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Alternatives to fittest-win and Moran processes as simple mathematical models of selection
When modeling selective sweeps as a micro-building block in models of macroevolution (not to be confused with misuses of this in creationist arguments), I use the fittest-win model of selection as a first approximation, or Moran process model when I want a more reasonable approximation.
In the fittest win model the probability for a mutant of fitness r to invade a host population of fitness 1 is 100% if r > 1 and 0 otherwise. In the Moran process model, the mutant of fitness r invades with probability $\frac{1 - r^{-1}}{1 - r^{-n}}$ for a finite population. Alternative in the limit as n goes to infinite, a mutant with r > 1 invades with probability $1 - \frac{1}{r}$ and 0 otherwise.
In general I am interested in simple models of selection of a single (or small concentration of) mutant invading an asexual host population of fitness 1 (with fitness constant and independent of frequency). Are there other common mathematical models for selection of this type?

I may suggest to give a look to game theory based model and their generalization from homogenous spatial diatribution to network like model. An easy review can be found in Martin A. Nowak's Evolutionary Dynamics (Harvard press 2006).
In particular you can see the classical Moran process as an evolutionary graph game going on a complete graph with identical weights. Changing the topology of the graph can give different results, though it is not necessary (and there're results showing in which case a graph behave just as a Moran process).
Graph related behaviour are, i.e., suppressing or amplifier of selection...


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Why dont "growing degree days" have units of degrees Celsius (or do they)?
From Wikipedia:

Growing degree days (GDD), also called growing degree units (GDUs), are a heuristic tool in phenology. GDD are a measure of heat accumulation used by horticulturists, gardeners, and farmers to predict plant and pest development rates such as the date that a flower will bloom or a crop reach maturity.

GDD is calculated as $\frac{T_{min}-T_{max}}{2}- T_{base}$ - so a quick check of the units would indicate that they are in the same units as T, i.e., degrees C. However, they are usually presented without units.
Why is this?

Actually, the units are °C days   or °F days. The units are mostly given in the typical name, Growing Degree Days where which temperature unit is meant is understood from the context.  Much more important is knowing the base temperature ("T_base") since this value can be different in different usages, even for the same type of organism.

source: Stack Exchange

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

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Can a living organism run on electricity?
Each time I'm too lazy too cook I think it'd be cool to be able to just plug myselt into an outlet. Yet I know it is not possible - I need amino acids and a lot of other stuff that electricity can't replace.
Can some simple organism live on electricity alone or is it just fundamentally impossible?

The cells would have to produce glucose directly from electricity. If we figured that out we could also solve our energy crisis.

I don't see how producing glucose from electricity solves the energy crisis; I would have thought that we want to produce electricity from glucose (efficiently) to do that.

I was mainly making a reference to the storage issue with clean energy generation.

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


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Computational/mathematical models for predicting phenotype from genotype
Karr, Sanghvi, et al. (2012) propose a whole-cell computational model for predicting phenotype from genotype in Mycoplasma genitalium. Their model simulates myriad cell processes such as DNA replication, RNA transcription and regulation, protein synthesis, metabolism and cell division at the molecular level over the life-cycle of the organism.
They achieve this by combining many existing mathematical and computational models into one piece of software. The article suggests that this is the first comprehensive whole-cell model at the molecular level in detail. They cite previous molecular-level models for their sub-modules, but don't go on to discuss more coarse-grained genotype-to-phenotype models. Their model is exciting, but the 10 hours of simulation on a top-end computer cluster to follow the life-cycle of a single organism is unreasonable for someone who wants to study evolutionary processes.
Are there prior reasonably accurate computational (or even better, analytic) genotype-to-phenotype models? If there are, what are some of the best coarse-grained genotype-to-phenotype models for commonly studied organisms such as E.Coli?

The Karr et al. paper attempts to capture most of the details in their model by combining features from the genome, transcriptome, proteome, and metabolome. This work heavily builds off of the coarse-grained models that you ask of especially on the work from Bernhard Palsson from which Markus Covert did his training. The answer to your question rests entirely on the type of question that you seek and what you want the model to do.
For the most part, most of your questions can be answered using COBRA, the COnstratins Based Reconstruction and Analysis Toolbox. You can get a good idea of what genotypes can be knocked out and see how it affects the phenotype as long as the phenotype is a known pathway that gets affected by that gene and you don't care about temporal and dynamic information.
There is also the E-Cell Project for E. coli. I personally don't know much about it but it has created some basic models for E. coli and that may be good enough.
If you want to build your own models, you should check out BiGG where all of the large-scale reconstructions exists. A good chunk of the code is stored at the Palsson lab website where you can attempt to use COBRA and start generating your own hypotheses.

The questions I seek are ones of micro and macro-evolution with more realistic models of genotype-to-phenotype mapping. I come from a background in EGT where the distinction is virtually non-existance. Your answer is very helpful, but I don't understand how it is about more coarse-grained models, aren't these models also at the molecular level?

I assume EGT is evolutionary game theory?

@ArtemKaznatcheev, I'm not entirely sure how you would be able to achieve any sort of genotype-phenotype mapping without having some molecular element in the modeling. Clearly, I misunderstood your question.

@ArtemKaznatcheev the paper you cited describes a model that uses many different molecular phenotypes to build a 'model' of whether cellular functions are affected by gene perturbations. Bob has cited several viable options for you to do a simplified model in E.coli, however if these do not help in answering your question then it may need re-phrasing.

@Luke in the question I ask what are some of the best coarse-grained genotype-to-phenotype by coarse-grained I mean more coarse-grained that the paper. In other words, something that doesn't go as far into the details as tracking at the molecular level. If no one suggests such a model then after a few days (and some more extensive search on my part), I will accept Bob's answer.

@ArtemKaznatcheev Ok, but I don't really see how you could quantify the effect you are having on the outcome without making a specific change at the molecular level. What is it you would actually like to measure, and what it is you would actually like to 'alter' to see an effect? Thanks!

@ArtemKaznatcheev, For a coarse-gained approach, I would still suggest looking at the molecular models and then placing constraints around key pathways using FBA. For the most part, a lot of those components can be treated as a "black box".


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How does one measure the length of telomeres?
My questions are:

What techniques are available for doing so?
Are they destructive ?
What is their accuracy ?

Again, not an expert, but I found this article seems to say it pretty well:
Telomere's are most commonly measured by qPCR of the repetitive regions with degenerate oligomer sequences such as "TTAGGG and CCCTAA repeats"  Although articles like this one appear to advance measurements in vertebrates, this reference from 2011 implies two techniques continue to be most common:
1) qPCR with the appropriate oligos and then running them on an agarose gel
2) Southern blot of a restriction digest that leaves the telomeres intact
Clearly sequencing techniques don't do well with repetitive sequences such as this, so in general this still seems like the most common method.
This would indeed be quite destructive, at least for the cells used, though a biopsy would be enough, though apparently micrograms of DNA are required.  Kind of a large amount.
The accuracy would then be limited to that of the gel or blot.  That would generally be a percentage of total length, I think 2% might be obtainable, but I'm not sure about that part.


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What can the timing of human urination tell about the human's physical condition and circadian rhythms?
I've noticed a peculiar phenomenon. A subject drinks 400 ml of water, then observes time until the urge to urinate is felt. The time is 15 minutes. The subject releases water. 14 minutes later another urge to urinate is felt. The subject releases water again.
I'm particularly interested in what kinds of biological systems are involved in timing of such events.
Does the time depend on how full the subject's stomach is? Does caffeine and other diuretics play a part?
Is it time of day (circadian rhythm) sensitive?
Does that predict anything about the suppression/release of diuretic hormones?
What I'm trying to understand is if the timing between human urges to urinate after water consumption can be used to make predictions about the human biological clock and the state of various systems within the body (for example the digestive system).
I will be conducting this experiment at different times of the day. My hypothesis is that at night, when diuretic hormones are suppressed, the timing would be longer for the same amount of water consumed. This is based on my limited research in the area.
Update: I did perform the same experiment at night, the time was 75 minutes for the same amount of water. The experiment was performed at the end of one of sleep cycles, which makes me think that 75 minutes was the duration of the subsequent sleep cycle.
I appreciate your input on the subject, along with any keywords that can help me advance my research in this area.
Thank you!

The fact that urine output (enuresis) and other kidney functions are circadian is well known, just search on pubmed 'circadian urine kidney'. This can be due both to the fact that liquid consumption is less during the night and to the fact that hormones regulating kidney function like aldosterone and plasma angiotensin II are circadian.

Thanks for a great answer! I got a glimpse that this may be circadian from a general scholarly paper, now I know precise keywords that I can search for.

I would suggest a couple of papers
Circadian rhythms in urinary functions: possible roles of circadian clocks? - Noh et al., Int Neurourol J., 2011
Circadian regulation of renal function - Firsov and Bonny, 2010
Neural regulation of the circadian vasopressin rhythm in cerebrospinal fluid: a pre-eminent role for the suprachiasmatic nuclei - Schwartz and Reppert, J Neurosci, 1985


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Are there "multi-frequency" signals within a human brain?
I know that neurons can exhibit tonic and phasic firing, and also that a neuron is sometimes called an integrator. This makes me interested to know if there are activities in the brain that depend on two or more signals of different frequency occurring at the same time. For example, in a telephone system, two signals with a different frequencies at once(DTMF) are interpreted as 1. Is there anything similar in the human brain?

Remembering that neurons don't generate sinusoids, just spikes (mostly)....
It depends on exactly how you want to define "depend on".  For instance, a downstream neuron receiving inputs from two neurons will be more likely to fire as it spatially/temporally sums the inputs from the two neurons.  Regardless of their specific rates, if their interaction is such that an impulse from each neuron arrives within a certain timing of the other, it may be sufficient to cause the downstream neuron to spike.  In this case, particular sets of frequencies of the two upstream neurons would be more likely to activate the downstream neuron and would do so at a particular rate for the downstream neuron.  Of course, the phase delay between the two neurons would be important too.
In a more general sense, one might consider the binding problem, by which many sensory inputs are bound into a single, higher level experience, such as an object or a biographical memory, which can then later be recalled (and thus activate all the lower sensory regions that encoded the memory in the first place, nearly recreating the experience).

