text:
Change of DNA concentration due to restriction digest?
Assume that you perform a restriction digest in a molecular biology lab: you combine genomic DNA, a restriction endonuclease (e.g., EcoRI), and the optimal buffer for that endonuclease and are about incubate the reaction at the optimal temperature for the endonuclease (e.g., 37 C).
Before you incubate the reaction, you measure the reaction's DNA concentration via a spectrophotometer. Then, you incubate the reaction for one hour and, afterwards, measure the DNA concentration again via a spectrophotometer again.
Q: Has the DNA concentration of the reaction changed through the restriction digest?
Most people would argue that the overall DNA concentration does not change due to the restriction digest, whereas the fragment distribution does, with the average fragment length decreasing through the digest. However, every time I have run this experiment with my students, we have observed a slight increase in the DNA concentration after the restriction digest. What could be the reason for this observation?

Did you clean up the reaction before the measurement? Have you tried running samples on a gel to make an estimation via a comparison of the bands?

@Chris Yes, we did both: after the restriction digest, we purified the DNA (i.e., removed any enzymes or other confounding components) via magnetic beads, and we compared the DNA fragment sizes before and after the digest via an agarose gel electrophoresis. The gel electrophoresis clearly showed the results of the digest: bands with smaller lengths than before the digest.

Summary
The poster wishes to know why spectrophotometric readings (presumably absorbance at 260 nm) on a sample of genomic DNA from an unspecified organism appear “slightly” greater after incubation with a restriction endonuclease, EcoRI. Assuming trivial explanations can be excluded — the effect is not statistically significant or results from components of the added enzyme preparation — it is evident that, under these conditions, absorbance measurement is not a measure of the concentration of DNA. The change would reflect an effect of the change of structure of the DNA on the absorbance, either as an intrinsic difference between intact and linearized species, or in their ability of the two strands to separate (melt) at the temperature and ionic conditions employed. Suggestions are made for cheap and simple experiments to clarify the situation.
More Detailed Consideration
Let me consider some different possibilities in turn.

The readings do not actually show a statistically significant difference.
The poster cites neither the magnitude of the effect nor the results of statistical tests done to show that the increase is significant. Without the latter we cannot be sure that there is any question to answer, and without the former we cannot judge whether a particular explanation could account for the observed change.

An increase in absorbance results from something in the preparation of restriction enzyme added. The poster argues against this on the basis of purification following the reaction, but more direct experiments are both possible and preferable. Comparison could be made between the reaction mixture at the end of the incubation and at the start, or after incubation with inactivated enzyme, and other controls are possible. A time course of the values of absorbance throughout the experiment would be useful to see whether the increase in absorbance correlated with the cleavage, as judged by the electrophoretic behaviour of the products.

DNA is being created during the experiment.
As the law of conservation of matter has been shown to hold at the molecular level, I reject this possibility. The obvious conclusion is then that ultraviolet absorbance is not a valid measure the amount of DNA, especially when comparing DNA of different structural forms. This point is developed further in 4, below. The question can be resolved by using an alternative method to measure the concentration of DNA — preferably a chemical method that is not affected by the physical form of the DNA†.

“When you have eliminated the impossible, whatever remains, however improbable, must be the truth.”
[Sir Arthur Conan Doyle — Sherlock Holmes]

The change reflects a change in the ultraviolet absorbance properties of different structural forms of DNA.
It has long been known that on heating double-stranded DNA so that the strands separate (melt) the absorbance at 260nm increases: the hyperchromic effect. This is thought to reflect the greater energy required for the π→π* transitions in the aromatic bases of double-stranded DNA, where the base stacking involves π–π interactions. It seems to me most likely that the changes observed reflect a change in the spectral behaviour of the bases in the DNA after the structure has been changed by cleavage into small fragments. This could conceivably be an intrinsic difference between the linear cleavage products and the original form of the DNA (supercoils etc.), unfortunately not specified in the question. I am not aware of reports of such differences, but this does not mean that they do not exist. Alternatively ‘melting’ of DNA could be occurring at the temperature and ionic strength used in the reaction, and the supercoiled or higher-order structure of the undigested DNA might be hindering strand separation and suppressing the hyperchromic effect.
In relation to the latter possibility, experiments are required with linear DNA (in the absence of enzyme) to see if there is indeed a hyperchromic effect on heating to 37C at the ionic conditions used. I would suggest three other main lines of approach to clarifying the situation. The first would be to employ different types of “genomic” DNA — animal, bacterial, viral, plasmid — in the digestion. The second would be to do a clean structural comparison without restriction enzymes. Plasmid DNA can be separated by gel electrophoresis and the supercoiled and linear form extracted. The spectrophotometric and chemical ‘concentration of DNA’ could be compared in the two cases, as could be their maximum percentage increase on melting at increasing temperatures. The third would be to
prepare linear DNA of different sizes, using either different restriction endonucleases or non-enzymatic physical shearing of the DNA. Indeed, experiments with sheared DNA would exclude the possibility of effects from the endonuclease preparations and allow experiments at temperatures and ionic strengths not possible with the latter.

Of course this is not Sherlock Holmes’ “all that remains”, as I am mindful of Shakespeare’s:
“There are more things in heaven and earth, Horatio,
than are dreamt of in your philosophy.”
[Hamlet]
Concluding suggestion
I would respectfully suggest that questions of this sort are framed in an explicit manner that clearly distinguishes between what was done, what was observed, and what conclusions were drawn.
––––––––––––––––
† This is something of a problem as the only chemical method I am aware of is the diphenylamine method, with the advantage that the reaction is with the deoxyribose ring. However this is several orders of magnitude less sensitive than spectrophotometric methods. The fluorometric method suggested in another answer depends on the interaction of fluorophore with the bases, and its access could well be different for single-stranded and double-stranded DNA.

As you did a clean up, then you lost some DNA in this process. There are always losses from clean up steps.
Note also that spectrophotometry is notoriously unreliable for DNA quantitation; it's more of a "there's roughly this amount of DNA there" sort of reading, especially as they are particularly prone to organic compound contamination (e.g. guanidine, phenol from your extraction) throwing your reading off. Interestingly, the original use for 280 nm measurement for DNA was for determining DNA contamination in protein samples. Have a look in Sambrook's Molecular Cloning: a laboratory manual for further detail 1.
If you want a more reliable reading, then you should use something like a fluorophore that is known to bind at a certain ratio to the DNA, as these are less prone to contamination problems and are more sensitive2.
Refs:

Sambrook, Joseph & Russell, David W. (David William), 1957- & Cold Spring Harbor Laboratory. (2001). Molecular cloning : a laboratory manual / Joseph Sambrook, David W. Russell. Cold Spring Harbor, N.Y. : Cold Spring Harbor Laboratory

Green MR, Sambrook J. Estimating the Concentration of DNA by Fluorometry Using Hoechst 33258. Cold Spring Harb Protoc. 2017 May 1;2017(5). doi: 10.1101/pdb.prot093567. PMID: 28461657.


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What is the fundamental difference between human genome and other genomes that makes human a self-conscious living organism?
DNA is considered to be the blueprint from which any organism can be created.
DNA carries the genetic information to construct a living body. DNA carries genes which represents the information that is used to produce proteins which operate and shape the body. So what exactly is the difference in human genome which sets it apart from other species
and makes it self-conscious ? Are there specific genes for self-consciousness that makes a particular animal conscious ?

I have edited your (naive) question, replacing your misuse of "genetic code". See the Wikipedia entry to get the answer to what the genetic code is. The secret of conciousness, you won't find an answer to.

DNA is considered to be the blueprint from which any organism can be
  created

It's the main blueprint, true, but in order for DNA to be functional it needs a complex composition of proteins, ions, membranes, sugars etc.. You know, all your cells have the same DNA, yet they all are different!
A friend of mine, a leading expert in stem cell manipulation, is even struggling to force a single differentiation of his stem-cells. So no, no one can create an organism solely from it's DNA.

So what exactly is the difference in human DNA which sets it apart
  from other species and makes it self-conscious ?

The building blocks of DNA, the 4 nucleotides, are the same for all living organisms.

Is there a specific gene for self-consciousness that makes a
  particular animal conscious ?

The interaction of genes is way to complex to point out a single most relevant gene responsible for consciousness. There is not a single gene that functions without the others. Anyways, the human brains function is heavily dependent on it's structure; the physical connection between cells. So if you want to search for genes that are involved in consciousness I would look at the group of structure/differentiation controlling genes. For example NOTCH2NL was found to be involved in control of the brain size. (The Notch protein family is involved in developmental differentiation and acts through cell-cell contact)

Biritsh Scientists have successfully created a new organism 'Syn61' from recoded genome. You can refer article published in Nature [https://www.nature.com/articles/s41586-019-1192-5.epdf]. So its possible to create an organism from its DNA.

@chaitanyabudkule: You've misunderstood that paper — they replaced the genome of a strain of E. coli with a synthetic version.  This would not work without the "machinery" (proteins, RNAs, membranes, metabolites etc.) present in the "host" bacterial cell.

While we likely do not know exactly what constitutes consciousness, we can likely surmise that other organisms are conscious (or at least show what we might call self-awareness), and we can probably agree that the brain (or at least a nervous system) is an organ critical to developing and maintaining consciousness in an organism. The Hox family of genes (and their associated DNA sequences) guide the orientation of embryonic cells and the subsequent development of the brain in most eukaryotes, including humans. Cites of relevance: 1) https://en.m.wikipedia.org/wiki/Hox_gene 2) https://www.ncbi.nlm.nih.gov/m/pubmed/20795329/ 3) https://en.m.wikipedia.org/wiki/Self-awareness#Animals

DNA may be the blueprint, but - like the blueprints used in construction - it does nothing without a whole bunch of complicated machinery, which we call a parent.

