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Glutamine analysis
I use to run a method to analyse all the amino-acids in a food sample. For that I have to hydrololyse the sample and in the last stage of the method I read the amino acids with a ion exchange chromatography.
However, when using this method, due to the hydrolysis, the glutamine transforms into glutamic acid, thus in my result I get a big peak for glutamic acid and I cannot read glutamine.
My question is if there's a method to quantify glutamine in a food sample.
Edit: it has been a while, thanks for the feedback!
In the kind of samples I have I need to measure the bound glutamine, not free glutamine. This imposes a problem during sample preparation when trying to separate the amino acids. I have made a few experiments and I have almost succeeded by using a 'enzyme cocktail' that does a total enzymatic hydrolysis. Next step will be to find out if I can quantify glutamine.

A Google search for glutamine assay reveals a number of commercial kits. Some of these refer to food assays. I don't know what the basis of these assays is however.

Maybe there's an alternate hydrolysis method that doesn't convert glutamine to glutamate?

I am not so familiar with enzymatic kits for quantifying glutamine, but most enzyme-based analysis kits come with a number of fairly strong assumptions on the enzymology involved, and in my experience they are difficult to use reliably. Commercial kits are hopeless to troubleshoot since their components are not disclosed --- you don't know what you're working with.
Are you at a clinical chemistry facility? If so you may have access to analyzers used to measure blood biochemistry parameters, and some models measure glutamine, for example this one. These instruments are also based on enzymatic assays, but they are carefully tested since they are used in human medicine, and so I would consider them more reliable than the average Sigma kit.
The best alternative I think is mass spectrometry, or NMR. Glutamine is easy to measure on any LC-MS or GC-MS setup (an old triple-quadrupole will do nicely), it ionizes well in positive mode electrospray, is well retained on a typical HILIC column, and isotope-labeled standards are readily available. I'm no expert in NMR but I know glutamine is measured routinely.
Another caveat with analyzing glutamine is that it decomposes spontaneously in water to form pyroglutamate, with a half life of about two weeks at room temperature, as shown in this paper. But I'm sure you're aware of that.


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What is the advantage of circular DNA in bacteria?
From what I understand, bacteria have circular DNA. What advantages does it have over linear strands like for eukaryotes?
Do there exist bacteria with more than one ring of DNA?

Interesting question!

closely related question: Is there an advantage to linear chromosomes?

Vibrio cholerae is known to have two circular chromosomes.
Bacteria cell division is a lot simpler and efficient as compared to eukaryotic cell division, partly due in part to the nature of their chromosomes. They don't have to undergo mitosis -- condensation of chromosomes, segregation, spindle fibre formation, attachment et al aren't involved in bacterial cell division.
Circular DNA also circumvents the Hayflick limit (thus allowing it to be "immortal"), which is the number of times a cell population can divide before it stops, presumably due to the shortening of telomeres, the sequences at the end of the chromosomes. Since circular DNA lacks telomeres, it does not get shorter with each replication cycle.
Circular DNA can also facilitate horizontal gene transfer such as Hfr mediated conjugation. Remember, conjugation is analogous to a "rolling-circle" type replication which is of course, only possible on circular pieces of DNA.

I made a minor edit to your answer, hope you don't mind.

interesting, but aren't fission yeast also immortal?

Yes- but they need telomerase to maintain their telomeric ends. Bacteria avoids this problem altogether by using a circular chromosome.

To expand a little bit the other answer, I would also add that bacteria can have other (usually circular) DNA segments aside from their main chromosome. These are called plasmids and are double stranded molecules of DNA that can replicate autonomously.
Plasmids often carry genes that allow an organism to survive in certain conditions, for instance they could carry the resistance to an antibiotic, or the gene that encodes for a specific nutrient that may be absent in the environment and so on.
As the other answer says, plasmids can be transferred horizontally between bacteria in a process called bacterial conjugation, and that is made possible by the presence of a specific plasmid, called the F-plasmid in the donor. The F-plasmid encodes, amongst other things, for the F-pilus protein pilin, that allows the formation of the pilus necessary for DNA transfer.
Because of their properties, plasmids are widely used in laboratory as vectors, to transfer genetic material to cells in order to give them specific "abilities" (e.g. you could insert a gene that encodes for a certain receptor normally not expressed by the cells to allow its expression and test its function).
Finally, it is worth remembering that plasmids can also be found in eukaryotes (e.g. in yeast).

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Why does milk contained in cartons of milk expand?
In the morning, I went to the fridge to drink some chocolate milk. At night, when I took out the same carton of milk, the packaging seems expanded, like some kind of air is inside. Explain please !

There are probably several reasons. One that I can think of is that spoilage bacteria may have introduced gases that increased the pressure inside the carton. Probably that's why you notice the bulging.

@user16893 say you have 1L of air at +4C temp (T=277K) and move it at constant pressure to room temp of +24C (T=297K). You should be able to calculate change in volume as PV=nRT, where P=const

Perhaps the culprit here is the packaging, not the contents.  Since you say 'carton', I'm assuming the ones with a square cross section, no?  So they're shipped, and on the shelves, packed tightly together and so hold their square shape.  Put a single carton in the refrigerator, and the sides slump a bit under the weight of the contents, since for economic reasons they're made no stronger than necessary.

The likeliest culprit here is fermentation carried out by bacteria present in the milk. Fermentation of a sugar, for example glucose, releases carbon dioxide (a gas) :
$$C_{6}H_{12}O_{6} \rightarrow 2 C_{2}H_{5}OH + 2 CO_{2}$$
Since this reaction produces a gas, the gas builds up in the milk carton causing it to bulge. This is not, generally, a good sign, make sure to smell the milk before drinking it!

Do the bacteria in milk undergo ethanol fermentation? It's always been my understanding that homolactic fermentation predominates, though that isn't actually based on anything.

@canadianer no idea, to be honest. I'd be interested in the answer if you look into it though!

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Viral mutation rates and replication
TL;DR
What's the relationship between the following?

Mutation rates (expressed as "mutations per year" for a virus like e.g. COVID-19 (SARS-CoV-2). E.g. this article mentions "The rate looks to be about 24 mutations per year"
Actual virion replication error rates in a single host cell, measured as e.g. error rates per released virion from the infected cell, i.e. (# of mutated released virions) per infected cell.

Assumptions
I would assume that mutations happen at a single virion-cell level because there are differences in e.g. nucleotides in RNA  between:

the virion infecting a cell (e.g. ACE2 for SARS-CoV-2)
the released virions from that same single cell

If so, wouldn't one argue that:

replication errors (at the nucleotide and thus released virion level) can easily happen, potentially billions of times during the infection of a single host organism
there is no "single successful" mutation or RNA variant within a host, rather, we have a distribution of RNAs, many of which could be simultaneously transmitted to another host organism?

Further context
I quote from e.g. this paper:

On a per-site level, DNA viruses typically have mutation rates on the order of 10E-8 to 10E-6 substitutions per nucleotide site per cell infection (s/n/c). RNA viruses, however, have higher mutation rates that range between 10E−6 and 10E−4 s/n/c

Again, wouldn't that mean that a single host could 1) easily generate many mutations of the same virus and 2) pass most of those uniquely generated mutations to another host? If so, how come we can simply say "24 mutations (over time) per year"?

Only those mutations which are themselves viable can be passed on. Most mutations are deleterious — evolutionary dead-ends, which do not reproduce. Thus you get a substitution rate calculated from the population of mutants that can reproduce.

Thanks @AlexReynolds but isn't it fair to say that on any single organism, you would still have a population (distribution) of viral RNAs, and not a single (even if dominant) mutation?

@AlexReynolds That sounds more like an answer than a comment.

Hi Amelio, I'd suggest taking a look at the difference between mutation rates and substitution rates, which is a subtle difference in terminology but which may help get a better comment to address your question. Hope this helps!

+1 I did here Thanks @AlexReynolds

Since no one else has done so, just gonna expand on what occurred here in the comments (mostly from @Alex Reynolds):
tl;dr: natural selection exists.
Longer version:

Mutations/replication errors/whatever will happen in the creation of new virus particles within a host cell. There is some distribution of number of mutational events that will occur as a function of the number of new RNA molecules created per cell and the replication error rate. Some subset of these RNA molecules will be packaged into new particles, yielding a new generation of viruses that get a chance to infect. Yes, this is potentially a large number of new mutations per infection event.
Some large proportion of these new particles will contain non-functional RNAs, due to inactivating mutations of one kind or another. Most of the new mutations will be worse at being a virus than the originally infecting virus (their immediate parent). So therefore, they will be outcompeted by non-mutated forms.
Among all those viruses which continue successfully infecting throughout the course of a year, on average we observe 24 substitution mutations in the genome over the course of that year. Every transmission chain included in the group of viruses at the end of the year must have remained viable for infection of hosts. In other words, it has survived natural selection.

In population genetics, this phenomenon is known as "mutation-selection balance"- e.g. new mutations arise in the population at a rate that is limited by the action of natural selection (at equilibrium).
Genotype-phenotype maps
What of course I am leaving unstated is exactly why "...new mutations will be worse at being a virus than the originally infecting virus..."
This is very hard to predict in many cases. In some cases it is very obvious why a mutant is bad at being a virus, if e.g. an essential gene is deleted from the RNA genome. But for many single mutations we don't really understand what their effect will be on virus function, we just observe that they drop out of the population due to negative selection.
If you are interested in this question, I recommend looking into genotype-phenotype maps. I know Jesse Bloom has done some work on influenza in this field, here is one example of such a paper. It is generally extremely laborious to do this kind of work, so relatively little is known about the functional effect of any specific mutation in any specific genome.
Hope it is helpful to have all that written out.

Thanks! This is perfect, and confirms exactly what I thought (the terminology here was confusing me so this is great!). Does the literature really use the term "mutation rate" to refer to both: 1) "population genome" mutation rates (for lack of a better term)  and 2) "per replicating virion" mutation rates?

