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Why are there six reading frames if only one strand of DNA is referred to as the ‘coding strand’?
We need to consider six reading frames when considering the potential of DNA to encode protein (three frames for each strand). But only one strand is transcribed into RNA — the so-called coding strand. It would therefore seem to me that there are actually only three reading frames to consider. Why, then, do people refer to six?
Another point concerning reading frames is the definition of Open Reading Frame — ORF. One text defines ORF as:

“An ORF is a continuous stretch of codons beginning with a start codon
  (usually AUG) and ending with a stop codon”

whereas another text defines it as

“An ORF is a continuous stretch of codons that do not contain a stop
  codon (usually UAA, UAG or UGA)”

It seems to me that the first definition is correct. Which is the generally accepted definition for ORF?

I have edited your question, not only to correct the English, but to clarify it. In a way, I have set it up so I can provide an answer (when I have a moment) that points out the source of confusion (not only yours, but also others'). However I think this is fair. I have also improved the presentation of the two alternative definitions of open reading frame (you should have defined the abbreviation, ORF, the first time you used it.) I see why you did it, but in general you should not ask two questions in one, because it can lead to answer being accepted which doesn’t  answer both parts well.

In my opinion this question reflects two things:

The difficulty students have in appreciating the historical experimental concerns of research workers in an area that is now well understood, and, hence, how it influenced the coining of new technical terms.
The way that the use of terms has changed with time as old concerns disappear and new ones arise. Thus, a term originally used in one sense may have subsequently been adopted to mean something else, even if this does not appear strictly logical.

What is a coding strand?
This is the crux of the first question, and the answer is that the term ‘coding strand’ does not mean anything (or at least is ambiguous) without context. Thus, I think the poster is assuming a genome context, and this is the fallacy of her argument.
If one talks (or thinks) about the ‘coding strand’ of a DNA genome, one is assuming that because many DNA genomes are double-stranded, if you separated the two strands (e.g. of a small DNA virus) and performed a conceptual translation (decoded the DNA into amino acids using a genetic code with T rather than U) one strand would have all the information for the genes and the other strand would have none. Another way of saying this is that you are assuming that all the genes in the genome have the same directionality (arrow direction on a genome diagram, such as that from E. coli, below). This is hardly ever the case. (The only examples I can think of are the genomes of single-stranded RNA viruses.)

So if you use the term ‘coding strand’, you must state that this is in the context of a single gene. Each strand of DNA in a genome (e.g. E.coli) will contain sections of DNA that are coding and some that are non-coding in terms of conceptual translation. (If you look at papers describing early isolations of genes you will find the words “coding strand” generally qualified by  “of the gene”
But cDNA has just one coding strand…
Historically one of the concerns was to sequence eukaryotic cDNAs, DNA copies of mRNAs. These would be monocistronic, i.e. encode a single protein. So here one strand would be coding and the other non-coding. Was it possible to reduce to three the number of reading frames it was necessary to analyse in this case? No! The fact that only one strand is coding was no help at all as there was no way of knowing which this was in the cDNA being sequencing. Likewise for a the fragment of any gene. You had sequenced a piece of DNA, cloned into some plasmid vector and there was no way of telling which strand the sequence you read out originated from. Hence you need to translate it in all six reading frames to find potential amino acid sequences.
So what is an Open Reading Frame?
Open Reading Frame is a term that is often used today in a manner distinct from the way it was used when it was coined. At the time it was coined one would be sequencing short stretches of cDNAs or virus or bacterial genes and there was a low likelihood that one would be sequencing through the C-terminus, i.e. the stop codon of the gene. One’s concern was to concentrate on reading frames that were not interupted by stop codons. This original usage is reflected in the definition of Open Reading Frame in Wikipedia:

“An ORF is a continuous stretch of codons that do not contain a stop codon (usually UAA, UAG or UGA)”

However as knowledge increased and technology improved, the focus switched to discovering genes in the genomic or long partial genomic sequences of organisms. Now one was working with long DNA sequences containing many whole genes. The focus became finding potential genes based on start and stop codons (and a cut-off length). This is reflected in the documentation for the EMBOSS program, getorf:

“An ORF may be defined as a region of a specified minimum size between two STOP codons, or between a START and a STOP codon.”

Note that even this last definition is ambiguous.
Which is correct? That is a concern of students. In the real world one must recognize that the meaning of expressions can change. If there is any ambiguity — as here — one must define the way in which you are using the expression.

The coding strand refers to the DNA strand with the same base order as the RNA transcript for a particular gene. As one gene is always entirely present on a single DNA strand there are indeed 3 reading frames possible in this strand, with only 1 actually containing the correct codon sequence for this gene.
However when we view an entire genome it is entirely possible for one gene to be present on one strand with another gene present on the other,  meaning that the coding strand for one gene is the non-coding strand for the other. This is why there are 6 possible reading frames for the genome as a whole as both strands can (and do) contain genes.
As to the ORF, both definitions seem to be in use. In the context of trying to discover genes by looking for long ORFs the first definition is probably more helpful as following the second definition could lead to a lot of falsely predicted genes (for an extreme example a long stop codon free sequence that has no start codons either would be considered a possible gene even though that should be impossible).

