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Definition of Phenotype
I'm not a biologist but, I'm trying to enter molecular biology from a perspective. I have noticed that concept of genotype is quite well defined while phenotype is not. If I understand well, gene expression builds up enzymes that ultimately control all chemistry inside the cell, and which are sensible to the environment. Then, how correct/incorrect would it be to state that "phenotype is the enzyme composition within the cell"? Is it at least a good approximate idea?

Phenotype is considered the physical/observable representation of the genotype.

Where is your quote from? The entire enzyme (protein) composition of the cell is correctly referred to as the proteome. As not all proteins play a role in individual traits, then no, that is a bad approximation of the idea.

Have you read this? If not, please do. If so, what specific questions do you have about it?

Genotype:
Simply genotype is the inherited genetic information an individual has, and is conceptually quite easy to grasp. For example, if height is determined by gene $A$ and there are two alleles (variants of the gene, $A_1$ and $A_2$), then the three possible genotypes at that locus are $A_1A_1$, $A_1A_2$, and $A_2A_2$.
Phenotype:
The definition of a phenotype is a little more difficult to grasp, in part because it's so broad. As a quantitative geneticist I would say its any characteristic of an individual that can be measured. There's an enormous variance in the phenotypes that are used, they can be characteristics that are physiological, morphological, behavioural, life-history, even fitness itself. Personally I've used phenotypes from gene expression, which is one of the "lowest" (most close to genotype on the bridge between genotype and phenotype) phenotypic levels, through to lifespan, rates of ageing, and lifetime offspring production. Phenotypes are determined by genotype and/or environment (all non-genetic effects). For example, height may be affected by several genes, but it is also affected by nutrition during development and growth (among other things). As an evolutionary biologist, I feel the need to point out that selection operates on the phenotype, it is because genotype often has some effect on the phenotype that we see evolution by inheritance of genetic information.
Correctness of your statement:

"Phenotype is the enzyme composition within the cell"

Would be sort of incorrect. It certainly wouldn't be appropriately defining phenotype as a general thing. It would be saying that phenotype means enzyme composition within cells, and the appropriate sentence depends on what you are trying to say. The following would say that, in the discussed case, the enzyme composition of the cell is what you consider to be the phenotype:

"In this study the enzyme composition within the cell is the phenotype."

Whereas, the following defined the concept of phenotype:

"Phenotypes are characteristics which could be, in principle, measured, such as the enzyme composition within a cell."

The problem of your statement is it makes it sound like phenotype, as a general thing, is enzyme composition within cells. It's kind of a problem of while enzyme composition of a cell can be a phenotype, not all phenotypes are enzyme compositions of cells. Similarly to all humans are mammals but not all mammals are humans.

Phenotype is the physical result that one sees that is the outcome of genetic makeup. Genotype is the code that is written in the DNA (or RNA if you are a retrovirus). Enzyme composition in the cell, hair color, proclivity towards certain diseases; pretty much everything is a product of genoptype. There are some other factors in the environment that affect gene expression, but you are very much the product of your genotype.

Your answer lacks references and completely ignores environmental effects and gene-environment interactions, which are large components of phenotype.

I also believe this answer can be improved if it includes external factors.


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Why is HIV associated with weight loss/being underweight?
It seems that people with HIV are often underweight, is there something (or multiple things) which cause HIV sufferers to lose weight? What is happening within the body as a  direct effect of HIV that will lead to increased weight loss?

"without all these headaches".. why? Do you plan to reduce weight by acquiring HIV??!! It sounds like that from your question. It is a disease which takes toll on the body. There are several AIDS related complications and the medicines can also have some side effects. Please improve your question.

This is the future, folks. People looking to acquire HIV so they can lose weight quickly. All the doctors hate it.

I've edited to make more about the mechanisms underlying weight loss in HIV patients.

Whatever you do, don't get HIV to lose weight. Dealing with HIV is going to be a much, much greater annoyance than losing weight is. I don't have it myself, but I know someone who does, and it isn't pleasant.

Here is a brief dissection of the causes of weight loss associated with HIV which are listed by AidsMap.com. Most were quite obvious (disease and side-effects of medicine often cause appetite loss, diarrhea, vomiting etc. - kind of trivial components of the answer) but the first two were more interesting (and new to me).

HIV can increase the rate at which the body uses nutrients (increased
  metabolism)

It seems that, at least in the early phases of HIV, the metabolic rate is higher. In one study, the resting energy expenditure of HIV patients was ~8% higher, and fat oxidation was increased. This will result in more calories being burned on a daily basis, and, to put it in perspective, ~8% of a males recommended daily allowance of calories is 200 calories, or about one 40g bar of chocolate. Patients will have to consume more calories just to meet their basic daily needs.

HIV can alter the lining of the gut, making it harder to
  absorb nutrients (malabsorption)

It seems the HIV virus is associated with inflammation in the gut, causing damage to the intestinal lining. The intestine is a major area of where we absorb nutrients from our food, if efficiency is reduced by damage and inflammation, then fewer calories will be absorb. Patients will have to eat more food to get the same amount of calories in to their system.

other gut infections can cause
  malabsorption and/or diarrhoea

Many illnesses that a HIV patient will contract will causes these problems.

you may eat less than you used to (and
  need to) because of loss of appetite during ill health

Simple one, less energy in = less energy to absorb, weight loss is all about calorie intake vs. calorie usage.

specific
  conditions may make it harder to eat, such as mouth and throat
  infections

Obviously some infections, such as herpes and canker sores, will make it unpleasant to eat. HIV leaves patients more prone to such problems so they will more frequently avoid eating because of the discomfort and pain.

some drugs may suppress your appetite or cause side-effects
  that put you off food, such as nausea, vomiting, indigestion or
  altered taste.

A lot of drugs, not just those that fight HIV, cause side-effects on appetite, vomiting, etc. Here is a list of various HIV/AIDS drugs and their common side effects. A quick eyeballing of that table suggests around 20 of 28 (~71%) are associated with some kind of vomiting or diarrhea.

why you mention "you" in answer? i am not facing HIV.

those are quotes from http://www.aidsmap.com/Unintentional-weight-loss/page/1044802/

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What does characterization mean in a genomics context?

"The resulting libraries of gene sequences allow CDC and other
  laboratories to compare the genes of currently circulating influenza
  viruses with the genes of older influenza viruses and viruses used in
  vaccines. Through this process of comparing genetic sequences, called
  genetic characterization, CDC can make informed assumptions regarding.."

I'm unsure what genetic characterization means. What do the researchers actually here?

I've made some edits to clarify your question a bit - are these suitable edits?

I think what I'm trying to ask is what genetic characterization really means.  Is it simply a comparison of genetic sequences to detect when they are different?  The CDC use of the term doesn't seem to apply in the context of genomics papers that I read but I could simply be mistaken (I am not a biologist, rather a software engineer trying to understand how the phrase is being used).

There's no technical definition for "genetic characterization". It is simply a phrase used by authors based on the normal meaning of the words: (1) having to do with genes and heredity, and (2) describing the essential character.  Of course the bounds of the genetics and the essence of their nature are entirely in the eye of the author and reader, so no particular definition applies across all papers in genomics (or in other fields).

True. The word characterization doesn't really have a defined meaning, the implication is that you've observed something and described the significance and meaning of what you've observed - so the 'essential character' here presumably refers to the likely consequences of change in the virus' genotype to it's phenotype.

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What physical or mental actions can be picked up by EEGs?
There certainly seem to be a lot of gadgets and gizmos leveraging EEG technologies to the control of devices.
This makes me wonder: what intentions/thoughts can be captured by EEG technology, and which ones can't?
For example: how about motor movements? If I am wearing one of these EEG devices, and I shake one of my fingers back and forth, is my brain generating waves that the EEG device will detect? Why/why not?

Many EEG responses are swamped in random brain activity, artifacts and background noise. A single movement typically doesn't evoke measurable activity, because its amplitude is so small with respect to background noise.
I think the potentials you are looking for are event-related potentials or ERPs (Fig. 1). During ERP recording, basically a regular EEG is registered, but certain events (presentation of stimuli or actions by the subject) are time locked with the EEG recordings. By repeatedly measuring (e.g., 25 times) the time-locked response to the event, an average EEG can be obtained. Assuming remaining EEG activity, noise and artifacts are random, the averaging process will decrease noise, but will not affect the ERP. The averaging hence leaves you with a clean ERP response (Yordanova et al., 2003).

Fig. 1. ERPs. Left are stimulus-evoked ERPs (auditory, visual) and right are ERPs associated with the motor response by the subject (button-press upon stimulus presentation). Source: Yordanova et al., 2003.
In Fig. 1, the reaction times indicated correspond to the subject's button press, so the intention to press the button in fact precedes the actual motor response. In fact, the covert (imagined) ERP response can be nearly identical to the overt ERP (the motor action), see Fig. 2 (Kranczioch et al., 2009).

Fig. 2. Overt motor-evoked ERPs (top three panels) and equivalent covert (imagined) ERPs (lower three panels). The three panels cover different electrodes. Source: Kranczioch et al. (2009).
By characterizing the exact shape and other characteristics of the ERP, computer software can be deployed to recognize this ERP wave within a normal EEG. This is done in computer-brain interfaces. By filtering the ERG outside the frequency range associated with the ERP a lot of the cleaning can be done on the fly in near-real time.
A list of various stimuli in ERPs can be found in Table 1 in (Goodman, 2010).
References
- Goodman, Atten Percept Psychophys (2010); 72(8): 10.3758
- Kranczioch et al., Human Brain Mapping (2009); 30(10): 3275–86
- Yordanova et al., Brain (2003); 127(2): 351 - 62

Thanks @Christiaan (+1) - one quick followup. A human can think about moving a particular muscle group (say, an arm or a leg), and then there is the process of actually moving it (not just thinking it). Can I assume that thinking about moving a muscle and actually moving it produce two distinct EEG/ERP signals?

