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Why is ATP the preferred choice for energy carriers?
Why is ATP the most prevalent form of chemical energy storage and utilization in most cells?

the energetics of the phosphate hydrolysis is more or less similar for most NTPs. Compared to GTP, ATP requires one less enzyme for its synthesis. Pyrimidine triphosphates are also high energy molecules but have specialized roles.

It might be worth while having a look at this great article by F. H. Westheimer Why Nature Choose Phosphates, published in Science in 1987

Thats an interesting paper, thanks for recommending it. IF someone wants with no access through a university wants to read this paper, see here: http://academic.evergreen.edu/curricular/m2o2006/seminar/westheimer.pdf

Although ATP is certainly the most common triphosphate synthesized, GTP is quite commonly used to drive reactions: GTP provides 2/3 of the energy for protein synthesis, which is a major energy expenditure for most cells. So I would argue the preference for ATP over other NTPs is not as strong as it might seem at first glance.

The academic.evergreen.edu link is broken, but the Westheimer paper still lives at http://archives.evergreen.edu/webpages/curricular/2006-2007/m2o2006/seminar/westheimer.pdf

I wonder if oxygen has anything to do with it? See MH Zhou's theory here: "Please look at and compare the chemical structures of adenine and ATP vs guanine...the oxygen level on [early] Earth was below 0.1% as compared to 20% nowaday. Therefore, adenine was far earlier than guanine appearred on Earth by billions of years on early Earth. It is because, adenine has no oxygen atom in its structure, whereas guanine has 1 oxygen atom in its structure...."

I really like this question as it is such a fundamental underpinning of all life on the planet, yet there is such sparsity of actual information on its origins and why selection rewarded ATP use over anything else. Here I am talking generally since no specific studies exist in ATP vs other candidates.
A lot of the below information is taken from a relatively old article mentioned in the comments by TomD that discusses: "Why nature chose phosphates." by Westheimer, 1987. The article is very influential and has been cited over a thousand times since publication. Another article that came out in the same year that this question was asked "Why nature really chose phosphate." by Kamerlin et al., 2013
Some of the below arguments are more convincing than others, but all of them should be thought of when attempting to answer this question.
Summary.

ATP has ancestral dominance. Most other reasons derive from this.

Alternative phosphate groups or other molecules may not provide enough energy.

Alternatives may be toxic.

Other molecules, particularly phosphates, are used for inefficient high energy bursts.

Pi is a "good" leaving group.

Phosphates are fundamentally able to be regulated through electrostatic manipulation.

ATP synthase can efficiently reattach the Pi to ADP.

Lots of Pi available to organisms because of it's ancestral dominance ("if it ain't broken, why fix it?" is at play).

ATP can provide more energy if needed; it's scalable to the situation. (ADP becomes AMP + Pi)

Easily usable by a variety of proteins.

Why ATP?
ATP is an efficient and relatively easily biosynthesised molecule that can fulfil multiple biochemical roles. Cells do have alternative energy carriers, some with more specialised roles, however, ATP is ubiquitous throughout our cells and inter-cellular spaces. There aren't a wealth of resources explaining why ATP is any better than other compounds, however, there is plenty of reasons why the phosphates are required.
Why not the alternatives?
Citric acids and their derivatives are a good candidate, with deductible groups and high bioavailability but they simply don't give enough energy to stabilise genetic material.
Another tribasic candidate is arsenic acid. This is a fundamentally toxic compound, though, which isn't particularly great for living things.
There are other phosphates too, and they are used in many organisms. In biology, they have specific functions, and not used as the general energy carrier. For example, creatine triphosphate provides a high energy phospho- anhydride bond, that is often used to quickly and anaerobically regenerate ATP, useful during high rate muscle activity for contraction.
GTP is structurally very similar to ATP. GTPases are used more to initiate cellular signalling pathways. It is sometimes used as an energy source. This is a good example of an alternative energy carrier.
Over the years, many proteins have specialised with a specific shape, and this chance is the primary reason behind ATP over GTP. In other words, the choice of ATP over GTP is primarily down to cellular preference of molecular shape. One of them had to emerge as being more widely used, and it was ATP that 'won'.
Efficiency and simplicity.
The reaction was once thought to be a relatively simple nucleophilic displacement. From the 2013 paper:

...this simplicity is deceptive, as, even in aqueous solution, the low-lying d-orbitals on the phosphorus atom allow for eight distinct mechanistic possibilities, before even introducing the complexities of the enzyme catalysed reactions.

Traditionally one will be taught that ATP is such a chemically efficient way of storing and transporting energy. This is due to the ATP->ADP & Pi hydrolysis reaction. The phosphate groups in ATP are full of negative charges and these are repelling one another. This means that the third phosphate is a great leaving group and breaking the phospho- anhydride bond is a favourable reaction. ...
...But the story is a lot more complicated than that. The above explanation isn't really satisfying because those same negative charge forces are repulsive of the nucleophile that is attempting to complete ATP->ADP & Pi. A more comprehensive explanation would go along the lines of 'although a negative charge repulsion exists between the nucleophile of the protein and the phosphate, that high energy barrier can be overcome by electrostatic manipulation'. This allows an "on-off switch" for the hydrolytic reaction by tweaking the electrostatic environment. This is another great regulatory tool that the phosphates provide. This regulatory feature is important for signal and metabolic/catabolic cascades.
When it comes to 'rebinding' the Pi to ADP, it is fairly easy since ADP seldom covalently binds to anything, which would require a lot of energy to recover the ADP. This also helps the bioavailability of free ADP to ATP synthase, an incredibly efficient enzyme, that uses membrane proton gradient to drive the production of ATP. Talking about actual numbers is difficult here as there is only data available from Rat hepatocytes. Who is to say mammals are representative of all organisms? The estimates of energy of hydrolysis range from ΔG˚ = -48 kJ mol-1 to -30.5 kJ mol-1. Note that these are considerable, but not exceptional values, so it's easy for many different proteins, that need not be very specialized, to break the bond all over the body. I couldn't even find the numbers for the synthase reaction per ATP, but a single ATP synthase can produce up to 600 ATP per minute.
The final point of this efficiency is that the elements in ATP are very abundant and established in the biosphere making it readily available. This makes the phosphates a convenient biomolecule.
Multi-functionality.
ATP is ubiquitous in the body, but in some cases more energy is needed than there are ATP available. In these times of need, ATP can be used to produce more energy, breaking another phosphoanhydride bond to become AMP+2Pi. AMP however is typically a signalling molecule.
With the low activation energy required to break the phosphoanhydride bond, a multitude of enzymes, far too many to list here, can make use of ATP in order to gain energy towards the activation energy for many other functions.

I think this answer mixes up the advantage of phosphates as energy carriers with the predominance of ATP. The case for phosphates is nicely made by Westheimer's 1987 paper; but there is little reason to suppose that ATP is chemically special compared to, say, GTP --- the prevalence of ATP over other triphosphates is likely just an evolutionary coincidence. And the argument that ATP is "a great biomolecue" because it is "abundant in the biosphere" is obviously circular.

@Roland Great points, but allow me to elaborate that when I say that abundance makes it a "good" biomolecule I am not making a circular argument. Once any compound establishes itself in the primordial soup and is propagated, it is more convenient/probable that molecule is used than an alternative. This is a valuable point, and is less circular than it would first appear.

It seems like you just accidentally explained why AMP is a signalling molecule. AMP signals low energy.

I really like how the top two answers start with their opposing views on whether or whether they do not like the question.

I don’t like this sort of question because I don’t think it can really be answered and I’m very suspicious of arguments that seem to claim ATP is the only or even the best solution to the problem. Nature generally demonstrates that there is more than one way to kill a cat, but if one way works adequately you don’t always need to look for another.
This is not necessarily the case, of course, if we consider an example from the postulated RNA World — which I shall presently — catalysis using RNA was supplanted in most cases by catalysis using proteins. So sometimes a better solution provides an evolutionary advantage, and sometimes if things work well enough they stick as the limiting factor is elsewhere.
So I tend to the view that ATP worked, so it stuck. It was probably chance it wasn’t GTP or CTP or UTP, as these work as energy sources in signal transduction, phospholipid synthesis, and glycogen synthesis, respectively.
But this raises the question of the function or necessity of the purine or pyrimidine ring in the nucleoside triphosphates. As far as I can see the answer is this serves no indispensible function. (Sure, it binds to enzymes — but all sorts of other structure are able to do this.) So I would like to fly the following kite (which must have been flown before, although I am not aware of a reference).

A nucleotide triphosphate (ATP) became the preferred energy source in
  metabolism after a mechanism of RNA synthesis evolved that used NTPs as
  substrates.

When the synthesis of RNA evolved to use the free energy of hyrolysis of a ‘diphosphorylated extension’ of its structural building block (NMP), a system of using a related hydrolysis was extended to metabolism. Note that I say ‘related’, as RNA synthesis (like other macromolecular syntheses) hydrolyses the alpha-beta phosphodiester bond (releasing pyrophosphate), whereas in metabolism it is generally the beta-gamma bond that is hydrolysed (releasing orthophosphate).
The hydrolysis of ATP would have displaced what it is thought to have been a pre-replication system(s) of energy generation because it would presumably have been better and allowed integrated energy metabolism. (The energy demands of replication would have been large.) But that doesn’t mean it’s the best conceivable method — working well and being convenient could have been enough.
Footnote
Although not part of my argument, there is another key molecule in metabolism that has what may be considered a ‘useless’ adenosine component — NAD (and NADP). The redox guts of this is the nicotinamide ring. Did this evolve from a form that was initially part of a ribozyme — perhaps involved in the formation of deoxyribose when the RNA genome was being displaced by the DNA genome?

