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Is DNA replaced after organ donation?
If an organ from person A is transplanted to a new human body B, is it possible that we can detect A's DNA in B?
How long until the organ's DNA is replaced by B's DNA so that we are no longer able to detect any signature of A?

The organ from person A will never have it's DNA replaced to match that of its new host B. This is actually a good thing, because many organ transplants are done to treat genetic diseases. If the new organ had its DNA replaced with the host's faulty DNA, the transplant would be ruined. As far as detecting the organ's foreign DNA in its new host, that depends on how the sample was collected. If you look really hard at DNA in blood samples, you might find some evidence of the donor's DNA in the host's blood, but how much probably depends on what organ was transplanted and other factors.

@user137 But cells of the new organ may die and be replaced at least. The new cells have the host's DNA or the new organ's DNA?

If the transplanted organ's cells die, they probably have to be replaced by other cells in the transplanted organ. These would carry the foreign DNA from the donor. The only way for new cells in the organ to carry the host's DNA would be if host cells colonized the new organ from the outside, which doesn't seem significant. There are cells that can colonize tissues, such as Kupffer cells in the Liver, but these don't make up the bulk of the liver, those are hepatocytes.

DNA will be never replaced (unless you are speaking about something, where DNA might be only trash, like in the case of blood transplantation or in the case when "organ" would be slowly replaced itself by host regenerative power and "organ" transplantation would be only something temporary, but then we are probably speaking about wider definition of organs).
For further evidence, you may look at cases of chimerism. That is, when young embryos fuse together and create single one with two different cell-lines, which later differentiate to create different organs.
https://en.wikipedia.org/wiki/Chimera_%28genetics%29
Furthermore, rather more common but with less drastic effect can be somatic chimeras, that is when (usually) early, when embryo is formed only by small amount of cells, one of cell has a mutation, then later in life, this cell again can give rise to organ or several of them. In that case, those organs will carry this mutation while rest of the body will not. This can be potentially more common as this can happen in any single time during development and even after it (in fact, cancer cells are sort of product of that).
More interesting cases here:
https://en.wikipedia.org/wiki/Mosaic_%28genetics%29
So, from simple fact that these cases exists and are well-spread, and basically means that several different cell-lines can live in the same body, the answer on your question, if organ DNA will be replaced after transplantation is no.
edit: In the case of whole cell replacement, they can be from both donor and host. However, there are a few problems:
Most of cells that we have are not totipotent, not even pluripotent or multipotent (see: https://en.wikipedia.org/wiki/Cell_potency), most of our cells are plain and stupid. This means that highly specialized cells of some organ would probably be replaced only by other highly-specialized cells of that organ (or their precursor cells that are kept for this solo reason, keep regenerativ ability of particular organ, as quite a lot of highly-specialized cells can't divide any more). However, there are a few documented cases with regnancy, where a few cells (embryogenic, thus with bigger "healing" power) migrated through placenta to mother's body and healed her diabetes. So theoretically this is possible, as well as host getting cancer from donor's organ. But again, reason why we are transplanting organs is because human body is not particularly great in regenerating itself and those organs won't grow. So theoretically possible, but not great concern (except for cancer).

DNA will be replaced as long as cells die. But new cells carry whose DNA?  It is possible an organ carry A's and B's DNA simutaneously?

@questionhang It's not just the DNA that's replaced, it's the cells that are replaced. And they are replaced by cell division. So they get the same DNA as the other cells of that organ have.

@yvide I know. The cells of the donor's organ die too. The new cells carry the host's DNA or the donor's DNA?

@questionhang: Did edit. Does that answer your further question?

@Colombo So it is possible the organ can have host's cells and donor's cells simulatenously? Many years later, the donor's cells will not be purged?

Yes, they can have donor cells and host cells simultaneously. Donor cells would not be purged. Unless host stop taking medicine to slow down immunity response, because donor cells are still alien and would be destroyed. And with them, whole organ.


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How is a bacterial strain defined?
When a species of bacteria is referred to by its strain, are they a clone of single founder or is a certain amount variation allowed?

In theory they're clones, but depending on the age of the strain(some strains are surprisingly old: ~40 years) there's variation inside strains.
The reverse is also true. Bacteria from a single species are isolated twice and named different things by different labs and the mistake can take years to even find, much less correct.

Bacteria effectively clone themselves so theoretically all clones are identical. However like every organism they're subject to Darwinian evolution so there's always a chance a random mutation happens. Since bacteria usually reproduce fast the rate of these mutations can happen fast resulting in the strain evolving to a (slightly) different strain.

Whereas a clone (or clonal population) is the current population of individuals descended from a single particular ancestral individual, a strain can be understood as the whole line of individuals down and up to that single particular individual.
But as noted in the other answers, even though the isogenic character is often taken as a more or less tacit approximation, none of those two concepts forbid genetic variation or assume that all the individuals of the said clone or strain are isogenic.
The concept of species for microbial organisms is more intricate.

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Gene and alleles
This is a multiple choice question:
Consider a gene, ABC, which codes for an enzyme involved in the metabolism of sugars. There are two known
alleles of this gene, ABC1 and ABC2. Which statement correctly describes the relationship between the ABC gene
and the ABC1 and ABC2 alleles?
a. The gene is a sequence of amino acids and the alleles are a very similar sequence of amino acids.
b. The gene is a trait and the alleles are a sequence of amino acids.
c. The gene is a trait and the alleles are a nucleotide sequence.
d. The gene is a nucleotide sequence and the alleles are a sequence of amino acids.
e. Both the gene and the alleles are a nucleotide sequence.
I thought the answer is b, but the correct answer is e. I can't figure out why so. Does anyone know?

Alleles are basically subtypes of a gene. At the time of Mendel, the molecular nature of inheritance was not known so the original definition of gene refers to "some" inheritable molecular entity inside the organism that is responsible for a trait. Alleles are different "flavours" of a given gene. For example there is a gene for flower colour, there can be different alleles which give rise to different colours (this is a highly simplified example). Genotype is a configuration of alleles whereas the phenotype is the effect that is seen.
With the knowledge of molecular genetics superimposed on these basic concepts a gene would basically be a well defined part of the genome (DNA) which is responsible for a molecular trait. Alleles are the actual sequence variants of this genomic region (not considering translocations here).
This is my justification on correctness and incorrectness of different points, based on current knowledge of molecular genetics:
a. Incorrect. Genes need not necessarily code for proteins. There are non-coding RNAs
b. Incorrect. Trait is a qualitative feature. Phenotype is the manifestation of a trait. Genes and genotypes are the causes of a trait and not traits themselves.
c. Incorrect. Same as above.
d. Incorrect. As per the definition, alleles are variants of a gene and they have to be of the same molecular nature as the genes. However, if we forget the semantics then this may seem like a more apt definition because the variations in traits arise not just because of the gene sequence but also the amino acids. However there is a flaw in this logic and the counter points be:

This scheme would not be inheritable (RNA editing/alternative splicing/PTM etc).
It has been shown that even synonymous mutations can have different phenotypes. (Plotkin and Kudla. 2011)
This does not consider non-coding RNAs

e. More or less correct (not in a very strict sense but fine for most discussions. Gene is not really a nucleotide sequence. Gene is an annotated region of a genome which has a defined sequence. This is similar to saying that object is mass. Object has a mass; object is not mass. This is just semantics and, as I said, not too important for general discussions.)

Both genes and alleles are sequences of DNA. A gene will code for a trait, say hair colour, while an allele will be the variants of that gene (say the alleles coding for blonde, brown, black, and red hair).
It's almost like cookbooks: two cookbooks (the DNA) might have a recipe (gene) for bread but they use slightly different instructions (alleles) resulting in different breads (traits).

That's a very good analogy imo

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Which of the following is NOT a type of tropism?
Which of the following plant movements is NOT a tropism?

Plant stem growing toward light
Plant structure growing away from light
Plant roots growing in response to gravity
Vines coiling around tree trunks
Leaflets folding after losing turgor pressure

Please help, I am stuck!  Thank u :)

Is there anything you can rule out definitively? Some thoughts about what you've tried will help us fill in what you're missing.

First two are ruled out for sure. I'd rule out the third, considering "Gravitropism", but some people are telling me it's the answer... So it's probably one of the last two.

The answer is #5, Leaflets folding after losing turgor pressure. This refers to a phenomenon called plasmolysis.
1 - positive phototropism, incorrect
2 - negative phototropism, incorrect
3 - gravitropism, incorrect
4 - thigmotropism, incorrect


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What are the basic skills required to pursue future studies in theoretical ecology?
I am a student and just about to choose a project for my Master's thesis in biology. I want to pursue studies in theoretical ecology in the future. Between field ecology and computational biology (as my two possible choices) what would be the best option to go for? Suggestions are needed as soon as possible .

I'm voting to close this question as off-topic

Theoretical ecology
From wikipedia

Theoretical ecology is the scientific discipline devoted to the study of ecological systems using theoretical methods such as simple conceptual models, mathematical models, computational simulations, and advanced data analysis. Effective models improve understanding of the natural world by revealing how the dynamics of species populations are often based on fundamental biological conditions and processes. Further, the field aims to unify a diverse range of empirical observations by assuming that common, mechanistic processes generate observable phenomena across species and ecological environments. Based on biologically realistic assumptions, theoretical ecologists are able to uncover novel, non-intuitive insights about natural processes. Theoretical results are often verified by empirical and observational studies, revealing the power of theoretical methods in both predicting and understanding the noisy, diverse biological world.
The field is broad and includes foundations in applied mathematics, computer science, biology, statistical physics, genetics, chemistry, evolution, and conservation biology. Theoretical ecology aims to explain a diverse range of phenomena in the life sciences, such as population growth and dynamics, fisheries, competition, evolutionary theory, epidemiology, animal behavior and group dynamics, food webs, ecosystems, spatial ecology, and the effects of climate change.
Theoretical ecology has further benefited from the advent of fast computing power, allowing the analysis and visualization of large-scale computational simulations of ecological phenomena. Importantly, these modern tools provide quantitative predictions about the effects of human induced environmental change on a diverse variety of ecological phenomena, such as: species invasions, climate change, the effect of fishing and hunting on food network stability, and the global carbon cycle.