There are many different mutation rates in the literature, and each of them has its purposes. For example, there is the "population mutation rate", https://en.wikipedia.org/wiki/Watterson_estimator, the rate at which new mutations arise at a site in a population. There is also the "mutation rate" which is closer to the "replication error rate", which is the rate at which mistakes/new nucleotide variants occur. There is also what is sometimes called the "substitution rate", handled elsewhere. And more. All have their proper domains, but figuring out which one to use can be confusing.

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How are epigenetic marks transmitted during cell division?
As far as I know, this is one of the biggest questions in the epigenetic field: how are the epigenetic marks like histone modifications propagated through cell division? A lot is already known about DNA methylation (e.g. as in How does “inheritance of methylation” of DNA and/or histones work?), but very little about histone modifications. What is the current state of knowledge?

I know this could probably fill a whole thesis, but a brief overview for someone who has an "advanced beginner" knowledge of genetics would be perfect.

As far as I understand Alberts, after dissociation from DNA at the replication fork, histones will randomly reassociate with the copy and the original, so half of the marked histones will associate with the copy in the region which was just replicated. Then you get HP1 and such propagating the modifications all the way to the ominous "boundary element".

I can get the ball rolling..
Found a nice paper which looks at this phenomenon in yeast.
So as a primer, 8 histone proteins come together to make a spool of sorts which DNA wraps around:

Histone proteins have many sequence variants, and each one of them can be covalently modified with methyl, acyl, phospho, SUMO, adp and many other sorts of chemical groups via a chemical bond.  Although its not yet clear exactly how it works its clear that these modifications can change the behavior of the histones which prevent transcription of the gene when they have the chromosomal DNA all wrapped up.
So as to the question a pattern of inheritance of modified histone patterns is indeed seen and has epigenetic effects.  (that is, it modifies the genetic phenotype of daughter cells which retain the histone modifications of the parent cells).  In this paper, newly synthesized (and labelled) yeast histone can be found incorporated into certain segments of the genome, which demonstrates that large segments of the histones are carried forward from the parent cell.
They also found a particular case of histone epigenetic labeling carried forward through division:

Furthermore, if the heterochromatin-binding protein Sir3 is unavailable during DNA replication, histone H3-K4

So there's evidence that histone configurations are transmitted epigenetically, In this 2011 paper, the author support a 'conservative distribution model' and compare it to a 'semi-conservative' model:

The conservative distribution model proposes that newly synthesized histone molecules form nucleosomes that are randomly inserted among preexisting parental nucleosomes.
The semi-conservative distribution model proposes that a hybrid nucleosome that contains both newly synthesized and parental histone H3-H4 dimers is formed, which facilitates the transmission of epigenetic information within the basic nucleosome unit.

They go on to say that a conservative model of histone inheritance allows for strong epigenetic inheritance as the remaining parent histones will tend to attract similarly labelled histones as the new histones incorporate themselves among the parental histones on the daughter chromosome.
Its still being worked out though...


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What is the prehistory of amino acids in cells?
As a followup to Why 20 amino acids instead of 64? and What is the smallest number of amino acids required for life?, I am trying to understand the prehistory of amino acids in cells.
All living cells now use 20 (or 22 if you include selenocysteine and pyrrolysine) amino acids. Perhaps in the past there were fewer amino acids used in cells, especially if the theory of a 2-nucleotide codon is to be believed.
Is there any theory as to the order in which these amino acids were incorporated into cells?
This paper (by Akanuma, Kigawi, Yokoyama, "Combinatorial mutagenesis to restrict amino acid usage in an enzyme to a reduced set", http://www.pnas.org/content/99/21/13549.full) suggest that the full complement of 20 amino acids are not strictly necessary by reducing the number of amino acids in a certain enzyme to 13, yet still retain functionality.

the quippiest answer might be ZERO since its been shown that RNA can reproduce itself, at least in theory and probably at some point in biological history as well.

If there ever was a 2 bp code - i think it would have not produced proteins as we know them - there simply isn't enough variety to make a structure as we know it.  Proteins would have done something else at that point.  Not sure what to make of the question at that point. Maybe it was all keratin...

@shigeta: check the paper I've added as a reference

Edward N. Trifonov is a professor at the Institute of evolution at University of Haifa, Israel. One of the main research topics in his group is the reconstruction of the origins of life. In one of his papers, The triplet Code From First Principles, he proposes the the chronological appearance of the 20 amino acids. There are a lot of hypothesis and testable predictions, among which is the theory of S. Miller that some biological compounds have been abiotically produced in the atmosphere. This prediction has been confirmed by imitation experiments, yielding ten different amino acids, as glycine and alanine being the prevalent ones.
The author tries to predict the chronological order in which the 20 amino acids appeared by taking into account various criteria (studies, hypothesis and viewpoints) that propose some order, as each one of them contributes to the consensus order to a certain extent. This contribution is described in the form of rank. He compiles a list of 60 rankings of 60 different criteria to derive the consensus order. Some of the criteria are:

N1’. Criteria based on various evaluations of complexity of amino-acids. N1, N34, N35,
  N37 – as in (5), and N44 (6). G, A, S, P, V, C, D, T, N, L, K, I, E, (MQ), H, R, F, Y, W
N2’. Criteria based on evolution of amino-acyl-tRNA synthetases. N2, N7 (5).
  (AG), (DFHKNPST), (CEILMQRV), (WY)
N4’. Criteria based on amino-acid compositions of various sets of presumably ancient
  proteins. N4, N26 (5), N41 (7), N45 (8), N47 (9), N48 (10), and N58 (11).

The first ten (earliest) consensus amino acids are the same as in Millers’s experiments. The amino acids appeared last have their respective codons borrowed from already existing ones. The derived consensus order is G, A, D, V, P, S, E, (L, T), R, (I, Q, N), H, K, C, F, Y, M, W.
The author also proposes a reconstruction of the chronological order in which the 64 codons had appeared.

This is an interesting paper. I've not picked through it in detail, but it seems to assume we started with the triplet code immediately and did not pass through a doublet code as other people have proposed ( http://www.imb-jena.de/~sweta/genetic_code_and_evolution/evolution.html )

Yeah, the assumption is that the earliest amino acids (ala ang gly) were encoded by triplet codons. Perhaps you can look at Trifonof's eariler literature to see whether he discusses this.


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E coli cotransformation efficiency
What is the E coli transformation efficiency for 2 plasmids? Are any studies that have looked at the correlation between number of plasmids transformed and transformation efficiency? Is there a commercial E coli strain that is better at co-transformation?
For example, electroporation with single plasmid yields around 1 × 10^10 cfu/μg. I would like to know what is the limit for co-transformation and whether it can be or has been improved.

Nothing to back this up with so just a comment: my understanding is that the cells which are competent take up a lot of DNA, so cotransformation is easy to achieve as long as you can select for both plasmids (if they have replication/segregation features from the same incompatibility group they will segregate rapidly). I once did a Tn5 mutagenesis experiment which required propagating the plasmid in a Tn5 strain, preparing plasmid, transforming a recipient at high DNA input and selecting for kanamycin resistance. Many transformants contained more than one plasmid but they resolved easily.

The efficiency is pretty low. You have to be able to select for both plasmids individually (for example plasmid 1 with ampicillin and plasmid 2 with choramphenicol or other possible antibiotics) otherwise the cells will rapidly loose one of the plasmids. Usually the shorter and less "energy expensive" stays, if it maintains the selection marker.

I've always understood for this process to be incredibly low. When you consider how much DNA is added and how many competent cells there are, if you have even 1% transformation efficiency, you'll always get lawns. Since we don't, that gives a rough estimate of the process.

I also make the previous comments into a nice answer.

There is no problem to transform bacteria with more than one plasmid. The usual methods (either chemical competent cells or electroporation) are working fine, although electroporation might give you better results, as the cells take up more DNA. On the downside you have to make sure that your cells are prepared nicely, otherwise the electroporation cell will produce a short circuit (of course chemically competent cells can be problematic, too).
What you will definitely need are two (or more) different selection markers. The easiest will probably be different antibiotics (something I used in the lab and which works nicely) or other like genes which provide essential substances for the cells. As long as the selection pressure on the cells is held up, both plasmids will stay in the cells, when you take away one of them, the corresponding plasmid will get lost within a few days.
Regarding the efficiency of co-transformations I haven't found any papers. There is however, some data available on factors which influence the effiency of single transformations and I don't see, why these shouldn't be applied for co-transformations as well.
First, there is the size of the plasmid. The bigger the plasmid is, the lower gets the transformation efficiency. The figure from Inoue, 1990 is pretty clear in this point:

So for this reason I would use plasmids as small as possible.
Second, the density at which the growing bacterial culture which is used to prepare the competent cells is harvested has a big influence on the transformation efficiency. Tang and colleagues (1994) found out that growing the cells to a higher density than the classical OD$_{600}$ of 0.6 (which for example Inoue recommends in it paper cited above) is not a very good choice in terms of transformation efficiency. They found an OD$_{600}$ of about 0.94 working much better, see the corresponding figure:

And finally the amount of competing DNA is a big factor. Hanahan, 1983 found out that the transformation efficiency gets lower, the more competing DNA is present:

So I would try to use as little of each DNA to work against this effect.

Thanks, Chris, but I was more wondering how high with efficiency (number of clones per ug DNA) you can get with co-transformation. For example for single electroporation the efficiency is around 1 × 10^10 cfu/μg so I would like to know what is the limit and whether it can be improved for co-transformation.

I haven't found any papers looking on this for co-transfections, but some data for single transfections. We can do some interpolation from them, I will expand my answer.


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Why are Lymphatic trunks part of the Cardiovascular system?
According to Wikipedia the Terminologia Anatomica (international anatomy standard) the lymphatic trunks are part of the cardiovascular system instead of the lymphoid system.
Why did they make that choice?