I'm not convinced that ATP is used more often than the other nucleotides because of chance. In the early stages of cellular evolution, there must have been competition for the nucleotide that gave the highest fitness, and it turned out to be ATP. Why? That's a very good question.

@rhody  You are quite justified in feeling that the answer to this unanswerable question is not chance. However, what is not justified, in my opinion, is the assumption that a non-chance answer is of the type you assume, namely that NTPs were the best molecule for the job, and that ATP was the best of the NTPs. In the latter case it could be e.g. that ATP was the 'cheapest' to synthesize, or that purines bound better to ribozymes than pyrimidines. And if NTPs were a consequence of the RNA structure of the genome, then selection occured at RNA, i.e. it was not 'pure chance'.

Preface
I have already provided an answer to this question, addressing one aspect of it: why a nucleotide triphosphate — rather than any other molecule — was the choice for an energy carrier. In that answer I suggest that the choice of ATP, rather than any GTP, CTP or UTP, was mere chance.
This second question has, in fact, been posed, but was regarded — incorrectly in my opinion — as a duplicate. I have recently become aware of research that suggests to me a possible reason for the preference of ATP over other NTPs, and, as it is independent of my previous answer, I would like to present it as a separate answer.
Why ATP rather than other NTPs?
I am starting from the assumption of an RNA world in which some sort of RNA genome had developed the ability to replicate and exhibit enzymic activity. The ribosome, and especially ribosomal RNA, can be regarded as a fossil of such a world. Harry Noller, in a review of this topic in Science in 2005, considers the bases that are involved in base-pairing in the many RNA double-helical loops, and those that are unpaired in such loops. Many of the latter are involved in ternary interactions in the rRNA, which has an overall protein-like structure. A significant fact that he mentions about the bases that are unpaired in the helical secondary structures is their skewed distribution:

“However, the unpaired bases are not distributed evenly among the four bases. In Escherichia coli 16S rRNA, for example, the proportions of unpaired bases for G, C, and U are 31%, 29%, and 33%, respectively, whereas 62% of As are unpaired, a tendency that extends to other functional RNAs.”

It transpires that many of these ‘unpaired As’ are involved in what are called Type II A-minor nucleoside interactions, which are illustrated in Fig 3. of that paper, below:

In the legend to this figure Noller points out that:

These precise lock-and-key minor-groove interactions between (usually) an adenosine and a Watson–Crick base pair are found extensively in 16S and 23S rRNA. They were first observed in crystal packing of the hammerhead ribozyme and in the P4-P6 domain of the group I ribozyme. A-minor interactions play an important functional role in monitoring codon-anticodon interaction by the ribosome via their unique stereo-chemical fit to Watson-Crick base pairs.

From this I conclude that adenine has unique structural properties that would allow it to form a more precise and stronger interaction to base-pairs in a ribozyme RNA than the other three bases. One of the features of any ribozyme involved in using an NTP to drive chemical reactions would have been to bind the NTP. (We see this in contemporary proteins with the Rossman Fold which binds adenine.)
The greater suitability of the adenine of ATP for this role may be why it, rather then GTP, CTP or UTP, became the major (I would assume initial) choice for energy carrier.

If this idea has been expressed before, I apologize for not acknowledging the fact. Let me know. Otherwise, you read it here first.


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Why is the function of lacA (encoding thiogalactoside transacetylase) not clearly understood?
It's almost half a century since the lac operon was discovered but isn't it weird that the precise role of transacetylase isn't clearly understood ?
Here a wikipedia article with a link to a journal article which proposes a function of this enzyme. This article was written in 2002 but in most of the text books I have referred to ( written well after 2002 ), no function is mentioned.
MY QUESTION : What are the difficulties that are not allowing us to understand the precise role of this enzyme ?

the mechanism of the reaction catalysed by this enzyme is understood. what is not understood is why is this reaction important. perhaps it increases the rate of lactose metabolism in some conditions. knockouts cannot always elucidate roles of genes because there may be only a set of conditions when they play an important role.

Note: This is NOT my field. However, given @biogirl's question, it appears that there aren't many people in this field in the first place. From what I can gather, here are the reasons why I think it has been difficult to study.
I. The lac operon has strong polarity. By this I mean that when the lac operon is induced, lacZ (the first gene in the operon) is translated much more than lacA (the last gene in the operon). Measurements have recorded the molar ratio of $\beta$-galactosidase : thiogalactoside transacetylase (the protein products of lacZ and lacA) upon induction of the operon at 3:1 to 5:1; i.e. when the lac operon is induced 3 to 5 molecules of $\beta$-gal are produced for every one of the transacetylase. If you factor in the relative length of each of these proteins ($\beta$-gal is 1024 a.a.s, transacetylase is 203), it works out that lacZ is being translated at least 10 times faster than lacA when the lac operon is induced. Sidney Altman's lab has attributed this to the fact that there is a cleavage site between lacY and lacA where RNAses can cleave the nascent mRNA transcript, removing lacA from the operon and reducing the production rate of transacetylase. So it appears the cell needs quite a bit less lacA than lacZ---if indeed they need it at all, see point 2---which makes it harder to study.
Sources: Brown JL, Brown DM, Zabin I. (1967). J Biol Chem. 242(18):4254-8.
Li Y, Altman S. (2004). J Mol Biol. 339(1):31-9.
II. lacA seems to provide only a small fitness advantage under somewhat contrived conditions. In A paper from the 70s researchers presented competition experiments between $lacA^{+}$ and $lacA^{-}$ strains in media with $\beta$-galactosides as the only carbon source. For 50 generations there was no competitive advantage of one strain over the other (ratio of $lacA^{+}$ : $lacA^{-}$ stayed at 1). When after 50 generations the researchers added a lot of IPTG, a non-hydrolyzable $\beta$-galactoside, $lacA^{+}$ outcompeted $lacA^{-}$; the absolute fitness of wild-type:mutant could be calculated to be $\approx 1.05$. This means that the wild-type produced 105 cells for every 100 produced by the mutant. I am not a population geneticist, so I don't know if that is a large value or not. For comparison, I used to work in cyanobacterial circadian rhythms, and the absolute fitness advantage for having a circadian clock with the same period as the light-dark cycle in the environment works out to $>1.11$, which is twice as advantageous as the one reported for $lacA^{+}$ over $lacA^-$. In any case, the experimental situation in which $lacA^+$ has a competitive advantage seems rather contrived: growing with $\beta$-galactosides as the sole carbon source with a significant amount of non-hydrolyzable analoges around gumming up the $\beta$-galactoside metabolic machinery.
Source: Andrews KJ, Lin EC. (1976). J Bacteriol. 128(1):510-3.
My read from these observations is that the physiological role of lacA is challenging for a biologist to untangle due to the small size of its effect on bacterial physiology. Fitness advantages of 5% may certainly be useful on evolutionary timescales, but they suggest that the benefit afforded by the enzyme will be very hard to discriminate from noise or other confounding factors in the system. The fact that lacA production is much lower than lacZ in times of lac operon induction also would make it hard to measure.
A postdoc I used to work with advised me, "don't go looking for 2-fold changes in biology," by which he meant don't spend too much time on questions where the size of the effect you are looking at is minor and very difficult to distinguish from noise, bias, measurement error, or other confounding variables. Obviously there are limitations to this advice; a lot can be learned from the the combination of several seemingly minor effects that have big cumulative consequences for an organism. But as a rule of thumb, it's so hard to get strong results when your effect size is so small that going after small effects is justifiable only if you have a good reason to believe there is some profound, fundamental biology behind them. My view is that the consensus of the scientific community up to this point has been that untangling the role of lacA in the lac operon and more broadly in bacterial physiology would involve too much work for too little payoff.

Thank you for your awesome answer ! I would like to point out that 1.1 isn't double of 1.05 so I don't understand how that's twice as advantageous.

Thanks! It's a great question that I'd wondered about, too, so I had fun thinking about it and looking it up. My reasoning for "twice as advantageous" is that the 1 in 1.1 or 1.05 you kind of get for free: the fitness number 1.1 or 1.05 means that 110 or 105 bacteria are produced in the more fit condition vs. 100 in in the less fit condition. So the fitness difference is really  only responsible for an extra 5 or 10 bacteria. So by that measure, a fitness of 1.1 is responsible for twice as many additional bacteria as a fitness of 1.05. Though that might not be the best way to summarize it.

Alright. You have really done a lot of work to find all those references !

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Is the poly(A) tail added while transcription is still underway?
I read in Campbell that

....splicing and poly A tail addition may also occur while transcription is still under way.

How can the poly(A) tail be added while transcription is still going on?

splicing is co-transcriptional not polyadenylation. You might have missed a clause in the statement :P

@WYSIWYG The whole statement says " In the cell, the 5 cap is added soon after transcription is initiated, splicing and poly A tail addition may also occur while transcription is still under way."

polyadenylation signals are present at the end of the gene. so it is not possible.. that means this textbook is wrong

@WYSIWYG Yup that is what I think too, but it would be better if we wait for some other people to answer as this textbook is a reputable source.

the textbook will have a reference for this statement. check that.

@WYSIWYG The textbook contains no references at all...

then it's a bad textbook :P

@WYSIWYG Wohoo !!

@WYSIWYG Wikipedia says " Polyadenylation occurs during and immediately after transcription of DNA into RNA."

let us continue this discussion in chat

It's slightly more complicated than the comments above indicate.

