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How does a gene "know" what to change to?
Excuse my ignorance but I've always been curious about this...
For example, a frog is red, but it starts living in a green forest. Over time the frog becomes green to camouflage. But a gene can't see and I'm sure there's no mechanism for color info to be transmitted to individual genes from the brain. So how does a gene know to pick green over, say, blue?

Colour adaptation does not involve changes in genes. Why you would assume this I really don't know but it makes nonsense of your question. If you want to know how colour adaptation works rephrase your question accordingly. But please never ask questions applying the word "know" to insentient objects. Take the trouble to express yourself in a scientific manner.

@David: you say the question is "nonsense", yet it has a number of upvotes, and very good answers, five of them at the moment of writing. I would also like to know what it means to "express yourself in a scientific manner"; and, is that a requisite to ask a question?

@David - just saying thanks for being ever vigilant and for your efforts in trying to keep the site's overall quality in check. Having said that, I also wish to share that your comments here are receiving flags [general tone, rude, offensive, yadiya, you know...].

@MartinArgerami - the high number of upvotes, as well as the high number of answers is more related to the fact that the question made it into the hot questions list than because of its quality. In fact,  the question has been downvoted 4 times too. The fact that some folks (like Remi) know very well how to generate excellent answers, doesn't take away the fact that the question itself testifies of a certain lack of scientificness.

@MartinArgerami — Please read what I wrote, which was that talking about "genes knowing" makes nonsense of the question. As genes are not sentient beings, this phrase is nonsense, and if you have a question (which may have some merit) including nonsensical expressions invalidates or "makes nonsense of" it. This is avoided if the idea that the poster wishes to express is framed in a scientific manner. I am not clear what the poster means, but an example of scientific expression might be "Is there a way in which electrical signals from the brain can cause genes to mutate in a particular way?".

As it is written, the question asks about change in colour over the course of an individuals life, but the highest voted answer discusses change in colour of a population due to evolution. The question should be closed as unclear until the asker clarifies it.

@canadianer - I totally agree, but vow against mod-closure :) The top answer now basically states - your question is based on the incorrect assumption that a gene has a brain

The pedantry here is absurd.  OP obviously knows "know" isn't the correct word, that's why they put it in quotes.  Not knowing how to refer to it or how mutation works is why they're here.  "You're ignorant and write nonsense" is not an appropriate response to someone trying to learn.  And a Q&A site is probably not the best place for those users who are interested in neither questions nor answers.

Is punctuated equilibrium relevant here? I'm surprised nobody mentioned it... but I'm not a biologist either, so...

I asked the original question (system doesn't let me post in the comment section.) I can't believe how quickly this devolved into an argument about the semantics of the question. If you are versed in science and esp. biology isn't obvious that gene's know know anything? Even I know that, and I'm not a scientist. I very clearly stated that i am ignorant on the subject, hence the question. If we knew how to ask all the right questions in the right way then we'd be much more advanced as a species. Anyway, I appreciate everyone who put semantics aside and answered the question. Thank you, it is mu

Using your example, the gene doesn't know anything. Mutations cause some of the offspring of the red frog to turn green, some to turn blue, some to turn fluorescent yellow, and some stay red. Birds can't see the green ones as well as the others, so more green frogs survive and make more green frogs. The red frogs, the fluorescent yellow ones, the blue ones, mostly get eaten. After a few generations, almost all the frogs are green -- not because the gene knew anything, not because the mutations went in any direction, but because all the other changes were counterproductive and got eaten.
The gene doesn't know anything. It's just a bunch of chemicals that randomly react with cosmic rays, chance, whatever. Most of the changes are irrelevant or actively bad, and the frog that's carrying those particular chemicals doesn't survive. But sometimes the change benefits the frog carrying the particular chemicals and then the frog sends those chemicals down to its progeny.
Obviously this is hugely over-simplified. A short and simple intro to the basics of evolution is Understanding Evolution, by UC Berkeley.

This is a good answer but I just want to add that this process is called "natural selection", and is fueled by "selection pressures".

Also in reality that one frog's offspring will be just a tiny bit more green, just a tiny bit more blue, or just a tiny bit more fluorescent yellow. (Though some might have a mutation that makes their colouring not work at all, so they become albino). It takes a lot of generations before you could actually see a green or blue or yellow frog. (If its kinda-green or kinda-blue or kinda-yellow ancestors didn't get killed by predators first)

@immibis: Not necessarily. The green gene could be recessive and initially rare. It wouldn't even require mutations, it simply would be a matter of the dominant red genes disappearing due to predation.

Unless female frogs prefer to mate with red frogs, then green frogs are out of luck, and frogs will more likely become extinct than "evolve" to become green.

@Peter: ...although those female frogs that don't prefer red mates so much will have greener offspring on average, and so more of their female offspring will survive to mate again. So the female preferences will tend to change over time, too, unless of course the frogs go extinct first. (But near-extinction events do tend to accelerate selection, since the last few frogs to survive are likely to be the greenest ones.) A bigger potential issue is that if there's a steady supply of red frogs migrating in from another habitat, that'll make it hard for a green subpopulation to get established.

Honestly, I'm not really sure this answers the question. When was the last time anyone saw, say, a green deer? If colors change randomly and it's just a matter of survival, then surely someone should spot randomly colored animals occasionally. The closest I've ever seen is white giraffes, which simply lack pigments. So it's easy not to believe natural selection as a layman. I think if you want this answer to be convincing, you should give some numbers as to how often you'd expect to see weird mutations if you are to be likely to observe a change that can be selected for over a span of N years.

Second @Mehrdad, plus: what about chameleons?

But fluorescent frogs don't get eaten because the birds assume they are poisonous...

This is the theory of evolution through randomness. It doesn't explain changes that require 2-3 major simultaneous changes for the survival of the mutated animals. Then one starts to think whether evolution really happens on a random basis.

@akostadinov if you genuinely don't understand this simple concept, ask another question and someone will explain it to you.  The comments are not  the right place to ask new questions (or to make old and long-debunked claims)

@iayork, I don't see a question in my comment. I was trying to point out a weak spot in your answer. Or maybe whatever in your answer is the thing much harder to explain.

@akostadinov (or to make old and long-debunked claims) - I was giving you the benefit of the doubt and assuming you might be genuinely ignorant, but since you first parroted the long-debunked creationist talking point and then responded with classic creationist obfuscation, I'll just point out (in case newcomers are fooled) that this "weak spot" is nothing of the kind and is a well understood concept, even though creationists constantly try to lie about it.

@iayork, as long as you don't provide evidence, your position is just an opinion or a belief. While some naive forms of "creationism" have been proven wrong, this didn't prove the "random" evolution theory in any way. The "random" theory in my opinion is equally naive as some "creationism" theories and has never been proved scientifically. I'm not going to write anything more. Anybody that can think and read can go on investigate and think for him/her-self.

Each offspring's color is a bit different from its parents.  Some colors help the frog survive, other colors tend to get it killed before it reproduces.  Over time, the species tends toward a color that improves survival because those that fit their environment better will reproduce and those that fit their environment worse don't reproduce at quite the same rate.

How does this answer a question that is clearly concerned with molecular mechanisms, even though it makes wrongheaded assumptions?  All you are saying is "it happens".

@David I don't think the question is concerned with molecular mechanisms, I think the questioner is just confused about how evolution works, in particular the genetic variation/mutations side of things.

@BryanKrause — Who knows? But the answer is terrible whatever the question. The question is clearly unclear and should be closed unless someone edits it. Don't you think?

I think this answer is just fine. It isn't perfect, and I think @iayork's answer is more precise in wording, but this one benefits from being short and to the point and accessible to someone truly new to evolution, like the OP appears to be. It's much better than your comment "Colour adaptation does not involve changes in genes" which is clearly wrong, of course adaptation involves changes in genes, just not in the manner the OP was thinking.

And although the original question shows a poor understanding, I'm not convinced it's actually a terrible question. I think there is almost certainly a duplicate someplace to close it with, but the OP's thinking and logic are clearly displayed, and they aren't asking for an answer that would be too broad or in-depth for this site.

Of course, as you know, a gene does not have any conscious, a gene does not know anything. It is all just a bunch of chemical reactions.
Central dilemma
First, you have to understand that a gene is a piece of DNA that will be transcribed in mRNA and the mRNA will be translated into a protein (this is a bit of an oversimplification). The protein is the molecule that is causing an action. The concentration of proteins in the cell is key in causing a phenotypic effect.
Regulatory mechanisms
The concentration of proteins can be affected by many regulatory mechanisms.
Gene expression regulation

Regulation of gene expression includes a wide range of mechanisms that are used by cells to increase or decrease the production of specific gene products (protein or RNA), and is informally termed gene regulation. Sophisticated programs of gene expression are widely observed in biology, for example to trigger developmental pathways, respond to environmental stimuli, or adapt to new food sources. Virtually any step of gene expression can be modulated, from transcriptional initiation, to RNA processing, and to the post-translational modification of a protein. Often, one gene regulator controls another, and so on, in a gene regulatory network.

Post-transcriptional regulation

Post-transcriptional regulation is the control of gene expression at the RNA level, therefore between the transcription and the translation of the gene.1 It contributes substantially to gene expression regulation across human tissues.

These include mechanisms such as

capping
splicing
Addition of poly(A) tail
RNA editing
mRNA Stability

Post-translational regulation

Post-translational regulation refers to the control of the levels of active protein.[..] It is performed either by means of reversible events (posttranslational modifications, such as phosphorylation or sequestration) or by means of irreversible events (proteolysis).

