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Has human skin pigmentation adaptation and evolution ceased?
Before asking this question read

Why human skin colour disprove natural selection?
Does darker skin color make it easier to live under sun?

though neither posed the same question or provide the answer to the present question.
In Modern Human Diversity - Skin Color published by The Smithsonian National Museum of Natural History the document in pertinent part states

As early humans moved into hot, open environments in search of food
  and water, one big challenge was keeping cool. The adaptation that was
  favored involved an increase in the number of sweat glands on the skin
  while at the same time reducing the amount of body hair. With less
  hair, perspiration could evaporate more easily and cool the body more
  efficiently. But this less-hairy skin was a problem because it was
  exposed to a very strong sun, especially in lands near the equator.
  Since strong sun exposure damages the body, the solution was to evolve
  skin that was permanently dark so as to protect against the sun’s more
  damaging rays.
...
The darker skin of peoples who lived closer to the equator was
  important in preventing folate deficiency. Measures of skin
  reflectance, a way to quantify skin color by measuring the amount of
  light it reflects, in people around the world support this idea. While
  UV rays can cause skin cancer, because skin cancer usually affects
  people after they have had children, it likely had little effect on
  the evolution of skin color because evolution favors changes that
  improve reproductive success.
There is also a third factor which affects skin color: coastal peoples
  who eat diets rich in seafood enjoy this alternate source of vitamin
  D. That means that some Arctic peoples, such as native peoples of
  Alaska and Canada, can afford to remain dark-skinned even in low UV
  areas. In the summer they get high levels of UV rays reflected from
  the surface of snow and ice, and their dark skin protects them from
  this reflected light.

Cases: Lighter skinned populations who migrated to tropical regions (for example, Mennonites in Belize, Boers in South Africa, Belgians in Congo (DRC)) and darker skinned populations which migrated to non-tropical regions (for example Africans in Britain, Africans in the northern U.S. States and Alaska, and Africans in Canada), where the diets of the populations take on the diets which in part led to the specific pigmentation, and the sun applies the same amount of light (UV; other spectrums) to the population as the population where darker or lighter skin adapted, or evolved.
Given the parameters provided, a lay person might conclude that they should be able to migrate to a specific tropic or non-tropic region of the world, take on the diet which led to the melanin production and skin pigmentation which the article states influences adaption or evolution, and over N fixed generations, or an unknown period of time, though eventually, their skin pigmentation will adapt or evolve to the population planners' desired pigmentation; that melanin production and skin pigmentation is not fixed, that evolution and adaptation as to skin pigmentation is continuously ongoing in the human population on Earth circa 2019 CE - and the claim is capable of being reproduced, observed and objectively measured using the scientific method.
Have any scientific studies been performed which substantiates or refutes by observable measurement the theory or claim that environment and diet have an effect on melanin production and skin pigmentation within the scope of any timescale ("One generation, two generations, ten generations, 10-20 generations")?

I downvoted because this question, despite its length, seems to strongly misunderstand evolution and because I suspect it is not asked in good faith. See a good reference on basic evolution like https://evolution.berkeley.edu/evolibrary/home.php

@BryanKrause Gather what evolution and adaptation are. Have no "faith" in anything. The question asks for facts: have any studies been performed to substantiate the claim presented as to melanin production and diet having measurable impact and influence over skin pigmentation; which obviously can be proven true and correct or false by examining the cases provided as example at the question.

"In good faith" is a phrase not related to the typical meaning of "faith" as religious belief. Saying I don't think your question is in good faith means I think you're probably asking it because you want to infer something about race, rather than having any actual interest in human evolution.

The claim is that melanin production may have been selected against in higher latitudes and selected for in lower latitudes. The evidence is that populations near the equator tend to have darker skin than those far from the equator, across multiple continents.

@BryanKrause Am fully aware that "race" has absolutely no basis in science and "it is a made-up label", etc. Do not self-identify with any fictitious "race". Am asking about the actual science. Yes, have an interest in evolution, though am not compelled to agree with every assertion made under the banner of evolution or adaptation. "The evidence is that populations near the equator tend to have darker skin than those far from the equator, across multiple continents." Is that true for Mennonites in Belize?  The question is: Is that process ongoing right now?

@BryanKrause Just re-read your comment and noticed the "may have been" ("used to say that something is possible or probable" http://www.learnersdictionary.com/qa/comparing-may-and-might). Does that intend to relegate the theory of human skin pigmentation adaptation and evolution proffered at the linked publication as just that: Merely a theory that has not been proven by way of the scientific method?

@guest271314 Are you asking whether, today, people with lighter skin have a lower fitness in areas where the solar radiation than people with darker skin (and similar questions for other UV and diet environments)?

Most evolution pressure has been divided by 10, maybe 50 recently due to medicine and life conveniences. good sunguards and no need to spend days out finding food makes white people able to live in the tropics, who have a max sun time of 1 hour, and very dark people can live without much sun thanks to vitamine D. Same goes for most other wild traits.

The originally linked page contains a bibliography: http://humanorigins.si.edu/evidence/genetics/human-skin-color-variation/bibliography

@Remi.b The question is clear. Am asking if the claim is measurable right now. If the claim of skin pigmentation being the result of diet, tropical or non-tropical residence is true and correct then the Mennonites in Belize and Dutch in Congo (DRC) and Boers in South Africa must be adapting and evolving darker skin in real-time, right now, and that adaptation must be observable and measurable. Similarly, the dark skinned people who migrated to Nordic countries, or Minnesota, Alaska, Canada, and so forth must be adapting and evolving lighter skin. If false, neither is measurable right now

@tsttst Which link in the bibliography provides a study which presents evidence that skin pigmentation adaptation and evolution is occurring right now?

You keep repeating “in real time, right now” which is at the best vague, and at the worst nonsense. “Real time” is a computing expression generally taken to mean “in a period of time that would not entail an unacceptable wait for the user”. “Right now” suggests today or even within the hour. Until you replace this by something more precise — e. g. 10-20 generations — I shall have to vote to close your question as unclear.

@David The question is clear. The conjecture that you are contriving does not make the question unclear. Yes, real-time in the computational manner that you gathered as a reference. Yes, "right now" does means today and tomorrow. Again if the claim is true that measurement must be possible, today, particularly as to the cases cited at the question. If in fact the claim is true even from one second to the next the claim must be measurable 10-20 generations are not necessary. The actual question asks if any studies have been performed which publish evidence to substantiate or refute the claim.

Pardon me, but “right now” and “in real time” qualify the studies you ask about in the question in your last sentence. This is not clear and would take little effort to clarify, assuming you are clear yourself about the timescale. Are you?

@David A cursory definition of "adaptation" "a change or the process of change by which an organism or species becomes better suited to its environment." Any timescale must be capable of being applied to the subject matter. If in fact the claim is measurable, from one second or one year to the next. Are Mennonites in Belize becoming darker and Africans in Scandinavia becoming lighter second by second, year by year, decade by decade, generation by generation? What terminology do you suggest to overcome what you interpret as being unclear to you about the terms "right now" and "real time"?

I told you. One generation, two generations, ten generations, 10-20 generations. You choose, it's your question. Evolution questions actually bore me, and I just check them for trolls to see if they need a close vote. In your case the question was so long I looked to the end to see if there was an actual question there. There was, but the "right now in real time" stuck out like a sore thumb. Comments on SE Biology are not for discussion but for asking for clarification or suggesting improvements in a question, and that is what I did. Take my advice or leave it, but that's enough.

@David Updated the question. Does that satisfy the criteria for substitution of "right now in real time"? Used your own suggestions. Am asking if any scientific study has vetted the claim by way of empirical evidence. If the theory was true in some arbitrary period of the past the theory must be true from that arbitrary past date through to and including 2019 CE, and must be true for any moment in time that a scientist decides to capture the raw data to vet using the scientific method.


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What makes the flowers glow?

I had learnt in a plant biology course that, all the flowers are actually originating from leaves, with several mutations. I wonder what makes a flower sparkly like this.
Photos belong to a Phalaenopsis Orchid (White) (under direct sunlight) . But I believe this can be observed in many plants.
When searched for it, I saw one explanation on that they shine right after they are watered. But I observed this long after the plant was watered. So I guess this is not the case.
Also I've read about the pigments that absorbs different wavelenghts and give the plant its color. But I couldn't find an explanation about this sparkling view.
Another thing I read was about the shiny views of some flowers, like buttercup flower. It is said that this is originating from flat cell shapes. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5332578/). But again, this is different than what I am asking.
Biology is not my major (probably as you have already guessed :)), so I might not be searching it with the right keywords. So I will be glad to get some help. Thank you :)!
Edit:
Another photo, taken with flash light. The shiny view is only in the side leaves (petals and sepals), not in the middle parts.

hi new user and welcome! please provide name of the flower, and also any research you did to asnwer this question yourself

Hi, sure. Actually photo was just an example, I observe this in many flowers. Still, I will edit my question. Thank you :)

Also what lighting conditions &c.  From a quick look, the "sparkles" look like they might be small drops of water.  Have you looked at them under a microscope?

There was a strong sunlight on them. I don't have a microscope :). So do you mean water droplets due to the air humidity ?

I'm not sure of the conditions in which the photograph was taken. That could be anything from wax on the leaf, or stomata.

I am adding a photo taken with a flash light. You can see that the shining part is only the petals (and sepals) not the middle part.

@GabrielFair this is something you can see with your naked eye in direct sunlight on daffodil petals as well as iris petals. I'm sure you can see it on many others but those are places I have seen flowers sparkle like this.

Could be water condensing from the air (dew), or it could be water released from the plants via transpiration: https://water.usgs.gov/edu/watercycletranspiration.html  But I'm just guessing...  Though Google Images has some similar pictures: https://www.google.com/search?q=water+droplets+on+leaves+from+transpiration&complete=0&source=lnms&tbm=isch&sa=X&ved=0ahUKEwi2u7iBu8ngAhUBqp4KHTVgBp8Q_AUIDigB&biw=1223&bih=952

@L.B. Yes it is exactly what I am talking about. I had thought that this was a very wellknown phenomenna through.

