of nucleotides in the transcribed mRNA from this strand of DNA molecule, doesn't that mean that this is the sequence of the template strand?

I'm assuming you are working with a small sequence, but for larger sequences, or if you want to double check your answer, you can use tools like this one: http://www.attotron.com/cybertory/analysis/trans.htm


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Can a cell survive temporarily without oxygen?
Can temporary denial of oxygen to a cell damage the cell? Will the cell continue to live in partially damaged condition if the supply of oxygen and nutrients are restored?

Can you provide more information as to what kind of cell? I am assuming you are talking about a human cell but please remember that there are many other cell types out there. Especially when we extend the conversation to bacterial cells that are able to grow/thrive in anaerobic conditions.

I was talking about human cell, thanks for responding.

This is really interesting because the answer largely depends on the severity of the damage, the length of the damaging condition, the type of damage incurred, and the type of cell incurring the damage.
For a real life example, irreparable DNA damage as by irradiation or drugs tends to be lethal to a cell. The severity of the damage may affect how long a cell has to live, however. For example, PBMC we irradiated with X gy tend to stay alive for 10-15 days (they actually don't divide though, due to the damage). Why did we pick that number? Too low a dose the cells persist, and too high you obliterate them. For reference, my experiements require my PBMC to be alive for a few days but disappear from the culture over time, so X gy is just an optimized value. Gy (gray) is an SI value for dose of ionizing radiation.
What you call a temporary denial of oxygen is actually referred to as intermittent hypoxia, or in a prolonged case just hypoxia. Human cells regularly survive in hypoxia by altering their metabolic pathways when OxPhos can't be utilized anymore. These changes are assisted by oxygen-sensing molecules that change the transcriptional profile of the cell. HIF1a comes to mind, a hypoxia inducible factor, which is regularly induced by PI3K and MAPK (typical cellular signals). It's typically kept in check by other oxygen sensitive proteins like VHL, but in hypoxia the effects of HIF1a action are entirely beneficial. So when the cell returns to "normoxia" it can typically reprogram into OxPhos (caveats exist, tumors for example).
So to answer your question yes, the cells will survive (in nutrient deprivation, too, but with a different mechanism), but they have to make a lot of changes first.


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Do different species of bacteria have distinct absorption bands?
Do bacteria of different species absorb different wavelengths of light? How different?
Most of my searching has lead to topics about Optical Dispertion which seems to be species independent as opposed to single species.

Did you do some research to find an answer? Please share them in your question. Low effort questions get closed on Bio SE.

Yes they do, as demonstrated by the fact that bacteria have different colors ! Moreover, some bacteria are photosynthetic and others aren't; the photosynthetic bacteria have a very specific mechanism for absorbing light that the others don't so it stands to reason they won't absorb the same wavelengths.
This page talks about it very nicely, with a list of different colors and bacteria that have them:
http://www.biotecharticles.com/Applications-Article/Colorful-Bacteria-612.html
Money quote :

Bacteria are pigmented or colored. Pigmented bacteria are also known as chromobacteria. Bacterial pigments are water soluble or insoluble; water soluble pigments are diffused in the growth medium. Chemically, bacterial pigments are pyrrole, phenazine, carotenoid, xanthophylls and quinine or quinone derivatives. The pigment molecules are synthesized in cell wall or periplasmic space. We can visualize pigmentation in bacteria in specific growth medium or my staining bacterial cells with a dye to observe under microscope. It has been proved that only aerobic and facultatively aerobic bacteria are pigmented because, molecular oxygen is essential for pigmentation. Therefore, anaerobic bacteria are nonpigmented. Pigment synthesis is also dependent on light, pH, temperature and media constituents like indicator dyes. They display all the colors from rainbow including light or dark tinges and unual colors like black, white, brown, golden, silver and fluorescent green, yellow or blue.

And the list:

Purple: Spirillum rubrum
Violet: Chromobacterium violacein
Indigo: Janthinobacterium lividum
Blue: Streptomyces coelicolor
Green: Chlorobium tepium
Yellow: Xanthomonas campestris
Orange: Sarcina aurentiaca
Red: Serratia marcenscens
Brown: Rhizobium etli
Black: Prevotela melaninogenica
Golden: Staphylococcus aureus
Silver: Actinomyces sp.
White: Staphylococcus epidermidis
Cream: Proteus vulgaris
Pink: Micrococcus roseus
Maroon: Rugamonas rubra
Fluorescent blue/green: Pseudomonas aeruginosa
Fluorescent yellow: Pseudomonas fluorescens

It appears some purposes of producing pigments, aside from photosynthesis, are to absorb UV light (i.e. absorbing a specific wavelength is the entire point) or mopping up free radicals.
An additional note, from the Wikipedia page for Rhodospirillum rubrum, the first bacterium in that list (which Wikipedia describes as "pink" but close enough):

The photosynthesis of R. rubrum differs from that of plants as it possesses not chlorophyll a, but bacteriochlorophylls. While bacteriochlorophyll an absorbs light having a maximum wavelength of 800 to 925 nm, chlorophyll absorbs light having a maximum wavelength of 660 to 680 nm.

https://en.wikipedia.org/wiki/Rhodospirillum_rubrum
And while that paragraph describes "chlorophyll a" as being a feature of plants, other bacteria do use it such as Chlorobium tepidum, so there you can see some wavelengths that are absorbed by one and not the other.

Hmm, but most bacteria will still be visible in monochromatic light, right?

I'm not sure what you mean. Most things are visible in monochromatic light aren't they ? They would have to be completely transparent to a given wavelength not to be, and bacteria are full of many different molecules so I doubt that would be the case.

Yes, they do, just as Rozenn Keribin has explained in her answer. In addition to the answer above, there is a 1954 research paper written by Shibata, Bensen and Calvin freely available from the Berkeley Lab of the University of California which should give you the theoretical background, experimental methodology as well as some data on the absoprtion spectra of different micro-organisms including bacteria:
The Absorption Spectra of Suspensions of Living Micro-Organisms


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Which DNA sequence will have higher melting temperature: CCCCCC... or GCGCGC...?
I tried this service to calculate temperatures. The nearest neighbour method consistently gives larger results for sequences like GCGCGC over sequences like CCCCC or GGGGG, while other methods don't give a difference. Is it nearest neighbour's feature or is there indeed a difference in melting temperatures?