The definition of "vascular" is as follows:-

of, relating to, affecting, or consisting of a vessel or vessels, esp.
  those that carry blood:

By this defninition, the cardio-vascular system doesn't need to include only the blood vessels and the heart. It includes all conducting and distributing vessel elements including those which carry the lymph-Lymphatic vessels. The cardiovascular system stands for the "circulatory system"+ the heart tissues and since lymph is an essential part  of the circulation (of nutrients, hormones, wastes etc), the cardiovascular system must include the lymphatic system.
Lymphoid system is a completely different entity which includes spleen, the lymphoid tissue (MALT), the lymph nodes and the lymph vessels. Hence the lymphatic vessels belong to both, the cardiovascular system and the lymphatic system, but the MALT and Spleen (arguable and disputed) are only a part of the lymphatic system and not of the cardiovascular system.
MALT= Mucosal Associated Lymphoid TIssue


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Is there any disadvantage to having a really low adipocyte count in our times?
The key feature of adipocytes seems to be energy storage. Today humans in Western countries don't have to hunger and have therefore less need to store energy in fat cells.
Do adipocytes have additional functions that still make them valuable?
Wikipedia lists 10–13% and 2-5% for men as essential body fat percentage for woman. What functions don't get fulfilled if the body fat percentage drops below that level?

You mentioned something odd in the tittle "adipocyte count", this was likely a mistake, but I will address it anyway. I recall something about liposuction not being preventative for
   diabetes:
You can have more adipocytes with less lipids in each cell, or fewer
   adipocytes with more lipid in each cell. Hypertrophy vs hyperplasia, just like in the question you asked on muscles elsewhere on this forum. Anyway, when a patient gets liposuction they decrease the number of
   adipocytes. Then if s/he gains the weight back the size of their
   individual adipocytes will be larger than it was before the
   liposuction. Somehow this was bad, and it increased insulin resistance. in a way, decreased "adipocyte count" is dangerous.

here is the other, obvious stuff on endocrine function of adipose tissue that you surely already know since your profile is very endocrine based, but anyway, here goes:
Adipose tissue has hormonal functions, secreting horomones (leptin, adiponectin, and resisting... these modify appetite as well as insulin resistance) and modifying them (converting testosterone to estrogen vi the enzyme aromatase).
The adipose-derived hormones are quite mysterious to me, I don't know much about them. The effects of the aromatase in adipose tissue are more obvious:

men will have increased estrogen levels (for example leading to gynecomastia aka man boobs, as a chubby guy I know this all to well)
women will have higher estrogen which will stimulate LH secretion from the pituitary stimulating theca intern cells in the ovary which will increase testosterone levels. The condition in women is known as PCOS.

In a person with little adipose tissues, there will be less conversion of testosterone to estrogen, so men will have less estrogen. Women will also have less estrogen, and less testosterone, aka they will not have PCOS in those women that already have PCOS, but thats not saying much :)

I may be wrong on some of this information, anyone please correct me.


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How much of the genetic differences between humans and chimpanzees are due to genetic drift?
Both natural selection and genetic drift play a part in changing our DNA over time. Are there trustworthy estimates how much of the differences over the whole genome between us and chimpanzees are due to genetic drift and how much is due to natural selection?

Interestingly, the rate of accumulation of new neutral mutations is independent on the population size and is equal to $\mu$ (per lineage), where $\mu$ is (also) the mutation rate at a given locus.

@Remi.b : Let's focus on the whole genome.

Note that most selection pressures will actually prevent divergence between two sister lineages as they act in the same direction. Only cases where selection differs between lineages will cause divergence. This type of selection is simply called divergent selection.

Following the neutral theory of molecular evolution, I would predict that most divergence is due to accumulation on neutral mutations. (+1)

@Remi.b I always learned that genetic drift is higher in smaller populations. This is discredited now?

@Rodrigo The loss of polymorphism through time (which is how one would quantify the concept of genetic drift) is higher in smaller population. Have a look to why-is-the-strength-of-genetic-drift-inversely-proportional-to-the-population-size.

@Rodrigo However, the rate at which neutral mutation fix is the same. The reason is that the probability of a neutral mutation to fix is $\frac{1}{2N}$. There are $2N\mu$ new mutations entering the population each generation and therefore the rate of fixation of neutral mutations is $\frac{1}{2N} \cdot 2N\mu = \mu$. This classic result is essential for phylogenetic reconstruction typically as we can infer time of divergence from the rate of neutral divergence without knowing anything about $N$.

The easiest way to track whether a particular protein-coding gene has diverged between two species because of drift or actively maintained selection is to look at the ratio of synonymous to nonsynonymous mutations within that gene. A synonymous mutation is one that doesn't change the identity of the amino acid within that protein; a nonsynonymous mutation is one that does. Synonymous mutations are neutral by definition; their presence gives us an idea of how much time has diverged and how frequently mutations in that protein coding region change over time.
A dN/dS (Nonsynonymous mutation to Synonymous mutation) ratio of 1 suggests that the primary driver of change between species is purely neutral change. That usually means that it doesn't matter what is going on with that protein and is a little unusual--I would primarily expect to see something like that in a gene that is on its way to becoming a pseudogene.
A ratio of less than one means that synonymous mutations are much more likely to persist in that region than nonsynonymous ones. This is usually a sign that purifying selection is happening--for whatever reason, it's important to the function of both species that those proteins stay relatively similar.
A ratio of more than 1 means that there is diverging or directional selection happening, and that that protein type is changing between the two species because selection is actively modifying one or both proteins.
Here is a paper specifically analyzing whole human and chimpanzee genomes using this metric.

You could improve this answer if you summarize what the linked paper concludes (in general, answers on StackExchange should stand on their own; links and references provide support, but we hope for answers here to outlast links that could change or go dead in the future).

"Synonymous mutations are neutral by definition" that's wrong. It doesn't change the shape of the protein but it does change protein synthetisation speed/amounts.

@Christian It's wrong in so far as it is a simplification/assumption, and a useful one at that.

@canadianer : I see no reason why there shouldn't be evolutionary pressure to increase or decrease the synthesis of a certain protein and that's what a synonymous mutations does.

Wildman et al. (2003) investigated 97 genes in humans and chimpanzees and show evidence that 30 of them (~31%) have evolved under positive selection. This is not per say an estimate of what fraction of substitutions are adaptive but it gives an idea.
Such estimates can be quite hard to get. I don't know any such estimates between human and primates but I know one on Drosophila.
Eyre-Walker and Keightley (2009) that about 40% of all substitutions between Drosophila melanogaster and D. simulans are adaptive.
Population sizes being larger in the Drosophila lineage than in the Hominidae lineage, I would predict that the fraction of substitutions that are adaptative would be significantly lower between humans and chimpanzees (prediction which agrees with Wildman et al. (2003)).
So, to the question How much of the genetic differences between humans and chimpanzees are due to genetic drift?, I would answer: More than 60%! But remain cautious realizing this is a vague estimate.


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What does it mean for muscles origins and insertions to be the other way around in the right than left limb?
Herbert Srebnik writes in Concepts in Anatomy:

In the right limb, the muscle's origin is proximal to the joint and
  the insertion is distal to it. In the left limb, the muscle's origin
  is distal to the joint and the insertion is proximal to it.
  (The text appears next to an image of the biceps brachii)

What does that mean? What does it tell this paragraph tell me as someone new to human anatomy?

Muscles span joints, and their purpose is to affect movement of that joint. Typically a muscle's origin is the more fixed or stable point of attachment to bone, while the insertion is on the bone which moves when contraction or relaxation of that muscle occurs.
Usually with the muscles of the limbs we think of the more proximal end of the muscle as being the origin, and the distal end being the insertion, because muscle action tends to move bones more distal to the limb joints. For example, for movement of the elbow joint you can typically think of muscles originating on the humerus and inserting on the radius and ulna.
However the nomenclature is somewhat arbitrary, because one can in a sense reverse the origin and insertion by fixing the location of the more distal bone and moving the upper body. For example, by placing your forearm still on the table and moving your upper body, because of the nature of their action in this position you might consider the muscles of the elbow to originate on the radius/ulna and have their insertion on the humerus.
I suspect this is what is described in the book. The biceps brachii attaches to the scapula and radius. Depending on whether it is the forearm or the shoulder moving with respect to the elbow joint, the insertion and origin could be considered at either end of the muscle. It is not that the origin/insertion is always opposite for the right versus left limb.


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How long does it take for Vitamin D3 to have physiological effect
As far as I understand Vitamin D3 has no direct physiological effect but has to be first converted. If a person if given a mega-dosis. (50000-200000 IU) of Vitamin D3, how long does it take till the body produces a physiological response?
Is it a matter of hour? Is it a matter of days?

This sounds like an upstream question... i.e., you want to know this in order to know something about what happens if someone takes a large dose of vitamin D3. Can you flesh out your question?

@DanHall I changed the question to be a level higher upstream.

I not sure we still don't have an X-Y problem here. Is this actually the thing you're trying to figure out? Or some thing that you are trying to find out in order to answer a different question. I'm making an attempt to answer, but give me a minute, since a quick search has shown one of my assumptions (that nobody would study that large a dose) to be false.

Well, it turns out I don't know the answer to your question, and I'm not comfortable offering an authoritative answer just by reading some new literature. In a different context, a patient with Vitamin D deficiency, it will take 3+ weeks before calcitriol levels normalize in response to oral Vitamin D3. That (normalized levels of calcitriol) is the physiologic response to oral Vitamin D3. The response to mega doses would likely be different, but I don't know what it would be. There's some work out there, but you'd have to draw some conclusions yourself.


text:
How hard is it to build a promotor in a DNA that initiates DNA transcription when specific hormones are around
I have an idea that you could find out which substances are within a sample in vitro that you are investigating by creating DNA that has a bunch of different promotors for different substances you are interested in.
After inserting those DNA strains you could do nucleotide sequencing and as nucleotide sequencing allows you to to read a lot of data you could read the sequencing behind the promotors.
How complicated would it be to build DNA with promotors for dozens of medically relevant substances?