In general, drawing analogies of how the brain might work from engineered telecommunication/computing system can be quite misleading.
I just wanted to add Izhikevich's FM modulation theory of communication, but I would say it is controversial.

Izhikevich E.M. (1999) Weakly Pulse-Coupled Oscillators, FM Interactions, Synchronization, and Oscillatory Associative Memory. IEEE Transactions On Neural Networks, 10:508-526
Hoppensteadt F.C. and Izhikevich E.M. (1998) Thalamo-Cortical Interactions Modeled by Weakly Connected Oscillators: Could Brain Use FM Radio Principles? BioSystems, 48:85-94

There is a somewhat-hypothetical phenomenon called cross-frequency coupling which has generated some interest recently. This has mostly been described in the hippocampus and in interactions between the hippocampus and neocortex.
http://www.cell.com/neuron/abstract/S0896-6273(13)00231-6
http://www.bio.brandeis.edu/lismanlab/theta.html


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Examples of intracellular parasites of medical or economic importance?
What are examples of intracellular parasites of medical or economic importance? I have read that Xanthomonas oryzae is an intracellular parasite in rice that produces proteins able to cause changes in the gene regulation of the rice cells in order to feed off the sugars produced by the rice cells.
I would like to know of other examples of intracellular parasites of medical or economic importance that would be potentially (even if not tested) able to interact with the host's genome in a similar manner.

All viruses are obligate intracellular parasites... I would closely watch that because they could soon become a very useful tool for medicine :)

As Armatus pointed out above, all viruses are obligately intracellular, and their medical and economic importance cannot be overstated.
Many bacterial species live intracellularly. The arthropod specific Wolbachia has a wide variety of consequences for its host, including alteration of reproduction and sex ratios, induction of reproductive isolation possibly driving speciation, and conferring protection from some viral infections.
Eukaryotes can be intracellular parasites as well: Malaria is a well-known example. Toxoplasma gondii is another intracellular parasite that uses cats as a primary host, but can use other warm-blooded animals (such as humans, rats, and birds) as intermediate hosts. T. gondii infection has been shown to induce behavioral changes in rats, causing an attraction to cats (thereby increasing the chance that the parasite will infect the cat and sexually reproduce). There is also some evidence that T. gondii infection in humans causes behavioral and psychological changes such as decreased reaction times, and links to depression and suicide.


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What does "cellular" mean in this context?
I came across a confusing word when I was reading a Scientific American story, “Controversial Spewed Iron Experiment Succeeds as Carbon Sink” (by David Biello). It goes like this:

“One key to the whole experiment’s success turns out to be the
  specific diatoms involved, which use silicon to make their shells and
  tend to form long strands of cellular slime after their demise that
  falls quickly to the seafloor.”

I'm wondering what “cellular” means in this context. Does it mean “of (diatom) cells” or “porous”?
Could someone kindly enlighten me on this?

My understanding is that the slime in question is formed of the bodies (the cells) of the dead diatoms. Where does porous come into it? Is it mentioned in a previous sentence?

Diatoms are generally porous, so perhaps that's why they thought it might mean that. But I've never known 'cellular' to mean porous.

Thank you so much for your answer, terdon. My original intepretation was that too. But since diatomite is renowed for its porosity (which was not discussed in the article), I am wondering if it could mean "porous" too?

Thanks for your comment too, Richard Smith. My Collins dictionary does include "porous" as a meaning for "cellular".

@Shummy, this is getting way off topic but I imagine your dictionary had "porous" as a possible synonym of "cellular". When talking about fabrics or clothes, cellular can mean something "knitted so as to form holes" (from NOAD). Porous could be taken a synonym of cellular in that, very specific, context but is not relevant here.

Thank you all for your answers and comments. You have helped me to get a much clearer understanding.

'Cellular' in this context simply refers to slime of (diatom) cellular origin. The word 'cellular' is not referring to porosity. It appears the author wanted to be clear that the slime is from the cell, and not of some other origin. Perhaps the distinction is necessary, because the author mentions that the cells are dead, and dead cells rarely produce metabolic products, like slime.


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Chromosome 2 fusion?
I read this article by Jeffrey Tomkins and Jerry Bergman claiming to debunk chromosome 2 fusion. Is there anything wrong with these conclusions?
" 1.The reputed fusion site is located in a peri-centric region with suppressed recombination and should exhibit a reasonable degree of tandem telomere motif conservation. Instead, the region is highly degenerate—a notable feature reported by a previous investigation.

In a 30 kb region surrounding the fusion site, there exists a paucity of intact telomere motifs (forward and reverse) and very few of them are in tandem or in frame.
Telomere motifs, both forward and reverse (TTAGGG and CCTAAA), populate both sides of the purported fusion site. Forward motifs should only be found on the left side of the fusion site and reverse motifs on the right side
The 798-base core fusion-site sequence is not unique to the purported fusion site, but found throughout the genome with 80% or greater identity internally on nearly every chromosome; indicating that it is some type of ubiquitous higher-order repeat.
No evidence of synteny with chimp for the purported fusion site was found. The 798-base core fusion-site sequence does not align to its predicted orthologous telomeric regions in the chimp genome on chromsomes 2A and 2B.
Queries against the chimp genome with the human alphoid sequences found at the purported cryptic centromere site on human 2qfus produced no homologous hits using two different algorithms (BLAT and BLASTN).
Alphoid sequences at the putative cryptic centromere site are diverse, form three separate sub-groups in alignment analyses, and do not cluster with known functional human centromeric alphoid elements."

I've also heard them say that there has to be a fusion in every living thing that evolved or evolution isn't true.  Is that true or not?
The article is here

Part one
Part two

You are describing two processes - one of general fusion happening now and then throughout history (which is common) and one of specific fusion, that was supposed to happen at a certain time in human evolution history (which is not sure, but possible).

@Jeff , could you include the reference to the story  you are asking about?

Thanks!  Let me take a crack at this, though @jkadlubowska has it in a nutshell here.

Regarding the Papers referenced above:
If the authors maintain that the evidence at the site of fusion is not clear and that explanations as to how this happened are flawed that is possibly concedable.   They would need to do more homework than these papers.  The discussion of vestigial centromere sequences and telomere motifs being inverted is interesting, though contrary views have been written up elsewhere.  I'm not going to review that evidence as I think its not primary to the question at hand...
I would point out that the centromere and telomere sequences are highly repetitive - they are so repetitive that they are often associated with unreliable sequencing in a typical genome build.  While its possible some will be found in future builds of the human genome, such sequences are just as likely to have been excised during mitosis or by mutation.  There would be strong selection pressure for them to be excised quickly; having two centromeres on one chromosome would probably be a fatal trait and the same is probably true for telomerase susceptible sequences in the middle of a chromosomal arm is too.  A lot has happened at the point of fusion and 150 kB of DNA seems to have included itself which is not from the original Chr 2A or 2B.
I think there is some confusion here: The fusion models examined do not predict the fusion from the local configuration of bases.  The main evidence for fusion has always been the fact that the two pieces of human chromosome 2 are nearly identical to chromosomes 2A and 2B of apes - typically 96-98% identical.  The genes are almost entirely in the same order, the inter-genic regions are very similar All along the 2A/2B length - millions of bases.  The site of fusion ad models for its occurrence is merely confirming what we already - there are two chromosomes somehow stuck together.  Since both papers focus on the site of combination and do not adequately address this primary piece of information, they seem to be missing this point.
The chances are infinitesimal that human chr 2 were to resemble those of other primates at random.   This is what you say in science when you mean 'impossible'.  One simply doesn't see a segment of DNA the size of Chr 2A and 2B being so similar for such a length when we look at rats, dogs, worms or any more distantly related living thing.  But for every primate the relationship corresponds to humans the same way.  In addition studies show that these highly similar blocks of DNA sit right next to the site of fusion and show a crossover where the fusion probably occurred.  Some recent hominids - Neanderthals and Denisovans had the chr 2 fusion as well.
I have to say is that there's always a chance that chromosome 2 fusion did not happen though in my view there's a tremendous amount of evidence that it did.  The second most likely explanation is that all the other apes had their chromosome 2 break into 2 pieces at some susceptible site.
I don't quite agree that chromosome 2 fusion is an indispensable or even leading piece of evidence that means that humans and the other primates are interrelated.  That question is a different kettle of fish and the relationship between Human chromosome 2 and the chromosomes of other primates is just one contributing point.  All the other chromosome sequences in primates are the same, and nearly every gene in human beings is closer to primates than to other animals.  If they had not found chromosome 2 fusion in the genome sequences few if anybody would have worried about it.
As to your last question - I don't know if its necessary that chromosomal fusion must occur in every living thing, but it appears that it has.  In fact what we see as we look at all the diverse chromosomes being sequenced, is that most chromosomes have been merged or rearranged over and over again.  Over long periods of evolutionary time, a typical chromosome looks like a patchwork quilt stitched up from pieces of other chromosomes.  These relationships are called synteny, which reaffirm the thesis that all living things came from a single point of origin, if you go back far enough.  Really, the fusion point of Chr2 is interesting because its a relatively new event; by picking through the pieces we might find some understanding of something that appears to be a common phenomenon in genome dynamics.