The dependence of melting temperature on different dinucleotide pairs was experimentally measured; the meting temperature calculator is based on those results. Based on these results, you would see that a GC dinucleotide pair would differ from GG and CC pairs. Possibly, this is because of steric effects and stacking conformations.
SantaLucia (1998; author of the nearest neighbour model) has referred to different experimental studies from which the values were obtained, in the Table-1 of the paper.

That answers my question, but I am curious whether triplets and longer sequences of nucleotides have also been tested experimentally for melting temperature?

@СашкоЛихенко I haven't checked if studies with triplets have been performed. However, I think that with longer stretches of nucleotides, there would be additional factors that would affect the binding (mostly arising from steric factors). For longer sequences (oligonucleotides) people do isothermal titration calorimetry (ITC) to calculate binding energy and other theromodynamic parameters. People also perform melting analysis by slowly increasing the temperature. This would provide the most accurate in-vitro estimate of melting temperature.


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Do men with an African ethnic background have larger penises in comparison to men of European ethnic background? If so, why?
Do men with an African ethnic background have, on average, a larger penis than their European counterparts?

That question is... not unusual. It's addressed on Wikipedia's page on human penis size (which, by the way, exists) of all things. https://en.wikipedia.org/wiki/Human_penis_size#Size_and_race

You might want to reformulate "black and white" men. This is a rather unscientific wording. Also, I find the title of your question rather amusing :) .. This is a perfectly legitimate, biological question just say what you would like to know and try not to step into the pitfalls of everyday language which unfortunately very often has a "racial/racist" bias. There is no shame in the human anatomy.

I think that 4 down votes (5 actually as there was an up vote) is a bit overreacting. Among the 4 close votes, only one states that because the post shows lack of effort (via the 'homework question' reason for closing) and 3 said the post is opinion based. I don't thin the post is opinion based. I agree that given the gigantic genetic diversity present in Africa, the category African ethnicities might be unclear though.

I am not a student. I would like to know the answer.

Quoting from Oarkwe and Ebuh 2007

The mean full-stretch penile length of the Nigerian Blacks was 13.37cm and the mean flaccid length was 9.36cm. Similar studies reported full-stretch penile lengths of 12.50cm in Italians, 12.18cm in Greeks, 9.6cm in Koreans, 13cm in British Caucasians, and 12.45cm in the American Caucasians. The penile length for Nigerian Blacks was longer than those of the other races, but the differences were only statistically different in comparison with the Koreans.


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What is meant by re-absorption?
It is said that PCT, DCT, Henle’s Loop reabsorb the filtrate. Does that mean they absorb the filtrate again? If it is actually reabsorbed to medulla then why it is said that PCT, DCT or Henle’s loop reabsorb the filtrate?

In the glomerulus of the nephron we have filtration occuring. The subsequent formation of an ultra-filtrate travels down the tubulus from Bowmans space; during this journey, the filtrate will be exposed to various transporters and forces such as solvent drags and diffusion gradients, which leads to the (re)absorption of this filtrate. Reabsorption occurs also in medullary tubules and later collecting ducts, until the filtrate (by now urine) reaches the calyces. (Note that secretion - that tubular cells permit the transportation of various electrolytes for instance to the tubulary lumen - also occurs in the nephron, giving it three ways to manipulate the its luminal contents: filtration, reabsorption and secretion)


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What is the meaning of "The Molecular Basis of Disease"
What is the exact meaning of The Molecular Basis of Disease? I have one assignment which involves presenting Molecular Basis of a Disease. I am not really sure what points to add.

It means 'what is happening at molecular level' to result into the concerned diseased state. If you add the disease you are interested in, the question might be answered otherwise it is too broad to answer(though it has received one).

There is an ELSEVIER research journal by the name of BBA Molecular Basis of Disease (link to journal). I think their synopsis of what the journal is about will illuminate what is meant by The Molecular Basis of Disease.

BBA Molecular Basis of Disease addresses the biochemistry and
  molecular genetics of disease processes and models of human disease.
  This journal covers aspects of aging, cancer, metabolic-,
  neurological-, and immunological-based disease. Manuscripts focused on
  using animal models to elucidate biochemical and mechanistic insight
  in each of these conditions, are particularly encouraged.

The keywords here are biochemistry and molecular genetics, so I would think of what kind of mutations, at what chromosomal locations can cause genetic disorders for example. Or in terms of biochemistry, what kind of biochemical environment can lead to alcoholic liver disease etc.


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Why do Asian people have black hair and Northern people have golden hair?
I have got two questions.

Why do majority of Asian people have black hair?
Why do majority of people from the northern countries (Sweeden, Norway, Finland) have light (golden) hair?

Thanks for an answer.

Please put a bit more research effort into your question and please be aware of generalisations. Where is it written that all people from Asia or all people in Scandinavia have black or blonde hair respectively. Try to add some sources. I am fairly certain that you will find loads of people with dark hair colour in Scandinavia and that you will find people with blonde hair in Asia. Perhaps you need to go back to the drawing board and think a little longer about what you actually want to ask, e.g. how is hair colour determined, what genes are involved etc.

I am not questioning your own personal observation but I do question that you have seen all people living in Asia in order to make the claim that you make in your question. Also, may I please remind you that this is a scientific knowledge Q&A website. The purpose of this website is not to validate your personal opinions, claims or observations. If you do hold one of the aforementioned things please do back it up with data or legitimate source (published / peer-reviewed).

I'm voting to close this question as off-topic because it lacks primary research and appears to be based on completely unscientific presumption.

All people don't have those hair colors. All people from those Northern countries aren't blond, and there are blond people outside of Northern Europe; I don't know if you count Melanesians as "Asian", but they have blond people among them:
https://en.wikipedia.org/wiki/Melanesians#Incidence_of_blond_hair_in_Melanesia
Still; there are two, really three, different kinds of answers to this type of question.
1) Human populations differ through random drift and assortative mating: populations that are separated will develop different mutations over time that make them look different, and different populations may find different traits attractive (including traits that mark them as part of that population), which would work to amplify those differences even when the populations interact. There is no deep reason for those traits other than "that mutation happened to occur and spread through this population".
2) Certain traits are more or less useful in different environments, and thus will spread through natural selection. The issue here is that this is the kind of explanation people intuitively love (every difference must have a reason for its existence) but it's actually very hard to separate it from the first explanation.
3) Certain traits can be considered "human-default", as in the common ancestor of humans had it, most humans still have it, so the question of "why does a human population have this trait" is less relevant than "why do some human populations not have this trait".
So having said that, black hair seems like the clearly ancestral state, and so Asian populations probably have black hair for the same reason almost all human populations have black hair. And black hair seems common in great apes in general - Orang Utans are the only exception I can think of.
As for Northern Europeans, blond hair and white skin are actually one of those traits where it's hard to separate random variation from natural selection. It is quite likely there are advantages to being fair in high latitudes where there is little sunlight; you need less protection from the sun in the first place, and you need to be able to get enough vitamin D from sunlight on the other. However this applies much more obviously to skin than to hair. Blond hair is the result of very few mutations, which are thought to have appeared around 11,000 years ago. So it could be that those mutations happened to occur and to spread through those populations and not others and that's why they're blond and most other human populations (Melanesians excepted) are not. Or it could be that once those mutations happened they spread particularly well in those populations because it was adaptive in their environment. The question isn't scientifically settled.
https://en.wikipedia.org/wiki/Blond#Evolution_of_blond_hair