@jamesqf As you had Said, that sparkles really look like tiny water droplets (nearly microscopic). Actually they more look to me like some cyrstals, like a snow surface.  I have looked those transpiration photos. I couldn't catch a simular image though.. Those droplets are very big and seems to be at the surface of the leaf. Mine seems like they are at the inner tissue. It might be because they are very small scaled. I also searched it as "petal transpiration" but couldn't find a simular image yet.

@jamesqf - I knew this was an orchid when I saw the first picture. It is not water. It has to do with surface cell shape, translucency and light. It's not an uncommon phenomenon in flowers.

@anongoodnurse hi, as far as I understood from the article I mentioned in the question the flat cell shapes provides a mirror like or buttered/polished like shiny surface.But here, I think we can see some obvious particles. Might they be some plant mineral crystals? I had also thought of dust particles but these particles are very homogeneous and can be seen also at the back side of the petals, which I wouldn't expect to hold much dust.

@user6069929: I was thinking of this image in particular: https://image.shutterstock.com/image-photo/close-water-drops-on-pumpkin-450w-1027095193.jpg Looks almost exactly like yours.  But try some experiments, like brushing the surface of the leaf/flower, or passing a razor blade over it.

@user6069929 - I don't think so. See http://bulbnrose.x10.mx/Heredity/KayPetals1981/KayPetals1981.html; look at the photomicrographs. Especially helpful are scanning electron micrographs of orchid petals.

@jamesqf I see. Mine are not even that obvious. Moreover they are independent of the temperature or the time of the day. Also when I tap on the surface with my finger, it doesn't give a wet feeling neighter the pattern is distrubbed. But okay I will try those :) Thank you.

@anongoodnurse Thank you for the source. I have skimmed it, I couldn't catch the SEM Photos of Orchids (might be as I am not familiar with the names.., I couldn't Google it all). But, i.e. the one with conical cells which the light is reflected only from the tips and generates a spotted-like pattern. There it's written that the photo is in x160 scale. Mine are visible with bare eye. What would you say on that?

I have seen the phenomenon you describe to some degree in many flowers: violets, daffodils, but most prominently (in my mind) on orchids. Look up "scanning Electrom micrographs orchid petals; with what the paper discussed, it should correlate.

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Structure of phosphates in nucleotides
Nucleotides are made up of a heterocyclic nitrogenous base, a sugar (only ribose or deoxyribose), and a phosphate. In nucleotides, obviously the nitrogenous base matters as its variations dictate the production of certain amino acids, and the sugar can only be ribose (in RNA) or deoxyribose (in DNA), but does the type of phosphate matter? I've seen that a nucleoside describes the nitrogenous base and the sugar alone, and there are nucleoside monophosphates, nucleoside diphosphates and nucleoside triphosphates.
Do these three variations differentiate; when it dictating the production of amino acids; when looking at any sort physical variation; in any sort of way; or are all three just the same as each other??
Also, do all of the phosphates have to look like this?
(https://en.wikipedia.org/wiki/File:Phosphate-group.png). Or can they look like this (https://en.wikipedia.org/wiki/File:Phosphodiester-group.png). If they can look like the second image, then similarly to the question above, does it make any difference?

Hi, welcome to the Biology Stack Exchange! Interesting question, do you think you could try and distill it down to one question? I'm not sure if you're trying to ask about phosphate (of which there is only one: PO4) or asking about nucleotides.

I have cleaned up your title and removed irrelevant tags. You are asking a very basic chemical question about chemical structures, the only complication of which is the ionization of the phosphate at physiological pH.  Read and understand the WIkipedia or Berg et al (NCBI Bookshelf) pages about the structure of  nuceotides, phosphate, and nucleic acids and you will be able to answer your own question, which will no doubt be put on hold shortly.

Do the differentiations of possible phosphates (e.g. mono-,di-,tri-, isomers) as components of a nucleotide affect the function of that nucleotide?

Is it often that nucleotides are found with more than one regular phosphate group (first link in question) as a component?

@LucasDyson-Diaz please do not ping everyone every time you respond. This is exactly why you can only ping one person per comment. You now have two very basic chemistry questions, which (again) can be answered by reading the relevant Wikipedia pages. The answer to both of your questions is yes.

@MattDMo (to the first question) How so? How does the phosphate group(s) it affect the nucleotide?

@LucasDyson-Diaz you'll have to read the resources we've all suggested to learn more about nucleotide mono-, di-, and tri-phosphates.

Well it turns out that when nucleotides are bonded together in a strand of DNA/RNA (nucleic acid) they ALWAYS HAVE only one phosphate group attached to their nucleoside (nucleoside = sugar + nitrogenous base (without phosphate)).
However, when they are by themselves, they are more often found with two or three phosphate groups as oppose to just the one. For this reason, the definition of a nucleotide is often misunderstood as it refers to containing one OR MORE phosphates, in reality, the official definition of a nucleotide states that only one phosphate group is present...
An example of a (so-called) "nucleotide" is ATP (adenosine triphosphate); it follows all of the rules that the misunderstood definition of a nucleotide states (these are; a nitrogenous base (adenine); a pentose sugar (ribose); and one "OR MORE" phosphate groups (triphosphate)). However, according to the official definition of a nucleotide, it is not, in fact, a nucleotide! It is instead considered a 'nucleoside triphosphate', since it is a nucleoside. with three phosphate groups (it is also a nucleotide with two additional phosphate groups, but I guess 'nucleotide-with-a-diphosphate' attachment doesn't roll off the tongue so well as nucleoside triphosphate).
Finally, as in nucleic acids and indeed anywhere else (according to the official definition of the nucleotide), there is only one phosphate group allowed to attached to each nucleoside (regular phosphate group) to form a nucleotide (officially). Therefore there is no variation allowed in the phosphate groups (since there's only one and they bond to other nucleotides, in the same way, every time (in nucleic acids)), furthermore in the pentose sugar the only variation allowed is whether it is a ribose (in RNA) or a deoxyribose (in DNA). So the phosphate-sugar backbone of the DNA strands and the RNA strands (nucleic acids) are consistent throughout the entire strand (and each strand of its type; differentiating only in the type of pentose sugar it consists of (ribose/deoxyribose)). Consequently, there is no phosphate-sugar backbone variation within DNA strands or RNA strands, for the phosphate or the pentose sugar to make any genetic difference to genetic material (those strands); only the nitrogenous bases and their sequences can make a difference to the genetic material...

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LacZ' selection: blue colonies despite ligation of insert
It has been suggested that bacteria transformed with pBlueScript vector, containing an insert in the middle of the lacZ' gene, can still give blue colour on X-gal, if the insert is small and ligated in-frame with the lacZ' gene (source: my course, ResearchGate).
I don't understand how it is possible that translation doesn't end at the stop codon encoded by the insert. Is this something to do with leaky termination? Moreover, even if leaky termination was possible, this would mean that there is ALWAYS a 1 in 3 chance of the insert being in-frame.

Transcription doesn't stop at the stop codon.

@canadianer Thanks! But why does it not? And also, if it doesn't stop at the stop codon, doesn't this mean that in 1 out of 3 cases, an insert would be ligated in-frame and the assay wouldn't work?

Transcription has nothing to do with codons. Perhaps you meant translation?

@canadianer Oops, this is awkward! Yes, this is what I meant!

Most inserts will disrupt beta-gal expression (by shifting the reading
  frame and introducing stop codons) and therefore remove the enzymatic
  activity required to cleave X-gal and produce the blue color.

Your source is agreeing with you - inserting a stop codon will stop translation (not transcription) and keep the white color.

Thanks! But the source also says that "In rare cases, when the insert is very small and does not disrupt the reading frame, beta-galactosidase activity will occur even in the recombinant clones, so blue-white screening becomes irrelevant." Am I interpreting this incorrectly?

I'm understanding the implication that, to still have beta-galactosidase activity, the insert needs to not have a stop codon. I think this is reasonable because the stop codon case is explicitly addressed in the previous paragraph.

But doesn't this mean that without a stop codon blue color will be produced in 1 in 3 cases (probability of in-frame ligation) and the assay is kind of pointless, so why would anyone use it like that?

The insert needs to not disrupt protein folding on top of being small, not having a stop codon, and being in frame.

@mxwsn You should add this to your answer.

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Allosteric regulation: why involve extra molecules
Why are molecules such as allolactose (for lac repressor) or 2,3-BPG (for haemoglobin) used for allosteric regulation rather than the actual molecules involved in biochemical pathways, such as lactose and 1,3-BPG? The formation of such "extra" regulators requires energy – what is the advantage of such organisation?

You might be interested in this.

@Metroplex Thank you! This is a great article. The argument makes sense for allolactose but I don't see how a similar one would work for 2,3-BPG or 2,6-biphosphofructose (regulating phosphofructokinase and fructose 2,6-biphosphatase).

It's an interesting question, and there are a lot of potential explanations.
I can at least hypothesize a little bit for the case of 2,3-BPG and 1,3-BPG. I think the key point is that it's not obvious to me why sensing the 1,3-BPG concentration would be useful. This concentration actually has to be maintained in a pretty tight range for glycolysis to function (note that the entire lower portion of glycolysis is very close to thermodynamic equilibrium). The reason that I think 2,3-DPG is a useful regulatory molecule is precisely because its levels can be regulated independently of the function of glycolysis. The activity of the enzymes in the 1,3-BPG -> 2,3-BPG -> 3PG shunt can controlled independently of the control of normal glycolysis and can be regulated by whatever physiological parameter you want 2,3-DPG concentration to represent.
One other thing to note is that typical red blood cell concentrations of 2,3-BPG are actually many orders of magnitude higher than 1,3-BPG. The very low concentrations of 1,3-BPG are a necessary consequence of the thermodynamics of glycolysis as mentnioned above -- if 1,3-BPG concentrations are too high, the GAPDH reaction will become unfavorable. Thus it may be that the typical concentration of 1,3-BPG is too low to be an effective regulator of anything (because it would have to bind very strongly). But I think this is a less important point than asking the question of "what does the concentration of my regulator represent".
There may be biochemical reasons at work in other cases -- for instance, some molecules may just bind better to the protein that you want to regulate, and that's why they're chosen by evolution. I think this is a case when it will be hard to come up with a blanket explanation -- it's better to look at each case, consider what signal biology is trying to measure, and look at the relevant constraints.
I don't know the answer for 1,6-FBP and 2,6-FBP, and note that in other species, 1,6-FBP does appear to be the major regulatory molecule. You could argue that by having 2,6-FBP be the regulator, there are more enzymes whose activity you can control and thus somehow you have more fine-tuned regulation </hand waving>.