The above image comes from a review of methods to identify syntenic regions.  It identifies regions of human chromosome 7 and similar regions of mouse chromosomes, identifying regions on mouse chromosomes 6, 9, 11, and 12 with substantial similarities as well as a little bit of chr 2.  Hu chr 7 is 158 million bases long, so even a small band (> 1/1000th of the full length) on this chart means 100,000s of bases.
If all these syntenic relationships are considered together they can construct chromosomal rearrangement events that compare with the phylogenetic tree and typically verify speciation events that separate the two organisms being compared.
Whoops - just found this.  Take a look at this Biology.SE question: it refers to Robertsonian translocation where the long arms of several of the chromosomes chr 14, 15, 16, 21 and 22 are known to sometimes fuse, resulting in viability.  The answer there is useful - these variants don't tend to produce offspring, but it only takes one time.  Its only happened once in the past 5 million years or so.  So another point of view there.
That should't discourage the authors from trying again.
All this being said, as a scientific question I'd rather have a discussion like this, based on evidence and facts that anyone can evaluate.  The authors did quite a bit of homework and read some of the literature that is out there.  This is the right direction some of the creationists are taking here and I personally hope that they keep at it.
If science is to have any merit (or fun) at all, its because any idea can be called into question and be re-evaluated at any time by anyone.

I'd really like to give you more than just one upvote.

Thanks for this.  Can you tell me, was the fusion of "two chromosomes" actually predicted before it was demonstrated in Chr 2, or was it discovered first and then taken as evidence in support of the lineage?

It was known. When you localize genes in humans and then in chimps the broad idea of a chromosomal fusion is referenced from 1995 on the wikipedia page http://en.wikipedia.org/wiki/Chromosome_2_(human)

This reply needs to contain a number of links to qualify each of my claims. Unfortunately this site won't allow me to include more than two links because I am a new user. Please see this post which contains the same response and all the necessary links as well.
I would be very careful trusting any claims published by the young earther Jeffrey Tomkins. In my experience, each of his claims needs to be thoroughly researched because I have found him to be less than rigorous (sloppy) in at least one other paper he has published. He has faced similar accusations from others in the past.
I'm not saying dismiss everything he says: I'm saying take all of his claims with a grain of salt, expect there to be exaggerations, errors and misleading claims (he has a young earth creationist agenda)
If you are ever concerned about anything he writes, you will need to look at the evidence for yourself. I will attempt to answer your questions here.

In a 30 kb region surrounding the fusion site, there exists a paucity of intact telomere motifs (forward and reverse) and very few of them are in tandem or in frame.

This is true, but it isn't surprising (at least not to me). To quote popular science blogger, Carl Zimmer:

The ends of chromosomes are very vulnerable places. If they simply dangle loosely, DNA-cutting enzymes can nibble away at them, destroying the genes they encounter. The dangling end of one chromosome can also get attached to the dangling end of another, fusing chromosomes together. We are mostly protected from such changes thanks to special proteins called telomerases. They tack on little repeating bits of DNA, which form a loop–a telomere–so that chromosomes end as a hairpin curve, rather than dangling ends.

It is this loop that prevents chromosomes from undergoing the type of fusion that we see in the second chromosome. Now telomeres naturally shorten and become mutated with age. If we encountered two fused chromosomes (with the telomeres joined end to end) we should expect that this could only happen where the telomeres are short enough and mutated enough to allow this to happen. Only when they can no longer form that protective loop, can they become fused.
Experiments like this have shown that defective telomeres with few repeats are vulnerable to chromosome fusion.
Here is what the fusion site actually looks like - the highlighted repeating elements (TTAGGG and CCCTAA) are those that are still perfectly formed. If I relax my criteria a little and also highlight those repeating elements that have just one single mutation, this is what the fusion site looks like. To raise doubts that what we are looking at here are a series of repeats of "TTAGGG" joined to a series of repeats of "CCCTAA" is either asinine or dishonest.

Telomere motifs, both forward and reverse (TTAGGG and CCTAAA), populate both sides of the purported fusion site. Forward motifs should only be found on the left side of the fusion site and reverse motifs on the right side

(Note: it is CCCTAA not CCTAAA)
This is just pure nonsense, I am tempted even to call it a lie but I can't be sure. I have looked into this claim by searching through the 20,000 bases that surround the fusion site.
In those 20,000 bases there is exactly 1 instance of TTAGGG that occurs before the fusion site and 1 instance of CCCTAA that occurs before the fusion site (No more than we should expect to occur by chance alone in any sequence this long).
After the fusion site (and away from it), there is 1 more instance of CCCTAA and 3 more instances of TTAGGG (No more than we should expect to occur by chance alone in any sequence this long).
Don't take my word for it. Here are 20,023 bases that surround the fusion site.

The 798-base core fusion-site sequence is not unique to the purported fusion site, but found throughout the genome with 80% or greater identity internally on nearly every chromosome; indicating that it is some type of ubiquitous higher-order repeat.

This sounds like more rubbish (even a lie perhaps). Using BLAT to search for the actual sequence, there is no location in the human genome except for this place on chromosome 2 where we see a sequence of repeating TTAGGG joined to a sequence of repeating CCCTAA. If the authors claim to have found another site like this, why have they not linked to it?
We could also use BLAT to search for an idealised sequence of perfect repeats. Once again, the only hit that includes both the TTAGGG and the CCCTAA is in this exact location on chromosome 2.
We do unsurprisingly find sequences of repeating TTAGGG but what makes this fusion site unique is that those repeats are followed by repeating CCCTAA - that isn't found anywhere else in our genome of over 3 billion base pairs.
Think about that for a moment. A sequence with a signature as unique as this, found in the exact place where scientists expect to find it!

No evidence of synteny with chimp for the purported fusion site was found. The 798-base core fusion-site sequence does not align to its predicted orthologous telomeric regions in the chimp genome on chromsomes 2A and 2B.

First of all, this claim doesn't even make sense. The 798 bases he talks about are just the telomeric repeats. If they are telomeric repeats then they will be found on the telomeres of chromosomes 2A and 2B. Perhaps he made a mistake here and was talking about the wider region surrounding this fusion site?
It is true that there is a lack of synteny in the wider region surrounding this.
This became well understood with the sequencing of the gorilla genome. There was a paper published explaining how this happened in 2012. If you prefer, here is the layman's explanation with diagrams.

Queries against the chimp genome with the human alphoid sequences found at the purported cryptic centromere site on human 2qfus produced no homologous hits using two different algorithms (BLAT and BLASTN).

This isn't true either. Where does he get this nonsense from? I have downloaded the alphoid sequences from the defunct centromere on human chromosome 2 and used BLAT (against Chimpanzee Feb 2011) to find their homologs in the chimpanzee. Unsurprisingly they are exactly where we expect to find them on chimpanzee chromosome 2B - where there is a functional centromere.
Think about that for a moment. The very same sequences that form a functioning centromere on chimpanzee chromosome 2B are found exactly where we expect to find them at a defunct centromere on human chromosome 2.
I am busy constructing a detailed write-up on this. I will update this post to provide a link to that.

Alphoid sequences at the putative cryptic centromere site are diverse, form three separate sub-groups in alignment analyses, and do not cluster with known functional human centromeric alphoid elements."

I can't comment on the first claim but it seems irrelevant anyway. I can tell you that these alphoid sequences occur frequently at centromeres all over the human genome from X to 22. More importantly they are appear almost exclusively at centromeres. For example, alphoid 2 appears at centromeres on the following chromosomes: 21, 9 (twice), 11 (twice), 20 (twice), 7 (3x), 22 (5x), 16, 14, 15, 5.
It appears once at an unexpected location on chromosome 9 where there isn't a centromere, but that exact location is rich in other alphoid sequences suggesting that it too is a defunct centromere (or was perhaps duplicated from another centromere).
This will also be covered in that detailed write-up I mentioned.
edit (2 Oct 2015):
I promised to follow up on this post with a detailed write-up on the fossil centromere on chromosome 2. I've done that now (A year and a bit later) - you can find the information I've compiled on the centromere here

You can add the links into the comments and we can add them for you. Just state where they should be located.

every claim should be taken skeptically in science really...

I've been able to add the links myself now :)

There's skepticism, and then there's refusing to consider extremely well-evidenced conclusions, simply because one doesn't like the conclusion.  With Young-Earth Creationists, you have to figure the latter is what's happening.

I promised to follow up this post with a detailed write-up on the fossil centromere. I have done that now. It turns out that there is an abundance of evidence for this centromere. You can find that here

If one looks at the sequence map in detail, at the fusion point we find both telomere and pre-telomere sequences. And what is particularly compelling, is that these main groups occur in the correct order.  That is, first you see a pre-telomere sequence, then a telomere sequence. Then we see the telomeres inverted and the inverted pre-telomeres after that. This is exactly what would be predicted for a chromosome fusion.  Yes, one can quibble (as Tomkins does) that within a particular group that the sequences don't "look exactly as they should".  But this would be consistent with ideas proposed here.  That these sequences MUST have undergone significant mutation in order for the fusion to even occur!  And then of course one would expect mutations to continue after the fusion event as part of normal evolution.


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High protein turnover rate and protease inhibitors?
I work with mice, and I want to see what happens to some specific proteins in the mouse brain after IL-1b injection (intracerebroventricular).
I have a problem: when I measure the mRNA and protein levels, I see that there are some differences between them.
It can be like:  mRNA (upregulated)  Protein (no difference)
Is it possible that these proteins have a high turnover rate? If so, how can I prevent that?
Can I (if it is possible) inject (intracerebroventricular) IL-1b mixed with protease inhibitors?

Scientists are recently finding (or coming to accept the notion) that, at least in eukaryotes, mRNA expression is poorly correlated to protein expression. There are several factors influencing translation regulation, such as siRNA or microRNAs, sequestering mRNAs while they are transported to various cell compartments, and others.  Even after the protein is made, there can be factors interfering with your expression reporter.  And as you mention, it may be degraded faster than you expect.  Cells try to keep proteins at certain expression levels, so if IL-1b is promoting expression without inhibiting the degradation pathway, degradation might kick into overdrive to bring the levels back down to normal.
Trying some protease inhibitors is worth a shot, since it's pretty simple by itself.  It should also increase your protein expression regardless of whether protein degradation is your limiting factor. If this doesn't work, or if it's prohibitively expensive to be sacrificing mice while you're working out a protocol (and is usually is), then I would turn to cell cultures and try and discern where you're getting blocked.  That kind of information will generally make a decent PNAS paper by itself.


