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How did butterflies evolve to have eyes on their wings?
Some butterflies, such as the UK native Peacock butterfly (Google Image Search) have markings on their wings that look just like eyes, complete with a white fleck to imitate a convex, transparency effect, as though the "eye" is reflecting sunlight.
Presumably, this pattern is designed to deter prospective predators, because the predator will see a creature with massive eyes looking at them and think twice before attacking.
But how did the pattern evolve?  Was the first one a fluke / a genetic mutation that happened to work, or is there another explanation?
For possible bonus points, is there any way of telling when this occurred, and therefore making a guess as to which creature's eye is being imitated?

All evolution is due to random changes which are selected for. Change is random, selection is not.

Kahn Academy does an amazing job at this one: Introduction to Evolution and Natural Selection

@Armatus love Kahn Academy

There has been quite a bit of study on the development of eyespots. How did they evolve is still unclear, but several experiments have elucidated the molecular mechanisms underlying their formation.
The Wikipedia page about eyespots gives a good basic introduction and some interesting references.
So, first of all, how does an eyespot form?
During the development of wings, eyespots arise at specific locations called foci (singular focus).
If you take cells from a focus in a developing wing, and transplant them into another region of the wing, an eyespot will develop at the transplanted site.

Adapted from: Pattern Formation on Lepidopteran Wings: Determination of an Eyespot - Nijhout, Dev. Biol, 1980
The photo on the left is a normal wing from an adult Buckeye butterfly, Precis coenia. In the middle and right photos, some cells of the big eyespots have been transplanted in a new position during development. As you can see, a third eyespot develops. Note that the middle photo is from an autograph, that is, the cells were transplanted on the same wing. This results in a shrinkage of the normal eyespot. In the right picture, instead, cells were transplanted in another individual, and this does not result in shrinkage of the eyespot.
The authors conclude that:

It is evident from these experiments that the development of the large eyespot on the forewing of Precis coenia depends on the presence of a small group of cells that lie at or near its center. This group of cells corresponds to a "focus": a small region, occurring in each wing cell, that is postulated
  to be responsible for the induction of most color pattern elements in butterflies and moths (Nijhout, 1978). Cautery experiments establish an upper limit for the size of this focus in the neighborhood of 300 epidermal cells, though it is probable that the actual size of the focus is much smaller.

They further speculate that a specific morphogen may be involved:

The response of the eyespot pattern to cautery or transplantation of the focus is most readily interpreted if we assume that the focus is the source of a morphogen that is somehow able to induce synthesis of specific pigments.

The idea that a morphogen was involved has been confirmed in later years.
From: Development, plasticity and evolution of butterfly eyespot patterns - Brakefield et al., Nature, 1996

The focus is proposed to be a signalling source for a morphogen, the levels of which determine the pigmentation of surrounding cells. Recent investigations have indicated that regulatory genes, such as the Distalless homeobox gene, are specifically espressed in the eyespot focus.

During the development of the wing the expression of the Distalless (Dll) protein (shown in green in the picture) corresponds to the location of the future eyespots.
Several mutations exist that will provoke changes in the eyespots patterns. Some of this with the evoking names of Cyclops, Spotty and Bigeye were analysed in the paper.
Now, without going much into insects genetics (which is far from being my domain of interest), you can clearly see that, although the number, position and size of the foci are affected by the mutations, their position always correspond with an increased expression of Dll during development.

Left column: ventral hindwing patterns of a wild type (top), Cyclops (middle) and Bigeye mutants. Right column: forewing pattern in a wild type (top) and Cyclops mutant (bottom).
From the conclusion of the paper (bold mine):

The selection experiments on B. anynana rapidly produced dramatic differences in eyespot size which were due to genes of small phenotypic effect. The mutants described here show that genes also exist with large phenotypic effect on eyespot development (including size) that have no perceptible effect on other wing or body patterns. It is likely that the evolution of eyespot patterns in nature involves both genes with large and small effects on eyespots development. [...]
  These observations suggest that the regulation of the eyespot developmental pathway is such that eyespot patterns can evolve rapidly and independently of other wing-pattern elements and body structures.

Finally, another interesting read is:
Wings, Horns, and Butterfly Eyespots: How Do Complex Traits Evolve? - Monteiro and Podlaha - PLoS Biol., 2009
where the authors propose that:

Complex traits require co-ordinated expression of many transcription factors and signaling pathways to guide their development. Creating a developmental program de novo would involve linking many genes one-by-one, requiring each mutation to drift into fixation, or to confer some selective advantage at every intermediate step in order to spread in the population. While this lengthy process is not completely unlikely, it could be circumvented with fewer steps by recruiting a top regulator of an already existing gene network, i.e., by means of gene network co-option. Subsequent modifications of the co-opted network could further optimize its role in the new developmental context.

Please note: I am not an insect development expert, so I may have missed some important paper/evidence etc. If you know some more that are worth citing please do!

You're correct with the genetic mutation bit. A basic explanation would be:
Some gene or genes became mutated that lead to the coloration you see, and the end result was that the butterfly or butterflies with the mutated gene were able to produce more offspring or offspring which survived better than the eyeless versions.
There are ways of dating genetic mutations by comparing one organism's genes to another, but accuracy can be an issue without some significant genomic study to confirm mutation rates and other aspects.
However, the butterfly wouldn't be purposefully imitating another creature's eye. It may be by chance and/or predator behaviors that the eyespots look like the eyes of another creature, but the adaptation wasn't a willful act. It was a random genetic mutation or mutations that lead to beneficial coloring, and the eyespots may have improved over time as more mutations occurred.

Is it possible that the butterfly could have been wilfully imitating another creature's eye, but that the conscious part was genetically mutated out later on?

Possible? I suppose it's possible.
However, the likelihood is zero. The chain of mutations and lack of evidence of similar behavior by other butterflies is a Sysiphisian mountain to overcome to prove it happened.
The easiest explanation, and the one observed in nature, is that a mutation causes unique coloration. Over time, the butterflies which have the coloration closely resembling eyes are left alone, while those that aren't get eaten - instantly taking them out of the gene pool and leaving only the ones with eyespots.
Much, much, much easier.

Good old Occam and his Razor.

I read above ;
''Some gene or genes became mutated that lead to the coloration you see, and the end result was that the butterfly or butterflies with the mutated gene were able to produce more offspring or offspring which survived better than the eyeless versions.''
But, for the genes to mutate randomly, an eye would not form, but a mess.
Further,  how strange it is, that neither the butteryfly nor the genes are able to see this manifestation. Yet any preditors, from above sees it clearly.
To apply that this random mutation and natural selection, makes up everything that we know, is in itself blind and calls for an eye.
I will state, it is positive variation and nothing more nothing less.
No lifeform goes downhill in terms of evolution. Random anything would render any 'random' lifeform , lifeless.

An eye doesn't need to form with the first mutation. If any marking gives an advantage over non-marked butterflies, that would be sufficient. Then natural selection would refine the mutations to an eye-shape. Evolution acts over multiple generations, always. The butterflies don't have to see what gives them the advantage - as long as an advantage is given, that's enough. I have no idea what you mean by "positive variation," and there's no such thing as "downhill" in terms of evolutionary biology - only better able to survive or less able to survive. Your last sentence is also meaningless.

But, for the genes to mutate randomly, an eye would not form, but a mess: do you have proof of that? An eyespot is a fairly simple round pattern, is not such a complex thing to encode.

You just delivered some pretty opinionated statements. What knowledge/science/evidence are you basing them on? Could you please provide references?

@MCM - you said 'If any marking gives an advantage over non-marked butterflies, that would be sufficient. Then natural selection would refine the mutations to an eye-shape'. I am sorry, but here you are inferring 'direction' via natural selection. Please, explain how nature performs this selection. The mechanics behind it please?

@Nico . An eyespot is geometric, geometric is nothing to do with random. That it should resemble an eye, is enough to suggest it is intended to be a 'fake' eye. Please afford me some evindence, of your mathematical formula, which acts on random operations, to form geometric patterns?

@Lubo I am basing them on mathematics. No mathematical formula exists which can operate on random numbers, to form complex organic geometric patterning. Please, can you prove i am wrong?

@user1310: I never mentioned any mathematical formula... you are the one who should provide references for your assertion that a pattern cannot arise from a random mutation. Anyway I will be writing a bit more detailed answer (should probably have time tonight), but essentially eyespots form because of gradients of homeogenes, there is quite a bit of literature at this regard.

@user1310: Directionality can occur in evolution, it's just not willfull direction. Say the first mutation creates an amorphous dark blob which survives better than the previous phenotype. Then another mutation occurs where the dark blob gets more circular, and that phenotype survives better than the amorphous. Continue in that vein until you have the current eyespot phenotype. As soon as the eyespot is no longer advantagous, another mutation could enter the population and produce another phenotype.

@user1310, again you make a statement without proof, and you happen to be spectacularly wrong. Fractals generate the exact type of patterns that you are referring to, and I refer you to the Wikipedia entry: Fractals. BTW, this is Q/A site, not a debate site, so if you have some knowledge to share, please provide the source of your assertions - a publication, well-known theorem, whatever.


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Human evolution: Where *exactly* did the first human come from, whose parents were not?
Layman here. So I have never really quite understood this facet of human evolution, (or any other for that matter), in that, I understand the evolutionary process, but I get lost on the 'border' cases.
For example, we, as humans, evolved from monkeys, (to use the colloquial term, I am not a biologist by any measure).
My question is, doesn't this mean that at some, discrete point, there had to have been a human, whose parents were not? If that is true, how does that work, in the sense that we now have species1 giving birth to species2.
If not, then how exactly does this border case work? The only other alternative I see, is that the borders are 'fuzzy', but then that necessarily means that the definition of a species is itself fuzzy, which I understand is not the case.
Thanks!

Take a bucket of blue-dyed water and start slowly pouring yellow-dyed water into it. Is there a discrete point at which it becomes green?

@RussellBorogove Interesting - please see my comment/question to Konrad on this matter though.

