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Why will tissue from identical twin be rejected in some cases?

Also, transplants from one identical twin to another are almost never rejected.
[ Source: Medline Plus ]

Why can a tissue from an identical twin be rejected ?

I don't think there is a reason in identic twins, since they have identic surface antigens on the cells.

MattDMo, I think you're right on.  Also remember the thymus is where T-cell recombination and maturation occurs during fetal development, and rates are highest during neonatal period through pre-adolescent childhood - long after sharing a womb.
The immune system keeps developing during childhood.  It's the immune system that's responsible for tissue rejection in transplant.
In our immune system, T cells attack and kill foreign cells in the body.  They're supposed
to ignore cells that carry molecules belonging to their own body.
T cells go through selection in the thymus during these years to eliminate the T cells that attack their own molecules;the rest of the T cells that recognize foreign molecules are allowed to live.
Next, consider that environmentally-induced epigenetics influence the expression of proteins and other products.  Even twins have different experiences and exposures, so there may be a difference in protein components in their bodies.
Also, this is conjecture, but the same concepts involved in autoimmune disorders (which are another topic entirely) might also be involved in some of these situations as well.

While Epigenetics play a role in the different expression of proteins and is different even between identic twins, the important proteins for determining own and foreign come from the HLA-complex. And these are identic in identic twins (but not in other, even closely related persons).

This was too long for a comment, but I have absolutely no evidence for what I'm about to say :)
It looks like that sentence was a little bit of hand-waving, as the author didn't want to categorically state that identical twin tissue would never be rejected. I suspect that in the early days there may have been reports of organ failure (esp. kidneys) in the recipient that were incorrectly identified as rejection episodes. I suppose there's also the slight possibility that one twin could have a mutation event very shortly after the separation of the twins in utero (when all the cells are still pluripotent) that could somehow change or (more likely) silence one or more of the HLA or other surface antigens involved in transplant rejection. This would almost certainly have to happen when the separated twin was a single cell. The mutated twin would therefore not express an antigen the non-mutated twin did, and if the non-mutated twin donated a kidney or other organ to the mutated one, its immune system wouldn't recognize the silenced antigen and could potentially result in rejection.
Like I said earlier, all pure conjecture :)


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What is the proper format for genus and species names in latin?
When using the latin nomenclature for a fish in printed materials (such as Sander vitreus for walleye), what is the correct capitalization of each word?
In this example, should 'S' be uppercase only, or both 'S' and 'V' be upper/lower case?

The correct latin nomenclature is Sander vitreus, with the genus capitalized and the species name in lowercase.  This is known as binomial nomenclature.

Carl Linnaeus chose to use a two-word naming system [...] binomial nomenclature scheme, using only the genus name and the specific name or epithet which together form the whole name of the species. For example, humans belong to genus Homo and their specific name is sapiens.  The first letter of the first name, the genus, is always capitalized, while that of the second is not, even when derived from a proper noun such as the name of a person or place.

Some scientific naming conventions:

Classification example (for Homo sapiens):

Adding to it: If you abbreviate the name its the genus which is shortened. In this case it would be S.vitreus.

Awesome -- thank you both SO much for the quick and thorough responses!

@Sbechet When you like the answer (and it answers your question) you can upvote it and also accept it. This way the person who answered it get the reputation credit for it and it is a nice way of saying thank you on the Stackexchange network.

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Size of DNA in phage
I have read that DNA(after recombination) is packaged in bacteriophages lambda only if it's between 40000 and 53000 bp long. This constraint can be used to ensure packaging of recombinant DNA.
I don't understand why shorter DNA can not be packaged.
Source : Lehninger Principles of Biochemistry

Does the Lehninger explicitly state that it is not possible?

These values relate specifically to lambda phage.

@Chris Yes. And as Alan Boyd states, this values are applicable only for bacteriophage lambda. (Edited my question)

For lambda:

If the distance between the two cos sites is less than ~37 kb, the resulting phage particle will be unstable. When the DNA is inside the capsid, it exerts pressure on the capsid. Likewise the capsid exerts an inward force on the DNA. If there is not enough DNA inside the capsid, it will implode from the inward force of the capsid. If the distance between the two cos sites is too far (~52 kb), then the capsid will be filled before the second cos is reached. The tail cannot be added because the DNA hanging out of the capsid is in the way and no infectious phage particle is produced.

http://www.microinmuno.qb.fcen.uba.ar/03-Bacteriophage.pdf
In contrast filamentous phage like M13 have no upper size limit, but since they get longer with more DNA they become physically fragile.

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Why does the stability of YAC increase with size?
From Lehninger Principles of Biochemistry :

The stability of YAC increases with size (up to a limit). Those with
  inserts of less than 100000 are gradually lost during mitosis.

Why does this happen ? (YAC refers to yeast artificial chromosome )

just guessing: perhaps small YACs have problem during mitotic segregation (too small for the cohesin and kinetochore assembly)

From The world of the cell by becker : Infact, YAC must carry at least 50000bp to be reliably replicated and segregated. This supports @WYSIWYG guess.

@user137 :P Edited it !

This is a question which is not easy to answer, especially the 50.000bp number (which I haven't found anywhere in there literature). However, I found some evidence, partly derived from plant and mammal artificial chromosomes (references 1 and 2), partly from the original publication from Murray and colleagues (reference 3).
The problems with small chromosomes seems to be their passage through mitosis and meiosis, where smaller artificial chromosomes tend to get lost. They are also not controlled very well in their number.
Murray states that YACs of 55kB in size are relatively stable in the yeast cells are relatively stable, but have a lower stability than natural chromosomes. When you are interested in the deeper details, I recommend reading the article.
References:

Construction of mammalian artificial chromosomes: prospects for
defining an optimal centromere
Alteration of chromosome numbers by generation of minichromosomes –
Is there a lower limit of chromosome size for stable segregation?
Contruction of artificial chromosomes in yeast.


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Are there special constants in biology that define organism's morphology?
In math, there are special numbers, like Pi (3.14159...) and e (2.71828...). In chemistry, there's numbers like avogadro's number (6.0221413e+23). For example a circle can be defined in terms of 2 * Pi.
Are there any significant constant numbers in biology that define the shape of an organism (ex: mammal)? I'm talking about stuff like shoulder to hip ratio or length of an organism, etc?
Here's an example that came to mind - different fetuses developing into different organisms. Is there any constant that is the same for these at some stage of development? Like the ratio of head to tail?

A fundamental idea of biology is individual variation. Though I don't know, I expect that there would be few, if any, constants shared between members of a group (outside of the molecular level).

The golden ratio turns up in a lot of places, if that's what you mean

To give context to the question: I'm interested if there are some numerical patterns to gene expression during organism's development.

I don't know if this is what you mean, but take a look at BioNumbers.
Also, mathematical constants like pi are different from physical constants. Mathematical constants are true in a mathematical (logic) sense, and do not need to be related to any physical quantity. They are derived by logic. Physical constants, on the other hand, typically describe an observed relation between two types of quantities. They are derived by measurement.

I think you have the direction of causality reversed. Due to either physical, chemical or dynamical properties of cells and organisms, it would certainly be possible to see patterns of constants emerge when making some measurements. I don't think you can say that the mathematical constants define any aspect of an organism. The Golden Ratio, or phi, was brought up as a recurring pattern in nature (e.g., the spiral pattern of snail. shells and sunflower seeds) but these are emergent properties of a physical system bound by physical constraints, and it so happens some pattern is used because it is efficient (in whatever sense that may mean).

There are lots of examples of human body parts demonstrating the golden ratio.

Any scientific references on the appearance of the golden ratio in nature? From what I know this is highly debated.

There are 20 references concerning facial symmetry and the golden ratio indexed on PubMed, and nearly 800 mentioning the golden ratio itself. I'm not sure there will be scientific evidence per se, since that would require experimental evidence. Instead, most of what I've seen about the golden ratio (or the associated logarithmic spiral or golden angle) are observational reports. The significance of this number is debated, but I don't see any arguments discounting its existence.


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How to study the effect on tau protein isoforms on microtubule based transport?
From what I read, A-beta plaques inhibit microtubule based transport of mitochondria when tau protein is present in the cell. How would I be able to do a test to see if one isoform of tau is more effective at conferring this A-beta sensitivity than another isofrom?

You can do a microscopy based assay to quantify the transport rate (both retrograde and anterograde). Mitochondria can be labeled with fluorescent proteins such as mito-dsRed, and its movement along the axon can be tracked by live cell imaging. You can check this paper; they have done this experiment. (Others have also done it but I remember this paper because someone told me about it recently).
How do you plan to see the effect of different isoforms? It may not be that easy. You will have to replace the common isoform with the others. It is not very easy to control splicing. So you may have to make lines that express only one variant (exon deletion). Though this study reports that alternative splicing can be controlled by using antisense oligonucleotides, the technology is not standardized yet; you can try it nonetheless, because making knockouts is difficult (you would have to make KO mice and then culture neurons from it).

Reference The transport is anterograde. I just need to think of an assay that will test which naturally occurring isoforms of tau will confer the greatest sensitivity to A-beta inhibition of MT based anterograde transport. Are you saying I would have to generate different lines, each expressing only one isoforms, and compare their vesicles transport rates along the MTs?

does this answer your question ? The test that you intend to do is not that straightforward

Could I just take a tau KO line and introduce different tau isoforms to different neurons and then measure vesicles transport rate and compare them?

You can do that too. But I am skeptical if tau KO mice will survive. Another trick is to intoduce loxP sites near exons/the gene and delete it by induction. You may also try working with neuroblastoma cell lines (e.g. Neuro2a) or PC12 cell line instead, for the ease of growing and manipulation. They can be differentiated to neuronal phenotype by retinoic acid/NGF treatment.