@smeeb - see the added Fig.2 for your reference

Thanks again @Christiaan (+1) - last followup, I promise (!): so are you saying that it is possible (using software) to distinguish between overt/actual and covert/imagined signals, or is this evidence suggesting the signals are too similar to differentiate them?

@smeeb - that would warrant an extensive literature search. If there is a specific event you are interested in you could tease out the differences and similarities. It will also be dependent on location of the electrodes; e.g. electrodes on top of the motor cortex may favor motor over imagined ERPs, while electrodes over frontal cortex may favor the reverse. My answer is more of a general answer to a quite general question :-)


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Regression to the mean and evolution
I don't have a strong biological background but, in studying statistics, I met the idea of regression to the mean. e.g. children of tall parents tend to be shorter than their parents, and so on.
Does this interact with evolution ?

Interestingly, statistics have evolved quite significantly in parallel of evolutionary biology. Galton, Pearson and R. Fisher are important names that contributed to both biology and statistics.

Have a look at Wikipedia > Heritability > Parent-offspring_regression.

When you talk about "regression toward the mean", do you refer to the modelling of data (linear regressions) or do you refer to the natural tendency for extreme values to be less extreme in a future measurement (origin of the term regression but rarely used with this meaning today)?

answers to this question are related: Is it possible for a child to grow taller than their tallest parent?

Actually i was referring to the tendency of values to be around the mean on the normal distribution curve.

"the tendency of values to be around the mean on the normal distribution curve". What do you mean? Do you mean the tendency of extreme data points to regress toward the mean in future measurements? If yes, then please let us know how it could affect evolutionary processes as it is not obvious for me. Also, your example does not match this. I am voting as unclear.

TL;DR answer: Regression to the mean doesn't always occur (children can be taller than either parent, as can be easily observed at any high-school basketball game), so it doesn't affect the theory of evolution through natural selection.
The observation of regression to the mean was of great concern to Darwin and early thoughts on natural selection (don't confuse "evolution", which is the observed phenomenon, and "natural selection", which is one of the theories proposed to explain evolution).  The problem has been effectively resolved since the rediscovery of Mendel's genetic work at the end of the 19th century.
"Regression to the mean" is inevitable if inheritance works through blending of features.  That was how everyone believed inheritance to work in the mid-1800s, and Darwin understood that it presented an insuperable obstacle to his theory.  That is, if blending inheritance was true, then natural selection could not be true.  Darwin puzzled over this quite a bit, and came up with some unsatisfying suggestions to overcome it, but at the end of the day, one of the predictions that his theory of evolution through natural selection made, was that blending inheritance could not be true.
Of course, blending inheritance is not true.  Mendel showed that in fact inheritance is quantal, not blending.  We now know that many traits of interest look, superficially, as if they're blending (which leads to regression to the mean), but are actually the result of multiple traits interacting.
With blending inheritance, the variation that is required for natural selection to work is lost, generation after generation; regression to the mean in an inevitable consequence.  With gene-based inheritance, variation (can be) preserved generation after generation; regression to the mean is a common but not inevitable consequence, because the variation in the original population is still present and can be re-created given appropriate selection pressure.

Interesting read on how Mendel was mostly wrong.

Mendel wasn't wrong on the key point that inheritance is not blended, which is what's relevant here.

That's true, I should have been more specific. I was just mentioning the article as possible interesting reading for those whose understanding of Mendel's work didn't go beyond high school biology. Your answer is actually pretty decent.

There is a concept known as "heritability" which essentially is a measure of how much of the variability in a certain trait that is due to genetic factors. This is closely related to regression to the mean. Now for length the heritability sometimes is estimated, by measuring the lengths of many parents and their offspring, to be around 0.7. This means that if your father is ten centimeters taller than the average man in your population and your mother is ten centimeter taller than the average woman in your population you are expected to be around three centimeters shorter than your same sex parent but still seven centimeters taller than the average for your sex in your population.
A heritability of 0.7 is very high so if it were a clear evolutionary advantage for an individual to be taller or shorter than the current average height the length of the population will be expected to change rather fast.
There are other traits, for instance the tendency to have one-egg twins, where the heritability is believed to be basically zero. This means that even if you are a one-egg twin and being a one-egg twin constitutes a clear evolutionary advantage the relative amounts of one-egg twins will not increase in the population because there is no heritability.
You could say that the higher the heritability, and thus the lower the regression to the mean, the faster a trait will change in a population in a certain direction if there is evolutionary pressure for it to do so.

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Why do leukemia and lymphoma cause "night sweats"?
One of the symptoms of these blood cancers is sleep hyperhidrosis (aka night sweats).  Also referred to as one of the B-symptoms, it may be used for prognosis.
What is the the mechanism behind the symptom?

Possibilities I came up with:

Body is more likely to be infected due to immune compromise and thus a bacterial or viral etiology
White cell counts may be very high causing release of cytokines which affect thermal regulation
Something else

Why is there more sweating at night and not so much in the daytime?

When the tumor cells infiltrate other tissues and then die, there's a good chance they release some pyrogenic molecules that cause sweating. But, I don't know why at night. Hence, though, it'd be considered a paraneoplastic effect.


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Can anyone Id this flower?
Small pink flower, started out as tiny buds, leaves look almost like Maple leaves..

Welcome to Biology.SE. Try to tell us as much as you can about this flower. In which country did you find it? Which environment? What season? Do you know if it is a wild species or an ornemental species?

Location information is extremely important to species id questions @LindaMarie

It's a mallow.

The leaves - they look like maple leaves - and the flower are identical.
Mallows are from the family Malvaceae, which includes food plants (okra, cocoa beans, kola nut), economic plants (cotton), and ornamentals (e.g. hibiscus) One species of this family (Althaea officinalis) is actually the original ingredient to make marshmallows.
I'm not sure which mallow it is (there are 243 genera with 4225+ species), but it's a common weed wildflower all over the world.

Nice answer - I agree on the classification, it's a shame theres so many species

@rg255 - Thanks. Yep. I've seen this one on my own property, and couldn't narrow it down further. There are so many. I've seen marsh mallow, rose mallow, and a bunch of others, but this one I could not identify.


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Why a striped baby is not the result of a white and a black parent?
Someone asked me:

If a striped cat is the result of a white and a black cat, why the result of a white woman and a black man is not a striped child?

I know the answer. I also know that the result of a black cat and a white one is not a striped cat. But I'm looking for a simple answer. I'm looking for an explanation without a genetics background required. I'm looking for a metaphor or something similar.

Perhaps metaphors should be sought on English.SE. I vote to close, as the question is not about the biological underpinnings. If it were, it is closable on homework grounds.

I disagree with the close vote - it's a biological question. Asking for a metaphor (perhaps analogy is a better word) is just asking for a laymans answer. Though if you can't explain it simply I would question whether you know the answer, and why you would want the answer to not require genetics training @Farzad...

@rg255 - I don't like the general tone, I don't like the fluff, and it is homework as there is no proof of any effort.

I'm not sure I really understand. "If X then why not Y?" is completely answered by "not X".  A complete answer to this question is "because that's not how you get striped cats". Everything else is "simple ways of giving basic genetics information to people".

I want an answer without genetics background required, because I want to explain it to the guy who asked me and he has no idea about genetics. I can explain it by the means of genes and alleles that the result of a pure black and a pure white cat (that's so rare) is whether a white or a black cat. But I just want to find a real-world analogue for it, and it's still science and it's still biology. @rg255

that's what I've given in my answer - also I'm one of the ones arguing that this question is biology related... You're best hope of saving this question is to edit it to show that you understand the genetics and biology of what's going on, and ask for a good layman's explanation

@Farzad your reasoning is not entirely correct. The pigmentation patterns in cats are more complex and if you do ask about them then this question would be opened. It is up to you how you explain your friend. I don't think they can understand the pigmentation patterns without knowing what neural crest cells are.

This is a good and funny question. Cats are not striped? But cats are with black parts and white parts. This can be quite pretty. What aren't humans generally like this? There is a rare case where humans do get parts of different colors: chimeras.

@Farzad you should really edit this question to make it suitable.

The reason that there are no stripes when black and white people get babies is the fact that the number of pigment cells is the same for black and white people. What is different is the amount of pigment produced, and it will be different in the kids as well (lighter than the dark parent, darker than the light parent) See references 1 and 2 for details on the melanocyte density. Skin color is a multigenic trait, so the genetic background of both parents and their effects on pigmentation come into full play here.
Besides this effect, humans do have stripes, although they are mostly not visible. They are called Blaschko's lines and look like below:

These develop from the migration pattern of the melanocytes (and their precursor cells) in the developing embryo. They can get visible in some rare genetic conditions or by diseases. See reference 3 for a more popular explanation and reference 4 for a review on this field.
References:

The Regional Anatomy of the Human Integument with Special Reference
to the Distribution of Hair Follicles, Sweat Glands and Melanocytes
General Biology of Mammalian Pigmentation
Blaschko’s Lines
Lines of Blaschko.

And aren't cat pigments controlled by one gene?

What about cats?

