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Father with mutated mtDNA- why isn't his offspring at risk?
Mothers transmit their mitochondria (and therefore mtDNA) to their offspring and fathers don't. Lets assume that father had a mutation of the gene that encodes mtDNA, would then be his offspring at risk? Why?
I also found the following statement:
"The current genetic advice is that fathers with mtDNA mutations are at no risk of transmitting the defect to their offspring."
How can that be true? Is it because of gene silencing?
Thank you in advance!

For that matter, the mitochondria replicates on its own unlike other cell components

...would then be his offspring at risk? Why?

No. Generally speaking, fathers do not pass on their mtDNA (Mitochondrial DNA).
Why? Because the mitochondria present in oocytes (egg cell) is the mother's, as every oocyte directly inherits the mother's mitochondria when they are made in the reproductive organs. The mitochondria that the sperm from the father carry to the egg do not enter the egg cell or are destroyed in the process.
It's also worth mentioning that, in general, mtDNA does NOT reside in the nucleus of cells, but in the mitochondria itself. It is not condensed during cell division, it is not spliced during Meiosis II, and it does not undergo recombination with another cell's mtDNA. Instead, when a cell divides, each cell takes about half of the mitochondria present in the cell and maintains them. That way only the mitochondria present in the cell before division will be inherited by the daughter cells, and thus only the maternal mitochondria present in oocytes (egg cells) before sperm instigate cell division will be inherited by any offspring.

Can you please cite references for the absence of mtDNA in fertilized cells? You have no references at all.

@anongoodnurse "Paternal Inheritance of Mitochondrial DNA in Mice" - Nature 1991. The truth is that some paternal mtDNA is passed along, but the undergrad level generalization is that "no" paternal mtDNA is passed because the amount is practically non-existent outside of rare cases. In those rare cases then mtDNA can cause metabolic issues, like the 28 year old case study by Scwhartz in 2002.

TL;DR: Ubiquitin.
Occasional occurrence of paternal inheritance of mtDNA has been suggested in mammals including humans. Clearly, spermatozoa have mitochondria; they make the energy needed for motility. Paternal mitochondrial DNA (mtDNA) does enter oocytes. It is a persisting fallacy that only maternal mtDNA is present in humans because only oocyte mitochondria are present in the product of conception.
This has been known for some time. According to an article in the Proceedings of the National Academy of Sciences, Nov. 1996, under Evolution:

In vertebrates, inheritance of mitochondria is thought to be predominantly maternal, and mitochondrial DNA analysis has become a standard taxonomic tool. In
  accordance with the prevailing view of strict maternal inheritance, many sources assert that during fertilization, the sperm tail, with its mitochondria, gets excluded from the embryo. This is incorrect. In the majority of mammals — including humans — the midpiece mitochondria can be identified in the embryo even though their ultimate fate is unknown. The "missing mitochondria" story seems to have
  survived — and proliferated — unchallenged in a time of contention between hypotheses of human origins, because it supports the "African Eve" model of recent radiation of Homo sapiens out of Africa.[1]

So, what happens to paternal mtDNA if it is indeed present in embryonic cells? Paternal mitochondria are targeted and destroyed.

While some confusion may still persist in popular science, research data clearly document that the paternal sperm-borne mitochondria of most mammalian species enter the ooplasm at fertilization and are specifically targeted for degradation by the resident ubiquitin system. Ubiquitin is a proteolytic chaperone that forms covalently linked polyubiquitin chains on the targeted proteinaceous substrates....Prohibitin, the major protein of the inner mitochondrial membrane, appears to be ubiquitinated in the sperm mitochondria.[2]

A finding of a patient with severe exercise intolerance in whom the mutated mtDNA in muscle was shown to be paternally inherited challenged the concept of strict maternal inheritance of mtDNA (the mtDNA harboring the mutation was paternal in origin and accounted for 90 percent of the patient's muscle mtDNA.)[3]

Paternal mtDNA inheritance may have gone unrecognized in cases of mitochondrial disease with no clear maternal pattern of inheritance because mitochondrial haplotypes are rarely investigated in diagnostic analyses.

However, a small study of 12 patients with mitochondrial myopathy failed to show Paternal mtDNA.[4]
It is too simplistic to say paternal inheritance of mtDNA does not occur. It has been shown in mice and other mammals.

The mitochondrial DNA of 172 sheep from 48 families were typed by using PCR-RFLP, direct amplification of the repeated sequence domain and sequencing analysis. The mitochondrial DNA from three lambs in two half-sib families were found to show paternal inheritance. Our findings provide direct evidence of paternal inheritance of mitochondria DNA in sheep. A total of 12 highly polymorphic microsatellite markers, which mapped on different chromosomes, were employed to type the sheep population to confirm family relationships. Possible mechanisms of paternal inheritance are discussed.[4]

We should not believe everything we read without more investigation.
[1] Misconceptions about mitochondria and mammalian fertilization:
Implications for theories on human evolution
[2] Degradation of paternal mitochondria after fertilization: implications for heteroplasmy, assisted reproductive technologies and mtDNA inheritance
[3] Paternal Inheritance of Mitochondrial DNA
[4] No evidence for paternal inheritance of mtDNA in patients with sporadic mtDNA mutations
[5] Further evidence for paternal inheritance of mitochondrial DNA in the sheep (Ovis aries)


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What to do if microarray t-test, ANOVA, SAM and LImma show various selected significant genes?
Need advice: how to approach discrepancy in differential microarray gene expression test results: what to do if ANOVA, ttest, SAM and Limma procedures show different results and especially more discrepant when using log transformations and normalization operations?

I wouldn't expect different methods to give the same results. Further, why are you even testing non-normalized datasets, the results of that are completely and utterly useless for any purpose other than showing that normalization is important. In addition, an T-test is a special case of an ANOVA (and of course limma is itself using a moderated T-test, though it's going to have significantly more power than the others), so I have to ask myself exactly what sort of design you're using that it's appropriate to substitute one for the other and still get apparently vastly different results.
In general, I would strongly encourage you to work with a local bioinformatician or statistician for what is presumably your first microarray analysis, particularly if you don't have a strong statistics background.

We are all academically educated in medicine and computer science, you know. However, we did 7 years of angiogenesis, not microarray research and started this theme recently, We have read many books, and advices are quite controversial. In routine, we do quantile normalization and log2 or log1o transformation for visualization. Design is simple: 4 columns of control bioichips and 6 of experimental data. Problem is that no up- or down- significant expression is achieved when using massive normalization, log transform, FDR and so on. Thank you for helping me.

source: Stack Exchange

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

sort: votes


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Can iGEM distribution parts be directly PCR'd?
The iGEM DNA Kit Plate Instructions say that there is only 2-3ng of DNA per well, which is already miniprepped and in plasmids.  Then it says that "there is not enough DNA in each well to perform anything but transformations".
Couldn't PCR be performed on an amount of DNA that small, given appropriate primers?  Is transformation truly the only thing that could be done with that DNA?  If PCR could be done on the DNA, why might they suggest otherwise?

You probably could do PCR on that amount of DNA, but if you screw something up you don't get a second chance. Transforming bacteria and doing a miniprep turns your 3ng into a few micrograms, which is enough to tolerate a few mistakes.

A failed transformation would have the same bad result - no second chance - so that leads to the (obvious?) follow-up question: Is transformation a lot more reliable than PCR?

Transformation with intact plasmids is usually ok. I only have trouble with transformations when ligating a plasmid together. Remember these plasmids have all been transformed into bacteria, grown, and prepped, so they are intact and ready to go back into bacteria.

What's the approximate percentage of success in PCR and in transformation, in your own experience?  Thanks again.

Guessing a percentage is hard, there have been times when ligating a plasmid when I was glad to get 1 colony. If the plasmid was intact I can get a lawn of colonies if I don't remember to dilute the cells. I can't guess a percent for PCR but there are more things that can go wrong, primer design, reaction setup, purification, etc. Transformation has about 1 step, add DNA to cells, much smaller opportunity to fail.

Here is the feedback I got from iGEM HQ:

Yes, we estimate there would be a total of ~3ng (on average) for a part sample in a well, and assuming a suspension with 10ul, there would be more than enough for PCR reactions. However, transformations are recommended over PCRing directly from the kit, because you can now store that part long term in glycerol form and you can prepare more of that part easily.

So the reason to prefer transformation over PCR seems to be long-term storage and future amplification.

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


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What is the most effective way to eliminate silverfish (g. Thysanura) from walls and floorboards?
I've had our home fumigated, but the silverfish seem to return unaffected.
Are their eggs unaffected?
What's the best way to eliminate them from your home?

This question does not appear off-topic to me. I just want to say that the question might also be a good fit on lifehacks.SE.

If you say "return", haven't they just re-populated your house?

Yes, return = re-populate.

They feed on fungi, which grow wherever there's high humidity levels. So the best way to get rid of them would be to lower the air humidity. For example, by increasing the temperature in your (presumably) bathroom.


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Does a man contain all the genes needed to make a woman?
This question is brought on by a Sci Fi novel I am thinking about writing. The plot device involves a colonist in charge of building a population on a new planet who loses his supply of embryos and so forth in the landing. With the artificial "wombs" intact, he populates the planet with clones of himself.
If he wanted to introduce enough variation (without making up new genes, only rearranging) in the population to allow them to be able to reproduce naturally without inbreeding problems, would he be able to? In particular, could he make a woman?
Alternately, could a woman (without a Y chromosome) do the the inverse?
At the risk of introducing bias into the answers, the plot as it stands assumes he is a male and he CAN'T do any of the above and he is restricted to clones.

If they're clones they'd be pretty much identical. He might have better luck making induced pluripotent stem cells and deriving them as gametes, then making embryos. Still have the same genes as he did, but at least the recessive/dominant allele ratios might change and could get some females out of it. Why not get DNA from the dead embryos?