Glover-Cutter, K et al. (2007) RNA polymerase II pauses and associates with pre-mRNA processing factors at both ends of genes. Nature Structural & Molecular Biology 15: 71-78

The authors present evidence that RNA polII pauses 0.5 - 1.5 kb downstream of the poly(A) site where processing factors are recruited (cleavage stimulation factor, or CstF, and cleavage polyadenylation specificity factor, CPSF). So the polymerase is still engaged with the template and the premRNA when processing is initiated, although it may not be actively elongating the transcript.

"Localisation of the active polII-3' end processing complex well downstream of the poly(A) consensus sequence agrees well with the cleavage of Chironomus BR1 transcripts after 600 bases of downstream sequence has been transcribed. This model is also supported by the fact that efficient poly(A) site cleavage requires an intact RNA tether linking the poly(A) site with the downstream polymerase." (references are cited in the original).

It is a semantic question as to whether you call this cotranscriptional processing.
[Incidentally this is yet another example which contradicts the commonly-stated idea that evolution acts to optimise everything to conserve ATP - here we have the transcription process discarding the energy from approximately 1000 phosphodiester bonds per transcript.]
UPDATE
@WYSIWYG The polymerase goes past the site where the poly(A) will eventually be added, and makes another 1000 bases of RNA before pausing to recruit factors that are needed for the subsequent cleavage at the pol(A) site which now lies "behind it". After that the poly (A) tail is added at the newly created 3' end. So the initiation of poly(A) addition (in the sense that the cleavage is an obligatory first step in the process) is accomplished while the polymerase is still engaged. I agree that the actual addition of the poly(A) cannot in any way be considered to be cotranscriptional.
I was trying to make the point out that it isn't simply a case of the polymerase encountering the cleavage site and dropping off to allow a second unlinked process to take place.

But recruitment of CstF or CPSF can't be considered as an event of polyadenylation. Splicing does indeed happen co-transcriptionally but it is theoretically impossible to have a co-translational polyadenylation for the accepted unidirectional transcription model. Besides, how would the polymerase sense the polyA signal 1.5 kb upstream without actually sensing it (or else it needs an accomplice); perhaps the assembly just happens as a result of processes initiated during transcription start.

IMHO it is still incorrect to say that polyadenylation happens during transcription. It is equivalent to saying that ovulation happens since the infancy of a female.

As others have stated, splicing does happen cotranscriptionally but you cannot be actively transcribing the RNA while it is being transcribed. However, it is generally accepted that a transcript can be polyadenylated while the RNA polymerase is still transcribing - this is called the torpedo model. The distinction is that the transcript has been cleaved between the polymerase and the polyA, but they were still part fo the same transcriptional event.  See the figure here...
http://www.nature.com/nsmb/journal/v11/n12/fig_tab/nsmb1204-1156_F1.html

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Which surfaces contain no epithelial tissues and which epithelial tissues are vascular?
Epithelial tissues are found on all the surfaces of the body; including external surfaces and surfaces of organs etc.
Are there any surfaces which do not have epithelial? I have read in my book that almost all the surfaces has epithelial tissues but there are some exceptions. What are the exceptions?
Similarly, almost all the epithelial tissues are avascular. But there are some exceptions which are vascular? Which epithelial tissues are vascuar?
*I'm talking about a human body.

Epithelial tissue is vascular, dead epithelial cells form the surface of skin, hair and nails.

no, epithelial tissues are avascular @Skippy-psI'mawoman. A few exceptions are vascular. I want to know what are these exceptions.

Well we have different understanding then.. perhaps you'd like to cite your source>

read the 4th line.
http://en.wikipedia.org/wiki/Epithelium

You answered a question on the body breaking down glucose. Why does it do this? What do cells require to maintain life. There are very few tissue types that have little or no vascular supply. Bone, cartilage and keratinized epithelial cells to name some off the top of my head.

Most of the epithelial cells do not have vascular supply because they are exposed to the external environment. They can easily be damaged and severe bleeding can occur.

vascular wall cells are called endothelial cells.

@Skippy-psI'mawoman Epithelial tissues get all their nutrients from the blood vessels in the basal membrane. All( almost ) epithelial tissues have a basal membrane.

Most people wouldn't consider osteoblasts as epithelial cells, thus many surfaces of bones could be said to be without epithelium.  Your going to get objections to that, however, on the idea that the periosteum is still a "connective tissue."

Also add to that serosa or mesothelium is also vascular despite being a layer of squamous epithelial cells...

I think you're talking about two different things.  I assume Rafique is referring to vascularized epithelium, but user4693 is referring to vascular epithelium.  Although the terminology is very similar, the difference is important.
vascular epithelium = endothelium of a blood or lymphatic vessel.
vascularized epithelium = epithelium with a blood supply, meaning that small vessels invade the epithelium (pass between epithelial cells) rather than simply occurring in the underlying basement membrane or connective tissue.
Most epithelia are avascular (lack blood vessels).  As far as I know the only vascularized epithelium in humans is found in the inner ear (1).  I've been told that the lips have vascularized epithelium (which is why they appear reddish), but I don't completely trust that source and I cannot find anything online to support it.
Also, some pathological conditions can cause vascularization of certain epithelia, like the cornea (2).

I suppose "vascular eipthelium" could be a correct term, but I've always seen endothelium (or endothelial as adj as @wysiwyg pointed out). Perhaps this helps prevent the confusion.

I've always used endothelium.  However, I noticed that some online sources (notably wikipedia) use the term "vascular epithelium".  I thought that may be why earlier comments disagreed, so I was trying to, hopefully, provide some clarification.


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Common Ancestry of ETCs and ATP Synthase complexes
Rickettsiales are widely regarded as the ancestor of eukaryotic mitochondria through endosymbiosis.
Cyanobacteria are widely regarded as the ancestor of eukaryotic chloroplasts through endosymbiosis.
These two organelles bear striking similarities in terms of structure and mechanics. There seems to be plenty of information regarding speculation on the endosymbiosis that led from these free-living organims to the organelles. However I can't seem to find much on speculated relationships between these organisms in terms of common structures.
My Quesions : Are the electron transport systems and chemiosmosis simply ubiquitous phenomena in prokaryotes, or are these similarities evidence of highly conserved common ancestry? Or is there another answer?
Is there any information regarding the phylogenetics of Rickettsiales and Cyanobacteria. Do these two organisms belong to a single small clade or were these biochemistries (ETCs, ATP Synthases, etc) ubiquitous at some point and have simply been preserved in these two organisms today?

photosynthesis and respiration both use electron transport to generate ATP. However, in photosynthesis the proton is produced by photolysis of water whereas in respiration it is generated by oxidation of organic molecules, The ATP synthase is essentially the same. Also, the electron carriers like quinones and cytochromes are very similar. The different proton source in these two reactions must be a resultant of habitat among other factors.
Assuming that you already know these details, I am unsure of what exactly you are asking.

Rickettsia and Cyanobacteria are not part of a small clade that share these features.  ATP synthases are present across all domains of life, and they are all homologous, i.e. derived from a common ancestor.  The means its fairly likely that the last universal common ancestor had some form of ATP synthase.
ETCs and ATP synthases are part of the chemiosmotic theory put forward by Mitchell.  Whats beautiful about this mechanism is that you just need a single ATP synthase to make your energy, and it can be used regardless of your metabolism, be it a Cyano or a Rickettsia.  All you need to do is somehow couple your metabolism to a proton motive force across your membrane, and then you just let the protons fall back down their electrochemical gradient, powering the formation of ATP.
Organisms from all corners of the tree of life use this strategy, so this is not some special common feature linking the organisms that ultimately became eukaryotic organelles.  Its worth noting that there are alternatives to ETCs and proton motive force-based ATPases, you can make ATP by substrate-level phosphorylation like in fermentation metabolisms.


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Do bigger animals have more testosterone?
I was wondering the other day outside, thinking about varieties of species and their aggression levels, etc.
I had a theory that since these highly aggressive, powerful, and viciously advantageous animals in fights with humans, such as lions, tigers, rhinos, elephants, etc. are so strong and aggressive in the wild compared to us humans and smaller animals, do they have more testosterone?
Like, in animals, does testosterone correlate with size, possibly explaining why a lion is heaps more slender, muscular, fit, agile, aggressive, and vicious than a typical human?
Basically, does the bigger size and aggression in wild animals correlate to their higher testosterone, such as larger size equal to larger testosterone in comparison to other smalelr or less aggressive animals, or is it different?

It is a good question. If I may ask, what instilled your curiosity?

Lions are more vicious than humans? What makes you think that? We are far more aggressive and violent than lions. Also, you may be surprised at how vicious and aggressive certain snakes and many insects are. Not to mention viruses which are little packets of aggression and little else. Finally,consider some extremes, the blue whale is the largest living animal and it is far far less aggressive than, say the praying mantis.