What do you mean by within a "probe"? Do you mean "sample"?   2) Are you thinking of these detector DNA molecules as being within an organism or in vitro?   3) Also note that typically when this type of experiment is done we would look at protein readouts since proteins can be fluorescent or have enzymatic activities that are easily measured. Is there some reason you want to do a sequencing based measurement and if so why do you think that would be preferable to just doing a standard test e.g. one based on antibodies?

@tyersome : I mean in vitro. You can't measure dozens or hundreds of different fluorescent proteins at the same time on the other hand if you have working promotors you could detect many targets at the same time. The cost of antibody based detection has stayed relatively constant over the last decades while nucleotide sequencing is a technique that fell a lot in price and there's hope of further price drops even if it doesn't fall faster then Moore's law anymore.

Dozens of fluorescent proteins might be possible, but I agree hundreds would be right out. —— I don't want to be a wet blanket, but are you familiar with what transcription involves? Transcription requires multiple components — doing this in vitro would require a mixture including: DNA, transcription factors§, RNA polymerase, and ribonucleotides. All of these macromolecules are subject to degradation and would typically be stored separately at -20°C before mixing. ——— §Note: For each hormone you would need a specific transcription factor that respond to that hormone and bound one promoter.

Promoters bind transcription factors (TFs) and RNA polymerase (or a related complex, in the case of eukaryotes).
The substances you are interested in testing would need to bind to DNA in the same way as TFs and RNA polymerase, in order to trigger RNA synthesis (which you might measure with RNA-seq experiments). That would seem to severely limit what you can test the presence of.
In any case, if you could make that happen for your substances of interest, you would probably also want to make sure to avoid degradation effects of short-length RNA, by removing associated proteins.
https://en.m.wikipedia.org/wiki/Promoter_(genetics)
https://en.m.wikipedia.org/wiki/RNA-Seq
https://en.m.wikipedia.org/wiki/Small_RNA


text:
Which organisms have introns?
From Wikipedia:

For example, introns are extremely common within the nuclear genome of higher vertebrates (e.g. humans and mice), where protein-coding genes almost always contain multiple introns, while introns are rare within the nuclear genes of some eukaryotic microorganisms,[8] for example baker's/brewer's yeast (Saccharomyces cerevisiae). In contrast, the mitochondrial genomes of vertebrates are entirely devoid of introns, while those of eukaryotic microorganisms may contain many introns. Introns are well known in bacterial and archaeal genes, but occur more rarely than in most eukaryotic genomes.

In my biochemistry course we learned that bacteria have no introns and eukaryots nearly always have them. What's correct?
Do viruses have introns as the Wikipedia article claims?

As a general rule, a blanket statement in Biology should always be considered false.
It so happens that bacteria do have 'introns' (or at least the intron genomic sequence has been determined) in the sense of the cis-acting autocatalytic Group I and II introns. These are sequences of RNA that adopt such a conformation to catalyze their own excision from an mRNA transcript, and thus may be considered ribozymes, enzyme made of ribonucleic acid.
Although not generally considered 'introns' segments of RNA are removed during the course of tRNA in both prokaryotes and eukaryotes.
Now introns that are removed by the action of the spliceosome are strictly found in eukaryotes, as bacteria lack the spliceosome.
There seem to be a considerable number of papers regarding the question of intron (particularly spliceosomal) phylogeny that should be relatively easy to find if you are so interested.
One example paper in which viral introns (Group I) are reported:
http://nar.oxfordjournals.org/content/22/13/2532.abstract

As a general rule, a blanket statement in Biology should always be considered false. I could not agree more.


text:
Why do people feel extreme cold at different temperatures compared to other people of same body structure?
I have seen some people shivering in the room temperature of 18°C while others of similar body structure do not feel that much amount of cold.
Of course the clothing of both people is similar if not same.
What can be the cause of such different body reactions?

Do you mean why does the same temperature feel different for different people?

@TAbraham exactly

First of all, this observation is the norm across human perception. While humans react in roughly the same way to similar stimuli (e.g. both a cranberry and a tomato are seen as red, the destruction of tissue is felt as painful), the intensity tends to be different. Also, many stimuli elicit not just a knowledge of the state of the world or one's body, but also a reaction (e.g. shivering when cold, or emotions like fear when physical pain is felt), and these reactions differ between humans too. So, on a very general level, it can be answered with "Because that's how human perception works".
I know that this is a very unsatisfactory answer, so here are some factors off the top of my head. For any given case, one or more of them will cause the difference, and you cannot tell which ones from casual observation.

Your observation of "similar clothing" could have been incorrect. For example, an acrylic sweater can look exactly like a sheep wool sweater, but warms much less. Or, slightly shorter sleeves can cause much cooling if they leave the wrist exposed. Layering is also very important, and we generally only notice the uppermost clothing layer.
Your observation of "similar body structure" could have been not precise enough. People who have the same appearance can have different amounts and distributions of body fat. Maybe one person is simply better insulated than another one.
The state of their circulatory system was different. Vasoconstriction and vasodilation will change the skin temperature, which is sensed by peripheral thermoreceptors.
Estrogen is involved in thermal perception. The gender of the person and the current point in the menstrual cycle (or pregnancy) in women will make a difference.
The circadian cycle of the two people is probably not perfectly synchronised. Core body temperature varies during the cycle, and thermoperception depends on core body temperature too, not just skin temperature.
A different metabolism will cause one person to create more body heat than another
Other hormones (beyond estrogen and the ones ruling the circadian cycle and metabolism) probably have an effect on thermoperception, but I can't tell you details here. Temperature is regulated in the hypothalamic-pituitary-adrenal axis, so the hormones from it are likely to have an influence.
Normal variations in the two people's neural networks will change the intensity of signal perception. People are born with very unconnected neurons, and build unique connections depending on the environment they encounter while growing up. As a result, each person's brain functions slightly differently when given the same input.
Differences in neurotransmitter sensitivity can account for the difference in intensity of perception. People sometimes react differently to the same level of neurotransmitter, or also their brains secrete different amounts of neurotransmitter as a response to the same stimulus. These differences exist on an average level (e.g. glutamate can potentially "do" more for me than for you) but are also affected by drugs and illness.
Attention is a major part of perception. The CNS can suppress information from sensory organs at a very low level if the brain is focusing elsewhere.
Habit: people can intentionally or unintentionally learn to disregard or misinterpret their body sensations.
Psychological stress increases the core body temperature
The above reasons all assumed differences between a pair of healthy individuals. Some conditions, for example running a fever, but also neurological disorders anywhere along the complex pathways from sensors to cortex (and the other way round!) or diseases which for some reason alter thermoregulation, will all change the feeling of hot or cold.

This list is probably incomplete. Also, some of the factors I listed will overlap to some extent (e.g. vasodilation is frequently mediated through hormones, and ingrained habits are reflected in neural network connections). But the take away point is: Human perception is an active process, very far removed from simple "reporting" of the state of the environment. It is unrealistic to expect two individuals to have the same perception when exposed to the same stimuli.
For an in-depth description of how thermoperception and thermoregulation work physiologically, see this summarizing paper.

Human body temperature is a measure of the body's ability to keep, generate, or get rid of heat as the need arises. The body is very adept at maintaining temperature within a narrow and safe range, despite occasional huge variations in the room temperature.
But some bodies are more efficient than others. Even bodies of the same height and weight may differ dramatically in the ability to maintain body temperature.
Humans also differ in their preferred room temperature. Some like it warmer, some cooler. This is called thermal comfort. Thermal comfort is not merely physical, but psychological too. In one's choice of preferred temperature, besides psychology, other personal factors come into the equation.
Also the feeling of cold or hot depends upon the DIFFERENCE between one's normal body temperature and outside temperature. And contrary to popular belief, different people have different normal body temperatures. It also depends upon the amount of muscle mass and fat, as fat stores heat (decreasing the normal temperature) while muscles dissipate it (increasing the normal temperature.
Following links might help:
http://www.mnn.com/health/fitness-well-being/stories/why-are-some-people-colder-than-others
http://www.medicalnewstoday.com/releases/5711.php


text:
Simulating Cell differentiation
I'm a computer programmer deeply interested in Biology.
I wish to write a computer simulation for cell differentiation. I understand there will be seemingly impossible challenges in doing this. But first I am looking for  answers to some basic questions.

I've learned that a zygote turns into 'embryonic stem cells' which results in the organism. How does the zygote turn into embryonic cells ?
What are the factors that determine the specialization of embryonic stem cells into more specialized types of cells and how does this transformation take place physically ?
Where is the data stored which acts as the "guide" for all these processes ? Is it stored in the DNA ? If it's stored in the DNA , is it known how the cells interpret the information in the DNA?
What are some textbooks I should be referring for this project ?

PS : Pardon my ignorance if these questions sound stupid, but I'm willing to commit time for learning anything needed to do this. Also , I understand all these questions cannot be answered in a few lines. Please provide references/pointers . Thanks !

Trying to answer this question in a few lines is a tedious task. Mostly I'm not sure that as of today we know all there is to know about it.
I'll try to give you some hints though.

The process is called embryogenesis. The zygote (or ovum) undergoes rapid mitotic divisions with no significant size growth which will lead to the development of an embryo. This process is called cleavage. Blastomeres are created during this process. On the third day - time may vary but not significantly - cleavage reaches the state of 16 cells. Cell divisions always occurs by parallel division (1 -> 2, 2 -> 4, 4 -> 8, 8 -> 16). Study the links I gave you and come back with more specific questions.
Again that's kind of impossible question to answer without explaining the entire process from fertilization to fetal development, because creation of tissues (cells) and organs happens along the way, not at once. However, it's documented.
Not sure.
Start with the wikipedia links and try to come back with more specific questions. I have a couple of text-books but I'm afraid they are not as detailed as you would want :-)

Good luck!