My two cents in addition to all these wonderful answers: The spectrum of phenotypical/genetic/epigenetic variation is always there, until natural selection hits the continuum and breaks it in to pieces (species) by destroying "unfit" elements in this continuum.
I may be dead wrong though, I'm no expert on evolution (aside from causing evolution to Pens/strep resistant bacteria in my incubator, that is. :) )

For a review of the definition of species (with application to human) have a look at How could humans have interbred with Neanderthals if we're a different species?.

Actually, your last paragraph is more the case than not.
There are currently three common definitions for delineating discrete species:
1) Phenotypically different from related species (looks or acts differently).
2) Produces viable offspring in the wild.
3) Some % of genetic difference.
There are strengths to all three:
1) Very easy to ascertain and measure.
2) Most common conception of a species.
3) Genes control the first two, so genetic divergence gets to the heart of the matter.
There are also weaknesses to all three:
1) Is notorious for mis-labeling and missing species.
2) Some species which can mate and produce fertile offspring under enclosed conditions do not do so in the wild (Tigers and Lions, for instance).
3) The amount of divergence has, thus far, been completely arbitrary. If there is a certain % or patterns of mutation required in the genome, science hasn't yet discovered it.
The fuzzy definition of species, combined in the not-exactly-intuitive generational-type thinking required for understanding evolution, and the answer to your question is (at least to the best of my understanding) the following:
Yes, at some point one of our ancestors gave birth to the first Homo sapien that was somehow genetically different from its parents. However, the magnitude of the difference is probably not as great as you might think.
We've already observed our closest evolutionary cousins, the Bonobos, making basic tools through flint napping: http://www.newscientist.com/article/dn22197-bonobo-genius-makes-stone-tools-like-early-humans-did.html
It's also possible that disputes between male chimpanzees are mediated by an older female: http://www.cpradr.org/Resources/ALLCPRArticles/tabid/265/ID/121/Primates-and-Me-Web.aspx
And that both Chimpanzees and Capuchin monkeys can be taught the concept of currency (which, somewhat comedically, they then used for prostitution): http://www.nytimes.com/2005/06/05/magazine/05FREAK.html?ei=5090&en=af2d9755a2c32ba8&ex=1275624000&partner=rssuserland&emc=rss&adxnnlx=1118160068-1EGJuan4FJH1LooxHYd5/g&pagewanted=all
Then there's the everlasting impact of Koko, the Silverback Gorilla who was taught - and perfectly capable of replying in - sign language: http://en.wikipedia.org/wiki/Koko_%28gorilla%29
The idea that humans jumped onto the scene with unforeseen amounts of intelligence and capability probably isn't what happened. Obviously we are capable of constructing and using the most advanced tools on the planet, but this is after several thousand generations of innovation. The very first human might have been more intelligent (or at least had the capacity to be), but otherwise probably fit in pretty well with its parents and other relatives since the vast majority of what we learn comes from our parents and personal experience.
Then over time the number of individuals with the capacity for higher modes of thinking increased as a result of the genetic inheritance of whatever mutation created the first human. The first human, to put it simply, was successfully able to pass on their mutation which gave them our unique traits, and their offspring were also successful - until you have an entire population of humans living amongst each other. Eventually our innovative capacity lead, step by step, to our dominant position on the planet.
Even now humans are yet evolving. Lactose tolerance (the ability to consume dairy products after childhood) is a very new trait among humans (and unprecedented among all mammals) only a few hundred generations old (roughly 10,000 years) that evolved twice in separate populations of humans (North Africa and Northern Europe). Our jaws are getting progressively smaller (which is why some people have to remove their wisdom teeth to maintain a straight smile - and some people don't have wisdom teeth at all), some muscles are disappearing (the Palmaris Longus is one example - it's present in about 80% of humans), and other subtle changes are occurring.
Just don't make the mistake of equating "evolved" with "superior." Evolution is dictated by the ever-changing demands of the environments we find ourselves in, and what's beneficial today isn't guaranteed to be beneficial forever.

Thank you, but let me understand you. You are saying that yes, there had to be a discrete point in history, where the first homo-sapien, was literally, born to parents who were not homo-sapiens? 1) What species were those pre-homo-sapien parents? 2) Was there just one instance of this first-homo-sapien being born? A figurative 'Adam'? Or were there multiple first-homo-sapiens being born at around the same time to different parents throughout the tribes/groups etc? 3) If (2) is true, why/how the sudden convergence of many homo-sapiens being born at the same time?

Are you also saying that even though those first-homo-sapien(s) were in face human and their parents were not, they most likely didnt act that different from their parents? In that, they had the capacity for everything we take humans for granted today, but this capacity was never used? 5) Silly question but I have to know, if they were humans and their parents were not, how did they look relative to their parents? If their parents were not human, but the offspring was... wouldnt their parents be hairy apes and the offspring not so hairy humans? Not being facetious, serious question! :-)

Don't want to be pedantic but Homo Sapiens is singular, no need to take off the s when talking about one (also because that is not the way plurals work in Latin). On a separate note, you may want to have a look at the Wikipedia pages for Mithochondrial Eve and Y-chromosomal Adam

It's hard to know for sure. It doesn't help early humans interbred with other close cousins, like Denisovans. The species prior to Homo sapiens (thanks Nico) may have only existed for a very short time and may not have left any records. 2) Probably, as genetic mutations are passed linearly from parent to child. However, the mutations could occur twice, though it is unlikely. As Nico points out, we have, indeed, found a "Mitochondrial Eve". 3) They weren't born all at once. The population most likely gained numbers steadily over generations. Humans generally follow exponential growth.

They probably acted like their parents because that's all they knew how to do. The capacity for creative problem solving probably came in handy, which is why they lived long enough to reproduce. However, it was probably later humans which really got the ball rolling is what I meant. 5) Probably pretty close, again. You're assuming, however, the parents were more ape-like than human-like, which wasn't the case. You would probably mistake them for humans if they were alive today! While apes are our closest living cousins, there's still MILLIONS of years of divergence. Lots of time for change!

@MCM As a guy constantly looking for more sound evidence I was very excited at first when you brought up another ancestor with signs of tool-making: "bonobos". In context, you were mentioning just prior to that about the homo sapien being different from its parents, and I thought perhaps I was going to find that Bonobos was a new addition to our fossil record. It was a bummer to find that you referenced a modern life-form and called it our ancestor instead. That's a non-sequitor. Please refrain from making incorrect logical links like this because it's hurting support for evolution. :(

@Jim - I didn't call them our ancestors. I called them our 'closest evolutionary cousins' as the species we evolved from are now extinct (although they did use tools as well - but we've known that for some time).

Bonobos are no closer to us than other chimpanzees

It's a mistake to say "humans" were born from "non-humans" and then  compound the mistake to say lots of "humans" all appeared in one generation. This is biology ala Marvel Comics. Much better to go with the spectrum analogies.

@NickKeighley - Humans were born from non-humans, but I specifically addressed why saying that is an issue in the first half. We call ourselves human, but defining a single "species" is extremely difficult on on a small scale. Yes, the spectrum is a better analogy that has more upvotes. :) Also, I didn't say that lots of humans appeared in one generation. I said the advantageous traits were passed on through many generations. Thanks, though. :)

words are discrete terms used to solidify an unending spectrum of meaning. like colors, blue, red, green, where does one stop and the other begin. you should understand that all words you use have different limits in the range of things they describe in different languages. that is why i feel this is an amator question.

but I get lost on the 'border' cases.

Not surprisingly, since there are no borders, and this is probably the greatest misunderstanding: Evolution is gradual. It’s not generally possible to say where a complex feature (or a species) starts and another one ends. We could in theory say, for individual mutations on the genetic level, in which generation they first occurred, or when they became fixed in the population. But we cannot infer from these atomic changes where our ancestors started becoming humans. So the whole concept of “first human” is not biologically meaningful.
The best analogy remains a gradient between two colours. Going from the left, where does blue end and red start?

By the way, you spotted this very well by yourself:

[if there is no first human] then that necessarily means that the definition of a species is itself fuzzy

Exactly, that’s the case. For more details on definitions of species, refer to MCM’s answer. But it’s indeed crucial to note that the definition of species (or any other biological classification) is an ever-changing approximation which tries to fit a definitive yes/no answer onto a gradually changing scale.

Hmm, interesting... but then let me pose the question in a different way... what distance between any two colors on this scale, when mated together, cannot give an offspring that can then reproduce?...Do you see what I am asking? What is this minimal distance? Perhaps this is then the true measure of 'specieness'.

There's no hard-line rule for that either. There are a large number of genetic and developmental factors that influence reproductive viability. You can have two closely related "species" that actually can interbreed successfully one in a thousand times. You can also have two members of a single species population that can't successfully interbreed. How many species are represented by a lion, a tiger, and a fertile female liger? (http://en.wikipedia.org/wiki/Liger)

@Mohammad Excellent question. Unfortunately, Russel’s answer is spot-on. For instance, some species of dogs cannot inter-breed simply because of size differences, not due to other genetic incompatibility. Some species of crickets could inter-breed but aren’t sexually attracted to each other due to different mating calls. Some species, such as the Larus gulls (technically, all one species) can both inter-breed with a third, but not with each other.

@KonradRudolph Perhaps I have phrased it badly - let me rephrase, de-emphasizing reproducibility - What is the minimal delta of distance between colors we might chose, so as to maximize delta, with the constraint of producing a viable/compatible 'all around healthy' resulting offspring? What is the distance at which the resulting offspring might still result in qualities of some respectibility, VS where this respectibility completely breaks down in some coarse optimality space? (Let us just use humans in this gedankenesperiment).

@KonradRudolph For example, if I was to take a human, and mate it with the first proto-mammal - I do not think that I would get anything worthy out of it. (Red on blue). In contrast, what if I mated a modern human with one from 1000 years ago? 5000 years ago? 50,000 years ago? 250k? Where does it start to break down?