It is not that easy. Off the top of my hat I can try to pinpoint a few fallacies in your theory:

Scaling of the body happens in three dimensions and thus to a power law. As such allometric equations have to be applied when dealing with the total amount of substance in the body. Different species have different correlation factors of body mass to total substance amounts.
Angiogenesis (the formation of blood vessels) is affected by Allometry (the relationship of body size to the 'biology')
Diffusion factors are similar in closely related species. This means in order for messenger molecules with a short acting range/half-life (e.g. nitric oxide), the total amount in the animal may indeed be likely higher and the messenger in question may be produced on-site (e.g. endothelium). Testosterone as the name indicates, is however produced in the testes and released in the blood stream.
The sensitivity and regulation of the receptors themselves (which react to a substance) can be different in different species. It may also be weakly responsive to begin with at the genetic and ultimately the folded protein level. A good example of that is the melanocortin receptor MC1R in a gross section of the white human population. Even if you were to produce the same level of melanotonin, the melanocytes wouldn't respond to the same degree as in Humans with darker skin.
Messenger molecules can be re-purposed and take over or be given additional roles and functions over evolutionary-time. Again, Melatonin may serve here as an example.
After all a given messenger is already evolutionary tested, especially in regard to cross-talk, Haptens, and other adverse molecular interactions in the animal species and comes with the full set of molecular machinery adapted to it, - a "luxury" a new messenger doesn't have. As such pressure usually exists to re-use given messengers.

Like, in animals, does testosterone correlate with size, possibly
  explaining why a lion is heaps more slender, muscular, fit, agile,
  aggressive, and vicious than a typical human?

I doubt you will find typical humans or typical human populations from a biological perspective. Your view may be skewed by economic factors.

Basically, does the bigger size and aggression in wild animals
  correlate to their higher testosterone, such as larger size equal to
  larger testosterone in comparison to other smalelr or less aggressive
  animals, or is it different?

To a large degree the behavior is determined by the niche the animal is in. As to which concerted molecular messengers make the "evolutionary cut", by best influencing an animals behavior in its given "time-domain" is another question. As the question is complex much is still researched.
Take this counter-example: A mouse and an elephant have very different masses resulting in different inertial forces. Fleeing from an enemy will take different strategies in regard to the central nervous system as well as the body, and demand different levels of messenger molecules at different places, at different times for both animals. Yet the substances in question will likely be similar.


text:
Is the book "Bioinformatics for Geneticists" outdated?
I am going to be working with genetics data in my organization's data warehouse next year and helping our biotechnology department.  I work in academic research, but I have very little genomics background.  I was able to find the book called "Bioinformatics for Geneticists" (Edited by Michael R. Barnes & Ian C. Gray) at a used book store for a couple dollars.  It looks like it was published in 2003.  Do you think this book is too outdated, or would I still get a good introduction to the subject?  If you think it's too outdated, what book(s) do you recommend?

I haven't read through all of it, but from the second edition, which I found available online here, it seems to me that it might be a good introduction, but (as expected from the publishing date) it is really missing out on all the next generation sequencing stuff. Which is important, not only because it is my favourite field.
I am not sure what you want to get from it? You say you have little genomics background, but then you got a book that expects you to know the genetics, but explains the bioinformatics.
There's a basic description of the background of sequencing at the NIH website, maybe that helps.

The hyperlink of "here" is not working for me.  Which country are you in?

Germany. It is loading slowly,though. But it works, and I checked, it is not as site we might have some kind of paid subscription for.

After it downloaded, I got an exe.  What happens when you run it?  I didn't want to open it at work, so I will wait until I get home and test it.

Well, for me it's just a pdf. Maybe you got an exe for a pdf-reader? I was looking at it from a Mac, so no exe at all.

Yah, maybe.  I'll try it tonight.  Yep, this was Windows.  I'm in the US by the way, but that shouldn't matter.  I was asking because of the latency.  It took several minutes to download.

Well, it is a whole book, with graphs and all. I guess you just need to be more patient or find a faster internet connection. ;-)


text:
Why does ice reduce swelling?
It is common practice to use ice packs on injuries that cause bruising and swelling. It seems to be  an effective method to assist in reducing swelling.
Why does ice reduce welling?

related http://skeptics.stackexchange.com/questions/7816/does-putting-an-ice-pack-on-an-injury-reduce-swelling

It may be due to vasocostrictory effect of cooling. As vessels would constrict less fluid would be lost from the blood.

@biogirl are you referring to the cells that enter the tissue during inflammation?

I am referring to narrowing of blood vessels which would reduce both loss of fluid from the blood and the entry of WBCs in the area.

there are also associated cells that bring fluid to the tissue when damaged

I don't know whether there are such cells that actually "bring" fluid to the tissues. I just know that histamine released by mast cells cause dilatation of capillaries which would cause fluid from blood to leak out. Are you talking about mast cells?

I'm too tired at the mo. it's 2.43am to have a discussion about the histology of inflammation.. I find it very interesting.. Please feel free to write an answer.. and I'm sure we'll catch up another day :)

Alright. Immunity is damn interesting :p

@biogirl yes it is, I have a horrendous autoimmune disease :/ this has caused me to read many journals.. :/ and much unhappiness.. in my case my body lays down collagen, to plug up the dmamage of destroyed cells, (my cells I have an immunity against).. Anyway.. this is WHY I didn't want to get started! LOL It's a better topic for chat (not the Q) inflammation.. the curse of my life :) Nice to meet you! I am usually on [pets.se] and [cogsci.se]

@biogirl ah and you're a fellow Aussie! :) I wish my kids were as interested in all this as you are! cheers

let us continue this discussion in chat

Swelling is one of the signs of inflammation. Inflammation involves release of histamine by mast cells present in the tissues. Histamine causes vasodilation and leads to leakage of fluid from the blood, along with which neutrophils and other WBCs also enter the area. They phagocytose microbes that might have entered with the injury.
Applying ice would cause vasoconstriction* (i.e. narrowing of blood vessels.) which would reduce the leakage of tissue fluid and hence swelling.
*If you wonder why ice(or any cool thing) causes vasoconstriction think why you turn pale in winter ? Vasoconstriction reduces blood flow to the particular area and hence the exchange of heat is reduced which conserves body heat in cold environments.

http://biology.stackexchange.com/questions/11325/what-happens-during-a-raynauds-episode

Just to add to this- the recommendation for healing using ice is to alternate ice and warm packs so that the fluid exchanges, swelling and then constricting to aid healing - that's where a lot of the relief comes from.


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Image analysis of GFP-tagged protein localization bursts
I'm reading an article (full text here) that analyze the dynamics of localization of a GFP-tagged transcription factor (Crz1) over the time at the single-cell level, by taking movies in a fluorescent microscope.
In Methods section they say:

Fluorescence cell images were segmented using a Hough transformation algorithm in Matlab, provided by Sharad Ramanathan. Localization score was determined by the difference between the mean intensity of the 5 brightest pixels in the cell and mean intensity of the rest of the pixels in the cell.

The segmentation process here seems to be the identification of cells over the background. They then calculate a localization score, for each frame of the video, for every cell. Now there's the part that I can't understand:

Bursts were identified by thresholding traces at >1 standard deviations above background noise, estimated from the lowest 20% of values.

I searched some definitions of "background noise", but I can't figure out what does it mean in this particular context. Moreover, "lowest 20% of values" of what?
Is it plausible that they define it for the lowest 20% of values of localization scores over the time, at the cell each time considered?
Maybe can be useful a screenshot of a single cell in a photogram of the video:

Yep, the Hough Transform is a way to pick out shapes you're interested in, in this case they probably have it set to find circles, and they use that to segment the image.
I think that you have interpreted their methods correctly.  For each cell they make a trace of localization score vs. time, localization score defined in arbitrary units as the difference between the mean of the five brightest pixels and the mean of the remaining pixels in the cell.  I think the lowest 20% refers to the frames in the video that have the lowest 20% of localization scores.  They take the lowest 20% of localization scores, calculate a standard deviation, and then for any frame that has a localization score that is more than 1 standard deviation above the mean of those 20%, you say that frame exhibits a burst of localization.  If I'm understanding this correctly, this process would be repeated on every individual cell.
My interpretation is that the 20% doesn't have anything to do with the signal intensity from the background pixels, and it comes from analyzing the series over time, not a single image.

I don't know a whole lot about signal processing but I am a little familiar with artificial intelligence. Perhaps this wiki would be helpful http://en.wikipedia.org/wiki/Image_segmentation. I am familiar with k-means clustering discussed there and as a trivial segmentation method it would indeed identify the cell versus the background of the photo. The Hough transformation would be more sophisticated and probably more useful for this application but if you want to get a sense of the process the naive k-means algorithm may be helpful.
I interpret the "lowest 20% of values" to refer to the localization score values, the lowest being those who are darkest in your image. That is, the background the cell is imaged on. The background noise refers to the fact that a signal processing algorithm without any preprocessing may try to identify patterns from the background of the image rather than the cell subject matter, which is the part the researchers are after. This is why they perform the segmenting.
For instance, imagine a k-nearest neighbors algorithm http://en.wikipedia.org/wiki/K-nearest_neighbors_algorithm for computing a "localization score" for image brightness. Your paper is interested in the intensity of GFP for a cell. In the image, pixels on the border of the cell with its background will have artificially low score values because of the background: the adjacent pixels that are in the background and not part of the cell are dark, but that doesn't mean anything related to the biology of the problem. This is the noise.
The lowest 20% of values, then, should refer to a single image, not to a series over time.


text:
Growing crops on the Moon
The short version of my question is this:

It's some time in the future. I go into my back garden and focus my telescope on the Moon. The surface is virtually covered with giant greenhouses, growing food to support the cities that have sprung up there. The question is: what plants are they growing in those greenhouses?