That's a cool idea with the pluripotent cells. Of course exact copies would be clones, the idea is that he could have technology for directly manipulating the genes, he just doesn't know any sequences that are not present in himself. Your point about the eggs can be easily explained away by a fire, but it makes be think of the point that there could be DNA from anyone else who was involved with the building or launching of the ship still aboard

And it wouldn't be hard to keep an electronic database of DNA sequences on a computer.

Another good point.

From a narrow, technical perspective, a man "contains" all the genes to "make" a woman (X-chromosome) while women lack the genes to "make" a man (a Y-chromosome). To actually make use of this is another question (for instance, producing gametes containing X & Y chromosomes), but for a SciFi novel this shouldn't be a problem. Epigenetic effects might also be an issue.

Related: http://biology.stackexchange.com/questions/17410/could-a-sperm-be-altered-to-contain-a-females-genetics/17435#17435

This answer also involves some speculations as the question is about a good theoretical framework for a science fiction.
You can find in this post about how sperm can be used to produce embryonic stem cells. It would still require an oocyte for doing that.
The question now is- Can you produce oocytes from a male?
You may fuse two X bearing haploid spermatids to form a diploid cell with XX. This cell will also have mitochondria and ribosomes — seems like a decent candidate. Gametogenesis has not been shown to happen in-vitro. Moreover a zygote will need a lot more cytoplasmic resources that you can get from a fused spermatid.
Plus there are imprinting issues as already pointed out by Chris.
Conclusion: Next to impossible
For your question "Does a man contain all the genes needed to make a women": yes he has but does not have the biological machinery to do that (exclusive of the womb).
However if you choose to send a female astronaut for this mission then there may be some hope. As Chris said, there are problems with homotypic fusions because of imprinting issues. But with a supply of ova there can be other ways:

Make clones using SCNT: limitation is that there would be very little variability.
Erase imprinting marks and fuse two oocytes: This has not been done yet but this is possible. At this moment we have technology (still incipient for therapy grade), for targeted genome editing. The basic principle involves fusing a DNA-endonuclease with a sequence specific DNA Binding Domain (DBD). Examples include Zinc Finger Nuclease, TALENs and Crispr-Cas. This study demonstrates an engineered system that can deaminate RNA in a sequence specific manner. Based on a similar principle it should be possible to link DNA-(cytosine/adenine)- methyltransferase or DNA-(cytosine/adenine)-demethylase to a sequence specific DBD 1. This system can be used for targeted epigenetic modification. This would have a little more variation than cloning because of meiotic recombination. Limitation is that there won't be any males, this would perhaps become an Amazonian Planet.

Make sure that your space-shuttle has a good biolab facility :P

1 Imprinting is generally implemented by DNA methylation which happens mostly on cytosines.

Thanks guys! All your answers have contributed a fascinating and realistic backdrop with which to write!

A woman (assuming no mosaicism) has two X chromosomes in the nuclei of her cells (except for oocytes). A man, in every cell with a nucleus (except for spermatocytes), has only one, pluripotent or not.
The only way he could make a female would be to either manipulate cells by  duplicating the X chromosome (very difficult to do) or remove/inactivate the Y (giving rise to an XO female). That in itself would introduce problems in the female.
Turner Syndrome XO Syndrome

If he could make pluripotent stem cells he could turn those into egg cells, half of which would carry his X chromosome. If fertilized, half of those would get another copy of the X chromosome and become female. Of course there could also be egg cells with Y chromosomes, which might still function if they get an X chromosome sperm, but a YY embryo probably wouldn't work well.

@user137 - May I ask why you believe pluripotent stem cells are haploid?

@user137 Stem cells are not haploid. Only germ cells are.

The question asks whether a man "...contains all the genes..." to make a woman, while this answer is mostly dealing with chromosomal makeup and the issue of producing haploid gametes. From a strict/narrow gene perspective, I think the answer to this question is yes.

It is possible to make haploid stem cells by injecting a sperm in an enucleated oocyte or artificially activating the oocyte without fertilization. See here

@WYSIWYG - that is wild; I never knew that! I did know there are some nearly-haploid cell cultures, but I did not know the manipulation of genetic material in oocytes was this far along.

@anongoodnurse It was one kickass paper. I was so thrilled while reading it.

@fileunderwater - true enough. I guess the answer would be (for me) even if he could get two gametes with X chromasomes, as a male, how will he introduce the genetic material into a manipulated oocyte? The clone seems maybe better. Some of this is new to me.

@WYSIWYG and anongoodnurse - guys, some interesting gems hidden away in the comments!

@anongoodnurse Here are some more references about making gametes from stem cells Ref 1 ref 2 ref 3

@Chris recently, I saw a paper on haploid pleuripotent stem cells (in Nature, I guess) .

Theoretically this should be possible as men carry both sex chromosomes. You would have to find a way to make haploid cells and then have them form a diploid cell with two X chromosomes. Your population would go through a genetic bottleneck which would soon cause a lot of other genetic problems as there is not enough variety.
But besides this rather theoretical approach, there is a real problem with this kind of reproduction: it won't work because of genetic imprinting. This takes place in the egg and as well in the sperm cell and consists of small modifications added to the DNA. This silences this gene and allows the expression of genes specifically either from the mother's or the father's copy of the chromosome.
An example for this would be the loss of a part of chromosome 15. Depending on which copy is lost, this either causes the Prader-Willi Syndome (inherited from the father) or the Angelman Syndrome (inherited from the mother). This article goes deeper into imprinting.
Due to the missing maternal imprinting, the cells constructed from the father will not be viable since the expression of some genes (which would come from the mother) is missing. Nevertheless it has been shown in mice that it is possible to overcome this problem. The researchers deleted the maternal imprinting on one copy of the chromosomes they used, mimicked the fathers imprinting and where able to breed viable off-springs from two female mice without a father. But this approach is rather technical and also error prone since you have to know the imprinting of the mother. The article can be found here.


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Which Papaya (Lechosa) plant (male or female) bears fruit?
I will be planting Papaya fruit seeds and I understand that there is a female and a male plant, so how can one distinguish which are the ones that will bear fruit and which I should just rip up by its roots as I have limited planting space?

@chrisstronks hermaphrodite should be added to the title.

@dustin - I will leave that to PO, or you are welcome to edi the question!

Male flowers have no ovary and do not produce a fruit but females need to be pollinated or the fruits will be aborted falling off when they are about golf ball size (1). Therefore, you will need at least one male or hermaphrodite plant with your female plants so you can manually pollinate the female plants. Also, note that hermaphrodites can pollinate themselves so you will not need another one or a male for fruit.
The article goes on to say that hermaphrodites are the preferred type but under certain circumstances a hermaphrodite can shift to a female.

Cool winter weather or high soil moisture can lead to a shift toward femaleness, where the stamens fuse to the carpels or ovary wall. The re
  sulting fruits become severely ridged (carpelloid, or “cat faced”) and hence are deformed and unmarketable (1).

Home gardeners should take steps to avoid having only a single papaya plant, in case it turns out to be a female. One way to accomplish this is have several plants in the garden, to ensure the possibility that at least one will be
  a hermaphrodite with pollen. If space is limited, allow several seedlings to grow to flowering stage in the same planting spot, and then remove all but the healthiest hermaphrodite plant (1).

that was the fastest answer ever....

@ChrisStronks I am used to math.SX. If you aren't fast, the the question will have 10 different answers before you even develop your approach.

but you don't really answer how the PO can differentiate between the (wanted) females and (unwanted) males.

A question about the answer...dustin, you say that "hermaphrodites can't pollinate themselves" but the picture text describes the hermaphrodite as "self-fertile"...it sounds like as if it is saying that the hermaphrodite can fertilize its own self, or am I reading it wrong?

@ChrisStronks the answer is in the picture on how to differentiate.

@x457812 I miss typed and corrected already. Hermaphrodites don't need the presence of a male to bear fruit. However, the article goes on to say under certain circumstances a hermaphrodite can shift to a female.


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Is it true that some organs "sleep" at certain times of the day and does this affect dieting or when to take medicine?
Is it true that some organs (such as the liver or the intestines) are less active at certain times of the day, regardless of whether the individual is awake or not?

I have removed the part of the question that was about health advice.

No, this is not true. The only "organ" (if you will) that needs to "sleep" is the brain, and even then it is still quite active. The body needs to rest.
When blood is needed in a prioritized manner in certain areas of the body - for example, during a marathon the muscles and the heart need more oxygen - mechanisms are in place to shunt some of the blood away from organs that need it less (the stomach and intestines, for example) to those that need it more. But that doesn't mean the GI tract is sleeping, or even resting.
There is no organ that "sleeps". The brain as a whole is highly active during sleep, even secreting certain hormones predominantly during that time.


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What does x in "Miscanthus × giganteus" name stand for?
I came across a species name that contains "x" in its name, namely Miscanthus × giganteus. What does this symbol stand for and is it commonly used in taxonomic nomenclature?

It means that the plant is a hybrid. Having it in the middle means that it is between species of the same genus, else the × (it's not the letter x but the multiplication symbol ×) would have been in front.
It is very commonly used in taxonomic nomenclature, namely every time you have a hybrid. This means you'll usually see it with plants, as animals very rarely interbreed.
Wikipedia says that your plant is a hybrid from Miscanthus sinensis and Miscanthus sacchariflorus. It is an easy place to look up most hybrids you might encounter.

Well, would be rather hard to eat due high cellulose content, but it is one of the promising spices for 2nd generation biofuels production.

Lemongras is also a tough gras, but still used as a spice, sometimes even eaten, http://cooking.stackexchange.com/questions/53671/should-lemongrass-be-edible-or-just-a-flavoring. I don't know why you'd look at spices when you choose biofuel sources though.

I'm working in research where we develop cellulase activity assays - the cheap, fast and quantitative ways to say what mixtures of enzymes will produce most glucose from lignocellulotic biomass in industrial context. Miscanthus is the sample we got from other research group and I got curious what the symbols in the name means.
In general finding a good energy crops for 2nd generation biofuels is an active and well founded research field [C. Somerville, H. Youngs, C. Taylor, S. C. Davis, S. P. Long, Science 2010, 329, 790–792.] [J. Wang, J. Xi, Y. Wang, Green Chem. 2015]

I think Klara is talking about a species name, not a spice's name.