Computational Biology
from wikipedia

Computational biology involves the development and application of data-analytical and theoretical methods, mathematical modeling and computational simulation techniques to the study of biological, behavioral, and social systems.1 The field is broadly defined and includes foundations in computer science, applied mathematics, animation, statistics, biochemistry, chemistry, biophysics, molecular biology, genetics, genomics, ecology, evolution, anatomy, neuroscience, and visualization.2
Computational biology is different from biological computation, which is a subfield of computer science and computer engineering using bioengineering and biology to build computers, but is similar to bioinformatics, which is an interdisciplinary science using computers to store and process biological data.

Field Ecology
Ecology can be studied empirically through data analysis, through lab experiments or through field observations and experimentations. Field ecology refers to this last point that is, it refers to empirical ecology in the field.
Conclusion
Potential Misunderstanding
In your post, you seem to suggest that field ecology is a subfield of theoretical ecology. It is not! Either you work as a theoretician or as an empiricist (and then eventually as a field ecologist). Of course many people do both theory and empiric work.
Note that whether you are theoretical or an empiricist working in ecology, you will need to have a good understanding of the theory behind the science of ecology.
Computational biology vs theoretical ecology
In opposition to empirical ecology and field ecology, computational biology and theoretical ecology do not have a hierarchical relationship. If you work in theoretical ecology you can make analytical modelling or numerical (computer) modelling. If you work in computational biology you could analyze data in genetics, you could model cell processes, you could simulate interacting populations in ecology and many other things.
What should you chose?
What skills do you need?

Do you like data analysis (statistics and R and python coding)? You will have to analyze your data whatever you chose!

Do you like numerical simulations (lots of coding, incl. languages like C++)? If no, then maybe avoid computational ecology!

Do you like analytical modelling (lots of math)? If no, then maybe avoid making analytical models in ecology!

Do you like messy, complicated, tiring field work? if not, then maybe avoid working as a field ecologist.

What would you imagine to work on?

What question would you like an answer to? Think about it and try to understand how you would address the question you are trying to answer.

My advice

Do not be afraid of any field, any technics, any programming language, etc... You are good enough and have enough time to learn what you do not know.

Do whatever you like most!

thank you for the answer. I am surely interested in analytical modelling. But at the moment I can only choose between field ecology and  computational biology (studying metagenomics) and am in a fix as to what will be the most effective option.

Oh ok... that phrasing sounds a little different from the original post. It seems that you know what you want (mathematical modelling in ecology) and are wondering what path will be best to reach this point. I would rather recommend computational biology and genomic data analyses as to stay in a field of theory related work. Note, I am a theoretician (using numerical modelling and not so much analytical modelling) and I would not want my preference to affect my answer. Good luck!

Thanks again:) It's always great to get advice from experts!

Feels like too much of a compliment. I am just a PhD student. I work in population genetics, not in ecology (might have been unclear from above).

I think knowing some statistics and R is good no matter what you're doing, mainly because scrolling past the statistical inferences in a paper (what's a p-value and a confidence interval? How'd they get those?!) feels bad, and the packages you can get add a lot of utility. Edx has am interesting course track on data analysis for life sciences, PH525, that can be taken for free with no obligations if you want to dive into something relevant and get a feel for some methods.

Just a warning on that edX, it's not necessarily beginner/entry so they do assume you know a thing or two about stats, R, molecular biology and related, etc. to begin with!


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Does evolution thinks?
I understand evolution as survival of the fittest rule , where its the nature and surroundings that shapes the life by extinction of species which are not fit to survive the nature at that period.
To me its analogy would be like soil passing though a net,where nature act as the net and the soil particles act as lifeforms. The particles whose shape and size are small (fit) will go through the net and live on while the bigger ones (unfit) will get stuck and hence go extinct.
Pretty clear so far.
However there are certain things that do not seem to make sense with this theory for me personally.

When we evolved from primates to humans why did we lose our body mass, muscles and hair? I mean sure we could be intelligent with the muscles and the
furcoat would keep us warm and hence more likely to survive.

The explanation I get for this is that we did not had any use of body hair and strong muscles over our intellect so we lost them, however how can WE make it happen ? Its not like intellect requires less muscles or something so how did we lose it from redundancy? whats the mechanism?
2.How does Genetical heritage evolve?
In a nutshell what I want to ask is does our actions (as a species) define our DNA in evolution? Apart from natural mutation and survival of the fittest is there anything that affects the biological evolution? It is believed that child of intelligent parent is supposed to be somewhat intelligent as well, is this linked to heritage or just the environment he grows in?

Pt. 2 of your question concerns the famous nature v. nurture debate; feel free to Google that, it's quite interesting. You said: "we did not have any use of body hair and strong muscles over our intellect so we lost them". That is wrong. Natural selection doesn't compare different traits within an individual and choose the ones among them that are the most "superior" (it doesn't "filter" body hair and muscles because we possess intelligence, unless intelligence somehow makes the former traits obsolete or if the traits are an unnecessary burden). Also, I suggest a title change for clarity

To answer the last question,  in my opinion,  genetically passed  intelligence is just a potenial.  However, the enviroment he grows  matters also. To be more clear,  intelligence just express itself based  on the "data" (static knowledge) in your brain.   Less data means less intelligence expression.  How google translate work ?  It is artificially intelligent.  However, its intelligence alone does not work well. Gtranslate continiously  read more and more  ebooks with the translations. So it can be more accurate.  Same intelligence, but different intelligence expression :)

Also, in addition to my previous post, I wanted to mention that species which are at a disadvantage don't necessarily go extinct, unless they are repeatedly at a disadvantage over long periods of time and therefore the allele frequencies dwindle to very small percentages, or because an environmental disturbance occurs to which they cannot adapt or recover from.

@ AleksandrH
Thats not my question. "we did not have any use of body hair and strong muscles over our intellect so we lost them" is what most people usually tell me.
"Natural selection doesn't compare different traits within an individual and choose the ones among them" is what I know as well, but what causes redundant features to be eliminated?

This is one of numerous other moments when I would love to downvote a few comments.

If I commented anything wrong, just let me know and I'll delete it.

This is a little ambiguous. A bit more detail would help

Welcome to Biology.SE
Issues with the question

It is impossible to correctly answer this question as the phrasing is so fantastically unclear, wrong and misleading (no offense, really). I will give a few points here that may help you but the only thing you can really do to answer your own question is take some time to follow an introductory course to evolutionary biology such as Understanding Evolution by UC berkeley (online and free) for example.
You probably want to work on the format of the question as numbering lines that have different number of tags looks pretty bad.
You are asking 9 different questions (there are 9 question marks at least) that are all relatively unrelated! A post should always be reduced to one single clearly defined question.

A few simple definitions

Population: A group of individuals.
Locus: A position in the genome.
Gene: A functional unit at a given locus that codes for a protein.
Allele: A variant of two or more variants at a given locus. Simplified example: At the locus where stands the gene coding eye colour, there are 2 variants brown eyes and blue eyes.
Evolution: Refers to any change in allele frequency in a population through time.
Phenotype: The manifestation of a gene on the world. In short: It is how someone looks like.

Does evolution thinks?

It is always quite difficult to define what "thinking" means. But really here, we won't need to debate the detail of the terminology of what is a thought. Evolution is a process, it is not an organism, it has no brain and can not think. The answer is "no".

I understand evolution as survival of the fittest rule , where its the nature and surroundings that shapes the life by extinction of species which are not fit to survive the nature at that period.

This is wrong! "survival of the fittest" is just a quick and dirty expression for referring to the process called natural selection. Natural selection describes the fact that alleles conferring higher fitness (that is having lower chance of survival and/or higher fecundity) to individuals carrying the allele, raise in frequency in the population.
Natural selection does not necessarily decrease nor necessarily increase the probability of a population to go extinct.

Apart from natural mutation and survival of the fittest is there anything that affects the biological evolution?

Natural selection and "survival of the fittest" refers to the same process.
Yes, there are other forces that affect evolution (and are absolutely essential) such as mutations and genetic drift.

I want to ask is does our actions (as a species) define our DNA in evolution?

It is unclear what you mean by "define evolution" and you probably want to replace "species" by "population". Yes, the current state of population (including the behaviour of its constituent individuals) affect future evolution of the species.

It is believed that child of intelligent parent is supposed to be somewhat intelligent as well, is this linked to heritage or just the environment he grows in?

This is an interesting question. I wrote an introduction into the concept of heritability (incl. the role of genes and environment in shaping phenotypes) in this post.

When we evolved from primates to humans why did we lose [body mass and muscles]?

You will have to ask this question on a separate post. In this post, you will have to make sure that we indeed lost in body mass. Note that human shape is nicely adapted for high endurance (hunting large mammals over long distance and period of time)

When we evolved from primates to humans why did we lose [..] hair?

This question is a duplicate of this very interesting post. Have a look!
Recommendation
To the risk of repeating myself, I'd recommend that you have a look at a very introductory source of information on evolutionary biology such as Understanding Evolution by UC berkeley (online and free) for example.


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How does the splicing enzyme recognize where to splice the introns?
When the DNA from the nucleus is transcribed to an mRNA, the mRNA is spliced by an enzyme before it goes outside through the nuclear pore. What is the name of this enzyme and how does it recognize where to splice the DNA so only the introns remain inside? Would it not need an instruction set itself to recognize exactly where to cut so the sequence does not change?