I don't know what your comment means, I'm sorry.

It means that if you have a string of DNA, it basically won't do anything unless it's imbedded in a cell.  And it has to be a cell of the proper sort.  Unless I've totally misunderstood biology, if you want to make a frog, you have to put the frog DNA in a frog egg cell.  If you put it in say a rat egg cell, I doubt if you'd get anything viable - though it might make an interesting experiment.  It'd be like handing the blueprints for an airplane to a housing construction crew :-)

I don't know what your comment means in the context of genomics or developmental biology, which is the crux of the question. If you have a better answer, please post it separately.

Nothing! If DNA is one way of doing life–which is not well defined–it has shown that in all its forms it has been creating organisms with some form of intelligence. If you can accept that there can be different levels of consciousness and intelligence, then it may almost be easier to ask which organisms have zero consciousness?
Here's a video showing that plants have intelligence in that they respond to current events and plan responses for the near future. Plants have their own kind of nervous system from Science Magazine.
Clearly, it must be like something to be a plant.

When you look in the mirror, you see yourself. That puts you in the company of animals like dolphins, elephants, chimpanzees, and magpies, all of whom have shown the ability to recognize their own reflections.
The mirror test is often used as a way of measuring whether animals possess self-awareness. Some fish have recently passed the test, which has left scientists confused about limits of "self consciousness".
https://en.m.wikipedia.org/wiki/Mirror_test
Other animals have far less of it, and it correlates with logical thinking and intelligence too. It's like a side effect or component of animal intelect and wit.
DNA codes intelligence hardware and number of neurons, just like number of teeth and pilosity. On the next hyperlink theres info about 22 genes for intelligence and "dna for brain volume"
Intelligence is the key to human survival since 500+ billion years:
Making spears, fire, tools, clothes, and avoiding death from other monkey tricks.
DNA of brain size and logical ability has incrementally been sharply selected and increased for humans.
https://www.google.com/search?ei=xP68XZfAEcLggweFsqTwAQ&q=intelligence+dna
Theres even articles on logic gates within DNA. Self-concious often signifies introverted emotion, so it's rarely used in biology journals. Self-aware is used in animal psychology tests, and is relative / not an exact science.

Are there specific genes for self-consciousness that makes a particular animal conscious ?

The mechanism of self-consciousness in the brain (in the cortex) is separate from the formation of the brain which is separate from the genetic control of the brain development. You want an answer for the genetic control of the brain development (cell differentiation, embryonic development) that will explain the mechanism of self-consciousness at the same time.
So; the short answer is "No, there are not".
It is clear that consciousness is the product of a brain structure which is made of complex connections between a high number of neurons. These neurons are formed and construct an organ (with other cell types) in the process of embryonic and fetal development. Neuron formation, placement and connection is influenced/guided by some genes. But that does not mean that "a couple of genes carry the information to construct a brain". Genes control the cell, not the organ. Genes affect the cell structure and cell's operation; cell structure and cell's operation affects the organ development; organ's structure affects its functions and products.
Some reading on organ development can be helpful to understand this point (for example; Forces shaping the Drosophila wing).
But, if you refer the genes which guide the brain development as genes that create consciousness, then yes, there are consciousness genes. But, of course, this won't solve anything.

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text:
How much of the Neanderthal genome is living on in humans?
I've understand that outside of African, most ethnic groups carry some (4% or less) Neanderthal DNA.  So en masse, across all living humans, what percentage of the original Neanderthal genome is still alive in human decedents today?

I think this question is meaningless. What is the point of calculating an average? It's as useful as calculating that on average people have one testicle.

Isn't it more than 90% same. All mammals have a lot of same genes. Neanderthal belongs to same genus even. So, answer needs to be more than 90%. There  can be just 1% difference in any homosapien gene population.

Even though individual humans only have around 2-5% Neanderthal genome, it's not the same 2-5% across people. In total, at least 20%, and perhaps as much as 40% of the Neanderthal genome could be recovered from modern human populations:

We identified Neandertal lineages that persist in the DNA of modern humans, in whole-genome sequences from 379 European and 286 East Asian individuals, recovering more than 15 gigabases of introgressed sequence that spans ~20% of the Neandertal genome

--Resurrecting Surviving Neandertal Lineages from Modern Human Genomes
However, there are stretches of the human genome that are almost completely devoid of Neanderthal genes. These include male-fertility associated regions (leading to the suggestion that male sapiens/neandertalis hybrids may be been subfertile or sterile):

Genes that are more highly expressed in testes than in any other tissue are especially reduced in Neanderthal ancestry, and there is an approximately fivefold reduction of Neanderthal ancestry on the X chromosome, which is known from studies of diverse species to be especially dense in male hybrid sterility genes. These results suggest that part of the explanation for genomic regions of reduced Neanderthal ancestry is Neanderthal alleles that caused decreased fertility in males when moved to a modern human genetic background.

--The genomic landscape of Neanderthal ancestry in present-day humans
And some brain-specific regions (suggesting that those are uniquely human):

Regions depleted of archaic lineages are significantly enriched for genes expressed in specific brain regions ... A large region depleted of archaic sequence spans 11 Mb on chromosome 7 and contains the FOXP2 gene (Fig. 4B), which has been associated with speech and language

--Excavating Neandertal and Denisovan DNA from the genomes of Melanesian individuals

I see the "~20%" in the quote, but where does the "as much as 40%" come from? Was that related to "Coalescent simulations for a broad range of admixture models suggest that 35 to 70% of the Neandertal genome persists in the DNA of present-day humans (figs. S1 and S2)" from that paper?

The comment from Anubhav Goel below the question is a good one, presumably that 20% is the proportion of the Neanderthal exclusive DNA in their genome that isn't shared by practically all humans .. so 20% of something like 1%, would that be right?

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What's the lowest atmospheric pressure a tardigrade can remain active in?
I'm not asking what atmospheric pressures they can survive (we now they can survive the vacuum of space) I'm wondering at what point a deficit of atmospheric pressure would cause them to enter one of their various states of metabolic suspension.


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RNA-Seq library normalization and experimental setup
I'm working on an RNA-Seq project and I am trying to figure out library normalization.  I'm aware of using the geometric means (e.g. cuffdiff) of the fpkm for the normalization.
However, I was wondering why people don't add some unique, known RNA sequence of known concentration into their sample prior to amplification.  Then after sequencing you would have some known measure by which to normalize your fpkm. I would think this would also be a way to minimize batch effects.
Is there a technical reason why this isn't done?

People do do that. Google "ERCC spike-in probes"

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Enzyme kinetics: Effect of immobilization on kinetic parameters
What is the typical effect of enzyme immobilization on the kinetic parameters of an enzyme's activity?
Can one assume that they'd stay approximately the same or is there a gross change? Any way to estimate the effect?
The native parameters are as follows:
kcat    0.5 1/min
Km      0.6 microM
[E0]    5   micro M
[S]     60  micro M

Could I expect to retain them after immobilization? Or are these too high for an immobilized enzyme?
If it matters, it is a 500 residue enzyme with a MW of approx. 65,000 Da

The main factor influencing the kinetics of immobilized enzymes is thought to be the rate of diffusion of substrate and product towards and away from the enzyme, respectively.
This has been discussed on ResearchGate and an article in Process Biochemistry from one of those in the discussion quotes figures for effects on immobilized laccase: approx. 100x increase in Km and 2–5x reduction in Vmax (as noted in the poster’s comment).
There are several theoretical treatments of the question:

http://www1.lsbu.ac.uk/water/enztech/summary3.html
http://link.springer.com/article/10.1007%2FBF02460071#page-1
http://www.amazon.co.uk/gp/search?index=books&linkCode=qs&keywords=9780849369872

Thanks! Those are great links. What I'd have loved to find was a study of the sort where someone had taken a bunch of enzymes, immobilized them and reported on the change in activities.

This snippet from your link is sort of what I wanted: "As expected, after an immobilization process, the apparent Km and Vmax values are significantly affected. In literature, for example, the Vmax value for immobilized laccase compared to that of the free enzyme is reduced of about 2–5 times compared to the free enzyme, due to substrate diffusion to the catalytic site, with an increase of Km value. The increase of Km can be explained as a result of diffusional limitation of the substrate or to conformational changes of the enzyme resulting in a lower affinity of the substrate for the enzyme"

Glad the links were of use. I'll flesh out my answer on the basis of your comment to improve it.

Did you get a chance to flesh out your answer? Any tips would help  a lot!

Sorry, just the reference. Been busy as was preparing to leave for a week. Currently en route to the French Alps.

Well! Lucky you! :)

Think of it as dedication to science. Effect of exercise at high altitude on human biochemistry.


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Is it possible to clone a Neanderthal?
As Neanderthal DNA has been sequenced, is it possible to create a living Neanderthal?

Not any time soon.  By far the greatest challenge is getting the DNA sequence from the computer into a form that could be implanted into an embryo.  Craig Venter's team was able to build a bacterial genome from scratch, but that was incredibly painstaking work, requiring the assembly of many small fragments of DNA into a single circular chromosome.  With current technology that process becomes prohibitively difficult for a human-like genome.  You would have to build each chromosome from scratch, these chromosomes are linear, and you'd need to associate with them the various histones and other proteins help tightly fold them together.
Another huge problem is epigenetics.  The next generation sequencing methods used for the neanderthal genome just give you DNA sequences, not what epigenetic modifications are present on that DNA.  Genomic imprinting in mammals is very important, and presents problems even in normal cloning efforts where genomes are taken wholesale from live animals.
Not to mention that 1% of the current genome is contaminated with human DNA (not meant as a criticism, its amazing what they have been able to do with a toe bone if this work stands up to peer review).
And none of this takes into account the ethical problems associated with this.  Would you clone it in a human?  Chimp?  Either way its got serious ethical questions.
Dont take my word for it though, here is the leader of the project commenting on this question a few years ago:

Paabo said because the Neanderthal DNA was scattered in imperfect
  fossils, the notion of cloning a Neanderthal was far-fetched.
"Starting from the DNA extracted from a fossil, it is and will remain
  impossible," he said. "There is not really an improvement on current
  technologies that would make that possible.