@Mohammad I had understood the question but the answer remains that 1. we do not know, and 2. it varies. Concerning your specific example, it’s not even known whether humans and chimpanzees (not ancestors, but closely related species) could produce viable offsprings. Many biologists are convinced that they could, even though their chromosome numbers are different. Of course, this is an impossible, because unethical, experiment. Mating modern humans with 250kya ancestors would almost certainly work.

There are points where speciation is final and abrupt though, aren't there?  I'm thinking of large chromosomal rearrangements and fusions.

@shigeta I’m uncertain – a single individual with a mutation does not a species make. That said, speciation can be fairly abrupt simply because (separated) subpopulations have to respond to sudden changes in environment.

I was just remembering that Mules (products of donkey and horse matings) are viable while both parents have different chromosome counts, so there has to be some forgiveness there.

There are cases of abrupt speciation, I think, when chromosomes are duplicated in a hybrid that would otherwise not be able to reproduce sexually. The duplication restores the ability to form viable gametes (the chromosomes can now form pairs during meiosis: http://en.wikipedia.org/wiki/Meiosis#Prophase_I). This is documented in plants, where vegetative reproduction allows survival of a sterile hybrid population until chromosome duplication occurs.

There are, of course, plenty of examples where different species in a genus can interbreed and produce fertile offspring.  The most familiar is probably the dog genus: dogs, wolves, coyotes, and other species all interbreed: https://en.wikipedia.org/wiki/Canid_hybrid

Ernst Mayr, distinguished elder statesman of twentieth-century
  evolution, has blamed the delusion of discontinuity — under its
  philosophical name of Essentialism — as the main reason why
  evolutionary understanding came so late in human history. Plato, whose
  philosophy can be seen as the inspiration for Essentialism, believed
  that actual things are imperfect versions of an ideal archetype of
  their kind. Hanging somewhere in ideal space is an essential, perfect
  rabbit, which bears the same relation to a real rabbit as a
  mathematician’s perfect circle bears to a circle drawn in the dust. To
  this day many people are deeply imbued with the idea that sheep are
  sheep and goats are goats, and no species can ever give rise to
  another because to do so they’d have to change their ‘essence’.
  There is no such thing as essence.

The barrier would not come suddenly. There would never be a generation
  in which it made sense to say of an individual that he is Homo sapiens
  but his parents are Homo erectus. You can think of it as a paradox if
  you like, but there is no reason to think that any child was ever a
  member of a different species from its parents, even though the daisy
  chain of parents and children stretches back from humans to fish and
  beyond. Actually it isn’t paradoxical to anybody but a
  dyed-in-the-wool essentialist. It is no more paradoxical than the
  statement that there is never a moment when a growing child ceases to
  be short and becomes tall. Or a kettle ceases to be cold and becomes
  hot. The legal mind may find it necessary to impose a barrier
  between childhood and majority — the stroke of midnight on the
  eighteenth birthday, or whenever it is. But anyone can see that it is
  a (necessary for some purposes) fiction. If only more people could see
  that the same applies to when, say, a developing embryo becomes
  ‘human’.

The Ancestor’s Tale Richard Dawkins,

This is quite fantastic! If only because images convey so easily what is so hard to convey in words! Thanks for this, it is clearer now. I will say however, that a legitimate aspect of confusion comes from the use of 'species' as a term. We cannot be told that there exist giraffes and men, and that we are of different species, only to then simultaneously be told that there is no border defining this difference of species we were originally informed about to begin with.

Hi @apoz - this answer is considered useful by the community but still needs to consist of more than direct quotes.

I'd just like to expand on Konrad and MCM's answers. If I understand you correctly, your main question is "what were the 1st human's parents". You cannot really get an answer to that because the question itself is wrong.
The idea that evolution moves in discrete bounds, that is that speciation occurs suddenly, from one generation to the next (also known as Lamarckian evolution) has been abandoned years ago. That is simply not how evolution works (our modern knowledge of epigenetics notwithstanding). The color analogy given by Konrad is indeed a good one.
So, there was never an individual 'proto human'. This is also the case for all other species. What you do get, usually, is that a change in a species' environment (e.g. temperature, atmospheric pH, the introduction of a new predator etc) causes a particular mutation, or set of mutations, to become advantageous.
One has to remember that a genome (an organism's genetic material, their DNA) is not stable. It is in fact extremely dynamic and constantly undergoing mutational changes. Most of these mutations are neutral, they do not affect the organism in any way. However, when an external change such as I mentioned before occurs, some of these mutations may become advantageous.
Imagine a random mutation that causes an individual of a species to be more resistant to cold. If this occurs at the beginning of an ice age, that individual is more likely to reproduce, passing the mutation to its offspring. Over time, since the mutation-carriers are likelier to survive and reproduce, this mutation will spread across the population and become "fixed".
At some point these changes accumulate past a certain indefinable point and we call a speciation event. This does not occur at the individual but at the species level. A good analogy here is the sorites paradox. How many stones does it take to make a pile?
So, to sum up, humans did not evolve from monkeys. Humans and monkeys at some point shared a common ancestor. Then, over a long time period, successive changes caused the two species to diverge. That is not the same thing. The linear concept of evolution that has one species morphing into the next is one of the greatest misrepresentations of a scientific concept ever perpetrated by the media and inflicted upon the unsuspecting public.

"[H]umans did not evolve from monkeys" - I strongly dislike this claim. There is no doubt in my mind that the common ancestor of humans and currently extant monkeys would be classified as a monkey so I think a more correct statement would be "humans did not evolve from any current living species of monkey".

@jackaidley The point is that the hypothetical ancestor does not exist. Whether it would have been classified as a monkey or not is moot. Humans did not evolve from the animals we know today as monkeys. In any case, it is the construction that really bothers me. Species do not really evolve from one another. They evolve. The "from" implies a sense of linear progress that is simply wrong as explained by the various answers on this page.

The hypothetical ancestor most certainly does exist. It's just not extant. Your point about "from" is a good one, but yet I don't see any sensible way to discuss the evolutionary history of species without without using it or a similar construct.

@JackAidley I just tend to avoid using a preposition to get around it. And no, it does not exist. It has existed, but it does not exist today. Both exist (in the present tense) and extant mean that something is in existence at the moment.

There seems little point arguing over the exact meaning of the words exist and extant, so I'll merely note my disagreement and leave it at that. As to the rest, how then do you convey the evolutionary history which is concisely described as "humans evolve from monkeys"?

Agreed, this is not the place for linguistic disagreements. I convey the history by saying that monkeys and humans share a common ancestor. Otherwise, you are implying that humans have somehow evolved from the monkeys we see today.

That's okay in the case where both are extant (although I think it misses the point that the common ancestor would have been classified as a monkey), but what if you want to convey evolution from a group now extinct?

let us continue this discussion in chat

There are a lot of good answers here, but let me try to streamline things a bit: @Konrad's analogy to the color spectrum is spot on - where does red begin in that spectrum? This is essentially your question - where in the continuum of generations does the Homo sapiens species begin?
Just like our definition of color is imprecise (we usually can identify bright red and deep blue, but we cannot be sure about the shades in between), our definition of species is imprecise. We can identify a modern human and we could identify a far ancestor as such, but if we were presented with somebody from an intermediate generation, we could not confidently say if they are Homo sapiens or not.
We could, arbitrarily, point to a particular individual and say it was the first human, but it would not have any scientific meaning.

Lucas, thanks for your answer. Yes, I am trying to figure out, where the biological scientific community draws a discrete like in the sand and says anything less than this is not human, anything more is human. (I understand that it can be somewhat arbitrary, but surely there is an agreed upon threshold, if only so that not everyone makes their own arbitrary thresholds in the literature?). And what exactly do you call them? Humanish? 64%human? 12%human? How does it work in the literature?

@Mohammad, I don't think this issue comes up for humans that often - after all our nearest species relative that is not extinct, is easy to tell apart from human, except maybe in a dark room :). As far as classifying prehistoric "missing links", giving them a percentage of "humanness" does not make any sense, since that would imply that we could accurately describe what a 100% human was and relate it to them. I suppose, if we suddenly discovered a remote populated island, whose inhabitants cannot reproduce with the rest of humanity, we might need to deal with that issue :)

Lucas, in other words, the actual physical lack of evidence from swaths of the spectrum (by virtue of extinction) has nicely delineated in a clear way what is a human, and what is not, and hasn't forced the issue onto the biological community. Fair enough, I suppose I can reluctantly accept that. :-)

@Mohammad, yes, I think you make a good point. To use the color analogy again, if all we could see was blue, red and purple, we could point to purple and say "this is not red".

The border is fuzzy.

but then that necessarily means that the definition of a species is itself fuzzy, which I understand is not the case.

The concept of species, applied at one moment (or brief period) in time, is (fairly) well-defined. It breaks down if you try to apply it over a stretch of millenia.
The most commonly used definition of species is "a population whose members are capable of interbreeding with each other". (This was Ernst Mayr's definition.) So, take a group of humans and a group of chimpanzees. Humans can make babies with humans, and chimpanzees can make babies with chimpanzees. A human and a chimpanzee can't make a baby, even if they try. There's no fuzziness or ambiguity here. They're separate species.
Yet we share a common ancestor. So some of our ancestors could mate with some of their ancestors. And the transition from that state of affairs to this one was fuzzy.
(The sort of thing that might have happened is this. Once upon a time there was a population of chimp-ish creatures. Then, some of them ended up on the other side of a canyon and stayed there. Gradually, whether through genetic drift or local adaptation to slightly different conditions, they became sexually incompatible. This might have started off as simply behavioural - even if they met, they wouldn't find each other sexy - but eventually became more of a genomic, biochemical incompatibility, such that even if they did try to mate, either (earlier on) the baby would be sterile or (later on) nothing would come of it.)

Actually, there are indeed fuzzy cases where this species concept isn't perfect, even when applied contemporarily. A fun one is this picture. There's a horseshoe-shaped mountain range, with salamanders that live on it. Salamanders in the green bit can't mate with salamanders in the purple bit. But they can mate with salamanders in the yellow bit; and yellow can mate with red; and red can mate with magenta; and magenta can mate with purple. So are all these salamanders a "population capable of interbreeding", or not? And how many species are they?
(There's a fun chapter about these salamanders in Richard Dawkins' The Ancestor's Tale, making the point about fuzziness.)