Ah I hadn't even thought of introducing loxP sites. That's a good idea. Thank you for all the help.


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Why does evolution not make our life longer?
Why does evolution not make life longer for humans or any other species?
Wouldn't evolution favour a long life?

Your question is a little unclear but are you asking "why do we age?/why hasn't evolution made us live forever?"

@GriffinEvo yes! why evolution not made us live more? Is not goal of evolution to make us better to let human kind live more?

Evolution has no "goal". It is "simply" the survival of the fittest under a given condition. What should be the advantage of living longer? Getting kids (=spreading the own genetic information) is done latest until the mid-40s after that we have not much biological meaning.

@GriffinEvo I'm waiting for your answer!

For the whole species it is advantageous that older individuals die to make more room (and not use up food) from younger generations. Evolution doesn't only work on an individual scale.

In addition to @Chris, not only does evolution not have a "goal," evolution doesn't necessarily mean "make us better!" It's absolutely possible to evolve negative traits.

A longer life span would eventually mean either less reproduction or more overcrowding.  It seems to me that the former would slow down evolution and make us less adaptive as a species, and the latter is simply suicidal.  Of course evolution didn't sit down with Excel and figure all this out.  But evolutionally, immortality isn't all it's cracked up to be.  :)

Related question on "Why do we die?"

I note that the question is incoherent in at least two ways. First, you've used "longer" without saying "than something".  If we replace "longer" with "longer than 100 years", or "longer than elephants", or "longer than lifespan 10000 years ago" we'd get three different answers.  Second, the question presupposes that evolution does not make life longer. Evolution has made life longer for humans than for many other species. Asking "why does X not happen?" when X does happen means the question cannot be sensibly answered. I would clarify your question.

There are a few benefits to aging and death. Firstly, if you have two coexisting (and non-competing) species, one that ages and dies, the other that is immortal and reproduces forever, you'll reach a point where all children of the immortal species die because the large number of adults out compete them. This leaves you with an immortal population with a very slow turnover of individuals and a population that dies of old age with constant genetic fluctuation, much more resilient to change and disease.

I agree with those who think it's not a good question; it sounds like something a creationist would ask, in order to get more arguments why evolution theory is nonsense. The whole premise is wrong: evolution is not a driving force, it's just a description of what happens.

@Chris what you say is true, but how is that relevant to the question? You're also assuming living longer wouldn't increase the number of fertile years, which doesn't have to be so.

@gwho It's a comment, not an answer. Besides that, our muh longer life is occurring only for a very short time period (less than 100 years), so evolutionary we haven't adapted to that. I might happen.

Evolution chooses the best out of available. It can't create best. That can only be a +ve mutation.

If this subject really interests you I would strongly suggest taking a look at the book: The selfish gene by Richard Dawkins. I had a blast reading this and in chapter 2 there is a section specificly answering this question, citing G.C. Williams as does the accepted answer.

@DartFeld Thank you for suggestion! I hope find a free time to give a look at it. :)

@cHao evolution does not care is something is detrimental to the species, gene level selection driving an species extinct is completely consistent with both evolutionary theory and observations.

@John: It is not, however, consistent with some longer-lived species being around to ask the question. :)

@cHao sure it is, it is perfectly possible to a species to drive itself extinct. Some would argue humans are already doing so.

@John: An extinct species wouldn't be around to ask the question. Still waiting for the relevance.

Why do we age is a classical question in Evolutionary Biology. There are several things to consider when we think of how genes that cause disease, aging, and death to evolve.
One explanation for the evolution of aging is the mutation accumulation (MA) hypothesis. This hypothesis by P. Medawar states that mutations causing late life deleterious (damaging) effects can build up in the genome more than diseases that cause early life disease. This is because selection on late acting mutations is weaker. Mutations that cause early life disease will more severely reduce the fitness of its carrier than late acting mutations. For example, if we said in an imaginary species that all individuals cease to reproduce at 40 years old and a mutation arises that causes a fatal disease at 50 years old then selection can not remove it from the population - carriers will have as many children as those who do not have the gene. Under the mutation accumulation hypothesis it is then possible for mutations to drift through the population.
Another hypothesis which could contribute to aging is the antagonistic pleiotropy (AP) hypothesis of G.C. Williams. Pleiotropy is when genes have more than one effect, such genes tend to cause correlations between traits, height and arm length probably have many of the same genes affecting them, otherwise there would be no correlation between arm length and height (though environment and linkage can also cause these patterns)... Back to AP as an explanation for aging, if a gene improves fitness early in life, but causes late life disease it can spread through the population via selection. The favourable early effect spreads well because of selection and, just as with MA, selection can not "see" the late acting disease.
Under both MA and AP the key point is that selection is less efficient at removing late acting deleterious mutations, and they may spread more rapidly thanks to beneficial early life effects. Also if there is extrinsic mortality (predation etc.) then the effect of selection is also weakened on alleles that affect late life. The same late-life reduction in the efficacy of selection also slows the rate at which alleles increasing lifespan spread.
A third consideration is the disposable-soma model, a description by T. Kirkwood of life-history trade-offs which might explain why aging and earlier death could be favoured. The idea is that individuals have a limited amount of resources available to them - perhaps because of environmental constraints or ability to acquire/allocate the resources. If we then assume that individuals have to use their energy for two things, staying alive via repair and maintenance (somatic-maintenance) and making offspring (reproductive-investment), then any energy devoted to one will take away from the other. If an individual carries a gene that makes it devote all of its energy to somatic maintenance then its fitness will be very low (probably 0!) and that gene will not spread. If the level of maintenance required to live forever costs more energy than an individual can spare without suffering from low fitness (very likely) or can even acquire and efficiently convert in the first place (also very likely) then high-maintenance alleles will not spread (and aging & death will continue to occur).
To go a little further, it is common for sexes to age differently (this is what I work on) and one possible explanation is that the sexes favour different balances of the trade off between somatic-maintenance and reproductive investment, this can lead to conflict over the evolution of genes affecting this balance and slow the rates of evolution to sex specific optima. This paper provides a good review of the area.
To summarise, evolution has not managed to get rid of death via genetic disease etc. (intrinsic mortality) because the effect is only weakly selected against, and those alleles may provide some early life benefit, and resource limitation may also reduce the potential to increase lifespan due to trade-offs with reproductive effort. Adaptive evolution is not about the survival of the fittest but the reproduction of the fittest - the fittest allele is the one which spreads the most effectively.
EDIT: Thanks to Remi.b for also pointing out some other considerations.
Another thought is that of altruistic aging - aging for the good of the population (the population is likely to contain related individuals, you are related to all other humans to some degree). In this model aging is an adaptive process (unlike in MA where it is just a consequence of weak selection). By dying an individual makes space for it's offspring/relatives to survive (because resources are then less likely to limit populations). This will stop excessive population growth which could lead to crashes in the population and so, by dying earlier, an individual promotes the likelihood that its progeny will survive. Arguments of altruistic sacrifice are often hard to promote but recent work suggests that this is a more plausible model than once thought.
Evolvabilty theories also suggest that aging is an adaptive process. These suggest that populations, composed of a mixture of young and old, have biases in how well adapted the members of the population are - where younger individuals are better adapted (because they were produced more recently it is likely that the environment is similar to the environment they are favoured in). Thus by removing the less well adapted individuals from a population via senescence and freeing up resources for younger better adapted individuals, a population evolves more rapidly towards it optimal state.

+1 I bet I would never have got 5 upvotes to my answer if you'd had posted your answer earlier $\ddot \smile$ . You don't talk about some hypotheses of the kind "Because our body is not so flexible (most cells are specialized (not very totipotent anymore)) we can't heal from many damages. The population where old individuals free places (by dying) for the younger individuals which are more fit will thrive compared to populations that don't do this (lineage selection)". You may not be so far from giving an exhaustive list of hypotheses that would definitely would make your answer perfect!

Regarding your third consideration; there are 3 things that an organism can spend its resources on: reproducing, growing and maintaining. The third consideration only works if growing is cheaper than maintaining (since if an old organism reproduces and dies a new organism must grow to replace it).

On the other hand, living a bit longer than reproducing can also be good for fitness because then you can help your offspring along until they are old enough to live on their own. (So your 40/50 year example gene might still have a bit of negative selection.)

@RichardTingle I would include both growth and maintenance in somatic maintenance - this is how it is regarded in the literature on the subject

@PaŭloEbermann yes, some kin/group selection arguments would reduce the negative effect of living long but it requires some social structure and group selection is generally weak so I chose not to delve to far in to that subject, but yes, if by living longer an individual increases the fitness of its offspring then there is a positive effect of long life via indirect selection

@GriffinEvo it seems strange to group them together.  If (for example) growth =10 units/year. Maintainance = 5 units/year then (other consideration aside) immortality becomes the optimum choice, whatever the cost of reproduction, since every year an old organism lives you have a net 5 extra units to spend in reproduction.  On the other hand if growth=5 units/year and maintenance=10 units/year (seems unlikely; although perhaps repairing a damaged organ could be more complex than building a new one from scratch) then a finite age makes sense

@richardtingle  your example doesn't give the full picture, it needs more info. if, within a population, the average individual takes up 10 units of energy which it can spend in its life, reproduction events cost 1 unit of energy per offspring produced, and the repair and growth costs 3 units of energy per reproductive cycle then the optimal strategy is to to neglect somatic maintenance (growth AND repair) and have seven offspring in one reproductive event - it's the way to pass the most copies of its genes with its limited budget

The evolvability ideas would suggest that, in a stable environment, lifetimes (and reproduction window) will get longer and longer. But we're not seeing this in any lifeforms at all, even in the most stable environments. So, there must be the other factors involved, i.e. that from some point it's easier to build from scratch than to repair, for the same reason that old buildings from the sixties are knocked down instead of being refurbished. About the last sentence: it evolves more rapidly towards a local optimum state. Evolution cannot find global optima in general.