Skin colour is determined by additive effects. That is, the amount of pigment is determined additively by the genes. For the basic genetics of it I will give a simple example, which is just illustrative and a gross oversimplification, it's probably much more complex (many loci all acting at once).
Imaginary example:
Suppose skin colour is affected by a single locus (at one position) within the DNA, which determines the amount of pigment produced. At this locus there are two alleles within a population, that is two versions of the DNA (e.g. ACGTCCATT and GACTTAACT are different DNA sequences). Allele one ($A_1$) produces a small amount of pigment, and allele 2 ($A_2$) produces a large amount. Thus people with $A_1 A_1$ genotype (people are diploid, i.e. they get a version from each parent) have light skin, $A_2 A_2$ genotypes have dark skin, and $A_1 A_2$ have an intermediate skin colour.
Analogy
This is analogous to mixing fruit juice with water - if you mix blackcurrant cordial with water the colour is determined by the proportions. If you put out two bottles, one with cordial and one with water, allow two people to randomly choose a bottle, and use their choices to mix a glass of drink, 50% of the time you will end up with 1/2 water mixed with 1/2 cordial, while 25% of the time just a glass full of water, and the remaining 25% of the time just a glass full of cordial.
Why stripes don't occur
Note: although stripes occur in animals including humans (see chris' answer), it's not I'm the way your question insinuates
For stripes to occur you would have to have structure in the skin with two different types of skin cell, where bands/stripes of type occur - alternating between expressing the allele inherited from the mother, and that inherited from the father. That would require structure in the skin and something called genomic imprinting so parent of origin could be a factor.
The analogy with the glass of cordial is what going on in each cell, for stripes you would have to have organised and alternating clusters of glasses (cells) which get their contents determined by one individuals choice of cordial, with the selector alternating with the cluster of glasses.

Why would black and white bands require genetic imprinting? How do cats have black and white parts?

because the cells in the offspring would need to be able to differentiate between the paternally and maternally inherited allele to be able to organise them in to stripes


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Under what circumstances does Batesian mimicry evolve?
Batesian mimicry is a form of biological resemblance in which a noxious, or dangerous, organism (the model), equipped with a warning system such as conspicuous colouration, is mimicked by a harmless organism (the mimic). An example would be unrelated species such as Myrmarachne plataleoides, the spider, and the weaver ant Oecophylla smaragdina.
Given that evolution is a random process that doesn't have any pre-defined targets the probability of such convergence in evolutionary history should be nearly zero. My argument is that the search space for a 'nearly optimal' Batesian mimic would be too large and hence any search algorithm would be unable to avoid the curse of dimensionality. Even the sampler, which would
need to sample from a wide variety of valid phenotypes in the parameter space would run into serious problems.
The problem of the curse of dimensionality for optimal sampling can be intuitively explained in the following way:

Let's say you have a straight line 100 yards long and you dropped a penny somewhere on it. It wouldn't be too hard to find. You walk along the line and it takes two minutes.
Now let's say you have a square 100 yards on each side and you dropped a penny somewhere on it. It would be pretty hard, like searching across two football fields stuck together. It could take days.
Now a cube 100 yards across. That's like searching a 30-story building the size of a football stadium.
The difficulty of searching through the space gets a lot harder as you have more dimensions.

Here are additional points to clarify what I mean:
My question is whether the Batesian mimic would need to initially be quite similar in morphology to the different species that it's converging to in morphology. In mathematical terms, if the parameter space for the visible morphological features is $(x_1,x_2,...,x_n) \in \mathbb{R}^n$ then convergence is probable if and only if the initial condition lies in a small enough neighborhood of the solution $(q_1,...,q_n)$.
One of the features of the fitness function is that I think there should be exponential payoffs in terms of reproductive success near the solution $\vec{q}$. Further, I think there are probably other very important environmental factors that might lead to such convergence. An arboreal jumping spider of similar size that shares the same environment as leaf-cutter ants is a good example. They would already have similar color among other features in order to blend in the same environment.

Well it is not too hard for it to evolve, because it has evolved, many times. What is your question? See my answer here regarding (what some people suggest are implausible) rates of evolution and adaptation. http://biology.stackexchange.com/questions/45005/approaches-towards-a-theory-of-innovation-in-evolution?lq=1

One of the (several) problems with your conclusion is that you assume the initial adaption needs to be "nearly optimal" to start with.  Assume instead that looking 1% more like a coral snake provides a harmless species with a 1% improvement in reproduction. Modeling that leads to efficient mimicry within a relatively short number of generations.

There are no question mark in your question :) It is a sign that the question is probably unclear.

@iayork What do you mean by 1% more? Let's just look at a silly example. Let's suppose you're just comparing two 3 dimensional shapes. How does a square become 1% more like a sphere?

@rg255 My question is whether the Batesian mimic would need to already be quite similar in morphology to the different species that it's converging to in terms of morphology to start with. In mathematical terms, if the parameter space for the visible morphological features is $(x_1,x_2,...,x_n)$ and we assume that each of these variables are differential functions of a parameter $t \in [0,1]$ then convergence is probable if and only if the initial condition lies in a small enough neighborhood of the solution $(q_1,...,q_n)$.

@rg255 This can probably be modeled as a monte carlo simulation once we have defined a suitable fitness function. One of the features of the fitness function is that I think there should be exponential payoffs in terms of reproductive success near the solution $\vec{q}$. Further, I think there are probably other very important environmental factors that might lead to such convergence. An arboreal jumping spider of similar size that shares the same environment as leaf-cutter ants is a good example.

@Aidan Rocke How does a cube become 1% more like a sphere? It rounds off the corners a little bit, obviously.   How is this a difficult concept? The same applies with mimicry.  The whole point about evolution is that tiny advantages, compounded, become large advantages.

@iayork Your argument is actually false. Show me the computation that determines that a cube is '1%' more spherical when its corners are rounded. Now, in general how are you supposed to do such a calculation of 'percentage similarity' assuming that some of the variables are independent from each other and some are strongly correlated.

@iayork There are many ways for a cube to become more 'spherical' but the computation would involve some distance measure not a percentage. If you're serious about saying anything correct about shape similarity measures you might like to google that first. But, I must say that this question is much more complicated than that. If you can't do a good job analyzing such a problem then I wouldn't join this discussion.

You're an engineer, aren't you.  Engineers, dentists, and physicists are notorious for (1) not understanding evolution, and (2) being too arrogant to try to learn about it.  As a result, they make incredible fools of themselves bloviating about things they don't understand.

@iayork it might be best to step away from the comments here, I don't think the mods will appreciate the way the thread is going.

@AidanRocke it's rarely good to try reducing evolution to computation, it's far more complex. I think the (very appropriate) point iayork is trying to make is that the mimic species doesn't evolve by jumping from a state of dissimilarity to perfect mimicry, but gradually becomes a better mimic - in other words, it will slowly evolve to look more and more similar to the species it mimics.

@rg255 I actually understand that point. But, my question is whether there must be special restrictions on the initial conditions in order to guarantee that such convergence is possible. There might be an advantage for a baboon to look like a lion for example as it wouldn't be bothered as much by hyenas and leopards but the cost makes such an evolutionary trajectory improbable. In some sense the morphological parameters of the mimic must initially be within a neighborhood of the morphological parameters of the target animal.

Then essentially your question is why doesn't mimicry always evolve - for example, why don't baboons evolve to look like lions? In such a case you are right, they look really different so it's hard (but not impossible) for evolution to produce that mimicry... see here: http://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont/35658#35658 and here: http://biology.stackexchange.com/questions/7932/why-are-there-no-wheeled-animals

@rg255 That's a related question. My question is under what circumstances does mimicry evolve. And can these conditions be made precise to a certain degree? Answering why mimicry doesn't always evolve is easier than explaining under what circumstances it might evolve.

Well the only requisite would be the presence of heritable genetic variance affecting phenotype, such that the two species could carry genes which have similar phenotypic results. Selection is not even a requisite, but it does help a lot; really good mimicry is less likely to evolve purely by random processes of evolution (e.g. drift). Even with selection favouring mimicry we cannot say that mimicry will evolve.

Mimicry and camouflage is an extremely efficient defense. If an insect gains a color fleck that makes it 1 percent less likely to be eaten, that color fleck will grow, diverge and change over generations.

While the attempt to consider this in a mathematical framework perhaps isn't so useful, it seems that the biological essence of your question is along the lines of:

Does a Batesian mimic initially need to be initially quite similar in morphology to the different species which it evolves to mimic?

The answer is no, morphology does not need to be similar, but it does help make mimicry likely. The only requisite to evolution is the presence of heritable genetic information with the potential for change, and this prerequisite is the same for any trait. Selection is not a prerequisite but mimicry is more likely to evolve by adaptive evolution than random evolution. Given that phenotype is often strongly affected by the DNA and that DNA has a potential to mutate, then any distance in phenotypic space can be covered so long as sufficient mutations occur. Sufficient mutations are more likely to occur when
a) the distance in phenotypic space between the two initial species is small (the ancestral form of the mimic species is similar to the species it will mimic)
b) a large amount of time is allowed to elapse (more mutations can occur)
The first of these is simply stating that there are fewer (or less extreme) mutations required to get the species to be perfect mimics. The latter simply states that time allows for a greater number of mutations to occurs, making it more likely that large phenotypic spaces can be bridged.
Consequently, allowing identical time, mutation rates, mutation effect sizes, and selection coefficients, two species that initially look similar are more likely to evolve mimicry than two species that initially look very different, because fewer steps need to be taken for convergence of phenotypes.
This is the same for any trait. One could ask can humans evolve to be ten feet tall, the answer is yes, as long as the genetic variance arises. One could ask can humans evolve to be 20 feet tall, and again the answer is yes. However, the latter is less likely because it requires a greater movement in phenotypic space. More time also makes both results more likely.

This answer seems reasonable. but, would you mind expanding on point a)? I mean can we quantify how small this distance must be in order for evolution of Batesian mimicry to be probable within a few generations?

It would involve too many assumptions that would be violated in nature, there's a major problem with trying to reduce some evolutionary problems to equations - nature is just too complex

I can take a look at point a tomorrow - it's explained a little in the last paragraph when comparing 10 and 20 feet tall people (as a very simple univariate example) - but if you want me to expand further then remind me tomorrow (bedtime here!) @AidanRocke


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Synthesis of an additional DNA in Pachytene and Zygotene
I've read, that in Pachytene and Zygotene additional DNA material is synthesized, about 0,3, 0,1% respectively. Why is it so?