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What ecological niche do disk shaped fish exploit?
I looked up "Early Triassic" to get a sense of what that meant and I ended up on this image of marine life at the time. I noticed some disk shaped fish (#8 in the picture:  Bobasatrania (durophagous actinopterygian)) that looked, to me, like Permit or a Sunny.
I wondered, what ecological niche are disk shaped fish exploiting? Why is this particular body type repeating itself 250 million years later?
EDIT per answers:
I view them as same thing. I don't mean to suggest an animal can only exploit one niche, nor that a given niche can only be exploited by one animal. For example, birds with short, thick beaks like parrots eat seeds that are tough to crack. They give up the ability, perhaps, to get at some more delicate flower nectars. Brightly colored poisonous animals are easier to spot, but they are poisonous. So, over time, they are, as a specie, less likely to get eaten. What do disk shaped fish give up by being disk shaped, and what do they gain?

large appearance especially in shoals, reduce side oscillations of the head and make them less detectable, ability to confuse predators by changing shape when they turn, display signalling, ability to use the current like a boat sail, some reasons like that, I don't know, giant opah, gourami, pirahna, discus, moon fish, piranha, silver dollar, thorn tails, trigger fish, butterfly fish all have that shape.

this is less like a birds beak an more like their wings, birds with the same style of flight develop the same shaped wings, even if only distant;y related. Such as long narrow wings of soaring birds, or short square ones in highly maneuverable ones. Tose shapes just work better for that activity and many different birds with different niches may focus on that activity for different reasons.

@John perfect.  So, what does that shape do for fish?  I don’t think it’s speed as the fastest fish are not shaped like that.

@dwstein you should read jdfinch3 answer it covers that quite well. It packs a lot of muscle into a  a short tail which makes for the fish equivalent of sprinters. Huge acceleration but not great efficiency.

I believe what you're referring to are fish with the compressiform body shape (fish with a narrow flattened body). The advantage to this body shape is that it allows the fish to swim very quickly for short periods of time. This would, I assume, be an advantage both as predator and prey in that it can use a quick burst to escape from something else trying to eat it and also allow it to use a quick burst to catch food for itself.
--added--
I just re-read your question and caught the "ecological niche" part, which is different from evolutionary advantage. I'm not 100% sure regarding this (I'd say 80% sure though), but I don't think that an animal has to fill a specific ecological niche in order to survive - it just has to...survive. Surely animals that fill specific niches can gain an evolutionary advantage by filling a niche, but it is not (to my knowledge) a requirement.

I view them as same thing.  I don't mean to suggest an animal can only exploit one niche, nor that a given niche can only be exploited by one animal.  For example, birds with short, thick beaks like parrots eat seeds that are tough to crack. They give up the ability, perhaps, to get at some more delicate flower nectars.  Brightly colored poisonous animals are easier to spot, but they are poisonous.  So, over time, they are, as a specie, less likely to get eaten.  What do disk shaped fish give up by being disk shaped, and what do they gain?

I'm not an expert on fish, but I definitely understand the process of evolution and how evolution plays a part in the survival (and death) of animals. So the following is a well educated guess as to the advantage and disadvantage to such a body shape: The advantage is what I stated in the answer. As to disadvantages, an obvious one is that they are extremely easy to see by predators. Another possible disadvantage (and this is pure speculation) is that having a shape that allows for short bursts of very quick speed may cause them to move more slowly at normal speed (kind of a trade off).


text:
Can a less fit species evolve from a more fit species, by living at separate places?
[EDIT] if the genetic mechanism responsible for bringing about evolution is random, and if the environmental favoritism of some heritable traits over others is non-purposeful (like in the example of the black peppered moth during the era of industrial revolution: see here), then one would expect to see some examples of evolution that results in emergence of species the members of which has lower fitness than those of its immediate ancestor species. What I mean by that is that the genetic material in the gametes of some members of some species undergo changes that results in the emergence of a NEW SPECIES the members of which has lower fitness, that can go live in a separate environment.
Are there such examples? if not then why?
I'm not asking here about examples of an offspring having lesser reproductive rate than its parents and yet that offspring belonging into the same species of the parents. Of course that is well known to occur, since many hereditary disorders clearly affects the reproductive rate and survival of the affected individuals. No I'm asking about the emergence of a NEW SPECIES the members of which has lower fitness than those of its immediate ancestor species. The reason why I've mentioned that members belonging to the new species go live in a separate place from that of its immediate ancestor species, is because if they live in the same place, then clearly members of the ancestor species having more fitness would overcome members of the newly emerging species, to result in their extinction by natural selection, that's why I'm asking if it is possible for members of the new species to travel to another environment where it can live, albeit being less fit than members of the ancestor species from which it emerged. I call that backward evolution, though the term is odd, to mean that the direction in that particular case of evolution was towards lesser fitness rather than toward increasing fitness of members of the newly evolved species.
Are there such examples in the history of Evolution.
I'm not asking if the mechanism of such a step in evolution is due to Natural Selection, I'm asking if that evolution step can occur? and if it had occurred? And what are possible mechanisms behind such a step?
With the founder effect, what I'm understanding is that migration is the cause of lessening in genetic variation of the original population, and that this can possibly further lead to emergency of a new less fit species.
What I'm asking about here is a little bit different, I'm asking if the emergence of the new species caused the emerging (less fit) population to migrate as to avoid competition with members of the more fit original species. And because of this separation in place both populations need not compete each other for available resources, since they live at distant places. In other words, if some mechanism caused the birth of some less fit individuals that belongs to a distinct species form its ancestor, and such that those less fit individuals migrated as to avoid competition with the more fit ancestors, and that by this migration they managed to survive and reproduce. So it is not that migration caused at the end the less fitness, as in the founder effect, No its the opposite, its the less fitness that caused the migration.
I hope the question became clear now.

Comments are not for extended discussion; this conversation has been moved to chat.

Frankly your edited question is still unclear, although it does add more emphasis on sub-populations traveling to new environments. Please explain how the founder effect (which has been mentioned already) doesn't answer your question.

And your question still has major terminology issues that make it hard to answer (despite all the efforts of commenters to make you clarify what you mean), chiefly your usage of species instead of populations and perhaps your confusion of evolution with natural selection,

@Fizz, thanks about reference to "founder effect", I've updated my question, I hope its understandable now. I'm not familiar with the founder effect, I'm not sure if what I'm asking is an example of it, but from the reference you've linked it appears to be 'change due to migration' while here what I'm asking is "migration due to change", i.e. that some genetic mechanism caused the emergence of individuals that has different genetic material from the original population, such that those individuals belongs to a different species that are less fit than the original population, that caused them

.. to migrate, in order to avoid natural selection, selecting against them in favor of the original species which is more fit then them.

its a kind of evolution avoiding natural selection, thereby produce emergence of less fit species from more fit ones. Can this happen? actually did this happen? and if yes, by what mechanism?

Your updated question sound a bit like shifting balance theory, which is itself hard to test, except that in your question you insist on some poorly defined lower fitness... Fitness depends on the environment; if geographic division occurs, the environment is not the same for the sub-populations (and eventual species) so it makes little sense to compare population/species fitnesses that way. In that regard see "is evolution progressive?"

@Fizz the fitness I'm speaking about is the average number of reproductions per individual in the population. So its not poorly defined. That's beside the two geographic locations might have similar environments yet be distinct in place. So comparisons can be allowed.

Ok, so compare the average number of reproduction per individual between coyotes and humans. And conclude what from that? (Your definition of fitness is another idiosyncrasy.)

And since my last comment was probably not educational/detailed enough on that confusion: http://gregladen.com/blog/2013/07/19/reproductive-success-and-fitness-are-not-the-same-thing/ That was also discussed here, in less detail: https://biology.stackexchange.com/questions/45248/whats-the-difference-between-evolution-fitness-and-reproductive-success

@Fizz, that's not my definition that's what's written in the introductory reference that was cited to me here including Wikipedia article on natural selection. second I'm speaking about the relative fitness of members of a species and those of its immediate ancestor, neither coyotes came from humans nor humans from coyotes. also see your references.

You have a lot of individual questions together, you may have better luck asking them individually. Generally only one question per question is accepted.

The question contains a fair number of issues as explained in the comments. I won't go through them here. I will phrase some specific questions which might be of interest to you and very quickly answer them

Can an offspring have a lower fitness than its parent?

Yes, of course. There is a whole load of environmental reasons for that but leaving them aside, the offspring might have inherited some new deleterious mutations

Can the offspring population have a lower mean fitness than a parent population?

Yes. Under constant environment, with an population of infinite size, without migration, without mutations, it would not be possible (unless some fancy linkage disequilibrium and epistasis) as, in such circumstance, the mean fitness of a population increases exactly by the additive genetic variance of the parent population.
However, populations are never infinite. Hence genetic drift is in play and can cause the mean fitness to randomly vary which may cause a drop from any generation to any next generation. Other things such as an environmental change or an extreme mutation rate may also cause the mean fitness to decrease.

Can an offspring have fewer offspring than its parents

Yes. Fitness is an expectation. There is variation from it. Whether or not the fitness of the offspring is higher or lower than the one of the parent, it still remain that there is variation from the expectation.

Can a mutation undo a previous mutation.

Yes.