There are two factors that involve the ability of enzymes to process RNA.
1) Structure see wikipedia
2) Binding affinitya
Let's take a look at the splicing process:

The active 'sites' (GU,A & AG) need to be in spatial proximity (point one), and the enzyme needs to be able to bind there, aka forming hydrogen bonds with the nucleotides, which is mostly the case if:
a) the nucleotides are 'free' as in they are not paired with other nucleotides
b) it is energetically favorable for the enzyme to bind and do its work, which factors like temperature, and of course on the correct nucleotides
If there were some mutations, the splicing might not work.

Comment for the enzyme: It's a complex, the splicosome. There is a cool movie about it: https://www.dnalc.org/resources/3d/rna-splicing.html

Simply add the additional information into the answer by using the edit function below it and do not put it in the comments.

There are several determinants. As you mentioned 5'-GU--//--[---]--//--AG-3' is the typical sequence of an intron.  There is also a polypyrimidine tract in the intron.


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Male-Male competition limited to breeding season?
I'm currently reading about sexual selection in the context of evolution. Unfortunately, the focus is always on animal behavior during the breeding season. What is 'normal' behavior outside of breeding season?
For instance: Red deer compete with their antlers. Are they doing that throughout the whole year, or just specifically during breeding season?
More general: Does male-male competition exist outside of breeding season?

It's strongest in the breeding season but male-male competition exists outside of the breeding season too, e.g. European Robins only breed in the summer, yet maintain territories year-round. It's pretty circumstantial, however sexual competition will only exist in the breeding season.
To address the Red Deer example, the deer only compete with antlers in the breeding season, but outside of the breeding season they aggregate in same-sex groups too, so most of the competition males will experience is male-male.
Normal behaviour will depend again on the species. Most birds I can think of have discrete breeding seasons and behaviour outside of this is rarely dependent on sex, generally including foraging etc. However I can think of many examples to this, such as Capercaillie, where the hens sometimes forage together. I suppose that 'normal' behaviour could be defined as any behaviour that is not part of the organism's motivation to reproduce.


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Is it possible to separate the binding and catalysis of an enzyme in two steps?
Is it possible to do the following:

Enzyme E binds to its substrate S without catalysis;
Add a controllable stimulus, such as light, adding or removing chemicals;
The enzymatic reaction is triggered by the stimulus.

The word controllable means I can add the stimulus at any time I want. Before I add the stimulus, the enzyme keeps binding to the substrate specifically but no reaction takes place.
This is what I mean by separating binding and catalysis in two steps.
In the case of allosteric regulation, some chemicals will inhibit the activity of an enzyme. For example, ATP will inhibit the activity of phosphofructokinase 1 (PFK1). But I'm not sure whether this allosteric inhibition also hinders PFK1's binding to the substrate, which does'nt satisfy my description above.

Interesting question, but need some more specifics. This depends strongly on the enzyme, are you focusing on FPK1? Do you consider the enzyme substrates themselves as "controllable"? (That gives you more options.) Must the enzyme bind all its substrates irreversibly in the inactive state (for FPK1, ADP and fructose-6P)? Is this for detailed enzyme mechanism studies in vitro, so the molecular dynamics is important? (For simply keeping the enzyme inactive in cells this seems unnecessary.)

@Roland Thank you for your comment. I'm actually focusing on methionine aminopeptidase (MetAP). I mentioned FPK1 because it is a typical example for allostery. The substrate of MetAP is a peptide with methionine as its N termini, which could be controllable if necessary (but how?). It is prefered if the binding is irreversible, but also acceptable if reversible. The assay is designed for an in vitro biotechnology. I don't think such a method is already available for MetAP, but any similar method may be helpful for me to adapt it to MetAP.

In that case you need to review the details of the reaction mechanism for MetAP. Some enzymes bind their substrates and cofactors sequentially, and if the peptide happens to bind first, you might achieve what you want by withholding a cofactor. But if peptide binding is the event that initiates reaction, this may not be possible. If the enzyme requires a posttranslational modificatin for activity (e.g. phosphorylation) that might be another possibility.


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How to understand Aposematism and Batesian mimicry
EDIT I want to understand the reason for intense animal colors. I.e. I don't want to understand the variety of the colors, just the intensity.
The Wikipedia page for Cethosia biblis says, the intense colors are a "warning" to enemies, which means the enemy is warned by the colors that eating that butterfly may result in death.

[...], while the intense color of the dorsal sides of the wings is a warning
  to predators that the Red Lacewing has a bad taste, deriving from the
  poisonous host plants of the caterpillars.

In general it would make sense to me, that animals have learned something like "intense colors means danger". Although, I don't know how good animals recognize colors, but that would be another question.
But poisonous animals don't have necessarily intense colors. E.g. Sydney funnel web spider is very poisonous, but doesn't have intense colors, while on the other side some very intense colored butterflies are not poisonous like explained here. As a result, the explanation given in the wikipedia article doesn't make sense to me. I estimate it very unlikely, that animals learned something like "intense colors means danger", because there are of course examples where this is not true.
Therefore, I don't think the "Golden poison frog" has survived because his enemies recognize his intense colors and conclude "eating this frog will result in death" are hence hesitated to eat him.
My question is: Why does wikipedia say then, the intense colors of Cethosia biblis are a warning for their enemies?
PS: I just found the correct terms for my thoughts ("aposematism" and "batesian mimicry" and are reading now the appropriate wikipedia article. I didn't knew them when I've asked this question.
PPS: to avoid confusion: @DavidBlomstrom answered this version of my question https://biology.stackexchange.com/revisions/42554/2

The question is hard to understand because it is a a bit poorly phrased. I would advice that you 1) start you sentences with capitalized letters. 2) Introduce a quotation before actually quoting. 3) Clarify the intention behind the use of " around the term "warning signal" or just remove them. 4) Clarify what you mean by "warning signal" 5) Don't use ==> but use language to express causation. 6) Clarify what you mean by "survival of the scar" 7) Use capitalized I for the first person in singular.

Make sure you make sentences. For example this: I mean, i doubt a simple "survival of the scar", because of the colorful, but not poisonous animals. is not a sentence. Being ESL (which I also am) might not help. I am voting to close as unclear.

While I don't understand the question I suppose that your question (assuming you know what you really want to ask) is very broad and is something Why are there so many colors?. As you are talking about toxic animals, you might want to focus on them and try to understand why they are colorful. Btw, poisonous and toxic are not synonym.

thanks for the feedback, i've updated my question accordingly. @Remi.b why are "poisonous" and "toxic" not synonym? The cambridge dictionary lists "poisonous" as alternative term for toxic.


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What is meant by electron transfer potential?
I was reading a text and came across the term. What does it mean? The sentence said 'The driving force of oxidative phosphorylation is the electron transfer potential of NADH or FADH2 relative to that of O2. '

https://en.wikipedia.org/wiki/Reduction_potential

the electron transfer potential is based on the difference in the affinity of elements/molecules to bind electrons. the affinity of the element derives from it's components as shown in the elements table, just like all other characteristics. for example, oxygen has higher affinity to bind new electron than carbon. the affinity of the molecule derives from the atoms that build it, their electric potential and the connections between those atoms.
this potential between the two elements/molecules (lets say: NADH, O2, iron–sulfur clusters) holds energy that can start a reaction which will never start otherwise.
I have tried to keep it simple. for more reading about oxidation-reduction ( reactions involve the transfer of electrons between chemical species) read TERMODINAMICS AND CHEMICAL KINETICS p.255 as suggested by @Roland.

Could you add a reference? Happy to upvote then

You should add the precise definition of electron transfer potential I think, as it's a relatively unusual term. Perhaps the best way is to describe it from the Nernst equation. Would suggest p.255 in this book: https://books.google.se/books?id=Gd1NIGrYOEoC&pg=PA255#v=onepage&q&f=false


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Are axons capable of endocytosis?
There is evidence for the uptake of toxic substances like prions from the cell bodies of neurons via endocytosis.  There is also evidence for prion deposition in white matter.  But I haven't been able to find a discussion of whether or not endocytosis is possible from axons.  Does anybody know if this is possible?

Are you asking specifically about the myelin sheathed region or are you also including the axon termini?

Short answer
In hippocampal neurons, endocytosis does occur in the axon, but only at the synapse and at varicosities.
Background
In cultured rat hippocampal neurons, Parton et al. (1992) showed that the cell body and dendritic regions are indeed capable of endyctosis. They used horse-radish peroxidase dissolved in an internalization medium. In the axon, endocytosis was only found to occur in the pre-synaptic region and in varicosities. Varicosities are points of synaptic release from the axon, outside the synapse proper.
Hence, axonal endocytosis is limited to regions where neurotransmitters are released. Presynaptic terminals often engage actively in neurotransmitter reuptake mechanisms to recycle released neurotransmitters.
Reference
- Parton et al., J Cell Biol (1992); 119(1): 123–37


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How many protons are pumped out per pair of electrons from NADH in oxidative phosphorylation?
I have searched the web and found that 10 protons are suppose to get pumped out during the electron cycle, but i'm a bit confused.
I'm trying to count, for every complex(1/3/4), the number of protons that are reduced in the matrix versus the number of protons added to the intermembrane space. The numbers don't add up.
my calculations:

complex 1: 4 protons reduced, 4 protons added.
complex 3: 2 protons reduced, 4 protons added.
complex 4: 2 protons reduced(not counting the ones that condens to H2O), 2 protons added.