It is very commonly used in taxonomic nomenclature, namely every time you have a hybrid. I second that, and I think I had better give an example everyone knows about: the beautiful Iris, especially the German one, Iris germanica L.. Dykes' taxonomy is most widely used these days, not seeing the plants as a "wild species" (as Linnaeus partly did) but as hybrids, e. g. Iris × germanica var. florentina' (L.) (Dykes) The × is particularly common with this very kind of flower.

@senderle Oh, thanks for catching it. I realized that there must be some misunderstanding after Klara's second comment, but I just didn't make the association with species

Thanks @senderle for catching the typo, I totally overlooked it and I was quite confused with rumtscho comment.


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What does to "evolve" exactly mean?
In this article, the author says:

Evolution isn’t “leading up” to anything, it just drunkenly limps along using the same set of tricks in slightly different orders.

On other occasions, however, the term "evolution" is often deployed as a process that develops gradually, typically from a simple to a more complex form, or from not adapted to more specialized and "fit".
These contrasting interpretations of evolution make me wonder how I should interpret "to evolve" and "evolution" in the context of processes involved in speciation?

Do you mean that the word is misused in biology, in the dictionary defintion, or in public/general use? To me, this is unclear from the question. 'Evolve' is certainly used in different ways with different meanings.

@Ooker - I slightly edited your question to improve wording. Feel free to roll back. it's just a suggestion.

In biology. I know that language is sometimes, erm, evolve and a word can adapt a new definition. But since the original definition of the word (develope from simple to complex) had had a long time before the biological definition appeared, and because of that, the former meaning dominates the latter in our mind. I suspect that even biologists are still using it wrong.

@Ooker I think you are misrepresenting and simplifying 'evolve' when you say that it originally (only) meant "...developed from simple to complex". The previous use wasn't this clearcut.

@fileunderwater that's the definition you will find in Oxford

@Ooker that is one particular modern definition, which doesn't take etymology or historical use into account. Look at http://www.merriam-webster.com/dictionary/evolve, http://www.oxforddictionaries.com/definition/english/evolve and http://www.collinsdictionary.com/dictionary/english/evolve?showCookiePolicy=true for other definitions, more in line with the biological use of the term.

@fileunderwater I don't get your point. All the dictionaries you give define evolve as I define, which means that I don't misrepresent or simplify it. Do you mean that evolve has adapted a new meaning and all we need is careful not to use the wrong definition?

@Ooker My point is that those other modern defintions are more inclusive and often explicitely refer to "biological evolution". Languages and the meaning of words always change (...evolve), and under current use the biological meaning is rather unproblematic. I think the most interesting part of your question is whether the biological adoption of the word (late 19th century) deviated strongly from the previous use.

I think this may be off-topic because it is about semantics, not biology.

In any case, as has already been pointed out to you, you cite just one definition and even that one only states that it is "especially from a simple to a more complex form." That does not mean exclusively. Other definitions include the specific meaning used in biology. Also, dictionaries do not define words. Usage defines words and those definitions are then included in dictionaries. Finally, there are many examples of evolution leading from a simple to a more complex organism, just like your definition suggests. I don't see an issue here.

@terdon I know that this question is somewhat off-topic, but as I say, I ask it here so that it can reach to more biologists. If it has to be closed, which site should it be moved to?

@Ooker The premise of your question is based on a misunderstanding. Biology uses the word "evolution" to mean something. Dictionaries that fail to record that definition are deficient. It's not the biologists who are deficient. You can trace the etymology of the word and muse about whether or not the initial usage in biological contexts was appropriate, but for a word that's as established as this one is now, there's really little point in disputing it.

@Mr.ShinyandNew安宇 thank you so much. Make it an answer and I will accept yours

Ooker, [elu.se] would be the best fit but you'd just receive the same answer as posted by @Mr.ShinyandNew安宇 above. Almost certainly by Mr Shiny himself. Feel free to post there or flag it and ask for migration. Just be warned: the ELU folks don't believe in the kind of prescriptivist ideas that prompted your question :). They're a firmly descriptivist bunch. You might also want to discuss it in the ELU chat room

I edited the question and hope for re-opening. I think it touches on such a fundamental principle in Biology that it deserves a round of evolution (and evaluation) itself.

@Ooker - my pleasure, but feel free to roll back. it's just a suggested edit and it may be totally off from your original intentions.

To put in my view on this issue, I disagree this is a semantics question. This question specifically identifies itself as requesting the biological definition of evolution, which is significantly different from a classical, non-biological definition.

A couple of comments, but maybe not an answer; I think misuse is the wrong word - alternative meaning is better. 'Evolve' as a word is much older than the theory of evolution, and has its origin in the Latin evolvere:

evolve (v.)
      1640s, "to unfold, open out, expand," from Latin evolvere "to unroll, roll out, roll forth, unfold," especially of books; figuratively "to make clear, disclose; to produce, develop,"
  from assimilated form of ex- "out" (see ex-) + volvere "to roll" (see volvox). Meaning "to develop by natural processes to a higher state" is from 1832. Related: Evolved; evolving.

from Online Etymology Dictionary. Implicit in that definition is the laying out of something predetermined, which can relate to going from simpler to more complex.
Also note that Darwin only used the word 'evolve' once in On the Origin of Species (1859), in the final sentence:

There is grandeur in this view of life, with its several
  powers, having been originally breathed into a few forms or into one;
  and that, whilst this planet has gone cycling on according to the fixed
  law of gravity, from so simple a beginning endless forms most beautiful
  and most wonderful have been, and are being, evolved.

The implication of progress was one reason why Darwin disliked the word 'evolve' and preferred "descent with modification".
The same root was then used as a name to the theory of Evolution, but then in a much more specific sense than the older, general meaning.
If you look back at the etymology above, it is quite clear that biological evolution (The Modern synthesis version) emphazise the connotations 'expand', 'produce' and 'develop', but not the 'unroll' and 'unfold' parts (which both to some extent imply something predetermined).

As far as I remember, Darwin also wanted to avoid the hard confrontation with the church by not using evolving.

@Chris Quite possible, but I don't know if this was a stated motivation. Do you know of an account from Darwin that express this concern?

@fileunderwater - it was most definitely the reason for his vagueness, and perhaps the only reason. As far as I know, people were hanged for questioning the 7-day Creation back in the days.

@ChrisStronks Sure, but his book was just as inflammatory by stating "descent with modification". Did the church use the word 'evolve' themselves in any way, or is there any account that they reacted particularly strongly to this word? I'm not saying that this wasn't the reason, I'm only wondering if there is any proof/account that this was the reason. The older implication of progress is a good enought reason for Darwin to dislike the term.

As far as I know he was concealing the true meanings by talking around it. Just as Sir Wallace did before him (Darwin stood on the shoulders of giants himself). If you are interested I can look up references?

I think it's alike with relativity. I remember that Einstein also hate using this word to say everything is relativity

Great question
I think evolution and its derivatives are among the most misconceived and abused terms in Biology. Evolution is often seen as the driving force that pushes life to perfection. For example, what I often encounter are things along the line: "Organism A has trait X, A has been evolving for Y years, thus X is evolved into a useful and optimal token for survival, so we have been exploring X... bladibla". No - the trait X is there because it may be useful at present, or it has been useful in the past, or perhaps it is simply there because it occurred by chance and hasn't proved detrimental in Y years. Evolution is not only survival of the fittest (X is optimized), it is, and probably even more so, the extermination of the unfit (X is not detrimental). The "termination of the unfit" may, in fact, be more apt than "survival of the fittest", as survival depends on out-competing (and hence terminating) others. The interpretation of evolution as "survival of the fittest" is, however, the most encountered interpretation, perhaps unfortunately.

do all biologists aware of this when they use the word evolve?

@Ooker - no, otherwise they would be more careful using the term :)

@Ooker actually, biologists are quite careful when using the term. It is just horribly abused by the popular press. Things like "more evolved" for example will not be used by people working in the field.

@terdon I have seen in many biological contexts, evolve means "optimizing", as Christ Stronks says.

I don't agree with your interpretation. Survival of the fittest implies death of the non-fittest by modus tollens.

@MarchHo - please elaborate - I love this topic. We could go on chat actually. But not now :)


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Are there any viruses that have infected all humans in the past or present?
Are there any known viruses that have managed to infect all of humankind either in the past or presently, either benign or otherwise?

Could mitochondria, ancestrally the result of a bacterial infection, be included?

Quick answer: yes. Research human endogenous retroviruses for more information.

Do ERVs count? None of the HERVs are functional viruses(anymore). And they didn't need to infect 100% of humanity to cross over, so they may not have. On the other hand, does gut microflora count? There are lots of those, even if they don't infect human cells there's probably one that's inhabited 100% of humans at one time or another.

You mean to say some virus that everyone has got infected with at one point of time or the other. I don't understand the point of this question. Even for a common infection like viral cold, there can exist people who have not contracted the disease. @MattDMo are ERVs same as retrotransposons?

@WYSIWYG according to Wikipedia, yes, to an extent - HERVs are one class of retrotransposons.

This shouldn't be closed - I found the answer. The HHV-6 family of herpes viruses infects almost all humans by the age of 2. Thankfully, it's generally a commensal and negative health effects from it are rare. See https://hhv-6foundation.org/what-is-hhv-6


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How much of the human body is processed sunlight?
So I believe (and correct me if I'm wrong--it's logic, not research) that the human body is pretty much all just processed sunlight based on the food chain.  How much, if any, of the human body is made up of materials that did not originate from the sun (e.g., various minerals or other trace elements)?

The atoms in our body do not come from the sun, but the energy to do chemistry on those atoms does. The material itself comes from other stars that exploded over 4.5 billion years ago.

So instead of saying we're made of sunlight, we're really just made of dirt.  Not quite as uplifting.

If you want to be inspired by the dirt remember that it was still made inside a star and then blasted across space by a supernova.