Can an entire population back to the exact same stage it was a few generations back.

If by exact same stage, you mean "exact same genome of the entire population", then this would be so fantastically unlikely that I will just say no.
Edit

I think you need to post that as an answer explaining why NS will "by definition" always acts to increase the frequency of more fit individuals,

NS is defined as the fitness differential among different genotypes in a populations. The change in allele frequency that results from this fitness differential. Individuals with higher fitness leave more offspring than those with lower fitness leading to a change in allele frequency, alleles associated increase in frequency.

I think you need to post that as an answer explaining why NS will "by definition" always acts to increase the frequency of more fit individuals, so that there cannot be an instance of speciation whereby a less fit species evolved from a more fit species.

You misunderstand the concept of speciation. Your sentences are so non-sensical that it is really hard to be of help to you. Really, you should just have a look at an intro course to evolutionary biology.

I find some difficulty in understanding how NS is "not purposeful", it seems to have a purpose to me, namely "producing more fit species from earlier ones", this is a kind of purpose.

The term "purposeful" is never used in science as it is very much undefined. The term feels to me that to have a purpose you need a conscience or a will. Obviously NS is not a small green creature hidden somewhere with the goal of making life evolve. It is just a natural phenomenon like many others.
You should just follow an intro course to evolutionary biology to understand what the terms natural selection, evolution, mutation, genetic drift and speciation mean.

By then if fossil evidence or laboratory evidence documents an event of what I'm saying here, it means that NS is false. right

I don't understand what you refer to by "what I'm saying here" either.
I highly recommend that you follow a short intro course to evolutionary biology (such as evo101 for example). It will take you a few hours and you will learn a lot. Also, you will be able to ask questions that don't give a headache to whoever is reading it :) Good luck!

Comments are not for extended discussion; this conversation has been moved to chat.


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codon optimization / enzyme active site improvement
Does one necessarily have to use de novo synthesis of DNA when attempting protein expression improvement by codon optimization? Or are there other ways?
e.g. Say the gene coding for the enzyme needed to synthesize a certain secondary metabolite is known & sequenced already. The standard cloning approach is to extract mRNA from (say) plant tissue, then construct a cDNA library & express it in E Coli using a suitable plasmid.
Now if the neucleotide sequence needs to be modified (to increase expression) does one have to start de novo or is there easier ways that can start from the mRNA / cDNA?
A variant of the same question is when I'd want to modify the gene because a protein docking study shows some ways to modify the active site of the enzyme by changing a residue or two in the amino acid sequence.

Kind of an old post, I'm surprised it doesn't have an answer yet.
There's no reason why you couldn't modify the RNA or cDNA directly, you just have to splice the gene correctly to make the changes you want. You're absolutely right that even a single amino acid change can have a huge difference if it's in the right spot.

Some questions are unclear and the best interpretation of them is that they are trivial and could be answered by the poster with a little research. In such cases As the Help on answering questions says, "Not all questions can or should be answered here". But if you do insist on answering I suggest you read that help, because your answer only expresses an opinion which, though it may be correct, provides no supporting references or explanation of why it is correct. Thus, neither the poster nor anyone else can tell whether it is so.


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Enzyme immobilization: Factors that help or hurt success
Are there any factors to consider that can help / hurt the chance to get a successful immobilized enzyme catalyst?
i.e. The relative attractiveness of a live host synthesis vs an immobilized enzyme.
Specifically, the product of interest is a secondary metabolite of MW approx. & the host of choice is S. Cervesae. The transformation is a single step, catalyzed by a single, known enzyme with the gene coding for it approx. 2000 base pairs.


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How to cut out a specific named gene from plant DNA
Suppose one has extracted RNA from a plant, converted it to the corresponding cDNA & amplified it but now wants to cut out a particular, already-sequenced gene out from it, how does one proceed?
i.e. How does one cut out that particular segment of the whole DNA which one wants? Does one always find restriction sites (or rather cleavage sites)  at both ends of the desired gene segment & then one treats the cDNA sample with those specific restriction enzymes?
To get the gene shown below I'd find an enzyme that cuts at the GGCCAC site and another to cut at AAAAAA?

You could also PCR amplify the gene using primers with fitting restriction enzyme recognition sites (+ some extra bases) on the ends.

PCR, as Chris suggested. Also, when you made the cDNA library, you don't really have "whole DNA" as you suggested, but many pieces of DNA corresponding to the mRNAs you extracted. Some of those should be the gene of interest and can be amplified.

@user137 Thanks! Must one go through the mRNA & cDNA  stages? Or is there an easier way to get the gene? e.g. Can't one extract the DNA itself from the plant cell nucleus. Why start from mRNA? Sorry if some of my questions are naive.

mRNAs are generally used because they tend to have a much higher copy number than genomic DNA and because the introns are already removed, so you are left with the coding sequence. You can isolate genomic DNA and do PCR directly off that, but the introns will be there, potentially making for a much much much larger gene. If you just want the exons, use the mRNA -> cDNA approach. It should be pointed out that if you want to express protein in bacteria, the introns will probably not be removed properly on transcription, so the protein won't be right.

@user137 Makes a lot of sense now the way you described it! Thank you.


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Yeast Strain with squalene synthase / farnesyltransferase (ERG9) gene deleted
I was interested in obtaining a yeast strain without the enzyme farnesyltransferase (Which catalyses conversion of FPP to Squalene). The Euroscraf database has thousands of yeast strains with individual genes deleted but when I search for "farnesyltransferase" I get a couple of hits that I am not being able to interpret.
Here's the link: http://www.euroscarf.de/search.php?search=farnesyltransferase&project=
What are all these different strains? In particular how does one interpret notation like which seems to be describing a particular strain:
BY4743; MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4

Seems like you should have searched for erg9 instead...

@MattDMo Ah! That explains it. Thanks! So what's the difference between these two strains that it throws up SC2489 and Y22884: http://www.euroscarf.de/search.php?search=ERG9&project= Are they both Squalene blocked strains? I still cannot interpret the "Genotype" goblydygook that the database entry has.......

Well, the genotype is simply describing what variants of certain genes the strain has - what mating type it is (MATa/MATα), what nutrients it requires in the medium and what it can synthesize for itself, and the type of mutation that occurred (or was engineered) to make the strain deficient for the gene you are interested in. You'll need to talk to someone much more familiar with yeast genetics than me to determine exactly what each notation means - I'm just remembering all this stuff from grad school 13 or 14 years ago...

Yeast strains have two mating types MATa (since it secretes a pheromone named 'a factor'), MATα (secretes pheromone 'α factor'). Both MATa and MATα strains are haploid and when they fuse together they form diploid zygote. A haploid yeast has only one set of genes and utilize chemicals like histidine and tryptophan (amino acids) and adenine (part of DNA, ATP and other molecules) for growing. Yeast strains mutant with any of genes to
make these chemicals they will not grow unless they can get these chemicals from their food (yeast media) or allowed to mate with strain having normal genes.
Interpreting the strain notation:
BY4743; MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; Met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4
Strain name: BY4743
Genotype: MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; Met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4
To understand clearly, you can dissect the genotype in individual strains
BY4743;MATa;ura3Δ0;leu2Δ0;his3Δ1;met15Δ0;LYS2;YKL019w/YKL019w
BY4743;MATα;ura3Δ0;leu2Δ0;his3Δ1;MET15;lys2Δ0;kanMX4
Yeast genetics nomenclature:

Normal or wildtype genes are written in capitalized form - MET15 in MATα
Mutated genes are symbolized with small letter and Δ - ura3Δ0
ura3Δ0/ura3Δ0 - allelic mutation:  mutation in same genes of both strains (MATa/MATα) - They are two mutant alleles in the same gene locus. Both alleles of same gene are knocked out, so even both strains mate, they need external source of uracil in media to grow. Defect in one strain is NOT complemented by the other.
Met15Δ0/MET15 & LYS2/lys2Δ0 - Non-allelic mutation: Defect in one strain is complemented by the other. MATa has Met15Δ0 (mutation in methionine gene) and MATα has wildtype MET15 gene, capable of met synthesis. Complementation works here.
YKL019w/YKL019w::kanMX4 - Critical aspect of yeast strain in functional complementation assays. In all commercially available yeast strains, one gene will be double knocked out (both alleles of same gene) and replaced with an auxotrophic markers like antibiotics - tetracycline, kanamycin, ampicillin - for selecting the diploid cells after mating two strains. It is similar to plating Kanamycin mixed LB media to pick E.coli colonies harboring Kanamycin resistance vector in it.

The gene that is replaced is the gene of interest, i.e. if I am looking to study role of putative PGPS in Plasmodium falciparum, I get yeast strain knocked out with yeast PGPS (pgsΔ). When I do complementation test, I provide external DNA template cloned with Plasmodium falciparum's PGPS to check whether it complements in yeast genome and yeast grows - gene essentiality study.
I am not sure of the gene YKL019w/YKL019w, but it implies that wildtype of YKL019 is replaced with Kanamycin - kanMX4.

Wow! That was an amazing answer. Thank you very much. I am still trying to digest all of it!