Skin colour changes in frogs
One such regulatory mechanism must be involved.
I really don't know much about physiology and molecular biology but I could find a large number of papers (including Taylor and Hadley 1969 and Fernandez and Bagnara 1991) showing that the colour change is mediated via production of the Melanophore Stimulating Hormone (MSH) produced by the hypophysis. Maybe a better physiologist / molecular biologist could give you a better answer.
If you are interested in the particular case of color change, you might also want to have a look at Neri and Castrucci 1997 and Skold et al. 2012.

Still doesn't explain why the mRNA transcribes one piece of DNA rather than another.

The mRNA is the result of transcription but it does not transcribe. 2) yes, it does (see gene expression regulation). There would be a lot to say about gene expression regulation, so for more information just have a look at the wikipedia page or at an intro course such as those by Khan Academy for example

Another fun example is a certain type of moth that used to live in Western Germany ("Ruhrpott") and other areas during the Industrialisation. Its main habitat are birch trees, i.e. mainly white tree barks. So the animal used to be white with a few black spots.
Sometime in the past, the Ruhrpott had an awful lot of coal production, and in some areas the birch trees actually went and turned black from all the pollution in the air. Lo and behold, after some time, the moth also turned black with white spots.
As has been mentioned, obviously this is just basic evolution. What is nice about your and mine example is that this is a very direct, clear connection. If the animal is clearly sticking out due to its color, it will be frequently killed. It is not the other way 'round, where a slightly positive bias gets slightly more offspring, but a clear-cut, straight "be red (or white) and get caught" fact.
The effect of this is that this kind of evolution works really fast. It may have a tremendous effect after only one or two generations (obviously). So, with such drastic changes of the environment, after a handful of generations there may literally be no white moths left, the dark ones then have the whole habitat for their own (i.e., lots of food/nesting places, whatever moths do to reproduce). Hence this kind of evolution is - in contrast to other developments, which may take hundreds or thousands of years - very visible to humans.
Another fun fact: after the Industrialisation, our air turned clear, the birches turned white, and the moths got eradicated again until they were white again. Poor animals...
Source: Peppered moth evolution. Interesting read; all of this was not "obvious" to people back then, and there is criticism to be found as well.

The change in colour may be caused by new mutations or by epigenetic changes (e.g. changing the diet of a pregnant rodent may change coat color of pups, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC165709/). If the change is epigenetic, it means that the blueprint for producing the new colour was already present in the animal's genes before the colour change was triggered in its offspring by a change in the environment. In the case of the frogs, it could have been that the red frogs had some green ancestors that evolved the ability to toggle their colour between green and red in response to an environmental factor (like the availability of some specific food).
I don't know what the commenter David means with his comment "Colour adaptation does not involve changes in genes.", though. Even if the change is epigenetic, it still affects the functioning of genes.

Intro
There are actually at least three ways in which the colour of a frog might change to adapt to the colour of its environment. I will layout briefly how the three work, because from some of the comments there seems to be some confusion between the three, and also because the question mixes up changes within the lifetime of an individual frog with changes to the genome of the frog. These three categories can be more broadly applied to the question of how animals adapt to the environment.
Evolution

Occurs over multiple frog lifetimes
Involves changes to the genes
Is inherited by the offspring

Evolution occurs through natural selection. Other answers such as @iayork's answer have explained this mechanism.
Gene Expression

Occurs within a frog's lifetime
The genome of the frog is not changed, and the changes are not inherited
The way a gene is interpreted changes

While the genes of an organism don't change over the course of their lifetime, the way they are expressed can. This can lead to changes in skin colour based on environmental changes. This is explained in Environmental Influences on Gene Expression.
This would be a pre-existing response to a particular set of conditions; thus they 'know' what to change to because the response to the environmental change is pre-determined by their genes.
How the gene expression is influenced by the environment would depend on the particular trait in question. The mechanisms for this are not well understood, at least for some traits, as seen in The effect of light on gene expression and podophyllotoxin biosynthesis in Linum album cell culture from Plant Physiology and Biochemistry Volume 56 (July 2012, Pages 41-46)
Background adaptation

Does not involve the genes of the animal except in as much as every biological mechanism is encoded in the genes
can occur rapidly

Background adaptation is the approach used by Chameleons, but some frog species, as well as various fish and crustaceans also have this ability. In essence the distribution of pigments in specialised structures in the skin can be changed to modify the colour of the animal.
In at least some species this process relies on the animals ability of sight, so it seems likely the information on which colour to take is transmitted through the nervous system. The Wikipedia article on Chromatophores gives more information in the section on Background Adaptation
Conclusion
The kind of change described in the example could not be through genetic change, as this occurs over many generations, rather than one lifetime. To understand how animals adapt to the environment it is important to separate this kind of adaptation from the longer term adaptation through natural selection.
In these more rapid changes the colours to which the animal can change are already encoded in its genes. One mechanism by which the changes to the environment can be conveyed to bring about physical adaptations is through the nervous system.
TLDR:

Changes to the genome of an animal don't happen over the lifetime of an individual, but natural selection combined with random mutations can cause changes over multiple generations.
Immediate changes in response to the environment like the changes in Chameleons (and to a lesser degree in frogs) are not caused by changes to gene expression, but by mechanisms inbuilt in the animal in question.
Over the lifetime of an animal the way genes are interpreted can change in response to the environment, but this is also an inbuilt mechanism and the changes are not inherited.

DNA contains if-then statements that direct the mRNA to transcribe one piece rather than the other. I'm no microbiologist so I'm glossing here, but the transcription-mechanism is what allows proteins to be build which are then somehow assembled into hormones, tissues and various fluids such as mucus, gall, etc.
The question is really, what triggers one branch of the if-then over the other? Temperature appears to be one: deer, for example, are sexually active only in the autumn. When the temperatures drop, they start producing high-levels of sex-hormones, which cause the males to grow antlers and fight each other.
Color perception must be another: chameleons and certain species of squid are very dramatic examples. Eyes contain various cells, which are sensitive to certain wavelengths (https://en.wikipedia.org/wiki/Color_vision). The cells transmit signals to the brain, which must somehow result in the production of hormones that in turn trigger the skin-cells.
Some chemical reaches the mRNA in the relevant cells that sets the variables seasonIsAutumn or environmentIsGreen to true and the deer start growing antlers and the frogs, chameleons and squid turn green.
Of course, these signals, of temperature or color, will only have effect on those species, subspecies and genders whose DNA contains a relevant if-then statement. Deer obviously do not possess a switchColor function, just as frogs or does do not possess a growBigAntlers function.

I would like to start my answer by saying never apologize for not knowing something.  There is nothing to be ashamed about and it's good to ask about things you don't know!  More people should do it, and you should not be criticized for it.
I want to address your example first, since I believe there is some (common) misunderstanding.  The scenario you have described is a type of Lamarckian evolution, which was actually the best attempt at explaining the mechanism of evolution before Darwinism.  Lamarck was a great biologist, and so even though we may mock his ideas, it was progressive for the time with the information he had available!  Anyways, Lamarck's idea was that organisms could change during their lifetime in order to adapt to their particular environment, and then pass these changes onto their offspring.  The very classic example is the long neck of a giraffe.  The Lamarckian thought is that a giraffe stretched his neck to reach the leaves high up in trees, and passed this newly-stretched neck onto his offspring (and hence all giraffes now have long necks).  Today we know that Lamarckian evolution is never observed and is not a supported or a sufficient explanation for complex adaptations.
Here is why this idea doesn't work:
All organisms carry a one-dimensional "code" in their cell(s) which act as a recipe for "building" that organism along with the organism's characteristics that make up their phenotype (which would include the color that you describe).  Most commonly this code is "written" and stored as DNA, a string of biomolecules called nucleic acids.  Information is read from this code via sophisticated biological molecular machinery and used to form every aspect of the organism and that organism's effect upon the environment;  that is to say the information flows from code to the environment and not the other way around (ie: it doesn't move from the environment back to the genes).  I should state that there are exceptions known as epigenetics, which while extremely interesting, is beyond the scope of this question.
You can think of it this way: imagine you have a recipe for a cake.  All the instructions to bake the cake are coded into a one-dimensional sequence of letters on a page of your cook book.  This is the code for making the cake.  You read these letters, and your brain interprets the meaning.  You use this interpreted information to carry out the actions required to bake the cake.  Now, once the cake is made, you cut a slice from it.  Of course, the act of cutting and removing the slice does not convey information back to the recipe.    You can imagine if it did, the next cake you made from that recipe would come with an already removed slice!
The point I want to get across here is that a frog which carries the gene for the red color cannot willingly or spontaneously change his color to green to match his environment.  There is no feedback to the frog's genes from the environment.  The ability to perform such a change would need to encoded within this frog's DNA and likely be part of a sophisticated mechanism that has evolved over millions of years.  For example, many birds have breeding plumage that changes color at certain times of the year, but this is a heritable trait that has been honed through the action of natural selection over millions of years and has nothing to do with the bird's conscious desire to be more attractive.
Please do not be confused though - an organism's environment (including the "genetic environment", the collection of genes in the gene pool) as well as things like the habitat, predators, etc, are the pressures which drive evolution by natural selection.  In this sense there is feedback from the environment, but it occurs within populations of species over many generations, not within individual organisms' lifetimes, and it acts through totally different means than those imagined via Lamarckian evolution.
This is a large topic and I could go on and on, but I hope that this is a sufficient answer to your specific question for now.  I recommend you check out the extremely engaging and informative book called "The Blind Watchmaker" by the illustrious Richard Dawkins.  My cake example was summarized from this wonderful book, and there are plenty more where that came from!