If you want to say it poetically, we're stardust held together by the sun. Condensed and continuously renewed by a giant nuclear forge.

I think that Carl Sagan said it best:

The nitrogen in our DNA, the calcium in our teeth, the iron in our blood, the carbon in our apple pies were made in the interiors of collapsing stars. We are made of starstuff.

The current view of cosmology is that every atom that isn't hydrogen, helium, or lithium was created in the fusion furnace in  the hearts of giant stars. These heavy atoms were then spread about the place by supernovas.
However, there's a lot more to the matter that makes up living creatures than just the atoms. The vast majority of the free energy that allows for the creation of intricate organic molecules with complex patterns of chemical bonds (e.g. protein, DNA, etc.) does indeed originate with our sun.


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Grapefruits and CYP3A4
Grapefruit juice contains furanocoumarins, which irreversibly inhibit CYP3A4.  For this reason, when one is taking certain medications it is necessary to not eat grapefruits because the inhibition of CYP3A4 can reduce how much of the drug is metabolized before it can get used, resulting in an overdose.   It apparently takes 24 hours after eating a grapefruit before the enzyme level is 50% and up to 72 hours for it to be completely normal.  So, it seems that eating one grapefruit a day would substantially impair one's CYP3A4 levels indefinitely.
Wikipedia says, the purpose of CYP3A4 is "to oxidize small foreign organic molecules (xenobiotics), such as toxins or drugs, so that they can be removed from the body."   It seems like inhibiting CYP3A4, from a biological standpoint, would reduce one's immune system or at least the ability to tolerate and eliminate certain toxins.   Are there other enzymes that take up the slack, or is there something in grapefruit itself which does the job instead, or is a daily grapefruit just a bad idea?  What are the effects of extended inhibition of CYP3A4?  Will the body perhaps build up a tolerance or immunity, or (perhaps with negative effects) pump out more CYP3A4 to try to compensate?

Keep in mind that CYP3A4 is one of MANY cytochrome P450s. Many substrates are capable of bind to more than one of these and being metabolized. Grapefruits would probably only be an issue for compounds that are only metabolized by the same CYP450 that gets deactivated by the grapefruit.

CYP3A4 is the most abundant cytochrome in the liver - and the most important for the metaboization of drugs.

Non scientific resources claim that 10% of the liver capacity is enough to do the daily routine detoxification. I guess grapefruit cannot inhibit the liver enzymes that degree. Afaik. nobody talks about grapefruit as a poisonous fruit...

http://en.wikipedia.org/wiki/CYP3A4#cite_note-Flockhart-29 According to wikipedia grapefruit is only a moderate inhibitor of CYP3A4.

Though a moderate inhibitor, high concentrations of grapefruits/grapefruit juice will irreversibly inhibit CYP3A4 - a grapefruit every day is not recommended.

@Michael - don't confuse "foreign organic molecules" with the "immune system" - I don't know of any deficiency or immune-related problems that could result from inhibition of CYP3A4.

In general, xenobiotic biotransformation (i.e. processing the xenobiotics aka drugs - detoxing the body) is accomplished by a limited number of enzymes with broad substrate speciﬁcities. In humans, for example, two cytochrome P450 enzymes— namely,CYP2D6 and CYP3A4 — metabolise over half the orally administered drugs currently used. (Gonzalez and Tukey,2006).
The various different CYP enzymes can act on various different foreign organic compounds with varying levels of efficiency. The CYP enzymes oxidise these organic molecules adding on -OH groups to make them more solube and thus more easily excreted.
Grapefruit contains compounds known as furanocoumarins that block the CYP3A4 enzymes. These compounds do this by irreversibly binding to the CYP3A4 enzymes, putting them out of commission. Like the wikipedia article says it takes about 24 hours for the CYP3A4 enzymes to return to normal levels after the average glass of grapefruit juice is consumed. During this time your body’s ability to process drugs for elimination is decreased because CYP3A4 is the main CYP enzyme for processing many drugs and toxins.
You might think that this could be used to reduce the dose for a drug, but the amount of furanocoumarin in your blood would vary widely (grapefruit isn't uniform in it's concentrations) and CYP3A4 levels vary between individuals.
 If you tried using grapefruit juice or another source of furanocoumarins to do this you'd be reduced to guessing how much of your prescribed drug is safe to take. Blood levels of the drug may rise, resulting in the risk for new or worsened side effects. it can essentially cause the normal, dose of a therapeutic drug to act like an overdose by increasing the bioavailabilty of the drug in your body. Better not to risk it.
Sources:

Gonzalez FJ, Tukey RH: Drug metabolism, in Goodman LS, Gilman A, Brunton LL, Lazo JS, Parker KL (eds.): Goodman & Gilman’s the Pharmacological Basis of Therapeutics. New York: McGraw-Hill, 2006, pp. 71–91. [I'm afraid I unable link you directly to it]

Textbook - Toxicology - the basic science of poisons, Cassarett & Doull (A PDF version of the textbook can be found here: https://ilmufarmasis.files.wordpress.com/2011/07/casarett-and-doulls-toxicology-the-basic-science-of-poisons7th-ed.pdf)
Half-remembered undergraduate lectures.


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Does the size or mass of a body affect the time it takes for rigor mortis to sets in?
Does the size or mass of a body affect the time it takes for rigor mortis to sets in? For example: compare a 300 pound man to 100 pound girl to 5 pound animal.

My work with mice suggests it can happen in less than 10 minutes, but I haven't had to euthanize any other types of animals.

One of the main factors that impacts rigor mortis is temperature. Basically, a smaller body would slow down the metabolic processes behind rigor more substantially. Also, one of the first things that happens in rigor is the stiffening of muscles. An increase in muscle mass would increase the time for rigor as well.
Refer to these links: wikipedia and another that talks about rigor mortis within the scope of forensic pathology.
Hope that helps!
n.i.

I think that a larger body mass with a corresponding smaller surface area to volume ratio would decrease the time for rigor mortis to set it since the body stays warmer for longer.

Yes I saw that but previously you said that a larger body mass increases the time for rigor mortis to set in.

@canadianer - thanks for catching that! I edited my answer.


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What effects does being cryogenically frozen have on a person's body?
I'm wondering what effects are known to happen to a person's cells when a person is cryogenically frozen, especially those that need to be overcome in order to "bring them back to life."
From a cellular and maybe even molecular level, is the person exactly the same as before?

It's not possible to freeze a person and bring it back to life later.

Possible or not, I'm still curious what effects have been observed - the study of Cryonics still seems to active.

@Chris wrong! Well, maybe. Check out this frog

You need to add details or stick to one domain- molecular/physiological. In any case since this has not been done on humans the answer can be based only on speculations.

@tel: More to point, we know that it is possible to freeze human sperm for later re-use. That leads me to wonder if we can someday freeze human BEINGS for re-use. After all,who would have ever guessed that we could clone sheep.

@Chris Can you prove that statement?

@JBentley Which one?

@chris I can only see one - "It's not possible to freeze a person and bring it back to life later."

Short Answer
Death!
Longer Explanation
In terms of the cellular and molecular level, many of the relatively weak interactions holding a person together are disrupted by cold temperatures. As a cell freezes, most of its  proteins and lipid membrane content will denature and "fall apart", the same as if you boiled it.
As with many things in biology, the problem is water. At room temperature, the lipid bilayers and proteins of a cell are held together largely by way of a complex network of interactions with the surrounding water. If the cell gets too hot or too cold this network of interactions between biomolecules and water falls apart. This leads to a disruption of the cell's overall organization*, which in turn can cause problems up to and including complete cell rupture and death.
So in order to preserve a living creature under cryonic conditions you need to replace the water in and around its cells with a different molecule that will maintain most of the normal intermolecular interactions even under conditions of extreme cold. There are protocols for freezing cell cultures that use various different substances as replacements for water, such as glycerol or DMSO, and there's a frog that loads its own blood with carbohydrates at low temperatures in order to turn it into a better cryonic medium.
footnote
*The disruption of a cell's organization at extreme cold is likely to persist even if the cell is brought back to room temperature. See Gulevsky, et al for a complete review of the thermodynamics of cold denaturation.


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Is it possible that a set of functionally related proteins in a pathway fulfill different functions?
Could it be that a given pathway of enzymes (or proteins in general) may fulfill different purposes in a cell by for shifting partners? Say protein A activates B, B activates C and C has a specific action X (e.g. X = phosphorylation of protein D). Now do pathways exist where, e.g., A can activate C directly resulting in action Y (e.g. dephosphorylation of protein D)?
At this time I am in need of real-world examples of this scenario, but I can't find any. Can anyone help?

Hello Costa, and welcome! I don't understand your question. What is supposed to connect to what, what do you mean by property? It's a very broad tem. And maybe you man exhibit, not execute. I know it's not easy if English is not your first language, but people can't answer if they don't know what the question is. You can edit it to add detail, else it's possible that it will be temporarily closed until you explain more.

Hi Costa Welcome to Stack Exchange! - Thanks for your question! @rumtscho is right. I took a bash at improving your wording a bit, but you may have to elaborate a bit yourself. SE users, and particularly those at Biology SE (myself included :-) can be picky in accepting questions :)

ps: please feel free to roll my edits back if it is not to your liking

Just summarizing my current understanding: A -> B -> C effects X. Then, through some mechanism, A -> C effects Y.

Do you mean C has two X and Y actions and this different actions results from its different stimulator?

I don't understand the question...

If Y can be seen as the inverse or absence of X function, it sounds to me like an incoherent type 3 feed-forward loop, where
A activates B
B activates C
A inhibits/reverses C
example from literature, E.coli: fnr as A, and arcA as B, cydAB as C
source: http://www.pnas.org/content/100/21/11980.long

I3FFLs are quite rare. I haven't really encountered an example of I3FFL. I1FFL is quite common. This you can intuitively guess because A acts as both inhibitor and activator. Though this phenomenon is possible it is not very common.