@evgenisergeev evolvability is in my eyes a weak argument to the adaptive spread of aging - at best I'd suggest it can offer very weak influences on selection. Like you, I think other factors play a larger roll in shaping the evolution of aging, but many of these above are not mutually exclusive ideas. *and nor do I necessarily agree with the ideas, but this site is about answers based on science, not my opinions :)

Do we know why exactly does a bacteria or eukaryotic cell, seen by itself, die of old age? Are its protein structures all crumbling? Is its membrane all wrinkly? Are its organelles cluttered with debris and have bits broken off? If that's so, then the only way an animal can live indefinitely is if it replaces all its cells every so often. And how many animals do you know that can do that?

@evgenisergeev RE the last sentence - you may have misinterpreted what I said, to clarify -  if we compare two populations, where the resources (inc. space) are limited and the rates of evolution are high such that young are better adapted than old. If in one population we remove the oldest individuals and in the other we remove at random (but equal rate) then (according to evolvability hypothesis) the selectively altered population should be better adapted after time has passed

@GriffinEvo I'm not sure I understand this concept of energy/lifetime. Why is an organisms total energy capped? As opposed to its energy/year. If we are getting free radical damage into the equation thats a reason for non infinite age but thats a seperate issue and something evolutions would try to overcome

@RichardTingle energy will be capped by the energy content of food, efficiency of energy conversion, ability to find and consume food (spatial and temporal limitations, including spending time doing other things like sleep and reproduction), resource competition... You can ignore the thought of free radicals in regards to this question, it is more why aging evolves (ultimate question) rather than why we age (on a mechanistic level)

@GriffinEvo Yes but that is all a cap/year not a cap/lifetime. If it takes 10 years (and 100 units of energy - 10/year) to bring an organism to sexual maturity and 5 units/year to maintain it and 5 units to reproduce. An organism is 10 years old, its total spend is 100 units and its got 10 to spend this year. It can (a) have 2 childern and die or (b) have 1 child and live to next year. If it chooses option (a) it will have 2 children; neither of which will reproduce for 10 years (and 100 units will be effectively thrown away). If it chooses (b) it can keep having 1 child a year indefinately

So in a decade from now there will be 2 sexually mature organisms either way. Option (a) it’s the two children and in Option (b) it’s the original organism and the first child. But in option (b) there are also children at ages 9 through 1. Of course all this breaks down if you’ll probably be dead in a year anyway (which in nature probably isn’t an unreasonable assumption).

Won't Individuals who are fittest get to reproduce more? If someone lives upto 40 and have 5 children vs if someone lives upto 500 and have 400 children...isn't 2nd one at advantage. Secondly, many life forms seem to live their whole lives without aging much...and i know of one that is actually biologically immortal...aging is no problem to it. Where is error accumulation in them?. I agree with the theory that for a group with limited resources natural selection would favor formula where weak gets replaced by stronger ones..However, more favorable group would be in which no one gets weak.

@RichardTingle The disposable soma model is a TRADEOFF scenario - in your example that does not happen (individuals have enough resources to reach 10 years regardless of strategy). The idea is that an individual can not secure the resources necessary to both produce the most number of offspring per reproductive episode and maintain/grow indefinitely.

@MuhammadUmer See above - the disposable soma is a TRADEOFF, an individual can either prioritise reproduction or maintenance because it is resource limited so it is not as simple as your example. As for biological immortality, it does appear in some species (lobsters is one example) and rate of aging varies between species. Immortality is probably not ubiquitous because it likely requires complex cellular machinery and species where it occurs could boom and collapse due to over-population/resource depletion.

@Griffin Under my example I'm assuming an animal does not become reproductively active until 10 years, what you're saying makes sense if you could have 1 child ever or live forever, but I don't see the mistake in my maths where you can trade off halving reproduction per year to increase life by 1 year (each year - so effectively half rate for immortality). The avoidance of boom and bust makes sense however

This is a very good question.
There is a big ongoing field of research called "evolution of aging/senescence" that tackles this question. I won't give you a complete overview of the different hypothesis the could explain why we age but here is a fundamental concept that is to know.
We'll assume that there is some extrinsic mortality, mortality against which a lineage won't ever be able to escape and I think it is not an assumption that is hard to meet. Therefore, an allele that has age-specific effect such as decreasing the fecundity at age 3 will undergo a higher selection pressure and will faster get eliminated from the population than another allele causing the same decrease in fecundity but at age 4 because some individuals would have died between age 3 and age 4. In other words, natural selection is more efficient at lower age than at higher age. Now, imagine in humans an allele that increases the reproductive success of an individual at age 20 by decreasing the survival at age 78. This allele will easily spread in the population. Such alleles are said to have age-specific antagonist pleiotropic effect. And empirical studies have shown that alleles that have antagonist age-specific antagonist pleiotropic exist.
In short, it is because there is some extrinsic mortality that natural selection acts with a different strength at different ages allowing some deleterious allele at old age to fix in the population especially if those alleles have age-specific antagonist pleiotropic effect. You'll find in this book mathematical formulation and more complete discussion of this effect
Other hypotheses exist which are based on lineage selection, group selection or on the mutation-selection balance.

Actually, genetically, there is no reason for animals to continue to exist after they have procreated.
If you look at salmon, they die immediately after procreating, which is probably the most efficient way to carry the best genes to the next generation.
In the case of mammals, they need to teach their offspring where to find food, where to find water and how to avoid dangers.
In the case of humans, that goes into the third generation, so most humans know their parents and their grandparents, and even they live with them in some cultures, since their experiences and ideas are taken as very important.
So maybe the question should be the opposite, why do we live to see our grandchildren grow?
Taking your same question to the opposite: why do people die? Why don't they live forever instead of reproducing? I can think of various reasons for this. Imagine a race that lives forever and another race who have a lot of children early on and then die. Now imagine a contagious disease that spreads among both populations. Which race has the most probability of survival?
Of course, the race that reproduces rapidly has a better chance.
And also, evolution works wonders for the race that reproduces rapidly instead of the race that lives forever. Meaning the number of years a species live has carefully been "designed out" by evolution.
Evolution would not work if it didn't stabilize around the best genes. And that's exactly what happens with humans. Most humans have the same traits: live around the same number of years, and have more or less the same abilities, most differences are almost irrelevant.

Another example for this line of argument: http://www.wired.com/2014/05/absurd-creature-of-the-week-this-marsupial-has-marathon-sex-until-it-goes-blind-and-drops-dead/

There is an exception to the statement that animals dont need to live after they have procreated, and that's in most social mammal groups, the older patriarchs or matriarchs use their memory to guide the group away from danger and towards food. Especially with humans, where the oldest naturally occuring individuals are about 80-90 that help to guide the group, see native american tribes for example. In other social animal groups, the oldest individuals often have a role to play in guiding travel,i.e. elephants.

I get what you're saying, but I must first object to "reason for animals to continue". This language is hard to avoid, but it does imbue a certain paradigm or assumption that genes are the purpose (there is no purpose in evolution), while the phenotype and the boday are carriers. It's a useful paradigm to analyze the essence of evolution, which are the genes, but that wording confounds and obfuscates clear thinking, which is necessary to tackle questions like these.

Animals after reproducing can have a "purpose" if they reproduce more. having multiple kids. If they can extend their fertile years, that would be reproductively advantageous, and help with those genes surviving. This is naturally assumed when anyone asks "why don't we live longer" with some awareness of evolution. If we live longer, they are also assuming fertile years be longer as well.

Here is an idea: if animals lived long past their fertile years, they would take up resources (less food, safe ground, etc), and leave less for the offspring which do/can reproduce. (Species may not compete for resources with vastly different species, but they certainly do compete with members of their own species.) Having a bunch of old, non-reproducing individuals would put a damper of the chances of survivability of their offspring. This is only one isolated effect to be superimposed with other effects which may take precedence or overshadow this effect.

Because evolution isn't about individuals: it's about species. What matters to natural selection isn't how long you live, but how many grandchildren you have. A long lifespan can be an evolutionary advantage, but like any trait, it's only an advantage to the extent that allows you to reproduce more.
It would seem that a longer lifespan would be advantageous anyway, because it would give you more time to reproduce. However, for reasons we don't yet fully understand, it doesn't seem to work out that way in practice. Most organisms (assuming they live long enough) eventually reach an age where they stop reproducing. Even humans do this, and although we've managed to increase the average lifespan quite a bit over the course of recorded human history (to say nothing of the millennia before that), the average age at which people stop reproducing apparently hasn't changed very much.
Why not? What makes this an evolutionary advantage over having more reproductive years? This is one of those things that we haven't really figured out yet. There are a number of competing theories, and the other answers here go into some of them. But the most direct way to answer your question is fairly simple: longer lifespans (and/or reproductive years) haven't given us, or our children, any more success at reproducing. Thus, there is no pressure on the species to live longer, and so it doesn't happen.

longer lifespans haven't given us more success at reproducing why do you say that?

Technically, evolution isn't even about species, but about aleles. Something can be an advantage to a gene, even if it provides no advantage to the species; for example retroviruses.