While the definition of species certainly is fuzzy, the process of species generation is easily defined: migration of a population part leads to two geographically isolated gene pools which do not communicate genetic information. Both pools will, through genetic drift (mutations/inserts/deletions), develop away from each other to the point that, if they were to meet again, they could no longer produce offspring with each other. Voilà, a new species.

The process of species generation, speciation,  is most certainly not easily defined. It is still the subject of many a PhD thesis. The definition you offer is only relevant to sexual species. Most species on the planet do not have sexual reproduction. Also, many of those that do can interbreed with other species. Quite a few examples of this have already been mentioned in previous answers.

Just one point: if species can interbreed with species, contrary to definitions of the speciation process, then it is plausible to hypothesize they weren't species to begin with.

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text:
What is the most complex plant form?
At school we were told on scale of 0 through 1000 the animal kingdom ranges from amoeba the simplest/primitive being at 0, and Humans the most complex animals at 1000; what are the equivalent complexity species (?) in the plant kingdom? What is the least complex plant, and the most complex?

"Complexity" is a notoriously subjective and difficult-to-define term. Complexity differences between amoebas and vertebrates are hard to dispute, but amongst plants is a different story.

That whole thing of being more complex is non-sense, you can't say that for animals and you can't say that for plants either. It all depends on how you look at it. Average number of cells? Size of genome? Size of the proteome? Adaptability to different environments? Mental abilities? You can't place human on the top of any of them (maybe we could argue about if you define it as mental abilities but that doesn't sound right) and you can't place amoeba at the bottom either.
Also, if you look at a phylogenetic tree, an organism is also not more complex by the number of nodes it has behind them (I've seen people thinking this means more evolved and associate that with more complex).

The venus fly trap would certainly appear one of the most complex plants.
The plant almost 'bridges' a lifeform gap.

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text:
RMSD during conformational transition in proteins
When I was investigating the differences between protein structures obtained by X-ray crystallography and NMR spectroscopy, I found the paper [1] compairing structures of several proteins resolved both with X-ray and NMR. The average root-mean-square deviation (RMSD) between NMR and Xray structures is 1.4Å (max. 3.6Å), and the average RMSD between different NMR structures for same protein is 0.4Å (max. 1.3Å). I've checked some proteins studied in this paper, and they are mostly within 100–200 residues long.
However, there are plenty of papers (e.g. [2], [3], dealing with similarly sized proteins) that base their statements about conformational transitions on structures with RMSD difference 1–2Å.
I wonder what is considered reliable RMSD between two structures to draw any solid conlusions about conformational transitions (e.g. upon ligand binding) as opposed to simple thermal fluctuations or perturbance caused by the method to obtain structure?
Of course, the best way (at least in my opinion) to distinguish actual conformational transition from thermal fluctuations is to measure its lifetime, but it is often not an option.

 Andrec M, Snyder DA, Zhou Z, Young J, Montelione GT, Levy RM. 2007. A large data set comparison of protein structures determined by crystallography and NMR: statistical test for structural differences and the effect of crystal packing. Proteins 69: 449–65.
 Grant BJ, Gorfe AA, McCammon JA. 2009. Ras conformational switching: simulating nucleotide-dependent conformational transitions with accelerated molecular dynamics. PLoS Computational Biology 5(3): e1000325.
 Kumaraswami M, Newberry KJ, Brennan RG. 2010. Conformational plasticity of the coiled-coil domain of BmrR is required for bmr operator binding: the structure of unliganded BmrR. Journal of Molecular Biology 398: 264–75.

The best way to distinguish "actual conformational transition from thermal fluctuations" in a protein is to (determine and) compare atomic-resolution structures of the ligand-free and ligand-bound protein.
http://www.rcsb.org/pdb/home/home.do


text:
Can the third sex be categorized as Male or Female?
Hijra are people who have a penis (not sure if sexually active) but look much like a female (perhaps for some feminine biological property). Wikipedia says they are "physiological males who have feminine gender identity"
Also, I just came to know there are some more types of third gender people.
Now, is there really any BIOLOGICAL third gender which cannot be categorized as male or female? Or its always possible to categorize them to male or female?

When dealing with humans, there are only two Biological genders as defined by the presence or absence of the Y-Chromosome. If the Y-Chromosome is not present, or through some process gets totally deactivated, the human will appear and function as a Female.
XX = Female
XY = Male
XXY = Male (Klinefelter's Syndrome)
XYY = Male (Aneuploidy - Normal Functioning Males)
XXX = Female (Aneuploidy - Normal Functioning Females)
X = Female (Turner's Syndrome - Generally infertile, other issues)
Y = Fatal (The Y-Chromosome is drastically smaller than the X-Chromosome, which contains many necessary genes)
XXYY = Male
...
The list goes on, since there have been records of up to XXXXX.
If there is a Y-Chromosome present, the human born will be male.
However, that is not to say that a person cannot psychologically identify as something else. It's also worth noting that the majority of known species are asexual and do not have genders, and that those which do have genders do not always follow the same rules (Fruit Flies, for instance, use the ratio of genes to determine sex).

That one is really a nice answer. I did not take biology in school (planned to be engineer) but I did know about X-Y chromosomes. However, I always thought its only XX and XY!

There is also the barr body test to determine sex. When present, the organism is said to be female. Using the barr body test XXY is female and X is male. There is a certain lack of consensus on what makes a sex male or female and we normally revert to how the individual identifies, which is not particularly scientific.

How do you deal with XX males without SRY gene and with infertility?

@Remi.b -- The missing SRY gene in a phenotypical male with XX chromosomes is a really interesting exception to the general rule I described above. Thanks for bringing it up in the comments! I didn't know it existed.

I think you might be confusing sex and gender. The terms are often used interchangeably, but strictly speaking, they have different biological meanings. Sex refers to the biological categorization based on genetics, reproductive organs, or similar things, whereas gender is based on social identity.
For humans, there are only two sex chromosomes, X and Y, and they determine the male and female sexes. But there are many situations that don't fall under the XX/XY categorization, and people with these conditions are usually referred to as intersex. These can include conditions such as congenital adrenal hyperplasia, androgen insensitivity syndrome, and 5-alpha-reductase deficiency. So in short, there is no biological third sex, but that doesn't mean you can always categorize a person as biologically male or female.
As you quoted, the hijira are usually physiologically male but have a different gender identity.

Yeah, I was not aware of the difference between gender and sex. But I mentioned Biological Gender which IMO implies the technical term sex as you explained. Thanks for explaining the distinction.

As I read the Wikipedia article you reference, its useful to remember that conventional chromosomal definitions of gender, the genitals are soft tissue which has many recorded morphological abnormalities.  hermaphrodites and a spectrum of tissue shapes do occur to the extent that the conventional gender identity is not acceptable.
Physiological definition of gender, despite the chromosomes do need to be medically and socially addressed.  I am not sure that all these 'intersex' people really should be grouped into a single 'third sex', but some way of recognizing their essential human rights should be out there in my opinion.

Adding to @MCM answer, there are also chromosomal crossover that might happen between non homologous. You can have some of the genes of Y chromosome going to X chromosome or elsewhere, for instance, further expanding the possibilities for different sexualities...

There is an actual third gender. That is true hermaphroditism. Some humans are true hermaphrodites. The most common cause of this? 2 eggs fusing, 1 male and 1 female before they start differentiation.
These have both male and female characteristics and so they can't be classified as either male or female.
Here is my source:
https://en.wikipedia.org/wiki/True_hermaphroditism

Do you have a source for this?

Yeah I just now added it

From your source: "There are no documented cases in which both types of gonadal tissue function."  Based on this, human "true hermaphrodites" can always be classified as either "reproductively male" or "reproductively female", never a mix.

Hermaphrodites don't occur in humans — you may be confusing this with intersexuality. 2) Eggs don't have a sex and I don't think there's ever been a record of an egg containing an Y-chromosome so this doesn't seem to make any sense. 3) if you have evidence that two egg cells have ever been observed to fuse and lead to a viable child please post it here – since even small trisomies are typically fatal or in rare cases only have severe developmental problems (e.g. Down's syndrome) the current understanding is that a triploid human is not possible.


text:
Is it possible to correctly identify presence of Y chromosome with external physical test only?
I asked a question related to the third sex, and I came to know that its always possible to categorize a human to male or female with presence of Y chromosome.
Now, I have another question. Is there a way to say if someone has Y chromosome only with external physical test? More specifically:

Someone has a penis, can we say that s/he will have Y chromosome?
Some one has Y chromosome, can we say that he will have a penis?

No, an external physical examination would be inconclusive. The reason is the TDF
gene. To be more specific, if a person has XY and the gene is not active then the subject
would have a female appearance. Also we cannot conclude that a person has a Y
chromosome even if it has penis because that gene could be transferred on the X chromosome.
Here is a reference: http://en.wikipedia.org/wiki/Testis_determining_factor.

Isn't it the SRY gene which expresses the TDF transcription factor?

Sometimes, the area which encodes this protein is referred as TDF gene, although I am not sure if this terminology is abusive. http://www.biology-online.org/dictionary/TDF_gene . Also see here http://www.ncbi.nlm.nih.gov/gene?term=testis%20determinding%20factor  a alias for the SRY gene is TDF.

An interesting condition is androgen insentivity syndrome. In AIS, the body is unable to respond to androgens, the male sex hormone, of which testosterone is the best known. The most common cause is a defective androgen receptor, and most of these diseases are X-linked. In extreme cases, complete androgen insensitivy syndrome (CAIS) can occur. Genetic males (XY) with CAIS appear outwardly as females due to the lack of androgens that would normally lead to masculinzation. However, the SRY gene (sex-determining region Y) that encodes TDF still causes testes to develop, although they are usually internal. Individuals with CAIS generally identify as females.


text:
How does a plant decide when to grow a branch?
As a plant grows, at some point the first branch forms. As it continues, branches grow new branches, and so on, in a seemingly random way. Is it random, or is it driven by the environment (heat or cold, sunshine, wind)? Or is it somehow defined in the plant's DNA, that each branch will grow at in such and such a direction, at such and such a time?
Does this generalize down to successively smaller branches, and eventually leaves?