Is it possible to cite where you read this?

that's from one book, in Russian, unfortunately. But i can look for english source.
UPD: Answer below gave us english sources, i guess.

About 0.3% of total DNA complement is synthesized during those 2 stages as a measure of replication repair mechanism.
Reference:
http://www.ncbi.nlm.nih.gov/pubmed/3731943
http://www.nature.com/nature/journal/v219/n5153/abs/219489a0.html

Could you expand on this a little? Why is that DNA complement synthesized, and how does it act as a repair mechanism (and a repair mechanism to what)?


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When was it discovered XY chromosomes decide the sex of a child in humans?
Several stories are told from before-genetic-age (books and movies are my reference, the one present in my mind is Marie-Antoinette by Copola) in which we can always see that women are blamed for giving birth to a girl - when it was a boy which was "required".
How did mankind's (man) society took the discovery of the fact that the sex of a human baby is decided by the Y or X chromosome carried in the masculin genes within the sperm fertilizing the female's egg. (at least this is what I learned in school decades ago).
When was this fact discovered and by whom?
(The occasion for this question is Nettie Stevens 155th birthday today)

For history of science questions there is another website: History of Science & Mathematics SE.

The discovery of genetic sex determination, and determination of sex via male gametes (in XY species, female in ZW), occurred over some time in the late 1800's and early 1900's. Advances were made with methods to stain chromosomes and, in 1891, Henking noted that wasps produced sperm with a varying number of chromosomes. However, he was unable to gather evidence that the "x-element" was determining sex. Nettie Stevens, in 1905, then used beetles and noted an odd set of chromosomes in sperm, which later became known as the sex chromosomes. This was the discovery of sex determination through male gametes.

"In 1905, while studying the gametes of the beetle Tenebrio molitor, Stevens noted an unusual-looking pair of chromosomes that separated to form sperm cells in the male beetles. Based on her comparisons of chromosome appearance in cells from male and female beetles, Stevens proposed that these accessory chromosomes were related to the inheritance of sex." - Link

In 1905, Beecher-Williams also made the same discovery, so they are both credited with discovering sex determination by the sex chromosomes. However, Clarence Erwing McClung also contributed to theory that Henkings X-elements may determine sex in 1901.
Thomas Hunt Morgan also contributed some major work on heredity and sex chromosomes, having been initially sceptical of Stevens' discovery. He found that eye mutations in Drosophila appeared to be sex linked, and concluded that the mutations were likely carried on the sex chromosomes.
There is a paper from 1910 where Michael Guyer concludes that accessory chromosomes (the sex chromosomes) likely determined sex in humans.

"It is probable that in man and certain other vertebrates, as in the insects, myriapods and arachnids, the accessory chromosomes are in some way associated with the determination of sex."

However, Theophilus Painter, in 1921, concluded for the first time that human sex determination was by the presence of X or Y in the sperm; Guyer had gone for an XO system. While Painter got the chromosome count wrong, being hampered by the techniques of the day (an issue that wasn't resolved until the 1950's), he got the sex determination system right.


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Chance of child inheriting at least one copy of an allele - heterozygote mother, unknown father
Our genetics professor has posted up working for previous examination answers, but I am not convinced that his answer is correct. My answer is close but may just be due to co-incidence.
Question: There is a dominant "risk" allele with a frequency of 5%; what is the chance that a woman with one copy of this allele, and her husband will have a child with at least one copy of the allele.
Heterozygote frequency: 0.095
Non-risk allele homozygote frequency: 0.9025
Risk allele homozygote frequencyy: 0.0025
Professor's answer:  0.50 (woman's chance of passing allele) + 0.095/2 (heterozygote frequency in population divided by chance of passing allele) = 0.5475
My answer:  There are three possible situations, that the husband is homozygous recessive, homozygous dominant and heterozygous. The probability that any child will have the allele in each situation is 50%, 75% and 100% respectively.
Hence my answer = (50% x 0.9025) + (75% x 0.095) + (100% x 0.0025) = 0.525

What is a risk genotype in a autosomal dominant disease - just the probability of being diseased?

To me, it is unclear whether the "disease" allele is dominant or recessive. Your statements "Homozygous recessive frequency: 0.9025" and "risk genotype (autosomal dominant)" could be impying that the disease is dominant, while the professor's answer is indicating that it's recessive. The answer also depends on whether you know the disease/carrier status of the father, and you and your professor are treating this information differently. [cnd...]

[cnd:] You could argue that the disease status of the father will be known (irrespectively of being recessive or dominant). Your professor's answer is based on that information while you are treating the fathers status as completly unknown.

I think the professor may have forgotten to also add the probability that the father is homozygous for the risk allele

It seems that what you are trying to do is calculate the probability of the child having at least one copy of the "risk allele" which I will denote as "A" (and it's counterpart "a").
First of all you know that the mother is Aa, and the child will get one allele at random. The probability that the mother passes on the A allele is then 0.5.
The tricky bit is the seemingly unknown genotype of the father. However, you do know genotype frequencies, which are the probability for the fathers three possible genotypes.

If the father is AA then it is certain the child will get the risk allele, and the probability of the father being AA is 0.0025.
If the father is heterozygous then there is a probability of 0.5 he will pass on the A allele, and the probability of the father being Aa is 0.095.
If the father is aa there is a probability if 0 that he will pass on the A allele.

Combined these give the probability that the father carries at least one A and will pass it to his child.
$$(1 \times 0.0025) + (0.5 \times 0.095) + (0 \times 0.9025) = 0.05$$
The probability of the child getting at least one A is then the probability of getting it from the mother plus the probability of getting it from the father.
$$0.5 + 0.05 = 0.55$$

I wrote out every possibility, and I agree with yours.
Mom passes good allele  50.00%
Dad is homo wt  90.25%
Odds of 0 bad alleles   45.13%
Mom passes good allele  50.00%
Dad is het  9.50%
Dad passes bad allele   50.00%
Odds of 1 bad allele    2.375000%
Mom passes good allele  50.00%
Dat is het  9.50%
Dad passes good allele  50.00%
Odds of 0 bad allele    2.375000%
Mom passes good allele  50.00%
Dad is diseased 0.25%
Odds of 1 bad allele    0.12500%
Mom passes bad allele   50.00%
Dad is homo wt  90.25%
Odds of 1 bad alleles   45.13%
Mom passes bad allele   50.00%
Dat is het  9.50%
Dad passes bad allele   50.00%
Odds of 2 bad alleles   2.375000%
Mom passes bad allele   50.00%
Dat is het  9.50%
Dad passes good allele  50.00%
Odds of 1 bad allele    2.375000%
Mom passes bad allele   50.00%
Dad is diseased 0.25%
Odds of 2 bad alleles   0.12500%
Odds of 0 bad alleles   47.50%
Odds of 1 bad allele    50.00%
Odds of 2 bad alleles   2.50%


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Negative feedback loop and oscillations
According to the textbook Alberts Molecular Biology of the Cell (5th ed., p. 902), negative feedback loops cause oscillations when they are long delayed. I just can't figure out why.
Except for that, in case of short delayed feedback, the inhibition doesn't seem to be full and to go down only mid-way, according to the attached plot. Why?

It is nice to see that MOBTC has included some stuff on systems biology. The edition that I read did not have these.

For that you would need to understand the dynamical systems theory behind the loop. The point at which the oscillation starts is called the Hopf-bifurcation. I shall explain this in simple intuitive terms. Lets assume that Protein-X activates the production of Protein-Y which in-turn causes inhibition of Protein-X production. This is a negative feedback loop.
X → Y
Y ⊣ X
Situation-1: No/little delay
You switch on the production of X. This leads to rapid production of Y which will in-turn quickly repress the formation of X. This would happen so quickly and all that would be observed is a reduction in the steady-state level of X (compared to an unregulated system). Mathematically, the eigenvalues of the system (jacobian matrix- denotes the slope of the function) evaluated at the steady state would be negative and real.
Situation-2: Some delay
In this case, it will take some time for Y to accumulate. This will cause X to shoot up above its final steady state level. This, in-turn, will cause higher production of Y. Because of higher production of Y, X will start getting repressed strongly when Y gets accumulated and starts acting. This will cause X to shoot down below the steady-state but the magnitude of this shoot-"down", will be less than the first shoot-"up". Finally, the system will settle to the steady state. This phenomenon is called damped oscillation. In this case, the eigenvalues of the jacobian are complex with negative real parts.
Situation 3: long delay
In this case the delay between production of Y and its action is so high that the system does not damp but sustains its oscillations. The eigenvalues of the jacobian are imaginary. These kind of oscillations are generally sensitive to different factors.
More robust forms of oscillations exist, called limit cycles. The network structures responsible for this are more complex than a delayed negative feedback loop. Typically it has a coupled positive and negative feedback. Understanding limit cycles is little bit more complicated and I shall not discuss them here.

Also, check out these reviews:
Tyson, John J., and Béla Novák. "Functional motifs in biochemical reaction networks." Annual Review of Physical Chemistry 61 (2010): 219.
Tyson, John J., Katherine C. Chen, and Béla Novák. "Sniffers, buzzers, toggles and blinkers: dynamics of regulatory and signaling pathways in the cell." Current Opinion in Cell Biology 15.2 (2003): 221-231.
and this book:
Alon, Uri. An introduction to systems biology: design principles of biological circuits. CRC press, 2006. ISBN 9781584886426


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Good pipetting technique?
Good pipetting technique is essential for many biologists, but it can be hard to get right. When I take 1 µl of liquid using a micropipette, I seem to always take less than 1 µl, and that amount is variable/inconsistent. I would like to know what could be wrong.
What is the proper pipetting technique? Could it be that the pipette is inaccurate?