@MuhammadUmer: It's interesting, just because it seems so counterintuitive, but if you look at the period over which human lifespans have been increasing, the birthrates have actually gone down, not up. Nowadays, many of the nations with the longest life expectancies actually have some of the lowest birthrates, and vice versa. There probably isn't a direct causal link here -that is to say, the birthrate probably isn't dropping because people are living longer- but the fact remains that lifespans are going up in some parts of the world, but where that's happening, birthrates aren't going up.

First i don't think this effect among humans, that countries with highest expectancy have lowest birth rate, is the result of evolution. But could be a hint as to why it may happen in Evolution. Shorter the lifespan in the country the poorer the population..The reason recent study discovered that poor like to have many children while richer parents often opt for 1 or 2 max, is because value of the Amount of wealth that gets divided among children goes very high as parents get richer...

...on the other hand poor man can have 10 children and they would still be relatively as rich as only 2 would have been. For rich the effect multiplies...if you were going to inherit 10 million if you were only one child...but if you had 9 other siblings you'd get only 1 million. Loss of 9 million. If you were poor, then instead of inheriting $5000.   you get $500 Both won't last more than a month.

@MuhammadUmer: I think you're right. It's not the result of evolution, but it may explain why evolution isn't going the way that the original question was asking about. It's just like you say: having fewer children is a good economic strategy if you are rich, because it means that you don't have to divide your wealth as much. But it is a bad evolutionary strategy (whether or not you're rich), because you can't get your genes out into the wider species unless you have many children. And so even though economic factors are helping people live longer, we don't evolve along those lines.

Wow, you should work in politics or PR. You've done a wonderful job of repeating the question without answering it, in a very eloquent way, giving the impression that you've said something smart or worthwhile.
Also, you start off by saying evolution isn't about the individual, and then directly contradict yourself, saying living longer would help you reproduce more. Of course it will help you reproduce more if you have more fertile years, barring other linked genes. Yes, it's about the individual. The individual shares genes with others, also making it about the species. It's both, not one.

@gwho: I did not contradict myself. I said that it seems like living longer ought to help a person reproduce more, but in practice, it hasn't worked out that way (i.e. that living longer actually hasn't helped people reproduce more). There is no contradiction there: it's a simple difference between what's intuitive -such as the original question's reasoning, which is why I mentioned it- and what works out. The question wasn't about the evolution of the aging process, but why evolution hasn't given us longer lifespans, and so I even answered that. Your attacks on me are uncalled for.

One factual inaccuracy here: Most organisms (assuming they live long enough) eventually reach an age where they stop reproducing. This simply is not true. It is true that fecundity decreases with age, but it is not true that it goes to zero in most species in the wild. Rather, humans are quite unusual in that human females go through menopause.

I think you're right. The true evolutionary stable strategy has people able to never get too old to reproduce. If a mutant woman who reproduces asexually and happened to have the right genome arose, her clones would outcompete the rest of humanity. After that, if another mutant woman who's like a hydra and could had a rate of death that remains constant at 1/3000 years under laboratory conditions and can keep reproducing until she dies, her clones would outcompete humanity. After they spread, they would have a rate of death by competition that remains constant at 1/30 years.

If you take the line of "The Selfish Gene - Richard Dawkins". Evolution doesn't care about individuals, it cares about genes. So as long as the genes are passed along reliably into the future, evolution may do it with 4 generations per 100 years or 100 generations per 100 years.

Lifeforms that we know tend to have a mature state towards which they rapidly develop, and then live for a while after that. What about a hypothetical lifeform, such that the longer an individual survived, the more successful it became? Suppose its tool of choice was intelligence, and it was a a whale with four human hands, and its brain kept growing and it became smarter and smarter every year... I guess there is still a limit at which it can't improve... But this thought experiment shows that if a lifeform can find a way to develop further during its life, its life expectancy will grow.

The evolutionary drive works on preferential survival of children. So in such a species such as you suggest, the children of older members would have to be preferentially selected over the offspring of younger members.

We can arrange that. Just as in countries with higher IQ, the life expectancy is longer, because they can organise better healthcare for themselves, perhaps the growing brain will improve the medical skills of this hypothetical animal, and it would preferentially provide medical help to its own children first. (Assuming it's a universally benevolent species; if it's partially or fully malevolent, you can also imagine how the cleverer older individuals' children will be better off.)

This then becomes involved in politics and the organisation of healthcare.

@user6571 I just commented OP to take a look at this book before even seeing your answer. Extremely good book on the subject.

I agree with your first principle of the replication/survival of the genes. However, your conclusion is unclear. What do you mean by "doesn't care about individuals"? Are you saying the individual life span is irrelevant to the gene replication/survival? That is a strong claim without proof. In fact, I contend thos is a priori wrong. If the life span of the individual improves the replication/survival of the gene, there will be the tendency for the gene to increase the individual life span.

There is no selection mechanism that would favor high age.
By the time it's apparent whether or not an individual can reach a high age healthily, they'll have ceased all reproductive activity.
Conversely, people who get cancer at 45 will have likely reproduced already.

This assumes an organism becomes long lived while still stopping reproducing early rather than the whole of life extending.

but shouldn't genetic variations result in individuals that are of higher age than average age at which they cease all reproductivity. Thus being at advantage..then why that advantage hasn't been represented among humans?..to me this conclusion is flawed.

To an extent it does; in that we live longer than our mouse-like ancestors. So the question becomes: why not keep extending it to immortality.
The key thing is that evolution cares only about the survival of your genes; so if you live for 1000 years or if 10 generations of your family have 1 individual's worth of your genes in each generation (each living for 100 years) this is equivalently successful.
But this assumes it's either-or that an organism can reproduce or live a long time, could it not do both? In principle it could but the resources of a particular niche are limited so in order to avoid mass starvation the reproductive rate must reduce as the average age of the individuals go up.
So this suggests having very long lived individuals is no better than having short lived individuals, but is it at least equal? Sadly not, if fewer new individuals are born then the rate of evolution of that species is reduced. A very long lived species is less able to respond to environmental changes. As such over an evolutionary timescale an extraordinarily long lived animal is likely to be outcompeted by a shorter lived species.
Of course there is a natural breakeven point; there is a considerable cost in bringing an individual from infant to reproductive adult so once they've got there it makes sense to keep them around for a while, but not indefinitely.

I am assuming that by longer life, you mean slower aging, because evolution can do little if a mountain falls on a person!
So, why don’t organisms have slower, or better, zero rate of aging?
The theory I am describing is based upon life history theory. Life history theory assumes that:

Resources available to any organism are limited,
Life processes like ‘reproduction’ and ‘repair and maintenance of the body’ are costly with respect to resource consumption, and resources directed towards one life process must be directed away from the other. Hence a trade off mechanism between the different life processes must exist.

Based on this data, one can infer that given a specie with a given death rate of extrinsic causes (causes beyond that of aging, like getting eaten), one can use a little mathematics to find the average life span of the organism if the organism does not ages. Simple…?
Now, given that the average life span of the non-aging specie is limited, do you really think that the optimum life strategy of the specie would be zero aging? Remember that to not to get old one needs to spend energy, and that all the energy gone in maintaining health will certainly be wasted in the form of dead bodies once the organism dies.
Hence, given a mechanism through which trade off of resources between life processes is possible, the organisms must invest a little more towards reproduction and a little less towards repair and maintenance? Why? Just to reduce the loss of resources in the form of dead bodies and to increase reproductive success, which is what gets counted in the end!
So, indeed, having zero rate of aging has disadvantages! It would be more advantageous if organisms age with a fixed specie specific rate.
Now, time to make few points clear:

This theory assumes Life history theory to be correct. I am not saying- “hello there- this is the correct reason of aging!” I am saying- “This is the correct theory of aging if life history theory is correct!” So, if you do not believe in life history theory, then get busy trying to prove it wrong. The theory I have discussed stands on the shoulder of a giant. On the other hand, if you believe that the theory I discuss does not follows from Life History theory, then lets hear your argument.
This theory also assumes that aging happens due to lack of repair and maintenance of constantly occurring body damages. The special thing about this theory is that it gives a non-altruistic mechanism through which aging can directly benefit the organism. Hence, this theory makes it easier for us to explain why aging got natural selection- because it has benefits!

I found this theory on this SE question, where the question has now been put on hold due to dubious reasons. Also, the OP mentions this book- Modern Biological theory and experiments on Celibacy, which, I think, was one of the reasons why the question was put on hold!

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


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How does a pine cone open?
When a pine cone is wet, it remains closed. However, when it's dry it opens again.
From the perspective of physics or biomechanics, what is the mechanism that allows a pine cone to open and close as I've described?

From How Do Pine Cones Open (Nature):

The scales of seed-bearing pine cones move in response to changes in relative humidity. The scales gape open when it is dry, releasing the cone's seeds. When it is damp, the scales close up. The cells in a mature cone are dead, so the mechanism is passive: the structure of the scale and the walls of the cells composing the scale respond to changing relative humidity.

As to the reasons why:

Pine cones usually appear open because this is considered a more favourable condition for the seed dispersal and germination. This usually happens when the weather is warm and when they touch water or in cold conditions, they tend to close to avoid destruction.

As to the physics/biomechanics of the pine cone opening/closing, there is an interesting article titled Hygromorphs: from pine cones to biomimetic bilayers that discusses objects that respond to environmental humidity to change their shape.

Using the pine cone as an example that opens when dried and closes when wet, we quantify the geometry, mechanics and dynamics of closure and opening at the cell, tissue and organ levels, building on our prior structural knowledge.


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What are Antihistamines doing in a baby?
In his song Lullaby, Tim Minchin sings:

Your nappy is dry and your tummy is full
  Of enough antihistamine to chill out a bull
  Yet still all this gringing

According to Wikipedia, antihistamines are used against allergies.
So, why is there antihistamine in his baby's tummy and why is it supposed to make her sleepy?