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


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Confusion about the role of capping and polyadenylation in nuclear transport
Before termination stage of transcription a GMP cap is added to the 5' end and poly-A tail to 3' end of mRNA.
The link(http://sciencing.com/role-rna-polyadenylation-5434666.html) says:

The poly(A) chain is important for transport of the mRNA from the nucleus where it is synthesized to the ribosomes where protein is translated.

I don't get this point. How does polyadenylation affcts the transportation of mRNA?
Wikipedia says abour capping's functions:

Regulation of nuclear export;
  Prevention of degradation by exonucleases;
  Promotion of translation (see ribosome and translation);
  Promotion of 5′ proximal intron excision.

I don't get how it plays a role in nuclear export.

What research have you done before asking it here?

Actually I read the importance of this activity but didn't understand some keypoints. I will edit it now.

@Mockingbird I really like this as a resource, I think you can start at the subheading Key steps in mRNA processing: http://jcs.biologists.org/content/joces/122/12/1933.full.pdf


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Identifying Some Kind Of Fossil
This was found off the coast of Ireland by a friend of mine. The running gag is it's some kind of fetish or totem and should be immediately discarded, but we're interested in whether it's perhaps a coronal section of a fish skull, a bivalve or something else entirely. Many thanks to anyone participating!
Attachments :
Image-1

(higher resolution)
Image-2

(higher resolution)
Image-3

higher resolution

Mostly speculation on my part but the patterns and configuration look like a sand dollar to me. Likely a species in the order Clypeasteroida.

I've shared a link of this to the EarthScience.SE chat room to see if we can get some geologist eyes on this as well.

looks like the fossil Brachiopod

The best page on the web to find fossil ID experts is: Fossil ID - The Fossil Forum ... There was a molar ID on this forum some time ago, and the fossil forum guys knew what it was the same day.

Coronal cross section of a fish skull to me!

I know this is quite old - but those two oval marks could be limpet home scars

I don't know what kind of fossil is this. But, I can help you with link to website called FossilID, here you just have to fill a submission form and Expert paleontologists will answer you and help you identify this one. Here's the link: https://form.jotform.com/221665322452047 Also, you can try downloading an app called Digital Atlas of Ancient Life. Available both on Apple App Store and Play Store. If you want you can use other online services.

looks like part of an echinoid aka sea urchin skeleton. there is a huge variety of shapes and patterns, especially when you start looking at fossil ones.


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New earliest life found, what are the implications?
So a couple of days ago it was announced that new fossils of microorganisms were possibly discovered around former hydrothermal vents. According to the paper these fossils "are at least 3,770 million and possibly 4,280 million years old" making them the earliest instance of life found so far. If the upper estimate is correct that would mean these organisms existed "only" ~250 million years after the formation of Earth.
Does this discovery shake up any of our previous ideas and/or provide new insights about the earliest life?

One can make a comparison between dating of extremely old fossils but IMO, no one can really answer to the question there new insights to be gained? as this very much depend on your specific interest. In other word, IMO, this part of the question is to broad.

I don't have access to Dodd et al. 2017 that you cite but I suspect they made comparisons with other recent discoveries. As you cite the abstract, you might have not read the paper. You should probably just try to read it.

@Remi.b I don't have access to the paper either :). I mean insights about earliest life/abiogenesis but yes I'll edit the sentence. I'm not so much looking for a copying of the article's discussion but more the scientific consensus on the importance of this find but I'm not sure if that exists yet.

Not a lot, the sample is not conclusively biotic in origin nor is it necessarily much older than known fossils, 3.7 billion vs 3.5 billion. The sample is a few simple hematite filaments, complex hematite filaments do form as a byproduct of oxygen using (aerobic) bacteria, they can also be formed by metamorphic processes. Subscribing these filaments to life and proposing oxygen must have been present far earlier than any evidence supports based on this is wishful thinking at best.
If it were correctly identified and as old as possible it would have only a small effect, it would make finding life on other planets more likely becasue it would mean life forms basically as soon as you have persistent liquid water. It might indicate oxygen earlier than suspected but that seems unlikely.

As I have not read the paper, could you please develop on the sample is not conclusively biotic to include a discussion of their sampling technic? Also, when you say is it necessarily much older than known fossils can you please provide referenced examples to allow a reader to make a comparison?

The OP's own linked articles discuss it. But I will expand.

Nice answer. However, could you add a reference on the different ways these filaments can be formed?