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Is there a vertical measure of appearance of a genotype over generations?
Is there some kind of a vertical measure of appearance of a genotype $g$ throughout ancestry, i.e. a measure of how many ancestors of $g$ had genotype $g$. Like for example in saying that on average each member of a population $P$ have 60% of its ancestors having genotype $g$ over 20 prior generations.
A clarifying example, lets take some genetic trait like color, suppose we have a population $P$, and suppose we know all of the ancestry of each individual $x$ in that population up to say six generations, i.e. we know specifically the color of each mother and father of $x$, the grandmothers and grandfathers of $x$, the first great grandmothers and the first great grandfathers of $x$, up to .. the fourth great grandparents, call the set of all those as $Ancestry^6(x)$, lets denote the set of all individuals of $Ancestry^6(x)$ that are $a$ colored as $Ancestry^6_a$, let's denote the total number of members of any set $y$ by $|y|$,
Now what I'm looking at is the proportion $p^6_a(x)$ of all $a$ colored members of the 6 generations ancestry of $x$, from that ancestry.
$$p^6_a(x)=|Ancestry^6_a(x)|/|Ancestry^6(x)|=|Ancestry^6_a(x)|/(2+2^2+..+2^6)$$
Now for population $P$ we'll look for average $p^6_a(x)$: $x \in P$, symbolized as $\mu^P(p^6_a)$ which is $$\mu^P(p^6_a) = \big{(}\sum^P p^6_a(x)\big{)}/|P| $$
In general the measure is $\mu^P(p^m_a)$, where $P$ is the population, $m$ the total number of generations in the ancestry of each member of $P$, $a$ is the genotype, and $\mu$ signify average, and $p$ for proportion. So $\mu^P(p^m_a)$ is: the average proportion of genotype $a$ in ancestry of each member of $P$ up to $m$ generations.

Question: is that measure directly proportional to fitness?

The idea is that if genotype $a$ is more fit than others, then it would appear more frequently in the ancestry of each member in the population.

I don't really understand the statistic that you are trying to describe but it sounds like you might want to read about "coalescent theory" (the usage of branching patterns to describe patterns of ancestry among individuals) and the "folder/unfolded site frequency spectrum" (SFS; frequency distribution of allele frequency in a population). The SFS is one of the many statistics for which we can get theoretical expectation from coalescent theory (see Watterson's estimator function maybe).

Remi.b, OK I've added a clarifying example, that defines it exactly.


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What is the definition of "Natural Selection"?
Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.
Natural selection, a process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype or genetic constitution.
Natural selection, then, can be defined as the differential reproduction of alternative hereditary variants, determined by the fact that some variants increase the likelihood that the organisms having them will survive and reproduce more successfully than will organisms carrying alternative variants.
Darwin's definition of natural selection his book "On The Origin Of Species By Means Of Natural Selection or the Preservation Of Favoured Races In The Struggle For Life" is:

The preservation of favorable variations and the rejection of injurious variations

In Evolution 101, natural selection is not defined, but rather the concept "evolution by natural section" is characterized as the outcome of variation, differential reproduction and Heredity, and a clarifying example is provided.
Clearly, the wording in each of the above is different!
I searched Biology StackExchange for any explicit statement of the definition of natural selection, I couldn't manage to find one. There are some discussions about whether it is a tautology or not, but even in those discussions, the definition of natural selection was not quoted.
I tried to search tags "natural selection" and "definitions" of biology StackExchange, and yet I didn't see any particular wording mentioned as the official definition of natural selection.
Actually, the tag [natural selection] mentions this definition in the tag information itself:
Natural Selection is a mechanism of evolution that leads to non-random spread of genes due to the effect that genes have on reproductive success
Natural selection is the process by which heritable traits that make it more likely for an organism to survive and successfully reproduce become more common in a population over successive generations.
Is there an official definition of natural selection that is adopted by biologists nowadays? and what is that definition exactly?

[EDIT] It came to my awareness that this question might be a possible duplicate of the following question: "How is Selection best defined", and indeed in the answers provided to that question the topic of definition of natural selection has been addressed.
I didn't know of this posting. I simply surfed for "natural selection", and not just for "selection", and I didn't notice it. But indeed what's presented in the answers does cover the question present here.
However there is some difference in the question itself from that present here. Here I wanted to know of what I thought would be an official definition, and I was asking in particular about "natural selection", while in the referred question, the question is more general, it's about what qualifies "any" force (apparently he means related to biology and especially evolution) to be labeled as "selection", including artificial selection, sexual selection, etc.., so it's a wider topic, at least as far as terminology is concerned.
Here in this question I've quoted the main results that one would see upon surfing the web for "definition of natural selection", and I wanted to know which one would be the official or as @Remi.b had put it, the most commonly used or referred to in biological research.
I still think, that for precision purposes, exact wordings are important, and such an extremely important concept like "natural selection", it would have been expected that it had an agreeable, kind of, official definition, by some convention or the alike.
Anyhow, I think, whether this question is a duplicate or not, can be better assessed by experts in evolution field present in this website, like those who provided answers, and others.
Thanks.

I think it's unrealistic to expect to find word-for-word congruence b/w definitions from multiple sources. All your definitions still describe the same phenomenon conceptually. From a broader viewpoint, no 2 textbooks (or at least few) define "simpler" biological concepts the same (e.g., even the word cell). The same can be said of common non-scientific words (e.g., see dictionary.com, OED, Merriam-Webster, etc. for any given word). In conclusion, there is no "official" wording for this definition or most definitions. This is why bio instruction emphasizes learning concepts not words...

Then there's the definition which pops up when you hover your cursor over the tag "natural-selection" at the bottom of this question.

@mgkrebbs, oh yes, thanks, i didn't notice that really. I'll add it.

Of all the definitions, I think the SE tag one is possibly the worst. Maybe @Remi.b would take a stab at editing it, if you agree?

As to whether it's a tautology: it's a tautology that the most fecund phenotypes will have more offspring, but it's not a tautology that there are more fecund phenotypes, or that heredity occurs, or that what qualifies as fit varies slowly (in fact, it might not). Nor is it a tautology that this is where adaptation comes from (or even primarily where it does), or that drift isn't also an important mechanism (which it is). These are all issues where evidence is key.

@J.G.: But fecundity, or reasonable lack thereof, really isn't a criterion for natural selection.  An organism can be extremely fecund, like the codfish with its millions of eggs, or humans (and other mammals) which only have a few offspring but make a large investment in post-natal care.  Either works: since both exist, they have obviously been selected for.

@Remi.b I think Bryan Krause was suggesting you to edit the the [tag:natural-selection] tag-info in SE.

@jamesqf Well, replace it with whatever you think succeeds under natural selection, but in any case I think you're conflating how species compare to how individuals in a species compare, which is what natural selection is all about.

Possible duplicate of How is "selection" best defined?

I think this is really related to the question linked above, and in this answer I name a couple of relevant sources to look at, and how to draw the line between natural selection and evolution by natural selection (which is sometimes fruitful).

Official definition

Is there an official definition of natural selection that is adopted by biologists nowadays? and what is that definition exactly?

I don't think there is such a concept as an "official definition" of any concept in science. There are common definitions though.
The definitions you cite
Let's go through your three definitions

Natural selection is the differential survival and reproduction of individuals due to differences in phenotype.

This definition lacks the idea that this fitness differential must be caused, in part at least, by genetic variation.

Natural selection, a process that results in the adaptation of an organism to its environment by means of selectively reproducing changes in its genotype or genetic constitution.

Part of the phrasing is about the consequence of the process rather than the process itself. The part that describes the process itself is "selectively reproducing changes in its genotype, or genetic constitution", which is a rather unusual phrasing and I would argue is slightly vague.
Note that while most authors refer to natural selection as the fitness differential, it is not impossible to refer to natural selection as the resulting change in allele frequency. I have never seen cases where this semantic difference matters though.

Natural selection, then, can be defined as the differential reproduction of alternative hereditary variants, determined by the fact that some variants increase the likelihood that the organisms having them will survive and reproduce more successfully than will organisms carrying alternative variants.

I have never encountered the expression "alternative hereditary variants". I think the author made it up. It sounds like the author tried to avoid the term "allele" by replacing it with "alternative hereditary variants". The author also seems to have tried to avoid the term "fitness" by replacing it with "likelihood that the organisms having them will survive and reproduce more successfully".
But overall the definition sounds correct to me. There is an important difference between the first and the third definition is that in the first definition, it emphasizes the fact that the genetic elements that explain fitness variance are doing so via its effect on the phenotype. The third definition just ignores phenotype. As such, I would consider the first definition more complete (and more compact).

Natural Selection is a mechanism of evolution that leads to non-random spread of genes due to the effect that genes have on reproductive success

Here, the definition is again very much based on the consequence of the process rather than the process itself. Only "due to the effect that genes have on reproductive success" refers to the actual process of natural selection.
I don't really like the term "random" here as the concept of randomness is somewhat unpleasant to define outside of a well-defined model. I don't really like the term "genes" either because selection doesn't only act on genes (but can act at any locus) and because the term "allele" would be more appropriate even if the phrasing would still remain unclear.
So in short, shame on us, the StackExchange definition is pretty bad!

The preservation of favourable variations and the rejection of injurious variations

I shall not talk here about how different is Darwin's theory of evolution from today's theory of evolution (which is called the "modern evolutionary synthesis"). I shall not talk either whether this single short sentence is a good summary of Darwin's representation of natural selection (see @Luaan comments for more information).
This definition is short and a bit vague. One would want to think of this definition as applying to a genetic variant, without regard to the phenotype, however, Darwin did not know anything about DNA.
My favourite definitions
Lewontin's recipe
A very simple way to think of natural selection is to consider Lewontin recipe. The Lewontin recipe says that natural selection occurs whenever:

Individuals in a population vary in terms of a given trait
This trait has a non-zero (additive) heritability. See this post for a definition of heritability.
The fitness varies (not necessarily linearly) as the trait varies

Single sentence definitions
If you prefer a shorter and simpler version I would personally suggest

Selection is the fitness differential among genotypes in the population.

This definition lacks the concept of phenotype but talking about the fact that an individual fitness is dependent on its phenotype (among other things) is, IMO, not required to mention in the definition of what natural selection is. Not that I also removed the term "natural". I don't quite like it because it leads people to think that natural and artificial selection could be fundamentally different. Same applies to sexual selection, IMO, but I shall not go down this slope now!
In a very similar post, I wrote the definition

Selection is a fitness differential associated to a genetic variance among individuals in a population.