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How does hibernation reduce risk of radiation-induced mutation?
A recent documentary (skip to 58:20) discusses the possibility that hibernation, if it could be induced in extrasolar astronauts, would reduce damage from cosmic radiation. The obvious reason this could happen is the shielding of hibernation chambers, but the documentary reviews evidence that even hibernation in the wild (e.g. bears) reduces radiation damage due to a slowed metabolism.
I would assume the connection is that reduced need for enzyme synthesis keeps DNA coiled up most of the time so its nucleotides are less exposed to radiation, but even if this is true it raises the question of how coiling shields radiation. (For example, is it less able to penetrate histones or the phosphorylated deoxyribose backbone?) Adding to my confusion, the documentary claims the mechanism is rooted in hydrogen sulphide, but doesn't explain either why this is more concentrated in the cells of hibernating animals nor how it reduces mutations.

This is still an area of active research, and there doesn't appear to be a single definitive answer for the mechanisms behind the reduction in radiation-damage during hibernation.
A recent review by Cerri et al. (2016) covers a lot of the known biology behind hibernation and resistance to radiation damage.
A few select quotes from this review:

At the cellular level, it is well known that cells irradiated in
resting state, and left undisturbed for 24 h after irradiation, are
more resistant than cells re-plated immediately after exposure. This
effect is known as delayed plating, and is generally attributed to the
potentially lethal damage repair (PLDR) in resting phase.
...
The oxygen level during hibernation may contribute to the enhanced
radioresistance. Hypoxia is a well know protective mechanism, and is
arguably the main reason of local control failure in radiotherapy.

Rockwell et al. (2009) discuss the underlying reason behind reduced radiation sensitivity in a hypoxic environment:

Molecular oxygen (O2) is a potent chemical radiosensitizer. This
radiosensitization does not result from any of the metabolic or
physiological effects of oxygen, but instead reflects the fact that O2
is an extremely electron-affinic molecule that participates in the
chemical reactions that lead to the production of DNA damage after the
absorption of energy from ionizing radiation [21,22].

My personal take would be that the reduced risk of radiation-induced damage is probably not due to the structural arrangement of DNA, but rather the overall cellular environment. This is perhaps linked to an enhanced ability to repair damaged DNA, but is also likely to be highly dependent on cellular oxygen levels.

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Amino acid structural charges

Hello,
I was wondering if i could get an explanation as to why the charge of this peptide is +2 and -2. How do you figure this out? What is it based on exactly?
Thank you

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why is DNA better for storing genetic info while RNA better for transmission of it?
I do know that RNA cannot be used for transmission since it is unstable, but how does it prove to be a better transmitter of genetic information?


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Frog species identification
A friend of mine came across this frog today. I'm not too familiar with frogs, can someone ID this? Please forgive my friend's abysmal use of English..
Location: Central Kentucky, USA.

I think is a Pickerel Frog - Lithobates palustris
Here some more pictures and habitat type
http://www.californiaherps.com/noncal/misc/miscfrogs/pages/l.palustris.html


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Can you "fight" a coma or serious illness?
In an article about the latest earthquake to strike Mexico, I read that a rescuer said to someone in a gurney, "Fight for your life, please!"
I've seen similar things in TV shows and movies where a character is in a coma or seriously injured or ill.
But how much—if anything—can mentally "fighting" a coma, injury, or illness do?


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Cancer and Evolution
Edit: just to clarify, I am asking what, if anything, the literature says can be gleaned about evolution by studying cancer, especially relating to how multicellularity evolved and the traits used to force cells under control of the organism.
Most of the original question details I had added were just my own thoughts on the topic.

Original question
Is there a sense in which cancer can be considered as a return to the unicellular "origin" of a cell?
It has always seemed to me like cancer is almost inevitable by the structure of the cell (its poor "design", essentially). The only thing standing in the way are the cellular controls: senescence/apoptosis (e.g. p53 pathway), immunosuppression (e.g. cytotoxic T lymphocytes), telomeres, etc...
So it seems like multi-cellularity did not evolve "ground-up", but was instead generated by slowly differentiating the functions of the various cells, while developing "top-down"controls against errant cellular behaviour.
Thus, cancer, which occurs when these protections fail, is in some sense merely a return to an ancient evolutionary root.
I suppose some arguments against this include the fact that modern cells are vastly different than their ancient ancestors (or even modern archaea/bacteria).
So the best we can perhaps say is that the core of the cell has been sufficiently preserved (ribosomes are still mostly RNA, are they not? :] ).
Further, it is hard to call some of the "micro-evolutions" of cancer (e.g. interleukin-8 production) as returns to primitive behaviour.
In these cases, I tend to see them as necessary occurrences to remove the "top-down" controls, rather than as integral to the destructive out-of-control growth characterizing oncogenesis.
But, debatably, perhaps not all of them are (e.g. extravasation in metastasis).
Obviously this seems very simplistic, but is there any literature thinking about it this way? Or directly debunking it?

Aside from anything else, your assumptions about multicellularity evolution seem off.  For example see The evolutionary-developmental origins of multicellularity (press-release version: From one cell to many: How did multicellularity evolve?)

While commending you for wishing to think about and discuss science, it has to be pointed out that this is question and answer site, not a discussion site. It is worthwhile reading the Help on What type of questions should I avoid asking to see why close votes are accumulating on your question. I would say it comes under the categoriy there of "there is no actual problem to be solved: “I’m curious if other people feel like I do.”" i.e. you are inviting discussion of an idea. Some other forum (Cynics?) may accommodate you.

@David I'm aware that this isn't a discussion site, which is why I asked specifically for literature. Thanks for your comment anyway though. I understand that the question is not exactly the cut-and-dry basic questions that this site seems to prefer. It may well be closed anyway, though I am not sure why it is so much worse than many of the other questions here....

Well, you seem to have changed your question and title now, and although I still think it's off-topic I'll leave things there. However I can't ignore the last sentence of your comment. Let me rephrase it: "Why pick on me officer? I wasn't the only one exceeding the speed limit. And some were going even faster."

Cancer and level of selection
Cancer results from the opposite action of different level of selection. There is selection on the population of multicellular individuals and there is selection on the population of cells within each multicellular individuals.
There is selection among cells within an individual for increase replication rate while there is selection among multicellular individuals in the population for controlled replication rate of their cells.
Major transitions
The passage from small unit of selection to bigger units is called a "major transition". Such transitions include the grouping of genes on chromosomes, the grouping of cells onto multicellular individuals, the grouping of multicellular individual onto colonies and, if there are several planets inhabiting life in the universe, then the grouping of life forms in every planet into a population of living planets. One can list other, more extreme or intermediate major transitions but there is quite a bit of debate on what really constitute a major transition.
Literature on the subject

[I]s there any literature thinking about it this way?

The keywords that will help search further information are group selection, kin selection, major transitions.
I recommend having a look at Major Transitions In Evolution by Maynard Smith and Szathmary and also The Major Transitions in Evolution Revisited by Calcott and Sterelny which is a book made of many small parts, each written by a different author on these same questions of level of selection.
You might eventually have a look at Evolutionary Dynamics: Exploring the Equations of Life  by Nowak as well.
These discussions of level of selection include discussion of what an individual is and what level is most important. The extremely popular and well written books by Dawkins will also bring you some light on the subject. Consider The extended phenotype for example.
For more book recommendations in evolutionary genetics, please have a look at Books on population or evolutionary genetics?.
If you like the sensation of thinking of the entire earth as an individual part of eventually a larger group of living planet, then you'll maybe enjoy having a physiological / ecological view of this living planet earth with Gaia by Lovelock


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What is the scientific name of this flying insect?
It looks like some relative of dragon fly.

To give an idea about its size I picked it by its wings

It had quite a flexible abdomen

I set it free after clicking the pics. I live in central India (If that matters)

Good on you for setting it free.

It seems that you were careful, but generally speaking try not to pick up insects by their wings, they are often the most fragile part and are one of the most essential for the insect's survival in many cases.

@ttbek OK I'll remember that!

@ttbek - that sounds nice in theory, but what else can you actually grab? Sure, for a hard beetle you can just grab damn thing by the body, but nearly everything else is too squishy for that.

@ttbek In general you are right, however dragonflies are about the only insects were it can't hurt to hold them by there wings (if done carefully off course).

Davor: I was wondering that I bit myself.... , but more in the sense of potential wing damage if one tries to hold on to somewhere else as they try to fly away.  The bodies are often not quite as squishy as you may imagine due the their exoskeletons, at least relative to the thin membrane that the wings often consist of.  Coyote Peterson often uses a special set of forceps for handling insects, and does grip them by the body this way, not a perfect reference but just from the top of my head for now.
RHA:  Yeah, dragonflies are pretty badass like that.

This insect is, indeed, related to dragonflies. This is a damselfly.
Damselflies are Odonata insects from the Suborder Zygoptera. Unlike dragonflies (Suborder Anisoptera), damselflies fold their wings when resting. This is the most noticeable difference between damselflies and dragonflies:

Regarding your specimen, I'd say that it is Caconeura ramburi, the indian blue bambootail. Here is an image for comparison:

The site where I found that image, conveniently called Odonata of India, is a good source of information.