I answered this in some detail in response to another question... http://biology.stackexchange.com/a/2646/430

Related topics: auxins, apical dominance.

Great answer Richard. Upvoted. You refer to a chaotic process that determines new areas of auxin concentration between meristems as the plant grows, so I guess the simplest answer to my question is "chance, within the confines of a system".  There doesn't appear to be any DNA-style central planning at work.


text:
What did Richard Feynman contribute to molecular biology?
Some time ago, I read James Gleick's "Genius: The Life and Science of Richard Feynman", a wonderful biography of Feynman and, by extension, most of modern physics.
In this book, the author mentions that Feynman spent a year working in a biology lab and that during that year he made an important discovery.
I remember that when reading the book as an undergraduate biology student, I knew the discovery in question well enough to be immensely impressed that it had been discovered by someone foreign to the field.
Unfortunately, I no longer have the book and cannot remember what that discovery was. Does anyone know?

Don't know the answer, but this has always made me lough a lot (and I deeply agree with Mr. Feynman)

@nico Tell me about it, the time I spent memorizing the names of all the myosins... I actually had an exam question once, asking what year the Origin of Species was published in. Not what the book said mind you, they were asking for information you can get by looking at the inside cover. This in what, at the time, was the best rated University for Biology in the UK.

According to Gleick, Feynman spent the summer of 1960 in Delbrück's lab at Caltech and discovered intragenic supression.
This is where the expression of a gene which has been knocked out by a mutation may be restored by a second mutation within the same gene.
Fenynman worked with the rII mutant of phage T4 and was looking for back mutations in E.coli strain K.
He noted some unusual plaques which he labelled idiot r's.
Feynman correctly deduced that these revertants were due to a second mutation which cancelled the effect of the first, but he did not publish the result, possibly because he had no molecular explanation for what was going on.
The Delbrück lab referred to these revertants as Feyntrons.
Cricks and co-workers in Cambridge, UK, correctly explained the phenomenon.  If, for example, a mutation caused a gene to be read out of sequence (a frameshift mutation) then a second mutation within the same gene could put the message back 'in phase', thus cancelling out the effect of the first mutation.
All the above is taken from James Gleick (1992) Genius.  Richard Feynman and modern physics, a great book.

That's wonderful, thank you. I have been trying to remember this for years. Are you sure about the book's title though? I can find no reference to it. See my answer for the one I remember and can find.


text:
How many human cells are there in our body, on average?
How many human cells are there in our body, on average?
Wikipedia says 1013:

Bacterial cells are much smaller than human cells, and there are at least ten times as many bacteria as human cells in the body (approximately 1014 versus 1013).

The Nobel site says 1014:

An adult human being has approximately 100 000 billion cells, all originating from a single cell, the fertilized egg cell.

The Physics fact book insists it's 1013:

(length of 1 bp)(number of bp per cell)(number of cells in the body)
  (0.34 × 10-9 m)(6 × 109)(1013)

Finally, Wolfram Alpha gives 1.0 × 1014 as fact:

Estimated number of eukaryotic (human) cells in the human body: 1.0×1014

I am quite confused: who is right here?

Well, the Nobel quote is wrong whichever way you turn it (for the reason outlined in the Wikipedia quote). But I wouldn’t be surprised that, even taking the average, there’s an uncertainty of a factor 10 about the correct number. Because all the factors used to determine the number are crude estimates indeed.

@Skivvz  Another interesting number is that of neurons in the human cerebral cortex: 16 billion, 8 billion pairs.  Fascinating isn't it.    Also, it is worth noting that one commonly cited number for cells in the human body, around 37 trillion is approximately 2^45; which means that if one cell divided to its Hayflick limit of 45, for argument's sake, then in order to maintain adult equilibrium, an equivalent number would need to die in a comparable period, of 6 or 7 weeks on average (for a cell type mitosing daily for instance).  ''Numbers'',  Isn't that an old Book or something?

Bianconi et al. 2013 give an estimated lower bound of 3.72 × 10^13 (which, by the way, is approximately the geometric mean of 10^13 and 10^14).
However, from the table in their Supplemental Information (where estimates for about fifty different types of cells are added up), it is clear that the vast majority of these are the erythrocytes, also known as red blood cells: estimated at 2.63 × 10^13. While the second largest class are the glial cells (from the nervous system), estimated at 0.30 × 10^13. Three other classes (endothelial cells {vessels}, dermal fibroblasts {skin}, and platelets {blood}) add up to another 0.58 × 10^13. These, in total, is about 3.5 × 10^13, and we can stop there, because the uncertainty in all these estimates swamps all the other cell type populations, which are much smaller.
This means that if we only consider the 5 most abundant cell types in the body, we already get a very good estimate. Is it likely that we have missed a cell type of which there are a trillion cells in the body? It's not impossible, but unlikely, because it would be hard to miss all these cells.
Maybe there is a long tail (i.e. a large number of minor cell types, each with a small, but significant population) that wasn't considered? Together, these could add up to a significant adjustment to the above figure. I don't know.
This estimate is for a typical human person: 30 year old young adult, 70 kg, 1.72 m tall and with a surface area of 1.85 m^2. For this person, the figure is given with roughly a +-20% uncertainty.
Given all the above, it's probably safe to say "30 to 50 trillion".
(This obviously doesn't take into account any of the bacteria mentioned above.)

That paper is behind a pay wall. Can you reproduce the contents of that table here? The data itself isn't copyright-able.

I was able to find a copy of the paper at http://nanoimmondizia.ge.ibf.cnr.it/UserFiles/documenti/Bianconi_AHB_2013.pdf

In Mike Lynch's "The Origins of Genome Architecture", he claims 10^13.  I forget the primary source he cited, and since the book is in my office I can't check it now.
** Found the snippet that contained the reference.  I think it's really worth including in its entirety.

A crude estimate of the amount of DNA within currently living
  organisms can be made by noting that the length spanned by one base of
  DNA is ~0.3x10^-12 km (Cook 2001).
The number of viral particles in the open oceans is ~10^30 (Suttle
  2005).  Assuming that there are twice as many viruses on land and in
  fresh water does not change the global estimate very much at the
  order-of-magnitude level.  Thus, assuming an average viral genome size
  of 10^4 bp, the total length of viral DNA if all chromosomes were
  linearized and placed end to end is ~10^22 km.
The estimated global number of prokaryotic cells is ~10^30 (Whitman et
  al. 1998), and assuming an average prokaryotic genome size of 3x10^6
  bp yields an estimated total DNA length of 10^24 km.
With a total population size of 6x10^9 individuals, 10^13 cells per
  individual (Baserga 1985), and a diploid genome size of 6x10^9 bp, the
  amount of DNA occupied by the human population is ~10^20 km.  Assuming
  there are ~10^7 species of eukaryotes on Earth (~6 times the number
  that have actually been identified), that the average eukaryotic
  genome size is ~1% of humans, and that all species occupy
  approximately the same amount of total biomass, total eukaryotic DNA
  is ~10^5 times that for humans, or ~10^25 km.
Given the very approximate nature of these calculations, any one of
  these estimates could be off by one or two orders of magnitude, but it
  is difficult to escape the conclusion that the total amount of DNA in
  living organisms is on the order of 10^25 km, which is equivalent to a
  distance of 10^12 light years, or 10 times the diameter of the known
  universe.


text:
What causes instinctive behaviour?
Some actions, almost behaviour, exist that are common across a species. For instance, based on personal observation, human babies try to taste anything new they encounter until they are a few score months old. Similarly most dogs will go round-and-round before they finally settle down to sleep.
We probably use the term 'instinctive' to indicate there is no conscious thought behind that action, albeit the action is not a reflex either. Anyway, what causes instinctive behaviour? Is it genetic in nature? Are there some basic rules/behaviour hard-coded into our brains sort of like BIOS in a computer?

If it's present across an entire species through multiple generations, then it implies that the behavior is inherited - so yes, genetics would play a role. If genetics play a role, then the behaviors are "hard-coded" into our physiology.

I just want to point out that behaviour is often divided into instinctive (including reflexes) and learned. Behaviour can be learned even if the species is not conscious, and repetetive behaviour can be learned. Remember that few species are conscious (maybe none, depending on your definition), so consciousness is not necessarily useful to discuss general instinctive behaviour.

This stuff is so interesting! The instinctive behaviour is also known as a fixed action pattern or FAP which is a collection of well-defined motor patterns that are activated in response to a stimulus, i.e. a group more eleborate reflexes [2]. FAPs allow the brain to concentrate on other things as they don't need require time or energy to be thought about. The theory is they've been selected for because they decrease choice and decision time, which can be particularly important to survival.
There are some cool examples here (http://www.cerebromente.org.br/n09/fastfacts/comportold_i.htm).

the bird is continues to perform parental instinctive behaviour in the absence of a brood of chicks because the similar stimulus of hungry open-mouthed fish is present.
Another article draws comparisons between different animals as to how much of their behaviour is fixed/pre-determined [3]. There can be a correlation between the size of the cerebral cortex, used for thinking and problem solving, and the amount of innate behaviour (i.e. the bigger your cortex the less you need to rely on pre-determined behaviours in certain situations).
These patterns seem to be for the most part genetically determined, however some studies with song-birds in the 70's demonstrated that a learning aspect can modify the innate behviour. Birds which have been reared in an environemnt where they cannot hear other birds of the same species sing still sing their typical song, but when allowed to hear others sing the song becomes more complex.
Investigating the genetic basis behind innate behaviours involve searching for Quantitative Trait Loci (QTLs) or stretches of DNA that contain genes (complex traits require the concerted actions of multiple genes) or are linked to genes that are involved in determining a specifc trait (in this case a behaviour). Classically this involves crossing two animals that differ in the trait you're interested in and looking at the segregation patterns in the offspring to try and pinpoint the specifc region of DNA/collection of genes that control the trait. I think quite a lot of this has been done in insects and mice which have high breeding rates and can be studied easily in the lab.
...at this risk of making this answer ridiculously long I've just included a snippet from another website on behavioural genetics which details the OMIM and some of the traits you can search for[4]:

Online Mendelian Inheritance in Man (OMIM) is a large, searchable, up-to-date database of human genes, genetic traits, and disorders. Each OMIM record contains bibliographic references and a summary of the scientific literature describing what is known about a particular gene, trait, or disorder. The following behavioral traits are included in OMIM. The six-digit number MIM number is used to uniquely identify each record.