Factors such as temperature, water, soil quality etc. can be controlled easily enough if you already have the ability to build sealed greenhouses in a vacuum. There are also a number of experiments on growing food in closed systems where air and water are recycled (the Biosphere 2 project being the best known). The low gravity can't be controlled, but there have been a number of experiments on plant growth in microgravity conducted on the international space station, so growing plants in Lunar gravity should be possible. There have also been some interesting results from growing plants in an Earth-based approximation to Lunar soil.
However, another important issue is the length of the Lunar day, which is 28 Earth days long, meaning that the Sun shines continuously for two Earth weeks, followed by two weeks of total darkness. I'm interested in what's known about how plants could adapt to this, but I haven't been able to find any research papers on the subject. Of course it would be possible to simulate an Earth day using artificial lighting, but the energy costs of doing this on a large scale would be rather high, so for economic reasons future Lunar farmers would likely want to keep it to a minimum.
So my first question is, has any research been done on the effect of extreme changes in day length on plant growth?
Secondly, is there any type of food plant that would be particularly likely to cope with such an environment (perhaps with some suitable genetic modifications)? For example, would normal crop plants such as cereals be able to build up enough sugar reserves in two weeks to survive the next two weeks in total darkness? If not, is there another type of plant that's more likely to be able to adapt to this? Or as an alternative strategy, is there any crop that grows fast enough that its shoots could be harvested after only two weeks of continuous sunlight? (Some individuals would have to be grown to maturity under artificial light in order to produce seeds, of course.)
Finally, I'd be grateful for pointers towards research on any other issues that I might have missed that are relevant to the problem of large-scale Lunar agriculture.

this question is quite long, perhaps you could make it clearer what you are trying to ask

@GriffinEvo are long questions considered bad here? If so that makes me sad. I think I've set out quite clearly what I'm asking in the final three paragraphs - could you please be more specific about what you found unclear?

There is no limit on length, I just feel that the key points you are trying to get to get a little lost and could be made to be more obvious, questions that are long or difficult to get to key point of are less likely to get good answers. So don't be sad :)

I suggest you rephrase your question to remove the reference to the moon. The obvious answer is that artificial light can be used and controlled so there is no reason why growing crops on the moon would be affected by its day/night cycle. Consider that if we have bases on the moon, we will already have lighting and the expense will be negligible compared to everything else necessary to make that possible. The question you are asking is how plants can/could adapt to different day/night cycles and it is a very interesting question but mentioning the moon distracts from it and confuses the issue.

@terdon I'm not talking about bases, I'm talking about large-scale agriculture. From basic thermodynamic considerations, providing a square kilometre of crops with full strength artificial daylight would require at least a square kilometre of solar panels, thus reducing the overall yield by 50%. Lunar agriculture might use some artificial light, but you'd really want to keep it to a minimum. I'll consider your suggestion, but I really am interested in the specific issues imposed by the Moon.

I agree with @terdon and think that the Q should be rephrased. Both "how plants cope with extreme day/night cycles" and "what plants that might be suitable for lunar greenhouses" are interesting questions, but at the moment your question is a bit unclear.

@Nathaniel the specific issues imposed by the moon also include the details of lunar soil (different pH, lack of bacterial species and nutrients etc, see here), the lack of atmosphere both as a source of necessary gasses and as a filter for UV. Since you seem to be exclusively interested in the effects of a different day/night question, I suggest you restrict your question to that.

@terdon I explained in the question that I'm aware of the relevant research pertaining to those issues (with the exception of the UV filtering, but that's trivially solved by coating the glass). However, there may be other issues that I haven't thought of. The question is about growing crops on the Moon, and these "I like your question but you should change it to a completely different question" comments are starting to bug me. I agree that a more generic question about adaptation to day length would also be interesting - please feel free to ask it yourself.

@Nathaniel I don't mean to bug you and you are, of course, welcome to leave the question as is. I am just pointing out that you are not making your point clear and that is reflected by the answer you have received and by the fact that you have already collected 3 close votes one each for unclear, too broad and primarily opinion based. Your call.

@fileunderwater if you can be specific about what you found unclear, I will gladly attempt to clarify it.

@terdon I expected better from this community, but if they choose to close it it's their loss. I'm an expert from another field with what I believe is a perfectly specific and well-defined (if somewhat speculative) question about biology, and if that's not welcome here then I guess this just isn't the site for me.

@Nathaniel don't take it personally! You may well believe that your question is clear but if people do not understand what you are asking, then it is obvious that others do not agree. Various people have already suggested ways of clarifying and there is clearly an interest in your question which I, personally, hope will stay here and get a good answer. You know how the SE sites work,this kind of back and forth is normal. You are also combining many questions in one which is bad form on all SE sites.

@terdon there is only one question. It is stated in a quotation block  at the top. The rest is clarification and background material - something which on most other stack exchange sites would be appreciated. I'm very happy to try and make it clearer, but if people keep just saying "it's unclear" without being specific about what they're having trouble with then there really isn't much I can do. Closing it would be perfectly reasonable if the question was against site policy, but it patently isn't, and the fact that the close votes are all for different reasons reflects this.

The question in the quote block is what plants are they growing in those greenhouses? which cannot be answered, there are too many ways of dealing with the various problems that lunar cultivation raises. You could have GM crops, airtight greenhouses, a terraformed moon, artificial gravity, unicellular chemosynthesizing algae, solar mirrors, artificial light, soil transferred from Earth, modified lunar soil, unmodified lunar soil with modified plants, the list goes on. What seems clear to someone outside the field can be very complex to experts who know more of the underlying complexity.

@terdon yes, the quoted part can't be answered on its own. That's why the following section on background and clarification is necessary - but then people complained it was too long, so I can't win.

@terdon again, most of the things you mentioned are already covered in the question. People keep bringing them up even though I already covered them, and I don't understand why. But Basically all the options you mention are possibilities, with the exception of artificial gravity, which is physically impossible (trust me, I'm an expert and know more of the underlying complexity) and artificial lighting unless it's kept to a minimum, for reasons already discussed. The question is aimed at someone with the knowledge and imagination to weigh those options up and arrive at a solution.

I think I can re-write it to be clearer, but it will have to wait until I'm at my computer, either tomorrow or next week.

@Nathaniel One can be concise whilst being being clear. Your question has too many unknowns to give a specific answer and you seem to be looking for an overcomplicated answer. The basic answer is simple, humans would have to adapt (by modifying conditions on the moon to resemble those found on earth) the plants would likely have to do very little adaptation.

@GriffinEvo the question I have asked is difficult and requires a considerable amount if expertise to answer. That is quite a different thing from being too broad, and I didn't think it was against the rules. It must definitely does have a specific answer. I completely disagree that it can be asked any more concisely than its current form, and when I edit it for clarity it will necessarily get longer. I have explained many times why modifying the day length won't work, and if you ignore that then you are simply not addressing the question.

@Nathaniel you think that getting to the moon, providing sufficient water (a resource not found on the moon [in any large amounts at least so far]), building farms and filling them with artificial atmospheres (from gases not found on the moon), providing a nutrient rich soil substrate (again I believe this is not already on the moon), dealing with low gravity, and starting human colonies large enough to maintain and require these farms across the entire moon surface (not currently on the moon) are all feasible... but we can't manage to produce a light source?

@GriffinEvo those things are all one-off costs. Lighting requires a continuous supply of energy. Maybe there are other options (fission, fusion) but the most obvious source for that energy is solar panels, and as I've discussed at length, the issue then becomes one of land area. The idea of agriculture is to maximise yield from a given area of land, and if half that land is occupied by solar panels then only half can have crops growing on it, which seems quite inefficient.

@GriffinEvo that's not to say there can't be any light. The sunlight that reaches a shady spot on a cloudy day on Earth is probably less than 1% (maybe much less) of the total energy provided by the Sun, and supplying that level of artificial light becomes much more feasible. But you still have to use plants that can cope with a 28-day dusk-daylight cycle.

About availability of energy needed to artificially light the plants during lunar night, I wouldn't worry much: it's probably a lot smaller than the energy needed to keep greenhouses warm during that night.

Plants are adapted to the conditions we have here on earth, therefore, for them to grow on the moon we would have to recreate the conditions found on earth (or at least find conditions that we can create and they can grow in). To do this we would need to replicate climate (temperature, air pressure, humidty etc.), provide (sun)light at the necessary intervals and intensity, provide water, air, and nutrients of the right composition, intervals and intensity. That is a simplified version...
In reality there is great variation in how plants require these things. Some cope with long dark periods better than others, some cope with drought better than others, some cope with chemical variation in the soil better than others so answering this question is hard. But generally growing plants on the moon will require the ability to recreate (to some degree depending on the sensitivity of the plant) the conditions a plant has evolved under on earth.
Thus to answer your questions:
Length of day can have strong effects on growth patterns, two weeks of darkness is likely to be a major upset for plants! Just transplanting plants of the same species from different latitudes can affect the growth patterns because of changes in length of day. Try putting some plants in darkness for two weeks and see what happens.
Plants all vary in their ability to meet the requirements of space growth. There will only be a short list of plants that could with "small" modifications to the moon's environment, the more we adapt (adding artificial light, watering, adding nutrients etc) the longer that list would become - the limitation is in our ability to adapt the moon.
See above for reasons why plants might struggle. Oh and we would need to consider the effects of reduced gravity too...
Here's a little something from nasa about how plants are used in space vehicles. And another on light and gravity.

Thanks, but I did mention in the question that I'm aware of research on most of these issues. I'm asking if there is any research specifically on the day length issue, and also about which specific types of plant are most likely to be able to adapt.