The effect of this hypothetical discovery (because I haven't seen the dating of the rocks yet) is almost non-existent. It just reinforces an idea already present in the origins of Life community for a lot of time-you discover life as soon as you discover solid rocks capable of creating fossils, so Life must have originated immediately after the cooling of the Earth's surface or possibly it simply originated elsewhere in the Solar system and was transported here by meteorites (there is solid evidence for this hypothesis in the ability of bacteria to survive extreme environments). What is important however is the reinforcing of the idea there is some "missing link" in the history of the transition of chemistry to biology which is definitely not in the fossil record!
The fact we can't discover some intermediary complex molecules between the primeval Earth and the bacteria means for most of the scientists that either Life simply "hitched a ride" on some comet or meteorite to come here from some other place in the Solar system it originated (possibly Mars) which in turn would imply that the entire Solar system gave rise to a single "type" of Life and therefore even if we find Life outside Earth it will probably be based on DNA and the central dogma and be too much like our own or that the emergence of Life was so fast it simply can not be by chance! I think the implications of the second case are greater but the first one can make a lot of "noise", too I guess (especially if they find bacteria on Mars and they turn out to be just like those here). I myself, however, am a little bit of an "heretic" here and believe the continuous occurrence of the same fossils everywhere in the ancient geological record (and in meteorites from Mars, too) may indicate a little bit different view of what Life can be defined as. What we are looking here are not evidence of cells, but rather evidence of metabolic products which we (not they by themselves) contribute to cells! Because modern cells can produce such products we assume they are produced by cells! But we don't have cells we can look at under the microscope in those rocks. We have thin bands of material we think comes from cells (it is the same with the Martian meteorites-science in a way becomes a "point of view" which you should consider isn't very "scientific"). But what if these bands were the result of metabolism, but is was not cellular! I myself think this is entirely possible, but most of my colleagues do not even consider this idea. This can easily explain the rise of products of metabolism early on but at the same time give enough time for the complexity of the modern cells to form under the influence of great competition among metabolic pathways themselves, rather than living cells-for which we seem to have direct evidence at a much later period. This hypothesis can also explain why are all the basic metabolic pathways in Life today so conservative (unlike the genes themselves which determine them-what is really more conservative-the gene or its role?) while the proteins coding for them can be coded under different genomic organization-e.g. different structure of the genome in different domains. The place of the gene can change, even to a certain extent its sequence, but what remains the same is their relationship to each other, e.g. their topology to respect of each other in the general graph of metabolism. Why? What if metabolism was more ancient than cells, but the evidence of this "metabolism evolution" was lost in the age before the cell(because there were no cells, no structures, no anything to leave fossils of the metabolism evolution, excepts its waste products (in a way its "coprolites"). I would like to think this evidence supports such hypothesis but again it is just an opinion.
I hope you like this answer.

Your answer is rather hard to follow, are you saying metabolism started inorganically?

Not exactly, actually I am saying what we perceive today as metabolism was the way the first form of life evolved in the beginning of its history. Actually, I (and not only me, of course) put forward the idea of gradual metabolic evolution whose waste products formed what we today find as the oldest fossils of living organisms. I think we don't have enough data to call them results of cellular activity, so they could well be the results of metabolic activity before the rise of cells. If metabolism evolved first, then its fossils can exist even if there weren't cells during that time.


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Would canines that consume the stomach of ruminant prey animals benefit from any of the bacteria and enzymes present in the rumen?
This question is inspired by the growth in popularity of raw diets for pet dogs. Green tripe is a common addition to these diets, with many claims of probiotic benefits.
Here's an example from a site that sells ground, frozen green tripe for pet dogs: http://greentripe.com/
Another article with some of the claimed benefits (I already know there is some misinformation in this article - it claims that dogs don't naturally produce the enzyme amylase, but that is false) http://ivcjournal.com/raw-green-tripe/
Do these claims make sense? I know most of the bacteria in the rumen would die after being exposed to oxygen, but would the rest of the bacteria, fungi, and enzymes present in the rumen be of any benefit to a canine when consumed?
What about after the tripe has been ground, frozen, etc?


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Do all proteins start with methionine?
Start codon AUG also codes for methionine and without start codon translation does not happen. And even the ambiguous codon GUG codes for methionine when it is first. So does this mean that all proteins start with methionine as the first amino acid.

You are correct in thinking that since the translation of mRNA begins with AUG, which codes for methionine, then all proteins should contain a methionine at their N-terminus (aka start site). But, it is indeed not so. First of all, I want to mention about variations in start codon. As you say, AUG is not the only, but actually the most common, start codon, and it codes for methionine in eukaryotes, or formylmethionine in prokaryotes but only at the start site. But, this start codon can also vary and become GUG or even UUG, coding for valine and leucine respectively. And the twist is, it still codes for methionine or formylmethionine1. In rare cases, such as heat shock, other codons like CUG, ACG, AUA and AUU, are also used for initiation 2. It is so because start codon itself is not sufficient to begin translation, other nearby factors, like the Shine-Dalgarno sequence, or initiation factors, also play a role. One such factor is the initiation tRNA. At the beginning of translation, tRNAMet or tRNAfMet binds to the small subunit of ribosome. So, whatever be the start codon, the first amino acid will be methionine3.
Now, coming back to the main question, N-terminal methionine, although being the first amino acid, is not present at N-terminus of all proteins. This is because of a process that is known as post-translational modification. After a polypeptide is completely translated from mRNA, it is modified at different places by different enzymes, which are regulated by different (internal or external) factors. There are more than a hundred post-translational modifications known4, one of which is the removal of methionine from the N-terminus of a polypeptide. N-terminal methionine is removed from a polypeptide by the enzyme methionine aminopeptidase5.
The question which immediately comes to mind is Why are proteins modified after translation? Well, there can be various different causes of it. First of all, post-translational modifications are regulated by many factors, and this process is called post-translational regulation6. Another point is cell targeting. Attaching different groups to polypeptides makes them more stable at their target location. For example, by attaching lipid molecules to polypeptides (in a process called lipidation) makes the polypeptide more stable and suitable for cell membranes4. A yet another factor is increasing stability. Yes, you read it right, in some cases, N-terminal methionine can destabilize a protein! For example, an extra N-terminal methionine not only destabilizes but also disrupts the native folding configuration of $\alpha$-lactalbumin7. There can be numerous other factors too, which promote removal of N-terminal methionine from polypeptides.
Thus, in short, No, not all proteins contain a methionine at their N-terminus. I hope this helps!
References:
 1. Touriol, C., Bornes, S., Bonnal, S., Audigier, S., Prats, H., Prats, A.-C. and Vagner, S. (2003), Generation of protein isoform diversity by alternative initiation of translation at non-AUG codons. Biology of the Cell, 95: 169–178. doi:10.1016/S0248-4900(03)00033-9
 2. Ivanov IP, Firth AE, Michel AM, Atkins JF, Baranov PV. Identification of evolutionarily conserved non-AUG-initiated N-terminal extensions in human coding sequences. Nucleic Acids Research. 2011;39(10):4220-4234. doi:10.1093/nar/gkr007.
 3. Sherman, F., Stewart, J. W. and Tsunasawa, S. (1985), Methionine or not methionine at the beginning of a protein. Bioessays, 3: 27–31. doi:10.1002/bies.950030108
 4. Post-translational modification - Wikipedia
 5. Liao, Y.-D., Jeng, J.-C., Wang, C.-F., Wang, S.-C. and Chang, S.-T. (2004), Removal of N-terminal methionine from recombinant proteins by engineered E. coli methionine aminopeptidase. Protein Science, 13: 1802–1810. doi:10.1110/ps.04679104
 6. Wolfgang Schumann; Wolfgang Schumann (Prof. Dr. rer. nat.) (2006). Dynamics of the bacterial chromosome: structure and function. Wiley-VCH
 7. Chaudhuri, T. K., Horii, K., Yoda, T., Arai, M., Nagata, S., Terada, T. P., & Kumagai, I. (1999). Effect of the extra N-terminal methionine residue on the stability and folding of recombinant alpha-lactalbumin expressed in Escherichia coli. Journal of Molecular Biology, 285(3), 1179–1194. doi:10.1006/jmbi.1998.2362

When ribosomes create peptides, Methionine is the starting amino acid. But, in many proteins, Methionine Aminopeptidases cut it off from N-terminus. This happens in cases when methionine is not required as starting amino acid (not required on N-terminus).
Source: https://en.m.wikipedia.org/wiki/Methionyl_aminopeptidase
I remembered the name of enzyme.