It seems like the mistake is in complex III. Look at this image from here:

It clearly shows the number of protons reduced in (and taken from) matrix and number of protons pumped into inter-membrane space. So the data becomes:
Complex I:
matrix: 2H+ reduced (from NADH + H+) + 2H+ pumped out
IMS: 4H+ pumped in
Complex II:
matrix: 2H+ reduced (from succinate)
IMS: 0H+ pumped in
Complex III:
matrix: 2H+ pumped out (when not considering complex II, you'd count 4H+ here)
IMS: 4H+ pumped in (2 from complex II)
Complex IV:
matrix: 2H+ reduced (to H2O, we won't consider it as you said) + 2H+ pumped out
IMS: 2H+ pumped in
TOTAL:
matrix: 10H+ subtracted/pumped out (with 2H+ to water, total 12H+)
IMS: 10H+ pumped in
This satisfies your statement that "10 protons are supposed to get pumped out during the electron cycle". I Hope this helps ;)
IMS = inter-membrane space

I just want to add a slight clarifying point to the previous member's already great answer. Keep in mind that these 10 protons that are pumped into the intermembrane space by the end are per one molecule of NADH. So each molecule of NADH will result in 10 protons being transported into the intermembrane space (as previously stated). For each molecule of FADH2, however, only 6 protons are pumped into the intermembrane space. This is because FADH2 skips Complex I (it feeds its electrons to ubiquinone "Q" through Complex II).


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Identify this large (swamp) fly?
Can anyone identify this large fly?
I encountered it in Okefenokee Swamp (Georgia, U.S.A.) on May 1, 2015.
Weather: 53-78°F (avg. 66°F), avg humidity = 60, dew point = 47°F.
The fly was about the size of an adult thumb (more accurately approx. 5cm long and 2cm wide) -- this fly was HUGE! It was fairly docile and allowed me to take a good close-up or 2.

Tabanus nigrovittatus as my initial guess. "Greenhead horse fly."

Source
This is probably the biggest give-away for the genus Tabanus (namely the features of the veins at the wing tip, denoted R4 and R5, versus other Diptera orders), still searching out a good identification key to solidify the ID. Furthermore, also known as the salt marsh greenhead, a swamp is a good candidate to find these (1).
So what's particular is entomologists have gone through and collected many specimens, and data about their wing venation, and based on the Comstock-Needham system, you can pin presence/absence of major veins, and branching of said veins to specific types on insects. In this case, R refers to the Radius or 3rd longitudinal vein, and the number refers part of the branching that reaches the margin of the wing. Pg 156 here helps us ID Tabanus vs other orders.
Problematic with identifying these spp. is you need to get a good look at the sternites on the under side as well, if you look at how they ID Tabanus sudeticus here, but the photos tend to match nicely with those of T. nigrovittatus you can widely find.

You should add a bit on why you think this a good fit (traits etc), but my first impression was also Tabanus sp. As the moment, this is more of a comment than a full answer. FYI it was caught by the low-quality review queue "because of its length and content".

Believe it or not it's really hard to find a good identification key for Tabanus species!

@Kendall could you comment what about the R4 & R5 wing features (i.e., what is unique about these features as compared to other genera's wings) that demonstrate that this is a Tabanus species?

@theforestecologist I've done so in an edit to my post, let me know how I can better clarify this!

@Kendall Great!! The Comstock-Needham system is very fascinating (and fairly easy to learn)! I don't get the nomenclature for the R2+3 vein though... Also, the vein nomenclature in the image you reference on p156 of the Hamilton paper does not match the nomenclature of the image you've presented here. Could you also provide the link to the image you included and perhaps a comment on the discrepancy. Finally, could you present a citation or key indicating the importance of sternites (and other characteristics). Thanks!!

@theforestecologist Most of the nomenclature discrepancy I suspect is  from the fact the article by Hamilton is trying to do something different. I can't quote you on when the distinction was made, but R2+3 means that the vein R2 and the vein R3 coalesce through their extent in a single vein. Here's your image source http://www.biodiversitylibrary.org/page/6270326#page/328/mode/1up .. for more on the nomenclature, here

It's  my thought while researching this that Tabanus is rather poorly defined!

@Kendall: your answer and subsequent comments have been very helpful (and interesting!).  However after having examined multiple photos of T. nigrovittatus and both photos /memory of the fly I saw, I Just am not convinced that the species is accurate. The wing veins do seem to support Tabanus. I will leave the question open (no accepted answer) to see if someone can provide additional expertise

@theforestecologist Unfortunately im not a specialist (just good at getting what I need out of the literature quickly). I did try quite hard to find an identification/dichotomous key, and outside of wing venation, the documentation is really scarce and photos simply don't help on average. Another good candidate: T. bovinus. The problem is distribution; the well-studied Tabanus spp. are often endemic to Europe/associated areas. "Salt-marsh greenhead" as T. nigrovittatus is often called fits the distribution, but you could viably contact an actual entomologist at a uni. department!

FYI (since this is the most relevant place I can think to place this cool find): here is a super cool website to look graphically at fly anatomical parts!! "Tha Anatomical Atlas of Flies"


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How are the two ATPs (properly 1.5 though) formed from oxidation of 1 FADH2?
Each ATP Synthase has three sites for binding three sets of ADP and Pi, so when the H+ pass through the a and c subunits are they (3 ATPs) not produced for FADH2 substrate?
Besides is the respiratory chain linked to the phosphorylation process apart from the trasfer of H+ ? How does the cell know which substrate has been oxidised and how much ATP is to be produced?

FADH2 substrate does increase the H+ gradient by 6, and so increases the ATP Synthesization "potential" by about 1.5 (6/3.3). the difference between the NADH and the FADH2 substrats are mainly the different path in the electron chain. NADH uses Complex1, and FADH2 is part of Complex2, which have different ability to to pump H+ out. (but of course there are many other differences).
About the second question, it's a really broad subject involving the Krebs cycle and Glycolysis among other subjects. it is mainly a matter of enzyme regulation. The regulation affect both the electron chain and the ATP synthase.


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Have scientists ever produce a new species in laboratory by means of natural selection?
I was wondering, if scientists ever produce a more complex species from a less complex species by means of natural selection? I imagine something like, bacteria which can't photosynthesis and oxygen (chemoautotrophs) to bacteria that can photosynthesis and oxygen like cyanobacteria.
If scientists have never done this, is this theoretically possible to be done in lab by means of natural selection?

If you have plenty of time and all the needed enviromental interactions, then, it should be theoretically possible.

There was a case I remember that involved genetic drift and not natural selection: https://en.wikipedia.org/wiki/E._coli_long-term_evolution_experiment

The term species is poorly defined concept (see here) and as a consequence the question is unclear. However, using the standard concept of species based on reproductive isolation, then the question has been asked (for Drosophila) here and your question is therefore a duplicate.

The question also suggests that you have a few misunderstanding about evolutionary biology. You might want to get some introductory knowledge in this field. Understanding Evolution (UC Berkeley) is a good (and free) online source of information.

@Remi.b I don't get your recent comments about species as a poorly defined concept. By the same logic you are applying here, all questions dealing with or mentioning species should be closed as unclear, which is hardly constructive. Irrespectively of your scepticism towards it, 'species' is fundamental concept in biology, and people should be able to ask about it here at Bio-SE without having to jump through hoops.

If I understand you correctly, the changes you are considering are huge evolutionary steps and not the type of changes you would normally see during speciation. You should also consider that species concepts in bacteria are usually quite different than those used in other taxonomic groups.

@fileunderwater There are ties when the exact definition matter little and times when it is important. You commented yourself on the species concept and what "kind of evolutionary change" is the OP looking for. This is here all I meant. Once the OP understands the concept of species, (s)he will understand why his/her question makes little sense. Note also, that I voted to close as duplicate and not as unclear.

Some people will argue HeLa cells fit this bill, but that's a subject of debate.

There are a few issues your question brings up.  First, the idea that species evolve from simple to complex is actually not a prediction or inevitable consequence of evolution by natural selection.  The terms "simple" and "complex" themselves are ill-defined.  For instance, if you defined "complex" to be size of the genome, the most complex organism found to date is probably a flowering plant from Japan.  This idea of arranging organisms from simple to complex hearkens back to a pre-Darwinian idea of the Great Chain of Being.
You may be thinking that since multicellular life, for example, evolved from single-celled organisms, mutlticellular life is more complex than single celled life.  The fallacy is that modern single celled organisms also evolved from the same single-celled ancestor.  In no evolutionary sense is modern multicellular life more evolved than modern single celled organisms. You can, of course, defined notions of complexity to make multicellular life more complex than single celled life, but such definitions have no evolutionary significance.
We can, of course, say that organisms evolved from earlier organisms.  So the second issue your question brings up is have scientists seen large evolutionary changes in a laboratory setting.  The example you bring up is whether we could observe the evolution of photosynthesis in a lab.
The short answer is no.  We would not expect traits which took millions of years to evolve to evolve in a lab in a shorter amount of time.  In the case of photosynthesis, we may not even have a good idea what selective pressures were involved early in the evolution of cyanobacteria.  Such traits do not usually evolve in their totality in one step.  Instead there are many steps along the way, each of which may be selected for in particular environments for different reasons.  Even if we had millions of years and a very large lab, we may not know of these early selective pressures to successfully recreate the evolution of a particular trait. (There's actually a bit more depth here which I am glossing over. Since the variation in the population is different, the same series of selective pressures won't necessarily yield the same outcome.  When traits evolve through convergent evolution, which is what you are suggesting, they virtually always have different genetic bases and underlying biochemistry.  But a digression into this is probably a distraction from the central point.)
So, you may reasonably ask, if we can not directly observe the evolution of these major traits in a lab, how do we know that they evolved?  There are multiple lines of evidence:

We can see smaller changes occur in shorter periods of time, so it seems likely that the same process creates larger changes in longer periods of time.
For many large traits, we see evidence of common ancestry and the same underlying biology being used for different purposes.
For some traits, we have the evolutionary history of that trait and can identify the sequence of events which brought that trait about (the best evidence generally comes from skeletal traits, where there's preservation).
More speculative evolutionary histories can still be examined through genetic techniques such as molecular clocks, which can indicate when species diverged from a common ancestor.