The answers to most of your questions are under active research and there are many unknowns. Understanding this process is one of the main goals of developmental biology. So, try to set reasonable goals for your project, mainly by seeing where you have sufficient data to work with.
I would start with reading some basic textbook on developmental biology.
Regarding the flow of information: Remember that starting from the zygote and onwards to the whole organism, the DNA sequence is generally the same between all cells. As a computer scientist it might help you to think about it this way:
Think of the DNA as a very complicated mathematical function $f()$ acting on cellular states. The current cellular state $S_i$ will be the total molecular components of the cell and will yield the biological function of the cell. So, you start with an initial cell state $S_0$ (could be a vector, for example) and then the daughter cells will be: $S_1=f(S_0)$, their daughter cells will be $S_2=f(S_1)$. This is not a perfect representation of the process (since at time point 2 you may actually have both $S_0$ and $S_1$ cells), but it emphasizes the point that although the DNA sequence "computes" the next step it is in fact constant, and the point that each cellular state dictates the next state. Seems to me like a Markov chain could be appropriate. Of course you can also try more sophisticated models - but it is better to start simple.
Also, I would suggest starting with C. elegans as your modeled species. This is because the full differentiation fate of each of its 1031 somatic cells is known - a remarkable achievement and something you will not have in other species.

I would start with Developmental Biology, 9th Ed. It's not up to the absolute cutting edge, as it was published in 2010, but it has a lot of good stuff in it. Wikipedia is a decent resource to get very brief overviews on certain subjects, but a lot of the life science articles I've read tend to be lacking, as opposed to the physics and math articles, for example.
As for question 3, yes, the "data" is stored in DNA. For a thorough guide, one of my favorite books is Molecular Biology of the Cell, 5th Ed.. It's a little dated now (published in 2007), but if you want to understand how DNA, RNA, and proteins work, it's a great overview text.

Note that the data is actually stored not only genetically (in the DNA sequence) but also epigenetically (e.g. modified chromatin).

@Bitwise - yes, I know, but I figured a short, direct answer was the best here, as the questioner is obviously very new to this field. I could spend a long time talking about DNA sequences vs. DNA modifications, the contributions of histones and their post-translational modifications, and the overall structure and organization of the chromatin in general if you'd like :)


text:
What did pangolin scales evolve from?
Were they developed anew or a heritage from fish?

Pangolin scales are certainly not retained from fish. Pangolins are within the clade Pholidota (Tree of Life page for Eutheria) and their nearest relatives are anteaters, sloths, and armadillos.
According to the University of California Museum of Paleontology, similarities between pangolin and armadillos are the results of convergent evolution. So the pangolin scales are a new feature that arose somewhere on the lineage leading to pangolins.

were they developed from hair or from skin folds?

They are keratinous scales, like hair and claws/nails. I'd suspect similar development to nails, but I'm not sure.

Their closest relatives are carnivores, not anteaters, sloths, and armadillos.  See DOI: 10.1186/1471-2148-6-93.


text:
Are there people cured of HIV by means of HAART?
I wonder if there people who were cured of HIV only by means of highly active anti retro-viral therapy (HAART) or other drugs rather than by bone marrow transplant?
I know that HAART can suppress HIV below detectable level but are there people who stopped HAART and did not experience the HIV levels rising?

This very recent (and freely available) review pretty much sums the problem up in the introduction:
http://dx.doi.org/10.1038/clpt.2012.202 (Barton et al., 2013: Prospects for Treatment of Latent HIV)
And here's an update more specifically on the problems with actually curing an individual of HIV infection, if you have access: http://dx.doi.org/10.1016/S0140-6736(13)60104-X (Katlama et al., 2013: Barriers to a cure for HIV: new ways to target and eradicate HIV-1 reservoirs)
Essentially, current antiretroviral therapy (ART) is able to nearly fully suppress active HIV, practically restoring the individual to a healthy status, including the prevention of transmission from them. However, the therapy needs full adherence (missing a dose can already cause viral loads to rise) and is lifelong. The reason for this is because HIV integrates into the genome of host CD4+ T cells, of which there are latent populations in places difficult to reach with therapeutics such as peripheral lymph nodes.
Apparently, some rare individuals actually achieve a "functional cure", i.e. the body is able to suppress viral replication for a given period of time (5 years) without ART. But these patients "are characterised by a favourable HLA profile and potent HIV-specific CD8 T-cell responses that are associated with a low viral DNA reservoir" (Katlama et al). They also mention another group of five patients who did not seem to have a favourable genetic profile and were still able to control HIV following cessation of ART for several years (http://dx.doi.org/10.1097/QAD.0b013e32833b61ba Hocqueloux, 2010: Long-term immunovirologic control following antiretroviral therapy interruption in patients treated at the time of primary HIV-1 infection). So it seems there are plenty reports of people who are able to remain free of detectable viral loads and maintain CD4+ T cell counts for a long time after treatment, but it doesn't seem like any of them stay permanently virus-free.

Since early March we know, that there is the first patient which has been cured by HAART. According to the paper it has been proven that the infant was infected with HIV. This was done by detecting the virus even after the first 48 hours, this rules out that the virus transmitted by the mother without infection.
The infant was first treated when it was 30 hours of age with a triple therapy (zidovudin, lamivudin and nevirapin). On the seventh day the therapy was changed to zidovudin, lamivudin and lopinavir/ritonavir. After one month of therapy no replicable virus particle could be found. The therapy was continued until the age of 18 months. The infant is now 26 months without a sign of a rebound of the HIV infection.
The approach was atypical, since they used a therapy scheme with not established high dosing of the antiretroviral drugs. They ruled out a innate HIV-immunity by certain HLA variants, since Mother and child had matching HLA-Haplotypes. But other genetic mutations are still possbile.
This is scientific progress, the answer to your questions changes in only 2 months.
[1] http://www.retroconference.org/2013b/Abstracts/47897.htm

Is not it the same as post-exposure prophylactic, which is used if a surgeon or a dentist get wounded when performing operation on a HIV patient? I know that one can be cured if the treatment is started within 48 hours after infection.

It seems what is important is whether the latent reservoirs were established.

It's not the same, since the infant was already infected, which was proven by detecting the HIV Virus on the 20th day after birth (the virus wouldn't persist so long otherwise). The treatment was started so early to give the infant the highest chance to be cured. PEP(post-exposure prophylactis) can prevent infection with HIV. But this was not a prevention, it was a therapeutic approach. This is also a big question in the paper, since a successfully PEP would be no big deal.

The authors of the paper claim that there are no latent reservoirs with high probability (by droplet digital PCR and undetectable HIV-specific antibodies). But you can never be 100% assured. Time will tell. But it sounds promising.

While it's difficult to prove a negative, I know of no cases where a patient has been treated with HAART to the extent that their viral load never rises again. Keep in mind that, if nothing else, such a study would be extremely hard to do, as proving you've "cured" someone would require extremely long term followup.
HAART is however quite good at suppressing HIV, and there's currently no known upper bound on the lifespan of an HIV+ individual undergoing treatment. Compared to a 10 year post-infection life expectancy a decade or two ago, that's pretty darn good.

I would add to this that any reported case of this happening, however spurious a publication it appeared in, I'm sure would attract great media attention.  When the reports came in of the bone marrow transplant cure, I remember it being reported by the BBC as the 'first cure'.

@RoryM Indeed - a drug-based 'cure' for HIV is hardly a finding that would go under the radar.


text:
Pedigree Probability of Autosomal Recessive Trait
Here is a pedigree:

The trait is autosomal recessive.
The question is:  What is the probability that the bottom 2 people (4 and 5) have a child with the trait?
I tried doing 2/3 * 2/3 * 2/3 *1/4 and got 2/27 but this is wrong. I thought that the probability of III 1 being a carrier is 2/3.  The probability that IV 4 is a carrier is also 2/3.  The probability that III 6 is a carrier is 2/3 and IV 5 must be a carrier.  So IV 4 and IV 5 must be carriers.  The probability that they have a child with the trait is 1/4. But I am not getting the right answer.
The right answer is 1/6.

You have now got sufficient rep to avoid new user restrictions so can post inline images yourself - you can either do this manually using markdown or there is a button on the WYSIWYG editor :)

Starting with the left hand side of the diagram:

III:2 is definitely a carrier (Tt) as one parent (II:2) is affected (tt).
III:1 is also definitely a carrier (Tt) as when mating with III:2 they produce an affected (tt) offspring (IV:1)
This means that we can work out the possibilities for IV:4 as we know the parent genotypes.  It follows the standard arrangement for two carrier parents giving the options of:

TT (1/4)
Tt (2/4 = 1/2)
tt (Normally 1/4 but in this case 0 as individual not marked as affected).

Therefore for this scenario, the probabilities for IV:4 are :

TT (1/3)
Tt (2/3)

Now if we look at the right hand side of the diagram.

IV:5 is definitely a carrier (Tt) as one of their parents (III:5) is affected.

This gives two possible Punnett squares to be examined:
|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

This gives nil affected offspring so we can disregard this option for your question (as we are ONLY looking for scenarios which produce affected individuals).
Therefore the alternative is:
|-------------------------------------------------------------------------------|
|                                        ♂ (IV:5)                               |
|                          T                                   t                |
|            -------------------------------------------------------------------|
|           |                                |                                  |
|         T |              TT                |                Tt                |
|           |                                |                                  |
| (IV:4)    |-------------------------------------------------------------------|
|    ♀      |                                |                                  |
|         t |              TT                |                tt                |
|           |                                |                                  |
|-----------|-------------------------------------------------------------------|

Giving 1/4 affected offspring.
As mentioned above, in order to have affected offspring then IV:4 must be Tt.  There is a 2/3 chance of this being the case.  If this is the case, then there is a 1/4 chance of the child being tt.
Both conditions need to be true for this to happen so we multiply the fractions:
2/3 * 1/4 = 1/6


text:
Introductory text for primatology
I'm looking for a book that provides a good overview of primatology, one aimed more at researchers rather than a popular science book. Ideally, I'd like something with an ethology/ecology angle with an eye towards phylogeny.
My preference would be for an e-book.