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Why are bacteria and archaea in different domains?
As I understand it, the main difference between the Bacteria and the Eucaryota domains are that eukaryotes have a nucleus and bacteria don't. I understand that bacteria and archaebacteria have enough of a genetic difference to be separate kingdoms, but why are they separate domains?

The reason that Archaea were determined to be a separate (and only the third) kingdom so late (1977 according to this reference) was because archaea often completely resemble eubacteria.  They are unicellular and have no organelles and appropriately they were grouped with other prokaryotes because of their morphology and cellular physiology.
But by the 1970s phylogeny becoming based on the sequence of DNA and RNA which were just becoming more available.  Based on a simple comparison of the sequences of 18S rRNA of 13 fungi, bacteria and archaea, Woese and Fox showed that the bacteria and the archaea were about as different from the eukaryotes than from the bacteria.  (see table 1).
Since then, the differences between bacteria and archaea have continued to be great.  The wikipedia diagram below is not to scale- the divergence of the three kingdoms is so far back that they pre-date the emergence of eukaryotes entirely. But you can see that fungi and other eukaryotes are more similar to archaea than the bacteria.
BTW, the idea that archaea are extremophiles is not entirely true - they are pretty much exclusively the only kingdom found in these conditions, but archaea have been found to coexist with bacteria and eukaryotes in the open sea and their detection heretofore in most environments may be only due to the fact that archaea are difficult to grow in the lab.
Just found this retrospective from Woese himself, who passed away recently.

I think the three kingdoms are prokaryotes/bacteria, eukaryotes and archaea...

Wikipedia entry for Archaea has a heading Relationship to other prokaryotes. Wikipedia entry for Prokaryote has: The division to prokaryotes and eukaryotes reflects two distinct levels of cellular organization rather than biological classification of species. Prokaryotes include two major classification domains: the bacteria and the archaea.


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Pharmacologically, can tricyclic antidepressants have a side-effect profile similar to neuroleptics?
Torticollis (wryneck, cervical dystonia) is a neurologic movement disorder causing involuntary muscle spasms in the neck. Often, neuroleptics can cause such a side effect.  I'm wondering if this condition could also be part of the side-effect profile of  tricyclic antidepressants, like amitriptyline.
Some potential indications:

Often the basal ganglia are associated with neurological conditions such as movement disorders. -> Do amitriptylines effect the basal ganglia?
Dressler and Benecke claim that "Of all patients treated with neuroleptics approximately 2 to 3% develop acute dystonic reactions within days of therapy initiation .When highly potent neuroleptics are used this rate may increase to over 50 %.Young men are at a particularly high risk. Cranial, pharyngeal, cervical and axial muscles are most commonly affected causing oculogyric crisis, grimacing, fixation of the jaw, retrocollis, torticollis or even opisthotonic posturing." -> Do tricyclic antidepressants operate similar to neuroleptics?
Geyer and Bressman claim that dystonia can be caused by certain drugs: "In addition to inherited forms of secondary dystonia (dystonia-plus syndromes and neurodegenerative diseases), a variety of acquired insults can cause secondary dystonia in previously unaffected individuals. Many cases are iatrogenic, resulting from drugs that block dopamine receptors; antipsychotic and antiemetic drugs are the most common culprits." -> even though amitriptyline doesn't seem to block dopamine, maybe there is some kind of connection?
Tricyclic antidepressants sometimes seem to be used to treat torticollis, so is the reverse effect of causing the condition also thinkable?

I'm not sure your question is allowed, and if it is, I'm not positive you'll get an answer. This sounds dangerously close to medical advice regarding possible side-effects, which only a trained physician or medical professional should give you. If you're curious about a specific mechanism of amitriptylines, then please specify. Otherwise, I suggest you take it up with your local M.D./D.O.

I can assure you that this I'm not seeking for medical advice by posting this question. I'm not sure either if I will get an answer here, but I didn't know a better place to ask for now. I have considered emailing the authors of the cited papers, but I think I'll try that a bit later.

Btw. if someone upvoted the question once more I could fix the links (only two links are allowed under 10 reputation).

I fixed the links for you and tried to rework the question a bit to make it more objective rather than advice-seeking.  See if it still carries the original meaning.

Torticollis can occur for several reasons, one of which is a side effect of certain drugs. Rather than highlight one specific drug it is perhaps better to talk about the mechanism of action by which this occurs.
Torticollis in a drug induced form is classed as an extrapyramidial side effect. Classically results from some medications which have anti-dopaminergic effects. The neurotransmitter dopamine is important for the regulation of movement. Different medications have different degrees of anti-dopaminergic effect. To complicate things further there are several different types of dopamine receptors and different drugs have different effects depending on their action on these receptors.
Classically drugs that have been associated with extrapyramidial side effects are some of the antipsychotics but there are case reports of this with trycyclics http://www.ncbi.nlm.nih.gov/pmc/articles/PMC489096/ however this appears to be a very rare, see http://www.sciencedirect.com/science/article/pii/S0924977X97004057.
The paradoxical treatment of torticollis might be dependent on the cause of the condition.  Tricyclic anti-depressants have anti-cholinergic effects, i.e. they block the effects of the neurotransmitter acetylcholine. This neurotransmitter works in opposition to dopamine in the basal ganglia (part of the brain responsible for movement control) as such might be used when the dystonia is as a result of doperminergic disregulation.
If you are at all concerned that you may be suffering side effects of any medication, then I highly recommend that you go and discuss this matter with your doctor. The above  is a simplified explanation of some of the reasons why these side effects may occur. It is not intended as information for the purposes of self diagnosis and treatment.


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Why is membrane potential not zero at equilibrium?
For the squid giant axon, the membrane potential computed by the Goldman equation is -60mV. And the Nernst potentials are (the differences between the K+ and the Na+'s Nernst potential and the membrane potential let the mechanism work):
  K+ = -74mV
  Na+ = 55mV
  Cl- = -60mV

I am wondering if the membrane potential is 0mV, whether the K+ and Na+ Nernst potentials still cause the mechanism to work, so can 0mV be a reasonable value? (That is, I think the value of potential is not important at all as long as the mechanism works well, is this true?)

You have to consider that there are plenty of voltage-sensitive channels that will open at 0mV so, no, you will not be likely to have an equilibrium at 0mV with the "classic" amount and type of channels on the membrane.

Not only are you battling the electronic potential, you're also battling chemical potentials. I'll let a cellular physiologist handle the answer.

Rephrased a little, why do neurons need to have nonzero resting potential, given that most of the driving force is in chemical gradients? See this answer: http://biology.stackexchange.com/questions/8811/why-do-neurons-have-a-negative-resting-potential

The value of the membrane potential does not affect the location of the resting potential.  The membrane potential affects only the fraction of channels that are open, thus allowing net current to change, which allows for the depolarization and repolarization of the membrane (the action potential).  During the action potential, the resting potential does not change.
The value of the resting potential is governed only by the distribution of ions (how many are on one side of the membrane vs. how many are on the other).  This is relatively constant even as ions cross the membrane for the action potential; it is really not a very large fraction of ions moving at all compared to the reservoir they are in, so the reversal potentials are preserved over time.


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What are the white dots on the tree in this photo?
Today in Kongens Have, I noticed a lot of white dots on bark of trees. There are plenty of them, and they were usually on 'bottom' side of branches. Does anyone know what this could be?
I took a photo:

I suspect some pupa of insects, but it is just a quess.

I'm not 100% sure, but I think they look like scale insects (Coccoidea). In particular it looks at bit like a hermaphrodite cottony cushion scale insect (Icerya purchasi)...

The white fluffy thing underneath the insects is the ootheca (egg case). The mature insect migrates to the main trunk of its host tree and attaches to the bark. It then secretes the cottony sack between itself and the bark. Hundreds of eggs are laid into the case, which eventually hatches and the nymphs disperse to the tips of branches where they feed on leaves. As they get older they gradually move first to twigs, then to branches and finally back to the main trunk to breed again.


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Does body mass have a bearing on reflex speed?
A reflex is an unconscious action in response to some specific stimulus, e.g., blinking an eye, or pulling the hand away from a hot pin
I know from school biology, and reading online that withdrawal reflexes are quick because

CNS is involved
Danger receptors send impulses to prevent inhibition of flexion

When a person is extremely obese, do these flexion impulses take longer?
Is a withdrawal reflex in an obese person noticeably slower than in case of a reasonably fit person?

Do you have some reason to suspect that it would be slower?

Merely speculating. An obese person probably does not generate extra nerves/muscles to support their extra mass. Rather any existing nerves may be compressed, and pre-obesity muscles might be distended(sp?) by the added mass already/

No, what would weight have to do it? An obese person has more fat than a person of a normal weight, but fat isn't innervated by nerves (or motor neurons, at least). What about very muscular people? In this case, they actually have more muscles that require innervation, and this comes from increased branching at the nerve terminal.
Since you mentioned muscles, let's focus on motor neurons (or motoneurons). Remember that the cell body of motor neurons is actually in the spinal cord. In the case of alpha motor neurons, which innervate skeletal muscle, the cell body is in the ventral horn. What you think of as a "nerve [bundle]" is really just a collection of cell axons. The axons can regrow if cut in the middle, but you don't grow more axons very easily.
Additionally, a spinal reflex is very quick because it involves the CNS, but not the brain. Look at the example of the patellar (knee-jerk) reflex. The stretch is sensed and transmitted to the spinal cord, causing contraction of the quadriceps while simultaneously inhibiting the antagonist muscle, the hamstrings.