I also like this definition because it highlights that selection acts on populations (and not on individuals or on species).
Mathematical modelling
You might want also to consider as a definition the mathematical modelling of the process. In absence of genetic drift (assuming infinite population size), assuming a bi-allelic locus with alleles a and A, one can model (haploid) selection as
$$p_{t+1} = \frac{p_t W_a}{p_t W_a + (1-p_t) W_A}$$
, where $p_t$ is the frequency of the allele a at time $t$. $W_a$ and $W_A$ are the fitness of the genotype with alleles a and A, respectively. Of course, you can extend this model to any kind of ploidy and any number of alleles. You can also extend this model to include genetic drift (typically done via the use of diffusion equations or via branching patterns).
For more information about these mathematical modelling, please have a look at an intro book in evolutionary genetics (see here for book recommendation).

@This is a very nice answer. I noticed that you skipped Darwins' definition?

@ZuhairAl-Johar Keep in mind that Darwin was simply defining his terminology for the book. This is similar to saying "James McKay (hereafter noted Defendant)...". The idea worked, the concept stuck, and the exact wording and semantics of the "definition" aren't important in the slightest - in general, in scientific thinking, the concept is far more important than the exact words you use to describe it. Scientists usually aren't language lawyers, they're just trying to communicate efficiently :)

@ZuhairAl-Johar It should further be noted that your cited part is the end of a whole paragraph where he describes what he means by natural selection (see https://counterbalance.org/evolution/direct-frame.html). And some of the definitions you showed focus on some mechanisms that we've found since Darwin's time - mainly, genetics (and the language of genetics). Darwin was talking about "individuals having any advantage ... would have the best chance of surviving", but that's equivalent to "some phenotypes promote survival" - just with more mature terminology and more insight.

@ZuhairAl-Johar You should consider reading the edit, which add discussion of the Lewontin recipe and add my own definition. Also, I quickly discussed "Darwin's definition" as you asked.

@Remi.b, why the first p in the equation is not in upper case?

@ZuhairAl-Johar It was a mistake. It is standard to use lower case p for allele frequency, so I changed all the Ps to lower case. Thanks.

I've adapted your definitions to another process that I think will be less controversial to you.

Eating is the intake of food by taking into the mouth, chewing, and swallowing.
Eating, the process that results in digestion by taking in food and chewing and then swallowing.
Eating, then, can be defined as the intake and digestion of food items, determined by the fact that organisms take in foods to the mouth and then chew and swallow them leading to digestion of those foods into nutrients used by that organism.

If you look up dictionary definitions of the verb "to eat" you will also get a variety of answers, but there is no controversy about what "eating" is: it's a concept you learn and agree on. Some of the definitions reach further, mentioning digestion. Some focus on the "just eating" part. However, they all agree with each other, there is no conflict. In fact, a lot of the words are just rearrangements of the same words into different grammatical constructs.
All of the definitions you cite are reasonable descriptions of the term; all of the sources you cite also go further into those definitions to describe the whole process. You should focus on that whole process rather than trying to find fault in the definition. Natural selection is not a tautology, and arguments that it is are misguided.

You've cited the same citation that I've cited. I'm not arguing that it is a tautology, I just wanted to know the definition, and all of your responses were great. Thanks

There is some variation as to whether it's thought of as acting on the phenotype or the genotype, although of course those two are interrelated.

As Remi points out there is not an official definition of anything as complex as natural selection in science. Science is a collective consensus, not a hierarchical structure, official things are rare and usually not directly connected to the science. The neo-Darwinian synthesis might count but that is far too large to be considered a definition, it is more a modern restatement of the theory.
I can offer the definition I use in class.
Selection: change in the heritable characteristics of a population due to differential reproduction of variations in said characteristics within a given environment
to break it down change in the heritable characteristics of a population... that's just a restatement of evolution essential for any consideration of natural selection.
...due to differential reproduction... so evolution happens because some things reproduce more successfully than other things.
...of variations in said characteristics within a given environment and this clarifies the cause of the differential, that variation in heritable characteristics exist and interact with the environment in different ways. Of course, it is important to understand the "environment" in this case is literally everything else, from other cells in the body to predators, to other genes on the same genome to abiotic processes.
Note authors tend to avoid the mention of genetics or related terms in the most fundamental definitions because natural selection is not reliant on nucleic acids it works with any form of heredity, an alien lifeform that has a different form of heredity will still undergo natural selection. Things like prions can also evolve via natural selection if a group of things has heritable characteristics that also vary in reproductive success natural selection will operate on those things.
Then you have the specification of "natural" selection. Which is simply selection not caused by human intervention. This has been an important piece of natural selection since the beginning mostly because people had little problem with the idea that humans could alter organisms by conscious choice but the idea that their natural environment could alter them simply due to survival and reproduction was not as easily accepted.
Differentiating natural selection and artificial selection is probably the vaguest part and has a tremendous amount of gray area. There is no Real difference between artificial and natural selection, it is all just down to human conceptual framing. Natural selection is just a response to an environment, but what makes up that environment covers everything from rocks, humans, members of the opposite sex, etc. Nearly anything can have an impact on survival depending on the circumstances. Because of this the only thing that differentiates natural from artificial selection is whether humans are the major environmental factor but that itself is vague, human mate choice and species that live around humans but are not domesticated( like cockroaches) make this imprecise. I have never found a satisfactory precise differentiation between the two forms of selection.

natural selection was an idea proposed by darwin a scientist. he said that nature select the fittest.
  he concluded following points after his research
  In a population, some individuals will have inherited traits that help them survive and reproduce (given the conditions of the environment, such as the predators and food sources present). The individuals with the helpful traits will leave more offspring in the next generation than their peers, since the traits make them more effective at surviving and reproducing.
  Because the helpful traits are heritable, and because organisms with these traits leave more offspring, the traits will tend to become more common (present in a larger fraction of the population) in the next generation.
  Over generations, the population will become adapted to its environment (as individuals with traits helpful in that environment have consistently greater reproductive success than their peers).

Quoted from the book
Darwin and Henslow
The growth of an idea
Edited by Nora Barlow

Thanks for this nice quote. But is this predictive? I mean suppose that it has always been a merry time for trait A and bad for trait B, then according to what you've said one would predict that trait A would prevail since it has more capacity to adapt to its environment and thereby survive and reproduce more. Now suppose suddenly an outbreak of a deadly disease spread that trait A happened to be susceptible to but not trait B, the outcome is final triumph of trait B, and the extinction of trait A.

What was usually the weaker trait, i.e. the less fit trait, prevailed in this example. Now a selection had been made, but for what? for what used to be the less fit trait? Its done by nature. So it doesn't appear that nature always select in favor of the most fit traits? isn't it.


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In bacterial conjugation, how do F+/F- cells detect each other?
I've just learnt about bacterial conjugation and while it is interesting info about early sexual activity in microbes, one aspect confuses me and doesnt seem to be mentioned in the material I read:
How do the donor/recipient pairs find each other?
While cells in a culture all can have physical contact as they move about, either the F+ cell inserts pili into various cells looking for some chemical stimulus or physical contact with a F- cell provides some data that lets it know it has touched a cell with which it can now perform conjugation.

F+ cells have mechanisms in place that inhibit them from making contacting with other F+ cells, therefore, a F plasmid cannot be transferred from F+ to F+. Source: https://www.ncbi.nlm.nih.gov/books/NBK21351/


text:
Does mung bean nuclease cleave a phosphate group when it's chewing off 5' or 3' ssDNA ends?
I'm looking to create blunt ends from sticky ends with mung bean nuclease for subsequent ligation.  Does anyone know full mechanism by which mung bean nuclease will do this?
In particular after the reaction, will the ends of resulting dsDNA have phosphate groups or will I need to phosphorylate the ends with an extra step for successful ligation?

According to Kroeker WD, Kowalski W, Laskowski M. 1976. Mung Bean Nuclease I. Terminally Directed Hydrolysis of Native DNA. Biochemistry 15(20):4463-4467

It was concluded that the products of the terminally directed hydrolysis of native DNA possess 5’-phosphoryl groups because: (1) greater than 99% of acid-soluble activity applied to the column was recovered in products which coeluted with 5’-terminated standards and (2) the w-monophosphatase activity of mung bean nuclease would have dephosphorylated 3’-phosphoryl-terminated products. The endonucleolytic activity of mung bean nuclease on denatured DNA also results in the production of 5’-phosphoryl-terminated products.

Also, from Promega:

Mung Bean Nuclease catalyzes the degradation of single-stranded DNA and RNA endonucleolytically to yield 5´-phosphoryl-terminated products


text:
Washing bacteria out with water
When I wash my running shoes by my hands,
I leave them near the window to dry them quickly.
Although they got sunlight in daytime and well dried after I came back from work, I could feel bad smell from them.
The smell was worse than when it was not washed for long time.
So I guess that the water increases the number of bad bacteria on shoes.
My conclusion is that water should be used to wash dirty things out only for a short time and
it should be dried as soon as possible.
Although our body is alive and can resist against bad bacteria on our skin which get nutrition from water, it seems that water should be used for a short time.
Am I right? Please advise on my thinking.
Thanks.

I think that "bad bacteria" isn't the right term to use here. Maybe mold is more accurate? What do you mean by "use water for a short time"? Do you mean dry out quickly?

It means washing with water for a short time, and we should dry out quickly as well, if water is helpful for 'the bad bacteria'. I had thought water was always helpful for removing smells in the past.


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Argentine Ant Trails
What is the maximum distance for an argentine ant (Linepithema humile) trail?  I imagine that there is some point where the ants are unable to make the return trip either through exhaustion or from the chemicals of the trail failing somehow.