Welcome to Biology.SE. You should try to give more info about the moment at which you realize you did not piped exactly one microlitre. Do you see directly in the pipette that you did not pipette 1 microlitre. Or do you sometimes have some leftover in the pipette and sometimes not. Do you think the pipette you are using might be in cause?

I wouldn't be surprised if your pipette needs some service. Some of the parts (rubber rings) that are important for proper function wear out and need to be replaced every now and then.

I've retracted my close vote, good pipetting technique is essential in a lot of biology. General pipetting technique information would be of use.

This post can be made a community wiki but I'll leave that decision with the OP and @rg255

What pipette did you use? Using a 10-ml one won't help you. Use the smallest one you can find. Also, when you use one single pipette to combine all solutions  and that one pipette has a systematic error (i.e., calibration needed, but not done) then there is no issue, as it is all about relative volumes. If you use multiple pipettes to combine fluids into a reaction mixture, then trouble arises.

Here's some step-by-step advice on good pipetting technique:

Make sure the pipette is set for the correct volume
Ensure the tip is firmly attached
Keep the pipette vertical when pipetting
Slowly and smoothly depress the plunger to the correct point (the first stop position)
Insert the tip in to the liquid to be pipetted. Ensure the tip is properly immersed in the liquid, but not touching/near any surfaces of the container
Slowly and smoothly release the plunger back, keeping the pipette upright, and tip immersed, and making sure no bubbles form - you can try pre-wetting (see video linked below, around 3:00)
Withdraw the pipette from the liquid
Carefully dispense the liquid in to the desired container by steadily depressing the plunger to the second stop position (fully depressed), making sure all liquid is dispensed without spills or splashes.

"Put the tip in a 45-degree angle onto the wall of the container; then
  start pushing down up until the first stop; then push through to the
  second stop; keep the plunger depressed and remove pipette and check
  whether the drop is in the container and pipette tip is empty" -
  Christiaan

Discard the tip using the release plunger

Also check you've got the right size/type of tip, and are using a suitable pipette (e.g. don't use a 10-100 µl pipette for 120 µl)
If this still causes incorrect measures then you could need to get your pipette calibrated.
Test a pipette by taking several samples. If the pipetted volume is consistent but incorrect (e.g. always 10% under the target) it suggests the pipette needs calibrating, it's probably not the technique that's wrong. If it is inconsistent (both under and over pipetting) then it's either technique or the pipette (bad/damaged pipettes can be inconsistent, poorly but good calibrated pipettes will more likely be consistent and only need calibrating).
Try using multiple pipettes, if they are each consistent but variance is among them (pipette 1 is always under by ~10%, pipette 2 is always over by 15%, pipette 3 is always over by ~2%...) then your technique is good, and you need better pipettes. Also get an experienced pipetter to check your technique and try the pipettes themselves.
Calibration can be done internally by lab techs or by external specialists, speak to your lab responsible person.

Also see this video which is well explained.

Additional point: care should be taken while pipetting surfactants and viscous liquids. Surfactant containing liquids should be properly mixed prior to dispensing and mixing by pipetting just before dispensing (with the same tip) should be avoided. Multiple rounds of pipetting creates bubbles inside the tip and leads to picking up of lower volumes. Viscous liquids should be gently pipetted and care should be taken to not let the liquid stick on the exterior of the tip.

It's also a good idea to practice your pipetting with serial dilutions of colored compounds, then measure the absorbance of each one and plot it. If your slope is off, you need to keep practicing, or fix your pipettes.

It's been a long time since I held one, but ref. step 8) - shouldn't you always put the tip in a 45-degree angle onto the wall of the container; then start pushing down up until the first stop; then push through to the second stop; keep the plunger depressed and remove pipette and check whether the drop is in the container and pipette tip is empty? Then give a few small taps to the container to make sure the drop is at the bottom of the container?

first of all i need to disclose i work for Andrew Alliance, but i answer for the sake of providing information and not for commercial purposes. What you experience depends - as we measured with our robot - from the humidity in the environment. if you have 1 nL of liquid water evaporating inside the tip, becasue the environmental humidity is low, it will become 1 ul of water vapour above the liquid level, so your sample will go down by the equivalent of 1 uL. you can verify this phenomenon by extracting the tip from the liquid, recovering air pressure and keeping the humidity inside the tip, and re-aspirating the liquid. This is actually why calibration laboratories work at 70% ambient humidity...

Interesting detail, I have never thought about it.


text:
Is NADH found in all type of cell in human body?
Is NADH found in all kinds of cell in the human body? I am curious about microglia specifically.

Can you add some background; especially about microglia. Why do you suspect that microglia would be any different?

As NAD+/NADH is involved in both glycolysis and in the tricarboxylic acid cycle it is difficult to imagine any cell capable of generating energy not having some NADH. (Are there any cells that are not capable of this? Calcified cells such as bone?)
A quick internet search for ‘microglia’ and ‘metabolism’ indicates that microglia have energy metabolism and so I would expect them to have NADH. How much (compared to NAD+) would depend on their metabolic state.


text:
Output of clustalo on (1.2.1) on ubuntu 14.04
I am trying to align the following 8 sequences using clustalo on ubuntu terminal using the following command. But I am not getting the right output.
clustalo -i sequence.fasta -o output.clu

My input file issequence.fasta with 8 sequences I downloaded from BLAST
My output file output.clu

The output I was hoping for outputOnline.clustal
Also I would appreciate if some can tell me how to share this kind of data in a question because obviously the way I have done is doesnot seem appropriate.

You just need to specify the output format with the outfmt flag.
clustalo -i sequence.fasta -o output.clu -outfmt=clu

should give you the desired output.

How to share data?
Try using an abbreviated example which people can copy&paste, for longer data you could use something like http://pastebin.com/ but the URL might expire.

gi|1709777|sp|P51780.1|PRIO_TRIVU MGKIQLGYWILVLFIVTWSDLGLCKKPKPRPGGGWNSGGSNRYPGQPGSPGGNRYPGWGHPQGGGTNWGQPHPGGSNWGQPHPGGSSWGQPHGGSNWGQGGYNKWKPDKPKT
gi|1709773|sp|P52114.1|PRIO_MUSPF MVKSHIGSWLLVLFVATWSDIGFCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWGKPSKPKT
gi|1709774|sp|P49927.1|PRIO_PIG MVKSHIGGWILVLFVAAWSDIGLCKKRPKPGGGWNTGGSRYPGQGSPGGNRYPPQGGGGWGQPHGGGWGQPHGGGWGQPHGGGWGQPHGGGGWGQGGGSHGQWNKPSKPKT


text:
How do traits with no negative effects get "weeded out" via evolution?
If only those who are most fit to reproduce are the ones reproducing the most, it makes sense that traits that prevent one from reproducing would eventually disappear from a population.
But what about traits that have no effect on reproduction, like the presence of wisdom teeth? Humans don't need them, but they don't inhibit us from reproducing either. So how do humans evolve past the point of having wisdom teeth or other similar traits with no negative effects?

Maybe in some cases the expression of the trait with no negative effects is linked to one that is, so thereby if the organism is expressing the negative trait it would also express the non negative trait, and then that would be selected against. I am just a layman though, I would wait for a more clear response...

They DON'T. Remi's answer down there is pretty comprehensive, but it really should point out with much more emphasis that non-negative traits can remain in the populations for millions of years, if not forever, unless a random mutation+drift removes it, which is a pretty low chance event.

Following up on the comment by @Davor vestigial organs are an example of useless traits sticking around. Having an appendix won't help your offspring to flourish, but it won't diminish their chances either

Oops I wrote a lot! This is almost a very brief introduction to some concepts of population genetics.
A little bit of terminology first
Locus
A locus (plur. loci) is a position on a chromosome.
Allele
At a specific locus, different individuals may have different variants. One individual might be ATTCTA while another might be ATTCAA for example. These variants are called "allele". The whole goal of evolutionary genetics is to understand the creation (mutation) and change in frequency of the different alleles in the population.
Heterozygosity
You probably know that in many species, we carry two copies of each chromosome. One individual can therefore carry twice the same allele at a given locus or can carry different alleles. Expected heterozygosity ($H$) at a given locus is the fraction of the population that carries two different alleles at this single locus.
Fixation
When an allele reaches a freuqency of 1 (100%), that is only this allele exists in the population (and therefore the other alleles have been wiped out), we say that it has reach fixation.
Natural Selection
The process you describe in your first paragraph is called natural selection.
Natural selection is a fitness (=a function of both reproductive success and survival) difference between different genotypes. As you said (but with other words), deleterious alleles will decrease in frequency through time and will eventually end up being weeded out from the population through natural selection.
Genetic Drift
There are other evolutionary processes than natural selection. Typically, the one we will be interested in to address your question is genetic drift.
What is genetic drift?
Genetic drift refers to the random sampling of a population in order to build up the next generation population. There are different ways to model genetic drift (Wright-Fisher model, Moran model, coalescence model) but without having to talk about the details of these mathematical models, it is important that you can conceive the role of random sampling in the change in allele frequency through time. For this, I invite you to first read Why is the strength of genetic drift inversely proportional to the population size? and when you have finished, come back to this post.
One the below figure, you can see the effect of drift through time. The below graph consider a bi-allelic locus (a locus where 2 and only 2 different alleles exist in the population) starting with an initial frequency of 0.5 (=50%). Each line is a separate simulation and shows the frequency of only one of the two alleles.