Hand skill, relative (handedness): (139900)
Hand clasping pattern: (139800)
Arm folding preference: (107850)
Ears, ability to move: (129100)
Tongue curling, folding, or rolling: (189300)
Musical perfect pitch: (159300)

[2] http://books.google.co.uk/books?id=aQvGXLPjMPAC&pg=PA44&lpg=PA44&dq=fixed+action+patterns+difference+reflex&source=bl&ots=TxaSYeIpTs&sig=RfsmHLWVlNiF8B-dH928-F0I5M8&hl=en&sa=X&ei=Bs1WUZeCFYiZtAbZ_IHYBw&ved=0CDcQ6AEwAA#v=onepage&q=fixed%20action%20patterns%20difference%20reflex&f=false
[3] http://www.grandin.com/references/genetics.html
[4] http://www.ornl.gov/sci/techresources/Human_Genome/elsi/behavior.shtml


text:
What is an organism?
The definition of an organism Wikipedia gives is

An organism is any contiguous living system.

I understand that these are not organisms according to this definition:

A bird and a tree it's perching on are living and contiguous, but they don't form a system.
All humans are living and form a system, but they are not contiguous.

But some things are unclear to me. My veins and my skin are contiguous and living. Do they form a system? I think so, at least according to what I read about systems in Wikipedia. They are definitely interconnected; they have behavior; and I believe they have structure, though I'm not really sure what structure is. Perhaps if we carefully define what we want "structure" to mean, we can save the definition from allowing (skin + veins) to be an organism?
Is (mother + her unborn child) an organism? I think it definitely is according to the definition. Is the unborn child an organism?
Is an apple that's just fallen off a tree an organism? Was it an organism before it fell?
Is (human + their microbiome) an organism? Is a human without the microbiome an organism?
I think the part of the definition that the least clear to me is the word "system", and in the definition of the word "system", it's the word "structure".

Cf. this question http://biology.stackexchange.com/questions/8745/polymorphism-in-cnidarians/9148#9148, and especially part B in my answer about "Organism Concepts"

I think the definition in Wikipedia is simply bad because it depends on another debatable definition.
I prefer something which follows from an observation made by Ricard Dawkins in The Extended Phenotype (the following is my definition, but I think Dawkins had something similar in mind):
An organism is any system of components which depend on each other for survival and cooperate in proliferating potentially unboundedly.
A single-celled organism is by this definition an organism since it proliferates by coordination of its components.
A single-celled organism with organelles deriving from endosymbiosis (think mitochondria) is an organism: even though mitochondria do proliferate on their own inside the cell, they don’t do so outside of the cell, hence have a bounded proliferation only; and they depend on the cell as a host. On the other hand, they cooperate with the cell division.
Endosymbionts, on the other hand, are organisms because even though they depend on a host (and the host on them), they may theoretically switch host or even survive a limited time without a host.
Similarly, the cells in a multi-cellular organism can sometimes divide independently (in organs) but they cannot survive without the rest of the organism, and the unbounded reproduction of any organ in fact requires going via the germ line of said organism.
A virus which depends on a host to proliferate does not form an organism with the host since it doesn’t use the host’s germ line; if, on the other hand, it does use the host’s germ line (consider virally derived pseudo-genes on our DNA) then, yes, it forms a common organism with its host.

Is (mother + her unborn child) an organism?

I wouldn’t say so, since the child is only temporally part of the host.

Is an apple that's just fallen off a tree an organism?

Interesting; I’d say yes, as long as it retains the potential ability to proliferate (it’s a separate organism from the tree though).

Is (human + their microbiome) an organism?

No. Humans can survive (albeit only shortly) without a microbiome; in the same vein, the bacteria of the microbiome can change their host.
Unfortunately, this definition also has a drawback: there are organisms which cannot reproduce because they are sterile, yet they are clearly still organisms.
Note that other definitions (e.g. “an organism is a collection of components sharing common genetic material”) also don’t work universally since they also break down – the example of genetic commonality would preclude mosaicism and organelles derived from endosymbiosis.

Thank you. I'm not sure I understand the part on mitochondria. Do you consider a mitochondrion an organism or not? You say "endosymbionts are organisms", but also "mitochondria . . . have a bounded proliferation only". Aren't mitochondria endosymbionts?

@ymar No. They form an organism with their host cell. Endosymbionts are organisms but mitochondria are derived from endosymbionts. They are no longer endosymbionts (according to the common definition of the term).

OK, I see. Could you explain what you mean by potential unbounded proliferation?

@ymar Literally, proliferation without (theoretical) limit. Mitochondria can try as hard as they want, they cannot proliferate beyond their host cells. On the other hand, humans can theoretically proliferate to the bounds of the biosphere, which, itself, has no fixed bounds (except the edge of the Universe if you’re so inclined).

I don't understand. Let's forget about humans for a moment because technology makes things complicated. But a cod cannot live on the desert unless there is a caring human that supplies water and food for it. There surely are limits to where cods can live and proliferate by themselves, right?

@ymar Sure. But a desert is not an organism which can proliferate by itself: mitochondria are restricted in their proliferation by the surrounding cell, but together with the cell they can proliferate beyond that single cell. The cod can proliferate more or less limitless within its biotope but the biotope itself isn’t an organism with which the cod can cooperate to reproduce further.

OK, this seems to be related to something I decided to leave out of my question. Can organisms be nested? Of course, an organism can live within another organism. But can an organism be a part of another organism? It seems to me that your answer is no.

I believe you are using the incorrect definition of "Contigous." The most common usage is basically "sharing a border," but it can also be:
-touching or connected throughout in an unbroken sequence contiguous row of houses
http://www.merriam-webster.com/dictionary/contiguous
You also need to include the part about what defines "living":
"... can react to stimuli, reproduce, grow, and maintain homeostasis."
Your organs form a system, which results in you. A mother and her unborn child could also be considered an organism under this definition. The apple would not, nor would the tree and bird combination.

I think that's the definition of "contiguous" I'm using. Why do you think it's not? I know all of my organs together form a system. What I'm not sure about is whether my skin together with my veins forms a system. Is being made of living cells enough for being living? I think it should be if a colony of bacteria is considered an organism.


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What is the role of Homocysteine in cognitive function?
I'm looking at this link : Homocysteine and cognitive impairments and am looking for more information on specific cognitive impairments associated with elevated levels Homocysteine. That article is not very clear on that point. I've seen some research papers about the study of this in elderly people and cardiovascular studies. I'm interested in average adults.
I've been fascinated with the effect/lack of thereof of vitamin B6 on dreaming and Homocysteine is the first thing that I've stumbled upon in quite some time that is directly related to the B family of vitamins. Has there been any research about what Homocysteine gets metabolized to if exposed to B-Complex vitamins versus Vitamin B6 alone?
Thank you for your input!

I'm not sure if this answers your question, but I'll give it a try anyway. Here's a diagram of homocysteine metabolism. Vitamin B12 is a cofactor for homocysteine methyltransferase, and folic acid is required for tetrahydrofolate (THF). As both vitamins are involved in homocysteine metabolism, the symptoms of folate and vitamin B12 deficiency are similar. Vitamin B12 deficiency can result in neurological symptoms due to abnormal myelin, but folate deficiency does not. Vitamin B12 also metabolizes methylmalonyl-CoA to succinyl-CoA as seem here, so the methylmalonic acid level is often measured to test for vitamin B12 deficiency.
Hyperhomocysteinemia is the condition of high levels of homocysteine, but it is usually due to low vitamin B12 or folate.

Thank you for a very informative answer! The diagram of    homocysteine metabolism confirmed that there are two possible ways that the amino acid gets metabolized and I will investigate this more thoroughly.


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Bugs' love for light
Do bugs love light bulbs because they resemble the stars or is it the sun? How do they sense the bulb? What is the purpose of this "brightophilia" that has evolved in insects?

I had previously heard in conversation that insects are actually attracted to the dimmest possible surroundings, which appears to be behind the light.

I think the answer to your question is relatively unknown. The answer I have heard the most often, which is largely the most accepted, is that many insects orient themselves in space using light. So if they are flying at night, the soft light of the moon tells them which relative direction they are going. Light bulbs end up confusing them, because they think they can orient themselves to it, but they are wrong.
http://www.npr.org/templates/story/story.php?storyId=12903572
Additionally, insects do have very similar photoreceptors as humans and vertebrates. Fruit fly eyes are a major research topic because of the similarity of the photoreceptor proteins as well as the amazing genetics that can be done.

This is similar to what I've heard most often, as well. I've always heard that insects use the moon or the sun to navigate, and artificial lights create a false version.

So they carry sextants in their invisible backpacks to follow the celestine map? Did you mean up with "orient" or positioning?


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Are there any effects of elevated Cysteine levels on cognitive function?
I'm looking at this diagram of homocysteine metabolism and see two distinct pathways that the amino acid may get metabolized to: with vitamin B12 it gets converted back into methionine, while with B6 it gets converted to cysteine.
I've followed the links for the products that Cysteine gets metabolized to and could not find any references to cognitive effects. Are there any cognitive effects of Cysteine or other amino acids that it gets metabolized to?