I don't think that the chemicals evaporating would be the limiting factor, because a trail isn't created by a single ant, it's created by many ants following the same track. Meaning as long as the trail is active the chemicals can be replenished. Offhand I would say a good indicator of the maximum length a trail gets is the amount of territory a single colony controls - but Argentine ants form supercolonies, so not only might this be hard to measure, but maybe they could share trails in which case ant exhaustion won't be a factor either. I will see if "Adventures among Ants" says something.

I was reading "Adventures among Ants", by Mark Moffett, to see if he said something about the length of the trails of Argentine ants and I was about to give up and give a general answer based on the other information about Argentine ants in the book, when I hit upon this quote by "Physicist turned biologist Jean-louis Deneubourg":

The Argentine ants' exploratory behavior is exceptional in that they mark continually and explore collectively. Whereas other recruitment trails are constructed between two points (e.g., nest and food), their exploratory trails have no known destination, progressively advancing into the unknown. They rapidly lead new explorers to the frontier between the just explored and the about to be explored zones, avoiding situations where ants will end up exploring the same zone twice, and help returning explorers reach the next directly. A wide corridor of the chemically unmarked area is thus systematically "swept' and marked in a minimum time with maximum economy.

The things to know about Argentine ants are, they form supercolonies in which all ants from the same supercolony can mingle indifferently, regardless of the nest they are from. There is no theoretical limit on the size of such a supercolony; if there is one, it is over thousands of kilometers:

The largest [Argentine ant supercolony] extends from Italy to Spain's Atlantic coast, a distance approaching 2,000 kilometers

This means that the length of an Argentine ant trail is definitely not limited by ant exhaustion or chemical evaporation, depending on what we mean by "trail". If interconnected trails can be counted as a single one you could theoretically have a 2000-km Argentine ant trail that is maintained by ants all along its length. In practice the trail lengths are probably still limited, but by their purpose instead of hard physical limitations. The Deneubourg quote says recruitment trails are built between two specific points, such as a nest and food: this example clearly implies a distance limited by nest density (the trail between a nest and food will be from the nest closest to the food, so if nests are all 10m apart the length of the trail will be 5m at most). This would be true of any trail that has a nest as an endpoint, and what other kind are there?
He also says exploratory trails have no fixed destination, but that doesn't mean they cover unlimited distance either: the exploratory front as described clearly moves forward gradually and deliberately, and as Argentine ants are constantly building nests within the territory of the colony, the exploration front will always be a certain limited distance from the nearest nest.
Then again we could also argue that nest density is itself determined by a physical limit on maximum trail length, which could indeed be ant exhaustion (or ant loss of efficiency at least), risk of the trail being perturbed, chemical evaporation (as in, a longer trail would need more ants to maintain it), etc. I can't speak to that.
Trying to find numbers on Argentine ant nest density I fell upon this paper, which gives more information about ant colony structure and gives the closest thing I think you will find to a definite answer to your question:
Nest connectivity and colony structure in unicolonial Argentine ants

In experiments using labeled food, and in a 3-year census of nests and trails, we found that food was shared and nests were linked by trails at distances up to 50 meters.

Note that this is "path distance", i.e. the length of interconnected sets of trails. I couldn't find statements on a single trail, but they show a figure and the longest trail on it is between nests that are about 12m apart.
As an aside, this very interesting paper breaks up the "supercolony" concept a bit; while supercolonies are defined by seeing which ants will attack one another, meaning you can legitimately drop an ant from one end of the colony into the other end and it will go to work unmolested as if it were home, the authors of this paper looked at actual worker movement and food sharing, and found that

Argentine ant populations do not function ecologically as single, large supercolonies, but instead as mosaics of smaller, distinct colonies consisting of groups of interacting nests.

It also says the distribution pattern of nests is seasonal (Argentine ants have very ephemeral nests to begin with); this could give some clue as to what determines nest density and whether physical limits on trail length play a role.


text:
What is the leaf venation of a scuppernong vine leaf?
I googled around and I didn't find anything that says its leaf veination. Anyone know?

2 hours later...;-; Does no one know?

Check this

Using the link, it's netted veination, though it doesn't say if it's palmate or pinnate. So I relied on using my own judgement on looking at my scuppernong leaf and it looks decidedly palmate. It would be better if I had confirmation from some site or such, but as it has main veins and smaller veins sprouting from those main veins, I think it's palmate.
Additionally, for all other botany question confusion, I finally found this website which may be useful: http://rampages.us/fieldbotany/2014/05/23/grape-vine-3/


text:
Brandywine Maple?
I'm collecting and classifying leaves for biology. Teacher took us on a 'walk' to help. She let us pick and told us one leaf was a Brandywine Maple and another later on, a different leaf, was a Red Maple. I'm googling around to classify, but everything says that a Brandywine maple IS a Red maple (different name).
What the?
Help please...

Perhaps you should talk to your teacher instead of asking strangers on the internets...

Wow. That was extremely helpful.
Not. What's the point of this site to students then? What if I want to finish this project this weekend before school starts again?
Not to be really harsh in tone. But I would appreciate an answer a lot more than that.

First, when your project is due is of no concern to us. If all of your research points to "Brandywine Maple" simply being another name for red maples, then perhaps you should speak to your teacher to find out why she was differentiating between the two. On the other hand, if the two leaves are clearly different, you should [edit] your post to include focused, well-lit, labeled images of each of them and a clearly-articulated question about them. "What the? Help please..." does not qualify, I'm afraid. You may want to take the [tour] and read the [help] to find out more about this site.

I'd also suggest reading our (rather brief, but to-the-point) homework policy. We are not a homework service, but with enough thought and work from you, we may be able to help point you towards an answer.

@MattDMo I disagree that this is a poorly researched homework question. The OP has clearly made attempts at answering the question (see the googling line), which is backed up by my own search.

@MarchHo I never said it was a poorly-researched homework problem, nor have I voted to close it as such. I was simply pointing out our homework policy.

It was kind of implied, whether you meant to imply such or not, in your comment. I don't see why you would point me to the homework policy otherwise (If you wanted me to tag it homework, which I neglected to do accidentally, you coulda just said so).
Also, I'm not telling you to be concerned about the due date (it's in fact not due tomorrow, it was just an example, that), but I was irked by the fact you left a basically useless comment.

According to the Missouri Botanical Garden and Washington State University, Acer rubrum var. Brandywine is a cultivar of the red maple, Acer rubrum.

'Brandywine' is the result of a 1982 cross (Acer rubrum 'October
  Glory' x Acer rubrum 'Autumn flame') conducted as part of a U. S.
  National Arboretum research project. It was subsequently introduced
  into commerce in 1995.

[...]

As a cross of the red maple cultivars ‘October Glory’ and ‘Autumn
  Flame’, the variant ‘Brandywine’ was released for its resistance to
  leaf hoppers. It turns a burgundy color later in the fall than the
  popular October Glory.
As with other red maple cultivars this one does well on many different
  types of sites. As such, red maple is well adapted to sites to that
  are wet.

Therefore, you are correct to say that a Brandywine maple is a red maple. However, it is not the alternative name for a red maple. All Brandywine maples are red maples, but not all red maples are Brandywine maples.


text:
What factors, other than its homochirality, make our "brand" of biology unique?
If humans were to discover organisms on another planet, it is supposed that (unless both we and they were seeded by the same source) we would have nothing to fear from alien pathogens, as they would likely be totally incompatible with our "brand" of life here on Earth. This is due to a set of fundamental particulars not inherent in all possible biologies (as apposed to physics, where characteristics are more omni-present). I know, for example, that the left-handed chirality of amino acids marks one such trait. There appears to be no reason why life could not arise with the opposite orientation. My question is, what other particulars make up this set?

Welcome to Biology S.E.! If you need/ want additional assistance, please visit The Help Center and take The Tour. I think you have a fascinating question here by the way!

I think the opposite list---what features of life might be reasonably expected to be the same elsewhere---would be much shorter. Nearly every feature of life on earth as I can think of it is arbitrary in the particular molecules.

DNA. Why only 4 bases? Why the bases that we have (ACTG)? Researchers are able to create organisms with expanded DNA alphabets even here on earth (1). Even if you believe that some form of molecular mechanism of heredity is a requirement for life, there is no reason it need be DNA. And while there has been plenty of controversy about arsenic-based life here on Earth, I don't see why there couldn't be arsenic-based life elsewhere.
Ribosomes. Why a combination of RNA and protein? There is a lot in the overall architecture of ribosomes that is locked in due to historical/evolutionary contingency, not any necessary feature of life.
The Central Dogma. Biology as we know it has certainly made great use of the ability to make temporary copies of messages, but I don't see why life orbiting Alpha Centauri would have to have arrived at a similar solution.
Phospholipid membranes. You could make the argument that some degree of compartmentalization is necessary for life to occur (to reduce complexity and allow evolution via drift and small-number effects to generate change), but I don't think they need to be phospholipids. I can also imagine all life on another planet contained within viral-like particles with purely protein (or some other alien polymer) coats.
Genes. Depending on the level one is arguing I can see this going either way. If a gene is just a modular set of instructions for a limited number of components, then perhaps this will show up everywhere---life on our planet is surprisingly modular, and it is hard to imagine life on another planet being able to get by without some modularity (though of course it is possible in principle). But certainly nothing is inevitable about the details of gene organization into promoters, coding regions (why a 3-base code?), introns and exons (I'm still surprised these exist on our own planet), operons, etc.