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Inter-codon mutations statistical analysis
I am looking for a statistical approach to inter-codon mutations. For example a 64*64 (64*63 actually) table, that contain the possibility of mutation from one codon to another codon (CCA to CAA or CGG... for example).
Is there any articles, databases or others that provide such table?
Please comment if my question is not completely clear.
I searched but didn't find an answer for this question in Google Scholar.

Yes and they are called substitution matrices. You might find some more information in this review.

@cagliari2005 I don't know if you're still active on the site, but this comment is IMO worth converting to an answer.


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Is it dangerous to rub closed eyes?
Phosphene from rubbing the closed eyes where first described at least since Ancient Greece, but I caught myself thinking that I wouldn't want to try it out. So I wonder, how safe it is to actually rub closed eyes or put pressure on the human eye in general? Can frequent but small, or rare but sharp, application of pressure cause myopia or other eye disorders? What is the maximum pressure before the eye is damaged? What happens with the eye if you accidentally hit it?
I remember several times during my childhood accidentally poking myself in the eye with a finger—the experience was very uncomfortable, I couldn't even open the eye for several minutes, but I don't think anything happened to my eyes since then, and my myopia was probably caused by any other factor than pressure damage.

According to scientific articles I read, myopia can be caused by light pollution at night, or not enough light during the day.
(In my case I had a small amount of black mold on my window, and its toxin caused a lot of health problems, e.g. diplopia, and probably myopia was a side effect as well. Now 2 days after the removal of the mold I don't need glasses anymore. I guess the complete recovery will take a few months, we will see.)

The answer is both yes and no, depending on how often and how hard one rubs his or her own eyes.
Occasional light rubbing is not a problem-- it stimulates tear production and relieves stress by lowering heart rate via the oculocardiac reflex.
Frequent hard rubbing is a problem-- it can worsen eyesight in people who already have progressive myopia, and worst-case-scenario lead to retinal detachment. For those with glaucoma, can interrupt blood flow and even cause nerve damage. It can (but rarely) scratch, tear, or deform the cornea leading to pain and distorted vision. It can lead to damage of small delicate vessels, causing a subconjunctival hemorrhage, which is benign despite its worrisome appearance.
It is generally recommended to just avoiding rubbing the eyes altogether!
References:

www.abc.net.au/health/talkinghealth/factbuster/stories/2012/09/18/3592456.htm
http://www.visioneyeinstitute.com.au/dangers-rubbing-eyes/


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How to do whole genome sequence alignment in R or Ruby/C++, any good language?
I need to perform tuberculosis mutation analysis. First step I need to do is to align sequences in fasta format against one reference file. i tried CLC genomics workstation --- it hangs on 60 000 lines of fasta reference file for entire day. Please advise what technology and tutorial to use to do that task.

I am a poorly trained molecular biologist, so when I build plasmids and have them sequenced I line up the sequences by hand in microsoft notepad. I know it's not a good way to do it, but haven't looked for anything better. What would you suggest for aligning up to a couple dozen relatively short sequences (~500 bases)?

Web VISTA tool designed for short sequences

Found a tool:  MUMmer is a system for rapidly aligning entire genomes.  The current
version (release 3.0) can find all 20 base pair maximal exact matches between
two bacterial genomes of ~5 million base pairs each in 20 seconds, using 90 MB
of memory, on a typical 1.8 GHz Linux desktop computer.
If you know a better programmatic approach, let me know, please

I think you incorrectly identified what type of analysis you want.  You mention that you have numerous sequences in a fasta file (you mention at least 60,000) that need to be aligned to a single genome.  So your not doing a pairwise alignment, your aligning DNA sequences to a reference genome.  The fastest known algorithm for this is burrow-wheeler transformation mappings which can be accomplished with tools such as bowtie, bowtie2, BWA, etc...
I'm assuming your experimental design is something like this: You have sequencing data from a number of tissue samples with half or some number of samples being a disease state, the other being normal.  So you want to create alignment files for each sample, and than determine where these alignments differ.
After alignment, you will need to create a variant file (VCF) which can be accomplished using samtools or GATK.  The VCF file will give you all bp locations with alternative alleles from your reference genome.  Which seems to be what your looking for.
Citations that could be useful:
Langmead B, Salzberg S. Fast gapped-read alignment with Bowtie 2. Nature Methods. 2012, 9:357-359.
Bioinformatics. 2011 Nov 1;27(21):2987-93. doi: 10.1093/bioinformatics/btr509
Li H. and Durbin R. (2009) Fast and accurate short read alignment with Burrows-Wheeler Transform. Bioinformatics, 25:1754-60. [PMID: 19451168]
Li H., Handsaker B., Wysoker A., Fennell T., Ruan J., Homer N., Marth G., Abecasis G., Durbin R. and 1000 Genome Project Data Processing Subgroup (2009) The Sequence alignment/map (SAM) format and SAMtools. Bioinformatics, 25, 2078-9. [PMID: 19505943]
https://www.broadinstitute.org/gatk/about/cited-by
The last url contains 145 publications that used GATK to look at population-scale variant differences.  These publications could be very useful to see how other papers have accomplished variant discovery for the use for scientific inference.
For User137 - since I can't comment on this board yet; you want to use a program called muscle.  There is an MS-DOS version and it can align short sequences extremely fast.

Thank you, I `ll read the recommended literature


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What do you call that part of the muscle that connects directly to the bone?
When you open up a chicken leg or a clam and you remove the meat, there is this little part that is connected to the bone and is not easily scraped off.
What is this part called and what mechanism does it use to connect to the bone or the shell?

The tendon is the part of the muscle that connects directly to the bone.

A tendon (or sinew) is a tough band of fibrous connective tissue that usually connects muscle to bone and is capable of withstanding tension. Tendons are similar to ligaments and fasciae; all three are made of collagen. Ligaments join one bone to another bone; fasciae connect muscles to other muscles. Tendons and muscles work together to move bones.

The image was taken from the wikipedia link.

The part of the bone to which the tendon connects is called esthesis

@CRags you mean enthesis?

Sorry spelled wrong, you are correct, it's enthesis


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What’s the reason for isovolumic contraction and isovolumic relaxation?
During cardiac cycle, there are two periods in which the heart volume doesn’t change, but there is a change in tension/pressure. It takes about 0.25-0.35 second to achieve this change.
I searched in Google and Wikipedia, but could not find the reason, so I decided to ask this question.

To put it in very simple words the reason for isovolumetric contaction and relaxation is to make the necessary pressure changes that is necessary to allow blood to flow into or flow out of the ventricles.
The basic formula you need to remember to understand this is:-

Fluids flow from high pressure area to low pressure area along the pressure gradient (Eg: Injecting a drug into blood stream - as the pressure in the syringe is higher than the pressure in blood vessel, the drug flows into the blood vessel)
Pressure is inversely proportional to volume (when temperature is constant) - this is Boyle's law. In a container with a fixed amount of fluid an increase in the volume of container will cause a proportionate amount of fall in the pressure in the container and vice-versa

Isovolumetric contraction:
The end-diastolic pressure in the aorta is in the range of approximately 90-100 mm of Hg. For blood to flow from left ventricle to aorta, the pressure in the left ventricle should exceed the pressure in the aorta.
As long as the pressure in the left ventricle is lesser than the pressure in the left atrium, the blood flows from Left Atrium to Left Ventricle. When Left Ventricle starts contracting the pressure in the LV rapidly overcomes the pressure in left atrium leading to closure of the mitral valve.
Now the pressure in the LV is greater than the pressure in the LA. So no blood flows in. At the same time the pressure in the LV is not sufficient to overcome the pressure in the aorta. So the semilunar valve remains closed. The ventricle continues contracting causing a time period in which there is increase in pressure without volume change as both inlet and outlet are closed. This period is called period of isovolumic contraction.
The isovolumic contraction ends when the pressure in the left ventricle becomes higher than the pressure in the aorta, which will cause the semilunar valves to open and blood to flow from left ventricle to aorta.
Isovolumic Relaxation:
The reverse happens in isovolumic relaxation.
As the blood volume in the ventricle decreases and the left ventricle starts relaxing the pressure in the left ventricle falls. When the pressure gets below that of the aorta, the semilunar valve closes. But the pressure in the ventricle is still higher than the pressure in the left atrium. So the mitral valve remains closed. So here too both the inlet and outlet are closed but as the ventricle is relaxing the pressure keeps falling. So till the pressure in the left ventricle falls below that of the left atrium, there is a time period volume is constant and the pressure keeps falling - this is called Isovolumic Relaxation.
This period is followed by opening of the mitral valve (as the pressure in the LV falls below that of the LA) and blood flows into the ventricle.
Take a look at the phonocardiogram linked in Majid's answer. It will help you understand what I explained.
Hope this explains your question

I have a question, when contracting the volume is constant and pressure is increasing. According to ideal gas/fluid law, doesn't it mean that temperature is changing (increasing, so the work done here is actually due to increased pressure over surface area and heat transfer) and the Charles law is more applicable?

@bonCodigo There will be a change in temperature, but the question is not dealing with the temperature. Besides, the heat generated by the cardiac muscles will be much more significant compared to the temperature change caused by the isovolumetric contraction or relaxation of such small chambers as the ventricles or atriums

You might have heard that a fluid is incompressible. That means that even if you push very very hard it will be impossible to contract a 1 L bottle to a half liter bottle.
If you imagine somebody squeezing your hand, you will feel a big increase in pressure, but your hand will practically not decrease in volume. It is the same that happens for the blood.


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Energy metabolism in Cancer cells
The TCA cycle intermediate Isocitrate dehydrogenase commonly undergoes point mutations in cancers. This allows IDH to reduce a-Ketogluterate to 2Hydoxygluterate, causing a reduction in pVHLs ability to hydroxylate HIF-1a, and a subsequent accumulation of HIF-1a. This leads to angiogenesis via VEGF. If the cancer cell is converting its a-KG away form the TCA cycle, how does the cell make up for the loss of TCA function, and subsequent ETC function for energy production? Why would the cancer cell prefer to lose high yield energy production in exchange for low yield energy production?