This song most likely refers to an off-label (and usually inappropriate) use for certain antihistamines like Benadryl. They are sometimes used by parents to sedate their children, functioning through the exact physiological mechanisms @Chris describes.  Parents use it inappropriately as a means of behavioral control for active or upset children to make them more docile or sleepy, such as for airplane rides, etc.  It's not recommended by most pediatricians, because even though adverse (bad) side effects are usually rare, it is an actual medication with another primary mechanism of action having effects on many body functions, not a medication designed as a sedative.

my mom totally used this method on me and my siblings lol

This is not only happening in babies...
In short (I will look for some references later and edit the post) the antihistamines are effective in the whole body and block the histamines there. The antihistamines which cross the blood-brain barrier do the same in the brain and hinder the small amounts of histamines which stimulate the nerve cells there from doing so. This results in the typical sleepyness.


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Why are embryonic germ cells considered stem cells?
In a class that I'm taking we were presented 3 types of stem cells.

Adult stem cells which come from bone marrow
Embryonic stem cells which come from embryos
Embryonic germ cells which come from testes

I understand that adult stem cells are a bit more specialized than embryonic stem cells, but I'm confused why embryonic germ cells are considered stem cells. From Wikipedia, the definition of stem cells is:

Undifferentiated biological cells that can differentiate into
  specialized cells and can divide (through mitosis) to produce more
  stem cells

But from my limited understanding of biology embryonic germ cells can't specialize into any other cells unless they fuse with another gamete, so why would they be considered stem cells? What am I missing here?

You are confusing germ cells, sperm and oocytes with Embryonic Germ Cells. EG Cells are diploid, while gametes are haploid. I explain what EG cells are in my answer below.

The difference in designation is the timing of the foundation of the cell line and the tissue that it was sourced from.
Embryonic Stem Cells are harvested from the inner cell mass of a Blastocyst around day 5 post fertilization. This is the first or second generation of cells to have started to differentiate, but they still have Pluripotency, which means that they can differentiate into any one of the three germ line cell types. [1][2]
Those  three germ cell types are:

Endoderm
Mesoderm
Ectoderm

Embryonic Germ Cells are "cultured from primordial germ cells obtained from the gonadal ridge and mesenchyma of 5- to 9-week fetal tissue...." [1] These cells are multipotent, meaning that they will usually only be able to give rise to mesenchymal derived cell lines.[3][4]
There are also differences in replicative ability. ES cells are for the most part immortal cells able to be maintained in in-vitro culture for long periods of time, while EG cells have a life cycle of about 70 to 80 cell divisions before they reach quiescence.[1] If I had to venture a guess as to why this was the case, I would say that EG cells have likely already reached a stage of differentiation where they are repressing or down regulating the expression of Telomerase. ES cells will be expressing telomerase, so they will not experience telomere shorting due to the 3' end replication problem during DNA synthesis in S phase of mitosis.
There are other cell types of Adult Stem Cells other than Hemopoietic Stem Cells, so I am not sure why your course is making the distinction. It could be that in practice, we have only really successfully used Hemopoietic Stem Cells in treatments for diseases by doing bone marrow transplants. You would likely have to have your instructor clarify this point for you.

Stem cells in embryos are the basis for the development of the organism i.e once the gametes are fused you have a produced a cell that will replicate and differentiate into every cell that body is composed
Any cell that differentiates into another cell can be defined as a stem cell. Yes, the testes only produced sperm cells but a localized group of stem cells will almost always be differentiated into the same type of cell over the course of the organisms lifetime.
In reality a stem cell is no different than any other stem cell as they are all pluripotent. What makes stem cells different are the location in the body and the differentiation signals that are prevalent there.
For example the hematopoietic stem cells in bone are responsible for producing all types of blood cells due, while the stem cells in the crypt of the villi lining the intestinal tract differentiate into absorptive epithelial cells and mucus secreting goblet cells.
To summarize, a stem cell's differentiation is based on signals. The type of signals are ultimately determined by the function of the particular location that the stem cells reside in. (It is more complex than just "signals" but if you decide to delve into a bit of genetics and biochemistry it will make more sense).

Adult stem cells are considered multipotent, not pluripotent. They have differentiated to the point where they can no longer give rise to other cell lines. HPSCs will not give rise to neurons. There are laboratory techniques that will induce cells back into pluripotency, but those do not take place within the organism, that we know of. ES cells are really the only pluripotent stem cells, and they arise early in development, and differentiate into the three different cell lineages. I would also hesitate to say that any cell that differentiates into another cell is a stem cell...

Monocytes are partially differentiated cells that can give rise to macrophages. Activate B and T-Cells can differentiate into effector cells and memory cells. There is also a temporal aspect to signaling and how it effects cell differentiation.

Stem cells are defined as having two properties: self-renewal and differentiation. This definition applies to hematopoietic stem cells just as well. As such, the substance of this response is incomplete.

Adult stem cells don't always come from bone marrow. In any or most adult tissues still have stem cells exist. Stem cell doesn't only mean it can specialize into other cells. Any cell, if it has self-renew ability and never grows old, can be called stem cells. So, for men's germ-line, even it has limit differentiation ability, maybe just could turn into sperm, but it has self-renew ability and never grows old. The is the reason that some old man, over 100 years old, they still can have a newborn....


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Dimerization of Immunoglobulin G
I would like to know the specific determinants for formation of IgG dimers. My understanding is the stem of the antibody is a homodimer of two heavy chains, covalently bonded through two disulfide bridges called the hinge region. Is there any association between the constant region? My reading would suggest no but I have not found a specific reference as such.

Do you mean disulfides linking constant regions?

No, of course each immunoglubulin-like domain has an intramolecular disulfide (stabilizing the beta sandwich conformation). I mean between two heavy chain molecules.

For human IgG1 and 4, the only inter-heavy chain disulfide bonds are the two in the hinge region. IgG2 has 4 disulfides in the hinge, and IgG3 has 11:

There are intra-heavy chain disulfides in the Fc region, and of course there are non-covalent bonds between the two heavy chains (as well as the light chains) to maintain structure, but aside from the hinge region the only other inter-chain disulfides are between heavy and light.
Here is an interesting review of classical (determined in the 1960s) and non-classical (more recently discovered) disulfide bond formation and structure in human IgGs.

What's the nature of the hydrogen bonds/non-covalent bonding between two heavy chains? Are they naturally aggregated in the cell?

What do you mean by nature? This bonds are formed in the cell, yes, during the assembly of the antibody.


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examples of chromosomal aberrations with lack of sexual chromosomes?
Are there any examples in animals where individuals survive having no copies of their sexual chromosomes?

In humans the Turner syndrom is a disease that occur when the carrier is X0 (has only one sexual chromsome, the X chromsome). But it does not answer your question I guess!

Are you talking exclusively about nullisomic during the diplontic phase of an organism? Otherwise before Turner syndrome occurs in the diploid individual, one gamete (haplontic phase) has to be nullisomic for a sex chromsome.


text:
What are the Gateway clonase enzymes?
The Gateway cloning system utilizes what Life Technologies refers to as "Clonase enzyme mix" to catalyze the BP and LR reactions.
What is in this enzyme mix? Is there a sequence for them?

I would imagine that if they're not listed on the datasheet, you're not going to be able to find out what they are...

@MattDMo The manual (publication number MAN0000282) does mention that they are "Int, Xis, IHF". Are these actual genes? I would expect they are engineered further, but do the native genes not work at all?

@Superbest they are recombinases. Usually the enzymes that are used in the lab are engineered to some extent, for better stability and efficacy.

The prototypes for these proteins are:
the bacteriophage λ proteins Int and Xis, required for, respectively the integration and excision of prophages. They are, as mentioned by @WYSIWYG, recombinases.

Genetic map of bacteriophage λ (source of image)
the original Ihf (integrative/integration host factor) was identified as an E. coli protein required for prophage integration.
As you might expect Int and Xis proteins occur in many phage genomes, and in integrated prophages in bacterial genomes, and Ihf, because it is involved in bacterial DNA replication, is ubiquitous. I imagine the actual source of the proteins used by Life Technologies could be a trade secret.


text:
Help explain multi alleles in terms of actual genetic code
I understand that someones genetic makeup at an allele is usually denoted as (AA,Aa,aa).
That means that instead of an A-T pair you get a C-G pair on none, 1 or 2 copies.
Now, what exactly happens when you have a tri-allele (as in blood type). Are they looking at two base positions? Or is it instead of an A -> C mutation, you get something weirder like an A->G mutation (and thus you need to account for directionality) etc?
Thanks!

All of these things happen, but triallelic SNPs (single nucleotide polymorphisms) refer to the case where a single specific base in the genome may have one of three bases. e.g.: A/G/C
Cases where more than one base in a sequence that changes.  This doesn't really have a name though: (e.g. AA -> GC ).
These can be called a/b/c alleles I guess.
The reason for this not having a name is probably because two bases don't really change at the same time as a common event.  If two SNPs are next to each other they probably changed at different times, which means that if you look around enough you will find AA, GC, and GA because the A->G happened first and then a few dozen generations the second A->C mutation happened.

Ah, I see, so if the sequence is TCGAT and that the 3 position by default is a G, but can be an A or T that would be tri-allelic. if it can be A,C,G or T, then it's quad-allelic? Can you go higher than a 4 way somehow?

@user1357015 not at a single point, because there are only 4 bases in DNA. However, any one gene may have from a few to hundreds of SNPs, each one creating a separate "allele."