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Where do all the NAD+s come from?
In the mitochondrial respiration (of plant cells) NADH is reduced from Nad+ as part of the TCA (converting malate to oxaleoacetate).
But where do the NAD+s come from?
The TCA cycle is working even in isolated mitochondrias by adding malate as a substrate, which indicates NAD+ must be present already.
I am also wondering if ADP and NAD+ can be transfered through the inner membranes of the mitochondrion without specific channels?

That NADH  (actually, NADH + H+) goes to the electron transport chain, donates the H+ and e- and comes back as NAH+. It's a cycle.

Reduce, reuse, recycle…

There is of course a pathway that synthesizes NAD+ de novo, usually from tryptophan, aspartic acid  or vitamin B3, or salvaged from compounds like nicotinic acid, nicotinamide. You can read more about it here: https://en.wikipedia.org/wiki/Nicotinamide_adenine_dinucleotide#De_novo_production
The fact that TCA works in isolated mitochondria is not necessarily the effect of de novo synthesis. The reason for that is the cycle-like fashion of NADH production in the TCA and consumption of that NADH for electron-chain reactions (which recreate NAD+) or other reactions involving oxidoreductases. Redox reactions do not change the overall amount of the coenzyme. But in a living cell, some reactions will irreversibly consume NAD+, ADP-rybosylation may be an example. Still, the cell prefers the salvage pathway over amino acid pathway, because it consumes way less energy.
ADP and NAD+ cannot pass through the membranes without channels. Both are polar molecules and only non-polar molecules such as steroids can freely pass through the cellular membrane without any help from transport proteins.


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Simple model of dendritic processing
[I striked through some passages that might be misleading, resp. where I have been misled.]
Is the following - very simplified - model biologically (or physically) plausible, explaining how spatiotemporal processing on dendrites works, especially how dendritic spikes and short-term potentiation modification of synaptic strength might work together? (I've read the wikipedia article on NMDA receptors but found it quite hard to digest. It's not a gentle introduction into the topic.)
Let the blue dots be two ligand- and voltage-dependent ion channels (eg. NMDA-gated channels) sitting on two synapses.
Let the green dot be a voltage-dependent ion channel that generates dendritic spikes.
Let the red dots be voltage-dependent ion channels that generate action potentials.
Without the green channel (generating dendritic spikes), two simultaneously synaptic inputs with depolarization V0 which sum up at the branching point of the dendrite would not suffice to generate an action potential:

But with it, two subsequent synaptic inputs (e.g. in two synchronous spike trains) would, because the postsynaptic response is stronger due to an additional voltage signal from the dendritic spikes.

At time  t2 another synaptic input and the dendritic spikes arrive at the blue channels. The resulting depolarization  V1 >  V0 suffices to evoke an action potential.

Is this picture correct in principle? Do such processes actually occur? Or are the real processes quite different? (Of course, they will be much more complicated and superimposed with other processes.) At least some NMDA receptors (which are ligand- and voltage-gated) sit on synapses.

You need to refine your concept of a dendritic spike. Perhaps you also then need to read about spike-timing dependent plasticity, and just replace backpropagating action potentials with dendritic spikes. Also note that you started by asking about plasticity but your drawings try to explain action potential generation. I think this confusion means that you need to better understand how synapses work and how they change.

@vkehayas: I didn't want to talk and ask about long-term plasticity, but only about short-term, maybe even ultra short-term "plasticity", i.e. potentation. But maybe I am misusing the term "short-term potentation". I explicitly did not want to "model" long-term potentation, but understand the short-term influence of dendritic spikes.

What I wasn't aware of is the existence of extrasynaptic NMDA receptors. This changes my picture a lot: non-synaptic ligand-gated ion channels? (Never heard of before.)

What we usually refer to as short-term plasticity has to do with pre-synaptic mechanisms. You don't necessarily need extrasynaptic NMDARs -and people don't generally consider this as the mechanism- in order to explain dendritic spike generation and synaptic potentiation through dendritic spikes (see REFs in my first comment). Having said that, this may prove interesting to you.

FYI, I found your previous question perfectly valid and interesting (it has a lot to do with what I work on). It's just that it's demanding and will take me a while to answer.

Allow me one specific question here (or would you mind continuing on chat)? In the wikipedia article on NMDAR I read "current flow through the ion channel is voltage dependent" (to explain that NMDAR is not only ligand- but also voltage-gated). Isn't this always the case, even for leak channels?

Let us continue this discussion in chat.

To whom it may concern: Any reason for down-voting is welcome! (Maybe too many and distracting edits?) Should I know the answer by myself (by carefully reading the literature)? But the literature is vast and not always gives a clear picture. Or is it about the form of my question (too much blah-blah)? Or is the question too speculative? (I would agree: it is speculative. But at least it is somehow precise.)


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Implanted neural recording system vs Electroencephalography
Can someone help me to understand why in nowadays the scientists develop implanted neural recording system to measure and collect neural signals? Why the use of the electroencephalogram is not sufficient to record neurons? Which is the difference between these systems?
Thanks in advance

EEG records a rough average of activity from a large area of the brain, because it is located far away from the actual neurons. There is no way to separate out the activity of individual or even small groups of cells; instead, you record lower frequency synchronous activity among whole populations.
Implanted systems can record from small groups or sometimes even single neurons, which greatly increases the amount of information available.
Depending on the purposes of the recording or research, EEG might be sufficient; in other cases, implantable electrodes are required. EEG is sufficient to monitor sleep/wake cycles, for example; there is no need to record intracranially to monitor sleep (unless perhaps you are studying mechanisms of sleep itself). Implanted electrodes are often used before surgery to remove parts of the brain that are causing seizures. Using ECoG (basically an "EEG on the dura" rather than on the skull) or depth electrodes allows the surgeon to know more precisely which area is causing seizures, hopefully leading to a more successful surgery and needing to resect less tissue.
Implanted electrodes are also commonly used in animal experiments to learn about how single neurons and small populations encode or process information.

Perhaps the OP was more likely referring to brain-machine interfaces, where recording from single neurons or populations may offer some advantages.

Perhaps; the answer is the same. I gave just two examples.

Thank you so much, Mr. Bryan Krause.Very good explanation!


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What type of worm is this?
Found this on the carpet in our office(North Carolina), no idea how it got there.
It is at between 8 and 12 inches long.

It looks desiccated and I think that's why it has this weird shape. Was it moving when you clicked this pic?

It was not moving.


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What is the name for when genetic deviation results in an organism that doesn't work?
There is a word for this, and it's escaping me. I want to reaearch more papers on it, but I can't find them or what the word is called.
It's typically used in the context of fitness and evolution. If there is a dead individual, it doesn't have a fitness and the mutation is called _____. ?? ( in some models could be given a zero or neg inf)

Hum... it is quite unclear for the moment. All individual have a fitness. Their fitness can be zero though. I am not sure what you mean by "genetic deviation". Do you mean a mutation? Are you looking for an adjective that qualifies a type of mutation, like a "lethal mutation" or maybe "recessive/dominant lethal mutation"?

Or are you looking for the term 'deleterious'?

LETHAL. That is the word. They are lethals. Hahah thanks!!!

If you are referring to the mutation
I think the word you are looking for is lethal.
A lethal mutation is a mutation that causes the death of its carrier. Now there are recessive lethal and dominant lethal. For dominant lethal mutations, all heterozygotes are inviable. For recessive lethal, only double mutant homozygotes are inviable.
If you are referring to the individual
An individual that is not able to survive and reproduce is said to be inviable (I already used the term above). However, the reason for it is not necessarily genetic.

lethal defines the mutation. I believe OP is referring to the whole organism (despite their comment, since the question in the title and in the body are different!)... If that's correct, the word I'd choose is "inviable", which is (almost) in your answer.

@GerardoFurtado Thanks, I attempted to clarify that lethal refers to the mutaiton. I also highlighted the use of the term inviable


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Wallace effect on human populations
Could sympatric speciation occur in humans, for instance, separating blue collar workers from white collar workers?

No, it won't happen
Even geographical isolation failed to allow speciation in humans (see Does it make sense to classify all humans in a single species?). So if there is some small reproductive isolation between working groups, it is definitely not going to be strong enough to cause speciation.
In an imaginary world
If there was strong reproductive isolation
In an imaginary world where there is a more important reproductive isolation that lasts for long enough between blue and white collar workers, sympatric speciation might be possible. Such reproductive isolation could be caused by very important social stigmas.
Wallace effect
Wallace effect is a type of speciation that is mediated by a reproductive isolation that has been selected for as fitness of offspring is higher when mating is assortative.
There is probably relatively little genetic predisposition to being blue collar or white collar worker. But in an imaginary world where there is very strong genetic predisposition to being a good blue collar or white collar worker, and where worker quality will affect income which will affect fitness, then yes, wallace effect could be a thing.
But really, we do not live in one of this imaginary world. In our world, speciation won't occur between blue collar and white collar workers.


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Resource for learning analysis of sequence data via QIIME 2
I am trying to study/learn metagenomics through 16s rRNA microbial data and I want to teach myself/review core biology concepts while also learning the QIIME 2 analysis pipeline, as the website suggests learning it instead of QIIME for beginners.
I found a great source : http://www.science.smith.edu/cmbs/wp-content/uploads/sites/36/2015/09/Tutorial-from-sample-to-analyzed-data-using-Qiime-for-analysis.pdf
but was hoping for something with an analysis I could actually work through on my own, as this one involves the use of a cluster, where as I only have access to a laptop of moderate power and also one that involves QIIME 2.
Also something free and maybe as hand-holding as possible would be ideal too.
As for the platform I am learning on, it is a virtual box instance of Ubuntu.