Which IDH protein are you considering? Mutations are frequently found in IDH1 and IDH2. IDH1 is not even mitochondrial and clearly not involved in the TCA cycle. IDH2 is mitochondrial, but not NADH-coupled, and therefore probably not the main TCA cycle enzyme. Hence, it is not clear that there is any disturbance to the TCA cycle.

Two things...
Rapidly proliferating tissues (esp tumours) rewire their energy metabolism anyway to aerobic glycolysis where you have energy being produced by lactic acid fermentation even if oxygen is present. This is called the Warburg effect.Here's the thing about "low yield" though - glycolysis chucks out less ATP per reaction at the end, but you can crunch through a lot more ATP by just having more of it going on.
Secondly, hypoxia in a tumour is generally rate limiting, and therefore the shunting away of alpha-KG with the consequence of increased angiogenesis is good for the tumour.

the loss of function mutation of IDH does not necessary mean that the oxidative phosphorylation ceases. The supply of TCA intermediates can still be maintained if other pathways are upregulated, e.g. amino acid degradation. One has to keep in mind, that the TCA is not solely standing, but there is a highly dynamic network with many entry gates (illustrated in http://www.cs.cmu.edu/~blmt/Seminar/SeminarMaterials/kegg.gif).
If you are interested in, the group of Eyal Gottlieb (http://www.beatson.gla.ac.uk/cancer-metabolism-growth-and-survival/eyal-gottlieb-apoptosis-and-tumour-metabolism.html) is investigating the metabolomics in cancer cells with truncated ability to run TCA. For example the showed upregulation of Acetyl-Synthetase 2 allowing acetate usage for cancer cell growth under metabolic stress.
With best regards


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How does DNA damage cause ageing in yeast?
As I understand it, in yeast ageing there is daughter cell and mother cell. The daughter cell is has newly "fresh" DNA and mother cell dies after some counts of replication.
What happens to the accumulated DNA damage in the yeast mother cell?
One of theory of human ageing is accumulation of damage in nuclear DNA. The daughter yeast cell is clone of mother, and has same DNA. What happens with this damage?
Edit to simplify: Why is the DNA damage not transferred at all to the daughter cell? The repair mechanism in humans is evidently not perfect, because DNA damage is one of major ageing theories. So if we die from this, how do yeast get around the detrimental affects of DNA damage that cause ageing in humans?

I can tell there is a good question here somewhere, but its hard to figure out exactly what you are asking. Are you asking if the DNA damage is transferred to the daughter cell? If you edit to clear up the question you'll probably get a good answer. Currently it sounds like you want to know about DNA damage repair.

I am asking about why there is no DNA damage transfer at all, to daughter cell. I wrote about the theory of damage in aging, so it couldn't be in any way question about repair - because if there was good repair - it wouldn't be in aging theory. I edited the question.

Unfortunately it is becoming less and less clear what you want to know. There are some assumptions your have made that are wrong compounded by difficult grammar. Furthermore ageing is a wildly understudied area of research. DNA damage is a very complex and broad field with a lot of case studies, science, and history behind it. Specifically: "Aging in yeast (and other eukaryotic) and DNA damage" is a massive topic. It sounds like you want to know everything there is to know about it, which is not suitable for this forum and the question could get closed after the bounty ends.

I have made an edit, feel free to roll back, but the grammar at least is much clearer, maybe someone will be able to grapple the question now.

Thank you Good Gravy. I just restore back the title, because I am asking about DNA only and not about all the aging process.

It is good practice to use a question rather than a statement title (only on these forums).

Perhaps you are confusing mutation caused ageing with DNA damage repair caused ageing?

I used only the world damage. No meter what damage. Some damage to DNA that leads to cell aging (loss of some activity) and death.

This is a massive question with a few key misunderstandings of the terminology, which to be fair is complicated in the field of ageing. OP kept moving the goal posts of what the question was (as can be seen in the comments for both answers), and I doubt any answer will be good enough.

In eukaryotic cells there is no difference between a mother and a daughter cell - the later is an exact copy of the mother cell. This is true for yeasts as well for example for human cells. The only thing that happens over time is that the telomeres at the end of the chromosomes get shorter (unless the cell has an active telomerase which most cells doesn't) and it reaches the Hayflick limit where every further division will lead to a shortage of coding chromosmal regions and thus cause problems. If cells do not acquire any other chromosomal damage and have enough ressources, this would be the limit for their lifetime.
Of course there are DNA damages occuring over time. Most of them are either repaired by the highly efficient DNA damage repair system of eukaryotic cells, which consists of different checkpoints during the cell cycle. These checkpoints are located at transition between the different  phases of the cell cycle. If a DNA damage is identified, the cell cycle is stopped to enable a DNA damage repair by special proteins and to prevent that damaged cells undergo mitosis (here the G2-M checkpoint is important). This works schematically like in this figure (from the Wikipedia article on DNA repair):

If the DNA damage cannot be resolved, cells will either go into senescence (basically go into a permanent dormant state) or undergo apoptosis. If there are damages which are (for whatever reasons) are either not spotted or occur during the repair of DNA double strand breaks by non-homologous end joining, these are then replicated and inherited by further generations. Unless these errors occur during the replication process mother and daughter cells are genetically identical.
So eukaryotic cells acquire DNA damage over time (one of the reasons why late pregnancies pose a greater risk than early), but we are different from yeast in one point: Yeast has an active telomerase, which is not active in most of our cells (mainly except in stem cells). If the cells collect too much chromosmal damages than they will die.
The references listed below go deeper into the topic and are interesting to read.
References:

Negative regulation of yeast telomerase activity through an
interaction with an upstream region of the DNA primer
Cell cycle control in the kidney.
The evolution of diverse biological responses to DNA damage:
insights from yeast and p53
DNA damage and decisions: CtIP coordinates DNA repair and cell cycle
checkpoints
Cellular Responses to DNA Damage: One Signal, Multiple Choices

Thank you Chris. But, like I wrote, one one the main theories of aging is DNA damage. So how is that? If the mechanism is so good, that keeping DNA of yeast fine for millions of years, why is in human its cause aging?

@Barbos you'll want to keep in mind the generation time of a yeast cell, vs. the generation time of a human being. The exact mechanisms or processes that are damaged and cause aging are under investigation. What you'll also want to consider is that yeasts and other multicellular eukaryotes have linear chromosomes that shorten with each replication at the telomere, and may become as above: cancerous, apoptotic or senescent. Check out the NIH website for aging.

I also figure it useful to add that senescent cells secrete cytokines, ECM hydrolases etc. to aid in their timely removal by the immune system. If there's a declining immune system with age, I'd assume the ability to remove senescent cells would decrease. Of course, the regular secretion of hydrolases and inflammatory compounds will produce it's own array of damage that may lead to aging.

@kendall - no, it's not the answer. Cancer? Telomere? Declining immune system with age? It is not what I am asking about. And about "generation time" - you have some source that says that because of this, yeast cells have so much less DNA damage than human? There is cells in mammals that divide and die faster that some eukaryote organisms.

Also, what the connection with generation time? This DNA lives, no matter in old cell or in new, daughter cell. It's same DNA that influenced by environment.

The mechanism is really good - humans only generate only about 30 new mutations in their gametes per generation (I can look up the paper which makes this estimation if this is of interest for you). This is an incredible small number...this happens because of damages that cannot be repaired correctly or where the wrong strand is corrected.

Why the downvote? Can you explain whats wrong? I can only work on the answer when I know the criticism.

Because it's really not what I asked, I know about this mechanisms (but you will get the bounty - thank you for answers anyway), There are really few central aging theories (3 main), one of them is damage in DNA. (not only mutations). Also there is damage in mitochondrial DNA. (Radiation, radicals, environment and more) So this mechanisms isn't perfect but yeast need to have just perfect system... Much more stronger than ours. Because if we have damaged DNA in cell, cell die - we live. If yeast have damage - he die.

@Barbos I have edited the question now - does it answer your question better? If not, please let me know which parts are still unclear.

@Chris, thank you, but now its worse - because your first paragraph is fully wrong. There is difference between mother and daughter cell - there is asymmetric division in yeast, also there is indication that bacteria has same thing. But it doesn't meter for my question. Also it is fully wrong to say that all what happens is telomeres shorting, there IS accumulating DNA damage, this bring cancer and aging (the last is theoretical). So human die from this, but yeast no. Why?

Most of our cells are not developing into cancer cells - otherwise we all would die from it. Assymetric cells division leads to differently sized cells, but the genetic material will be the same. There are indeed some indications that this is different in prokaryotic cells, where the damage accumulates in one cell. This article is interesting in this context.

No. No. That where my question coming from. The asymmetric division not lead to same cell! Because the cell of mother yeast AGING. And when we talking about aging, one of theories is accumulating DNA damage.

Then you should edit your question again to make clear what you really want.

All are in the question.  "Why there is no DNA damage transfer at all, to daughter cell?"

Your assumption is wrong - there a transfer of DNA damages to daughter cells. It's rare, though.

If the  transfer of DNA damages is rare - why is it one of major aging theories? I just say the same things again and aging ...

It was my understanding that it was unclear whether the shortening telomerase was a cause or an effect of ageing. Is there evidence that shows cause?