@MattDMo ah, I see. So a single point can be at most tri-allelic but a gene can be multi-allelic. In fact, if a gene is N bases long, it can then be 3N-allelic? Is that correct?

yup - you got it.  additional point is that each new addition to the allele is a separate mutation - it just happened in the same place

There are only 4 bases of DNA, but you can have insertions and deletions as well.  You can also have alleles that differ at multiple points, so no, there are a lot more than 3 x the length of the gene possible alleles.  Of course, you will only see so many possibilities in a real population.

@swbarnes2 Yes, I should of clarified. Assuming only point substitution mutations are allowed on a gene N units long -- that gene can have at most 3N alleles. Does that sound better?

Sound better?  Of course not.  You aren't limited to a single nucleotide change, and at every point, you can have 4 letters, not three.  How does it help to assume things that aren't even close to real?

Many models, for the sake of simplicity only deal with point substitutions. That's what I'm considering at the moment. Now, since each position is only 4 bases (and one is the "canonical"), there are only 3 mutations possible for each position. Since an "allele" is an alternative conformation, and there are only 3 alleles possible for each base (as one is the original one), why is 3N incorrect?

At a given point 4 alternative alleles are possible. its pretty rare is all.

@shigeta: I'm a little confused by the terminology then: Why at a given point 4 alternative alleles are possible. I thought an allele is an "alternative form". So there's the canonical base and then there are 3 possible mutations. Or is it that by "alternative" they mean including the canonical?

ok - well four alleles in any case.  triallelic means 3 possible alleles, bi-allelic 2 possible alleles.  in all these cases one would be most common for a given population. I do tend to think of all the alleles as alternatives to each other.

I understand that someones genetic makeup at an allele is usually
  denoted as (AA,Aa,aa).

No. That's what you learn in high school, because it's easy, and because it's what Mendel worked out for the 7 traits he studied in pea plants.  Real life is a lot more complex.  Most phenotypic differences cannot be explained in terms of exactly two alleles, one of which is classically dominant to the other.

That means that instead of an A-T pair you get a C-G pair on none, 1
  or 2 copies.

Not necessarily.  Two alleles might differ at many many points in their sequence.
And you seem to be a bit confused about how people write out DNA sequence.  Even though DNA is a double helix, when we talk about what the sequence is, we refer only to one strand, like this
GAGCCATGGGGCGCCATGTTGCCACCAGCTGCCACGTGGCCTGGCTTTTGGTGCTGATCT
A mutation might turn that last T into an A, but we don't say "oh, nothing happened, it's still an A-T pair" because it matters which strand has which letter.

Now, what exactly happens when you have a tri-allele (as in blood
  type).

Well, blood type is more complicated that just ABO...but here's a pretty old paper with some helpful details
http://www.ncbi.nlm.nih.gov/pubmed/2333095
"Here we present a molecular basis for the ABO genotypes. The A and B genes differ in a few single-base substitutions, changing four amino-acid residues that may cause differences in A and B transferase specificity.  A critical single-base deletion was found in the O gene, which results in an entirely different, inactive protein incapable of modifying the H antigen."

I'm not sure you've got a really solid understanding of what an allele is, so let me blather a bit and see if it helps.
The gene that codes for the enzyme that puts the "A" type of carbohydrate on a red blood cell is called the "IA" allele of the gene.  This gene is about 1065 base pairs long. If you were to spell it out, it would look like:
CAATGGCCGGGTAATTAAAATTGACGAC...
GTTACCGGCCCATTAATTTTAACTGCTG... (keep going to 1065 letters)
The most common O allele has the same series of base pairs, except one base pair (G_C) is lost at the 261 position. This is a deletion mutation.
The most common B allele is the same gene sequence, except there are seven single base substitutions within the coding sequence at base pairs 297, 526, 657, 703, 796, 803 and 930. These are substitution mutations.
Does that make sense? The basic ABO blood-type gene is almost the same in each allele, but has slight changes that result in different phenotypes.  And this is the simple version. Now that we can easily sequence genes, we can look in lots of people, and see that there are at least TWENTY different gene sequences with small changes in base pairs that still result in type "A" blood. You can see a figure with examples in this paper: http://www.ncbi.nlm.nih.gov/pubmed/12014997 (open-source)
So, since one gene has hundreds of base pairs, there are often many more than two, three or four alleles for that gene. You can add base pairs, delete them, change them, switch them in chunks from other chromosomes -- all kinds of stuff happens.


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How does an axon "know" it's not connecting to its own neuron?
I recently read about an experiment where they removed the dendrites and axons from rat neurons and placed them on a grid. After a while they started reconnecting and were able to learn things.
Since I'm trying to create a model simulating this, I'd like to know (as much as is needed to make it look at least a little bit realistic) how they reconnected. As far as I know some molecules are secreted attracting or repelling axon growth cones.
I think I can model that part, but the problem is that the axons can easily grow back to where they came from, so how do the axons in a brain 'know' they are not growing back to the neuron they originated from.

Grid is a 2D thing. I think this is a probabilistic problem. Brain is 3D thing. Probability is less there for the reconnection of axons.

Can you give us citations on the study you mentioned?

@Memming http://neural.bme.ufl.edu/page13/assets/NeuroFlght2.pdf, http://edition.cnn.com/2004/TECH/11/02/brain.dish/

@Lennart_96 that study was done with dissociated cortical culture; they formed random connections. (I happened to work with both authors, and did some modeling study myself, but not on the neurodevelopment side.)

@Memming Wow, that's pretty awesome. Do you mean by random that the axons just started growing in all directions or that there is no possible way to predict which neurons will connect?

@Lennart_96 I'm not a particular expert on neurodevelopment, but it seemed to me that they pretty much grew in many random directions. There were no extracellular matrix or chemicals that would give an overall structural guide to the neurons (though there were glia multiplying simultaneously).

If I understand correctly, based on neural simulation papers, sometimes neurons do connect to themselves, and this is supposedly an important type of connection. I'm not an expert as of yet so you should of course double check this.

I think I can partially answer you question. As far as I'm aware, there are many surface receptor molecules such as ephrins that are responsible for axonal guidance and dendritic repulsion in developing organisms such as flies (Drosophila). As you can tell this is extremely crucial since its important for neurons to spread their dendrites and axons as far as possible, evenly spaced out with axons bifurcating (separating) correctly and not sticking together. This is for example important in the Drosophila brain for axonal projections into different lobes.
One such surface receptor, which helps achieving the above is Dscam (Down syndrome cell adhesion molecule) (schmucker et al 2000 Cell). Dscam gene is expressed in over 38000 isoforms (through complex alternative splicing of Dscam mRNA) in flies. It is the homophilic binding and subsequent repulsion of Dscam protein isoforms that enables an intrinsic self-recognition for repulsion of same-cell axon. As far as I understand it, if a number of similar Dscam isoforms are present on axons or dendrites of a neuron, this is self recognised and the dendrites and axons get repelled from one another. This is the molecular pathway that ensures sister dendrites are not adhered together or become concentrated in one area.
In the absence of Dscam or when Dscam protein isoform diversity is removed flies die during larval stages and the early embryonic axonal patterning of the fly nervous system is clearly disrupted. In the absence of Dscam protein, Bolwig's axons exhibit frequent axon pathfinding errors at a specific intermediate target. Most of these processes are conserved in mammals.
For further information please look at Schmucker & chen, 2009 Genes and Dev

In cases of severe head injury where a large portion of neurons and their connections get shredded. I don't think a neuron would be very choosy  when presented with quite a few axons and lots of intracellular fluid
There are coup and the contra coup (p silent) brain injuries that occur because the brain bounces back and forth in the skull. The contra coup, other side contusion (bruise) is usually worse. A lot of axonal injury occurs in the brain stem and since the basics of life (breathing centers) a severe injury to the brain stem can cause not surviving the injury.
Probably speed of healing I is the priority. I forgot which journal it was in but those with a college education were 60% more likely to have a good recovery while those with just a high school diploma have only 10-20% chance of having a good recovery. It's a similar ranking when it comes to neuronal connections.
Thank you for answering my curiosities on how indeed does one heal from Diffuse Axonal Injury (DAI) on a molecular basis. I was a 1sr yr. radiology resident when I had a severe TBI or Traumatic Brain Injury. TBI is the fancy way of saying brain damaged. But now we know victims of severe head injury can recover and even grow new neurons until old age.

nice answer!  some references would really help tho ;)


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Why do insectivorous birds migrate?
Living in northern latitudes, I have always wondered why do migratory birds invest so much time and energy to travel twice a year the vast distances between their breeding grounds and wintering areas. The most commonly found explanation, and the one I am grown accustomed to, is the scarcity of resources, resources meaning food and nesting places.
For years I have considered this a quite convenient explanation but recently I came to rethink it.
As you know, many of the longest migrating birds are insectivorous such as European Pied Flycatcher that breeds in much of Europe and western Asia but spends winters in western Africa. While it is easy to see the scarcity of food (insects) in northern breeding areas during winters, it is more difficult for me to see the scarcity of food in southern wintering areas during summers. - Take, for example, ants, that I expect, are abundant in those places all year around. Considering their total biomass, they would seem to hold a potential for a stable food source for masses of insect eaters with minimal food gathering effort required. So why migrate?
Is it that ants (or any other seemingly overly abundant invertebrates such as termites and mosquitoes) are not nutritious enough? Or are they too stingy and poisonous perhaps?
As for nesting places, I am aware that many birds defend their home range (thereby setting an upper limit for population density), but I imagine that such behaviour could be subject to change (or never had emerged in the first place) if there was no need to compete for other resources (mainly for food).
Or are the primary constraining factors disease and predation that would follow from a larger population density?
So in short, my question is, what is (/are) the primary reasons(s) for insectivorous birds to migrate instead of staying in their wintering areas and feeding on (seemingly abundant) local resources such as ants?