I went into this with the same assumptions that jello did, but I found two studies that had some interesting results.
Isojärvi (2010) found that in obese and under-exercised adults, physical fitness level predicted, among other things, a significant proportion of the variance of nerve conduction velocity and F-wave latency.  So, these individuals may theoretically have a slower response to noxious stimuli.
While Type II diabetes is not always a result of obesity, there is often a high correlation between the two.  Oltman (2005) found that, in "Zucker diabetic fatty" rats (an animal model of Type II diabetes), motor nerve conduction velocity in the sciatic was significantly slowed.  This effect, too, would affect the rate with which an individual could withdraw a limb from a noxious stimuli.
So, I don't think that anatomical changes in the bodies of individuals who are obese would have any effect, but clearly there are physiological changes in the neurons of these individuals.

References:
Isojärvi H, Keinänen-Kiukaanniemi S, Kallio M, Kaikkonen K, Jämsä T, Korpelainen J, Korpelainen R. (2010). Exercise and fitness are related to peripheral nervous system function in overweight adults. Med Sci Sports Exerc. 42(7):1241-5.
Oltman CL, Coppey LJ, Gellett JS, Davidson EP, Lund DD, Yorek MA. (2005).  Progression of vascular and neural dysfunction in sciatic nerves of Zucker diabetic fatty and Zucker rats. Am J Physiol Endocrinol Metab. 289(1):E113-22.

That's really interesting, thanks. I didn't realize there would be such measurable changes, even in the larger nerves. Diabetic neuropathy causes serious problems for people, initially in the hands and feet, due to their distance from the brain. But apparently excess weight can cause negative physiological changes to nerves.

@jello Yes, I learned a few things I didn't know.  My mention of you wasn't a critique in any way, it was more saying that you'd already covered 95% of it, so I wouldn't rehash the info.

I didn't take it that way, no worries :)


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What is the known maximum ranging distance of a bat's sonar?
Bats are known to navigate by using echo-location.
How far away can a bat detect an object by its sonar?

This paper finds some species can detect as far as 67 meters, but the range varies between species.
Note that the bats can actively change their range of detection and trade off range for resolution (low range with high speed resolution for hunting in closed, cluttered spaces or high range with low speed resolution for hunting in open spaces), as explained in Wikipedia's article on Animal echolocation.
Cool stuff.

Are you sure they can switch between CF and FM calls? It was my understanding that CM bats are different species than FM bats.

@terdon the wikipedia article link which I gave says so. In fact it says that both can be combined in a call.

Sorry but I'm intrigued :). I cannot find any reference to a bat switching between CF and FM in the wikipedia article, in fact it refers to either CF or FM bats. There do seem to be some bats that use both but they don't  switch from one to the other either, rather their call has a CF and an FM portion. See here.

@terdon you are probably regarding changing between CF/FM, I am not expert on the terminology. However, in my answer I was referring to what they mention in the article as the "Pulse interval". The article says that bats can change the pulse interval and thus determine the maximum range they can detect objects.

Ah OK, I see now, thanks. Cool stuff indeed :).


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Does our DNA change during our lives?
As far as I know, DNA is the construction protocol of all organisms on Earth.
Does it change when influenced by time and environment (physical laws)?
As parents with schizophrenia are more likely to have children with schizophrenia and an individual with no genetic predisposition for schizophrenia can suffer from such a condition because of drug abuse or environmental influence, does this prove that human DNA is changing during our lifespan?

This question is more appropriate for a biology Stack Exchange. But the answer is that "yes, each cell's DNA changes over time." I think what you might mean though, is "does all my DNA change in precisely the same way?" and the answer to that is "no."

Changes in your DNA occur pretty much every minute of your life. You have trillions of cells, each of which contains about a meter of DNA. Tiny changes happen all the time.

I think this perspective in Science about genome mosaicism is appropriate here PMID:23888031. Basically, not only our genomes change, but it changes differently for each cell.

This related post will probably interest you

To quickly answer your question, yes DNA changes over the life time of many organisms including humans.  You have a whole host of mechanisms in your body that try to prevent your DNA from changing, but they are not perfect.
A good example of this is DNA degradation due to aging.  When discussing aging in biology, we use the technical term senescence.  Of interest here is the shortening of telomeres due to mistakes made in your cells as they continue to divide (copying the DNA to each new daughter cell).
In a grown adult, there's not some master well of DNA somewhere such that if you change it there it will immediately change the DNA throughout your body.  Most of the cells in your body have DNA in them (red blood cells are just one example of cells that don't have DNA in the traditional sense). Most of these cells can and will divide over time (mitosis) to produce new cells with copies of that DNA.  However, there are also plenty of cells that don't divide often or at all in healthy adults.  If one is concerned about schizophrenia, it would be important to note that many neurons in the CNS are in this group of static cells.
Considering environmental effects, there are plenty of things that can change your DNA. Radiation, gamma and x-rays in particular, do a great job of disrupting, degrading, and occasionally mutating DNA.  The class of chemicals and physical agents that can change DNA are called mutagens.  This shares a root with the verb mutate, which is when something is acting on genetic material to cause it change.
You will note that I said genetic material, and not DNA.  Without getting too far into the debate of what is "alive," DNA is most certainly not the only "construction protocol" for earthly organisms.  RNA is one common alternative, but there are weirder ones that are hard to describe like prions.

I have read that in parents DNA there is a code that guarantee their children to will more likely be proned to be better musicians or have better logic or just be better in something specific than other children.
If this is true does it mean that during my life part of my  way of thinking , my gifts will affect my DNA over time?
So for example if my 10xgrand mother was musician and my 9xgrand mother was musician and so on untill i was born
Does it mean that im proned to be musician and its coded in my DNA because of DNA changes in our geneological tree

@Flux your last comment makes no sense. Yes, you inherit characteristics (including, possibly, musical ability) from your ancestors. That does not mean that events during your life time will affect your DNA. Your DNA will change during your life because of damage and mutations but not because you become a better musician.

@terdon: see my comments to vonMises's answer. Epigenetic changes to the genome happen because of environmental changes, mutation is not the only way to change genetic information.

@nico of course, but do you really think that learning to play an instrument will result in inheritable epigenetic changes? And whether or not epigenetic changes are actually changes in DNA is debatable. Anyway, my main point was that I simply could not understand the OP's comment: "I have read that in parents DNA there is a code that guarantee their children to will more likely be proned to be better musicians or have better logic or just be better in something specific than other children." Can you?

@nico Darn.  After reading his comment, I was thinking about coming back to include info on epigenetics, but you beat me to the punch.  There are of course some really good questions not being asked here which are the subject of current research.

@terdon: I doubt there is a specific change for "piano playing ability", but I would not be that surprised whether there were changes to, say, genes involved in neurotransmission in cognitive areas of the brain. As for whether epigenetics changes are or not changes to DNA... well definitely methylation of DNA is a change to the DNA, that is really not debatable. I guess that strictly speaking histone modification are modifications of chromatin and not DNA, but that's nitpicking...

@nico I just said it was 'debatable', I did not specify my position in the debate :).

A DNA change will only be passed on if it occurs in a germ line cell (the cells that become eggs or sperm). If you have a mutation in, say, a liver cell, that will not be passed on.
But I dont think thats what you are talking about. From reading your question and comment closely I think the answer is "no". A person who becomes schizophrenic because of drug use does not become any more prone to having schizophrenic kids than a person who doesnt do drugs. Drugs can upset the chemical balance in your brain and that can mimic certain genetic diseases, but what happens in your brain because of drug use can absolutely under no conditions be passed on to your child.
In your piano comment things are slightly more complicated. Being good at playing piano is a result of a complex interaction of many factors, some of which may be genetic. A long line of pianists generation after generation may be a result of genes that, say, sharpen a persons auditory perception so they can hear and interpret notes better. However, I am sure that the parents encouraged piano playing and practice for their children, which is just as important.
But most importantly, playing the piano a lot will not in any way cause changes to your DNA that will make your children better at playing the piano. Your genes dont care how well you play the piano. Mutation is random, and that is the only way DNA can change.

A person who becomes schizophrenic because of drug use does not become any more prone to having schizophrenic kids than a person who doesnt do drugs. This is not that obvious. First, if drugs are taken during pregnancy/nursing they may as well influence the child. Second it is now well known that many drug can produce epigenetic modifications that, in certain situations, can be transmitted transgenerationally.

Mutation is random, and that is the only way DNA can change.. This is not true. Mutation is not necessarily random, mutagens may be more or less selective. Also, again, mutation is not the only way DNA can change, there are plenty of epigenetic changes that can play a big role in shaping behaviours. Just as an example, you may want to have a look at this paper: http://www.ncbi.nlm.nih.gov/pubmed/22941276

in response to your first comment, you completely ignored the second half of the sentence. I dont care that drugs can affect a fetus, they are not specifically going to change the fetuses DNA so that it has a schizophrenic gene

I understand the need to nit pick, and you are correct, but unless there is an epigentics paper that comes even close to doing what the OP is asking, I think saying "yea but sometimes..." will only mislead him.

sorry, but how can you say that it is impossible for a drug to affect a foetus so that it becomes schizophrenic? I can see many biologically plausible mechanism for that. Your answer is misleading because you are saying that the effect of the drug "can absolutely under no conditions be passed on to your child". Which is not necessarily true.

The key word is "specifically". What you are talking about is a non-specific effect of drug use. The fetus would be schizophrenic by chance. The asker is not looking to find out if a non-specific effect of drug use can be passed on. He is looking to find out if the DNA is specifically changed to a schizophrenic phenotype because of a specific trait acquired by the parent. The answer is an unequivocal "no". The fetus would be schizophrenic because of DNA damage, or brain damage done by the drug. It would not be "inherited" from the parent in any sense of the word

I see the question as much more general. "Does DNA change during our lives?". The answer is yes. Schizofrenia is meant to be just as an example...