I'm interested in learning what are the possible effects of pharmacological (50mg - 100mg) doses of vitamin B6 on this metabolic cycle, while folate and B12 levels stay at the baseline levels. It seems to me that if vitamin B6 is more readily available, there will be a higher chance of homocysteine metabolized into Cysteine. Is this assumption correct? What are the implications to this metabolic cycle that may be caused  by elevated levels of vitamin B6, while keeping folate and B12 at baseline levels?
I'm particularly interested in the implications of this process on dreaming. There has been numerous reports among dreamers that 50-100mg of vitamin B6, taken in the 3rd-5th sleep cycle produces very intense and vivid dreams, sometimes featuring spontaneous awareness (lucid dreams), while B-complex vitamins (B6, B12, Folate, Niacin, etc) appear to produce the opposite effect - very vague dream recall.
I'm trying to understand if there is indeed a connection between the metabolic pathway that homocysteine may take and the vividness of dreams, capacity to recall them clearly and the phenomenon of being able to spontaneously realize the fact that the person is dreaming while still asleep.
Thank you for your input!
Diagram obtained from here

Thank you for that great article. I've read it and see that they are using all 3 vitamins, although the B6 levels are indeed elevated 1000% (20mg/day for 2 years) but the B12 levels are 5000% daily recommended dose, and folic acid is 2000% daily recommended dose.

Your shown homocysteine pathway is way too simple. Especially the production of the neuromodulator H2S from excess sulfur amino acids is not shown. In the last years many more enzymes and reactions have been discovered. I have summarized human sulfur amino acid metabolism in reactome.org, so please use this link to discover all the details and new papers. I'll also append some of the relevant papers below.
Brosnan, JT, Brosnan, ME The sulfur-containing amino acids: an overview 2006 J Nutr PMID 16702333
Remethylation of homocysteine to methionine can also happen using betaine as a methyl donor. This reaction is also part of choline catabolism.
Li, F, Feng, Q, Lee, C, Wang, S, Pelleymounter, LL, Moon, I, Eckloff, BW, Wieben, ED, Schaid, DJ, Yee, V, Weinshilboum, RM Human betaine-homocysteine methyltransferase (BHMT) and BHMT2: common gene sequence variation and functional characterization 2008 Mol Genet Metab PMID 18457970
Bearden, SE, Beard RS, Jr, Pfau, JC Extracellular transsulfuration generates hydrogen sulfide from homocysteine and protects endothelium from redox stress 2010 Am J Physiol Heart Circ Physiol PMID 20817827
Dominy, JE, Stipanuk, MH New roles for cysteine and transsulfuration enzymes: production of H2S, a neuromodulator and smooth muscle relaxant 2004 Nutr Rev PMID 15497768
Stipanuk, MH, Ueki, I Dealing with methionine/homocysteine sulfur: cysteine metabolism to taurine and inorganic sulfur 2011 J Inherit Metab Dis PMID 20162368
Chiku, T, Padovani, D, Zhu, W, Singh, S, Vitvitsky, V, Banerjee, R H2S biogenesis by human cystathionine gamma-lyase leads to the novel sulfur metabolites lanthionine and homolanthionine and is responsive to the grade of hyperhomocysteinemia 2009 J Biol Chem PMID 19261609


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Biological Pathway of Lipid Hypothesis
I've read a lot on both sides of the debate of low carb vs low fat diets trying to make some sense of what is being proposed. The lipid hypothesis runs roughly along the lines that we have lots of observational epidemiological evidence that eating a high fat diet correlates heart disease/obesity/enter disease of choice.
An alternative hypothesis is that high carbohydrate diets cause these things. Since the studies haven't been done, there is not the correlation to point to. This hypothesis is believable (to some people) due to the well-understood biological pathway: Carbohydrates turn to glucose, which causes an insulin release, and insulin regulates fat storage, so high carbohydrate diets lead to weight gain (see a biochemsitry textbook for a more detailed explanation).
My question is: Does the lipid hypothesis have any biological pathway for which there could be proposed a causal relation rather than just a correlation? Of all the speakers/writers on this topic, the low carb advocates always clearly describe the causal relation, whereas the low fat advocates never say why eating fat should cause weight gain.
Note: I'm not interested in discussing the merits of the studies, but rather the proposed causal mechanism.

I think you're confounding two separate things.
The Lipid Hypothesis is about the creation of atherosclerosis (only atherosclerosis) and was proposed as an explanation for why plaques of cholesterol, fatty acids, and somatic cells form in arteries. It does not try to explain adipocyte behavior, which would result in weight gain.
For the Lipid Hypothesis, after the glycerol has been removed from fatty acids, they are free to diffuse into the blood and can start plaques.
Weight Gain/Loss due to adipocyte behavior is significantly more complicated. One of the weight-related regulatory hormones present in adipose tissue is Leptin: http://en.wikipedia.org/wiki/Leptin
And a more scholarly article from 1995 discussing Leptin:
http://www.nature.com/nature/journal/v395/n6704/abs/395763a0.html
Leptin helps inhibit appetite, along with Ghrelin and a host of other molecules that control hunger and keep track of nutrient levels. However, as the wiki article states, Leptin and Insulin based activities are the primary functions of adipocytes, so a high-fat diet would conceivably deal with either or both of those molecules.
One of the quirks of Leptin is that fad dieting or starvation techniques have a very undesirable affect on Leptin levels (for years after a starvation diet, sometimes) that cause adipocytes to accumulate lipids that they normally would not have.
Obesity can also cause Leptin resistance (which might be aggravated by Fructose intake: http://www.ncbi.nlm.nih.gov/pubmed/11723062 ), much the same way that a diet rich in simple sugars can cause Type II Diabetes: http://www.ncbi.nlm.nih.gov/pubmed/8532024  The Leptin levels are at the expected concentrations in obese individuals, but the proper neuro-receptor activity isn't taking place.
Come to think of it, this may be what you're after. High fat diets will result in more Leptin and thus quicker/more Leptin resistance. Once Leptin resistance occurs, the mechanisms for controlling hunger are no longer as effective as they once were, resulting in more food intake and more weight gain.
However, the actual satiatory signal of Leptin is still debated. Some researchers have proposed that it's more of a "starvation" signal than a "satiation" signal, and thus Leptin resistance might be a normal condition when energy-dense foods are widely available: http://www.ncbi.nlm.nih.gov/pubmed/19644451

Ah. Interesting. I'm going to be a pain. I understand the Lipid Hypothesis was originally about atherosclerosis, but due to the strong correlation between obesity and heart disease most (all?) proponents of low fat diets believe that eating fat causes you to get fat. At least this is the widespread U.S. belief. So I think this has been absorbed into the modern lipid hypothesis. You will have answered my question if you point out why eating a high fat diet leads to more Leptin. I had heard that fructose causes Leptin levels to increase, but haven't seen that fat can cause it too.

If that is all the Lipid Hypothesis really is, then would you consider it fairly well debunked? Our modern understanding describes pretty well that the types of lipoproteins that come out of eating fat are not the type that lead to plaque on the arteries, but the type formed from eating a high carbohydrate and/or high sugar diet are.

Well, my personal opinion is that the proponents are mistaking a high fat diet for a surplus-Calorie diet high in fats. You can gain weight off of almost any food, but fat has more than double the energy density of carbs and protein (9kcal/g vs. 4kcal/g) - so a "High Fat" diet is probably a "Calorie Surplus" diet to begin with. That said, more fat in your system also means more adipocyte activity, which could include fluctuation in Leptin levels sufficient to trigger resistance. I couldn't find any articles, but it is plausible to me...

...for the same reasons that Type II Diabetes, while often seen in obese patients, is not exclusive to obese patients. It's just an over-abundance of simple sugars in your system, combined with genetic predispositions, that results in Insulin resistance. Even if you burned off all of the Calories from sweet foods, if you only ate sweet foods you have a chance at developing Type II. Normal weight people, to the best figures I can find, make up about 10% of newly diagnosed cases.

Given that possibility, though, my personal opinion is still that it's debunked. A high-fat diet will not make you fat on its own, but it's certainly possible to underestimate the Calories involved. There might be some merit to low-carb diets, which show better weight loss over the short-term, but after 6 months there's no difference besides minor HDL and Triglyceride levels: http://www.nejm.org/doi/full/10.1056/NEJMoa022207

As a bit of a tangential addendum, here's an article from on of my constant haunts (Science Based Medicine): http://www.sciencebasedmedicine.org/index.php/whats-for-dinner/
It doesn't go in-depth into the Lipid or Carbohydrate Hypothesis (it looks like you were correct, the Lipid Hypothesis included more than I remembered), but it sums up my feelings well.

Thanks! I think of the calories in-calories out hypothesis as separate but related to the two I mentioned. If it is true, then it would make sense that a high fat diet would more easily lead to weight gain due to calorie density, but I find it hard to buy due to how closely linked how much you eat and how much you burn is. I wish the low carb trial you linked didn't have so much attrition and poor adherence. It could have shed some better light on this. It seems somewhat likely that the weight loss would continue in the long-term if people stayed on it.

You are mistaken in that the "lipid hypothesis" has no physiological basis like the carbohydrate biological pathways. Lipids and carbohydrates are produced and catabolized mutually from each other in the body. It's all the calories that matter (okay, proteins have a few too). Once the fat is in the body it gets turned into an energy source but it appears you are more interested what comes before. I'll quote from Wikipedia:

Digestion of some fats can begin in the mouth where lingual lipase
  breaks down some short chain lipids into diglycerides. The presence of
  fat in the small intestine produces hormones that stimulate the
  release of pancreatic lipase from the pancreas and bile from the liver
  for breakdown of fats into fatty acids. Complete digestion of one
  molecule of fat (a triglyceride) results in 3 fatty acid molecules and
  one glycerol molecule.