Reason for Migrating Birds:
Migrating for a Meal
Food scarcity: If birds will stay and eat all the bees they find, there will be no bees to feed on for the next generation. So, they fly away to take advantage of these places where there is abundance of food. And when the insects or replenish they come back.
Migrating for Family
Flocks of bird can be easy prey as they are small and are in a huge number. Also for the young ones who can't fly it is very dangerous. (Though they abandon the young one as soon they can fly)
Migrating for better Climate:
Some of the species fly away to sustain the temperature and come back when it is suitable for them. So, Northern birds migrate to tropical places for the winter and come back to north for the summer to lay eggs.

There are too many other theories for bird migration. It had been confirmed that migration is often due to genetics than any other reason.
Further Reading: THEORIES OF BIRD MIGRATION
Sources:
[1] http://birding.about.com/od/birdbehavior/a/Why-Birds-Migrate.htm
[2] http://en.wikipedia.org/wiki/Bird_migration

Just want to mention, not all insectivores are abandoned once they can fly. Specifically Magpies are still fed by their parents for 3-4 weeks after they learn to fly.
http://www.rspb.org.uk/discoverandenjoynature/discoverandlearn/birdguide/name/m/magpie/life_cycle.aspx
They fledge after 26 to 30 days, and are fed by the parents for a further four weeks after leaving the nest.


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If I sent a bag of rice to the bottom of the ocean and brought it back, could I eat it?
Suppose I filled an oceangoing container with rice and sunk it to the bottom of the ocean… say, a kilometer or so, then brought it back up.
Would it be edible?
Would it retain nutrients?
Do these things depend on how long it's been down there (at very low temperatures, mind you).
Asking for myself because, you know, I think ocean-bottom rice would be tasty.
Thanks!
Edit (after Doctor Whom's answer): I guess I should have mentioned that wrapping it in plastic is an option.  The pressure is what I was most interested in but I did a really poor job conveying that.

How much time do you plan to keep it there? Is it cooked or just plain uncooked rice

...asking for a friend.

Uncooked rice, certainly.

Depends on the container.  The bottom of the ocean has three main properties that would affect the rice:

Water
Salt and floating materials
Pressure - at the bottom of the Mariana Trench, the pressure is 1000x that standard atmospheric pressure at sea level.

Rice is absorbent.  Depending on the container, if it is permeable to water, then both seawater and pressure will affect the rice.
Rice + Water = soggy rice with a different texture than cooked rice.
Rice + Brine in Seawater = soggy rice that absorbed salt and fine particulate materials from the surrounding water.  (Cooking this would probably taste just like using seawater to cook rice.)
Rice + Intense pressure = the water, salt, and other materials would be absorbed on its way down more quickly due to the increased pressure, and any air within the grains would be replaced with water as the grain is compressed.
I do not believe it would work at all like a pressure cooker does due to the cold temperature; I am fairly certain that it would be only the grainy soggy rice - cooked rice is different from dry rice because of changes to the starches by the heat when cooking (and obviously the absorption of water).  The rice itself is a starch, so the carbohydrates would not likely respond differently to the pressure in the absence of heat.
I am curious if anyone might come up with anything on the chemistry of carbohydrates under pressure at near-freezing temperatures - whether any chemical bonds may be altered (like deformation of the beta-1-4 glycosidic linkage).  That's beyond my level of chemistry/physics knowledge.
But the duration of the journey would likely result in mush by the time it came up.  There are not many nutrients to white rice in the first place, other than the carbohydrates, so the nutrient change would be what it gains in the brine.
If I am missing something, please point it out.  But I believe this is the extent of the effects on the rice.
However:
If your rice were in a sealed container capable of withstanding the pressure without collapse or leaking, I am fairly certain that the rice would arrive back to the surface completely unchanged.  Humans are able to go down to the sea bottom in specially designed vehicles.

Thanks for your thorough reply!  I guess I should have said that watertight sealing is possible if it helps (which it certainly seems it would, by your answer), so the part I was really interested in was this: If your rice were in a sealed container capable of withstanding the pressure without collapse or leaking, I am fairly certain that the rice would arrive back to the surface completely unchanged. -- thanks, that's what I wanted to know!

Humans who scuba dive deep or are exposed to significantly higher pressures than sea level have some issues of gases esp. nitrogen that dissolve in the blood due to pressure; upon rising can exit as gas and cause all sorts of problems including air emboli - the phenomenon (not just emboli) is called "the bends" and can be serious, which is why we rise slowly when depressurizing.  But in a sealed can, there's not really much of a change in pressure if any.  http://deepseaadventures.com/photos/opportunities05/DualDeepWorker.pdf


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Inbreeding Coefficient and Coefficient of Relationship
Wikipedia gives the following formula to calculate a "path of coefficient of relationship" between an ancestor $A$ and an offspring $O$:
$$\rho_{AO} = 2^{-n} \left( \frac{1+f_A}{1+f_O} \right)^{1/2} = \left( \frac{1}{2}\right)^n \sqrt { \frac{1+f_A}{1+f_O}}$$
, where $f_A$ and $f_O$ are the coefficient of inbreeding of the ancestor and the offspring respectively.

Question
Where does the term $\sqrt { \frac{1+f_A}{1+f_O}}$ comes from? Please explain why this multiplicative term is $\sqrt { \frac{1+f_A}{1+f_O}}$ and not something different such as $\frac{f_A f_O}{2}$ for example.

In his paper Wright presents this as an alternative to other (existing) formulas. The ultimate test is whether it predicts herd health well and because of broad assumptions underlying the model it may be hard to tell how good a formula is. In general we want something close to 1 unless there is strong homozygosity somewhere. Yours won't work because it would likely be very small.

Great Question! If you have solved this, please gives us the complete derivation.

No I haven't solved it yet. Thks a lot for coming back to this post. I'll read your answer in 48h as I won't have time before!


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How important is the womb's environment?
- Background -
Talking about one phenotypic trait, the total phenotypic variance $V_p$ is decomposed into genetic and environmental variance for this trait, represented by the symbols $V_G$ and $V_E$ respectively. Also the covariance between genes and environment affect $V_p$ but we'll ignore it for the purpose of this question.
$$V_p = V_E + V_G + O(Cov(E,G))$$
The genetic variance $V_G$ can be further decomposed into dominance and additive variance. Similarly the environmental variance can be further decomposed into for example, for the mammals, the variance in the womb $V_W$ and the other environmental variance $V_{OE}$.
$$V_p = V_w + V_{OE} + V_A + V_D$$
$$h_N^2 = \frac{V_A}{V_p} = \frac{V_A}{V_w + V_{OE}}$$
One could measure $V_W$ by looking at correlation between dizygotic twins.
- Question -
What part of the environmental variance in phenotype is explained by the variance in wombs' environments? i.e. what are the estimates of $\frac{V_w}{V_e}$ or what are the estimates of $\frac{V_w}{V_p} = \frac{V_w}{V_w + V_{OE}}$?
Of course the answer will depends on the trait and on the species. I welcome either a general idea/estimation or any such measure for any specific trait.

Variance in womb is dependent on environmental variance. Some environmental effects are suppressed (some inflammatory modulators) whereas others are not. I am afraid your question is too broad. Moreover you are bringing in a lots of concepts together.

The womb environment depends on the non-womb environment (and probably on the genetics). Yes, there are covariance terms between $V_w$ and $V_E$ (and probably between $V_w$ and $V_G$) just like there are covariance terms between $V_E$ and $V_G$. It doesn't change the fact that there is a true $V_w$. My question might eventually be too broad because I don't specify a given phenotypic trait of interest. I edited my question to welcome answers about any phenotypic trait. I don't fully understand why my question mix up many different concepts? It sounds pretty straight forward to me. Thks

By "a lot of concepts" I mean that this question can be asked in a rather simple way. It would be straightforward to you because you posed it and you work on the area of population-biology. If I am not wrong this question has more to do with physiology (basically how well is a mammalian embryo protected against the environmental changes). Now it depends what those environmental changes are- temperature, chemicals (drugs), inflammation etc.

Now the second part is whether these changes that are relayed (with some attenuation?) to the embryo, will have an effect on some trait. So there are several environmental effects. You can break the question down that way; nonetheless you have to specify some environment variable else it gets too broad. Trait is still predictable if you fix the environmental factor.

Standard studies that aim at measuring the underlying genetic/environmental variances of variance in phenotypic trait do not look at the physiological mechanisms but only tries to determine the statistical associations. Also, typically these studies measure heritability through parent-offspring regression but does not make any consideration of specific environmental variables. You talk about "the second part of my question". Are there two parts in my question?

While I am defending my post, I have to accept that it has been asked 7 months ago and you are the first to even comment (Thank you) on it so you might somehow be right, or at least reflect why people did not answer.

Let us continue this discussion in chat.