It's become quite clear that your active genome changes all the time, due to various effects.  There is also gathering evidence that epigenetic changes can occur in somatic cells and be inherited by the offspring.  But these seem to be stress-related.
So, for schizophrenia: If the family had a gene that triggered schizophrenia, which was normally inactive, then stress/drugs could cause an epigenetic change which would make the "schizophrenia gene" active.  And this epigenetic change could conceivably (see what I did there?) be passed along to offspring.

+1, however it is to note that stress (depending on the definition of stress that you want to use, some are rather large) is not the only stimulus that can generate epigenetic changes. For instance maternal behaviour is well known for having epigenetic effects (e.g. http://www.ncbi.nlm.nih.gov/pubmed/15220929). Surely, you may say that at the end it is stress-related, as you modulate GR, but it is not directly caused by stress (again, you should define stress more clearly so we know we're talking about the same thing).

http://biology.stackexchange.com/questions/53406/any-dna-changes-inconsistent-with-its-genetic-ancestry

Are there any stimuli of any kind that have been observed to change a certain gene to change in a specific manner (specific chain). Can lived daily experience change an individual's spermatozoa genetic makeup (say over the course of days)


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Would a plant survive if it was watered using hard-water?
Hard water is water with high mineral/salt content. I'm told that a potted plant watered with a salt solution dries out sooner or later. Is this true?
If so, would a plant survive if watered using hard-water?

It would depend on the content of the hard-water. If the water contained heavier metals like lead or radioactive elements like tritium (Hydrogen-3), the plant would most likely die. Most land plants cannot survive when watered with massive amounts of salt water as the salt would absorb the water from the leaves.

I'm sorry, I do not understand. Do you mean the flow would be backwards out of the root - or would the salt in the water accumulate at some location/s within the plant and absorb the fluid locally?

The salt in the leaves would accumulate  like any other mineral would. However, the salt would attract the water molecules to them and prevent them from carrying out their job (transporting other nutrients throughout the leaves and stem), thus robbing the plant of necessary nutrients like phosphate and nitrogen. Does that answer your question? I'm not an expert on herbology unfortunately.

Hard water normally refers to water with high concentrations of dissolved calcium or magnesium and consequently has a slightly alkaline pH. Plants which are adapted to growing on limestone or similar alkaline substrates (calcicoles) will be fine with hard water, whereas those plants which are specific to acidic soils (e.g. carnivorous plants) will likely die slowly.

Tap water contains chlorides and fluorides and many hard tap waters contain high levels of calcium making it too alkaline for carnivorous plants.

Most plants are tolerant of a fairly wide range of pH and mineral levels and will cope fine with hard water.
Salt water is another issue and again depends on the plant. Most plants will eventually be killed by a buildup of salts in the soil and the plant tissue but halophytes (around 2% of all plants species) from coastal and desert environments can handle high levels of salt.


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Does a plant have to be alive for its roots to prevent erosion?
One argument often given in favour of saving current and planting additional plants/saplings is the roots hold soil together and prevent soil erosion.
Unlike plants that may be uprooted, a large tree may only be chopped down; its roots continue to remain buried. Do these, now dead, roots continue to prevent soil erosion, or does the plant have to be alive and kicking?
My guess is the latter, perhaps because absorption of water possibly 'compresses' the soil over the root.

You don't need to deprecate yourself like that, if a question is truly off the deep end, someone will comment. :)

The roots do actually continue to hold soil without being alie.  The stabilizing properties are structural in nature.  You begin to lose those though as the roots decompose, and the important roots against erosion, millions of fine root hairs, will go first. But leaving the roots in on a dead tree will help for a bit, but isn't a long term solution.

Here's a study that gets at this question, examining how root decay of felled trees impacts slope stability. http://www.springerlink.com/content/q328v49v72w14762/


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Are mature trees as susceptible to mutation from exposure to radiation as seedlings?
If a plant, say a ficus or a teak, as a sapling were exposed to radiation, and a tree of the same species were present at the same distance, which of the two would be more likely to mutate?

Aren't they all trees in the end, anyway?

Either is an ecosystem in itself.

Hehe, yeah, but I'm saying if you want to compare trees and plants you should have a true exemplar of each.

Erm )+: I don't have an example ...

Don't worry about it, then, it was just a suggestion.  See if you get any answers with it as is.

All trees are plants, I'll rephrase the question. Please let me know if it doesn't meet your intentions.

Ionizing radiation is harmful because of damage to genes. It's thus far more damaging, to everything, earlier in the development cycle; down to the point of the very first cell, where relatively small doses of radiation can render the potential organism non-viable (like killing the cell outright). Random mutations all over a tree are unlikely to amount to much

Ben raises a good point about this question actually - @Everyone are you interested in the effect of radiation on a single cell sampled from a large tree (compared to a single cell in a sapling), or on the organisms as a whole? If it is the whole organisms, Ben has the correct answer I believe; mutations (and thus radiation) will be less of a problem to a plant once it is larger, as any cutting of the plant could go on to form a new tree; each individual cell becomes less important. (See http://biology.stackexchange.com/questions/2055/do-trees-age-on-a-microscopic-level/ out of interest)

Depending on what plant/tree is concerned, I could also imagine things like bark absorbing some of the radiation  being emitted.

@Luke: The overall effect and any inheritable changes were what I had in mind.

@LanceLafontaine: Visualizing the bark as a radiation shield is a great idea! Anybody know whether it is possible/tested?


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What marine animals exhibit deep hibernation/aestivation?
Do marine animals exhibit deep hibernation/aestivation as land-based creatures do?
If not, Why?

Turtles and frogs do, if you classify them as "marine" animals...

Fish are ectothermic, and so, by definition, cannot hibernate because they cannot actively down-regulate their body temperature or their metabolic rate. However, they can experience decreased metabolic rates associated with colder environments and/or low oxygen availability (hypoxia) and can experience dormancy. For example, epaulette sharks have been known to stay dormant for long periods without oxygen (reference) Turtles in freshwater lakes have been known to hibernate by burying themselves in mud (reference). The mechanism through which turtles can experience several months of hypoxia or anoxia is explained in this paper. The Antarctic fish (Notothenia coriiceps) has been found to be able to activate and deactivate their metabolic processes independent of body temperature and hence enter a state of dormancy similar to hibernation through metabolic suppression (reference).


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What does self-preservation stem from?
Self-preservation, or preservation anyway, probably happens throughout the animal kingdom, and perhaps through the plant kingdom as well (some plants/trees, apparently, produce chemicals to repel bugs).
Where does self-preservation stem from? Is it only about a biochemical imbalance?

Could you expand on your question a bit please? I cannot understand what you are asking here.

self-preservation in what sense?

Saving one's own life by avoiding starvation/discomfort(extremes of temperatures for instance)

This is a prototypical case of evolution by natural selection. Any trait that prevents the organism from being eaten or destroyed will probably make that organism more likely to reproduce* than similar organisms that do not have that trait**. This results in self-preservation traits becoming more prevalent in the population and eventually ubiquitous.
* Or they reproduce more, or are able to provide for their offspring better, etc. Self-preservation behaviors that reduce reproductive success are not selected for and generally aren't common (unless they are a special case of some general trait that has a net reproductive benefit).
** Assuming that the trait is reproductively favorable after considering any trade-offs such as increased energy expenditure.

I would argue procreation is a side-effect ...

A side effect of what?


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Effect of single-gene overexpression in the cell's response
Which are the factors that modify the overall gene differential expression by introducing a vector for single-gene overexpression?
If you overexpress a gene for a protein involved in signal transduction (e.g., a kinase, scaffold, or receptor) by vector cell transfection, then you overdrive the cell using this signaling pathway, it's useful to isolate the pathway and study them.
Is there any way to modify the overall gene expression or cell differential expression pattern by gene transfection? I think this would work if you delivered a gene for overexpression in proteins involved for RNA processing (e.g., splicing, ribosomal proteins, etc.), RNA transcription (e.g., TFs) or protein translation.

This sound like all of genetics.

Looks very similar to Metabolic Engineering

Single protein over expression, was the main strategy to get information about protein function. I do my research in signal transduction, and we use this method. but this is the trick question, every member in our lab get in seminars.

Which are the factors that modify the overall gene differential
  expression by introducing a vector for single-gene overexpression

This is a very relevant question and the field of experimental biology needs to revisit the experimental strategies.
One of the explanations that you gave is correct- that the overexpressed protein might override the cellular processes.
Another problem that this practice gives rise to is incorrect inference. We are mostly interested in knowing what a protein does in a cell at general physiological conditions. If the stoichiometry is altered wrong results will definitely pop up.
For example in the case of a repressor/activator with multiple targets: At its general physiological concentration it may not really activate gene-X because of low affinity but in high concentrations it just may, and we end up concluding that gene-x is a target of repressor-1 by an OVEREXPRESSION experiment.
A synthetic biological approach is very good in studying small signaling/transcriptional modules. The entire module can be cloned and expressed in a cell under an inducible/constitutive promoter. This can be implemented in a heterologous cell also. A mathematical model generally helps in making certain predictions.
Other strategies which can be used instead of overexpression:

using sensor constructs harboring a functional or non-functional
target sites instead of overexpressing the upstream protein
downregulation experiments

There are lots of different overexpression vectors (usually they're promoters/regulatory elements upstream of the transfected gene). Here's an example of an overexpression vector (overexpression vector pCAMBIA1300S) that was used to overexpress a transcription factor called NAC in rice, resulting in large phenotypic changes (drought and salt tolerance): http://www.ncgr.ac.cn/articles/2009ZhenXN_NAC.pdf

Can you expand a little bit maybe giving some example of how the modulation of a single gene can subsequently affect many others?


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Has the age at which menopause occurs changed throughout history?
I was reading recently that the age of menarche has decreased in the last 150 years, and was wondering if the age of menopause in humans has also changed recently?
Would there be selective pressure for it to increase currently, given that the average age of women having their first child is increasing in the West anyway?