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fast metabolism and law of conservation of energy
Usually if person take more calories with food than he spends, he is gaining weight.
But if he has fast metabolism, his weight stays the same.
Where these calories go? Maybe food is not completely digesting?
PS. How it related to Basal metabolic rate?

"fast metabolism" usually refers to the daily energy expenditure, also known as the metabolic rate (https://en.wikipedia.org/wiki/Basal_metabolic_rate)  Incomplete uptake of nutrients ("not completely digesting") is distinct from metabolic rate. So it sound like your question is whether metabolic rate or nutrient uptake is the key factor?

@Roland, I just want to understand how this metabolism works, why people can stay slim. So you saying that they waste more energy, so they have low energy conversion efficiency?

No, I'm not saying that (and I don't know what you mean by "conversion efficiency"). I'm trying to figure out more precisely what you're asking. If a person has a high caloric intake and does not gain weight, then obviously there is either high energy expenditure ("fast metabolism"), or there is incomplete uptake of nutrients, or both. This varies between individuals. Are you asking for population data / studies on metabolic rate, or on digestion, or ... ?

@Roland, I'm interested in fast metabolism mechanics, how it's actually works in simple terms. About Energy conversion efficiency: https://en.wikipedia.org/wiki/Energy_conversion_efficiency

probably relation with Basal metabolic rate

One known mechanism is how efficient your mitochondria are, or more precisely how leaking your mitochondria membranes are. https://dl.sciencesocieties.org/publications/jas/abstracts/87/14_suppl/0870064

@John, tried to read, but difficult to understand

It is alright, most of mechanisms are still poorly understood but one that is is the the membrane that the ATP pump sits in, it varies in how effective a barrier to protons it is. brown fats cells have mitochondria that leak like a sieve so they they just pump protons endlessly and make very little ATP but in the process make a lot of heat. That's an extreme case but there is some variation in normal mitochondria as well making the more or less efficient at producing a proton gradient to run ATP pumps. How much of an impact this has is still under investigation.

@John, so it's losing some energy by heat? maybe you can write something like this as an answer?


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Loss of nerves in asthma
This site says:

VIP [vasoactive intestinal peptide] nerves are absent in severely asthmatic subjects. Mice with targeted deletion of the VIP gene exhibit histopathologic features of airway inflammation (Said et al., 2010).

So can we consider asthma as a neurodegenerative  disorder?
What will be the mechanism of destruction of nerves if the above statement is true? If the above statement is not correct then how there is reduction in VIP ? I think of two possibilities either VIP is not synthesised in the neurons (Gene is down regulated, if so, by what?) or it is readily destroyed after its synthesis?
Could anyone please correct me?

You also have to consider if the nerves were there to begin with, and whether it's an issue of development rather than degeneration. I think an overarching suggestion is that while asthma is mediated by immune cells, there are other events including neurological that mediate the response. And this is for me a good source, though not recent.


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Can Eskimos be regarded a distinct species from Kalahari Bushmen based on morphological differences & geographic isolation?
I was motivated to ask based on the answer to another SE Biology Question that uses the following argument to conclude that two varients of snake are indeed a different species:

To test whether [Dendrelaphis ashoki and D. girii  were a separate
  species of snake] they (Vogel and van Rooijen, 2011) compared 9
  individuals of D. ashoki with 34 individuals of D. pictus, and found
  statistically significant (p<0.05) differences in five morphological
  characters....

Further:

The authors didn't rely just on morphological evidence: they note that
  D. ashoki, which is found in the Western Ghats, is also geographically
  isolated from other populations of D. pictus, which are found in
  Northeast India, Myanmar and South East Asia.

Minor differences in morphology of a snake: Why designate it a different species?
My question is, why can't we on the bases of an analogous argument conclude that (say) Eskimos & Kalahari Bushmen are, forget the race debate, but two entirely  distinct species?
I mean if "number of infralabials touched by the first sublabial" can count as a legitimate species-distinguishing morpohological factor, then so can heights, eye colors, hair texture, skin color etc. right? And we won't even have to fish too hard to gain statistical significance given how different Eskimos are from Kalahari Bushmen morphologically.
Further, the geographical isolation must have been pretty strong too.

The quick answer is "because not all characters are equally informative". A great example of this is classifying dogs on the basis of their coat colours -- I don't think you'd think of a fawn-coloured chihuahua as similar to a fawn-coloured Great Dane. However, this is a great question for delving into derived characteristics, and I'm hoping someone comes up with a really great, detailed answer!

@Gaurav Thanks for humoring all my questions. To pick your brain a bit more, when you say "not all characters are equally informative" that begs the question (to a layman like me): Informative of what? What's the basic attribute that we are getting down to here? In other words, the "morphology" is means to what end?

@DavidBlomstrom Thanks! Is it though? Then it would be more straightforward but then why do we get so much elaboration & statistical significance testing of morphological differences & geographic isolation?

@curious_cat I may be wrong, but I think the general idea is to look at overall similarity, i.e. over all possible criteria. Of course that's impossible, but I think the traits that are chosen as relevant are those that have been observed to correlate with differences in other traits. So when mammals are defined based on milk or a specific bone shape instead of, say, color, it's not because traits were picked arbitrarily, it's because it was observed that plenty of very different animals share a color and nothing else, but all animals that give milk are also similar in many, many other ways.

@RozennKeribin Thanks. When you talk about features like "animals that give milk" sure that's a substantive criterion. It's at the level of individual species-defining criteria that I'm skeptical. e.g. When two snake species are differentiated on the basis of the feature "number of infralabials touched by the first sublabial" can we be sure this wasn't something picked arbitrarily? Is that a relevant trait for snakes?