By most definitions Rick Lenski's Long Term Evolution Experiment has produced a new species in the lab.


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How can binaural beats change mental state?
Can anyone tell me how binaural beats of 10 Hz can cause a person to calm down and one of 40 Hz to cause someone to heighten their attention. All I know is that they work on the principal of Brainwave Entrainment. I am confused as to how can a 10-Hz difference in 2 sounds cause the brain to change its state of mind! A detailed but simple explanation would be great.

It is thought that binaural beats entrain the brain in the frequency of the binaural beat. These beat frequencies show up in the EEG.
The EEG in turn represents synchronous activity in the cerebral cortex (Fig. 1).

Fig. 1. EEG frequency bands and their associate mental states. source: Conor Russomanno
Now if you look at where 10 Hz EEG waves show up it is in the alpha frequency band associated with a relaxed mental state. The 40 Hz band on the other hand is associated with beta activity associated with an alert state.
Indeed, presentation of beta-frequency binaural beats have shown to improve the performance on psychophysical tasks and performances were better than when binaural beats were presented in the theta-delta range (Lane et al., 1998).
Reference
- Lane et al., Physiol Behav (1998); 63(2): 249–52

I will put here a link that I think explained this phenomenon more fully by looking at a huge number of different scientific studies done on the matter...
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4428073/#!po=11.3861
If you find the article too long, read the last paragraphs to find their conclusions.

Please summarize the major points of the link here. It's also good to provide a citation in your answer. Both ensure that your answer remains useful in the future if your link dies. Thanks


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Why is metabolism of ethanol catabolism? Could it be also detoxification?
Detoxification is the physiological or medicinal removal of toxic substances from a living organism, including the human body, which is mainly carried out by the liver. Additionally, it can refer to the period of withdrawal during which an organism returns to homeostasis after long-term use of an addictive substance. (Source: https://en.wikipedia.org/wiki/Detoxification)

Ethanol is metabolised in liver with ADH, which oxidises ethanol to acetaldehyde. The latter is a toxic substance and can cause tissue damage, therfore, it must be further oxidised by ALDH to form a non-toxic product, acetate.
Ethanol can be an addictive substance.

Why is ethanol metabolism catagorized as catabolism? Could it also be detoxification (according to the assumptions above)? Why not?
Is ethanol metabolism a catabolic metabolic pathway because it provides NADH and acetate (which can be activated to acetyl-CoA) for anabolic reactions? Or is there another reason?

These are somewhat loosely defined terms, but I would say catabolism is any metabolic process that extracts energy from a substrate. Ethanol conversion to acetate (via alcohol dehydrogenase; see this schematic) is an oxidative pathway which extracts energy in the form of NADH, so yes, it is a catabolic pathway.
I guess you can also call this process detoxification, since it removes a (mildly) toxic metabolite. Anyway, I think the "classification" of a pathway is less important than understanding the actual biochemistry.


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What are the determinants of tumor metastasis
Under what conditions do tumors migrate? Is it due to hostile microenvironment conditions, drug application, mutations, or other causes? Are there any migration probability values (I am doing an in silico research) or equations to determine this?

There are a lot of mathematical approaches to understanding metastasis.  Review articles might be a good place to start.  The long and short of the biology of metastasis is it depends.  Tumors are highly variable, some metastasize easily and in particular ways, others do not.  It is a heavily studied area of medicine.  I will add that it is probably not a "hostile microenvironment" that encourages metastasis; it is probably better to think of the proximate causes rather than such ultimate causes.

You might also want to read about the epithelial-mesenchymal transition as an initiator of metastasis.

So here's a sort of review article that may help you https://people.maths.ox.ac.uk/maini/PKM%20publications/367.pdf .. and perhaps this one as well http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4626809/


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How does a Plasmodium move?
Plasmodium sp. does not have any locomotory organs. So, how does it move? What biochemical process allows it to move?

Short answer: Only some stages of plasmodium are motile.  These use "gliding motility".
Gliding motility relies on actin filaments, which enable the organism to deform it's shape, facilitating movement.
This video provides a good visual representation of the filament-based motility.

"Gametocytes develop into gametes in the insect midgut, and then fertilize each other to form motile zygotes, which escape the gut."

The ookinete and sporozoite are motile.  The merozoite is non-motile.
Then of course there is the circulatory system of the host.
Source:
https://en.wikipedia.org/wiki/Plasmodium
http://www.sciencedirect.com/science/article/pii/S0092867400812817

You did not answer the OP's question.

What makes the sporozoite and ookinete motile? Are there any filaments responsible for cell movement?


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Why do Major and Minor grooves exist in dna strands?
I've been trying to find what causes the periodic appearance of major and minor grooves in DNA but have not yet been successful. Geometrical explanations would also be appreciated as I cannot understand any of the geometrical explanations I have come across so far. As far as my knowledge of DNA is concerned I know of all the high school basics (e.g complimentarity, bonding between the individual components of a nucleotide etc.)

Please [edit] your question and explain what you have learned so far, and where exactly you're stuck. As it stands now, this question is too broad.

It is all explained here in Wikipedia. You are referring to Watson-Crick base pairs in the B-DNA structure.


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What is working definition for female infertility?
I've studied infertility and found that its quite complex to define. However, I came to know about a useful working definition of infertility; which was " Failure to achieve pregnancy".
Few days later I've hit upon a idea that proves that definition wrong. As I studied the turner syndrome, in which condition was XO but individual was infertile female. Further I studied that if they are subsequently treated with Gonadotrophin hormones, they have menstrual periods as well. There I found that if a fertilized egg is implanted in their uterus, pregnancy would be achieved. Now how would we call that female infertile?

Infertility is defined as the inability to conceive after one year or longer of intercourse without the use of contraception or therapeutic donor artificial insemination.

That definition does not include a state of permanence.  That is, with treatment, fertility can indeed be achieved in many cases.

You may want to consider the term sterility as a definition, which has a permanence to it. But even then, if you consider tubal ligation (female sterilization) or a vasectomy (male sterilization), then you'll quickly conclude that sterilization can be reversed.  At that rate, you may want to state "irreversible sterility" where a genetic basis cannot be overcome with treatment/intervention.  Even then definitions may vary.

As you've discovered, even some genetic-based infertility can be overcome with IVF.  In terms of your genetic interests, the condition of XX male syndrome, resulting from loss of the SRY gene during crossover, causes the inability to produce any sperm (azoospermia).  There is no existing treatment for that or even a reasonable theoretical one.
This could get more complicated/interesting as new medical therapies mature.  If one were to clone a human for example, is that a type of reproduction? Likewise, there is gene therapy, which could overcome some types of genetic-based sterility.
Sources:

http://medical-dictionary.thefreedictionary.com/Infertility
http://medical-dictionary.thefreedictionary.com/sterility
http://www.acog.org/~/media/For%20Patients/faq011.pdf


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What is 'noise'?
In both my psychology, biology and neuroscience classes, professors are constantly talking about 'noise'. For instance, our perception is limited due to 'sensory noise' in our neurons.
I am utterly confused about this concept. What is 'noise'? Can someone please conceptually describe what is is in laymen's terms?

Maybe they meant noise as a type of interference, like when you have everyone in the same room with the same type of wireless mouse, there is interference with the signal. Thats just a Wild A$$ Guess though...

The term noise can mean a number of different (more or les related) things is used in a number of different fields such as signal processing, psychology and statistics.
Outside of its context, it is impossible to say for certitude what you professors were referring to.
The quotations below come from wikipedia > Communication noise, wikipedia > Statistical noise, wikipedia > white noise and wikipedia > noise
Psychological noise

Psychological noise results from preconceived notions we bring to conversations, such as racial stereotypes, reputations, biases, and assumptions. When we come into a conversation with ideas about what the other person is going to say and why, we can easily become blinded to their original message. Most of the time psychological noise is impossible to free ourselves from, and we must simply strive to recognize that it exists and take those distractions into account when we converse with others.

Psychological noise

Physiological noise has to do with distractions from the natural effects of the body, such as being tired or hungry.

Physical noise

Physical noise is any external or environmental stimulus that distracts us from receiving the intended message sent by a communicator (Rothwell 11). Examples of physical noise include: others talking in the background, background music, a startling noise and acknowledging someone outside of the conversation.

Semantic noise

This is noise caused by the sender. i.e., the encoder. This type of noise occurs when grammar or technical language is used that the receiver (the decoder) cannot understand, or cannot understand it clearly. It occurs when the sender of the message uses a word or a phrase that we don't know the meaning of, or which we use in a different way from the speakers. This is usually due to the result that the encoder had failed to practice audience analysis at first. The type of audience is the one that determine the jargon one will use.

Statistical noise

Statistical noise is the colloquialism for recognized amounts of unexplained variation in a sample.

White noise

In signal processing, white noise is a random signal with a constant power spectral density.1 The term is used, with this or similar meanings, in many scientific and technical disciplines, including physics, acoustic engineering, telecommunications, statistical forecasting, and many more. White noise refers to a statistical model for signals and signal sources, rather than to any specific signal.

Noise in its everyday use

Noise is a variety of sound. It means any unwanted sound. Sounds, particularly loud ones, that disturb people or make it difficult to hear wanted sounds, are noise. For example, conversations of other people may be called noise by people not involved in any of them; any unwanted sound such as domesticated dogs barking, neighbours playing loud music, portable mechanical saws, road traffic sounds, or a distant aircraft in quiet countryside, is called noise.