The above graph considered a population of size $N=100$ individuals. Below, the same types of simulation with a population size of $N=25$ individuals. As you can see that the genetic drift is stronger

Every single locus is subject to genetic drift whether it is under selection or not. However, if a locus is under strong selection, then genetic drift with have little power to explain what allele will get fixed in comparison to when the locus is neutral.
Genetic drift and loss of alleles
It is clear from the graph above that genetic drift also wipe variant out of the population. We just don't know for sure which variant will be wiped out. To be more accurate, the expected heterozygosity due to genetic drift is reduced by a factor $\frac{1}{2N}$ each generation. One can make plenty of calculations from basic models of genetic drift. For example the expected time to being wiped out is $\bar t(p_0)=-4N\left(\frac{p_0}{1-p_0}\right)\ln(p_0)$, where $p_0$ is the starting frequency of the allele of interest.
A interesting result is that the probability of an allele to reach fixation is equal to its frequency. If there are $N$ individuals in the populations, there are $2N$ alleles (but not $2N$ different alleles). If there are, say 235 alleles A in the population and $2n - 235$ alleles B in the population, then over the long run (so that one will necessarily fix) the probability of fixation of the allele A is $\frac{235}{2N}$ and the probability of fixation of the allele B is $\frac{2N-235}{2N}=1-\frac{235}{2N}$.
Wisdom teeth
In your question, you are interested about a supposedly purely neutral locus. You talked about wisdom teeth I suspect more as an example rather than because you are interested to this trait.
Let's assume that the presence of wisdom teeth is completely neutral. Note by the way that as a rule of thumb if $2 N s << 1$, (where $s$ is the selection coefficient on a given allele) then the allele will behave essentially as if it was a neutral allele. So, if wisdom teeth is neutral, then the probability of this trait to disappear over the long run depends on the frequency of the allele causing this trait. So far, I have assumed that we were interested in a single locus only. In reality, variation in many traits are caused by variation at several loci. In such case calculations are a little less straight forward (but still feasible). I do not know the genetic basis of wisdom teeth, so I cannot make good predictions for the evolution of this particular trait.
Other evolutionary processes
Here are a few example of interest
Gene flow
Note of course that there are other processes to consider when trying to predict the fate of a given allele or trait. For example, in a given population you might have a flux of migrants that come from a population where one allele is fixed therefore affecting the allele freuqency in the focal population. This is called Gene flow.
Hill-Robertson effects
Never forget that a locus is not alone on its chromosome. It is physically linked to other loci and selective pressures at other loci will affect the allele frequency at the focal locus. This is called Hill-Robertson effects.
Mutations
Of course, when a locus is not polymorphic (has only one allele), mutations is the ultime source of variation. When a locus is polymorphic, then it is likely the mutations will have a minor effect on the allele frequency (although it depends on the size and type of locus and depends on whether mutations can make up new functional alleles).
Pleiotropy and covariance between phenotypic traits
Phenotypic trait do not evolve independently. If wisdom teeth is a consequence of the activation of the molecular pathway for resistance to HIV (which it very probably is not), then wisdom teeth will not evolve as a neutral trait. A locus that affects several traits is said to have pleiotropic effects.

You are correct in thinking that traits that improve (impede) ones reproductive rate should be spread through (removed from) the population by selection. However, the process of evolution rests upon more than just selection.
There are four mechanisms by which evolution operates; mutation, migration, drift, and selection. Mutation brings new variation in to populations, with changes occurring in the DNA (e.g. an A becomes a T in the genetic sequence). Migration can both add and remove variation from populations, but is a within species mechanism of evolution (by definition there should be no genetic migration between species). Drift is the change in genetic variation that comes from random variation in reproductive success. With drift there is no link between the genes and the rate of reproduction, i.e. carriers of one allele are equally likely to reproduce equally well as carriers of alternative alleles.
Selection operates when there is covariance between reproduction (fitness) and the genes one carries, i.e. there is a tendency for the carriers of one allele to produce more offspring than the carriers of an alternative allele. This might arise because, for example, the gene improves fertility.
When you are considering the evolution of neutral (or nearly neutral) traits you are considering evolution via the first three mechanisms (mutation, migration, drift). Small populations are prone to losing genetic variation by drift more so than large ones, here is a simulation of 10 populations over 250 generations, where the population size is 200 on the left, and 2000 on the right. You can see that the smaller populations have a higher tendency for fixation of one allele, this is with no selection occurring.
Many neutral traits persist for many generations because it is just a lottery, eventually they should be lost from the population, but we can't tell when.

Furthermore, the genes that cause neutral variation may be under no direct selection, but could be in linkage with loci under selection, thus be affected by indirect selection, or they could have multiple effects (pleiotropy; e.g. the gene causing the expression of a neutral trait also affects the expression of a selected trait).


text:
Species Identification: Waterborne larvae, Texas USA
Can you help identify this worm?
It was found in a cup of water at a restaurant (unpleasant, yes), likely came through the water system. (Location: Texas)
Found these images of it online (in which they were also found in water systems - dog bowl, sink), but none of the sites identified it.
Significant features: black head, black pointed tail, clear body with grayish intestines visible, tiny (2-3 mm)
Similar larvae that don't match:
-Mosquito larvae
-Midge larvae
Any insight is appreciated, including if you are familiar with similar looking larvae. Thank you.

The larvae are moth flies (Psychoda sp.)

The black head, black pointed tail, clear body with grayish intestines visible and also their small size 2-3 mm can be seen on both pictures.
Where they can be found in nature:

In nature, moth fly larvae, Psychoda sp. (Diptera: Psychodidae) normally occur in aquatic habitats that experience intermittent submersion or flooding. The larvae develop in polluted, shallow water or highly moist organic solids where they feed on decaying organic material in mud, moss or water.

Where they can be found in households:

In homes, the adult flies, which resemble tiny moths, are most likely found on the walls of bathrooms, kitchens, basements and other locations where sewer drains and plumbing fixtures are located. The flies are poor fliers and usually are found close to the drain or area from which they came. Moth fly larvae are known to live in drain traps, garbage disposals, toilet tanks, sides of drain pipes and overflow pipes in homes, wet areas around leaky pipes, sewer lines, and septic tanks where they feed on stuff that might accumulate in such areas. The moth flies that live in Michigan do not bite and are not known to transmit disease of any sort.

What to do against them:

The best way to control moth flies is to eliminate or reduce the larval food sources by thoroughly cleaning drain lines and plumbing fixtures. Pouring boiling water down the drain where larvae are suspected to be may help to reduce their numbers. Adults can be controlled with the application of a household aerosol insecticide (like Raid) or a good flyswatter. Be sure to read and follow all instructions and safety precautions found on the label before.

There are various other methods which are far more precise, listing how to eliminate moth flies from drains.

But what happens if someone drinks them along with water?

@rishabbairagi I suppose that your stomach acid can deal with them, worst case scenario would be internal myiasis which could cause cramps, vomiting and diarrhea,.

@JordiZambrino My concern is that the article you quote only says they are found near dirty water, nothing you'd want you to drink. If your drinking water is full of maggots, what other pathogens are floating around in that?

@user137 Pathogens that would be floating around in drinking water; I'd suggest they could be MSSA and MRSA Staphylococcus aureus

These are moth fly larvae (Psychodidae). They live in sinks, bathtubs etc. See
http://bugguide.net/node/view/201443/bgimage

Please include an image that shows this is the right ID, as well as additional supportive evidence, such as that its distribution overlaps with the location of OP at the time of sighting etc.


text:
Speciation of humans?
Since we homo sapiens (and all other species) are continuously evolving, are humans undergoing speciation based on our environment? OR has there been any difference across people that could say speciation has already happened?
PS: I am asking this question because I have recently seen a documentary in which some Chinese anthropologists claim that Chinese people are a different species altogether. Ref: Incredible human journey (Section Asia)

We are continuously evolving and a speciation could occur, but, by any definition of species that I am aware of, all populations of humans can be considered one species - generally accepted that for two to be considered different species they should not produce viable offspring (though as you alluded to in your other Q - speciation borders are hazy)

From the wiki entry: "The study initially hypothesised that the modern Chinese population evolved from Homo erectus in China but concluded that the Chinese people did in fact evolve and migrate from Africa like the rest of world's population."

Are you asking if Homo sapiens is undergoing speciation right now?

See also Does it make sense to classify all humans in a single species?

While its possible humans could speciate into two distinct groups at some point in the future, it hasn't happened recently (100 kya) and it doesn't seem to be happening now. If it were happening we would see two or more distinct populations that didn't interbreed and over time accumulated increasing differences.
These skin colors track most of the evolution we've done in the last hundred thousand years or so, and none of the people from different parts of the globe have any difficulty reproducing with any of the others. If speciation is happening it hasn't happened yet. I doubt speciation could happen given how much gene transfer there was between populations just on foot and boat, never mind planes and trains. Although, speciation does not require physical isolation to occur. See Wallace Effect and sympatric speciation. If there's enough pressure agaist hybridization, human speciation could occur. Think blue collar versus white collar worker and the disappearing middle class.
Speciation has certainly happened with humans before. Not with 'evolutionarily modern' humans, but 'evolutionarily modern' is mostly defined as 'humans since the last speciation event', so that's tautological. But Homo erectus, the neanderthals, the denisovans, et cetera(seriously, there's a lot of Homo species) were all descendants from one common ancestor.
As for the idea that Chinese people are a different species, or descended from Homo erectus? See the geneticist from the documentary who mapped out the genetics of the Chinese population. Archeological and skeletal evidence is easily blurred, but the genetics can't be explained without an out of africa theory.


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What's the correct name for the war of sexes in evolution?
I'm searching for the correct term for the part of the selfish gene evolution regarding sexes. In nature, this means the evolution of the traits such as the ducks' adaptation to "trap" the drakes' penises in order to restrict the male from attending to other females.

Sexual dimorphism  (?)

The correct term is sexual conflict (but if you see my answer you will see that sexual dimorphism is related) @SciEnt

Sexual Conflict is the word you are looking for!
Sexual Conflict occurs whenever the optimal mating strategy for the female and the male differ. For example, in Drosophila, it is beneficial for a male to mate as much as possible, while it is beneficial for a female to mate only a few times.