Background to the different theories of ageing.
This video, from a senior lecturer at the University of Liverpool who specialises in ageing, discusses the theories of ageing. He touches on the DNA damage theory.
DNA damage theory of ageing.
Note that when talking about DNA damage theory, we are specifically talking about damage to the process of cell renewal by DNA damage repair mechanisms in stem cells.
Mutation ageing is not the same as DNA damage causing ageing and cannot really cause ageing in yeast. The idea that cells acquire damage over time due to mutated DNA is fundamentally different to the DNA damage theory of ageing. The mechanisms that lead to DNA damage are covered very well in @Chris' answer.
The suggested systemic effect that DNA damage has in the human body causes an inability to renew cells due to a lack of viable stem cells. This contributes to the process of ageing in the organism.
In yeast, this stem cell depletion process does not happen (they are single cellular mostly). In the comments it appears that you are actually talking about mutation based ageing in your original question. Mutations are passed to daughter cells. But these daughter cells don't appear to age or to die quicker (If the parental cell is 5 days old, the daughter cell does not appear to be 5 days old). This is the fundamental reason why this form of ageing remains less studied - it doesn't really make sense that general mutations cause ageing.
Summary
To directly answer the question: "How does DNA damage cause ageing in yeast?"
The question doesn't quite capture the whole picture and confuses DNA damage theory of animal ageing with general DNA damage at a cellular level.
There are many theories of ageing. Nobody knows which ones have more or less influence on ageing. Yeast is a good model for some kinds of age theory modelling, but perhaps not in the case of DNA damage based ageing. Although they experience DNA damage in the form of mutation, this doesn't cause ageing in the same way that DNA damage might cause ageing in humans because they are single celled organisms, and don't experience the same inter-tissue relationships that more complex organisms have.

Edits
This answer has been changed extensively since its first draft based on additional questions and queries from the OP in the comments. I decided to keep some important points that were raised and dismissed.

Why there is no DNA damage transfer at all, to daughter cell?

DNA damage can occur and is transferred to the daughter cell. Damage is very rare though.

So how yeast survive? Human stem cells aging and die, or get cancer. But yeast no. Human start from one cell. And die. Yeast start from one cell and live forever (dividing again and again)

Edit After Comments:
Single cell
In yeast there are no inter-tissue systems. Mutated damage is simply passed on if the cell is viable. Also the assumption that they live forever isn't entirely accurate. But the DNA is passed on in its mutated or damaged form.
Multi cell
DNA damage based ageing is a big problem for animals. (Dolle et al 2013) Showed that DNA damage to a single repair pathway causes accelerated ageing, (but note that there was not an increase in mutation during this ageing).

but you talking about cancer, it's not so good example, my mistake.  But in humans aging NOT like cancer - it occur in ALL the body and all the cells. So in all cells there are some DNA damage.

Another edit: You were right to talk about cancer in this context. The DNA damage theory of ageing is that small changes (damage) in our DNA accumulate over time and damage cell types by damaging various DNA repair pathways.
Damage accumulates and over time less stem cells for renewal are viable and cellular repair of other damaged cells slows down.
Also this same fundamental principle of mutation damage happening over time can lead to mutations that switch off cell control mechanisms and lead to cancer. Although these these mutations do not increase in rate with age (Hill et al., 2005).
For example the naked mole rat lives 10 times that of comparable species (less ageing) and have not been observed to naturally acquire cancer (less cancer). The theory implies that the two things are quite linked because of the way DNA changes, but not that specifically mutation is a cause or result of ageing.

I talking more about aging. Because there is aging in yeast. And one of aging theories for human - accumulating DNA damage. So what Chris writing is that it's really rare.

**Stem cells are damaged. ** I'm no longer entirely sure of what you mean by ageing in yeast. Yeast aren't reliant on a limited number of stem cells for cellular renewal, they don't age in the way you might be thinking. They simply proliferate the mutated cell type. There is no impact to a larger organism like in human ageing.
DNA damage. Yeast is a very helpful organism for understanding the underlying biochemistry and genetics of ageing, not the overall ageing systems. These are two different fields of study. It is unclear which you are talking about at this point.

Also there is aging in places where no stem cells - like brain - no renew of cells, just existing cells age, damaged, die, and not replaced.

Dolle 2006 found that spontaneous DNA damage in relation to age happened in the liver but not the brain.

Also you telling us that there is no cancer.

No & No. The damage is rare, but it does occur so much that cancers may develop naturally in animals and may cause ageing over time. Remember cancer is a huge field of different diseases.

So how yeast survive? Human stem cells aging and die, or get cancer. But yeast no. Human start from one cell. And die. Yeast start from one cell and live forever (dividing again and again)

thank you for edition, but you talking about cancer, it's not so good example, my mistake. Sure there is no cancer in single cells. I talking more about aging. Because there is aging in yeast. And one of aging theories for human - accumulating DNA damage. So what Cris writing is that it's really rare. But in humans aging NOT like cancer - it occur in ALL the body and all the cells. So in all cells there are some DNA damage.

First of all, thank you! About yeast aging and "limited number of..". The yeast has limited number of divisions, mother cell die after some count of them. I am not asking why, I just taking ONE of the theories of human aging (accumulating DNA damage) and asking, if the same theory is right to Yeast, how is it possible that daughter get no damaged DNA, when mother die because it (one of theories).

About the main part "don't accumulate as much damage" - but the DNA lives 'forever'. It's the same DNA - what meter if it in old cell or in new? One mutation  transferred to daughter. Accumulate new damage (already 2), transfer to new daughter, another damage (already 3) ....

In my answer I explain that the DNA damage theory of ageing is not directly applicable to yeast as DNA damage theory of ageing affects stem cells and stops repair of tissues, so the whole massive 37 trillion cell human organism suffers. In yeast, the DNA damage doesn't have this affect and 'ageing' in that context does not occur despite there being DNA damage passed down the lineage of cells. What do you mean "DNA lives forever"?

I don't agree about  repair of tissues. DNA damage leads to problems in cell that damage occurs in. Doesn't meter if it steam or not. Damaged DNA can't make some protein or do bad one. So it's directly  applicable to yeast - in my opinion. Damaged DNA, not producing of important proteins - death.

About DNA lives forever. You say that there is no time to damage to accumulate because short life. But the DNA it self doesn't have short life. DNA (lets say one of single string) lives forever. And the second string is just a cope. Lets say we have a small damage in mother (G instead of C) and it doesn't influence. It pass to all the daughters. One of daughters take another damage (one A to T) so now we have already 2 damages in DNA. And it's go forward accumulating more and more. It doesn't meter that the initial cell already dead.

Unfortunately, it doesn't matter what your opinion is; The most current form of the theory of DNA damage based human ageing is that long lived stem cell stocks are depleted. For regular DNA damage you are right. It happens in yeast and humans. But ageing in humans is a more complex systemic and generally predictable process rather than random changes to random proteins. And always remember, this is one of many theories of human ageing and it possible many of those theories are right.

Damage in stem cell = stem cell not working. Same damage in yeast cell = yeast cell don't work. Also there is aging in places where no stem cells - like brain - no renew of cells, just existing cells age, damaged, die, and not replaced. Aging of stem cells cause by DNA damage (one of the causes) so in the same way it cause damage to yeasts. I talking only about DNA damage and not other theories. The DNA damage have some part in it - that is the theory. So in the same way it need to affect yeast too.

Damage in stem cell = stem cell not working = no cell renewal = ageing? The brain does not age quicker when DNA damage is increased (see modified answer, Doll et al 2013). Fundamentally you are misunderstanding that yeast and humans propagate in different ways. Another misunderstanding is that this form of ageing does not apply to yeast. But I hope I have helped a little. If you have any more questions or thoughts, feel free to move this to the discussion.

Thank you, Good Gravy. I will dive dipper in this topic. But about the brain, for example, in wiki "Accumulation of DNA damage with age in brain has been reported during the period 1971 to the present in at least 29 studies" (http://en.wikipedia.org/wiki/DNA_damage_theory_of_aging) there is a lot of studies that talking about accumulating damage in all body cells (not just stem). "The source of the DNA damages ... appears to be reactive oxygen species, produced as byproducts of normal cellular metabolism." Yeast produce same  reactive oxygen. Wiki talking about damage to single, not stem, cell

This is why there are many theories; each has evidence for and against it. Nobody know which contributes the most to ageing. Here we are discussing DNA damage only. The mutation theory is different. Perhaps open another question?

What meter how many theories is? Also I didn't talked which one more important.. I getting answer to questions that I didn't asked. I telling again and again. DNA damage is one of the theories of aging of single cell in human body (not only stem, regular cells). Because of all the DNA damage (mutation,oxidation,mistakes, doesn't meter) cell lose the function and die. Why it isn't happens in yeast? All your answers very interesting -but that not what I am asking for. There is similarity between yeast cell and human cell. They both get DNA damage, for example from reactive oxygen from metabolism

"This is why there are many theories; each has evidence for and against it" How is that connected to my comment? I wrote just about one thing - DNA damage.


text:
Why asexual reproduction?
When I took a course on genetics and evolution, I learned that recombination and sexual reproduction is advantageous compared to asexual reproduction. Sexual reproduction allows more combinations of DNA because of recombination, allowing more variations of species, causing natural selection to "choose" different variations of species to reproduce and share their genes to help the species from dying out. On the other hand, asexual reproduction doesn't allow recombination. So species can only rely on mutational changes to keep a species safe from extinction. Therefore, why don't we see more sexually reproducing species than asexually reproducing species? Sexually reproducing species have an advantage, don't they?

The most obvious disadvantage is that of sexually reproducting organisms, since half of the population cannot reproduce directly (i.e. reproduction will be 50% lower compared to an asexual counterpart), which is why "the mystery of sex" has become a issue. So in evolutionary biology, I would argue that explaining the value of sex has been the bigger issue.

There is one thing that both of the answers so far do not say and you kind of have to just think of, but except for the fertilization event, all development in animals anyway is asexual cell division guided by chemical signaling. So even in a human with its trillions of cells, only the fusion of the male and female gamete occurs sexually, the rest of the organism is made through controlled cell division. That program is probably the most important part of the genetic code of an organism, otherwise it will fail to develop.

"Sexually reproducing species have an advantage, don't they?"  - To be corrected to  "A(!)-sexually reproducing..."?