Thank you! It's all much clearer to me now, and the argument about 2,3-BPG is very interesting.


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Homologous structures under Lamarck
I've read that Lamarck's theory doesn't explain homologous structures.
But, what about the following hypothetical under Lamarck's theories:

A population develops an adaptation to its environment
Part of the adapted population moves away
The adaptation is passed onto the population's offspring
All offspring of the original population have the adaptation, regardless of whether or not their ancestors moved away

Isn't this adaptation a homologous structure?

I agree with you that I can't see why Lamarck's hypothesis could not explain the presence of homologous structures.
The link you offer also claim that Larmarck's hypothesis would fail to explain "Biogeographical diversity patterns". While this expression is a little vague, I would fail to understand why Lamarck's hypothesis would fail to explain patterns of biogeographical diversity.
The phrasing of your scenarios (absence of the term allopatric speciation, usage of the term "develops" instead of "evolves" of just "adapts") suggests that you may take advantage of an intro course to evolutionary biology such as the short and good course by UC Berkeley called Understanding Evolution


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Possible complications due to gene-therapy?
Edward Lanphier, CEO of Sangamo BioSciences mentions here(https://youtu.be/dJ1B8XnyEnM?t=1215) that scientists can now specifically target cells, change the genome within a cell. Say you want to cure a type of disease, which can be linked to your genome. You have successfully removed the faulty gene in your genome (GenomeA), replaced it with a correct gene resulting in a improved genome (GenomeB) in a single cell. The next step will probably be to put it back into the human body. However, as I understand it every human cell contains your faulty human genome (GenomeA).
Question:

Even if you put a few cells with the correct genome sequence (GenomeB) into your human body, it is probably going to be overwhelmed by the other cells that contain your faulty genome (GenomeA). Cells containing the correct genome (GenomeB) will divide and multiply but so will cells containing the faulty genome (GenomeA). In this “genomic war” will the fewer cells containing the correct Genome (genomeB) ever win? Or will you need period infusions of cells with the correct genome "forever"?

How would you guys think about this?
Optional questions:

Even if it wins, it will probably take a very long time to completely replace all the cells with the faulty genomes. How much time is required before you can completely replace all the cells with the incorrect genomeA, with cells containing the correct genomeB?
Say you realize that you have a faulty genome (GenomeA), and you attempt to replace your genome with a correct genome (GenomeB). After 2 years, you have another disease and realize that you have to again correct your genome with GenomeC. However, 2 years is not enough to replace all your cells with the incorrect GenomeA, with the correct GenomeB. If you attempt to undergo genetherapy, now you will have to introduce another group of cells with GenomeC. Now you have cells with multiple different types of genomes floating around: genomeA, genomeB and genomeC. Are there any complications that happen due to the presence of multiple types of cells with different genomes in your body?

good questions... but way too many posed in a single entry... can you try and focus your question? it's very unlikely that anyone will answer all of them in one post.

I feel the question is useful and raises good points and those points shouldn't be removed.  Even if a person may not answer all of them in one post, he or she may answer some of them, with other answers to be obtained in other posts.  In terms of the question, I don't see why only a few cells can be put into the human body.  What technology can do to one cell at a time now, it should be able to do to thousands or millions at a time in the future.

Hi Vance, you are right, my question is a bit broad, since my specialization is not biology/gene-therapy. Since 2 people pointed out that the question is a bit broad, I only highlighted the first question and left the 2nd and 3rd questions as optional. It kind of a compromise, so as to address Sterid's request as well.

Your question is too broad. It is better to take some specific example.
Not all cell's in the body divide. If you take cell out of the body and want to return it back, it must divide. So we probably could talk about stem cells for example. The stem cells don not really sit in one place. And it almost impossible now to get such cells from the place that they sit in it, and then return in back. It is possible with bone marrow for example.
If we take some example, like ALS - some percent of the disease is thought to be genetic. But the mutation is in all the body cells. Mostly it's affects astrocytes, microglia and motor neurons. You cant take them out of the body, fix and return back. The only chance to fix is to work inside the body. For example by using some sort of virus (AAV for ex.) And CRISPR.
However, if we follow your story and we insert cells with genomB, they will live together with cells with genomA, if there is not some bigger mortality of the original cells.

Thanks for pointing out some use cases. My specialization is not biology, and I am coming in from a 30000 feet so you are right that the question is perhaps a bit broad.  I guess my intuition was kindof right. It seems you do need some kind of periodic infusions of modified cells or viruses carrying the modified genes, as pointed out by this article. http://www.nytimes.com/2005/07/03/books/chapters/more-than-human.html?_r=0


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How do Sertoli cells protect sperms?
I was reading Developmental biology by Gilbert and stumbled upon a fact that Sertoli cells provide protection to the developing sperms with no futher explanation.
I googled it and found a few books mentioning that it protects sperms from cell mediated immunity and antisperm antibodies. Yet I found a website called fertilitypedia that said:

Sertoli cells do not only control the process of spermatogenesis, but they are also responsible for creating so called immunologically privileged area in the testicles. It means, that Sertoli cell manage to keep blood separated from seminiferous tubules through the connection between them, called tight junction. Tight junction keeps bloodborne substances from reaching germ cells, so all stages of germ cells are protected from the body immunity. Tight junction also keeps surface antigens found on developing germ cells from eluding into the bloodstream so no autoimmune reaction could happen. Since Sertoli cells form the block between the blood and lumen of seminiferous epithelium, they are also in control of the entry and exit of nutrients, hormones and other chemicals into the tubules of the testis.

I'm unable to verify this explanation from the cited sources as none contain the mentioned information.
So my question, how does it actually protect the sperms?

Have you tried Wikipedia? I know Wikipedia is far from an ideal source but that page has some references as well as links to other wiki pages that are relevant to your question such as one on the blood-testis barrier.

@BryanKrause you can write an answer if you want, then I can mark it as solved.

@BryanKrause I gave it a second thought, things written in Wikipedia, something I didn't consider at first, there are suppositions without any citation. So I think they are not good references.

Did you try my suggestion to search google scholar for reviews? This isn't a particularly controversial issue, it seems pretty well established and agreed on. The Wikipedia pages are not fully cited line by line but all the information is likely in the books and papers that are cited if you actually read them.

Found one.@BryanKrause

The Wikipedia pages on Blood-testis barrier and Sertoli cells have some information relevant to your question, with some academic references included.
You could also search for reviews on Sertoli cells on Google Scholar - several of the first returned results seem relevant, if you are able to access them.

Can you consider editing? I'm afraid but this doesn't answer the question ''How does it actually protect the sperms?''.

Doesn't your question contain that answer? Tight junctions between the Sertoli cells keep a barrier between the immune system and the developing sperm to prevent autoimmune reactions, because the sperm express antigens not found in the rest of the body.


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Immunology Book Suggestion
Which book will give a brief account about B-cell development so that it covers two questions about the following cells:

Plasmablast
Plasma cell
Memory B cell
Marginal zone (MZ) B cell
B-1 cell
B-2 cell
Regulatory B (Breg) cell

Where do they lie in the course of B-cell development and differentiation?
What are their functions (outline)?

P.S. I need to know the development part in details rather than the functions.

http://www.amazon.in/Kuby-Immunology-International-Judy-Owen/dp/1464137846/ref=sr_1_1?s=books&ie=UTF8&qid=1477876761&sr=1-1&keywords=kuby I feel is the best for learning.. But as said, for something like immunology, you must complement a text with nature reviews

You should probably check out a review. Most basic textbooks will not delve into the various subtypes. Wikipedia has entries on all these types of cells. Did you not find that informative?

@WYSIWYG Not really, that's why I posted here. Besides I'm skeptic about wikipedia. It doesn't always contain the right information.

In this case, the wikipedia articles are not stub and they cite relevant sources. Perhaps you can clarify what exactly you are looking for. If you want detailed information then you should go for a review. For e.g. this is a recent review on B-reg cells.

@WYSIWYG Well I have already put that in my post, questions 1 and 2. The problem with these reviews is that they though mention what the functions are but don't highlight where the cells lie in the course of B-cell development. However as a last resort I have thought of reading Kuby Immunology. I have been avoiding it because its too much detailed.

The question - "what are their functions" needs some elaboration. You can go into great level of detail with that. Kuby Immunology does not have these details; at least the version that was available 8 years ago.

Perhaps you should check this review out: http://dx.doi.org/10.1146/annurev-immunol-020711-074934

This question is a possible duplicate, as we also have a question about that: http://biology.stackexchange.com/questions/13729/modern-immunology-textbooks

I have been through it once before. That's related but not duplicate. It's a more broad question.

@WYSIWYG Thank you but I don't have access to the review article. Besides I've edited the body to make more suited to Bio SE..

I have found a book that explains in a quiet simple way the entire B-cell development and differentiation stepwise and covers the two questions I was looking for. It is Kuby Immunology, 7th Edition.
Except the Breg cells which is a recent discovery every cell was well discussed. I went through this to learn what the functions of B reg are.

The best immunology book hands down is Janeway's Immunobiology. There is no debate among the immunology community.  The middle section is devoted to B cell development.

Best books for Immunology

Cellular and Molecular Immunology
Roitt’s Essential Immunology
Kuby Immunology
Janeway’s Immunobiology
Basic and Clinical Immunology

source: Best Book for Immunology

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


text:
Liebig's law of minimum
I was reading from Odum about Liebig's law of minimum.
It said that

the law is appicable in steady state condition i.e. when the inflow of energy and material balances out the outflow.

I got two questions:
1.Here what is actually in steady state? Photosynthesis? or Plant community? or Biotic community?
2. Inflow of energy and material balances out the outflow.
What is the net material/energy that is flowing in an out of a system? Could it be amount of light absorbed and amount of glucose and O2 produced respectively? He used the word balances which means they are not equal actually but proportionate I suppose.