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Coefficient of relationship and path of coefficient
A path of coefficient of relationship is defined as
$$\rho_{AO} = \left( \frac{1}{2}\right)^n \sqrt { \frac{1+f_A}{1+f_O}}$$
This SE post discusses this definition
From this, the coefficient of relatedness between two individuals $B$ and $C$ is defined as
$$R_{BC} = \sum \rho_{AB} \rho_{AC}$$
, where $A$ is (I think) the last common ancestor of $B$ and $C$. The sum is over all possible path coefficients.
Source: Wikipedia

I am a little bit confused, I don't really understand this formula. One reason is the following. Let's assume that  $B$ has 2 paths and $C$ has 3 paths to go to $A$. If we denote $\rho_{AB,i}$, the path $i$ (or the $i^{th}$ if you prefer) between $A$ and $B$,
$$R_{BC} = \rho_{AB,i} \rho_{AC,i} + \rho_{AB,j} \rho_{AC,j} + \rho_{AB,k} \rho_{AC,k}$$
But the path $\rho_{AB,k}$ does not exist because there are only 2 paths between $A$ and $B$ (which are denoted $i$ and $j$). Also, there is no reason to count the path in a specific order and not another one. If we change the order we count the paths between $C$ and $A$, we can get:
$$R_{BC} = \rho_{AB,i} \rho_{AC,j} + \rho_{AB,j} \rho_{AC,i} + \rho_{AB,k} \rho_{AC,k}$$
, which is obviously different from the previous calculation of $R_{BC}$
Can you help me making sense of these formulas?

http://www.genetic-genealogy.co.uk/Toc115570135.html. The notation is confusing and the Wiki site is not helpful (imo). This site is better (many examples) and mentions Wright's original paper.

It would be more like: $\sum_i (\rho_{AB}\rho_{AC})_i.$

Wright's 1922 paper. http://aipl.arsusda.gov/publish/other/wright1922.pdf

Your comments and links helped a lot! Thanks. genetic-genealogy offers a perfect "for dummies introduction" I don't quite know how to answer my messy question though. You can give a try if you want and I'll check it. Otherwise I might just delete it. I still don't understand this and that though.

The expression $f = 2h-1,$ coefficient of inbreeding (COI) is a measure of homozygosity. Since in a randomly breeding herd (of cattle) we expect 50 per cent heterozygous and 50 per cent homozygous, the minimum for $2h-1 $ is 0. If the cattle's genome is purely homozygous (aa, AA) we have $2h-1 = 1.$ (h is total homozygosity--see Wright's paper, linked below.)
As we can see from this site, a basic calculation of relationship coefficient may not deal with f at all. For two descendants B, C, the quantities $f_B,f_C$ are an attempt to factor in existing relative homozygosity that the coefficient of relation (COR) would otherwise not capture. Likewise $f_A$ measures preexisting homozygosity in the common ancestor of B and C. If animal A is the product of siblings then the homozygosity could already be quite high and this would maybe have measurable effects on the vitality of a cross between B and C.
Now $f_A$ and $f_B$ vary between 0 and 1 so $s = (\frac{1+f_A}{1+f_B})^{1/2}$ varies between $(1/2)^{1/2}$ and $(2)^{1/2}.$ Note that the important thing here is relative homozygosity of an animal and its ancestor:
a. If the ancestor A and descendent B have the same known preexisting burden of heterozygosity we can disregard s (and f) entirely. Their COR will depend only on path distance.
b. The homozygosity of the ancestor A  tends to increase COR while that of B tends to decrease COR.
The expression $r_{BC }= \sum p_{AB }\cdot p_{AC}$ is somewhat confusing. On page 334 of one of Wright's earlier papers we can get a clear idea of the use of the coefficient.
He defines $p_{BA} = (1/2)^n (\frac{1+f_A}{1+f_B})^{1/2}.$ If the path from C to A is $p_{CA} = (1/2)^m (\frac{1+f_A}{1+f_C})^{1/2}$ then the total path BAC would be
$$ p_{AB,AC} = (1/2)^{n+m}(\frac{1+f_A}{1+f_B})^{1/2}(\frac{1+f_A}{1+f_C})^{1/2} $$
$$= (1/2)^{n+m}\frac{1+f_A}{[(1+f_B)(1+f_C)]^{1/2}}  $$
So the expression for the sum of such paths would be
$$r_{BC} = \sum_i p_{AB,AC} = \sum_i (1/2)^{k_i}\frac{1+f_{A_i}}{[(1+f_B)(1+f_C)]^{1/2}}   $$
in which $A_i$ is the ith ancestor through whom B and C are related. The total path length for a given term is $(n_i+m_i)$ which I abbreviated $k_i.$
So a less confusing expression for $r_{BC}$ might be:
$$r_{BC }= \sum_i p_{A_iB}p_{A_iC}. $$
Note that the sum is over all common ancestors back to some arbitrary generation.
A good example of this is Figure 11 at link 1 above.
It's really not ``dumbed down'' at all, it just leaves out the factor s, which for a carefully maintained herd may be close to 1 anyway.


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Inbreeding depression and dominance
From this article,  second paragraph of the second page

A classic theoretical result is that the mean of a character controlled by a single locus i with two alleles Ai1 and Ai2 is only affected by the value of f if there is some degree of dominance.

where f is the Wright's inbreeding coefficient.
The authors then add:

Assume that the trait is scaled such that the values for the genotypes Ai1Ai1, Ai1Ai2, and Ai2Ai2 are -ai, di, and ai respectively. The quantities ai and di measure the effect of the locus on the character and the degree of dominance of the locus, respectively. With two alleles, there is a linear decline in the mean of a trait
  with increasing f either with overdominance (di > ai) or if the allele associated with an increased value of the trait is dominant or partially dominant (ai ≥ di > 0). With additive joint effects of different loci on the trait, this conclusion can be extended to a polygenic character; inbreeding decline occurs if the average value of di over all i is positive.

I don't understand why "[..] there is a linear decline in the mean of a trait
with increasing f either with overdominance (di > ai) or if the allele associated with an increased value of the trait is dominant or partially dominant (ai ≥ di > 0)"
Can you please explain why the mean of a character controlled by a single locus is only affected by the value of "f" if there is some degree of dominance.

man i should be able to answer this. i didnt take that class though. I could write a doctor who knows the answer but i doubt he would respond.

Recap of the question:
Looking at a single locus trait ($A$) controlled by two alleles, $A_1$ and $A_2$, the phenotypic mean is only affected by inbreeding depression, $f$ (Wright's inbreeding coefficient), if there is some degree of dominance, $d$. Why?
Answer:
If we take inbreeding as a higher than expected frequency of homozygotes, such that if the frequencies of alleles $A_1$ and $A_2$ are $p = q = 0.5$ the expected frequencies of the genotypes in an outbred population, $P_{outbred}$, would be $p^2 = 0.25$, $2pq = 0.50$, and $q^2 = 0.25$.
Each genotype has the following phenotypic result on a trait $A_1A_1 = 5$, $A_1A_2 = 7.5$, $A_2A_2 = 10$... this is an additive trait with allele $A_1$ having an additive effect of 2.5, and $A_2$ an additive effect of 5.
We can then compare an inbred population of 100 individuals, $P_{inbred}$ where the frequency of $A_1A_1 = 0.5$, $A_1A_2 = 0$, $A2_A2 = 0.5$, to $P_{outbred}$ , where I use $\bar{X}$ to symbolise trait means.
$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 7.5) + (50 \cdot 10)}{100} = 7.5$
$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 7.5) + (25 \cdot 10)}{100} = 7.5$
So when the trait is additive the population means are equal. It is onlt when we add dominance to the situation that the population means will differ as a result of inbreeding. Continuing from the above example, the populations are the same size and structure, but $A_2$ is now completely dominant to $A_1$ such that $A_1A_2$ individuals now have a trait value of 10. Now
$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 10) + (50 \cdot 10)}{100} = 7.5$
$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 10) + (25 \cdot 10)}{100} = 8.75$
Thus inbreeding has affected the population mean in a trait which has dominance, it is basically because the heterozygotes are less common in an inbreeding population and this is where dominance effects are seen.

"there is a linear decline in the mean of a trait with increasing f... with overdominance (di > ai)"

This is because in the case of overdominance, the outbred population mean becomes even more elevated - if we say now the $A_1A2$ trait is a phenotype of 15 the means become
$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 15) + (50 \cdot 10)}{100} = 7.5$
$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 15) + (25 \cdot 10)}{100} = 11.25$

" there is a linear decline in the mean of a trait with increasing f... if the allele associated with an increased value of the trait is dominant or partially dominant (ai ≥ di > 0)"

The mean will increase if the dominant allele produces a smaller phenotype. Here we say $A_1$ is now completely dominant,
$\bar{X}_{inbred} = \frac{(50 \cdot 5) + (0 \cdot 5) + (50 \cdot 10)}{100} = 7.5$
$\bar{X}_{outbred} = \frac{(25 \cdot 5) + (50 \cdot 5) + (25 \cdot 10)}{100} = 6.25$
I hope that answers the question, I tried to answer last night but was too tired to think - this is just what I came up with on the walk to work today so I haven't had the time to check it/overthink it

Yes, that answers my question. It is actually a very good "for dummies" explanation of a fairly complicated text. You answered so many of my questions this week. Thanks a lot!

haha - there's been a bit of activity to try and get the unanswered Q's reduced, there was a comment in the chat room that probably the only person to answer some of your unanswered Q's was me so I set myself the challenge of answering 5 this week... two to go! @remi.b


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How can toddlers expend seemingly boundless energy when they eat so little?
A toddler's food intake seems very little: only milk and water and some solid food. Therefore, from where does this energy come?

They don't eat little. Consider the volume of milk / food they consume as a ratio of their weight. Quite the contrary they are ravenous machines and their consumption is much higher than an average adult. All cellular energy comes from the hydrolysis of ATP, and the production of ATP comes from the breakdown of glucose. The glucose comes from a sugar found in breast milk, called lactose.

... in grams consumed per baby weight.

Just to add to the answer from @buzrw:
Using data from here and here I have estimated recommended calorie intake per kg for a 2 yr old and for an adult. I've used figures for males and assumed 70 kg for the adult weight which is the "international standard man":

toddler: 120 Cal kg-1
adult: 40 Cal kg-1

So yes, the energy intake of toddlers is higher than that of an adult.