Quick answer: Yes, but not in the last 150 years.
There seems to be no clear link between age at menarche and age at menopause (taken from [1]):

While earlier studies were able to establish an association between
  early age of menarche and later menopause (Frisch 1978; 1987), more
  modern studies have not been able to confirm this effect (Whelan et
  al., 1990; van Noord et al., 1997).
Aristotle's assessment was similar to those of Hippocrates and also
  Roman authors, so it seems that 2000 years ago most women entered the
  menopause in their early 40s. Mediaeval authors, however, gave the 50s
  as the age when menses ceased-much closer to the timing for twentieth
  century women.

Jean Ginsburg in [2] states (emphasis mine):

In the past 100 years data from schoolchildren have shown a steady
  fall in the age at menarche in industrialised communities. Has
  there been a corresponding change in the age at the menopause?
  Unfortunately, reported surveys of the menopause have suffered from
  methodological defects. [...]
Nevertheless, those studies least subject to bias show a striking
  agreement that the median age at the menopause is currently around 50
  in Western industrialised societies. In Britain it is 50.78, in the
  United States 49.8 and in white South Africans 48.7 with little
  apparent change over the past century. In non-European women, however,
  the menopause seems to occur earlier-in South Africa and the United
  States black women have an earlier menopause than white women.

So, while early menarche is, apparently, irrelevant, age of onset of menopause has increased since antiquity but has remained relatively stable since the middle ages. Therefore, there have been no significant changes in the age of onset of menopause in the time frame you defined (150 years).
Finally, Bengtsson et al [3] state that:

Our study has, thus, not supported the view that the menopausal age is
  rapidly changing.

C. Keck, Predictive Factors to Determine Age of Onset of Menopause, PAMJ
, 3, 2005
Ginsberg J. What determines the age at the menopause? BMJ. 1991 Jun
1;302:1288-9.
Calle Bengtsson, Olof Lindquist, Lasse Redvall, Is the menopausal age rapidly changing?, Maturitas, 1(3), February 1979, Pages 159-164


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What is benjamini
I was doing some gene expression analysis using this tool http://david.abcc.ncifcrf.gov/summary.jsp. However, I have a confusion about what benjamini is. I fed it some gene list and it gave me some potential pathways the genes belong to(KEGG pathways). However, I have a confusion what this column called benjamini is. What does it denote? Any suggestions?

Probably from Yoav Benjamini and something to do with a statistical test of False Discovery Rate.

please don't cross-post with BioStars without acknowledging it in your question -- http://www.biostars.org/p/64888/

It is a Benjamini-Hochberg q-value, similar to a p-value corrected for multiple hypothesis testing using the false discovery rate.


text:
What gases are needed for humans to breathe?
I will be beginning a science project about sustaining life on space stations. I already know that pure oxygen is harmful for humans but would $O_2$ + $CO_2$ be enough for humans to breathe in or do humans need other gases as well?

For a start, in addition to the International Space Station (ISS), also look at gas mixtures used in scuba diving and breathing gases.

Yes that what my science project is about, it's about sustaining life on Mars so I just needed to know what gasses are required for human respiration respiration


text:
What is the composition of human feces?
Are there any studies or general information on the composition of human feces?
I'd specifically like to know the percentage of carbohydrates and amino acids relative to the amount that was ingested in diets of various types and amounts.
Any additional facts are also welcome.

This is a bit hard because the usual composition statements are a combination of different types of molecules.
Most of faeces are, by dry weight, bacteria (30%), undigested food and fiber (30%), fat (10%-20%), inorganic matter( 10-20%), other protein(2-3%). (reference)
As you can see the bacterial portion contains proteins (amino acids) and other types of molecules.  the inorganic matter includes bilins which are part of the used up hemoglobin from red blood cells which have been retired.
There's also a lot of variation from one sample to the next - 10% seems pretty common here as you can imagine).  What makes faeces so dangerous is the bacterial portion, which can pose quite a health risk.


text:
Can Taq polymerase be used instead of polymerase Vent exo (-)?
Instead of using  polymerase Vent  exo (-), can I go with the usual Taq polymerase?
Do the PCR conditions change (the temperature and master mix concentrations ) in the these two conditions? Do the primers (sequence and concentrations) change if we use vent exo instead of Taq polymerase and vice versa? If the primers are designed specifically for Vent exo (-) how can I modify the PCR conditions so that I can use the same primers (meant for vent exo) using Taq polymerase?

Can you describe what you need the PCR for, what your requirements on accuracy and other factors are?

SNP detection, using ARMS PCR

I haven't done ARMS PCR myself, so my answer is based on theory and there might be other practical factors I overlooked.
The characteristic feature of the Vent exo(-) polymerase is the lack of exonuclease activity compared to the regular Vent polymerase. ARMS uses the fact that a mismatch at the 3' position prevents primer extension. For this to work it is important to use a polymerase without exonuclease activity, as such a polymerase could "repair" the mismatch and the whole method would not work. Taq polymerase also doesn't have any exonuclease activity, so in theory you should be able to use it for this experiment.
The primers don't have to be changed for different polymerases, the polymerase buffer though is different and I wouldn't recommend using the wrong one.


text:
Why does getting certain chemicals in cuts hurt?
More specifically, shampoo. What are the mechanics of detecting a noxious chemical stimulus in terms of which receptors recognise what, how do they do it, and how is this information relayed to the nerve cells?
Why is the pain (and so signal, I presume) larger if one is having a hot shower at the time?

I edited the question a bit, as I don't think the sensation is specific to shampoo, but this is interesting.

I guess the second part has to do with hot water dilating blood vessels, facilitating extravasation

Shampoo is a detergent. Detergents emulsify lipids, including those in membranes. Skin cells are probably a bit more resistant to detergent than other cells. When it gets in cuts, the shampoo is probably causing rapid cell injury and/or death. I think pain is a perfectly proportional response to that.

@ChinmayKanchi I'd be happy to accept that if you post that as an answer I (perhaps with an extra link).

@Alyosha There you go...

Shampoo contains surfactants, chemicals which cause lipids to emulsify. The cell membrane is composed primarily of phospholipids, which are vulnerable to action by surfactants. In fact, sodium dodecyl sulphate (SDS, often labelled SLS on shampoo bottles), an integral component of many shampoos is also used in the lab (albeit at substantially higher concentration) to achieve cell lysis.
The outer layer of skin is composed largely of a very tough type of cells called keratinocytes, which form an impenetrable barrier to potentially harmful chemicals like surfactants. Once the skin is ruptured, the surfactant can act on cells that don't have the protection of keratin, causing damage to cell membranes, and perhaps even cell death. This will obviously lead to an immune response and inflammation, which is likely to be the source of the burning sensation/pain that one feels.
The inflammatory process involves various immune system-related mediators such as bradykinin and prostaglandins, which act to increase the sensitivity of neurons to pain.
With other chemicals that cause a burning sensation, the mechanism of cell injury might be different, but ultimately, the immune mechanisms kick in, causing inflammation and pain.
Kid & Urban (2001) reviews the processes that cause inflammatory pain in great detail (full text is available for free).


text:
Which bacteria have the highest mutation rate?
From my reading on M. tuberculosis, I know that this organism has a pretty high mutation rate due to uncorrected sloppy replication, which leads to a high rate of development of spontaneous resistance to treatment.
Are there species that can beat M. tuberculosis in this degree of mutation, due to polymerase sloppiness or other mechanism?

Do you have a reference for the "sloppiness" under normal conditions, or are you talking about in the presence of antibiotics like Moxifloxacin?

Indeed, the above was from memory. After a second look it appears that it's mainly a sloppiness during DNA repair following UV and especially oxidative stress. (PMID 12705867 and 21516081)

the other way of having a high mutation rate is to be around a lot of ionizing radiation like D radiodurans... it is true that organisms 'throttle' their mutation rate by changing up their dna repair systems. Darwin's gas pedal...  Given that fewer than 0.1% of the bacteria are known that exist (0.001%? the jury is still out), its possible some amazing discoveries will turn up later too.

You seem to be assuming that mutation rates are somehow constant over evolutionary time. They are not. Mutation rates will change according to the stresses a species is subjected to. If you take a bacterial population and place it in a stressful environment (high/low temperatures, oxidative stress, lack of nourishment or whatever) you are likely to see an increase in the mutation rate.
That said, this review and references therein might interest you:
E. Denamur and I. Matic,Evolution of mutation rates in bacteria,Molecular Microbiology 60(4), pages 820–827, May 2006

From my reading on M. tuberculosis, I know that this organism has a pretty high mutation rate

Huh, that's news to me. In fact, Mtb has a rather low mutation rate and rather low genetic variance. See the paper by Sherman & Gagneux in Nature genetics. The paper does state that mutation rate in latent infection is higher than expected or previously assumed, but that's a different story.
That said, mutation rate depends strongly on the genomic context. You can have mutator strains in E. coli or other bacteria that exceed the mutation rates of other strains by orders of magnitude.
A clinical example of a bacterium with mutator strains that help in acquiring resistance is Pseudomonas aeruginosa. More on that in the paper by Ferroni et al..


text:
Is there a detectable amount of bacterial DNA in the blood of infected persons?
With which bacterial infection in humans has it been shown that bacterial DNA can be found in the blood?
If any is found it is likely not to be very much, and even difficult to distinguish from human DNA, but presumably recent advances in sequencing should have made it possible.

Even difficult to distinguish from human DNA. Hmmm... a simple PCR for a bacterial-specific gene would easily distinguish human from bacterial DNA.

Yeah I think qPCR is a fairly routine diagnostic for determining a strain.

@nico so which exclusively bacterial gene would you pick out?

@rwst: hmmm... I'm sure there are tons of them. 16S for bacteria vs 18s for human would be easy enough.

Better than DNA detection to show existence of bacteria may be doing a MALDI-TOF of the blood to detect bacterial metabolism products like lipopolysaccharides or extracellular proteins.