@curious_cat "animals that give milk" sounds substantive but does "three middle ear bones"? That's also a criterion for defining mammals. The criteria for defining a clade will obviously get finer and finer as the clade gets smaller, and species are (almost) as small as clades go. The thing about species (or any other clade) is, there is no reason for there to be a single factor that uniquely defines them. All members of a clade will be more similar to each other than they are to any other member of the clade, but that's across all traits overall, not a single one (...).

For example, almost all mammals are land-based... except for cetaceans, but cetaceans are still more like other land-based mammals in way, way more ways than they are like other things. It so happens that you can usually find a trait that does include all members of a clade and excludes all non-members, but it isn't a logical inevitability; it could be that it so happens that all the traits are like "land-based" for mammals, or "four-limbed" for tetrapods. It also means that in the search for "that one defining trait", you might end up coming up with something that looks totally arcane (...)

@curious_cat not because that trait is more important than all the others, but because it's the one that happens to uniquely characterize that specific group, and "number of infralabials touched by the first sublabial" is still easier to work with than "shows up in this cluster of the principal component analysis on these 1024 measured traits".

I think that species delimitation is not a science, or at least not a coherent one. Different fields use different criteria, for practical or historical reasons. For instance, in plants, loads of fertile hybrids exist between species. It seems that botanists do not split based on the traditional biological definition of what a species is: they apparently tend to split more (see the splitters and lumpers notion).
My intuition is that humans are generally interfertile. There even seems to have been interfertility between H. sapiens and H. neandertalensis which have been (or maybe still are?) considered as distinct species. But how are the actual genetic exchanges across the human populations?
In my opinion, if it were proven that genetic exchanges between human populations living very far apart and having evolved very different ecological adaptations (like populations from the arctic and from the Kalahari) were almost reduced to zero, then it would not be absurd to call them different species. Humans would form a continuum that can be considered a unique species (if interfertility is to be taken as a criterion), but with isolated extremes being in the process of forming separate species, somewhat like the extremes of a ring species. Maybe there even is some degree of reproductive incompatibility between very divergent human populations. The thing is that it is not ethically acceptable to experiment with this. We need to rely on "natural" experiments happening. Globalization could potentially tell us in the future, by facilitating encounters between individuals from very distant populations, whether such reproductive incompatibilities exist or not. That said, I doubt that the origins of parents are recorded in a scientifically usable manner when a couple has problems having children.

Thanks. If species definition is not a science is it even relevant to modern biology? e.g. When someone conducts a statistical analysis of a sample of snakes and publishes an article that purports to establish a different species of snake based on some set of distinguishing features like "number of infralabials touched by the first sublabial" is that useful? Or does it just get the guy a publication? Do we make progress by defining  Dendrelaphis ashoki seperate from D. girii?

@curious_cat Giving distinct names to distinguishable subsets of a species is definitively useful. Giving these names species status may not necessarily be a scientific progress, but it can have practical implications. I remember having heard at a conference a case where the issue was whether some particular edible bivalve on the coast of Brazil and Africa was or not a single species. I don't remember the details, but this had implications on whether or not the species could be used in aquaculture or something like that, due to Brazilian environmental laws.

Though globaluzation has/will also increased gene flow :p.

Welcome to the difficult concept called "Species".
Let me ask a simple question are tigers and lions different species?

They look different (Lion is a solid light brown. Tiger is a darker
  brown with stripes. Male lions have a mane. Male tigers do not)
They are socially different. (Lions live in prides. Tigers are
  solitary)
They are behaviorally different. (Tigers climb, Lions do not. Tigers
  love water and swim. Lions do not. Tigers always attack from behind.
  Lioness have elaborate ambushes as they hunt in groups.)
They live in different environments (lions in Savannah, Tigers in
  forest)
They rarely interbreed.
Yet when they do...tiger-lion offspring are viable. The males are
  sterile. But the females are fertile. So gene flow between the two
  population is possible although limited.

So are lions and tigers different species?
This is the problem with the concept of species.
A lion and tigers are clearly different species of animal.... but why? Is it because they look different? Because of historical reasons? Perhaps because they cannot freely interbreed. Or is because they do so rarely or with difficulty?
If yes, to rarely... how difficult/rare does it need to be for it to be a different species not not simply different populations?
Biology as a field has not come up with a comprehensive answer. The botanist have their own criterion (Because plants can tolerate polyploidy relatively and thus make hyrbid easily). The microbiologist have their own (because DNA can move from wildly divergent bacteria very easily). And so forth.
As to your question (paraphrased) "why scale structure and not hair colour?"
Not all biological traits are equal in the ability to change. Some traits are virtually impossible to change (number of limbs) while others are relatively easy (fur colour).
The reason boils down to the genetic programming of those traits. How interdependent one trait is with other traits. So an extra set of limbs... would also require changes in the brain to control said limbs, it would also change the walk cycles of body for a 4 now 6 legged animal. etc.
Hence traits like fur color is not useful as it changes easily with the time.
Thankfully, we now have genetic testing... and we can determine the degree of genetic flow between two populations to help make the final call if a population is one species or possible two or more.
But genetic testing takes time and a lab. So if there is some visual aid that would be helpful in the field. And these is where counting scales comes in.

Thank! Compelling explanation. What is your opinion on the alternative: We keep speciating on minor differences because it gets people publications and taxonomists a way to justify their existence?

The best I alternative I like, is that two species is defined as two population having biological or behavioral barriers that limit gene flow between the two to a level below Y% per generation (And there is big debate of how much Y should be). However... this definition would make every cell of some bacteria (which rarely exchange DNA or mate) different species. So it does not quite work either.

I like this quantitative approach you mention but it will be a cataclysmic change in the current taxonomy I am sure. Taxonomists won't like a DNA-based definition, right? It would put them out of business. The scale-counting on snakes would become redundant.

Actually they are slowly going out of business as it were. DNA based definition is moving in. This is why we now consider the orangutan to be 2 species even when morphological they look nearly the same. The problem with a DNA based definition is that it was very expensive to do until very recently for a single genome. Far outside the budget of most labs. Probably still is as you have to genome sequence not one animal but a population. Funding to study a specific plant or animal species is also very limited. So counting scales if backed by DNA sequencing (even if limited) would have its place.