Your second question isn't a question. Please reformulate as a question.

The question is beneath the statement that is numbered 2.

Your question is not directly related to Liebig's Law of the Minimum. Instead you ask about a conditions under which the Law holds according to your quote.
From the quote it is clear what is in steady state: it is the total amount of energy and material. If the the amount of energy and material flowing into a system equals ("balances out") the amount of energy and material leaving the system, the total amount in the system does not change, that is, it is in steady state.
This does not mean that other quantities in the system are necessarily in steady state. For instance, the species composition of a bacterial community may fluctuate or evolution may cause the community to change.
An example of the sort of systems we are talking about here is the chemostat. A chemostat is a device for culturing microorganisms. It consists of a culture vessel connected to a feed bottle. A solution of nutrients (the growth medium) literally flows from the feed into the chemostat. Microorganisms in the chemostat will grow and reproduce (if the concentration of nutrients is sufficient). A mixture of microorganisms, unused nutrients, and byproducts of growth leaves the chemostat in the effluent flowing out of the outflow of the vessel. The rate at which this happens is the same as the rate at which medium flows into the vessel. Typically, after a while the concentration of microorganisms and the concentration of nutrients in the chemostat and effluent do not change anymore (if the inflow is constant, that is). The chemical conditions in the chemostat have then become static (hence "chemostat"). The concentration of nutrients and microorganisms are then at steady state.
In the case that the microorganisms are phototrophic, the nutrients may be inorganic and energy is added to the system through light. The light absorbed may then be considered as the energy flowing in, and the energy flowing out is then the chemical bond energy in the organic material that make up the microorganisms and the byproducts, and heat.
Chemostats are culturing devices, but are also models of natural systems such as lakes or ecosystems.
Liebig's Law of the Minimum says whichever resource (nutrient of light) is in short supply determines the growth rate of an organism. For instance, if nutrient concentrations are in ample supply but light levels are low, changing the nutrient concentrations will not change the growth rate of the organisms, however, changing the light levels will. The quote of Odum suggests the Law only holds under steady state conditions, but I do not understand very well why this would be so.

Thanks for the answer. I don't have time to read it now. I'll let you know if I have follow up questions in a few days.


text:
What is the difference between Reservoir and paratenic hosts?
Paratenic host
'In parasitology, the term paratenic describes a host that is not necessary for the development of a particular species of parasite, but nonetheless may happen to serve to maintain the life cycle of that parasite' until they are transferred to an obligatory host.
(from Wikipedia and Parasitology: A Conceptual Approach book)
Reservoir host

Reservoir hosts are such animals which accumulate in themselves the invasive larvae of the helminthes and contribute to their transfer to the definitive host, not being however an obligatory condition for the complition of parasite ontogenesis.

(from Proceedings of the First International Congress of Parasitology: Roma, 21-26 September 1964)
The source however says that Reservoir host is same as paratenic host which contradicts other sources
(like General Parasitology by Cheng) which says:

Reservoir host is an animal that becomes infected and serve as a source from which other animals can be infected. (the only difference I presume is that it may or may not be obligatory)

In many other books (book 1 & 2) a parallel definition is mentioned that a reservoir host is a host that harbors parasite until their transmission to human beings.
This inturn brings forth another question, is a reservoir host a biological vector then?
So the question : Are paratenic host and reservoir host same or different?
P.S. I don't know what the standard books on parasitology are which could have solved this issue. Reference to one such book will be really appreciated.

Reservoir host: The host of an infection in which the infectious agent multiplies and/or develops and on which the agent is dependent for survival in nature; essential host for maintenance of the infection when active transmission is not occurring.
Paratenic host: A host in which a parasite survives without undergoing any additional development (a transport host only)
Source: Diagnostic medical parasitology, pg 1161

and

Any animal that harbors an infection that can be transmitted to humans is called a reservoir host, even if the animal is a normal host of the parasite. Source: Pg no:4

So, we can conclude that paratenic host is different from reservoir host due to following differences:

Paratenic host don't harbour infective stages , if they harbour them, then they would be called as reservoir host but not paratenic host( see second definition)

No development takes place in paratenic hosts, whereas in reservoir host development and multiplication takes place( see 1st definition).

Is a reservoir host a biological vector then?

I too asked the same question, its answer is here.


text:
Which literature/study/myth spurred the idea that urine is sterile?
There is a seemingly unfounded mantra that a person's urine is sterile who is not suffering from a UTI.
So far I have found convincing evidence to the contrary; urine is not sterile. This poster abstract and publication by Hilt et al., 2014 shows that urine may not be sterile. They list 6 other articles (references 3-8) that also found evidence for microflora in healthy urine, the urethra, and the bladder. In some of those studies males were used, and some used females. This makes a convincing case for non-sterile urine.
But why does this mantra persist; where does it come from? Is there a paper that demonstrates the sterility of urine that I have missed? Even if it is old literature, or pop culture, I'd appreciate it.

You answered your own question. Hilt et al's paper and others have had more than convincing evidence that urine is not sterile. As to why this idea persists? Overall, because of ignorance: either people don't put in the effort to learn real facts or (in the case of other biologists) they don't keep up with the literature. You also can't ask any biologist (e.g., a cell biologist or ecologist) if they believe urine is sterile and believe they know much (any) more than a non-biologist

As there definitely are uropathogens, you can at least be sure urine is not always sterile. I have heard people talking about obligate pathogens in the urine and they definitely found microflora in healthy urine. But that was personal communication (and as far as I know the group studying their own urine because they needed to know whats there before using it to grow other bacteria, so not a study setting to be published).

I think the main point about the sterility myth is that is around for a long time. And it took the group, which finally found the bacteria quite a while to proof this. So to this point nobody was able to find bacteria, thus is was declared sterile. We could have know better, since we are populated with bacteria.

In a healthy person urine is sterile up until the point it leaves the bladder through the urethra. At least, that's what I thought. It depends on where in the system you are looking at it. After it leaves the kidneys it must be sterile.

@Christiaan According to the citations I found there are bacteria in women's bladders[1, 2]. Men are somewhat less studied since UTIs are far less common. Sorry to be a party pooper, but I'm after a reference that supports your statement.

@James - Just sharing what I know - nothing to be pooped. That's why I comment only. Won't go for an answer as it's not my expertise.

@Christiaan My last comment came across quite aggressive, apologies! I thought sterile bladder urine was the de-facto case too until these papers were pointed out to me, but I can't find anything (peer reviewed) to support urine sterility.

It's a good question. +1

But why does this mantra persist; where does it come from?

Behind this line of inquiry is a fascinating observation about the disconnect between the laboratory and the clinic. The basic answer, from my perspective, goes like this:

It is doctors who talk with people about their urine, and any testing thereof;
for doctors, urine is practically1 sterile; and
among those who are aware of the microbiologic reality, doctors inevitably gloss details when explaining laboratory results to patients.

The average clinician learns most of what he knows about his patients' urine from urinalyses. Most clinical urinalysis assays show negative nitrites and negative leukocyte esterase in normal people. A glance at the reference ranges for a clinical assay will demonstrate this. (See also the clinical review below.)
Ideally, urinalyses should not be performed in patients without relevant symptoms, but they are sent anyway, and they're mostly negative.2  Even in people who have symptoms possibly suggesting a UTI they're frequently negative.  Furthermore, urine cultures from properly collected specimens grown on the media used in clinical laboratories mostly return at 72 hours: "no growth". This point is emphasized in the abstract by Hilt et. al. linked in the question. Of the cultures that grew in their "expanded quantitative urine culture" protocol,

90% of these specimens were deemed "No Growth" by the standard urine culture technique, highlighting its limitations.

The last phrase "highlighting its limitations" is an interesting one. It appears to me to be yet to be proven that this is a clinically meaningful "limitation" of such assays. Without attempting to refute these data  — fortunately this question doesn't require me to do so — I will note that the two linked studies aimed to show that people with overactive bladder are characterized by increased urinary flora. The explicitly stated hypothesis is that this may contribute to symptoms. Even in this study demonstrating the existence of such a micro-biome even in normal people, then, it is understood as a potentially pathologic state.
The reason this "mantra persists", then, is that it remains true for clinical purposes. In contrast to most (all?) other bodily discharges, urine is not packed with bacteria, and the commonly used assays reflect this fact.  Medicine and laboratory science have different "modes of discourse", each calibrated to convey levels of precision that are appropriate to the outcomes of interest.

Notes

1. In American English at least, that adverb is ambiguous, meaning either "for practical purposes" or (idiomatically) "almost". Both senses are intended here.

2. Of course, there are plenty of data in various populations demonstrating that some substantial minority of urinalyses among asymptomatic people return positive, "proving" that we shouldn't be checking them (amen!). But this is not the point. The gestalt remains: normal = negative.

3. The nitrite parameter in particular is not especially sensitive. It is, however, quite specific (92-100%), meaning it reliably returns negative in people without infection. (See review, below.) Of course, negative nitrites does not mean sterile in the sense that the OP has used it; see "modes of discourse", above.

Reference

Simerville JA, et al. Urinalysis: A Comprehensive Review. Am Fam Physician. 2005 Mar;71(6):1153-1162.

Really great, satisfying, answer.


text:
Circulating Tumor Cell vs Circulating Tumor DNA
I'm a little confused about the wording of these two phrases and under which context the epithelial-mesenchymal transition occurs.
For example:
Is it the circulating tumor cell that releases the ctDNA so that it undergoes EMT?
Or
ctDNA from the CTC somehow creating new instructions for the EMT phenomenon to occur?
I think there is something I am fundamentally confused about and or I am mixing several or different concepts and phenomenon together and would like to get some clarification on this.
Thanks.
EDIT: So this is my new hypothesis / thinking..
So when EMT occurs, CTCs are more likely to develop in the context of cancer, and so when CTCs circulates throughout the blood stream CTCs may be apoptosed of necrosed as a by-product thus leaving ctDNA in the bloodstream and or possibly through out the body.
Is that a correct explanation to my confusion?