When you say, why don't we see more sexually reproducing species than asexual, I presume you are referring to bacteria, protists, archaea, some fungi, etc.
Most multicellular organisims do reproduce sexually, which makes sense since an organism would need to be multicellular to have cells specialized for gametes. As you stated, the advantage is that sexual reproduction offers an advantage by allowing more rapid generation of genetic diversity, allowing adaptation to changing environments.
However, look at the single-celled organisms that reproduce asexually. Asexual reproduction is beneficial in many circumstances in that it can create individuals rapidly and in large quantities. For example, yeast can duplicate every hour under the proper conditions. For yeast, that means survival by sheer numbers. For us, it means we can make bread in a few hours.
If you believe asexually reproducing organisms are at a disadvantage due to lack of genetic diversity, consider bacteria and antibiotic resistance. The rapid generation times allow mutations to be selected for in particular circumstances. Penicillin was introduced in 1941. Two years after this landmark event, strains of Penicillin-resistant S. aureus had already emerged. Now, perhaps 2% of Staph. aureus (SA) is susceptible to penicillin, and some SA are "superbugs" with multidrug resistance: good for Staph, bad for us.
Also, it is possible for single-celled organisms to "share" DNA through mechanisms sometimes likened to sexual reproduction; lateral gene transfer occurs through conjugation, transformation and transduction.
Thus, both asexually and sexually reproducing organisms are well-suited to their ecological niches.

You forgot to mention that one part of the Yeast life cycle is sexual. You can have a mating type cells fusing with alpha mating type cells to produce a diploid cell. When resources are scares the diploid yeast undergo meiosis form an ascus with four haploid spores, two a-type and two alpha. They go through meiotic recombination the same as multicellular organisms. It is felt that this is done to increase genetic diversity and improve survival chances during times of unfavorable growing conditions.

I would also probably bold your entire third paragraph. I know we disagree about paragraph 4, but resistant SA mutants likely already existed in the population well before Fleming worked out how to extract Penicillin. Remember that SA and P. rubens have been an arms race for millions or even billions of years, so if P. rubens had a chemical to defend against SA, there were likely already SA in the population that had resistance to it.

This just in addition to @anongoodnurse's excellent answer. It was mentioned in the OP that asexual organisms do not undergo recombination; this is not true. Recombination is used for integration of foreign DNA into prokaryotic chromosomes and for repair.
Also, don't underestimate the power of mutational change in rapidly reproducing organisms. While mutation rate is low, consider the effect when it is applied to millions of individuals.
Finally, just an interesting example of the ability of bacteria to evolve. Many organisms can rearrange foreign DNA for their benefit. I will mention the specific example (because it's what I work with) of transforming B subtilis with a plasmid containing an antibiotic resistance marker and somewhat toxic gene. Often you will find transformed bacteria that have rearranged the plasmid to delete or inactivate the toxic gene while still retaining the resistance gene. Thus they can still grow in the selective medium and manage to be of no use to me whatsoever!

@anongoodnurse Well I wouldn't say that, but thanks! (I +1'd yours as well)

Good point about mutational change. In multicellular sexual organisms, only mutations that happen in the germ line (relatively few cells) can be useful for evolution, while every single mutation in the entire population can potentially have an evolutionary impact in unicellular, asexual organisms.

Sexual reproduction probably evolved because an asexually reproducing species of bacteria evolved an evolutionary stable strategy and then there was a rapid change in the environment and only the mutant individuals that could reproduce sexually could evolve fast enough to survive which later evolved into sexually reproducing animals. Also, sexually reproducing species are more likely to be able to evolve fast enough to avoid extinction when there's a rapidly changing environment. However, the true evolutionary stable strategy for any species probably has the species reproduce only by parthenogenesis. Indeed, some bacteria probably didn’t evolve to reproduce sexually and then evolved into an asexually reproducing animal species which still exists like the New Mexico whiptail and Mycocepurus smithii.
If an asexually reproducing species happens to have the right genome, it will already be adapted to all those future rapidly changing environments that will happen like the spread of a deadly parasite assuming the Sun won't get brighter or die. The ones with a slightly faster mutation rate will very slowly outcompete the ones with a slower mutation rate because they can evolve the trait that's best for the current environment faster but once the next sudden change in environment occurs, the ones with a lower mutation rate will survive because they remained adapted to the change. After enough sudden changes to the environment occurr, the ones that survived the most recent sudden change in the environment will be the ones that had a genome that prediced that that environment could occur already was adapted to it because it was adapted to the sudden changes that already happened and there is a pattern in which changes in the environment already occurred.
Another advantage in asexual reproduction is that a mutant asexually reproducing individual who happens to have the right genome in a sexually reproducing species could rear 2 kids and pass all their genes onto them if the species was already at an evolutionary stable size. However, once the asexually reproducing individuals outcompete the sexually reproducing ones and reach a new evolutionary stable size, each individual on average could only rear 1 kid.
Another advantage in asexual reproduction is that any mutation that's advantageous for an offspring is also advantageous for their off spring and the mutation rate is very low making the strength of genetic drift very weak so there would probably be less of a tendency that the more of one advantageous trait there's genetic drift against that a species has, the less of another advantageous trait there's genetic drift against it can evolve to have. For example, an asexually reproducing human could outcompete all humans other than her descendants and then evolve a genome that gives them immunity to malaria without the possibility of sickle cell anemia. An sexually reproducing species if it evolved resistance to enough past diseases doesn't necessarily have to be more prone to the spread of a deadly parasite than a sexually reproducing species. Frequency dependent selection could easily select for mutations that make some individuals different from others in order to have resistance to a deadly parasite that already evolved to spread through some individuals.
The smaller an animal is, the faster it can run without ever getting too hot because the faster it can get rid of heat. However if it exceeds the speed it can go without ever getting too hot, then the faster it runs, the shorter the distance it can run before it collapses from heat exhaustion. A larger animal that exceeds the speed it can run without ever getting too hot can run longer at that speed before it gets too hot than a smaller animal running at the same speed.
I read that a wolf never gets too hot in its chase if it's not too hot outside so a mutant asexually reproducing wolf probably would have a huge evolutionary advantage for chasing rabbits as long as the air's not above 30°C. It would be able to evolve into a poikilotherm so that it can do away with having fur so that it can get rid of heat faster so that it can chase rabbits faster so that they'll be less likely to escape and to burn less energy when it's cold out.
A cheetah on the other hand builds up heat way faster than it can get rid of it during a chase so a mutant asexually reproducing cheetah would probably also have a hug advantage. It could evolve to be a poikilotherm so that it can have a lower core temperature at the beginning of a chase during times the air is colder so that it can chase its prey for a longer time before it gets too hot to continue the chase, and also evolve to not have fur so that it can get rid of heat faster after a chase so that if a prey animal happens to come sooner after its chase, it can chase it. That's because the expected amount of energy it will gain from continuing the chase is larger than the expected energy it will burn in continuing the chase. I think they could actually get rid of heat way faster because they could walk to speed up the loss of heat after a chase because the air would be freely circulating around them.


text:
How many different kinds of polypeptides, each composed of 12 amino acids, could be synthesized using the 20 common amino acids?
How many different kinds of polypeptides, each composed of 12 amino acids, could be synthesized using the 20 common amino acids?
The book's answer is $20^{12}$.
However, I disagree. This result distinguishes the following two polypeptides even though they are exactly the same polypeptide:
(Met)x11-Glu
and
Glu-(Met)x11
Am I right? How would I otherwise answer this question? My background in probabilities is very weak.

Judging from what you have said, I assume that combinatorics is not a problem to you.
I believe your problem is that you think Glu-(Met)x11 is equivalent to (Met)x11-Glu, just turned around. However, that is not a correct mindset. Amino acids are not symmetrical molecules, therefore reversed linear combination does not create a turned-around (be it chiral or not) form of a similar amino acid. My guess is that you write amino acid names in consecution when representing peptides. This method has a small problem that it does not incorporate directionality of molecules. Drawing the whole molecule may be a solution, but that is too much chore.
My solution is to add a small mark (perhaps an arrow, or a > mark) to represent a specific side of the amino acid molecule (amine group or carboxyl group), so that mirroring the sequence (so that the mark would be at the "other" side of each amino acid) would actually create a peptide molecule different from reversing the sequence (so that the mark is still at the "normal" side of each amino acid). If you think that doesn't look good, you can draw a frame around each amino acid, where one side of the amino acid has a dent and the other side has a bump (to represent the amine and carboxyl groups) so that only a bumped side can connect to a dented side. Mirroring the sequence would also reverse the positions of the bumps and dents, thereby creating a different peptide molecule than merely reversing the sequence while keeping the positions of the bumps and dents in place.

Tricky indeed. Very detailed and visual explanation. I forgot about the difference between the C- and N- terminus. Thanks.

Think of the amino acid choices as 12 seats. In the first seat, we have 20 choices. In the next seat, we have 20 choices, and this continues. Therefore, we have that
$$
\underbrace{20\cdots 20}_{12\text{ times}} = 20^{12}
$$
For your question about the the polypeptides, (Met)x11-Glu is not the same as Glu-(Met)x11, order matters.

Up to this point, we have considered the sequence of amino acids that make up a protein. This is the first of several levels of protein structure, illustrated in Fig. 4.4. The sequence of amino acids in
  a protein is its primary structure. The sequence of amino acids
  ultimately determines how a protein folds [1].

The individual amino acids are not symmetrical. Thus, your two example peptides are not chemically equivalent, and the $20^{12}$ figure is correct.


text:
How semi-synthetic cell with artificial DNA works
I know that by now this is old new but I heard that a cell that used a synthetic pair of nucleotides, called X and Y, have been made. My question was, how did the cell understand the X and Y nucleotides during translation and how was it even represented in mRNA? It must have been represented differently, possibly using X and Y nucleotides only. That's the only way I can think of that causes the cell to make 172 amino acids instead of the usual 20. By the way I read this in the Discover magazine, January issue.

The altered E Coli still only made use of the regular 20 amino acids (presumably).
Looking at the original citation, Malyshev et al didn't characterize the RNA in their altered E Coli at all. All they did was add free X and Y to the E Coli's growth medium and add a gene to the E Coli that expressed an algal nucleotide triphosphate transporter. Malyshev et al then demonstrated that replication (copying of the DNA) proceeds normally and in such a way as to preserve the X and Y content.
So no information as to whether any of the products downstream from the DNA (ie mRNA, proteins, etc) were affected by their modifications.