@Nathaniel I think if we get to the point where we can realistically inhabit the moon and modify it to grow some plants, then we should be able to get it to the point where most can grow. Whether it's wheat, corn, or oak trees, there will have to be some significant modifications made by us to the moon before we can grow any. Once we can grow one then small tweaks to the system will be needed to grow the others. Feels like its more how we could adapt the moon than how the plants can adapt. It's likely small simple things would be easiest for us to grow but crop plants would be most necessary

Sure - my thinking is that factors like water, soil quality, atmosphere etc. are easy enough to control if you already have the technology to build sealed greenhouses in a vacuum. Gravity can't be controlled at all, but if we can grow plants on the ISS then it should work on the Moon. That leaves the day length, which can only be changed using artificial lighting, which will need an expensive source of energy. So my guess is that the choice of which crop to grow would be mostly determined by its ability to cope with weeks of darkness.

@Nathaniel I can't find any research testing such long periods of light deprevation but my gut feeling is telling me not much would do well. These shade tolerant plants still need a few hours of sunlight per day http://www.motherearthnews.com/organic-gardening/shade-tolerant-vegetables-zm0z11zsto.aspx#axzz2jr6hxNjP

something like this might work... http://www.nytimes.com/1993/01/12/science/russians-to-test-space-mirror-as-giant-night-light-for-earth.html?pagewanted=all&src=pm


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At what temperature does DNA re-anneal?
If primers weren't present in PCR at what temperature would DNA re-anneal? I am wondering how primers manage to bind on DNA strands before DNA manages to anneal back together.

To answer your second question, one of the main reasons primers anneal before your target re-anneals to itself is not because it binds stronger, but because you add primers in large molar excess to their targets.  The primers will find your template faster than your template will find another matching template, and once the primer is annealed the template cant bind onto another template even if that reaction is more energetically favorable.  This molar excess is a requirement for the exponential amplification in PCR, and when you start to lose the excess primer concentration you lose exponential increase due to your targets re-annealing (and you get the production of unwanted PCR artifacts like chimeras).  As for the temperature, it depends on your template, but I guess it has to be somewhere between the primer annealing temp and the temp of your melting step.


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Difference in length of Okazaki fragments
The length of Okazaki fragments in the lagging strand is about 100-200 nucleotides in eukaryotes and about 1000-2000 nucleotides in prokaryotes.

What (molecular mechanism, enzyme type ) determines the length of
  these Okazaki fragments?
Moreover, which, longer or shorter, fragments would be more
  advantageous (energetically and considering accuracy)?

Longer fragments means less use of DNA ligase, DNA polymerase-I (prokaryotes) and other enzymes required to convert the okazaki fragments with dispersed RNA primers into a normal strand, and hence lesser scope of mistakes during replication in the lagging strand. Shorter Okazaki fragments improve telomere longevity, by reducing the capped-off portion after every division. Which of these views is correct?

Do you think it has to do something with our dna molecule being linear ? If there are shorter okazaki fragments there will be shorter telomere. There is no need for short okazaki fragments in prokaryotes as their genomes are circular and thus there are no telomeres.

@biogirl I guess it is the length of the telomere portion that is capped-off at every division, that will be reduced with shorter Okazaki fragments. Anyway, improving telomere longevity possibly could be a reason:)

First off, eukaryotes aren't "more evolved" than prokaryotes, just specialized in different ways. If anything, prokaryotes like E. coli with doubling times of as little as 20 minutes might suggest that they are "more" evolved than slow-growing eukaryotes for the basic aspects of growth, such as DNA replication. So the fact that prokaryotic Okazaki fragments are longer might actually suggest that longer Kkazaki fragments are better for DNA replication efficiency, and that they got shorter in eukaryotes due to some other tradeoff. It's pretty much useless to infer adaptivity in this fashion.

@A.Kennard Corrected in the question.

@SatwikPasani No worries. Sorry to be pedantic; I've worked exclusively with bacteria so far and I can get overly defensive of the little critters ;) Wish I could help actually answer your (interesting) question!

I think you are thinking too much into this. Not everything needs to give an advantage :) There is a famous paper about why one should not assume every part of an organism is meant to give an advantage http://rspb.royalsocietypublishing.org/content/205/1161/581.abstract I would say the length of fragments is more a result of processivity, binding constant of enzyme doing the priming, enzyme concentration etc rather than it being a result of an adaptation to anything in particular.

@vonMises True and probable, but the fact that the difference in replication between prokaryotes and eukaryotes in other factors involved in replication is quite pronounced, definite and attributable in many cases to the improved efficiency in case of eukaryotes.(eg. better repair, regulation owing to multi-factor control of initiation). So, maybe length of okazaki fragments belongs to that class of differences, especially so since the difference in length is of an order of magnitude (about 10 times)!

@SatwikPasani Just wondering ... Could this possibly also be a reason why bacterial replication is a lot faster than eukaryotic ?

Okazaki fragments is based on the interaction between dna primase or dna helicase,in eukaryotes interaction is more so length is short as compared to prokaryotes.

I have found one more possible reason from Bruce Alberts' The Molecular Biology of the Cell: (Ch. 5 page 254)

Nucleosomes are spaced at intervals of about 200 nucleotides pairs along the DNA strand , which may explain why new Okazaki fragments are synthesized on the lagging strand at intervals of 100-200 nucleotides in eukaryotes, instead of 1000-2000 nucleotides as in bacteria.

As already discussed by me and @SatwikPasani in the comments, increasing telomere longevity in eukaryotes by reducing the length of okazaki fragments, and consequently reducing the part of telomere cut-off after every division might be another reason for having shorter fragments in eukaryotes as compared to prokaryotes which do not contain telomeres.
EDIT : Having thought over it again, the relation between Okazaki fragment length and telomeres do not seem logical as only RNA primer length is important when considering telomere length.

Balakrishnan and Bambara (2013) explain the regulation of (and differences between) prokaryotic and eukaryotic Okazaki fragments in detail.

@satwik I was thinking over this question again and I think what I said about telomere length is wrong. Okazaki fragments don't influence telomere length, it is just the RNA primer of the lagging strand which is not replaced and thus leads to shorter telomeres. So, I don't see any relation between shorter Okazaki fragments and  telomeres.  What say ?

@satwik But it would be interesting to find out whether the RNA Primers used in eukaryotes are shorter than those used in prokaryotes.

true. I would certainly be interested in finding a similar trend of lengths for the primers.

@biogirl I was wondering the same thing regarding variation in  the length of Okazaki fragments. Your discussion has been helpful. Thanks.
As you mentioned, did you find any relation between variation in  the length of RNA primer and telomere longevity?

An addition: the lagging strand synthesis involves bending of the ssDNA such that it aligns in the direction of the replication fork. The nucleosomes (and the condensed eukaryotic chromatin) can hinder this bending such that only short stretches of bent ssDNA is available for the lagging strand synthesis.

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


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What happens during a Raynauds episode?
Raynaud's phenomenon can be a serious health issue, as the blood flow to the extremities, mainly the fingers is compromised, causing fingers to blanche, and then turn blue. Severe Raynaud's can cause gangrene in illnesses like progressive/ diffuse scleroderma.
I am not asking about connective tissue disease per se, but what occurs during an actual Raynaud event (for a better way of putting it), not what precipitates the condition to occur within a particular person and not another.
what are the underlying biological processes that cause the blood flow to be compromised like this?

^^^ please note the tag of neuroscience, this condition  involves the autonomic nervous system.

It is due to vasospasms that lead to constriction.

@biogirl care to provide an answer?? :)

The Raynaud phenomenon is a recurrent vasospasm that is associated with cold temperatures and emotional stress [1]. Excessive vasoconstriction leads to hypoxia. The cause of vasoconstriction is a hyperactivation of the sympathetic nervous system [2] and probably the lack of parasympathetic response. The mechanism is thought to involve both central neural issues and peripheral impairment (subclinical polyneuropathy) [3]. The resulted chronic hypoxia leads to pain, atrophy and sometimes even ulceration [2].

References:

Bakst R, Merola JF, Franks AG, Sanchez M. Raynaud's phenomenon: pathogenesis and management. J. Am. Acad. Dermatol. 2008 Oct;59(4):633-53. doi: 10.1016/j.jaad.2008.06.004. PubMed PMID: 18656283.
Wikipedia contributors, "Raynaud's phenomenon," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Raynaud%27s_phenomenon&oldid=613954124 (accessed June 27, 2014).
Koszewicz M, Gosk-Bierska I, Jerzy G, Bilińska M, Podemski R, Budrewicz S, Adamiec R. Peripheral nerve changes assessed by conduction velocity distribution in patients with primary Raynaud's phenomenon and dysautonomia. Int Angiol. 2011 Aug;30(4):375-9. PubMed PMID: 21747356.


text:
Which mountain range was formed first (historically) and which the pedigree is correct?
Source 1:

Source  1 shows a map of a particular area. In this map you will find the  mountain ranges 1 and 2, the species P, Q and R. Two possible pedigrees of  the ancestral history of the species P, Q and R are drawn .
Which mountain range was formed first (historically) and which  pedigree is correct?

1 might have formed first and I think pedigree 1 is correct.

If mountain range 1 was formed first, pedigree 1 is correct.
If mountain range 2 was formed first, none of the two pedigree seem correct.
If mountain range 1 was formed first you would first have the split of the initial population into population P and the population Q+R. Then, the formation of mountain range 2 split the population Q+R into Q and R. Therefore, Q and R are more closely related than they both are to P. Therefore Pedigree 1 is correct.
You can apply the same kind of reasoning by guessing that mountain range 2 was formed first and you will realize that you would expect a pedigree different than Pedigree 1 and Pedigree 2. If mountain range 2 appeared first then, the correct Pedigree would display the population/species/lineages P and Q more closely related to each other than they both are to R.