Everything depends upon the infection and on the general immune status of the patient.
Generally, the prerequisite for DNA to freely circulate in the blood is the presence of bacteria themselves in the blood (bacteraemia). This means that the infection left its original site (where it is usually kept isolated from the blood flow by the immune system). Depending upon the body reaction to this breakthrough, sepsis and/or SIRS can be the consequences.
Under these conditions (not necessarily as severe as sepsis, but in case of proven bacteriemia), the bacteria cells get attacked by the immuno cells, that leads to their eventual lyzing and releasing their content to the blood.
PCR can be used as a method to prove the existence of bacterial DNA. (Here is a publicly available paper on this topic).

Thanks for the ref. Barbars are they, let the rats gulp CCl4, nasty stuff...

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


text:
Is extreme cladism a mainstream position in the species debate?
In the philosophy of biology it has been claimed many times that a popular position regarding the question of what species are, among biologists, is cladism. For my current purposes, the defining trait of cladism is captured in the following quote:

According to cladism, a species becomes extinct whenever it sends forth a new side species. (LaPorte 2004, 54)

So, for example, if Homo floresiensis is truly a species, and it derives, via a speciation event, from Homo sapiens, then, after the speciation, there is no Homo sapiens: there is Homo floresiensis and a new species, very similar to sapiens. In general, whenever there is speciation the mother species disappears.
I am under the impression that this description of the situation is not the one most mainstream biologists would endorse. I take it that a more common description would be one under which, if a number of Homo sapiens get isolated in an island and go on to form a new species, Homo sapiens exists both before and after this speciation event. I would like to know whether cladism, described as above, is really a popular position, or whether I am right about what most biologists would say about the relation between floresiensis and sapiens.
It might also be that biologists declare themselves cladists when explicitly theorizing about the nature of species, but fall back to a less extreme form of cladism in the actual practice. Evidence in favour of or against this possibility (coming from biology, not the philosophy of biology) would also be appreciated.
As Noah has pointed below, what I have called extreme cladism might be very far from cladism, as usually interpreted. This is precisely the kind of claim I would like to see substantiated.

LaPorte, Joseph. 2004. Natural Kinds and Conceptual Change. Cambridge University Press.

Sorry, the following comments got toasted in a testing catastrophe - my fault: "Depending on how strong the emphasis is on monophyletic concepts, it would have the consequence that has been pointed in the question: if the "mono" in "monophyletic" indicates a single, non-branching stretch in the evolutionary tree, a species cannot survive its "sending forth a new side species", as LaPorte puts it." & ...

"that seems to me to be very far from the defining characteristic of cladism. Instead I'd says cladism is characterized by emphasizing monophyletic concepts (archosaur or ray-finned fish) over polyphyletic ones (like reptile or fish) and emphasizing the arbitrariness of Linnaean ranks (calling everything a clade instead of phylum/class/etc.)." - many apologies :/

I've never heard of it, actually - though I can't speak for my professors or researchers I know, none have ever presented the Cladism argument as an argument for the delineation of species.
As far as I'm aware, the attempts to define a species fall along three lines:
The ability to produce fertile offspring in the wild.
Distinct physical characteristics.
An arbitrary amount of genetic divergence.


text:
Do all sea creatures that have scales have to have fins?
Do all sea creatures that have scales have to have fins?
Do we know of any sea creatures that have only scales without fins?
I'm especially interested in fish that have scales but no fins.

The 'fish' part of this question may be circular, since fishes are a paraphyletic group. From wiki: "A fish is any member of a paraphyletic group of organisms that consist of all gill-bearing aquatic craniate animals that lack limbs with digits". In that definition, 'lacks limbs with digits' is a near-synonym of 'has fins' (the alternative being 'has lost all limbs'). If the group 'fish' were defined in the normal way (i.e., by phylogeny), then all of the groups mentioned in @Alan Boyd 's answer would count as fishes!

Very interesting question. It is stated in the Mishna (Ancient Jewish Texts) [Chullin 3:7] that there are no fish that have scales and not fins. Of course the definition of fish they were referring to was the swimming variety (not slithering or crawling). Later commentaries say that it was thought that the scincus marinus actually had scales and not fins. But it was redacted, due to the "skink" having legs, making it more of a lizard than a fish. So to answer the question, currently there is no fish (using the commonplace definition) that has scales and not fins. Plus a bunch of Rabbis put the

How about marine reptiles? Sea snakes have a paddle-like tail, so perhaps you would claim that as a fin, but maybe marine iguanas would qualify? And, of course, sea turtles.

Thanks Alan. Maybe you know of fish that answer the criterion?

Definitely not. Since the tail is the caudal fin, this hypothetical finless fish would have no means of locomotion.

Eels, but they have caudal fins... Would you consider rays to be finless?... Just checked, a ray's wings are considered fins...

Chitons have scales,but not like fish.


text:
Text/resource with information on all skeletal muscles and their motor units
Something analogous to an encyclopedia on baseball players with a list of all thier stats would be ideal.
I'm not looking for just generic muscle names, locations and illustrations.
Good answers would include links to resources, textbooks etc. which include stats for most or all of the following of every skeletal muscle in the human anatomy:

Language of origin/LOO definition
Labeled by ? shape, location, size etc.
Type of Shape (i.e., fusiform, pennate, bipennate, multipennate, convergent, parrellel etc)
Angle(s) of pennation (if applicable)
# of motor neuron innervations
# of proprioceptors in muscle
# of fibers
Length of muscle
Length of fibers
Typical fuel system reliance (determined off of biomechanical placement and architecture..CPr, oxidative, etc.)
Biomechanical function (structure of corresponding bone/tendon anchors and corresponding movement manipulation)

I'm not inclined to think that there is a "Compendium of All Muscle Data" out there, unfortunately.  I'm looking forward to an answer as well if there is.  Much of the insertion point, etc. data can probably be found in any medical anatomy text, but the fiber/fusiform/spindle/motor unit data may not be readily available for humans in one place.  I know Robert E. Burke at the NIH has devoted an entire successful career to exploring the motor unit anatomy and physiology of the cat preparation.  A pubmed search should give you a number of papers in that regard.

You can try Biomechanical models used in software frameworks such as OpenSim.
Here is an example of a combined upper and lower body model in XML: ULB_Project.


text:
Tool use by animals: research history
I was under impression that data about quite a lot different species using different tools is a fairly modern phenomenon, i.e., all of the research is fairly recent.
Around 50 years ago it was widely believed, by scientists too, that it was only apes that are able to use tools. I was recently told that it's basically nonsense and scientists have been studying different tool-using animals since the beginning of the 20th century or earlier.
Where could I get more info on research done in this area? I'd be especially thankful for those done in USSR, since it used to be my country and my knowledge on everything was basically limited by the Iron Curtain. However, I am also interested in research done worldwide as well.

Best tip I can give you is buying a textbook or popular science book about ethology. That should give you an overview about research done in the past decades. Konrad Lorenz was a pioneer of ethology, so a book should summarize his work, e.g. this one
For more current stuff look up some journals in this field:

Animal Behaviour
Journal of Comparative Psychology

Animals having a small brain compared to mammals but nevertheless showing very intelligent and reflective behaviour like this rook are currently interesting research objects. This kind of research is not really tricky or expensive as you see, it just has to be done by a student :) But behaviorism as the leading paradigm in the middle of the 20th century has probably made a lot of more fruitful research approaches impossible.


text:
Mutation-immunity in Luria-Delbruck experiment
If experiments like those of Luria and Delbruck on E. coli and T1 phage are the main source of our confidence in the mutation-immunity model, is it then highly unlikely that there are other types of bacteria for which an encounter with a phage is the mutagenic (or immunity-conferring) event?
Are the two possibilities in principle mutually exclusive?

No. There was a recent surprising paper on a bacterial adaptive immune system. I cannot find it, unfortunately.

No. Surprisingly, there is an adaptive immune system in prokaryotes. This is still widely unknown. The newest review is
S. Al-Attar, E. R. Westra et al: Clustered regularly interspaced short palindromic repeats (CRISPRs): the hallmark of an ingenious antiviral defense mechanism in prokaryotes. In: Biological chemistry. 392, 4, April 2011, 277–289. doi:10.1515/BC.2011.042. PMID 21294681. (Review).
Cited from abstract:

Many prokaryotes contain the recently discovered defense system
  against mobile genetic elements. This defense system contains a unique
  type of repetitive DNA stretches, termed Clustered Regularly
  Interspaced Short Palindromic Repeats (CRISPRs). CRISPRs consist of
  identical repeated DNA sequences (repeats), interspaced by highly
  variable sequences referred to as spacers. The spacers originate from
  either phages or plasmids and comprise the prokaryotes' 'immunological
  memory'. CRISPR-associated (cas) genes encode conserved proteins that
  together with CRISPRs make-up the CRISPR/Cas system, responsible for
  defending the prokaryotic cell against invaders.

and

An application of the CRISPR/Cas system is the immunization of
  industry-relevant prokaryotes (or eukaryotes) against mobile-genetic
  invasion. In addition, the high variability of the CRISPR spacer
  content can be exploited for phylogenetic and evolutionary studies.
  Despite impressive progress during the last couple of years, the
  elucidation of several fundamental details will be a major challenge
  in future research.


text:
What molecular processes are involved in pseudopodial extension?
I am curious as to the processes and mechanisms involved in the extension of pseudopodia in amoeba. How does the cell know and control the direction and extent of pseudopodia formation at a molecular level? I am not particularly interested in the taxes that amoeba recognize, but rather the mechanism of response to these taxes.

The extracellular cue signal must be relayed to the cell by Rho family of GTPases, like in the case of filopodia and lammelipodia. This causes local actin polymerization leading to extension of pseudopodium.
For a casual reference you can check the wikipedia page on Rho family of GTPases. Cell biology books like MBOTC also have information on mechanism of cytoskeletal dynamics.