In electronics, there are concepts of signal and noise; what is not signal is noise. Signal is an "intended" or expected impulse or waveform; noise is any other impulse or waveform - unwanted or unintended.
Taking this into a biological context, sensory noise would then be sensory impulses, whatever the cause, which don't convey useful or meaningful information.


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What is vascular cambium?
I'm confused over the two terms vascular cambium and intrafascicular cambium.
Is vascular cambium the same as intrafascicular cambium?

Intrafascicular and vascular cambium is the same.Intrafascicular is primary meristem but interfascicular is secondary as it developed from pith ray.

I know nothing about plant physiology but I googled your question and here is what I found
Vascular cambium
From wiki

The vascular cambium (plural cambia) is a plant tissue located between the xylem and the phloem in the stem and root of a vascular plant, and is the source of both the secondary xylem growth (inwards, towards the pith material at the center of plant, often dead and/or deteriorated, that is composed of parenchyma tissue) and the secondary phloem growth (outwards [to the bark, rough or smooth, of the plant]). It is a cylinder of unspecialized meristem cells that divide to give new cells which then specialize to form secondary vascular tissues.

Intra fascicular cambium
From Biology.easlife

The cambial strip which is present between the primary xylem and primary phloem is known as the intra fascicular cambium. The intra fascicular cambium is also known as the vascular cambium. During the secondary growth the cambial ring is formed by the inter connection of the intra fascicular and inter fascicular cambium. - See more at: http://www.biology.lifeeasy.org/5040/what-is-intrafascicular-cambium#sthash.aY3SPblI.dpuf

What is the difference between fascicular cambium and inter fascicular cambium?
From biology.lifeeasy

The cambium present within the vascular bundle is called intra fascicular cambium or vascular cambium. It is present between the primary xylem and primary phloem. The intra fascicular cambium is primary in origin.
The new strip of cambium which is formed from the permanent cells of inter fascicular parenchyma is called the inter fascicular cambium.  The inter fascicular cambium is secondary in origin since it is derived from the permanent cells of medullary rays.

Need more?
If the above definitions don't help, you should include in your question why these definitions don't help and what is unclear.

The Vascular cambium is responsible for secondary growth, which is growth in thickness. Whereas, primary is growth in length. Once, the length-wise growth of the xylem and phloem are accomplished, growth in thickness or growth inwards through the vascular cambium occurs; it occurs in wood-based plants.

This doesn't address the question of intrafascicular cambium.

Vascular cambium is made of two parts. one is interfascicular vascular cambium and other is intra fascicular vascular cambium. The part between xylem and phloem is called intra fascicular vascular cambium.


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How to predict Protein-Protein Interactions from a pair of gene symbols?
I have a list of pairs of gene symbols who interact (putatively) and would like to assign each pair a score (and record other details) based on the predicted Protein-Protein Interaction (PPI). The existing PPI webservers I've looked at (ClusPro and HADDOCK) require that I use PDB ID's as input. Unfortunately, PDB ID's don't always exist for the gene symbols I'd like to compare. I believe I need either:

a way to generate PDB files myself (perhaps with a folding program?) and then connect/upload them to a PPI webserver.

or

a way to find the most similar sequence that does have a PDB ID and upload it to a PPI webserver.

Am I understanding my problem correctly? Are there resources that can help with 1 or 2?

I don't understand what you mean. What kind of interaction data do you have and what kind are you after? Are you starting by a list of interacting genes and want to check whether their protein products interact as well? Is your question just about how to get predicted PPI interactions for pairs of gene names? If so, there's no need for PDB IDs, the vast majority of PPI databases use other identifiers. Please [edit] and clarify and then leave me a comment and I should be able to help. Make sure to include examples of your input IDs.

This may or may not be possible, depending on what proteins you are considering. Generating a PDB file means predicting the structure of the protein. There are no methods for predicting protein folding accurately from plain sequence data, so you will need some experimental data on the structure of your proteins.
If your proteins have not been structure determined, the next best thing is some kind of homology model, that is, a prediction of your protein structure based on a known structure of a homologous protein. These can be more or less accurate, depending on how close the homolog protein is. If specific domains are interacting, it may be enough to create a model of the domain only.
There are online tools available for homology modeling, for example swiss-model from the expasy site. This is not an automated process though --- creating an accurate model requires some skills. You should read the publications describing these tools and make sure you understand the process and error souces, and perhaps contact an expert if in doubt. Good luck!


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Atlas from human brain structures to 3D coordinates?
I would like to visualize specific human brain structures in the three dimensional space and compute specific geometric properties of these brain structures (size, centroid, etc).
Therefore, I am looking for an atlas that maps human brain structures to 3D coordinates (in Talairach or MNI coordinates).
I saw online a lot of websites allowing the inverse mapping, which is from coordinates to brain structures. So I know that this data should be somewhere but I was not able to find it.
Any lead would be greatly appreciated.


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Do antioxidants interfere with chemotherapy?
Since most of the chemotherapy drugs kill cancer cells by damaging their DNAs by means of free radicals. So antioxidants, which will detoxify free radicals, should theoretically decrease the efficacy of the chemotherapy.
However clinical trials are proving the opposite. Saying, antioxidants does not decrease chemotherapy efficacy but also make chemotherapy more effective, thus increase the survival rate.
http://www.ncbi.nlm.nih.gov/pubmed/17283738
The question is, why antioxidants do not interfere with chemo, while they are supposed to do ?

That reference doesn't look very authentic. Four authors all named Simone (a family enterprise?), from the "Simone Protective Cancer Institute", which appears to be just a website (www.drsimone.com). This Dr Simone (self-appointed as "cancer's worst enemy") says he is endorsed by Ronald Reagan and claims broad expertise ranging from "the truth" about cancer to "how to save yourself from a terrorist attack", and peddles various anti-cancer diets (?) as well as health insurance plans. Stay away ...

Since it's a very broad argument I'll try to summarize in a few sentences.
First of all the sentence:

Since most of the chemotherapy drugs kill cancer cells by damaging their DNAs by means of free radicals. So antioxidants, which will detoxify free radicals, should theoretically decrease the efficacy of the chemotherapy.

is a bit inaccurate as of today. The chemotherapy today uses the "classical" chemotherapy drugs which IN PART use the mechanism of free radical but there are a lot of mechanism such as microtubule damage and so on which do not depend on free radical toxicity. Today there are also a lot of biological drugs and inhibitors of tyrosine kinase inhibitor which use a completely different pathway.
You cite a paper from 2007, a bit dated, I cannot access full text because it's an abstract. It seems it's not performed in a systematic manner (it's a not a systematic review or meta-analysis) and is published in a journal of alternative medicine. Maybe there are more recent paper but unfortunately at the moment I cannot have the time to check.
Finally you are comparing the effects of a chemotherapy drug administered usually in high dosage to the use of antioxidant which I cannot recall are sold as drugs used regularly, so it's a potential interesting biological question but practically it's a bit difficult to compare the oxidative effect of a cancer drug with the effect of an antioxidant one in real patients since I don't think there are randomized controlled clinical trials comparing chemotherapy to antioxidant alone.

There are many ways to damage the DNA of a rapidly proliferating population of cells; oxidative damage is one example—albeit a very broad example not especially specific to cancer cells, the cells we would like to eliminate.
Many non-targeted chemotherapeutic drugs exploit other mechanisms of depriving cancers cells of a high-fidelity genome, therefore reducing their competitive fitness or outright killing them due to a lack of functioning copies of essential genes. For an overview of such classes of drugs, see the Wikipedia page on Chemotherapy.
Alkylating agents covalently modify the DNA (along with protein and RNA) of affected cells, causing misreading errors to accumulate as DNA is replicated. Alkylated DNA bases cause misincorporation of nucleotides on the newly synthesized strand that sometimes escape proofreading, causing mutations to be passed on to all daughter cells. Also, if such survailance systems are working in cancer cells, alkylated DNA can cause cell cycle arrest or even programmed cell death.
Antimetabolites disrupt necessary cellular metabolic functions. One common mechanism is to interfere with any chemical reactions catalyzed by the folate family of vitamins/enzymatic cofactors. Folate is necessary for synthesis of some new nucleotides, which are necessary for replicating the genome. A lack of these nucleotides can cause low-fidelity DNA replication (introducing deleterious mutations into the genomes the cells) and cell cycle arrest, blocking division and proliferation.
Anti-microtubule agents interfere with the dynamic behavior of microtubules, a subcellular structure responsible for properly sorting the chromosomes during cell division; microtubules also contribute to cell shape and tissue-invasive locomotion. Preventing microtubules from functioning normally can lead to chromosomal missegregation during cell division, depriving some daughter cells of whole chromosomes (gene loss) and leading to genome instability, which can cause cells to loose fitness or loose genes necessary for life.
These are some examples of chemotherapeutics that do not rely on broadly oxidative mechanisms for their cell-killing action. The point of chemotherapy is to be more toxic to malignant cells than to the rest of the body's cells. Since malignant cells often divide more often than normal body cells in adults, many chemotherapeutic agents are employed with the idea in mind of being more toxic to rapidly-diving cells and less toxic to slowly diving cells.


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How is HIV evolutionarily viable despite its extreme virulence?
How does HIV survive natural selection? And how has it managed to kill far more than any non-airborne virus in recorded history?