Could you elaborate on why you think so?

@user4847 Update! Does it make sense to you?

I approve it....


text:
Genetic variation and sensitivity of wild cabbage

1: Is it true that the genetic variation of kale plants is smaller
  than wild cabbage?

I think so, because of human selection of the kale plants.

2: Are broccoli and cauliflower more sensitive to changing
  environmental conditions than wild cabbage?

I think so, because domesticated crops have a lower genetic diversity than wild varieties. Genetic diversity is useful for adaptation

3: Is it a good recommendation to grow new Sprout plants from the
  seed of wild cabbage plants?

I don't think this is the best idea, because genetically engineered Sprout plants could be much better.

sounds like homework - could you provide a little of the background please?

I am going to assume that Kale is a plant derived from wild cabbage and has been selected upon for certain attributes by humans for 1000's of generations.
1 There are two principle reasons why genetic (allelic) diversity might be lower in the kale subgroup than in the wild cabbage. Firstly, strong selection imposed by humans may have diminished allelic diversity. Strong selection can drive alleles to fixation. Secondly, if the kale has come from a small sub-population of the wild cabbage it may have been through a genetic bottleneck, this is likely to reduce allelic diversity because, unless all alleles from the original population are captured in the founder populations, some alleles will be lost by genetic drift.
2 Generally allelic diversity is a "good" thing in an unstable environment. It allows different trait combinations and variation in traits to occur. If the environment changes drastically then it could impose severe selective forces on the population, those with high allelic diversity are likely to come up with a combination of alleles that survives.
E.g. Humans only allow the cabbages over 18cm in diameter to reproduce in to the next generation. 5 loci affect cabbage size, each having a "large cabbage" (C) allele and a "small cabbage" (c) allele. Having 5 c alleles gives a cabbage size of 15cm. Each C allele adds 1cm. If a population has fixed the c allele at 3 loci (i.e. there is low genetic diversity) then none of the cabbages will be >18cm. If a population has both the C and c allele at all loci then some of the population will be over 18cm.
3 The final question is difficult to answer, it depends on what you define as "a good recommendation,"  that is very subjective. If the aim is to maximize allelic diversity then yes, if it is to maximize cabbage size it is probably no (because the "genetically engineered" plants have been selected upon for large cabbages - they might have the C alleles fixed in the populations!)

Could you be a bit more clear on which parts of your answer are responses to which subquestions?

@user4847 there you go


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How to learn molecular biology through pubmed research articles?
Instead of using a textbook, is there an alternative curriculum, that simply lists a set of pubmed research articles for each topic covered in a typical undergrad molecular biology course?
I am currently learning molecular biology by reading a textbook.  Different chapters focus on different topics such as Cells and Genomes, Cell Chemistry, Proteins, DNA, Gene Expression, etc...  However, I'd prefer to learn these topics directly from research papers on pubmed.

For example, I would imagine the DNA "chapter" of such a curriculum would include the Watson Crick paper on DNA.
As another example, searching for "Protein" in pubmed reveals a ton of research papers, but which subset of them cover the topics taught in an intro molecular biology course?

Note: The pubmed articles don't have to be free or open access, I'm ok with getting the papers through my university library.  Also if an alternative curriculum such as this doesn't exist, maybe there is a supplemental one?  Or maybe you can recommend a set of papers that you'd include in such a curriculum?

I love this idea, but I think some things may just be better learned from a textbook, like the basics. But if you find something interesting I highly encourage you to look for a review article on that topic. The problem is that journal articles, even reviews, are meant to be specific. You may not be able to find a review on just 'mRNA' for example, but you can easily find reviews on topics like mRNA decay and mRNA splicing.

Tom Silhavy would use a similar method in the first year graduate Molecular Biology course.
His text was basically a set of papers bound into a book "The power of bacterial genetics: a literature based course".  I'm not sure its in print anymore, but a used copy can be had.  If you find a copy you can just fetch the papers if you like.
You can't do much better than finding excellent papers to read.
Briefly, the class covered the development of selection for mutations and mapping them onto genes - use of bacteriophage and replicate plating.  The papers started in the 40s and went on from there to the heyday of molecular biology.
It was an awesome course to take... an awesome baptism of fire.
As they say... Whatever doesn't kill you, will select you for a distinguishing phenotype.

If you are interested in quantitative/systems biology, the reading list for a course like this at Princeton has been published (with some context for each paper). I know this course reading list has also been taught at Stanford. They definitely look like good papers, and some of them are fairly recent.

Edit: I remembered another book of classic literature I've heard is good: Landmarks of Cell Biology. If you look at the Table of Contents, you can get quite a few of the articles straight from PubMedCentral, and with a reasonable university license you can download the rest. It's been an inspiration to at least one rising star professor at UCSF (link to a fun bio-sketch).

this is cool - Silhavy's class was there too.

There are in fact various books where each chapter is written like a published review. These are not text books, but they are very technical. Off the top of my head I can think of this one for example:

Hatfield DL, Berry MJ, Gladyshev VN. Editors. (2011) Selenium: Its molecular biology and role in human health, 3rd Edition. Springer.

Like all such books, it consists of various chapters, each of which is a short review of the relevant topic by leading authors in the field. The problem with this is that a certain level of knowledge is assumed. Using your example, you won't be able to understand the original DNA paper if you don't understand the results of X-Ray crystalography experiments. Published articles assume that the reader is already an expert and they won't explain basic concepts.
A better way would be to read your textbook and then, once you have read and understood a chapter, look into that chapter's references and read through those. Most serious textbooks include published articles at the end of each chapter, if yours does not, get a new textbook.
Finally, another choice would be to read a review article. Those of the Trends and Current Opinion series are particularly good. They tend to be very well written and, most importantly, highlight the seminal papers in their references. Just pick one that is about a subject you are interested in and then look at the references. The important papers in the field will be marked with • and seminal works with ••. So, read the review and then read the •• papers.


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Energy flow in an ecosystem
What are the mistakes in here?
The image below shows a part of the energy flow diagram in an ecosystem.

1. Part P of the biomass of the primary producers does not get consumed. Give a concrete example of how this energy can get to the decomposers.
I think this energy can get to the decomposers, because the biomass simply dies. E.g. dead animals, dead trees, etc.
2. The amount of energy that is represented by R may end up with the decomposers in different ways. Name three ways.
I can come up with natural cell dead (dissimilation after assimilation).
3. The energy that is released through dissimilation, is not only released in the form of heat. What can this energy 'Q' be used for by the organism?
I think this energy (e.g. dissimilation of glucose) could be used for movements by the organism.

The energy released as Q will be used by the organism to do any task not just movement. Energy R can also be consumed by other organism which may later die and then be consumed decoposer

What makes you think there are mistakes?

You are right but a small correction: P represents primary producers. So the answer is just dead plants or tissues such as broken branches.
Death, excretion because of turnover (which includes urine or other metabolites), tissue turnover (shedding of dead cells, molting etc)
Maintenance, locomotion, repair, immunity


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Strange looking mushroom found in a dead tree
I'm trying to identify this mushroom my sister found at her campus' lawn. It is brown, looks somewhat like a turtle or a brain and is growing inside of a dead tree trunk. Geographically the campus is in Haifa, Israel in case that helps. Any ideas?
Images:

Is it too dark to be Boletus subtomentosus ? (another pic here)

Have you tried mycokey? Looks like there are a lot of factors that can't be seen in that picture which might be important.

Possible Species: California Fungi - Gymnopilus luteofolius

Source:
http://www.mykoweb.com/CAF/species/Gymnopilus_luteofolius.html
http://mushroomobserver.org/174362?q=28kZM


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How closely correlated is the level of an snRNA with the level of its corresponding snRNP?
Let's say I am growing cells under two conditions, and let's say I measure U1 snRNA levels in both using digital PCR.  If the U1 snRNA level is reduced in one sample, how safe is it to say that U1 snRNP is also reduced in that sample?


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Shortest route for a Nitrogen atom from fossil fuel to a protein in your body?

Millions of years ago fossil fuels originated from plants. A nitrogen
  atom from fossil fuel is now inside in a protein molecule in your
  body. What is the shortest path that the nitrogen atom could have
  taken starting with plants that lived millions of years ago, until the
  protein molecule in your body. Use those points:

consumers
producers
reducers
fossil fuels
$NO_x$

I guess the route could be producers -> reducers -> fossil fuels -> consumers -> $NO_x$
But this could be wrong, because NO does not have to be produced by consumers.

producers-reducers-fossil fuels-NO-producers-consumers.

fossil fuel is out of question.. it is a byproduct not a precursor for a metabolite.. atmospheric nitrogen can be fixed to nitrate by physicochemical or biochemical processes

Fossil fuel -combustion-> NOx -deposition-> plant -> person


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Is there a limit to how much concise information a human can learn adequately?
Like, I am trying to learn more chemistry, but also computer programming from the higher-level programming methodologies, frameworks, languages, APIs, XML, web development, and I'm also hoping to improve especially with computer hardware/electrical engineering, and I am trying to improve my pixel art/graphic design/animation skills all at the same time, that is no set schedule for any, and just learning whatever I get my hands on.
Is it possible to learn this way for a human, or will this eventually become too much, and I'll have to sort them/order what I learn separately?
I have not been seeing very much success, but I do keep learning. The problem? Well, I can't get a good grasp on any subject because I am interchangeably attempting to learn all of the aforementioned subjects sporadically, interchangeably, and without any fine schedule. Is this a wrong way for a human to learn, or is the human brain capable of constantly & linearly learning anything in any order very well?