After that, fatty acids are packed into chylomicrons and transported through the blood to where they are catabolized.
This process, however, is strongly dependend on the right mixture of bile acids and pancreas enzymes. Any deviation from the ideal leads to undigested fat in the intestine, which is usually then partly digested by bacteria (winds as byproduct) or simply excreted as fatty stool.
http://en.wikipedia.org/wiki/Digestion#Fat_digestion
http://en.wikipedia.org/wiki/Fatty_acid_metabolism

First, nowhere in my question do I say the lipid hypothesis has no physiological basis. If so, I wouldn't ask the question. I said that defenders of the lipid hypothesis do not explain what the pathway is. Second, this explains (as you point out) how lipids are catabolized which I already knew. I'm wondering what the proposed pathway from ingesting fat to fat accumulation is, not how fatty acids are turned into an energy source. It would also be nice for people who stumble on this to be able to read an answer if you understand this rather than dig through a Wikipedia article to find it.

Now it's getting clearer what you want to know. I'll add to my answer.

Thanks so much for your time! Sorry if the question wasn't clear.

I think my question is still unclear. It is not about how fatty acids are digested or turn into energy. I think the "Lipid Hypothesis" wasn't explained well enough. The lipid hypothesis says that there is something about eating fat that causes you to get fat, i.e. if you eat the exact same amount of calories, then eating fat will cause you to gain weight (get heart disease, etc). The carb hypothesis has a particular pathway that leads to fat accumulation that does not happen from eating fat. My question is what is a proposed pathway for the lipid hypothesis?

First, dietary fat itself accumulates without big biochemical modifications: indeed dietary triglycerides are preferentially uptaken in white adipose tissue according to Bickerton et al. Diabetes 2007 56(1):168-76. So no complicated pathway: you eat fat, you store fat. If you eat more fat than the amount you dispose, you accumulate fat and get obese.
Second, continuted ingestion of dietary fat, and particularly saturated fat, facilitates insulin resistance. Therefore, insulin is less effective to drive glucose entering in the cells. Sometimes, you may want to eat something sweet as well, but because insulin is less effective, more glucose remains in the blood driving the typical complicances of the metabolic syndrome.
At this point, the increased glycemia causes the same interferences described in the carb hypothesis.

That second article is pretty horrible. It seems to be a survey of the literature, tons of which find no link between dietary fat and insulin resistance. Moreover, there is no proposed mechanism for why this should happen. I'll need more time to read through the first.

I cannot subscribe to the statement that all fat is simply absorbed. There are environmental differences in the stomach that influence fat intake like LPL activity. The first article states they modeled after LPL, so they clearly thought of this. Also, there is the symptom of fat stool---how can you get that if all fat goes straight to adipos?

In biology, 'all' does not exist. You may better figure out that some 'excess' fat is accumulated in WAT, some 'excess' in stool, some 'excess' in atheromas etc...


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Do twins "run in the family"?
My wife and I recently found out that we are going to have twins and so nearly everyone asks if we have a family history of twins.  Now I know that the answer for me is that it doesn't matter—as a man, I have no influence on my wife's tendency to hyper-ovulate.  And, of course, if we turn out to have monozygotic twins (we don't know yet), genetics plays no part.
Therefore the question only matters on my wife's side and only if dizygotic twins are known in her heritage. As it happens, we don't know of any twins on her side.  Given that many factors besides genetics are relevant to twins being born and we only know her family history for a half-dozen generations with any confidence, what are the odds that we would observe twins in her family history if she is genetically predisposed to having them?
Or, to put in another way, can I respond that nutrition and other factors were probably more important than genetics?

I admit to being amused that you say you "only" know her family history for something like 6 generations...:-)

The propensity for heterozygotic twins seems to be driven primarily by genetics, with additional factors playing a role (http://152.98.160.29/contents/p/staff/CV162Lewis_UQ_Copy.pdf', info site):

hormones ("Mothers of fraternal twins tend to be taller, and have earlier and shorter menstrual cycles")
ethnic background (which is really genetic) - African women are more likely than Caucasian women to have them, and Caucasian women are more likely than Asian women to have fraternal twins
mother's age
nutrition
previous births
fertility drugs

I also found a link to a genetic study published in Nature that claims to have linked a DNA region to dyzotic twins, but the Nature website seems to be down - maybe it will work later: A region on chromosome 3 is linked to dizygotic twinning - Nature.
Note that the father does not contribute to the chance of having heterozygotic twins, but a male offspring could pass the gene to daughter.

Do you have a source for: The propensity for heterozygotic twins seems to be driven primarily by genetics?

The Nature site is working for me.  An interesting quote: "Intra-uterine selection may be responsible for the Hardy−Weinberg deviation and we may in fact be dealing with a gene involved in the intrauterine survival of dizygotic twins."  I'm not sure I understand that, but it sounds like this study doesn't link genetics to hyper-ovulation, but survival in the womb.  Most of the information I've read so far point to a genetic link to the number of eggs released instead.

@JonEricson, added a couple of sources. It is my own impression from reading the sources that genetics is the most important. One way to think of it - without the genes for it, there is virtually 0 chance of it happening. In other words, it doesn't seem possible to just eat a bunch of soy beans, let's say, and have twins as a result.

@JonEricson, I don't think they try to establish any kind of causal relationship between the gene and hyperovulation. They simply found a suggestive correlation, but for the purposes of your question that would indicate a strong genetic component, I think. The study was geographically localized, which makes it more difficult to reach a general conclusion. The interesting thing that I noticed: they throw some doubt on the 'maternal lineage only' hypothesis. The quote you mentioned, I think it simply gives an alternative explanation for the disequilibrium in the alleles that they found.

I think it would help if some of your comments were added to the answer.  I particularly appreciate: "it doesn't seem possible to just eat a bunch of soy beans, let's say, and have twins as a result."  On the other hand, the practical aspect of my question is really a statistical one.  Are the genes for twinning very rare or do they just rarely produce twins?

Nutrition and environment don't have a huge affect, if any, that I could find. Age can, as women above 35 have a greater propensity for bearing twins. http://en.wikipedia.org/wiki/Twin#Fraternal_.28sororal.2Fdizygotic.29_twins
However, because fraternal twins can be the result of a gene on the X-Chromsome, the answer is yes in this specfic case. http://genetics.thetech.org/ask/ask86  If a mother is, herself, a fraternal twin then her chances of bearing fraternal twins is 2.5x higher than normal and it can be inherited from the mother's side even if she's not a twin herself. It's definitely not guaranteed, as the normal chances are so low to begin with, but there is definitely an increase.
However, for all other types of twins I have not yet been able to find anything implying there's a genetic component.

Hmm... I read those references as well and my impression was that nutrition did have a significant effect.  The age factor sounded more like a function of fertility treatments than age itself.  (We were actually trying to hold off on more children as it happens--our birth control failed.)  It does seem like a reasonable thing to point out is that my wife is not herself a twin.  But I'm more curious about the question of whether searching back through the family tree is a waste of time, statistically speaking.

I am still catching up on this topic but there are (atleast) 3 documented towns with greater than average rate of twinning: Cândido Godói, Kodinhi and Igbo-Ora. A published study on the Brazilian town might also be of help. It might be informative to look at familial twinning in these examples as beginning clues.


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In a vertebrate chimera, are particular organs homogenous genetically?
I have read that a chimera is an organism with two or more sets of DNA, with every cell having one of the sets. Is it possible and common for the two or more sets to be present in the cells of a single organ? I'm confining my question to vertebrates because I don't remember much about the biology of invertebrates from high school, but please don't hesitate to add anything interesting about them.

Chimerism (or genetic mosaicism if the cells come from the same zygote) is possible in the same organ or tissue. I don't think you will see a homogeneous distribution of the chimeric tissue because the tissue in any vertebrate organ is rarely homogeneous to begin with. Microchimerism may occur in a small number of cells. That's about all I know.

Could you add references to your answer?

@roryM, the links don't count?

@bobthejoe I read through them and couldn't find any reference for the chimerism can happen in the same organ/tissue point, plus the second is a wikipedia article, I'd rather see their references directly linked to.


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What does vitamin B6 and B12 absorption depend upon?
I'm looking at my question about homocysteine metabolism and am doing a followup inquiry into vitamins B6(Pyroxidine) and B12(Cyanocobalamin). I've found this interesting bit about vitamin B12 and am looking at its implications:

Approximately 56% of a 1 mcg oral dose of vitamin B12 is absorbed, but absorption decreases drastically when the capacity of intrinsic factor is exceeded (at 1–2 mcg of vitamin B12)

Quote from vitamin B12 fact sheet
I'm trying to understand the implications of an intrinsic factor involved in B12 absorption. Lets say that a person gets vitamin B12 from both food and a single supplement pill. Will taking that pill "use up" the absorption factor and prevent food's vitamin B12 from being absorbed over time?
This is the first time I'm hearing of additional "factors" that may limit vitamin absorption in the human body. Is this common across vitamins, or is it B12 specific?
Thank you for your input!

Vitamin B12 (cobalamin) is a water-soluble vitamin required for homocysteine methyltransferase. In order to be absorbed, it must bind to intrinsic factor (IF), which is produced by the parietal cells of the stomach. The absorption of the vitamin B12-IF complex occurs in the terminal ileum (of the small intestine). The quote just means that if there isn't enough IF, then you can't absorb vitamin B12.
There are many things that limit absorption of vitamins, and even vitamin B12. Because vitamin B12 is found in animal products, vegetarians and vegans may need to supplement it. Pernicious anemia is an autoimmune disease that destroys IF or the parietal cells, Gastric bypass surgery can lead to vitamin B12 deficiency. Anything that affects vitamin B12 absorption in the terminal ileum, such as in Crohn's, celiac disease, or enteritis, can lead to deficiency.
To answer your question, no. Yes, it will use some IF (provided you have IF), but that would allow your body to absorb vitamin B12. For people who have diseases mentioned above, they can take vitamin B12 via injections, subligually (under the tongue), or intranasal gels, according to the fact sheet you cited.
Because all the B vitamins and vitamin C are water-soluble, they are easily absorbed through the intestinal wall. Excess amounts are usually excreted in urine. I believe vitamin B12 is the only vitamin that needs to be bound to a factor, due to its larger size. It can be stored in the liver for several years. Fat-soluble vitamins (A, D, E, K) are absorbed with lipids.