Human Immunodeficiency Virus is a mutated form of Simian Immunodeficiency Virus. In simians (Apes and Monkeys, not including humans), SIV is not pathogenic, in most cases, however, when the mutated form made the jump to humans, it became highly contagious and virulent. You can find a basic description in the wikipedia article here: Simian Immunodeficiency virus.
As for your second question, I would likely say that influenza has killed more humans in total than HIV, so you would have to provide a reference for your claim.
However, because HIV is a retrovirus that incorporates into the genome of the immune cells of its host, it can survive in the body for long periods of time in a dormant state. A person may not know they are infected for months or years, and they can pass the virus on to other people. Slow killing viruses such as HIV are very dangerous, as they can be transmitted to large swaths of the population before people are aware they are sick.
Update:
Based on comments, there may be a misunderstanding of the term virulence. From The Karolinska Instetutet medical subject heading (MeSH) definition:

The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.
-The Karolinska Institutet; Virulence

The emphasis is mine, but virulence also refers to the ability of the virus to infect its host, and does not necessary lead to the hosts death. The virus that causes the common cold is highly virulent, but for almost the entire human population it causes nothing more than discomfort.
A virus like Ebola on the other hand is highly virulent in both senses of the term. The reason that there are far fewer cases of Ebola is that it kills the human host so quickly, that an afflicted person will on average only go on to infect about two other individuals, mainly because victims 1) die quickly, 2) are only contagious after symptoms manifest themselves, and 3) requires direct contact with the infected person's bodily fluids.
Contrast that with Influenza which a single person can infect tens to hundreds of people and is contagious before they are displaying symptoms and spreads it with casual contact, or as stated above, with HIV, where a person can be contagious for weeks, months, or even years before they are aware that they are infected, and you see why HIV is very sustainable in the Human population.
HIV also has the added weapon in its arsenal that it can lay dormant in cells for long periods of time so as to escape the detection of the host immune system, and as the disease attacks and kills immune cells, when the dormant virus activates again there are far fewer specialized cells to address the active infection.
Another thing is it is the comorbidity with other diseases that often results in the death of a patient with an HIV infection. AIDS results from other diseases having the opportunity to go unchecked after HIV has decimated the host immune system.

I don't think that answers the question. How is HIV viable? Virulence is selected against.

@Anonstudent - Perhaps you intended something different, but the answer answers the question you asked. Virulence is not always selected against, as shown in the answer.

@Anonstudent You might be thinking of the rate of mortality or pathogenecity (rate an infection causes a disease) -- which also aren't always selected against. There are many niches to fill between the extremes.

@Anonstudent - High pathogenicity is not selected against -- that's a widespread but incorrect belief.  Pathogens are generally selected for transmissibility; in some cases, higher transmissibility is associated with lower mortality, but the reverse is also true in some cases.  Viruses with extremely high mortality rates, like rabies, are perfectly viable on a population basis.

But rabies isn't viable among humans.

@Anonstudent -What's your point? Rabies is viable among dogs and many other species, in which it has a 99.9999% mortality rate.  Viruses like rabbit calicivirus are viable in rabbits in Australia, where there is a 90% mortality rate.  Again, both evolutionary theory, and trivial observations, show that pathogen evolution is linked to transmissibility, not mortality rate.

My point is that, in the long historical term, there aren't any highly virulent viruses that infect humans.

Smallpox was successful in humans and was "highly virulent" by any measure.  You keep making dogmatic claims that are trivially refuted -- you claim that "virulence is selected against", which is false; you claim that virulent viruses don't exist, which rabies disproves; you then claim that there are no virulent viruses in humans, which smallpox disproves.  And, of course, HIV itself disproves all your claims in the first place, for any except the most willfully ignorant denialists.  If you actually have an argument, and not merely a set of constantly-moving goalposts, please make it.


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Does a gene that regulates itself necessarily be a transcription factor?
I am not a biologist, so please pardon the overly noob question. Some genes are transcription factors (TF) and regulate other genes. My question is: if a gene is NOT a TF gene, can it regulate itself? E.g. given a system of 3 genes {g1,g2,g3} where only g1 and g2 are TF, then in a gene regulatory network, what are ALL possible parental sets of g3 (where in this GRN, you put a directed edge from the regulating gene to the regulated gene)? Will it be {{g1},{g1,g2},{g2},{}} or {{g3,g1},{g3,g1,g2},{g3,g2},{g3}}

There is no one answer to this question. Some non-TF proteins signal through negative feedback loops to eventually downregulate their expression when they're no longer needed/there is a lack of substrate/etc. Others don't, and are regulated through other means.

First of all you need to clarify what exactly is the output that needs to be regulated. We often say regulation of expression of a gene but what expression ultimately leads to is the activity of the gene (whatever it might be: enzyme based catalysis, cytoskeletal rearrangement, response to an extracellular signal). Activity of course depends on the expression level of the gene but it also depends on other factors such as covalent modifications, interactions with other genes (like dimerization) etc. Moreover, for genes which code for proteins, expression also has two stages.
Coming back to your question:

If a gene is NOT a TF gene, can it regulate itself?

Yes it can. There are many modes of gene activity regulation as I already mentioned. Examples where a non-TF gene can regulate itself:

Feedbacks in cell signalling which happen via activity modulation by protein phosphorylation [1].
Regulation via post-transcriptional regulation via RNA binding proteins (RBP) or regulatory RNAs such as miRNA. MAPK signalling pathway has a feedback via the RBP, Rnc1, which upon phosphorylation binds to and stabilizes the Pmp1 mRNA. Pmp1 is a phosphatase which dephosphorylates Rnc1[2]. This loop contains regulation by both post-translational modification and post-transcriptional mRNA stabilization. There are many other examples involving RBPs. An miRNA, let-7 is post-transcriptionally regulated by Lin28 (promotes degradation) which in-turn is post-transcriptionally repressed by let-7 [3].

There are many examples of metabolic feedbacks too which operate via allosteric regulation of the enzyme activity.
If you are only interested in regulation of gene expression then you can ignore phosphorylations and allosteric regulation but there are several examples of post-transcriptional regulatory interactions which also contain feedbacks.

References

Dougherty, Michele K., et al. "Regulation of Raf-1 by direct feedback phosphorylation." Molecular Cell 17.2 (2005): 215-224.
Sugiura, Reiko, et al. "Feedback regulation of MAPK signalling by an RNA-binding protein." Nature 424.6951 (2003): 961-965.
Rybak, Agnieszka, et al. "A feedback loop comprising lin-28 and let-7 controls pre-let-7 maturation during neural stem-cell commitment." Nature Cell Biology 10.8 (2008): 987-993.

I don't understand your system of 3 genes regulatory network question, but I can answer your general question regarding transcription factor self-regulation of transcription/gene expression.
Yes, in biology, there are transcription factors that bind to their own gene's promoter-proximal region (on DNA) and regulate their own gene's transcription. There are examples of positive feedback loop transcription factors (e.g. FOXL2) and negative feedback loop transcription factors (e.g. Oct4, Nanog, & FoxD3; also Irf8 with Cebpb).


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Nicotine levels in non fruit/edible parts of plants (that are not tobacco)
I am an ex smoker who now vapes (uses e-cigs). Various authorities are equating vaping with smoking by calling it a 'tobacco product' - which is in a sense true given that the majority of nicotine sold is extracted from the leaves of tobacco. I am interested in the practicality (or otherwise) of extracting nicotine from other botanical sources.
Of course, it is not just tobacco that contains nicotine, it is common in other plants of the nightshade family, as suggested by The Nicotine Content of Common Vegetables & Nicotine: Occurrence and biosynthesis. The second source notes:

Nicotine is a natural product of tobacco, occurring in the leaves in a range of 0.5 to 7.5% depending on variety.[84] Nicotine also naturally occurs in smaller amounts in plants from the family Solanaceae (such as potatoes, tomatoes, and eggplant).[85]

Reference 85 points back to the first link, which shows this table.

But looking at the numbers, it seems unlikely. At even .5%, the 'low nicotine' tobacco leaf comes in at 5 mg/g, which is 5,000,000 ng/g - around 50,000 times more concentrated than eggplant. In fact, here is a graph of the log10 value (2 is ten times larger than 1) of each.

On the other hand, the ability of a plant to produce nicotine is retained and handed down to ancestors because nicotine is a pesticide that ..discourages insects from eating the plant, and larger herbivores will also get sick if they eat too much of it. Logically, levels of nicotine would be higher in the leaves and stems of a plant than in the fruits/food that we & animals are more interested in eating. That again makes sense, since most fruits are 'designed' to be put through the stomach of a larger animal as part of the process of regeneration.
That logic seems to be borne out by the levels of nicotine in tomatoes, that start around 40 ng/g in green tomatoes, but end up at just over 4 ng/g in ripe tomatoes (not sure what's going on with that 'pureed tomato' level of over 50 ng!). The drop suggests to me that's the plant's way of preventing consumption while the fruits are still developing, but making them safe(r) to eat once ripe.
But what about the nicotine content in the leaves of those plants? Logically they might have a higher nicotine content. Does anyone know of studies of the levels of nicotine in the other parts of plants of the nightshade family?

Apparently someone thinks this question is less than optimal. Would appreciate any suggestions on improving it..

It might be an opinion about nicotine in general. This question has quite a bit more data than an average question, but I'm not aware of large nicotine levels in other parts of plants. I assume tobacco will still have the highest nicotine levels, because that's what people have been selecting for for centuries. I also assume that the FDA doesn't like e-cigarettes because they still have nicotine, regardless of source. Nicotine is addictive at low doses and toxic at high doses. They really don't like candy flavored nicotine products that might attract children.

"..I'm not aware of large nicotine levels in other parts of plants. I assume tobacco will still have the highest nicotine levels, because that's what people have been selecting for for centuries." I suspect therein lies the answer. "I also assume that the FDA doesn't like e-cigarettes because they still have nicotine," As do nicotine patches, lozenges, gum and puffers (inhalators).. "Nicotine is addictive at low doses and toxic at high doses." Not much. There is no single instance of getting a lab rat addicted to it. It is largely the other things in tobacco smoke (like WTAs) that ..