The QIIME 2 tutorials are the place to get started - see here.

So do you think those tutorials could take someone from layman to decent? I read on your profile that you teach bioinformatics so I am willing to take any other advice too. Thanks

They will teach you QIIME 2 without assuming much background knowledge. If you're new to the idea of studying microbiomes, you'll probably want some other resources too, possibly including Gut Check and An Introduction to Applied Bioinformatics. (Disclaimer: I'm involved in both of those projects, but all content is free.)


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How does natural selection explain how organisms that are poisonous evolved?
Natural selection makes perfect sense when describing the evolution of say camouflage. For example 2 bugs of the same species live on a tree. One is mutated to look slightly more like a tree, so the bird misses it and eats the one that sticks out more.
This logic seems to fail for poisonous animals though. For example, two bugs are equally visible but one has developed a mutation to be poisonous. Since they are both easy to spot they both get eaten. Now the poisonous mutation has died out. How does natural selection explain the poison mutation overcoming the initial hurdle?

@BryanKrause I don't think my question is a dupe of that. I'm asking how poisonousness becomes a species-level change, not why it happens at an individual level.

This should be informative, especially the section on evolution: https://en.wikipedia.org/wiki/Aposematism

@canadianer As a matter of fact what originally brought on this question was the Eastern Red Spotted Newt which has exactly these traits

There is a lot to say on this question. I will try to keep it short, to the risk of oversimplifying the problem. I can think of three main reasons:
1. Predation does not necessarily means death of the prey
Most of predation does not directly kill the prey. Typically herbivory, will often damage the prey but a single individual won't kill the prey entirely. In such systems, being poisonous may eventually either directly stop the predator (because the predator quickly sense it is poisonous or because the predator immediately dies) or will ensure that the predator remembers not to attack this same individual.
2. Kin selection
kin selection (aka. Group selection although there are a few authors who do not equate them), is selection above the level of the population of individuals (see also unit of selection; see this recent answer for some book recommendation on the subject).
In very short, under kin selection, an individual who dies of predation but can either cause suffering to the predator or just kill it, will protect its close relatives that live nearby from the same predator (who is iether dead or who may have learned to avoid these particular plants). As close relatives share of lot of DNA in common, a gene for toxicity - even if it fails to protect the individual being preyed upon - can protect the copies of itself present in the siblings of this individual.
3. Side effect
Let's not make the mistake of assuming that a trait has necessarily come to high frequency because it was selected for the specific purpose we associate this trait with. A plant may happen to become toxic for reasons that are unrelated to predation. While toxicity is often costly to the plant, it may sometimes eventually just be a by-product. Unfortunately, I would not be able to cite an example where toxicity is simply a side effect.


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evolution of advanced math ability
I am trying to convince a friend that human beings evolved from primates, and he challenged me that advanced mathematical ability couldn't have been the product of mutation and natural selection because this ability wouldn't have conferred any reproductive advantage until the last few hundred years, and the process of mutation and natural selection would have taken much longer than this to produce the extensive genetic basis of advanced mathematical ability. How do we refute this?

What is his definition of advanced mathematical ability?

I think, advanced mathematical ability is more an effect of the social evolution, that is a consequence of the brain evolution anyway.

Your friend is incorrectly assuming that all evolutionary developments directly contribute to the organisms success. Also, the burden of proof should [initially] be on your friend, and not you, for him/her to establish that "advanced mathematical ability" is even a relevant criteria to determine the plausibility of evolutionary behaviors to begin with. Lastly, as your friend mentioned, and which argues against their own case, is that mathematics is new, which could then very easily suggest that it's a recent emergent property of logic & reasoning, of which primates do [seem to] have.

Your question may be valid, but give up on thinking that you will convince your friend of anything. Believe me, it's a waste of time. In cases like this people believe what they want to believe — rationality or logic doesn't come in to it.

@David How come you voted to close if you think the question is valid?

@Remi.b  — I didn't say it was valid I said it may be (or may not be — understood). I voted to close because it was a request for debating ammunition which I do not consider appropriate to SE or ultimately useful for the OP. A pity, as your answer was interesting.

Mathematics is the queen of all sciences, of engineering roofs, of counting arrows, geometry of tools, counting days and reserves for travel, trading pelts, so all those survival skills benefit from increased maths and geometry. maths reasoning is qualitatively the same as geometry planning. not all humans are equal at programming, or have the same brain size, ask him why dolphins swim like dogs and breathe air and have milk, and treat him like a child with too many questions. maybe he will rationalize clearly one day.

Just to avoid misunderstandings
Just to avoid potential misunderstandings on your side, I wanted to talk about the saying that

human [are] evolved from primates

Humans are primates, so did our common ancestor with other primates.
Our ancestors are different from modern day primates. Chimps for example (which are great apes, like us) are not our ancestor more than we are their ancestors. We just share a common ancestor (who lived about 13 millions years ago).

Spandrel, exaptation and panselectionist arguments
Your are doing two mistakes. 1) The mistake of the spandrel (named after the title of the famous and old paper Gould and Lewontin (1979)) and the exaptation and 2) a panselectionist mistake.
1. Spandrel and exaptation
Spandrel

In evolutionary biology, a spandrel is a phenotypic characteristic that is a byproduct of the evolution of some other characteristic, rather than a direct product of adaptive selection

See also What is the “Spandrels” debate about?.
Exaptation

Exaptation [..] describe[s] a shift in the function of a trait during evolution.

While the existence of a spandrel in an evolutionary process does not necessarily cause the existence of an exaptation, but I will not go into these semantics details for simplicity.
Consider for example the two following wrong statements.

Birds have feathers to fly. It is impossible that birds evolved feather to fly because early feathers would have served no purpose to flight.

Bird feather actually probably first evolved for temperature regulation. Once this was done feathers were an exaptation for early flying tools.

Humans have nose to wear glasses. It is impossible that nose would have evolved because there was no glasses before

Noses evolved for another purpose and happen to be an exaptation for wearing glasses.

Humans have a big brain for advanced mathematical skills. It is impossible that humans evolved such big brains as such mathematical skills were useless in a time where we did not invent/discover much of the most basic math concept yet.

Humans evolved a big brain, mainly for social reasons incl. social hunting and social communication and probably because it was/is under sexual selection (see wikipedia > evolution of human intelligence). It just happen that logical reasoning, abstract thinking and other cognitive skills are an exaptation for advanced math skills.
2. Panselectionist view of evolution
I just want to highlight that there is much more to evolution than just mutations and natural selection. Not every trait has been selected for (otherwise we would not have any genetic disease).
On this subject, you might want to have a look at the paragraph Did you say Natural Selection? of this answer to Why don't mammals have more than 4 limbs? and to Why do some bad traits evolve, and good ones don't?

There is no such thing as "advanced mathematical ability" as a separate ability of the human brain. Advanced mathematical ability is formed by aspects of the general human intelligence. Given that not everyone is able to do advanced maths, it's a moniker for the high end of these aspects of human intelligence.
I can't give you a perfect description of all the aspects of human intelligence that are important for "advanced mathematical ability", but maybe a few examples will suffice:

The ability to abstract.
Reasoning by analogy.
Logical reasoning.
Spatial or geometric imagination.

All these abilities are pretty obviously useful, even in our far evolutionary past. Especially the first two abilities underly pretty much all our thinking.

Why did humans become increasingly intelligent long past what they needed to hunt prey? A large part of it is the intelligence needed to outfox other humans without being manipulated themselves. After language developed, we were our own greatest selective pressure. Indeed, no matter how smart we became because of this mechanism, it would continue to select for greater intelligence still to out-think the brains of the present. Going back to the spandrel point, the reasoning in mathematics may be a side-effect of this.

Thanks to B for posting this question -- I asked him to post it to biology.stackexchange, so that our interaction might be useful to others. My answer is a quickly-typed email but might be useful anyway.
My answer follows:
Hi B -- briefly, advanced mathematical ability WASN'T the product of mutation and natural selection.  Neither was writing, poetry, symphonic music, representative democracy, genius comedy, etc. etc. yadda yadda.
All of these cultural achievements are the product of a very long line of causes, very roughly,
A. general human physical and mental traits
B. hundreds of thousands of years of co-evolution of human brains, societies, and fundamental human technologies like the making of spearpoints, fishing hooks, clothes, rock art, etc. in stone-age, hunter-gatherer societies
C. farming and subsequent large, high-densities human societies
D. writing
E. well-organized governments, nation-states, and subsequent "space" for "high arts" (science, math, opera, whatever)
F. substantial economic and technological progress (better ship-building, international trade, the Mediterranean mercantile revolution before/during the Renaissance)
G. A long history of cultural development within each of the specialities in (E). Each of these began seriously building and expanding, generation on generation.  E.g. for math specifically, we only really got going seriously with the introduction of Arabic numerals, the idea of the numeral "0", etc., into the context of the European economic and academic structure, and their linkage to the general Scientific Revolution (e.g. the massive success of Kepler, Galileo, Newton etc. in applying math to physics and astronomy)
H. A concurrent massive expansion of organized, formalized educational system, ranging from childhood education through to university and postgraduate education
I. Massive growth in the human population, and generation of a huge leisure class, creating a relatively large number of people that can do advanced math.  Most of us still can't!
I suspect that advanced mathematical ability is roughly on a bell-curve.  Most of us have the aptitude/ability/focus to do things like counting, which would have been useful even in stone-age times, and which clearly exist even in animals.  It is relevant to know that you have better odds getting by 1 lion, instead of 10 lions.
The rest of the explanation of math ability is mostly due to the cultural factors above, which, through massive training (20 years plus for advanced math), take human's general counting abilities, language ability, good memory, etc., and produce mathematicians ranging from OK (like me) through to amazing (Einstein or someone).
Natural selection only has a role in explaining A and B.  The rest is culture, which (very slowly) built on humans' general intelligence, language ability, sociality, etc.
Repeat this explanation for any other remarkable cultural achievement.
And, anyone else wondering about evolution and some major cultural achievement, should ask themselves the following:

Can I myself produce a similar cultural achievement in the same area? Is everyone as good as Mozart and Einstein were in their specialties?  If not, why not?
For humans, language is easy, but any non-trivial math is hard.  But for computers, math is easy and language is hard.  Why is that?  Hmm, which one was useful back in the Stone Age?
Similar question: Why is math hard for most people?  Why is producing new advances in math basically always hard, even for extreme experts?