Lucas, I put more of a professional spin on this so it's not as much of a "shopping"-type question.

@jonsca I appreciate your effort, but you did change the nature of my question. I definitely want a good book, that is very important, it really does not matter if it is a canonical text or not. The ability to soundly judge things good or bad is the true value of professionalism ;)

well, maybe of expertise, but that didn't fit :)

Your changes to it are fine, thanks for your feedback!

I've had some experience with Karen Strier's 'Primate Behavioural Ecology', and it's solid. It's a nice overview with (obviously) a strong ecology/ethology bent. I don't think it comes in ebook though.
Here's the Amazon link.

Sweet Jesus that's expensive. Not unusually so, but I'd managed to forget how much academic books are.


text:
Does culling badgers restrict the spread of bovine tuberculosis?
The British government has announced that it plans a large-scale badger cull which they argue are implicated in the spread of Mycobacterium bovis - so-called bovine tuberculosis. Any cattle that contract this disease need to be slaughtered under EU regulations.
However, the link between badgers and cattle doesn't seem that clear to me. What is the evidence that badgers spread tuberculosis to cattle? Also, what is the evidence that badger culling will have a significant effect on the spread of the disease to cattle?

I have added the second part of my question which I left out - apologies.

This is apparently a debate since decades in the UK. As to the pathology:

Eurasian badgers (Meles meles) are an important wildlife reservoir of
  tuberculosis (Mycobacterium bovis) infection in Ireland and the United
  Kingdom. As part of national programmes to control tuberculosis in
  livestock, considerable effort has been devoted to studying the
  disease in badgers and this has lead to a rapid increase in our
  knowledge of tuberculosis in this host.

L. A. Corner, D. Murphy, E. Gormley: Mycobacterium bovis infection in the Eurasian badger (Meles meles): the disease, pathogenesis, epidemiology and control.'' In: ''Journal of comparative pathology. 144, 1, January 2011, 1–24. doi:10.1016/j.jcpa.2010.10.003. PMID 21131004. (Review).
A summary of the pre-1997 debates is here:
http://archive.defra.gov.uk/foodfarm/farmanimal/diseases/atoz/tb/publications/krebs.htm
The up-to-date DEFRA informations are at:
http://www.defra.gov.uk/animal-diseases/a-z/bovine-tb/
For an alternative approach see:
http://www.ncbi.nlm.nih.gov/pubmed/19846226 (in short: educate them not to piss everywhere)
I have been asked to give also a summary. Tuberculosis is probably one of the nastiest bacterial infections in existence. It is a prototype of those diseases which are called latent: you can be infected for decades without symptoms, but when your immune system falters (or you have to take immune suppressants) it breaks out and kills you. One third of the human population has such a latent infection with Mycobacterium tuberculosis, and the HIV wave plus the high mycobacterial mutation rate with following extreme resistances make for interesting epidemiology. But this is also a result of our lifestyle, depending on huge cattle herds, as cattle can be cross-infected with human TB. In the west we have succeded to cut human infections by controlling cattle infection with human TB. Still, cattle can get bovine TB, and this may be economically disastrous. One of the pools of the infection is the badger population which can get bovine TB too and spread bacteria with their urine. It is unclear if protozoa may be an even more important pool. It is likewise unclear if culling of badgers would be successful for cattle TB control; the government bases its decision on a long-term study of regions where culling has happened. Alternative approaches include vaccination (which only affects uninfected animals), different cattle grazing regimes, habitat manipulations and badger latrine management. Physical exclusion of badgers from farm buildings is suggested as the simplest, and potentially most effective, method of reducing contact and opportunities for disease transmission between badgers and cattle. The government expert opinion clearly concluded that without such additional measures, culling won't be successful in reducing cattle TB.

This doesn't answer the question...

Much better :) +1 For an even better answer you could summarise the main points?


text:
What is meant in biology by the term "evolved"?
A student asked me this the other day and I thought that I would ask it again here. If one organism is said to be "more evolved" than another, what exactly does this mean?

Just to be clear: are you specifically asking what “more evolved” means or what “evolved” (generally) means?

politics, history and humanities uses this sense of the word evolved - as an improcement - more than biology does

Highly related: Are we “more evolved” than present-day bacteria?

"More evolved" is actually meaningless in all contexts. See terdon's answer for a good explanation.
In the strictest sense, an organism can be said to be more divergent than another when comparing both to an outgroup, such that there is an inferred most common ancestor in reference to which to make the comparison. In this case, one organism is more divergent if there are more changes to this organism than the other, relative to the reference point.
However, when speaking, many people get lazy, and use "more evolved" as shorthand, wishing it to mean something like "more divergent". Even "more divergent" is meaningless in the following contexts:

when there is no outgroup understood
when describing increasing complexity (obligate parasites have lost complexity and have had more evolutionary changes than their non-parasitic relatives)
when the outgroup is poorly chosen. Mammal vs reptile comparisons should not, in general, use prokaryotes as the outgroup.

Edited 2013/12/06 to reflect the precision in the answer by terdon.

Can you suggest sources about evolutionary comparative methods?

I disagree, your definition refers to more diverged evolved is not qualitative. You cannot be more or less evolved unless you are actually comparing generation numbers.

Strongly agree/like this statement. Would also like to add: please emphasize teaching your students that evolution is not something that is worked towards, so much as naturally selected. I think heavy, heavy emphasis on natural selection is what you should explain, until your students demonstrate that they understand things "evolve" simply because they survive, and they survive if they are fit.

I cannot improve on Thomas Ingalls' description of when "more evolved" is appropriately used, but the inappropriate/lazy use of the phrase is so prevalent that it deserves further comment. In my experience, the most common use of the phrase "more evolved" is when describing the increased complexity of one organism versus another. This usage is not just meaningless, but wrong and harmful, and springs from a misunderstanding of what evolution implies. Evolution is emphatically not the same as increased complexity.
I try to avoid saying "more evolved" and tend to favor "more complex", "less simple" or "less primitive." "Primitive" has its own problems, since it sometimes brings with it the connotation of evolution (a "primitive eye" or "primitive nervous system" are common phrases), but it at least avoids an explicit misuse of "evolved."

“more complex” unfortunately suffers from similar problems.

@KonradRudolph Do you mean that "more complex" has the same problems as "more evolved"? Or rather that it has the same problems as "more primitive"? Can you expand? What phrase do you prefer? I think "more complex" is very near to what people actually want to say when they use the term "more evolved." It does come with a bit of a value judgment about what complexity means, but I have a hard time thinking of a phrase that has much less baggage. If one is careful to specify the dimension, I think it can be reasonable to discuss the relative complexity of different systems.

Well, the first question is: what is complex? Genome? Phenotype? Specifically, behaviour? And how do you measure complexity? Once you have agreed on that (but people don’t) – what does this actually tell us? In reality, not much. People just use it as they would “more evolved”. In reality, it makes much more sense to speak about specific features, not about an ill-defined, poorly-understood and not comparable whole.

@KonradRudolph I agree with you in general, and I was not advocating using "more complex" when comparing whole organisms. But I stand by using "more complex" when discussing specific features. It's true that complexity is a flexible ill-defined concept, but at least a speaker can specify how they are using the phrase. I think it's important to have some way to express the concept of relative complexity, which is meaningful if defined for a particular domain/feature.

There is no such thing as more or less evolved. At least not outside popular media. The only reasonable comparison one can make is comparing generation numbers. You could say that a species that has undergone X generations is less evolved than one that has undergone X*2 generations. It just doesn't mean much.
Evolved is not a quantitative term, you cannot really be more or less evolved than something else.

It is a phrase in common parlance without scientific meaning, fitting in the same category as devolved or devolution. It is as @terdon said:

There is no such thing as more or less evolved.

In a scientific context you should always find the evolutionary measure in question and the methods for quantifying that measure.
In a biological context the phrase would fail to find meaning, when evolution is a function of fitness. In such context fitness is inevitably tied to environmental parameters. The more complex these parameters, the more niches may be available for potential species, with temperature being one of the strongest factors (See: Effective evolutionary time Hypothesis ). Take this assertion with the necessary caution, as it is far outside my expertise.
Mostly I have come across the phrase more evolved in reference to large, tangible species, and also in science fiction.
Tell your student, to always be aware that in the end the unicellular species make life for us on this planet viable - we coevolved. But they also eventually consume/recycle us in one way or another, and surely will outlast us. It takes extreme effort and finesse for a large, energetic multicellular host to obtain, maintain and retain its niche on this planet. In all of the field of molecular biology there is nothing quite like Immunology.
For a mind experiment, let the student imagine soil with different pH, of the same plant species which equal seeding-times.
The outcome may be something as shown below. The phrase "more evolved" clearly fails to describe such a scenario of one generation of plant species, and hence is not suitable in an objective description of evolution.
Sidenote: Al3+-ions are toxic to plants, stuning root growth and phosphate intake. With increased pH, more aluminum dissolves.

I have mostly seen it used to mean "possessing features that appeared most recently in the historical evolutionary record". Thus a human is considered more evolved than a chimp because our bipedality, hairlessness and large brain appeared more recently than the features of chimps, and a chimp is more evolved than a fish because fish very similar to ones alive today appear in the record before anything resembling an ape, and so on.
I think it's pretty poor use of language, frankly, since it suggests linearity and ordering to evolution that is simply not there, conflates gross morphological change with change in general and incorrectly implies that stabilising selection is not evolution.


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Are there any motile plants?
There are numerous examples of sessile animals (sponges, barnacles etc.) but are there any examples of motile plants? If not, why not? Surely mobility would have conferred an evolutionary advantage to some plant species. I am specifically thinking of locomotion here.