I'm not sure the relationship you are trying to build between EMT and cancer cells.
Yes some "healthy" cells undergoing EMT could (due to specific underlying mutations) result in cancer cells but such a phenomenon is not a "hard and fast" rule.
The majority of ctDNA would likely be (as you suggest) from lysed cells, however, should mutations occur that allow for the aberrant export of DNA, then the latter could occur (I would assume this is rare but based on the currently available literature this possibility cannot be discounted).
Thus your "new hypothesis" seems to be the most likely.

Okay thanks for your input!

Welcome to Biology.SE! This looks like a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


text:
What is meant by "heads" and "tails" in the context of gene orientation?
I have a hard time understanding what this paper is talking about when it says:

We observed maximal cleavage at sites oriented tail-to-tail and separated by -10 bp to +30 bp (Fig. 2d). Finally, adjacent sites on the same DNA strand (head-to-tail orientation) did not show damage by NHEJ

Then it shows a figure/chart that I don't understand. I don't know the head and tail or the gene is, in terms of what it is relative or with respect to.
Any help would be appreciated.
Thanks.

The heads and tails, in this paper, refer to the orientation of sgRNA binding sites. If there are two tandem sites in the same orientation then they are referred to as head-to-tail (end of the first site followed by the beginning of the second site). It is also apparent from the excerpt that you have included in your question.
Head-to-head and tail-to-tail refer to the site pairs that are placed in the opposite strands; the former (H2H) refers to a configuration in which the beginnings of the two sites are closer whereas the latter (T2T) refers to the case where the ends of the two sites are closer.

Regarding your question about the placement of sites within -10 to +30 bp of each other:
I think the point of the paper is that the two cuts by the nickases should be close enough and in the T2T orientation for a maximally disruptive double strand break. If the distance between the single stranded cuts (nicks) is increased then they effectively are just two single strand breaks which are repaired efficiently. The authors also conclude that using two nickases in this fashion produces has lower chances of mistargeting compared to that of a normal Cas9 (that makes double strand cuts).


text:
What phosphorylates tau protein & and what causes tau to be phosphorylated?
I want to know what phosphorylates tau protein and its 6 isoforms.
I know kinases cause phosphorylation events, and in tau it can be phosphorylated in a healthy neuron in the trans conformation, but when it is hyperphosphorylated it becomes the cis conformation of tau.
Do the same or different kinases cause the normal phosphorylation / abnormal hyperphosphorylation of tau? Is it completed by a single kinase or multiple kinases?
----Edit---
So I've done a lot of reading of many different papers and have uncovered that there two types of broad spectrum kinases classified as:
Proline-directed kinases, such as CDK5 and GSK-3beta
Non-proline directed kinases
Source: https://www.hindawi.com/journals/omcl/2015/151979/
But I read in this paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601591/
that Cdc2 can also phosphorylate tau
My new question is a follow up to my existing previous question, I guess why is tau phosphorylated at all? What causes tau to be phosphorylated at in the first place?
Thanks.

I recommend checking out PhosphoSitePlus's entry on tau protein. Click on the "Upstream" tab to see a list of confirmed (SRPK2, Syk) and putative kinases (PKA) and their associated phosphosites (i.e. the specific amino acid they phosphorylate). The Wikipedia page for tau protein also lists more kinases, as does this 2013 review by Noble et al. As for why Tau protein is phosphorylated, [its phosphorylation is a key


text:
What is meant by bionomics of a vector?
What is supposed to fall under the title Bionomics (The study of an organism and its relation to its environment; ecology.)?
Suppose we are dealing with a vector, Anopheles sp. are the following going to be included in its bionomics:

Life cycle
Interaction with parasite (Plasmodium sp.)
Mode of transmission of parasite by this vector
Control
Diseases caused ?

Bionomics is indeed the 'thorough' study of living organisms and their relationship with the environment/ niche they thrive in.
Aim of Bionomics is mainly to decipher the driving factors for an organism to prefer a given niche. Given this key goal, it is apparent that one needs to focus on all aspects of an organism's life cycle and community dynamics.
So the answer to your question would be: Yes, one will need to focus on all the five points pertaining to Anopheles sp. (the 5th point i.e diseases caused) will more be an information resulting out of the study of its interactions with other living/ non-living forms), than a specific focal point for Bionomics.
References:
A good article on Bionomics
An amazing and detailed report on Bionomics of Entomophagous Coleoptera
Other references:
The dominant Anopheles vectors of human malaria in Africa, Europe and the Middle East: occurrence data, distribution maps and bionomic précis. Sinka et al., 2010
Description and Bionomics of Anopheles (Cellia) ovengensis (Diptera: Culicidae), a New Malaria Vector Species of the Anopheles nili Group from South Cameroon. Awono-ambene et al., 2004


text:
What does self-perpetuating mean?
From Wikipedia

The community begins with relatively few pioneering plants and animals and develops through increasing complexity until it becomes stable or self-perpetuating as a climax community.

From Wikipedia again,

Self-perpetuation, the capability of something to cause itself to continue to exist, is one of the main characteristics of life.

What I  don't understand is every organism has the capability to perpetuate (except the sterile ones, which are not under consideration) even a seral community does then why is climax community specifically labeled self-perpetuating?

Here self-perpetuating means that the community is able to sustain it'self and continue, more or less, as it is. A seral community is an ever changing one, so it can't be considered a self-perpetuating one.

"Climax community" suggests a long enough history to have tested, and perhaps evolved, relationships between the member species such that a high degree of stability exists. Among other needs, members have enough to eat, places to live and controls on overpopulation. It suggests a dynamic equilbrium between the member species. It should be noted that the concept of climax community, although having theoretical uses, is currently "abandoned" as an actual construct in favor of terms like "old growth".  https://en.wikipedia.org/wiki/Climax_community

The key here is to recognize the distinction between a community as a whole and the individual species within that community. Just because individuals have the capability to self-perpetuate, doesn't mean that a community as a whole does.
For example, imagine an island with a whole bunch of caterpillars. Now imagine that you introduce a non-native caterpillar-infesting wasp. On the mainland, the caterpillars have evolved resistance to this wasp and so can fight off the infestation. But on the island, they never evolved that resistance, and rapidly succumb. Upon introduction of the wasp, you have a "community" of wasps and caterpillars. The caterpillars can reproduce, as they have been, so they're self-perpetuating within their species. The wasps can also reproduce by laying their eggs in the caterpillars, so their species is self-perpetuating. But the wasp infestation is killing caterpillars faster than they can reproduce, so the community is unstable. Over time, the population of both wasps and caterpillars will crash as all the caterpillars die off. Each species can self-perpetuate, but the wasp/caterpillar community, taken as a whole, does not.
That, in a slightly more complex way, is what happens with non-climax communities. The pioneer species change the environment in a way that permits other species to grab a toe-hold. These species are more suited to the changed environment, and thus push the pioneer species out.
For example, species which can survive in nutrient-poor soil grow and die in that soil, enriching it with nutrients. Now that the soil is no longer nutrient poor, faster-growing plants can grow in the soil, and push out those species which started there. Each individual plant can reproduce, but the community as a whole is changing from one which favors the nutrient-poor adapted plants to the nutrient-rich adapted ones.
It's only in a climax community where the members of the climax community create/maintain an environment which is most conducive to the climax community species. This is why it (the climax community) is being called "self-perpetuating". The community as a whole is maintaining an environment which favors those species which make up that community.
Wipe out the climax community species (e.g. through a forest fire), and you no longer have an environment which favors the climax community species. A new set of species comes in, changing the environment, which then allows other species to come in, changing the environment further, which then ...

'The community as a whole is maintaining an environment which favors those species which make up that community' to forever last, at least theoretically ?

@SanjuktaGhosh Well, "forever" is a very long time. The concept of a "climax community" is no longer well accepted by ecology researchers, for this very reason. Many think it's inaccurate to pick out a particular community as "climax", as no community lasts forever due to fires, floods, storms, plagues, etc. But the use of the term "climax community" - in as much as it has any meaning - implies that the community is stable, ignoring "outside" influences like fire, etc. -- it's part of the definition of what a climax community is.


text:
What is the structure of DNA polymerase III?
According to Snustard and Simmons the structure of DNA polymerase III is the following, where the clamp loader( γ -δ complex ) is present on one side:

But according to Lehninger the clamp loader is centrally located:

Which one is right? Besides where can I find a correct diagrammatic representation of DNA polymerase III?

I recently found this paper which supports the second mentioned structure of DNA pol III.

I don't know the answer myself, but if you have access to Nature Structural Biology I would start with this recent paper and work back from it if necessary. (I found it by searching the Protein Data Bank (PDB) for E.coli DNA pol III): http://www.nature.com/nsmb/journal/v24/n2/pdf/nsmb.3348.pdf .

It's a problem then.You might try looking at the visualizations available in the various PDB entries, but it would probably be much more work than is justified. Hope there's someone on the list that works in the field and can tell you or reproduce an appropriate figure.


text:
Explanation of ecological parameters with some model examples
I think an ecological parameter is:

A variable, measurable property whose value is a determinant of the characteristics of an ecosystem.

From eea.europa.eu
But what could these parameters be? In other words, what are some examples of 'parameters'?
I assume they possibly vary with ecosystem.

I am not sure I understand your question. Do you not understand the definition you gave? Are you looking for examples?

@Remi.b Yeah, examples for a particular ecosystem.

For a particular ecosystem, a variable will take a value. Are you looking for a description of a random ecosystem?

Any ecosystem. I just want to know how it works. There's no information on internet. At least I found none.

So you are basically asking "What is the average temperature, soil acidity, rain intensity, average daytime, .... in the toundra (or in the savannah or in other ecosystem)?". You can find many of these descriptions on wikipedia.

No, I'm not. I wanted to know what these parameters could be (like the ones you have named) ? My previous comment is kind of misleading. I just want some of their names from an authentic reference or an expert user and I'll do the rest, find out how they work.i.e how they help determine the condition of an ecosystem.