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Subset of Protein Crystal Structures (from PDB)
Is there a well-accepted subset of the Protein Data Bank set of protein structures that:

Has only "high quality" structures (may be differing metrics of this; e.g. resolution, size, or structural completeness)
Has minimal redundancy (e.g. nothing with exact sequence identity from the same species)
Is still as large as possible, spanning as many molecules and species as possible
[Optionally but better] Is not too biased (e.g. certain classes of proteins are highly over-represented in the PDB)

It is possible to download the entire PDB and make up rules for myself, but this seems like something people might have already considered reasonably extensively. I'm hoping for a dataset I can just download and cite, in the best case. :)

Richardsons' Lab has a top8000 list.
See their paper from 2016.
They also have top500 list, but it hasn't been updated for many years.


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Why African species are larger in size compared to other parts of world?
Why are African species larger in size compared to other parts of world?
Best Example: African elephants are very famous for Giant ears.
So many African Animals listed in Guinness World of Records. (Source)

When it comes to mammals this cannot really be evaluated without taking the Megafaunal mass extinction into account. This mainly refers to the extinction of large mammals from the Pleistocene Megafauna, which affected different parts of the world differently. More species were extinct in the Americas, Australia and northern Eurasia, and fewer species in Africa and southern Asia. One of the reasons for the differential extinction is thought to be the shorter evolutionary history together with humans in the areas that were more affected (since over-hunting is though to be one of the main explanations, see e.g Sandom er al. 2014).
If you only look at currently extant animals, you ignore the Wooly mammoth, the Woolly rhinoceros, Ground sloths and many other large species inhabiting higher latitudes, and this will give a very biased picture when searching for evolutionary reasons for the differences in body size between continents.

The organisms listed in the question (elephant and the snail) are found in warm tropical regions (Africa is not completely hot continent 1). The organisms dwelling in tropical region shows adaptation for loosing excess heat by having longer extremities. This is known as Allen's rule 2.
This explains larger ear of African elephants.
In case of snail, probably it has to be vast resources which are available in tropics. The large amount of resources would cause a larger population to exist, resulting into more competition. The larger size of snail must be conferring increased fitness to snail.

But India & adjacent areas that are home to the smaller-eared Indian elephant are also warm tropical areas.

@jamesqf: Well that is true. In fact Asian animals are bigger than African animals. For example one horned rhinoceros is the biggest of all. Small size of Indian elephant could be due to several probable reasons:

Indian forests were quite dense and hence in order to move through the forest, the evolution favoured the small sized elephant

Continued....
2) India was densely civilized with great kingdoms and tribe and they hunted big and fierce animals which led to selection of small sized elephants on Indian subcontinent.

I was really just thinking about the size of the ears :-)  But there are two distinct species of African elephants, the large bush elephant (Loxodonta africana) and the much smaller forest elephant (L. cyclotis), with the Asian elephant (Elephas maximus) being intermediate in size between them, so there must be more at work than just climate.

@jamesqf Well in that case there is this circumstantial evidence (and we know these circumstantial evidence are only sometimes right) that forest species are shorter for easy movement.

But then we might have expected the Asian elephant to have evolved down to about the size of a deer, or the now-extinct dwarf elephant species that lived on Mediterranean islands.

@jamesqf Yes that may happen (can't deny possibilities in evolution). But evolution (which is dependent on fitness) is directed by many forces. In case of Asian elephant, the access to resources were ample and that encouraged increase in body size at the same time a very large size would hamper movement. This resulted into size of present day Asian elephant.


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Is female the default sex in humans?
I was taught in school that female is the default sex in humans based on the following logic:

Development into a human male requires the activation of the SRY gene in the foetus. If that doesn't happen (because there is no Y chromosome, or for some other reason) then development into a female occurs.

For historical context on the use of the term default, please see this article:

Female sexual development ... was thought to proceed as a “default” in the absence of Sry.
The English word, “default,” means “failure to act; neglect” or “a preselected option adopted […] when no alternative is specified” (Oxford English Dictionary, 2011). In the case of sex determination, “default” became the prevailing model for female pathways—i.e., an ovary results in the absence of other action...

Is it reasonable to say that female is the default sex in humans? If so, is the SRY gene all there is to it?

What if I say the same thing about FOXL2?

In the same vein you could argue humans have tails by default as embryos develop a tail before white blood cells break it down again. It really depends on your perspective in my opinion.

If a whole bunch of genes didn't activate in proper order in the human foetus it would result in abortion or stillbirth. Is the default state of humans inviability?

Please define what you mean by “default sex”. Despite the extensive answer by @canadianer the term by itself does not mean sufficient to me to be the basis of a discussion. It is not clear to me whether you are asking any more than whether it is true what you were taught about the SRY gene at school. Too many questions on this list end up as semantic arguments because of imprecise formulation.

I think the answer is Yes, the difference between male and female is that females can reproduce, it easier to not do something than always doing all the work, so genetically, males are a subset of a female without the reproductive features.

Summary:
The idea that primary sexual determination defaults to female was proposed several decades ago and is primarily based on the observation that, in the absence of Sry, ovarian development takes hold. However, more recent models suggest that both ovary and testis development require complex genetic regulation and neither can really be said to occur by default. Furthermore, maintenance of sexual determination is apparently a life-long process.

Quote from a Review (Yao 2005):

We have just begun to glimpse into the mechanisms underlying ovarian development. Convincing evidence challenges us to reconsider the existing paradigm that describes ovarian development as a default system. The default concept was first proposed in the early 1950s when Jost performed the groundbreaking experiments to demonstrate mechanisms of sex differentiation of reproductive tracts (Jost, 1947, 1953, 1970). The term “default” was not originally intended to describe the developmental status of the ovary. Instead, it is referred to the female reproductive tract or the Mullerian duct based on the fact that the female reproductive tract forms in both XX and XY individuals in the absence of gonads. Indeed, now it has become evident that early ovarian development is an active process involving intrinsic cell fate decisions and complex crosstalks between germ cells and somatic cells. Most intriguingly, the appearance of testicular structures in XX individuals where Sry and its downstream components are absent further raises the improbable question: Could the testicular development be default after all?