Cheers!
Nick Matzke
nick.matzkeATanu.edu.au


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Specific primer design
I'm designing primers for species-specific amplification (inside ITS1-ITS2 region). The problem is that when I blast (GenBank) my primer pair, the Forward primer anneals with some isolates (of the same fungus species that i'm targeting) that have one base polymorfism:
Ex:
Predicted Tm= 58-61ºC
product length = 189
Forward primer  1    TTCATCTCCGACTCGCATGT  20
Template        130  ........G...........  149
Reverse primer  1    GAATACCAAGGAGCACAAGGT  21
Template        318  .....................  298
My goal is to amplify only the 100% specific sequences. Would a higher annealing TºC be able to prevent this unspecific binding?
Question 2: The fungus species i'm targeting have isolates with a diversity of polymorfisms (deletions, insertions, one nucleotide substitution,..) and sometimes the predicted amplicon lenght may vary: 189bp, 190bp, 191bp. Will it be problematic for a RT-PCR quantification assay?
Thanks in advance

If your primers are not specific enough, you should design other primers. Try shifting a few bases upstream or downstream. Also, you can add a few extra bases to your primer, you can safely reach 68C as annealing temperature.
If you want your PCR to be able to distinguish a single base mismatch, then the mismatch should occur at the 3' of your primers, ideally one of the three last bases.
If your goal is just to quantify the initial DNA, then RT-PCR will be ok. But if you want to detect the composition of the different polymorphisms, then you should go for sequencing.

Q1: You need to provide more information. How much sequence identity is shared between your target and off-target? What is the purpose of your primers?
Generally, yes a higher annealing temperature would minimise mismatches - you could try a drop-down in T_a for increased specificity during the first few rounds of amplification.
Q2: I doubt it. The difference of 1-2bp is so small that it is highly unlikely to introduce bias.


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Pretty Flower Fungus in Oak Tree

Found this on a nature walk in the town of Lincoln, MA, USA. Is this edible? I believe it is a type of fungus.

It is not a good a idea to take advice from the internet about things being edible. Maybe ask for the species first and see whether there is consensus.

I believe it is a type of fungus.

Yes, this is a kind of fungus. Specifically, I believe it's of the genus Laetiporus sp., and is commonly known as "chicken of the woods" and "sulfur shelf". Notice that in both images the mushroom is growing on an oak tree.

Is this edible?

I strongly recommend that you watch this and this video. Collectively, they provide more than enough information on how to properly ID the fungus, how to harvest & cook, any potential look-alikes, and even possible medical applications.
IF my suggested identification of your posted organism is correct, then yes, it's edible.

aka , sulfur polypore.


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What is dendritic processing good for?
Can - on a very coarse level - the functional role of dendritic processing as a whole (at least one of possibly many functional roles it might play) be described as rewarding spatially coherent synaptic inputs when creating action potentials?
This would make sense, when the mapping of neurons to synapses was neighbourhood preserving (in the sense of topology): the efferent synapses of two neurons in close vicinity (in other parts of the brain) sit in close vicinity on the dendritic trees of their common target neurons.
Then it would be desirable, that when a group of $n$ neurons in close vicinity to each other (e.g. a nucleus) projects to a subtree of the dendritic tree (i.e. synapses in close vicinity) and those neurons are firing at the same time, this should evoke an action potential in the target neuron, but not, if $n$ synapses spread randomly over the dendritic tree are active at the same time. To achieve this could be the (or one) function of dendritic processing.
As I said: this is a very coarse level of description, and to be taken with some grains of salt.
(The whole question would break down if there is no such neighbourhood preserving mapping from neurons to synapses.)
References
I've read the following articles (but maybe not carefully enough to be able to pin them down to the short form above):

Buonomoano/Maass, State-dependent computations: spatiotemporal processing in cortical networks
Stuart/Spruston, Dendritic integration: 60 years of progress
Poirazi et al, Pyramidal Neuron as Two-Layer Neural Network (this article comes closest to the spirit of my question)
Magee, Dendritic integration of excitatory synaptic input

In lieu of a keyword for future google searches, the phenomenon you are describing is referred to as "synaptic clustering". I would rephrase the title of your question to reflect the main text into something like: "Is synaptic clustering reinforced by dendritic spikes?" Dendritic spikes can in principle have other functions as well, so your title suggests a more broad issue than what you are actually asking.

As you point out, a separate issue is if there is synaptic clustering, which is one of the 7 questions you asked here. Perhaps you should ask this in a separate question.

Is dendritic processing only done by dendritic spikes? In Rall's model there is dendritic processing but no dendritic spikes, isn't it? And I consciously didn't mention dendritic spikes.

It depends on your definition: dendritic spikes, NMDA spikes, NMDA plateau potentials. 'Dendritic processing' is better, my point wasn't to remove that part.

Action potentials are always based on coherent synaptic inputs. So dendritic processing means rewarding specific coherent subsets of synaptic inputs.
So to me it makes more sense to frame dendritic processing as allowing neurons to detect several different patterns (alternatively or at the same time).
In that case each dendritic spike encodes a different pattern. This allows a neuron to play roles (or maybe the same role) in several different contexts (or possibly in different combinations of contexts). If this is the case the neighbourhood mapping you describe doesn't have to exist (though it still might).

I added "spatially" to make clearer what I mean. BTW: How can a spike encode a pattern?

If a neuron always spikes when a certain pattern of other neuron activations occurs, this neuron's spike can be said to encode the pattern. The pattern is not encoded in the specifics of the spike, just in the fact of the spike.

So do you mean "dendritic spikes" (of which there are many) or "action potentials" (of which there is only one - in response to a certain pattern)? The latter is what I understand when a neuron spikes.

I mean that dendritic spikes encode for specific patterns, but these dendritic spikes may lead to the neuron spiking. So the neuron is able to encode many (combinations of) patterns.

This would be the second step of understanding. My question concerns a first step.


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T lymphocytes and HIV-AIDS
in studying maturation of lymphocytes into two different types-T LYMPHOCYTES and B LYMPHOCYTES. it is mentioned that if a lymphocyte matures in thymus gland it becomes T LYMPHOCYTE and becomes B LYMPHOCYTE if matures in bone marrow {bursa region}.
also HIV virus attacks helper t lymphocytes . I was thinking that if we could make the initial immature lymphocytes in thymus made outside in vitro  { like from stem cells or likewise from clone etc or some other alternatives} and then inject them in patient so as to overcome their deficiency .
is it possible?

The deficit here is that HIV invades and depletes arguably the most important immune cells you've got: CD4+ T lymphocytes. The concept behind your question is sort of like an expensive bandage you always have to get when your CD4 counts drop into AIDS territory. Does that make sense? It's like feeding the virus more host cells without addressing the virus.

@CMosychuk, my point was regarding replenishment of depleted t-lymphocytes. We have produced clones, we know about totipotency of cells. Also hiv virus should be given some other treatment. What do you think? Do make me aware about this. Thanks


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What kind of spider has colonised my timber framework?
I'm in the south east UK. I have a site I'm doing intermittent timber work on, that's been left idle for much of the summer. When I came back it has huge webs strung from walls to beams and across the open spaces, everywhere, with the spiders in this picture sitting in them.
At a a guess they are about 30 - 40mm across (maybe 25 when 'sitting' with legs curled at rest close to body?). They sit in the middle of the webs, not hidden at the edges. The webs are quite strong and look like they are durable, as webs go.
Any ideas?

You've encountered a very common spider, found all over holarctic.
Common names: European garden spider, diadem spider or cross spider
Scientific name: Araneus diadematus
link to wiki:
https://en.wikipedia.org/wiki/Araneus_diadematus
They can bite, but are hard to provoke.
If bitten it will feel similar to a wasp sting.
So nothing to worry about, unless you are allergic.
picture from underneath:

source: http://c8.alamy.com/comp/H45CTY/spinning-network-garden-spider-araneus-diadematus-bottom-side-animal-H45CTY.jpg
picture from above:

source: enter link description here


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Raw food diet digestion
I haven't really paid attention to the raw food diet and the claims of its supporters until now. A passage from this website says:

The basic premise behind preparing raw food is not to cook food above 118ºF. Cooking food denatures both the protein and the fats. So instead of your body using the food it simply stores it.”
  When food is cooked above 118ºF, 85% of the food's natural enzymes are destroyed. This forces your body to generate the enzymes necessary to digest the food. This results in partially digested foods that can clog the body's intestinal tract and arteries.