Part of the confusion lies in the fact that parameter can be used both in a technical sense (parameter in an explicit theoretical model) and in a looser, general sense ("...there are many parameters to consider when buying a car..."). Note also that you shouldn't mix up parameter and variable (which is also done here in the comments), especially in statistical models. Technically, a parameter is a fixed value, used to define a model (model parameter), while variables are things that are measured (and allowed to vary) - short summary: http://www.bmj.com/content/318/7199/1667

@fileunderwater I'll read it.

Here are some examples of ecological parameters:

temperature
yearly maximal temperature
rain intensity
Longest period without precipitation
soil acidity
salinity
nitrogen pollutants
average daytime
maximal wind speed
solar irradiance

You can just have a look at the description of any biome of interest on wikipedia to get an idea of what are the most common parameters used to describe biome. Precipitation, temperature and how their seasonality are very typical descriptors of an ecosystem.

Is it always related to the non-living components? Can there be something related to biotic components as well, like species diversity?

In the description of biome you typically assume some kind of equilibrium in the sense that the non-biotic environment is fixed and most fit species will assemble into the right communities. When making description of of te environment a specific individual experiences, then yes, biotic parameters are of great importance.

Nearly all ecological parameters (at least the ones I can think of) qualify for ecological factors.


text:
Phoresis and mechanical vectors
According to wikipedia and Human Parasitology
By Burton Jerome Bogitsh, Clint Earl Carter, Thomas N. Oeltmann

Phoresis: In this type of symbiotic relationship, the phoront, usually the smaller organism, is mechanically carried by the other,usually larger organism the host.

So can the host acting as a carrier be called a mechanical vector?
On searching google.books I found some books mentioning:
Like Clinical parasitology

Hosts that transmit parasites to man are vectors. Those that are essential in the life cycle are biologic vectors; those that are not essential are phoretic or mechanical vectors.

Cheeky bump for my own paper: http://rstb.royalsocietypublishing.org/content/372/1719/20160085 :)

A mechanical vector just as biological vector transfers a parasite to its obligatory host but carrying it on the surface of its body while the host in phoresis is not necessarily carrying a phoront to an obligatory host (for parasitic interaction).
A parasite-mechanical vector relationship is possibly a kind of phoresis.


text:
Basic understanding of cell cycle (mitosis) phase
Update

This is for a diploid cell (2n).
At G1, cell growth before the DNA is duplicated.
At S, DNA replicated. Chromosomes doubled!
At G2, cell growth
Then Mitosis; Prophase, Metaphase, Anaphase, Telophase, Cytokinesis
Could anyone explain if the chart is correct or incorrect?

Closevoters: please read the actual text of the close reason. The OP here has clearly shown their attempt at an answer.

I agree with @terdon, this might be not the greatest question but there is no reason to close it.

can you explain what mlcl means?

Further one chromosome does not contain the whole genome just a chuck of it (however sometimes a whole genome can be on one chromsoome in the case of simple life forms such as bacteria) can you please specify  the organism you are talking about?

Mlcl= Molecule. and idk what organism is. It wasnt specify. Initial chromosome number was 6 (which i believe 2n=6).

how do you count the number of genome copies?

All chromosomes form the genome (https://research.cip.cgiar.org/confluence/display/potatogene/What+is+DNA,+a+gene,+a+chromosome+and+a+genome) ps you can tag me next time so I will get a notification (using: @Rick Beeloo)

@RickBeeloo Thank you so much for the link. It was definitely helpful. So since chromosome has 6 according to my question, then number of genome copies would be 6 in G1 phase. I know number of chromosomes increase in anaphase (# of chromosomes would be 12 in anaphase). I'd like to know if im on the right track.

The total set of chromosomes (in this case thus 6) is the genome (maybe the answer to this question will help you: http://biology.stackexchange.com/questions/24126/do-human-cells-contain-only-one-copy-of-the-genome and read the comments) so 6 chromosomes is 1 genome copy and 12 chromosomes are 2 genomes copies (only for mitosis then)

@RickBeeloo i have updated my answer. I think i get what you're saying. i see that in this case, only in anaphase the number of genome copies would be 2 since there is 12 chromosomes if 2n=6. On other cases, number of genome copies would be only 1 since there is 6 chromosomes in G1,G2,Metaphase, and after cytokinesis. Correct?

I think your chromosomes and genome numbers are correct now (you can look a this great explanation about human chromsomes during mitosis http://datbootcamp.com/biology-strategy/chromosome-and-chromatid-numbers-during-mitosis-and-meiosis/ ) I'm not sure what you mean with number of DNA molecules?

You might want to clarify that "DNA molecule" here refers to the entire double helix, with both strands. Since the strands are not covalently bound to each other, some would say that the double helix is made up of two molecules, one for each strand.

# DNA molecules
A chromosome can have either 1 DNA molecule or 2, this depends upon what stage the cell is at that moment. It actually might help to know what chromatids are:

A chromatid (Greek khrōmat- 'color' + -id) is one copy of a newly
  copied chromosome which is still joined to the original copy by a
  single centromere. (wiki)

This means that the number of chromatids is directly related to the number of DNA molecuels.

Before replication, one chromosome is composed of one DNA molecule.
  Following replication, each chromosome is composed of two DNA
  molecules; in other words, DNA replication itself increases the amount
  of DNA but does not increase the number of chromosomes.(wiki)

We can now add another row which indicates the DNA molecules, chromatids are directly related to the number of DNA molecules thus from left to right:
 46        92         92        46

These are the basics, now in some more detail about mitosis:

So based on the number of chromatids and your chromosome number you can figure out the nubmer of chormatids and thus the number of DNA molecules:
Thus before replication (G1) = 6, then after S phase (G2) = 12, then metaphase = 12 and after cytokinesis = 6. Just as in your table so that part is correct!

# of chromosomes
You can read these from the table, however I think it's important to understand what is happening. In simple words chromatids and chromosomes are related in this sense:

It is only when sister chromatids separate – a step signaling that
  anaphase has begun – that each chromatid is considered a separate,
  individual chromosome (source)

The phase in which the chromatids seperate is called anaphase, so after this seperation:

we consider the previoulsy chromatids as chromosomes. Thus anaphase and telophase contain the double number of chromosomes as the amount you started with. However anaphase and telophase are not mentioned in your table. So let's go back to the phases in your table. During metphase the chromatids are still connected to each other, meaning that we consider them as one chromosome (the same is true for G1 and G2, because we did not seperate anything). So that part of you table is correct too.

# genome copies

The human genome is the complete set of nucleic acid sequence for
  humans (Homo sapiens), encoded as DNA within the 23 chromosome pairs
  in cell nuclei and in a small DNA molecule found within individual
  mitochondria.(wiki)

However read this question and the answers,  some say 1 genome per cell and some say two genomes per cell, this confuses me too so I'm not sure about this one, however based on the wiki it would say that 2n = one genome, which would make sense because the two pair of chromosomes are not equal and when saying you have two genomes per cell you are actually counting mitochondrial DNA twice.

I think the number of genome copies is correct on my chart. What do you think?

I think it is @Chris


text:
How do aminoacyl-tRNA synthases distinguish between similar amino acids?
How do aminoacyl tRNA synthases recognize the right amino acid for their tRNA? What is the structural reason behind the selective recognition? I have difficulty in seeing how, for example, leucine and isoleucine can be selectively recognized by different binding pockets when they exhibit similar hydrophobicity, molecular volume etc.

I have rewritten the title so it reflects the question and tightened the wording .

Aminoacyl-tRNA sythetases are highly specific to their corresponding amino acid. First, the activation site, where the amino acid binds, constitutes a complex network of intermolecular interactions. For example, threonine, catalyzed by  threonyl-tRNA synthetase, is very similar to valine and serine. Valine has a methyl group instead of the hydroxy group of threonine, and serine, on the other side, has no additional methyl side group. Uniquely to threonyl-tRNA synthetase, it contains a Zn2+ ion that exhibits an interaction structure specific to threonine. Nonetheless, the threonyl-tRNA synthetase could still be mischarged with serine because the zinc ion site is not specific enough, leading to 1% mischarged tRNAs. For this purpose, aminoacyl-tRNA synthetases have a second, editing site that proofreads the charged tRNA.  The editing site can recognize serine and cleave it from the tRNA.
Figure: Interaction network of the activation site of the threonyl-tRNA synthetase in A. pernix. The  threonine-AMP  is shown in green.

Sources:
a Berg JM, Tymoczko JL, Stryer L. Biochemistry. 5th edition. New York: W H Freeman; 2002. Section 29.2, Aminoacyl-Transfer RNA Synthetases Read the Genetic Code. Available from: https://www.ncbi.nlm.nih.gov/books/NBK22356/
b Nagaoka, Yoshiyuki, et al. "EVOLUTION AND tRNA RECOGNITION OF THREONYL-tRNA SYNTHETASE FROM AN EXTREME THERMOPHILIC ARCHAEON, Aeropyrum pernix K1." Viva Origino 1.31 (2003), http://www.origin-life.gr.jp/3101/3101062/3101062.html


text:
Is there a biological environment that we can we assume glutamate exists as glutamic acid?
In the body we almost always assume that glutamate exists as glutamate rather than glutamic acid. It is so commonly glutamate yet glutamic acid and glutamate share the abbreviations of Glu and E. From the wikipedia page:

The side chain carboxylic acid functional group has a pKa of 4.1 and therefore exists almost entirely in its negatively charged deprotonated carboxylate form at pH values greater than 4.1; therefore, it is negatively charged at physiological pH ranging from 7.35 to 7.45.

Glutamic acid:

Glutamate:

Given that the pKa of glutamate is 4.1, is their any biological situation (a cell type, organel etc.) that glutamic acid is preferred?
Additionally, does this have any large biochemical implications, or is that outweighed by the (relatively speaking) "extreme" acidic environment?

I'm confused by your question. Glutamate predominates at physiological pH.

Completely got them mixed up as I was writing, whoops! The underlying point is "where does the protonated form occur biologically, and does it matter?"

I figured as much. I might search for some examples later, but here's some speculation on where you might find it: proteins naturally found in the digestive track, acidophiles, active sites during catalysis. 4.1 is the pKa of glutamate free in solution. In a protein, this can change depending on interactions with other residues.

http://onlinelibrary.wiley.com/store/10.1111/j.1432-1033.1995.0839a.x/asset/j.1432-1033.1995.0839a.x.pdf;jsessionid=13F89FDABD001B72EC378584D072499C.f01t02?v=1&t=i5tvptqb&s=4913cff97a3d52693972c1e0917f3222bd9c67f4

lysosomes, stomach acid.