That's true of most species, where reproduction is extremely energy costly -- compared to insemination.

I would like to expand a little on Remi.b's answer and point out that there are two key forms of sexual conflict.
Sexual conflict arises when the sexes have different routes by which they maximise fitness.
In the case of the ducks (and many other species) the males increase fitness by mating as much as possible, whereas females may optimise fitness by slowing the males rate. These sorts of conflict where behaviour or phenotype of one sex is beneficial to one sex and harmful to the other is called interlocus sexual conflict: the effects of one locus have consequences for other loci. The bed bug is a fantastic example of coevolutionary dynamics between the sexes resulting from interlocus sexual conflict - males use traumatic insemination and females appear to have made multiple adaptations in response.

"In inter-locus sexual conflict, the sexes experience opposing selection pressures on one or more traits, but the genes affecting the expression of the trait probably differ between the sexes."

Alternatively there is intralocus sexual conflict; when the evolutionary interests of either sex differ within loci. In this case selection favours different alleles in either sex. Genetic covariance needs to be reduced for the sexes to be able to move towards their own phenotypic optima, with such sexually antagonistic selection leading to sexual dimorphism when covariance is reduced.

I wasn't aware of these terms. Was worth expanding on my answer +1


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Is there a difference between macroevolution and group selection?
I encountered two different attitudes towards macroevolution:

The first one included long-term microevolution such as the evolution of Cetacea.
The second one included only macroevolution in terms of group-selection - that is for example the evolution of altruistic behaviour (the groups - families or tribes survived more likely if they were altruistic and shared the resources).

What about for example evolution of the parental instinct? Would it be considered a macroevolutionary (because it is about the evolution of families) or a microevolutionary trait?
And in general, am I getting macroevolution right with the second attitude?

Your first definition of macroevolution is correct. Macroevolution is really not specific to group selection but included any evolutionary process (including neutral  processes).

Can you please link to where did you encounter the term macroevolution that excluded any process that was not group-selection? I suppose it was a paper talking about long term consequence of group selection but while focusing on that, they probably did not want to exclude other processes from the definition of macroevolution.

Is there a difference?
Yes, they are quite different things.
What is group selection?
Group selection is an view of evolution where selection acts at the level of the group, rather than the individual. It suggests that selection is mediated by fitness of the population, and leads to conclusions of things occurring for "the good of the species". It is generally excepted that group selection arguments can rarely be invoked (but see haplodiploid social insects and kin selection). There is a long and controversial history to group selection and it's well worth reading about in further detail if you are interested in the history of science!
What is macroevolution?
Macroevolution is the evolution which occurs at larger scales, things like speciation, extinction, and the history of life. It often involves comparing species or lineages for example.

"Macroevolution generally refers to evolution above the species level."

Microevolution on the other hand is, generally considered, evolution which occurs within lineages, or (more often) within populations. Researchers of microevolution would consider problems of adaptation for example.

"Microevolution is evolution on a small scale — within a single population."

Macro- or microevolutionary trait?
I've never heard anyone refer to something in this way, traits can be studied in both micro- and macroevolutionary contexts.


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Can I figure out the identity of my grandparent from this information?
I know all my family up to my grandparents, with the exception of the grandfather on my mother's side. At the time my mother was conceived, my grandmother was having an affair so no one in my family knows for sure who the grandfather was.
In high school we learnt that blue eyes are a recessive trait and brown eyes are a dominant trait, as such I should be able to figure out who my grandfather is, but I only studied up to that level and I want to check with someone more knowledgeable than myself if it is correct.
So here's my reasoning:
I have blue eyes, meaning I have two blue eyed genes and got one from my father and one from my mother.
My mother has brown eyes, meaning that she has one brown eyed gene and one blue eyed gene to pass it on to me.
My grandmother has blue eyes, so she passed one on to my mother.
One of my potential grandfathers had blue eyes, so if it had been him my mother would have received two blue eyes genes and have blue eyes. But she has brown eyes so it must be the other potential grandfather (who's eyes I don't know the colour of).
Can someone tell me if this is correct, and if not, why not?

All of your grandparents could have been brown eyed. Your having blue eyes only requires that one grandparent on the maternal and one on the paternal side were carriers. Note though that eye colour is not as simple as dominant and recessive.

Related: Is it possible for a brown eyed parent to have blue eyed child?

You are trying to work out who your mother's father was. You know that your mother's mother had blue eyes, but your mother had brown eyes. You also have blue eyes. You make an assumption that eye colour is a Mendelian trait, with a dominant brown allele (A) and recessive blue allele (a) such that AA and Aa are brown-eyed, while aa gives blue eyes.
To have blue eyes you must have gotten an a from each parent, so your mother (who is brown-eyed) must have been Aa. You know that her mother was aa, because she had blue eyes. Your mother must have inherited her A from her father, therefore, your mother's father had brown eyes.
Can this information identify your grandfather? Maybe, depending on the list of candidates (e.g. you have two men and you know that one of them is the grandfather, and one has blue eyes, the other has brown eyes). However, it's based on an assumption that eye colour is a Mendelian trait, with a dominant brown-eye allele and recessive blue-eye allele, and that a mutation has not occurred which gave your mother brown eyes. That assumption is flawed, eye colour is not Mendelian (it's polygenic), and you cannot rule out mutation in eye colour genes. That said, you are more likely to resemble the people you are more closely related to, so resemblance in eye colour could offer some clues (as would other easily visible characteristics like skin type, hair colour, hair type, facial features, height, physique). In short, you cannot identify your biological grandfather by eye colour, but it may give some slight indication.
See also:

Blog post on eye colour genetics (with referenced papers here and here)

One of my potential grandfathers had blue eyes, so if it had been him my mother would have received two blue eyes genes and have blue eyes.

No, this does not necessarily follow, because eye color genetics are more complicated than just one dominant-recessive gene. See, for example this article from a someone at  Stanford University on How Blue Eyed Parents Can Have Brown Eyed Children. It isn't common, but apparently it does happen.
Solving your inheritance just based on eye color with 100 percent certainty is not possible.

On a high-school level you are right. Still, the answer to your question is no.
As you may have already noticed, nothing in reality is as simple as schools tell us. Eye colour is generally determined by one gene, but there are other genes which can modify the effect. Think about this question: if there were just two alleles, blue and brown, where would green-eyed and grey-eyed people come from?
If you want to investigate your who is your biologic father, you can ask them both to take a genetic test. If they decline or cannot comply, try comparing many traits, not just one. Ask for photographs of you mother and both possible fathers when they were your age and make a list. What is everybody's hair colour? What is their height? What is the shape of their faces? the proportions of bodies? the skin colour? shape of mouth, nose, eyes? Do you know everybody's blood type? Maybe you just look a lot like one of the men, then you can assume he's your father. Maybe you look a lot like your mother and there are only subtle differences which point to one of the men? Remember that this comparing does not give you certainty, only clues.


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What is the difference between options protein and replication in the NCBI database?
After checking the NCBI help page, I am still unclear about the difference between protein and replication interactions for HIV.
http://www.ncbi.nlm.nih.gov/genome/viruses/retroviruses/hiv-1/interactions/

I'm not entirely sure what you're asking. What is your specific question? That help page seems clear enough.

What is the difference between options protein and replication

I've suggested a pretty major edit. Feel free to role back, but I think the question is much clearer now.

These edits provided by users are good, perhaps the OP could add what their interpretation of the two terms are so it is easier to identify where the misunderstanding is.

what is OP?????

@Rishika You are OP=Original Poster i.e. the person who starts the thread. In SE this just means the asker.

Interactions denote protein-protein interactions, which means physical association between proteins. By nature, these networks/graphs are undirected.
Replication interactions (actually a not very good term) denote gene regulatory interactions that affect HIV replication. These sets also include the regulatory effects of HIV genes on host genes (and hence the terminology is unsuitable). These networks are directed as well as signed (positive or negative interactions i.e. activation or inhibition respectively).
You can see for yourself, from the dropdown boxes and the interaction lists in this page.

So its basically just PPI not leading to virus replication versus PPI that lead to virus replication??

@Rishika in the PPI networks the final outcome is not considered. The "replication" interactions are more about proteins regulating transcription (which happen basically via protein-DNA interactions).


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Why aren't gene drives extremely common?
The ability for gene drives to sidestep the Mendelian mechanism and rapidly spread through populations (even if the gene is slightly fitness reducing) is extremely powerful. Why aren't normal populations riddled with parasitic gene drives?  What mechanism keeps naturally occurring gene drives suppressed to (apparently) very low levels?

You are going to need to provide references to back up the claim in your first sentence. If you mean this, it is because you need to edit the genome of the organism in order to accomplish the task.

Yes, by "gene drives" I mean "gene drives".  As described by Wikipedia.  To introduce new artificial gene drives you need to edit the genome of organisms.  But gene drives also occur naturally. (Mentioned here, for example.) The question is, why don't these dominate? Edits made artificially by experimenters can also occur naturally.  (Or if they can't, why?)

From what they are describing, this is double-stranded break repair. You need a break to occur in the locus of the gene for it to happen. And as only about 1.5% of the human genome is protein coding, random breaks are more than likely not occurring in genetically important regions. For it to happen non-randomly you need an endonuclease to make a break in the chromosome. There are a few examples or genes where this occurs naturally, but more often times you see it as a viral mechanism to integrate into the host chromosome. It is estimated that upwards of 8% of the human genome is viral DNA.

And to be passed on, all of these changes need to occur in germ line (sex) cells. If they occur in somatic (body) cells, then either they will be killed by the immune system if they are deleterious, or they will just sit there until the organism dies and they are lost.

OK, but double-stranded breaks occur naturally, and you only need a handful (or even one) gene drive created through chance to take over a population.