I think you get the idea. In fact, it's really hard to envision any feature of life on earth that doesn't smack of contingency in some way or other. Astrobiologists have held on to water as an essential ingredient for life as we know it, but still, that's "as we know it."
I am really tempted to make some sweeping speculative statement about what features I might expect to be "inherent in all possible biologies" (a fascinating idea to think about), but that is way out of my depth. Right now I find it hard to come up with good candidates.
(1): Malyshev D et al. (2014). A semi-synthetic organism with an expanded genetic alphabet. Nature 509: 385-8.


text:
How pain can stimulate the vagus nerve
I'm trying to find out why a prompt, severe, short pain is causing a stimulation of the vagus nerve. What could the physiological explanation be?
Is that because the pain is triggering the sympathetic system (Huge stress because of the pain), and directly after that the parasympathetic system is trying to balance it, but it's overreacting? and then the sympathetic system is going back to normal when parasympathetic stays high ?
Is there a physiologic explanation ?
Thanks

Could you elaborate on where the pain is and what symptom accompanies the vagus nerve stimulation?

Hello, it's quite a theoretical questions. If I'm not wrong. Syncope can be triggered by strong and sudden pain, sudden Heat, see of blood. I think that in those 3 example, the reason of the syncope will be stimuli of the vagus nerve. But how those 3 things Are doing this stimuli, physiologically talking? A 4th example is by applying directly pression on the vagus nerve pulse will go down, vasodilation, and syncope. In this last case, it's quite clear how the vagus nerve has been stimulated, but not the previous ones. Hope it's more clear now. And thanks

Short answer
Given your comments you are referring to the cause of fainting after being triggered by certain stressors. The reason is a sudden drop in blood pressure due to parasympathetic nervous system activation (vagus nerve activity). This leads to reduced blood flow to your brain, which results in a brief loss of consciousness (Mayo Clinic).
Background
There are various types of fainting (syncope) with various causes. The type you are referring to is neurally mediated syncope (Arthur & kaye, 2000). It is evoked by emotional activation due to stressors (pain, fear etc.) Stress responses are accompanied by the release of stress hormonses, most notably Adrenaline (epinephrine). Epinephrine release results in sympathetic nervous system arousal, resulting in increased blood pressure, increased pulse and sweating. It also increases amounts of blood being funneled to peripheral organs. These mechanisms aids in the fight,fright and flight response, as more blood in the periphery allows more glucose to be transported to the muscles (Agarwal, 2007). The funneling of blood in the periphery (venous pooling), however, can reach a point in which venous return of blood to the heart falls too sharply. This in turn can lead to a substantial increase in the muscle activity in the ventricles, as they are likely struggling to pump the small available amounts of venous blood into the heart chambers. The increased muscular activity in the ventricles is believed to activate mechanoreceptors that would normally fire only during stretch.
Stretch of heart muscle is normally associated with a high blood pressure. The warning message of a high blood pressure by the mechanoreceptors is sent to the medulla in the brainstem, which in turn leads to parasympathetic nervous arousal. As a part of the parasympathetic response, the vagus nerve is stimulated which reduces heart activity to reduce blood pressure.
However, when the mechanoreceptors are stimulated due to the overt contractility of the ventricles due to a low blood volume, they sent the same neural input to the medulla which normally signals hypertension, thus causing vagus nerve stimulation and hence a paradoxic parasympathetic arousal that results in low blood pressure (hypotension), low heart rate (bradycardia), and ultimately fainting (syncope) (Grubb, 2005).
References
Agarwal et al., Postgrad Med J 2007;83:478–80
Arthus & Kaye, Postgrad Med J 2000;76:750-75
Grubb, Circulation 2005;111:2997-3006

Why the downvote? Downvotes are great, but they should help to improve an answer. Isolated downvotes without comments  don't help.

I elaborated my answer to try to make it more clear.


text:
Is it possible to accurately measure micronutrient levels with the blood volume from a Dermal / Capillary puncture?
I have not been able to find much information beyond what tests are normally done with Capillary puncture sampling, as opposed to what tests are possible.
Could we test for a single micronutrient, or maybe some subset of nutrients with the blood drawn in this way? Is the issue purely volume, or are there other factors?
Thanks!

Welcome to Biology! What exactly do you mean with micronutrient? An example would be best, as trace elements may have very different detection limits than vitamins.

Thanks :) And by micronutrient, I was referring to any nutrient you would see on a nutrition label (yes, I know that's broad). Is there a good resource/chart that has micronutrient specific-info on testing methods / requirements? Or even just a good place to look for that kind of thing (I can do the research, as soon I can find a good place to look :) ).

Detection methods are constantly getting better, requiring lesser amounts of blood to make a determination. In newborns, a heel blood sample (of capillary blood) is used to detect up to 40 (sometimes more) disorders from maple-sugar urine disease and hypothyroidism to hemoglobinopathies and organic acid conditions. If such large molecules can be detected in capillary blood, smaller molecules should as well.
There are differences in central venous sampling and capillary blood sampling, but it could be argued that since the capillaries are the site of exchange of nutrients, this is the most accurate site to determine availability of micronutrients in blood.
One reason labs take more blood than required for the test is to run a second analysis if the first is abnormal. Although it's not done for every abnormal, clinicians often want to confirm significant abnormals before treating a possible lab error.
Newborn screening tests
Newborn Screening
Conditions Screened By State
A Layperson's Guide to Tandem Mass Spectrometry

Hey thanks for the answer and links! Would love to dig more into the specifics on the differences between central venous sampling and capillary blood sampling, re: nutrients and blood content -- any resources you could recommend?

@mattmattmatt - Gosh... I started learning about that, um... in 1977. Google scholar using the words "arterial, venous, capillary blood X" should help! :)


text:
Selection Pressure on Orca Whale Coloration
What is the proposed selection pressure that leads to the distinctive coloration of Orca whales? I can find nothing in the literature.

Hello. I want to remind you that natural selection is not the only process important to evolutionary processes. There are probably several posts that discuss that. You will find a paragraph in the first answer on this post for example.

Adding to Remi.b's comment, not every trait is adaptive. We've most recently discussed this here in this answer to a question about rose thorns.

Assuming the pattern of color would be adaptive (to a certain degree), here are few guesses. It sounds likely to me that such coloration would have evolved in reaction to recognition and signalling. Eventually due to sexual selection or to kin recognition. It may also be under selection for camouflage. Indeed orcas are black on the back and white on the belly and preys seeing from above would see a black background and those seeing from below would see a lighter background.

Clarification: I am familiar with concepts such as genetic drift and non-adaptive mutations. Given that the Orca is an apex predator, I could certainly believe that coloration doesn't confer much interspecies competitive advantage. If I were pressed to guess, I would actually guess sexual selection. I was just hoping someone actually had a theory (i.e. with some evidence) on which evolutionary process governs it.

Also, @Remi.b, I totally agree, countershading makes perfect sense. I guess was referring more to the black and white eye spots and the other well-known splotchy patterns.

Not every trait has to mean something. Orcas could have been red for no good reason. By "no good reason" I mean genetic drift, population bottleneck or something.

You can find a discussion of this topic in the literature:
Mitchell, Edward. 1970. Pigmentation pattern evolution in delphinid cetaceans: an essay in adaptive coloration. Canadian journal of Zoology 48(4): 717-740.
Perrin, W.F., 1972. Color patterns of spinner porpoises (Stenella cf. S. longirostris) of the eastern Pacific and Hawaii, with comments on delphinid pigmentation. Fish. Bull, 70(3), 983-1003
Caro, T., Beeman, K., Stankowich, T. and Whitehead, H., 2011. The functional significance of colouration in cetaceans. Evolutionary Ecology, 25(6), pp.1231-1245. http://web.csulb.edu/~tstankow/Caroetal2011.pdf
And related helpful article:
Evans, W.E., Yablokov, A.V. and Bowles, A.E., 1982. Geographic variation in the color pattern of killer whales (Orcinus orca). Report of the International Whaling Commission, 32, pp.687-694. http://www.kasatka.com/kirsten/ColorVariation.pdf
I'll let you explore these and their citations.
Remember, Google Scholar is your friend.

It would actually be better if you summarized the main points of the articles.

@kmm I was simply addressing the second part of the question: demonstrating sources in the literature. We don't have to handhold through the entire learning process...


text:
Why do four spermatids have different genomes?
It's been a while since my last class in genetics, so I've forgot most of it. However, I found myself studying human reproduction and I've the following doubt concerning spermatogenesis:
the process begins with a spermatogonium, a diploid cell (i.e. it contains 23 chromosomes and the corresponding homologous), which, through mitosis, generates the primary spermatocytes. The latter undergoes meiosis generating the two secondary spermatocytes; these are haploid, one of them contains 23 chromosomes and the other the corresponding homologous.
Since a chromosome A and its homologous B contain the same genes but with (generally) different alleles, the two secondary spermatocites have different genomes. Now, each of them splits into two equal cells (spermatids), through mitosis. My textbook says that the four spermatids have all different genomes, but shouldn't there be only two genomes?

You're forgetting about homologous recombination during meiosis.

Look at this post. I explained what could be the result of homologous recombination in mitosis and this is similar to what would happen in meiosis.

Spermatogonia contain 46 chromosomes (not 23) Spermatogonia increase their number by mitosis and one of Spermatogonia grow by increasing it's size to form primary spermatocyte. Primary spermatocyte undergo meiosis to produce spermatid. In 1st meiotic division secondary spermatocyte is formed following it in 2nd meiosis spermatids are formed. Both primary and secondary spermatocyte have 23 chromosomes.

Welcome to SE Biology. Your answer sounds, and may well be, correct, but as this is not my area, how am I to know? And that is the basic reason why we require answers supported by external authoritative sources (when it’s not just a question of logic). You just need to reference a Wikipedia article or book excerpt available on the internet, or quote from a printed edition. Have a look at the Help on answering questions. We look forward to your amended answer and future contributions.