At typical physiological pHs glutamate does exist as glutamate.
Broadly the acidity in the digestive track is enough to reduce glutamate to glutamic acid. The stomach for example has a healthy pH of between 1.5 to 3.5.
Canadianer points out in the comments that the active site during catalysis are protonated. There are obviously a lot of examples of this and sensitive evaluation by looking at the isocontours and surface potential of the protein structure are needed to draw conclusions if this might be important.


text:
Which hydrophobicity scales are best for detecting transmembrane regions, and why?
There are many hydrophobicity scales for protein analysis.
Broadly, I gather the differences between them are from the experimental method to acquire the data and the normalisation (or lack thereof) of the data.
To detect/predict transmembrane segments one method is to use a window of 19-20 of these residue scales to detect a region of hydrophobicity above a threshold. The Eisenberg et al. scale is used by uniprot for example.
Uniprot don't seem to explain their choice of using the Eisenberg et al. scale.
Why might one use a certain scale over another when predicting transmembrane segments?

In addition to hydrophobicity, alpha-helices formation should be considered.

This has been studied by some of my labmates in Why is the biological hydrophobicity scale more accurate than earlier experimental hydrophobicity scales? I am not involved in their research, but here is the gist of the paper:
Different scales are, as you say, developed based on different criteria. In particular, Eisenberg scale is one of the consensus scales, that is hopefully at least as good as all of its components. It was believed that there were no big performance differences between scales. This could be why Uniprot doesn't specify their choice of scale: at the time, it didn't matter too much. A study in 2009 showed that the new UHS scale was actually better than others.
The results of the benchmark are that the differences are indeed not so big: roughly $\pm2\%$ in difference in prediction accuracy. The overall winner? Hessa, scoring $1.29\ \sigma$ over the average of the scales, but closely followed by UHS, PM1D and PM3D. Eisenberg performance, by the way, is average.
Final note: they found that a near optimal window size for all the scales was 21 with double the weight in the central third.

This is exactly what I was after. Thanks. I don't have access to the journal at the moment. Does the article comment on Kyte & Doolittle's, or von Hiejne's scale?

@GoodGravy Kyte yes, and it is similar in results to Esenberg; von Heijne no (but it is indirectly present, as it is one of the components of Eisenberg).


text:
Dyes to bind to double stranded DNA?
Are there any commercially available fluorescent dyes that will bind only to double stranded DNA (not RNA, single stranded DNA etc.) for studying in vitro using confocal microscopy?

Most of the dyes used for visualization bind with a much higher affinity to dsDNA. This would be SybrGreen, EtBr (although this will bind RNA as well).
There is a pretty comprehensive website from Life Technologies about Nucleic acid stains that is worth a look.
There is as well a publication on this topic: "DNA Staining for Fluorescence and Laser Confocal Microscopy"

YOYO, TOTO join the list, I believe they have 1000-10000x binding/fluorescence efficiency in presence of dsDNA than ssDNA

You may also want to look at acridine orange.  It binds both single stranded and double stranded DNA, but fluoresces green when bound to double sided DNA, and orange when bound to single stranded DNA/RNA, making it very easy to see both in the same image.


text:
Why do specifically bananas go brown quicker in the fridge?
Perhaps the title should be: Why don't all fruits containing phenol residues go brown quickly when left in the fridge?
Bananas go brown over time because of the oxidation of phenol residues.
Bananas go brown quicker in the fridge than left at room temperature. This seems to contradict the first point since the reaction should be slower at colder temperatures. Dialogue from the naked scientists briefly explains why my line of thinking might be wrong.

Emily: Well it’s a good question and the answer is that they will
  brown faster in the fridge.  It’s mainly due to the formation of ice
  crystals, so if you put your banana in the fridge, the ice crystals
  grow, and they actually rupture the cells of the banana skin. This
  releases an enzyme called polyphenol oxidase and as the name suggests
  it acts to oxygenate phenols, which have a ring-like structure, into
  quinones, and these quinones can then all join together or polymerise
  and produce a black, brown, or red pigment called polyphenol and this
  is what gives it the brown colour. So, if you have your banana in the
  fridge, this will occur and you'll get a brown banana.  But another
  interesting thing about bananas is that if you have them in the fruit
  bowl, they'll release ethene and this will make the other fruits in
  the bowl ripen faster because it’s a ripening hormone.
Chris:   So, the question is though, if this is a chemical reaction
  making this brown pigment, if you slow down the reaction by lowering
  the temperature, then it should happen more slowly, therefore, going
  in the fridge should make the bananas go black slower?
Emily:   I can see why you're thinking that but actually, it’s more
  the rupturing of the cells.  So if you have a banana on your table,
  the cells are going to be intact, the enzymes contained, and the
  reaction is not happening at all whereas if you put in the fridge, the
  enzyme is released and the reaction can happen – although yes, it
  might happen slower.

At the risk of channeling people into a yes or no answer, could someone clarify for me if the following statement is true maybe with a peer-reviewed source, which I've had no luck finding:

TLDR Bananas go brown quickly in the fridge because cell lysis, caused by ice crystal formation at cold temperatures in the fridge, releases Polyphenol oxidase (PPO) into the surrounding area which freely causes more browning.

This leads me to another seeming paradox and the question I would like answered: Why doesn't this rapid browning in cool temperatures happen for other fruits and vegetables? What is special about bananas?

That is a good question indeed, but funding bodies are likely to be industrial, and they generally don't care much about writing papers, and often choose to go for patents instead.

@AliceD... I am going to flag you for using the There is no money in basic research argument. I don't know that I buy Emily's argument completely. Most fridges will not go below 4°C. I have actually observed this phenomena in my freezer and seen the brown bananas (Makes really good banana bread that way), but I just don't see ice crystals forming before you get to 0°C. There has to be something else going on. Maybe the enzyme is more stable at colder temperatures? Seems counter intuitive, but maybe it is an adaptive response to frost.

@AMR Not even microcrystals? Also, I don't think bananas originate from countries that have frost, so perhaps that's the key. Other vegetation can withstand or cope with microcrystals, bananas can't.

You are aware that we have had ice ages... While domestication is only about 7,000 years it is likely the plants that they were selected from had to endure periods of cold. As for microcrystals, they have cell walls which should provide a decent amount of structural support before you hit the freezing point, and you get significant expansion in volume.

@AMR Perhaps bananas are particularly vulnerable to microcystal formation somehow... I meant to say that whilst some plants like potatotoes were agriculturally selected for hardiness and yield through colder seasons, banana farmers never had to worry about that and cold resistance could have gone 7000 years without being selected for. It could have taken perhaps a handful of bottlenecks and frost resitance could be diminished. I'm not sure I agree with what I just said, but it's a possibility!

We also have had frosts in Florida that wiped out citrus crops, My thought was that maybe it hastens the decomposition of the fruit so that nutrients can go to maintaining the plant and when the fruit rots and falls off it can go back into feeding the plant. That was my line of thinking in how it may be an adaptation to frost. Protection for the plant to survive, the fruit is expendable.

If you freeze and thaw a tomato, it is pretty awful, there the ice definitely breaks down the fruit. I can't say I have tried other fruit that were frozen... But I think you have the same problem with berry.

@AMR I agree that there are a lot of foods that taste, feel, and look different after freezing (even carrots, which I would expect  to be very resistant to frosty conditions, taste powdery almost). But with bananas this happens well above freezing point. We have a relatively warm fridge at 7+ degrees and the bananas were completely brown and mushy overnight. I think there is something unusual about bananas, although I bet it's not limited to bananas.

Maybe it is the confined space, Ethene concentration is allowed to build up to higher concentrations in the enclosed space of the fridge. Try this experiment. Seal a banana in an airtight plastic bag at room temp in the dark, maybe with a slightly damp sponge to simulate the humidity in the fridge, leave one out, put one in the fridge, and one in the freezer and compare after 24 hours.

@AMR- I may have been unclear. What I meant was that I think chances are slim basic scientists have bothered with it. Food industries may have.

@AliceD NIH is sponsoring programs for scientist to learn to market their science to industry... The US thought we lost a lot of ground when we defunded stem cell research... Wait until they see the kind of science we start to do when we are expected to sell it.

+1. It can also be added that banana skins go completely black when frozen, even though freezing them will stop the enzymes from catalysing the reactions. The same does not happen for cut apples, despite the same explanation (polyphenol oxidases) being put forward for the browning of both fruits.