You need to distinguish an ambitious learning schedule with lack of focus and concentration. What you describe in your last paragraph sounds more like the latter - try to set aside large blocks of time for each subject and read more in-depth.

if you just put in some little effort this post can become a good question.


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How to determine if a plant is autotrophic or heterotrophic?
How do you determine if a plant is autotrophic or heterotrophic, and are there any traits in particular that can be used to classify species?
As two examples, how should Melampyrum pratense and Orobanche be classified?

It is difficult to understand what you are asking. Please elaborate.

What is you overall reason for asking? Are you interested in these species in particular or for a more general application?

This in part depends on how you define heterotrophic. The most common definition is the inability to synthesise energy-containing molecules, most commonly by fixing carbon through photosynthesis (but dont forget chemotrophs). However, I've sometimes seen definitions that also include dependency on external sources for nutrition (e.g. nitrogen) but also to supplement carbon sources.
Using the first, main definition a lack of chlorophyll is a sufficient trait to define heterotrophic plants, which clearly places Orobanche (lacks chlorophyll) in the heterotroph category. If you use the second definition you will include more species, but it also becomes much more tricky to draw the line between autotrophs and heterotrophs. I know that Melampyrum pratense is a hemiparasite, but don't know exactly to what extent, and therefore cannot say if it is accurate to label it as heterotrophic (using the second looser definition - it has fully functional photosynthesis). Checking whether a hemiparasitic plant can establish, survive and reproduce without its host should be a useful way to establish if it is a obligate or facultative hemiparasite (I suspect that Melampyrum pratense will be found in the latter category). Myco-heterotrophy can also be obligate and facultative, and can involve transfer of both carbon sources and nutrients, see Merckx et al (2009) for a review. Insect-eating plants such as the Venus flytrap are however sometimes called partial heterotrophs, based on the fact that they get part/most of their nitrogen from insect trapping, while still obtaining their energy from photosynthesis.


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Measuring fitness / lifetime reproductive success (LRS) in Drosophila
I am planning a fitness assay of Drosophila melanogaster. I'd like to get a good measure of lifetime reproductive success (lrs) but I don't want to count all the offspring produced over a lifetime by 100's of focal flies. The solution I am toying with is to count offspring production over the first few days or weeks. But before I commit to this I need to know if there is existing research material on the following:
Does early reproductive output correlate well with lrs? (this could be a low correlation if a fly trades early-life offspring production for late-life offspring production)
How much of a fly's reproductive output does one need to count before they have a good estimator of lrs? (does counting the offspring produced in the first day of life correlate well to overall lrs or do I need to count more - 5 days, 10 days, 50 days...)

Just finished an experiment (yesterday) where I measured lifetime reproductive success (LRS) of a few hundred flies, with measures taken from 24 hours of production every 7 days over the entire life of the fly. From this I can now answer the question.
Correlations of time interval to total offspring production (reproductive success [RS]):

Correlation of Week 1 RS         with Total LRS:    $\rho $ ~ 0.7
Correlation of Week 1 + 2 RS     with Total LRS:    $\rho $ ~ 0.9
Correlation of Week 1,2 +3 RS    with Total LRS:    $\rho $ > 0.9
Correlation of Week 1,2,3 + 4 RS with Total LRS:    $\rho $ > 0.95

Approximate conclusion (at least from my data - it may vary depending on experimental conditions and specific flies) is that LRS can be well estimated by measuring three to four weekly intervals.

I haven't done LRS but I don't see a reason why you couldn't make that measurement over only a few days, if you keep this method consistent through out all your populations. Just as a control you might have to do a complete LRS to see if you get any patterns in their egg laying behaviour, which I assume/believe is a decreasing pattern over time but just check the pattern of your WT and make sure your food is the same throughout all your experiments as changes in yeast % can completely distort your results as fly lay eggs like crazy when given yeast!! so use the same batch of fly food.
Although I'm no expert at this, if you look at female ovaries and do some molecular/phenotypic characterisations, you might get some interesting data if you are already observing a huge difference between your populations although you would have to look at the literature for this but having played around with these stuff a little, you find a surprising amount of data! This is in a way nice since you take the males out of the equation as the reproductive fitness could be compromised by either males or females in a population. To determine this you need to cross the males and females of your population of interest to WT flies and count the embryos (although this is slightly dangerous since if males are not performing well, females can lay lots of unfertilised eggs, blanks, and they are indistinguishable from fertilised egg so maybe count the hatched offspring and immediately discard them although that presents its own set of challenges and variables and to be honest its not likely to happen since you usually get this blanks in virgin females that have not yet courtshiped). If you observe lets say no changes in embryo numbers when your male populations are crossed to WT females but significant changes when females are crossed to the WT males, you would know the problem is with the males in your population.
Hope this helps!
EDIT: So I looked a bit further into this and came across this paper (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0024560). If you look at Fig 6, I think it answers your question. I'm basically quoting the paper here. They measured the correlations between adult LRS and cumulative and short-time measures of fecundity and offspring production. Correlations of the short-time measures of fecundity and offspring production with adult LRS were highly dependent on the time of measurement. For young females the correlations were low, but when measured from older females, the correlations were much higher (up to 0.67 for short-time fecundity and 0.83 for short-time offspring production). For both short-time fecundity and short-time offspring production the highest correlations with adult LRS were reached when the female age was about 50 to 80 days. The length of the time frame had only a minor effect: the correlation of the 10-day measure with adult LRS was generally only slightly higher than that of the 2-day measure. The short-time measures performed well in comparison to the cumulative measures of fecundity and offspring production. So in short if you let your females age a bit and measure their fecundity, then it should be representative of their LRS.

Just edited the answer so hopefully thats more helpful.


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Generalism - specialism index in microbial ecology
I am doing research in Lipid metabolism in different yeast species and I would like to look into ecology of them.
I would like to classify them to a Generalist/specialist based on different Parameters (growth on carbon sources, pH, temperature,...).
I wonder if you have any experiences with that classification and if any of you know which indexes are used for that in microbial ecology?
Thank you very much for your answer!
Martin

Can you expand a little on your classification desires, you're not very specific.  There has been plenty of research on lipid metabolism, including in yeast.

I've published a paper comparing different measures of specificity, if that is of any help. But if you plan to have, e.g., measures of performance on carbon sources, pH, and temperature, then you'll have three measures of specificity (i.e. one for each).
Also, worth to have a look at Graham Bell's inconsistency and responsiveness, as used by Venail et al. to classify specialists and generalists.


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Which statement about phenotypic plasticity is false?
This was a test question, and I'm not too sure about the answer.
Which statement about phenotypic plasticity is false?
a. Because the plasticity of a phenotypic trait may be costly to maintain, it will not be favoured in stable environments.
b. A trait that is an adaptation will not vary with environmental conditions within one generation.
c. Phenotypic plasticity can itself be an adaptation to varying environmental conditions.
d. Variation in phenotype among populations of a given species across different environments is only caused by phenotypic plasticity.
If you could explain the answer to me, that would be great.

When you say phenotypic plasticity, do you mean developmental phenotypic plasticity? Do you exclude phenotypic flexibility (lifetime REVERSIBLE and adaptive change in phenotype in response to environment)?

What did you answer and why?

what level was this question set at? (what is the group being examined.. undergrads, post grads, high school??). I think B would be false if it read "A trait that is plastic will not vary with environmental conditions within one generation."

Horrible phrasing of options.

@fileunderwater right, whoever wrote the exam should be ashamed.

If you can change teachers, do. That is a horribly worded question and very unclear. You can make arguments that everything is false depending on how you interpret the terms used. IN any case, D is 100% false with all interpretations so if the "teacher" only wants one answer, choose that.

I'll try to answer but I'll encounter some difficulties: first because I don't know what you mean by "plasticity". Does it mean non-reversible developmental plasticity or reversible flexibity. Then, because, I don't really like the word adaptation! Anyway'll try...
a: Plasticity  is some kind of mechanism allowing organisms to adapt to various environment. If the environment is stable and under the assumption the plasticity is associated with a intrinsic (physiological for example) cost, then a population would tend to evolve so that they always display the most optimal phenotype. I would argue that this is under the assumption that we gave enough time for the right mutations happen and under the assumptions that such mutation might exist!
b I don't really understand this statement. Does it mean that between two generations (which mean in one generation time) an adaptation cannot vary.…in what terms? in frequency? Through time any trait vary because of selection, environment, genetic drift and mutations. And to what environment is the trait under consideration adapted for? Can we accept that the environment is changing from one generation to the other in this question? What does this question has to do with plasticity? I guess that when one says that a trait is an adaptation it means (among other things) that the population has no more variance for this trait. Therefore, only mutations would bring variations if there were no environmental change making the trait not adaptive anymore.
c: Well, yes. Plasticity is an adaptation to fluctuating environment. It allows to display a rather optimal phenotype in multiple different environments.
Answer d is wrong for sure. There is variation within a population due to genetic variance and non-adaptive environmental variance (and their interactions). Variance due to plasticity is just some kind of subset of the variance du to the genetic-environnment interaction
Hope this helps a bit!

Agree with you there @Remi.b - A (with caveats) and C are true, D is definitely false (Phenotype = Genotype + Environment + GE... Plasticity is just one component of GE) and B doesn't make much sense (especially given the question is about plasticity).

I think the answer should be (d) as variation in phenotype among populations of species living in different environments are not caused only by phenotypic plasticity, they may also be caused by genetic differences which arose due to different selective pressures.