How are you defining motility?  Many plants "climb" or otherwise send out shoots, but I think most plants are dependent on a steady root system.

I was thinking specifically of examples of plant locomotion. Will edit question.

I can think of brunsvigia, which pollenates, and then dries out and dies. The dried husk then detaches from the stem and the wind sends it cartwheeling across the desert, dispersing it's seeds as it goes. Here is a video. It is locomotive like a sailing boat. Other examples given are actually just photo/geotropism and are directed growth rather than locomotion.

As to "why not", it's mainly because directed locomotion is energy-intensive, and plants don't have much energy available. Animals make use of energy that's been pre-concentrated, either by plants or by other animals; but plants just have a slow trickle of energy from the sun and need to be very sparing in its use.

It depends how you define locomotion.
If you take it to mean moving from one place to another, then yes, almost all plants do this at some stage during their life cycle. Primarily seeds and pollen move around, and generally they do so by harnessing either natural forces like wind and rain, or by manipulating animals to do the leg-work, e.g.:

by recruiting pollinating insects
by having barbs which snag the fur of passing mammals
by producing tasty fruit so monkeys eat them, seeds included, and deposit them with a dollop of fertiliser somewhere else

If you take it to mean moving around under ones own propulsion, then yes, some plants do this. The example that springs to mind is the gametophyte generation of ferns:

The prothallus (i.e. the gametophyte) has rhizoids on the underside and uses them to slide around and find some space in which to start the next generation. I have seen this happen when fern spores are germinated on agar - when they reach the tiny prothallus stage, they start sliding around to avoid overlapping with one another. I can't find any references for this, but I'll keep looking.
Another example of self-directed locomotion in plants is the motile sperm of bryophytes. The male sex cells have flagella, which they use to propel themselves through water to the female sex cells (reviewed by Renzaglia & Garbary 2001).

Renzaglia, K.S. & Garbary, D.J. (2001) Motile Gametes of Land Plants: Diversity, Development, and Evolution. Critical Reviews in Plant Sciences. [Online] 20 (2), 107–213.

Many plants crawl by sending out ground vines and replant themselves in neighboring positions. But that's not what you are asking I think.
I don't know if there are any land dwelling leaf bearing plant forms that move.
In the water most chlorophyll bearing algae have flagellae and can migrate through the water.
Reference:
http://science.jrank.org/pages/205/Algae.html

Plant movement can be measured by a crescograph. This mov is not only due to plant growth but also as response to stimuli.
Talking of growth itself  roots frequently go around a rock while the grow, and plants lean towards a light source when kept in shade.
Creepers and climbers do display a kind of locomotion  of the part if not the whole, Partial motility is available to leaves of certain plants(They clasp shut in night)and flowers (Sunflower).The few carnivores we know add to the example.
Free floating aquatic plants have movement though it may not be called locomotion


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Can a deletion occur on only one strand of a human chromosome?

Hello. Is it possible that a deletion can occur in the middle of only one strand of a human autosomal chromosome?

When people say "strand" in DNA, they refer to one sugar-phosphate backbone with one series of nucleotides. DNA is typically double stranded and RNA is typically single stranded. But when you talk about a "chromosome pair", you're not talking about a pair of strands, you're talking about a pair of chromosomes. Each chromosome is double-stranded. So, what do you actually mean in your question?

I have altered the question title from "Can a deletion occur on only one strand of a human chromosome pair?" by deleting the word "pair".  This matches the version of the question in the body and makes the most sense as a question.  It is also the question that had been addressed by the two answers that had been posted at the time I made the change.

This is a somewhat semantic question. In terms of WHEN a deletion happens, I think it's commonly on only one strand as most mutations are caused by a collision from radiation or sometimes a chemical.  That will typically only affect one base.  BUT there are repair mechanisms that come in and can cause a deletion on both strands or repair the damage.  In the long term the repair mechanisms work pretty hard to make sure both strands are the same in the end.

As it appears that most deletions occur by mechanisms that do not involve large-scale strand separation (e.g. during crossing over or by translocation etc.) this is unlikely to happen (see e.g. Wikipedia article). These vary in length from perhpas a dozen base pairs to thousands or more, and differ from mutations caused by radiation and chemicals.  Any small deletions on one strand (e.g. at single-strand breaks) need to be filled in if replication is to occur.


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Alternatives to ethidium bromide for staining small nucleic acids?
While ethidium bromide works well for staining larger single-stranded RNA or double-stranded DNA molecules, it doesn't stain smaller nucleic acids very well. I observed that at around 20 bases and below single-stranded nucleic acids are difficult to see with EtBr-staining unless the nucleic acids are highly concentrated.
What are good alternatives for observing small nucleic acids in polyacrylamide gels? The main consideration would be ease-of-use, and it should be possible without any unusual equipment.

A list of dyes is available here and a list of dyes specific to nucleic acids is available here. I think you have two choices the SYBR Gold nucleic acid gel stain (S11494) which can be detected under UV light (not sure if it can be used with polyacrylamide gels). Your other option which can be used with polyacrylamide gels is the SYBR Green II RNA gel stain (S7564, S7568, S7586), this stain can be detected with UV light post-electrophoresis. It states RNA in the name but it can also be used for ssDNA.
Hope this helps

I would think GelRed or GelGreen would be an option too.  They claim to be more sensitive than EtBr and certainly less toxic (even moreso than SYBR Green).  I haven't personally used them against such a small bp product though.  GelRed has basically the same excitation/emission wavelengths as EtBr so no equipment change is needed.
Product sheet
Store link

I have heard several people complaining about GelRed being less sensitive than EtBr. Also, an interesting blog post about the toxicity of EtBr and SYBR Green: http://rrresearch.fieldofscience.com/2006/10/heresy-about-ethidium-bromide.html.

Interesting. I haven't done a comparison so I can't speak one way or the other.  But I do remember a similar article sometime back saying a similar thing (EtBr is not as bad as you think, and SYBR Green really isn't a "safer alternative" as advertised).


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Are there proteins that stabilize mRNA:RNA polymerase or mRNA:ribosome complex?
Actinomycetes are known for their ability to produce rich variety of natural products, and particularly, polyketides. Many of the genes that encode the biosynthetic pathways are pretty big, as they could reach 20kb. These bacteria most probably have some kind of mechanism that would ensure efficient transcription and translation of these long ORFs. This could be done in two ways: either by stablizing the mRNA:RNA polymerase complex, or by stabilizing the mRNA:ribosome complex. Have any of you heard of such mechanisms in bacteria?

What makes you think this is so? Where did you read it? There is a specific mechanism for termination of translation and release of ribosome subunits. I may be wrong but I see no reason that ribosomes would fall off long mRNAs.

A professor I talked to at a conference mentioned it, so I know they exist, I just don't know how they are called. And it definitely makes sense for them to exist, since these ORFs are so long.

Don't believe everything you hear from professors. And don't be so definite about your logical rectitude. Does the RNA polymerase need extra proteins so it doesn't fall off the DNA when transcribing longer genes?

I am not saying they exist 100%. I am just saying that it makes sense.

To me it raises as many questions as it answers. For example how do these proteins distinguish short from long mRNAs?

That's a very good (and interesting) question. Will let you know if I find the answer.

One obvious candidate is the PABP (poly-A binding protein) that interacts with the cap to circularize and stabilize the RNA (in Eukaryotes). Ribosome recycling factors also play some role but I am not sure about an Actinomycetes specific mechanism. And nothing at all about proteins stabilizing RNA-ribosome complex. Moreover, I believe that these long genes are polycistronic.

There is indeed a gene, called nusG which is believed to be antiterminator of RNA transcription. NusG binds to RNA polymerase which leads to increased RNA elongation rate, decreased time in which the polymerase is into short-lived paused states, and suppressed long-lived stabilized pause states 1.
NusG has been shown to be important for natural product discovery and biosynthesis:

Overexpression of nusG in C. cellulolyticum enabled the isolation of seven novel analogues of closthioamide, named closthioamides B–H86. These new compounds are truncated and partially O-substituted derivatives of the antibacterial parent hexathioamide compound, but have substantially lower antibacterial activity 2

Furthermore, nusG-like gene is found in the Myxococcus xanthus gene cluster eccoding myxovirescin (TA) antibiotic. One of the polyketide-encoding genes in this cluster is ~27kb long [3]:

Herbert, K. M. et al. E. coli NusG inhibits backtracking and accelerates pause-free transcription by promoting forward translocation of RNA polymerase. J. Mol. Biol. 399, 17–30 (2010)
Peter J. Rutledge    & Gregory L. Challis. Discovery of microbial natural products by activation of silent biosynthetic gene clusters. Nature Reviews Microbiology 13, 509–523 (2015)
http://mibig.secondarymetabolites.org/repository/BGC0001025/index.html#cluster-1

I have searched for information on this topic as I used to work in the area of protein biosynthesis, but without success. However one argument against there being a tendency for ribosomes to fall off mRNA is the very specific mechanism for ribosome release after the stop codon has been reached (described here).
There are other possible problems with very long mRNAs:

Possible degradation of (prokaryotic) mRNA during a long translation time. I would imagine that the mRNA would have to contain structural features that prolonged its life.
Possible misfolding and precipitation of the protein product before the whole protein is completed. I think there are probably chaperone proteins that protect hydrophobic regions or encourage folding of domains to prevent this.

As a footnote, the longest mRNA is thought to be that for the muscle protein, titin. The assembly of that on the sarcomere would not be typical of polyketides, say, but other problems encountered might be similar.


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Why does pETDuet-1 only have one T7 terminator but two T7 promoters?
Why does pETDuet-1 only have one T7 terminator but two T7 promoters (vector map below)? Is there any advantage of having only one terminator? There are going to be two mRNAs transcribed from this vector: one polycistronic (with two genes) and one monocystronic. Also, presumably, there will be more RNA for the gene expressed from the second promoter compared to the gene expressed from the first. That could lead to higher expression of the second protein, provided that the RBSs are the same. Is there experimental evidence confirming/disproving that hypothesis?
Is there any advantage over using polycistronic mRNA vs moncystronic? Have Duet vectors been used for heterologous expression of long (>40kb) biosynthetic pathways?