Not without endonuclease activity. There is meiotic recombination that could easily delete the driver in the next generation, assuming that the gamete that had the mutation fertilized/was fertilized to form an embryo. Also if a gene is not under selection, especially when it comes to duplications, they rather quickly become pseudogenes through genetic drift. If the random driver confers a significant survival or reproductive advantage, then natural selection will select for it, otherwise it has far less of a chance of being maintained than the wild-type gene, as it is just a numbers game.

Are you saying breaks don't occur spontaneously without endonuclease?

Are you referring to the same thing as meiotic drive?

Spontaneous ds breaks occur and are repaired, but there are billions of possible locations that they can occur in higher Eukaryotes, so the odds of those breaks occurring in a productive way in the germ line without an endonuclease to specifically localize the break are slim. Also, there are other DNA repair mechanisms that do not go through Homologous recombination, such as non-homologous end joining, or even apoptosis (cell death) due to chromatin damage, that too reduces the probability even more. The key to the technology for synthetic drivers is specific breaks and providing template DNA.

Ok, you have started to sketch an answer, but its still not at all clear that those suppressive effects are nearly sufficient. Analogously, there are many ways that cells repair DNA and protect against cancer, and if you just listed those mechanisms and said "therefore it's highly unlikely cancer will ever develop", you'd be wrong. In the case of cancer, one can argue that the suppressive mechanisms will drive the rate to be low enough to allow procreation, but for gene drives there is no such argument (unless you go with group selection).

Compare: "The only way you can have a de novo mutation in the species is through a spontaneous event in the germline, and the chance that this would lead to anything useful is slim. Furthermore, there are lots of DNA repair mechanisms the cell uses which reduces the probability even more. Therefore, usefu de novol mutations cannot appear in a species."

I have a feeling that the OP is confusing naturally occurring so-called selfish, or parasitic genetic elements and the CRISPR/Cas9-based gene drives that have been making news as potential tools to eradicate disease vectors like the aedes mosquito. My answer is working from that assumption.
The big difference between naturally occurring "parasitic" genetic elements (including bacterial CRISPR elements and things like transposons) and the gene drives that are being tested as vector control revolves around what we put inside the latter class of gene drive.
The OP hit on this difference in his question, when he mentioned the decrease in fitness caused by engineered drives. In the naturally occurring drive-like elements, there is rarely ever a decrease in fitness in the organism and when it does occur, it is unlikely to be passed on to future generations.
Transposons, for instance, are largely active in somatic cells, whose DNA is not passed on to descendants. Semi-randomly occurring genetic changes are sometimes passed on, but this is relatively rare and evolution favors those that are either neutral or that increase fitness. A brief search doesn't turn up, and I can't think of, any cases of naturally occurring deleterious genetic alterations caused by something like a transposon having been found to remain in a population long enough to be studied.
Engineered gene drives, on the other hand, particularly in the cases of those meant to combat mosquitos, are purposefully designed to reduce the fitness of their target host.
The last question, of what keeps naturally occurring drives at low levels, requires either a rather vague, or a very long answer. I'll go with vague and provide some links to longer ones. Briefly, our genomes have evolved a lot of ways to maintain genomic integrity, in the forms of proteins responsible for proof-reading DNA, repairing breaks, and destroying any "free" pieces of DNA found outside of a chromosome. We've also evolved a lot of mechanisms to maintain genomic integrity through small non-coding RNAs.
Here are some good papers (without paywall) on the subject:

How p53 restrains mobile genetic elements
Proteins that function to restrain mobile genetic elements in rice
Good review of transposons in general
Finally, how people are engineering gene drives to combat malaria

Hope that helps!

Thanks very much for your answer.  In my defense, I don't think I confused anything so much as I just didn't state my question in the standard terminology.  This obviously is not my field, so thank you for filling in the gaps of my knowledge and answering the clearer version of my question.  Your paragraphs 2-5 point out that most naturally occurring parasitic gene elements have neutral, rather than negative, effects on fitness.  This is useful to know and much appreciated, but of course it just makes my question more pointed.

Paragraph 6 sounds to be essentially the sketch of an answer described by AMR in the comments on my question.  It may be that there simply isn't a clean, precise answer known.  But, as I pointed out there, an analog of this sort of argument exists for cancerous mutations, yet cancerous mutations are common.  And it does not explain the essential mechanisms by which lab-engineered gene drives can avoid these natural protections which are apparently so effective against natural parasitic genetic elements.

@JessRiedel - sorry for the radio silence. With respect to your original question, I wouldn't think of cancerous mutations as a 'gene drive'. Most cancers only occur after child-bearing age, so doesn't have much of an effect on an organism's fitness. That holds for both hereditary and acquired mutations, the latter requiring a long time to develop. Exceptions, like childhood leukemias, are interesting but quite rare.

Regarding lab-engineered gene drives, I doubt that they avoid cellular defenses, although it would be hard to measure that. Essentially, they overcome defense mechanisms by being targeted to a specific site and by carrying active payloads. That is, when they integrate, they do so in a functionally important location and deliver genetic code that has a measurable effect. This does not hold for many transposable elements. Although sometimes an endogenous TE gets lucky: http://www.the-scientist.com/?articles.view/articleNo/32298/title/Jumping-Genes-a-Cause-of-Cancer-/

To be clear, I am not considering cancerous mutations to be gene drives.  I was drawing an analogy between (a) the explanation suggested here for the rarity of naturally occurring gene drive with (b) an argument that cancerous mutations should not arise.  We know that (b) does not actually rule out cancer, so it would seem that, without further detail, (a) does not rule out widespread natural gene drives.


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How is the subunit molecular weight different from the native molecular weight?
I noticed that the native molecular weight for an enzyme is different from its subunit molecular weight. Why are they different? Aren't the genes needed to express the enzyme the same in the native organism and in the heterologous expression system?
Does the heterologous expression system happen to affect the molecular weight of the final enzyme product? If so, how?

Can you provide a source? It could be listed differently for a number of reasons

Can you please say about which enzyme you are talking? And what is the heterologous expression system in this context?

This paper: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065158/ Table 3 in page 3. Please help me. I am very confused with the terminology and how expressing an enzyme from Neurospora crassa in E. coli makes it have a different molecular weight than if it was in its native Neurospora crassa.

Your question is answered in the paper, the protein likely exists as a homodimer in vivo and denaturation (such as performed with SDS PAGE -> Western Blot) separates the dimers into monomers:
"To determine the quaternary structure, size exclusion high-performance liquid chromatography was performed using an Agilent 1100 series high-performance liquid chromatography system with a Bio-Sil SEC-250 column (300 by 7.8 mm) and a mobile phase of 0.1 M Na2PO4, 0.15 M NaCl, and 0.01 M NaN3, pH 6.8. A Bio-Rad standard was used to standardize the column's retention time with respect to molecular mass (supplemental data). All experiments were repeated twice with <0.05 min of deviation in the retention times. The molecular mass of XR was calculated from its retention time to be ∼53 kDa. Monomerization could be induced in the presence of 15% SDS, causing XR to elute as a single peak, with a retention time corresponding to a molecular mass of ∼34 kDa. The data suggest that the native XR is a noncovalently linked dimer. The significant difference between the calculated molecular weight of the dimer and its apparent molecular weight is not uncommon for XRs from other species (7, 21, 33), which also typically exist as dimers. However, to be certain of the protein size, N. crassa XR was subjected to mass analysis by electrospray ionization-quadrupole time of flight mass spectrometry. The highest abundance peak had a value of 38,381 m/z, corresponding exactly with the predicted molecular mass for the His6-tagged XR with the N-terminal fMet removed (supplemental data). Additionally, a 2M+ peak of about 20% abundance at 76,759 m/z corresponds well with the predicted mass of the dimeric form of the enzyme (76,762 Da)."

Also, smaller differences are common when eukaryotic proteins are expressed in bacterial systems due to differences in post-translational modification (esp glycosylation).


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Species Identification: Snake, New Mexico
The snake is about one and a half inches in diameter at its widest, a half inch at the head, and about two feet long. I found it in central New Mexico. It's hard to see the head in the pics, but it wasn't triangular or any bigger than the body/neck

did you notice whether the snake was a fast mover?

@rg255 yes, very fast

Coachwhips seem to be noticeably fast

It's difficult because the image quality is low, but there are some key features that can be made out which suggest it to be a Western Coachwhip, or "Whip snake", Masticophis flagellum testaceus.
There is not a huge number of species in New Mexico, and most have quite clearly different patterns and coloration, which brings it down to just a couple of species. With respect to colour and pattern, the main candidates are Western Coachwhip, New-Mexico Ridge-Nosed Rattlesnake, Mojave Rattlesnake, and Prairie Rattlesnake.
We can rule out the rattlesnakes because of the shape of the pupil; like most poisonous snakes, the rattlesnakes all have a "cats-eye" pupil, while in the second picture of yours it's fairly clearly a round pupil, which is a feature of the Western Coachwhip.
The slender head is a very telling feature that suggests Coachwhip.
The length is also about right (I'm going to suggest though that the one in your photo is perhaps more than 2 feet/60 cm - it looks bigger to me using the surroundings as relative measures); Coachwhips are in the region of 1-2 metres (3-6 feet) when fully grown.
The range is also perfect for the Western Coachwhip, though Sonoran Coachwhips are also found in southern areas of New Mexico. However, you list this as central New Mexico, so that virtually rules them out.
It seems, given that your picture is in the daytime, that it is diurnal (unlike many species in New Mexico which are nocturnal).

I'm bad at estimating length, thinking back, it's very possible it was closer to 3 feet or a little more

From the picture on your link to nmherpsociety.org, it's definitely the Western Coachwhip. I didn't even know we had these snakes here. Thanks for the research and the answer!