Banana fruit is very susceptible to chilling injury (CI) and this can occur at relatively high temperatures: CI may occur at  12oC and under. Typically the banana skin turns brown, but in addition there may be pitting and the fruit may not soften (Wang et al., 2013).
Oxidative Stress & ROS
One generally accepted theory it that oxidative stress, due to the accumulation of reactive oxygen species (ROS) such as H$_2$O$_2$ (hydrogen peroxide), O$_2$$^−$ (superoxide) and OH$^{\bullet}$( the hydroxyl radical), is a primary cause of  CI in bananas. (Wang et al, 2003, 2016; Pongprasert et al., 2011).
ROS may give rise to lipid peroxidation, enzyme inactivation, membrane rupture and, ultimately, cell death.
One possibility is that the effect of lowering the temperature is to decrease the activity of key enzymes involved in the 'normal' plant response to ROS.  In other words,  it is postulated that low temperatures cause key enzymes involved in the stress response to ROS to become sluggish, allowing the build-up of  reactive oxygen species that (indirectly) lead to cell death and browning (Wang et al., 2013).
However, plants also respond to cold-induced stress and a key player is the amino-acid proline (Verbruggen & Hermans, 2008; Chen et al., 2008).
Proline has a  key role in maintaining plant cellular integrity in times of stress, and it has been proposed that it does this by acting as an osmolyte, by scavenging ROS, by maintaining protein structure, and by buffering pH (see Verbruggen & Hermans, 2008).
Two key biosynthetic enzymes (starting with glutamate) are pyrroline-5-carboxylate synthase and pyrroline-5-carboxylate reductase (Verbruggen & Hermans, 2008).  A key degradative enzyme is proline dehydrogenase.  Although an aside to this answer, it is nevertheless interesting that proline biosynthesis occurs in the cytoplasm, but proline degradation occurs in the mitochondrion (Verbruggen & Hermans, 2008)
Biochemical Aspects of Stress Response
Plants have an intricate antioxidant defense mechanism to counter the dangers of ROS.
Non-enzymatic antioxidants include ascorbic acid (Vitamin C), polyphenols, the reduced form of glutathione, and α-tocopherols (Pongprasert  et al., 2011). Key enzymes of the antioxidant response include superoxide  dismutase (SOD), glutathione reductase (GR), catalase, peroxidase,  and ascorbate peroxidase
In addition, another important enzyme is phenylalanine ammonia-lyase (PAL).  This enzyme catalyzes the conversion of phenylalanine to trans-cinnamic acid, a key intermediate in the biosynthesis of polyphenols and (many) other plant secondary metabolites (Chen et al., 2008)
As will be seen below, many of the strategies employed to counteract CI involve  pretreatments designed to increase the levels of non-enzymic oxidants and to  increase the expression/activity of key enzymes involved in the stress response to ROS.
The Browning Reaction
It is almost universally accepted that the browning reaction is the result of the action of (the copper-containing) polyphenol oxidase (PPO). This enzyme oxidises mono-phenols and di-phenols to ortho-quinones that  non-enzymically polymerize, via  a free radical mechanism, to give a dark brown or black compound(s).
In normal undamaged tissue the enzyme is latent and, furthermore, does not have physical access to its phenolic substrates due to subcellular compartmentalization (Promyou et al., 2008; Hind et al., 1995).  In damaged tissues, however, the enzyme is activated and comes in contact with its substrates, perhaps through membrane rupture. The resulting  brown, structurally complex polyphenol product is thought to protect plants from pathogens and herbivores (Hind et al., 1995).
Thus the brown color is the response of the plant to irreversible tissue damage as a defense mechanism against further degeneracy.
(Polyphenol oxidase is sometimes referred to as tyrosinase and catechol oxidase, and the reaction catalyzed by PPO is similar to that catalyzed by tyrosinase in the (human) formation of melanin from tyrosine).
Prevention
A number of innovative methods have been used to prevent low-temperature browning. Many attempt to induce an increased stress response to ROS  prior to storage at low temperatures.
UV-C Irradiation

Pongprasert and co-workers have shown that  irradiation with UV-C light increases the expression of phenylalanine ammonia-lyase and other key ROS stress-response enzymes, and pretreatment with UV-C seems be a very effective method in reducing CI (Pongprasert et al., 2011).

Heat Pretreatment

Chen and colleagues demonstrated that heat pretreatment (38oC for 3 days) induces chilling tolerance, and they attribute the effect (at least in part) to an increase in both the activity and expression of phenylalanine ammonia-lyase (PAL).  (Chen et al., 2008)

Hot water

Promyou and associates have shown that hot water pretreatment is a practical method for preventing CI, and they attribute the effect to decreased polyphenol oxidase activity (which they call catechol oxidase)  (Promyou et al., 2008).

Modified Atmosphere packaging

It has been shown that  modified atmosphere packaging, where ethylene and CO$_2$ levels are lowered, alleviates the problem (Nguyen et al., 2004). The effect is attributed to  a lowering of polyphenol oxidase and phenylalanine ammonia lyase activities in the peel of bananas packaged in the modified atmosphere.

Nitric Oxide (NO)

In a detailed an innovative study, Wang and co-workers have shown that pretreatment with nitric oxide (NO), itself a free radical, greatly diminishes CI in bananas.  They demonstrated that key enzymes of ROS metabolism are elevated by NO treatment. In addition, the activity of phenylalanine ammonia-lyase (PAL) is increased as is the activity of a key proline biosynthetic enzyme (pyrroline-5-carboxylate synthase), but the activity of a key enzyme of proline degradation (proline dehydrogenase), decreased in activity.

Summary

The browning of banana skin is due to polymer formation by the catalytic action of polyphenol oxidase on mono- and di-phenols in response to irreversible tissue damage by reactive oxygen species (ROS)
ROS accumulate at low temperature due to a lowering of plant defense mechanisms.
The brown polyphenol product is formed only when tissue damage occurs as a plant defense mechanism against further abasement by pathogen and herbivore attack.

Key References
Chen, J.Y., He, L.H., Jiang, Y.M., Wang, Y., Joyce, D.C., Ji, Z.L. and Lu, W.J. (2008). Role of phenylalanine ammonia‐lyase in heat pretreatment‐induced chilling tolerance in banana fruit. Physiologia Plantarum, 132, pp.318-328. [PMID: 18275463]
Hind, G., Marshak, D.R. and Coughlan, S.J. (1995). Spinach thylakoid polyphenol oxidase: cloning, characterization, and relation to a putative protein kinase. Biochemistry, 34, pp.8157-8164 [First page]
Nguyen, T.B.T., Ketsa, S. and van Doorn, W.G., 2004. Effect of modified atmosphere packaging on chilling-induced peel browning in banana. Postharvest Biology and Technology, 31, pp.313-317. [pdf]
Pongprasert, N., Sekozawa, Y., Sugaya, S. and Gemma, H. (2011) The role and mode of action of UV-C hormesis in reducing cellular oxidative stress and the consequential chilling injury of banana fruit peel International Food Research Journal 18, pp 741-749   [pdf]
Promyou, S., Ketsa, S. and van Doorn, W.G. (2008). Hot water treatments delay cold-induced banana peel blackening. Postharvest Biology and Technology, 48, pp.132-138. [pdf]
Verbruggen, N. & Hermans, C. (2008). Proline accumulation in plants: a review. Amino acids, 35, pp.753-759. [pdf]
Wang, Y.,  Luo, Z., Du, R., Liu, Y.,Ying, T. & Mao, L. (2013)
Effect of Nitric Oxide on Antioxidative Response and Proline Metabolism in Banana during Cold Storage,
Journal of Agricultural and Food Chemistry,61, pp 8880-8887. [PMID: 23952496]
Wang, Y., Luo, Z., Mao, L. & Ying,T. (2016) Contribution of polyamines metabolism and GABA shunt to chilling tolerance induced by nitric oxide in cold-stored banana fruit.  Food Chemistry 197, pp 333-339. [PMID: 26616957]

Really interesting thorough answer! Thanks.

What's interesting with this one is we don't really know very well the mechanism behind what's called chilling injury. It happens to a range of fruits, like bananas, peaches, avocado, or apples. The belief is that the chilling alters membrane permeability to storage vacuoles inside the plant cells. Try On Food and Cooking, pp.269, and Puig et al. (2015) for references here.
Now the membrane permeability to the storage vacuole changes (it gets leaky), and inside these vacuoles are phenolic compounds. In the cytoplasm of the plant cell, there's an active enzyme called polyphenol oxidase (PO). The reactions it catalyzes end up with a compound called melanin, a brown/black pigment:

Fig A. An overview of what a PO might do.
So the phenolic compounds leak out and PO goes to work catalyzing reactions that start building up the dark pigments associated with browning. Being said, I can't at this moment find a good paper that says "look, this is how the entire process happens," but I'll be attempting to read a little deeper into the matter.
Keywords: flesh browning, enzymatic browning, chilling injury, polyphenol oxidase, storage quality, storage conditions


text:
Do mutated c-sis oncogenes only affect cell growth?
Since c-sis regulates only cell growth, a mutation there should only lead to an out of control growth of the cell, but the cells would still be mature, since c-sis does not regulate the function or maturing of the cell.
However a mutation in c-sis leads to cancer, and cancer is not just cells that grow out of control, but also don't performe their function (are not mature). Can someone explain how a c-sis mutation still leads to cancer please?

Hello and welcome to Biology.SE! Currently, the title of your question is quite broad, but the content of your question seems to focus on the c-sis oncogene. Are you expecting an answer only for the c-sis oncogene? If so, please be sure to edit the title of your question to reflect that.

Any oncogene that regulates growth only, I used c-sis oncogene as an example because that is the only one I know that has this function. I changed title, thanks for the feedback!

Cancer is not a disease like the flu or E. bola, where there is a single quick and easy cause for the disease which you can locate and describe in a single sentence.  Cancer consists of malignant cell growth, it is true, but why are the cells growing out of control?
The fact is that there is not one single cause.  At some point along the way, some cell experience a mutation to some gene which resulted in a slightly higher rate of proliferation than normal.  However, this in and of itself is not even enough to produce a tumour.  It simply gives the cells a higher number of daughter cells, and consequently, a higher risk of having more mutations.
At some point, one of those daughter cells acquires a mutation which results in higher levels yet of proliferation, or a mutation which encourages angiogenesis, or (in the case of epithelial cells, for instance) a mutation which allows the cell to escape typical anoikis pathways and perhaps perforate its basement membrane without dying.
Even the process of metastasis requires multiple mutations to happen, and yet if a tumour does not metastasize, it is typically regarded as benign.  The point is, cancer is not caused by a single mutation to an oncogene or otherwise.  It is caused by an accumulation of mutations which permit the cells to proliferate much faster than normal, to recruit the body's resources, and to live in tissues all around the body.
In the case of the particular gene that you mentioned, the exact role of the c-sis oncogene in cancer prevention is still unclear; in fact, according to the OMIM page,

The protein product of the c-sis gene has not been identified.

...though the gene is very similar to platelet derived growth factor genes, some of which have been identified as mitogenic factors.  Theoretically, therefore, it is possible that a mutation to the c-sis results in excessive mitogenic stimulation, resulting in an increase in cell division and proliferation.  But that last sentence is speculation, not hard science.
TL; DR:
We don't know, but it's possible c-sis encourages faster cell division.

Sources:

Platelet-derived growth factor, beta polypeptide; PDGFB on OMIM.org
Josephs SF, Guo C, Ratner L, Wong-Staal F. 1984. Human-proto-oncogene nucleotide sequences corresponding to the transforming region of simian sarcoma virus. Science 223(4635): 487-491.