Sounds like the manufacturer could answer these questions much better than we can.

Not sure it can. But waiting from reply from them as well.

One of the duet user manuals (https://www.emdmillipore.com/CA/en/product/pETDuet%E2%84%A2-1-DNA---Novagen,EMD_BIO-71146#documentation) says that they are useful for studying protein complexes. I'm assuming it allows for more optimal co-translational assembly processes, and possibly favours 1:1 stoichiometry.

@Jory But in that case why is there a second promoter?

OK so I didn't really read up on this last time I answered. As you said the downstream ORF isn't translated as much, so it wouldn't favour 1:1 stoichiometry. I have a feeling the expression of the shorter transcript is to compensate for this effect, but I'm not sure.

Can you add the plasmid map? Overlapping genes would actually cause lower expression.

@WYSIWYG Added vector map. The genes are not overlapping.

Apparently the expression of the second protein in a polycistronic mRNA is lower compared to a two-promoter system (Ref). Anyway, this still doesn't answer why a single terminator is present.

Could they be thinking that the transcription complex from ORF1 would fall apart when hitting an new transcription complex that is being assembled on promoter/RBS 2?

I think the presence of a single terminator is related to the high processivity of T7 RNA polymerase.
T7 RNA polymerase will transcribe a circular plasmid repeatedly before dissociating. The T7 terminator after ORF2 ensures that the transcript terminates efficiently.
Based on your schematic, these are the potential mRNA transcripts from that construct:
Transcript from T7 promoter #1
 5'---RBS---ORF1---STOP----RBS---ORF2---STOP---[T7 terminator]---3'

Transcript from T7 promoter #2
 5'---RBS---ORF2---STOP---[T7 terminator]---3'

It is doubtful that this vector will produce precisely equimolar concentrations of each protein product, however, the topology ensures that there is at least some of each protein produced. Of course, this could be tested empirically.
I hope that helps!


text:
What is the highest number of genes expressed under one T7 promoter?
What is the highest number of genes expressed under one T7 promoter? Also, what is the longest polycistronic mRNA? I am interested in the context of heterologously expressing biosynthetic gene clusters in E. coli.

does T2A/P2A peptides work for your case?

@aaaaaa Not really, since I would like to avoid adding extra sequence to the coding region.


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Does muscle get bigger by increase in size of individual cells or increase in number?
Somewhere in the back of my mind, I have the claim that a muscle never increases its amount of cells but, if the muscle gets bigger, it's simply because individual cells get bigger.
The book Anatomy Trains on page 36 cites "Changes in sarcomere length and physiological properties in immobilized muscle by  Williams et al" when it makes the claim :

Stretched, a muscle will attempt to recoil back to its
  resting length before giving up and adding more cells
  and sarcomeres to bridge the gap.

Is that true? Do muscles increase the number of their cells in that way?

This is what we currently know: http://www.gssrr.org/thesis/10.pdf . It suggests that both hypertrophy and hyperplasia happens. You might find the answer about whether stretch causes hyperplasia.

@inf3rno - I got to page 22 without seeing hyperplasia. Might you direct me to where in this paper hyperplasia is given as a means to increase muscle mass in adults?

@anongoodnurse page 7 - "One look at the current state of professional bodybuilding adds substantial evidence to support that hyperplasia actually occurs given the fact that bodybuilders keep adding substantial muscle mass that could not be otherwise gained through the mechanism of hypertrophy. There appears to be a threshold that governs hypertrophy and once the ceiling of adaptation has b een met, other mechanisms for growth such as hyperplasia must be considered (Engel & Franzini - Armstrong, 2004)." - I don't have the time now to read further that's why I did not wrote an answer.

@anongoodnurse ctrl+f and "hyperplasia", I run over the text, it says that by the adaptation of untrained people is due to hypertrophy, which has a threshold. after that threshold it is most likely that other mechanisms work, like increasing fiber length, or increasing cell numbers. it claims that currently there is no proof, because we lack of studies on professional bodybuilders.

@inf3rno - "One look at the current state of professional bodybuilding adds substantial evidence to support that hyperplasia actually occurs given the fact that bodybuilders keep adding substantial muscle mass that could not be otherwise gained through the mechanism of hypertrophy." I have any number of reputable papers in peer-reviewed journals that refute this. Even this thesis parer does not emphasize that theory (and muscle builders are not scientists).

@inf3rno - if one looks hard enough, one can find evidence for almost anything. This is one such example. If you look at the body building 'literature', you'll see the same claim.

@anongoodnurse "I have any number of reputable papers in peer-reviewed journals that refute this." - I checked the links in your answer, but found nothing that rules out muscle cell hyperplasia. Do you have a study which have the conclusion that hyperplasia does/can not happen in muscle?

@inf3rno - yes. Just about any in the links in my answer. Rule out hyperplasia? They all state it does not happen. Just like you will not find  paper ruling out ovaries splitting in two before conception of twins. There is no evidence for either.

@anongoodnurse Yes, it did not happen in those experiments, but it might happen by different conditions. I think I can agree with your answer, usually hyperplasia does not happen.

A quick survey of the above info points to measured stress and overload can cause the natural body responses into growth :)

The "back of your mind" is correct: "if the muscle gets bigger, it's simply because individual cells get bigger."
Growth of muscle can occur in three ways:

by an increase in muscle cell numbers
by an increase in muscle fiber diameter
by an increase in fiber length.

However, growth in cell numbers is limited to the prenatal and immediately postnatal period, with the animals and man being born with or soon reaching their full complement of muscle cells.

[G]rowth occurs by either hypertrophy of the existing muscle fibers by adding additional myofibrils to increase the muscle mass or by adding new sarcomeres to the ends of the existing muscle fibers to increase their length. Both of these mechanisms occur during the growth process. Growth in the girth of the muscle fibers... may be stimulated by development of stress creating an unequal pressure with splitting at the Z-band and development of additional SR and T-tubule systems. This adds to the diameter or girth of myofibers without any hyperplasia. The growth in length occurs at either end of the fibers and results in addition of new sarcomeres. In both cases, new myofibrillar protein must be synthesized and deposited in the muscle cells.

Adding or removing sarcomeres and myofibrils is determined by exercise, that is, the degree of force a muscle can generate which is in turn dependent on the degree of overlap of the thick and thin filaments. Thus, the amount of tension would control the number of in-series sarcomeres and the number of myofibrils in a single muscle fiber.
Nutrition is also known to play an important role in muscle growth, but growth (that is, increase in girth) cannot occur without exercise.
The exact roles of GF and IGF-I are not completely clear.
Muscle size does not increase by the addition of new muscle cells:

The results show that the increase in muscle cross-sectional area from childhood to adult age is caused by an increase in mean fiber size. This is accompanied by a functional development of the fiber population: the proportion of type 2 fibers increases significantly from the age of 5 (approx. 35%) to the age of 20 (approx. 50%), which, in the absence of any discernible effect on the total number of fibers, is most likely caused by a transformation of type 1 to type 2 fibers.

Activation of satellite cells, a claim made by body builders, is mis-represented by them. The satellite cells seem only to aid severely damaged muscle cells to heal, not to increase in number.
Muscle growth and exercise
Muscle hypertrophy
Growth and development of human muscle: A quantitative morphological study of whole vastus lateralis from childhood to adult age
Regulation of muscle mass by growth hormone and IGF-I

A tissue can undergo two types of quantitative growth:

hypertrophy - cells increase in size
hyperplasia - cells increase in number

There are tissues that grow as a result of one of the above processes and there are tissues that grow because both processes happen.
A Google search for muscular growth yields as first result Muscle hypertrophy. And this is the process that happens to muscle tissue of an adult body under physical exercise.
But muscle tissue can undergo hyperplasia too if stimulated by specific hormones like IGF-1 and human growth hormone (Wikipedia:Hyperplasia).
Muscle hyperplasia can occur also under physical activity in animals but this hasn't been proven for humans (Antonio J, Gonyea WJ. 1993). Stretch overload seems to be the most important trigger of hyperplasia (Kelley G., 1985).


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What are the biochemical processes occurring when food spoils?
Let's assume for a minute that microbes themselves and their direct toxic products (i.e. endotoxins) aren't toxic to humans. Let's also discount any innate immune responses the body mounts against the invading microbe (i.e. inflammation and production of cytokines).
What happens to food molecules (mechanistically) as it spoils and what deleterious effects do these "spoil products" have on the body if ingested? I'm looking for compounds that can result from the spontaneous breakdown of food or the byproducts of microbial metabolism (that is NOT a "direct" toxin) that is harmful to the body.
For example, do the proteins in food break down into some toxic nitrogenous substance?

It is mostly oxydation as far as I know.

During putrefaction of animal tissue, lysine is decarboxylated into cadaverine and arginine is decarboxylated into putrescine. These compounds are deemed to be toxic.
A serving of meat contains 8 g of protein, corresponding to 640 mg lysine and a little bit less of arginine. Let's go straight and say that a spoiled meat serving contains 640 mg cadaverine and a little bit less of putrescine.
In rats, the acute oral toxicity for both polyamines is around 2000 mg/kg, let'assume that this is valid for humans also. According to these rough calculations, to have an acute toxic effect, a 70kg man that is resistant to the direct toxic effects of microbes, should eat 140 grams of cadaverine, corresponding to 218 smelly rotten meat servings.
[composition and toxicity data taken from wikipedia]

Cadaverine...hah. what a clever name.

Cadaverine and putrescine are legendarily foul-smelling. I do not think I could keep down 140 grams of pure cadaverine. That's like an orange, made entirely out of the solified scent of death.