.. are so addictive. Most people that can transition from smoking to e-cigs typically drop the nicotine levels gradually. Not a great sign of an 'addictive substance'. "toxic at high doses" Yes, The dose makes the poison, and a 2014 study estimated an LD50 dose of 500 mg for an adult human. It is not to be treated lightly, and should be kept in bottles with child-proof cap, out of reach of children. "They really don't like candy flavored nicotine products that might attract children." Umm.. nicotine lozenges are designed in yummy ..

.. flavors, and check this graph of adult taste distributions for e-liquids. Further, a) kids often vape with no nicotine, and b) in states of the US where vaping is restricted, show a slower drop in smoking rate. Since the 1970s, tobacco controllers have recognized that "People smoke for the nicotine, but die from the tar". E-cigs have no tar, no carbon monoxide, and when used responsibly, provide an effective and 95% safer way for smokers to satisfy their desire for nicotine. Thanks for bringing those matters up. :)

BTW - I recognize that you were speculating about what other people might be thinking. I suspect the same reason was behind the down vote. The thing is, there are powerful forces aligned against the e-cig industry at the moment, including the CDC, FDA, ALA, AMA, CTFK.. and states deeply in debt to the MTSA.. They spread much fear, uncertainty and doubt for ..whatever reasons. That's why I'm investigating 'nicotine from other sources'. It has become a largely political point that nicotine is sourced from tobacco. Next stop would be, synthetic..

Note that the nicotine is not the problem and never was the problem. There are, apparently, some studies that link nicotine itself to certain cancers but the reason that smoking is bad for you is overwhelmingly because you smoke it. Take away combustion and most of the problem basically disappears. Therefore, the source (or even presence) of nicotine is essentially irrelevant. That said, please don't use this forum as a soap box to tout the improvements of e-cigs over smoking. I happen to agree with you 100%, but this is not the place for it.

Would look forward to finding out more when you get back to your computer, @kheironiscus.

why would hte lack of nicotine in other plants be relevant, many plants produce high concentrations of specific compounds that is relatively rare in most other plants.

.. I'm not aware of large nicotine levels in other parts of plants. I assume tobacco will still have the highest nicotine levels, because that's what people have been selecting for for centuries. .. - user137

That logic seems compellingly sound.
Based on that, why would a researcher even bother to measure the nicotine content of the other parts of non-tobacco plants?

They are not being eaten by consumers & thereby have little or no risk of poisoning them.
The levels of nicotine would be expected to be so far lower than the 'commercially viable' tobacco leaves as to be of no interest (purely for their nicotine content).

So in answer to my own question.

Does anyone know of studies of the levels of nicotine in the other parts of plants of the nightshade family?

No, because it is unlikely any such research has been performed.

Tomato leaves have something like 184 ng/g of nicotine, in the same ballpark as tomatoes (the fruit) and not close to tobacco.  I think this is not peer-reviewed, but it cites other papers that are: Nicotine Analysis in Several Non-Tobacco Plant Materials
And this is a PDF of a slide deck providing a simple presentation of the results from the same article: Nicotine Analysis in Several Non-Tobacco Plant Materials - PDF

"I think this is not peer-reviewed" No problem here. I've read enough papers from people in tobacco control that have passed peer review, which completely disagree with other peer reviewed papers, that the 'not peer reviewed' status does not bother me in the slightest. Thanks for your answer!

I take issue with the previous answerer's assertion that it is extremely unlikely that previous research on nicotine concentrations has ever been performed; in fact, it was very well established decades ago that alkaloids in Nicotiana (and other Solanaceaes) are predominantly synthesized in the roots and, in the case of grafting studies, translocated through the stalk into the scion, which findings rest on measurements of alkaloid levels throughout the plant.  The research is very much out there.
Reference
G. R. Waller and E. K. Nowacki,“Alkaloid Biology and Metabolism in
Plants,” Plenum Press, New York, NY, 1978. Pages 121-141 for the nicotiana grafting discussion.  No doubt there is more recent work out there, though.


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Droppings of mystery: What are they
I have noticed the droppings below, quite visible on snow, next to an inner-town building situated next to this place in Luxembourg, central Europe. There are quite a few, but I have not noticed them anywhere else. What animal creates these and why do they have this red color which stains the surrounding snow? Is it a cat being fed colored food?
Local wildlife is mostly city pigeons (with digestive tracts of steel), huge flocks of crows (inhabiting parks and occupying the construction cranes at nightfall), maybe a few stray foxes and rabbits. House dogs and cats of course although these don't run around unattended.

How big are they? Is the snow melting? (Otherwise it looks like whatever left it did it without leaving tracks.)

@picapica As big as the the half the pinky. The snow is not melting in this picture, temperature about -4°C. The picture shows the border of a decorative plant-holding trough, rather overgrown, so it's likely there are mice living in there and probably cats doing regular inspections.


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How do CAM plants keep stomata closed by day and open at night?
I understand how plants open stomata, with the H+ ion removal and the resulting K+ ion influx in the guard cells to induce turgor (wikipedia article here), though not how this process relates to presence/absence of light.
However, I don't understand how CAM plants manage to keep their stomata closed during the day and how it relates to CAM photosynthesis (if at all). I know that malate ions are involved in the opening of the stomata in C3 plants, could the malic acid production in CAM photosynthesis contribute to this?
So my question is: How do CAM plants induce closing of the stomata and what signal triggers this?

This isn't homework, I'm just genuinely curious. CAM and C4 photosynthesis isn't part of the Scottish curriculum, so I haven't covered this  and nor can I find anything about this online.

Yeah I've been searching for this casually for about 3 months now and am yet to find anything, thank you for the link but it hasn't turned over anything new. I apologise if the wording makes it out to seem like I haven't done reading of my own. I asked my interviewers at a university interview this question and they said they knew someone who could answer my question, so I know this has been answered and I'm just hoping someone on here will know it.

I think the biggest problem is we don't know the signal transduction pathway in CAM plants in response to CO2 levels.

Is it known what conditions in the cell trigger the H+ ion pumping in normal plants? Again something I've been looking for

@Phototroph Blue light phototropins activate the membrane H+-ATPase through phosphorylation events (1). Therein voltage-gated potassium channels open in response to the membrane potential generated by the H+ pumping.

As others already say in comments, the complete answer to this question is still unknown. However, the basic mechanism has been understood and has been summarized in the following diagram (from Wikipedia):

As you see, the mechanism is regulated by temperature instead of presence of light, keeping in mind that high temperatures are generally observed during the day and low tempertures at night. Temperature regulates, at the expression level, the activity of an enzyme PEP-C kinase. This enzyme phosphorylates PEP carboxylase (or PEPCase in short), which increases its activity. So lets see what happens when temperture is high:
During day:

high temperature inhibits expression of the enzyme PEP-C kinase, which decreases the activity of PEPCase.
activity of PEPCase is further reduced by an enzyme PEP-C phosphatase (this enzyme is active all the time, but its effect is reversed by PEP-C kinase).
due to respiration and photosynthesis, the amount of cytoplasmic malate is reduced (malate is converted to pyruvate to yield NADPH for photosynthesis, and pyruvate is used up in TCA cycle, whose by-product, $\ce{CO_2}$, is used up in calvin cycle).
due to this, malate is released from vacuole into the cytoplasm. This malate is not only used up in photosynthesis and respiration, but also further inhibits activity of PEPCase and expression of PEP-C kinase.
because PEPCase is inhibited, it results in depletion of malate in cytoplasm as well as vacuole.

During night:

at night, stomata open leading to increase in amount of $\ce{CO_2}$. Also, low temperature is unable to inhibit expression of PEP-C kinase.
when activity of PEPCase increases, PEP is converted to malate, which is then transported into vacuole. Also, increased concentration of $\ce{CO_2}$ increases photosynthesis.

Where is light required? As already said, the exact mechanism is still unknown. The mostly accepted mechanism is potassium ion pump hypothesis, but problems arise when we think about the initiation of this process in CAM plants. There are many hypotheses regarding this, and I will follow the one presented by Lee, 2010. Lets begin with the diagram (don't pay attention to the spellings):

initial stomatal opening is mediated by phytochrome in guard cells. The $\ce{H^+}$ pump in guard cells is also activated by darkness.
the maleic acid synthesized in other cells is also transported to the vacuoles in guard cells. There, the intracellular $\ce{H^+}$ (from maleic acid) is exchanged for intercellular $\ce{K^+}$.
increased concentration of $\ce{CO_2}$ also regenerates glyceraldehyde-3-phosphate and ribulose-1,5-bisphosphate, which lead to formation of sucrose via calvin cycle.
this sucrose is again transported to vacuole of guard cells, adding up to osmotic pressure. However, the major effect comes from maleic acid.
increased $\ce{CO_2}$ concentration and increased activity of PEPCase (as already explained) form malate and lead to further increase in the osmotic concentration. All this causes stomata to open.
during the day, malate is decarboxylated to pyruvate (as already explained), leading to decrease in osmotic pressure and thus, closing of stomata.

I hope this makes the concept more clear, but bear in mind that the above mechanism could later prove to be wrong as further studies on CAM plants help to find out the actual mechanism.

It's unbelievable that this answer was here for almost 1 day, with 500 views, without a singe vote. People upvote like if it was paid...at StackOverflow it's even worse! (I'll delete this).

Problem solved! Joking apart, new users normally forget to vote and experienced users apparently see each other like competitors. They don't understand that the gamification aspect of SE, despite a lot of people denying it, is what maintain SE sites active and it's what incentives people to write (good) answers.

@gerardofurtado +1 for explaining what I call healthy competition :)