It's possible this passage, which is from a chef describing the main benefit of raw food diets, misquotes the chef or wasn't phrased properly. I am assuming that the chef is talking about plant-based foods, like vegetables and legumes, when she says food. But given what's here, I read this as:
'-When cooked food (food prepared above 118ºF) is eaten, denatured proteins and fats are not 'useful', other than fat (storage).
-Food has natural enzymes (and the speaker may be equating proteins and fats with enzymes?); they get destroyed by cooking.
-Digestion that occurs via the enzymes an eater creates are ... bad? Not as efficient as the enzymes that are 'naturally' in the food?
-Digestion via the enzymes that an eater produces lead to partial digestion.'
My shoddy recollection of biology class is that we produce saliva and related enzymes to break down food items we ingest, like a tomato cut from the vine. Those items will not produce enzymes within themselves that will aid digestion inside other animals that consume said tomato. Why would it?
My question is: do I have the wrong understanding of digestion? Should humans rely on the "natural enzymes" that are in uncooked plant food for digestion and good nutritional benefits?


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By what mechanism can two chromosomes fuse?
What condition(s) would likely exist which could cause 2 chromosomes in the newly fertilized egg of a placental mammal to fuse? Assume this is more likely than having the same chromosome pair fuse in an individual egg, as well as an individual sperm.

Chromosome fusions (as well as fissions and other changes) usually take place during cell division or pairing, therefore, it's very unlikely that two chromosomes will fuse in an already fertilized egg. If they do such, this egg would probably be aborted.
One factor that may lead to chromosome fusion is loss of thelomeric sequences (telomere = chromosome extremity) (O'Sullivan and Karsleder, 2010) - but probably not in an fertilized egg.

As I trashed a recent answer of yours, I felt like I had to show myself nice by adding a reference to this answer! +1


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Why are humans so variable in appearance
Most animals look almost identical to their peers. To distinguish lions we record the spots on their face; with whales we look at the blemishes on their tail or flukes. In other words, we have to try hard to distinguish one lion from another.
In the case of dogs, we have created many different looking breeds - but within each breed they look the same: one poodle looks very much like the next one.
On the other hand, with humans we have not only the different races (cf. dog breeds), but even within one race no two people are alike. And, not only are the faces different, the body shapes vary equally much. We use face and body shape (and voice) to recognise each other. Most other animals use smell or sound.
I thought the reason for our uniqueness might be that, with civilisation, we are not constrained us to look the same. However, even in hunter-gatherer tribes each person looks different from every other one.
So what is it in human evolution that made us unique in this regard? And, are we unique? I cannot think of any other species with as much variation as ours, but are there others?

This really isn't the case.  Humans do look pretty much alike.  Take for instance blonde Hollywood actresses: most are perfectly interchangable, and their male counterparts only marginally less so.  You only think humans look different because you have long practice (mostly unconscious) in recognizing the small differences between them.  Apply the same effort to studying e.g. dogs, and you will likewise begin to recognize the differences.

"Most animals look almost identical to their peers." That's our perception, not theirs.

Because we as humans are really really good at picking up small differences in humans and really really bad at detecting them in anything else.
Animals are often quite good at telling each other apart, far better than humans are, birds in particular are known for this. Just because you as a human are bad at it does not mean they are.
There is a pretty strong evolutionary pressure for humans to be able to tell other humans apart and not much of an advantage for being able to tell two lions apart. We need to be able to tell mates, rivals, relatives, and strangers apart easily. We don't need to differentiating one black bird from another.
We also spend a lot of time around other humans, so we are more familiar with their differences, but the same thing happens to animal researchers whale researchers who spend a lot of time around whales can easily tell two whales apart at a glance. this is also part of the reason some people have trouble telling individuals from a different "race" apart, they are to unfamiliar and uninterested to spot differences. Or the way a car guy can spot the difference between two models at a diffrence but someone else might not.
You see the same effect chimps can tell each other apart but can't tell humans apart, unless they spend a lot of time around humans then they can. They can also match voice to face meaning the can recognize both.
Then of course you have the fact you are focusing on vision, try to tell two people apart by smell and you will likely fail but a dog will have no problem with it. likewise many monogamous song birds can identify their mates from song along, just as we recognize others by voice, penguins are another example. Humans are very visual creatures so much of our identification ability relies on vision we see the same thing in other visual species, animals tend to use whichever sense are their dominant ones. Saying organisms are more visually similar because organisms with far worse vision than humans can't tell them apart by vision alone is simply an unreasonable conclusion.

I wouldn't say that humans are inherently bad at recognizing those small differences in other species, it's just that most don't invest the amount of effort needed to learn to recognize them - a learning we do unconsciously by growing up among humans.  But if you grow up on a dairy farm, for instance, you learn to recognize cows as individuals.

We are generally worse at recognizing difference in other species mostly by comparison because of how good we are at each other, there is an entire aspect of our neural processing keyed to notice things about faces.

I didn't say animals can't recognise each other; I said they use smell and sound, whereas we use vision. Is that the main reason for our variability?
I take your point about chimps. But, do they use vision or smell? Ignoring faces, what about body shape - is there an animal species with long/short, thin/fat, muscular/flabby individuals? But I suppose evolution will rule that out in other animals

@hdhondt if you had read the linked paper you wild see they are suing vision,, in fact the same portion of the visual cortex we use, size and robustness variation is quite common in animals it is by no means unique to humans. You are assuming a lack of variation that just isn't there.

@John: Maybe your neural pattern recognition circuitry only recognizes faces; mine seems to work differently.  But how is it determined that this is innate, and not simply a matter of practice training a general-purpose pattern recognition circuitry?  Because those who have sufficient practice can make the same sort of distinctions among animals, or inanimate objects.

@John that article only says they have a built-in "face filter" like us. The chimps were asked to "select the faces of unknown apes from other objects". That is not the same as proving they use vision to recognise each other. They may do so, but the article does not state that.

except there is no reason to evolve face recognition unless you are using it for identification, and I was refering to the pubmed paper not the nature one , this one.. https://www.ncbi.nlm.nih.gov/pubmed/18085867

@jamesqf If you want to ask this as a separate question I would be more than happy to go into it, there are well documented brain injuries that impair the ability to recognize faces without impairing the ability to recognize objects and vice versa, the fact one can be damaged without affecting the other means they are separate. The condition is called Prosopagnosia.

For those familiar with prosopagnosia, which results from damage to the fusiform face area (at the fusiform gyrus), one ought to also be familiar with the area not being exclusive for facial recognition (perhaps only initially in development) but that it is also recruited for visually discerning things that we spend time on: xray images in radiologists, chess positions in grandmasters, dog faces in dog breeders, recognizing shapes related to playing music on instruments in musicians, cars and birds in enthusiasts, etc!


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Is the famous singer Taylor Swift currently the most beautiful woman in the world?
Is Ms. Taylor Swift currently the most beautiful woman in the world? Is she even in the top 10 or even the top 100? And if not, who is currently the most beautiful woman in the world? I apologize if this question may seem stupid, but I believe it is on-topic because sexual attractiveness in animal species, including humans, falls within the province of biology.

No. She is not. I never knew who she was, but I looked on Google Images. I live in Russia and see women more beautiful than she in the street every day.

The answers that could potentially be received by this question will most likely be completely subjective. I would suggest that you instead explore how various cultures assess attractiveness, since this does vary by culture, to ultimately find a culture that would find Taylor Swift's characteristics most appealing. From there, you would then identify all other women who also share strong expressions of these features, to then attempt a ranking that would establish a #1 most attractive woman. But even then, this ranking would be specific to the culture. So no, she's most likely not. VTC.

If you go on dirty sites, your hypothesis is easily disproven

Remember the old saying about beauty being in the eye of the beholder?  Different cultures, and different individuals within cultures, have very different ideas of what constitutes beauty.  Consider the (IMHO overweight and flabby) "beauties" portrayed by Renaissance painters, for instance, or the apparently commonplace "butt enhancement" often reported in the news (when it goes wrong).
From a quick glance at Google Images, Ms. Swift is, to me, no more than moderately attractive.


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Half-life and production rate of ion channels
There are "not millions, not a few hundred...somewhere in between (some tens of thousands)" of ion channels in a neuron.
Given the number of ion channels per neuron, knowing the  half-life of ion channels allows to calculate the production rate of ion channels, and vice versa.
I am looking for estimates of tpyical half-lifes of ion channels, somehow like this: "not years, not seconds... somewhere in between" but with better upper and lower bounds: months, weeks, .... minutes, hours.
Alternatively: estimates of production rates: "not thousands per second, not one per second ... somewhere in between".
[I know, that all numbers - number of ion channels, production rates, effective half-lifes - can change over time for a given neuron - this may have to do with long-term potentation. So I am talking about neurons in steady-state over a period in which no long-term potentation takes place. But I guess this won't change the rough estimates I asked for too much.]