Some Details:
Sex determination in mammals involves the development of a bipotential gonad into either a testis or ovary. Sertoli cell differentiation and thus testis formation is under the control of the regulatory gene Sry (Koopman et al. 1991). The Sry gene product was later shown to upregulate the expression of Sox9, which is key in testis development (Sekido and Lovell-Badge 2008). On the other hand, ovarian development is centered on β-catenin stabilisation by WNT4 signalling, which is thought to inhibit Sox9 expression (Bernard et al. 2012). Because Wnt4 is expressed basally in the genital ridge and testis development apparently depends on Sry expression, the ovarian pathway has often been described as default; in other words, the pathway that the gonad would take in the absence of Sry.
However, ovarian development is in fact an active process requiring the correct balance of many factors, including a transcription factor called forkhead box protein L2 (FOXL2) (Yao 2005). Studies in mice showed that Foxl2 is expressed in the ovary, both during development and in adulthood. Knockout of the gene prevented granulosa cell differentiation during development, leading to ovarian failure (Schmidt et al. 2004) and increased expression of markers for the testis development pathway (Ottolenghi et al. 2005). Furthermore, mutations of this gene are responsible for XX sex reversal in goats (polled intersex syndrome, PIS) (Pailhoux et al. 2001). Taken together, these experiments indicate that Foxl2 is required for ovarian development and that its absence can favour testis formation.
Many developmental process are dependent on correct timing of gene expression. Sry, particularly, must be expressed within a specific time interval or ovarian development will take hold (Bullejos and Koopman 2005; Hiramatsu et al. 2009). Research by Uhlenhaut et al. (2009), however, shows that this is not necessarily the case for Foxl2 mediated ovarian development, maturation and maintenance. A homozygous floxed Foxl2 mouse strain that expresses Cre under tamoxifen induction allowed conditional knockout of Foxl2. Three weeks after induction, cells of the ovary had transdifferentiated, adopting a morphology and gene expression pattern consistent with Sertoli and Leydig cells (which are normally found in testes). Notably, Sox9 expression increased drastically. Immunostaining showed that, while Foxl2 expression expectedly decreased after Cre induction, the increase in Sox9 was not observed until a day later, indicating that the expression of both is mutually exclusive and that FOXL2 may directly regulate Sox9.
This research presented a novel model for the maintenance of female ovary differentiation. During primary sex determination in females, activation of WNT4 signalling stabilises β-catenin allowing expression of female specific genes and the inhibition of Sox9 (Bernard et al. 2012). In adulthood, FOXL2 actively represses Sox9 expression in gonad cells, maintaining the granulosa phenotype. A similar model of maintenance has been proposed in males due to evidence that the loss of the transcription factor Dmrt1, which normally represses (and is also repressed by) Foxl2 expression, induces transdifferentiation of male mouse Sertoli cells to granulosa cells (Matson et al. 2011). In the case of both males and females, primary sex determination is not just a process that occurs during development but rather requires active regulation for the duration of adult life. This involves collective antagonism between various female and male sex determining factors, including Foxl2 and Dmrt1, and may dispel the notion that ovarian development occurs by default.

Further Reading:
The Genetics of Sex Determination: Rethinking Concepts and Theories
Genetics of sexual development: a new paradigm (Blecher and Erickson 2007)

References:
Bernard P, Ryan J, Sim H, Czech DP, Sinclair AH, Koopman P, Harley VR. 2012. Wnt signaling in ovarian development inhibits Sf1 activation of Sox9 via the Tesco enhancer. Endocrinology 153:901–912.
Blecher SR, Erickson RP. 2007. Genetics of sexual development: a new paradigm. Am J Med Genet A 143A:3054-68.
Bullejos M, Koopman P. 2005. Delayed Sry and Sox9 expression in developing mouse gonads underlies B6-YDOM sex reversal. Dev. Biol. 278:473–481.
Hiramatsu R, Matoba S, Kanai-Azuma M, Tsunekawa N, Katoh-Fukui Y, Kurohmaru M, Morohashi K-I, Wilhelm D, Koopman P, Kanai Y. 2009. A critical time window of Sry action in gonadal sex determination in mice. Development 136:129–138.
Koopman P, Gubbay J, Vivian N, Goodfellow P, Lovell-Badge R. 1991. Male development of chromosomally female mice transgenic for Sry. Nature 351:117–121.
Matson CK, Murphy MW, Sarver AL, Griswold MD, Bardwell VJ, Zarkower D. 2011. DMRT1 prevents female reprogramming in the postnatal mammalian testis. Nature 476:101–104.
Ottolenghi C, Omari S, Garcia-Ortiz JE, Uda M, Crisponi L, Forabosco A, Pilia G, Schlessinger D. 2005. Foxl2 is required for commitment to ovary differentiation. Hum. Mol. Genet. 14:2053– 2062.
Pailhoux E, Vigier B, Chaffaux S, Servel N, Taourit S, Furet JP, Fellous M, Grosclaude F, Cribiu EP, Cotinot C, et al. 2001. A 11.7-kb deletion triggers intersexuality and polledness in goats. Nat. Genet. 29:453–458.
Schmidt D, Ovitt CE, Anlag K, Fehsenfeld S, Gredsted L, Treier A-C, Treier M. 2004. The murine winged-helix transcription factor Foxl2 is required for granulosa cell differentiation and ovary maintenance. Development 131:933–942.
Sekido R, Lovell-Badge R. 2008. Sex determination involves synergistic action of SRY and SF1 on a specific Sox9 enhancer. Nature 453:930–934.
Uhlenhaut NH, Jakob S, Anlag K, Eisenberger T, Sekido R, Kress J, Treier AC, Klugmann C, Klasen C, Holter NI, et al. 2009. Somatic Sex Reprogramming of Adult Ovaries to Testes by FOXL2 Ablation. Cell 139:1130–1142.
Yao HH-C. 2005. The pathway to femaleness: current knowledge on embryonic development of the ovary. Mol. Cell. Endocrinol. 230:87–93.


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What is the proper pronounciation of the scientific name of the ground elder / Aegopodium podagraria?
A audio sample would be great. As a kind of bonus: I would appreciate a kind of database, which contains a lot of botanical plant names.

I'm voting to close this question as off-topic because  it is only about language/pronunciation, not biology. Also scientific species names are pronounced very differently around the world. The only "proper" pronunciation would be the original latin/Greek, but then this is a question about those specific languages.

@fileunderwater for me it is part of biology when you are able to communicate in a proper way to the community. It's like asking for information around biology, like literatur. And I think the probability that question got be answered, is higher in biology.stack exchange as in english- latin- or oldgreek.stackexchange. proper means for me that somebody can understand, to get a idea how it sounds like. thanks for your thoughts.

Here is a american database which offers sound samples for a lot of scientific plant names.

for me the question is now answered. and i will close in 2 days when stackexchange allow me to do. but anyway other sources are still welcome.