The rate varies with channels and channel subunits, and you can also distinguish between membrane half-life and degradation half-life, because channels can be cycled bidirectionally between the plasma membrane and internal membranes like the ER. For many (most likely all??) channels these processes are under the control of phosphorylation and/or ubiquination.
For a rough estimate of magnitude though, the relevant time window is hours to days. I'll include a couple references below to support this time frame.
References

Bedford, F. K., Kittler, J. T., Muller, E., Thomas, P., Uren, J. M., Merlo, D., ... & Moss, S. J. (2001). GABAA receptor cell surface number and subunit stability are regulated by the ubiquitin-like protein Plic-1. Nature neuroscience, 4(9), 908-916.
Colley, B. S., Biju, K. C., Visegrady, A., Campbell, S., & Fadool, D. A. (2007). Neurotrophin B receptor kinase increases Kv subfamily member 1.3 (Kv1. 3) ion channel half-life and surface expression. Neuroscience, 144(2), 531-546.
Huh, K. H., & Wenthold, R. J. (1999). Turnover analysis of glutamate receptors identifies a rapidly degraded pool of the N-methyl-D-aspartate receptor subunit, NR1, in cultured cerebellar granule cells. Journal of Biological Chemistry, 274(1), 151-157.


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Glia/Neuron ratio
Research seems to indicate that the further we go up the evolutionary ladder, the higher is the glia/neuron ratio, to the point that in humans glial cells conforms 90% of the brain.
Now, if the glia/neuron ratio is somehow related cogntive capabilities (considering it is higher up in the evolutionary ladder), and since the ideal of a brain made solely of glial cells and no neurons seems absurd, how high can the ratio glia/neuron get before it starts to be detrimental?

TL;DR The glia-to-neuron ratio is not sufficient in order to distinguish humans from other primates or mammals.

The figures of the glia-to-neuron ratio (GNR) being 10:1 come from old studies that either used guesstimates for the number of cells in either category or used methods that have since been improved. The newest estimates range about a 1:1 ratio for the whole brain as reviewed in von Bartheld et al. 2016. These authors comment on the evolution of the GNR:

[Comparative studies have] shown that brain size does not scale universally
  with neuron number, that different mammalian species
  such as primates and rodents scale differently, that cell
  numbers in cerebral cortex and cerebellum evolve in a
  coordinated fashion, and that glia density and sizes
  vary much less than neuronal density and sizes. The
  GNR is highly conserved between structures and species,
  pointing to an important and close regulation of
  glia numbers (scaling) in response to, or regulated by,
  neuron density and neuron sizes.

At least in the cortex, cell numbers and size are kept to a minimum, as they take valuable space from what really matters, dendrites and axons (Chklovskii et al. 2004).


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Distribution of dendritic spike generating ion channels on the dendritic tree
Is there evidence that dendritic spike generating ion channels are distributed unevenly on the dendritic tree, with higher density near the branching points of the tree than along the unbranched segments? Or the other way around? Or is there no observed correlation between density and local geometry of the tree?
If there is, i.e. if those channels tend to condense near branching points: which mechanism drives them to do so?
[I believe it could make sense to have the spike generating channels condensed at branching points: there they could act as local logical gates, summing up the inputs of the afferent branches (see Poirazi et al, Pyramidal Neuron as Two-Layer Neural Network).]
[There is also a figure in Larkums article on A cellular mechanism for cortical
associations in which at least one electrode is placed close to a branching point. Maybe because there are extraordinarily many spike generating channels?]

Larkum is likely recording near that branch point because they are trying to record potentials in the distal dendrites, but the technical ability to patch those very distal dendrites is incredibly more difficult than patching the large apical dendrite.


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Are Richard Lynn's estimates of African IQ inherently innacurate on the basis that most Africans aren't mentally retarded?
I've been looking at Richard Lynn's studies on average African IQ, and he seems to estimate really low IQs in the 60s range (e.g. http://www.sciencedirect.com/science/article/pii/S0160289609001275?via%3Dihub).
However, is this inherently wrong, as somebody who would score that low in a Western country would no doubt be mentally retarded (and this isn't the case for most African people)?

The study has been heavily criticized e.g.
Wicherts and his colleagues examined over 100 published studies, concluding that there is no evidence to back up Lynn's claims. Amongst other flaws, Lynn used selective data by systematically ignoring Africans with high IQ scores (Controversial study of African IQ levels is 'deeply flawed')
Lynn replied to the criticism but not at all convincingly. No one seems to have taken him very seriously outside of racist hacks looking to support their bigotry

I am not sure this really is a biology question. Sounds more like a question of social demography.

IQ is just a measure of how good you are at taking IQ tests, that's it. Those tests are usually culturally biased towards middle income first world citizens (among other things). Think of it this way, questions about mortgages, supermarkets, airplanes, or such thing presuppose the person being questions knows a reasonable amount about those things, this is not a reasonable assumption in many places around the world.
The classic "a train leave chicago at 10:00..." is a perfect example since the reader needs to know what a trains is, that chicago is a place, and what 10:00 means additionally they need to be familiar with reading exact measures of time and velocity, that they have already been taught basic math, are familiar with abstract questions, and that they are experienced readers, these are all fine assumptions for the New York suburbs but pretty bad ones for sub saharan subsistence farmers.
People who try to write the questions for said cultures often run into the reverse problem, we think of travels as a steady rate but to people who travel by boat know allowances need to be given for things like the speed the stream is moving, or the paddler taking breaks for lunch, information the writer may wrongfully assume or not understand. I recall a question about two people traveling along the same road that was consistently wrong because people in that culture thought is was proper for the faster person to slow down to match the slower for the safety of both (the norm in said society) so they constantly calculated their speed as the same, something the writers never anticipated.
There are millions of these differences across cultures and these cultural differences quickly snowball in to large differences when taking identical tests. So you are not seeing a real difference in intelligence just an artifact of culturally biased testing.

+1 That and when the metric becomes the goal, it's no longer a good metric.

Yeah, it's like trying to judge my intelligence by asking questions about TV shows or popular music - to which my answers would be a universal "Duh?" :-)

How do you define being "mentally retarded"? In order to minimize the difference in measured IQ that might be due to people growing up under different circumstances in different cultures you could try to measure how people with different ethnic backgrounds achieve in a multicultural society. Citation from a paper regarding school results in Florida, USA:

The number of ill-prepared students in Florida remains troubling, as
  do the differences by race and ethnicity: 38 percent of black students
  currently read at grade level. That compares with 53 percent of
  Hispanics, 69 percent of whites and 76 percent of Asians.

http://www.maswired.com/florida-lowers-standards-for-latino-black-students/
Obviously being able to read at some level does not have to correlate with IQ in a simple fashion and people in Florida who are reported to be "white" or "black" might have a mixed ethic background. I do not know if any large scale investigations trying to link IQ with ethnic background in countries such as the USA are done, as the subject might be deemed as controversial. If there are differences in school results, SAT-scores etc. that might at least give you a hint of how large the differences between different ethnic groups might be.

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


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Seizures and blood pressure
A seizure is basically a synchronized firing of neurons as opposed to the more common unsynchronized firing taking place during normal neural activities. However, I am uncertain if the exact technical definition of a seizure restricts this synchronized nerve activity to the brain only .
I wonder whether a wave of synchronized firing can propagate up to or occur in the area of brain controlling the blood pressure level and hence affect the blood pressure of the individual going through a seizure? Or can the impact of a seizure propagate to other areas and hence affect other functions like cardio-vascular system and hence the blood pressure? Or can neurons connected to heart, but not necessarily present in brain, exhibit synchronization as in a seizure and thereby affect the blood pressure of an individual undergoing seizure?
Summarizing my question is: can seizures affect blood pressure?

Yes, seizures can affect autonomic function including blood pressure. Such symptoms can even result in death. Note though that not all seizures are the same: there are many different types with many different causes, and they can affect different parts of the brain. There can also be different effects before, during, and post-seizure.
The effects described seem to be more related to overall discharge rates rather than synchronous firing in the periphery per se. The autonomic nervous system does not directly control heart rate, for example, but rather modulates the rate. The heart beat or vasculature would not entrain to any sort of seizure activity, for example, because the neurotransmitters involved in autonomic regulation of heart rate and blood pressure are comparatively slow-acting relative to the rate of seizure activity (essentially those functions are taking a moving average of neural input, rather than responding specifically to each impulse).
The relationship between autonomic function and seizures need not be unidirectional, either; circulatory changes can also be triggers for seizures.
References

Devinsky, O. (2004). Effects of seizures on autonomic and cardiovascular function. Epilepsy currents, 4(2), 43-46.
Nei, M. (2009). Cardiac effects of seizures. Epilepsy currents, 9(4), 91-95.
Penfield, W., von Sántha, K., & Cipriani, A. (1939). Cerebral blood flow during induced epileptiform seizures in animals and man. Journal of Neurophysiology, 2(4), 257-267.

Thanks a lot . Does this kind of synchronous firing occur in neurons in any other part of the body ,other than the brain ?

The brain has some network architecture that isn't really found elsewhere. You could possible make some analogies with fibrillation in the heart, but the actual structure and causes are completely different. In other nervous tissue like that of the gut, a particular synchronous rhythmic pattern is important for gut motility and digestion, and you can certainly have cramping that occurs with overly synchronous activation along a stretch of gut tissue, but again, the networks aren't constructed the same as in the brain so I think it would be a distant analogy at best.

So no known cases where a synchronous oscillation of brain propagates to other neural networks ?

I'd hesitate to say "no known cases" - that's a pretty big leap that I can't make (hard to prove a negative), certainly you can have rhythmic clonic muscle activity in seizures, so does that count? It just isn't how the CNS is coupled with autonomic functions that makes me think it's unlikely you would have that sort of propagation. Like if you were driving a car and rhythmically pump the gas quickly, the car is going to speed up fairly continuously, because the engine doesn't respond immediately to the accelerator press and the velocity doesn't respond immediately to the engine.