Thank you Koen. Your mean about the first question is some genes (coding genes? I'm not sure") are located on the non-coding strand, yes?, could you please tell me some example gene?

@Mary It isn't that genes are on the "non-coding strand" its that either stand can be a coding strand. Imagine a book arranged like this: on all the right-hand pages, the text is printed as normal, but on the left hand pages, a different, unrelated text is printed upside down. You would consider that side to be the "non-reading side". But behold! rotate the book 180 degrees and now suddenly the "non-reading side" is the reading side and vice-versa. Both strands can be coding strands, but you have to read them in the opposite direction.

@KoenvdH — I think your answer is correct. The reason I posted one of my own was to focus on what I think are the causes of confusion. It's an attempt to give a historical context, which I am able to do because of my, er, history.

@David Hah I reckon your answer is far better for clearing up the terminology confusion.


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How do we know that our genetic similarities to other species is actually due to common ancestry?
I know all about how the fossil record shows more human-like species coming about over time, and how modern testing proves we have genetic similarities with other animals.
All that says is we have similar genetic blueprints to animals in the past and present. How do we know these similarities are caused by having a common ancestor?

I don't believe in evolution, it's like saying 'similar' => 'come from'. But every various things inherently have similarities and dissimilarities. don't they?

That's why people in science field keep looking for physical evidences and study them. It's a very very long process and will take years to know the answers..... it's like you're studying the vast universe and wondering if there are alien life forms out there..... so difficult and still unknown.

@ChanKim Your implication reveals a massive misunderstanding of evolution and, in evolutionary terms, is plain wrong. No wonder you do not "believe" in it.

You should have a look at this highly related post and at Demonstrable and repeatable examples of evolution

If you want a short and very introductory course to evolutionary biology you should have a look at Understanding Evolution by UC Berkeley.

I think a major misunderstanding that could be coming in to play here is the misconception that DNA is like a engineering document, e.g. "this strand of DNA says i will have an arm with 5 fingers of certain proportions, this strand of DNA says I will have a facial structure like this.", and not realising that it appears our DNA is full of junk "data" that doesn't appear to be active or serve any purpose, and that even this "junk" un-used DNA is common between believed-to-be ancestors. It would be like throwing a dice in two sets of a thousand and getting results that are 80% the same order.

We don't know, and we never will. Science doesn't work that way. But evolution is the simplest hypothesis that is both falsifiable and consistent with lots of experimental data. Therefore it is the currently accepted scientific theory.
I would agree that genetic similarities between current species does not in itself suggest that they evolved from a common ancestor. But knowing the genome sequence of various species let's you do much more than simply measure pairwise similarity between species. The structure of genetic variation (losses, duplications, inversions, mutations ... ) also fits with evolutionary models. And crucially, genome sequences confirm predictions made by the evolutionary theory --- evolution is not just a post-hoc explanation of data, it has actually been tested many times over, and has never been falsified.
A good example is the sequencing of the human and chimpanzee genomes. We knew long before any genome was sequenced that humans have 23 chromosomes (23 pairs), while chimpanzees have 24. If the theory of evolution is correct and we do have a common ancestor, then that ancestor should have 24 chromosomes, like the chimps do, and it must be that in humans, one chromosome is a fusion of two ancestral chromosomes$^*$. This is a strong, testable prediction: if we don't find this arrangement of chromosomes, then evolution is proven wrong! In the 1980's, the sought fusion chromosome was found using high-resolution cytogenetic banding: it's chromosome 2. Modern genome sequencing later localized the precise fusion point on the human chromosome.
Also, the fossil record provides a timeline, not just a bunch of more or less similar organisms. In general, we don't find old fossils of modern-day animals (including ourselves), but we do find old fossils of species that no longer exist today. And when piecing together the findings, it looks like there is a sequence of gradual changes over time. That's a pretty good clue. What hypothesis might fit this data?
If you are suspicious about the theory of evolution --- which is fine, you should think critically about everything in science! --- then you must look for an alternative hypothesis which is falsifiable and fits the data. (Note that "god made everything" is not a falsifiable hypothesis, since it makes no testable predictions, and therefore not relevant to science.) If you come up with anything, let us know!
$^*$ As pointed out in comments, a priori one could imagine other rearrangements between the ancestor genome and the chimpanzee/human genomes that give the same result, but I believe this is the simplest hypothesis.

Just to clarify, we "don't know" in the same sense you can't know whether it's better to leave an apartment through the front door, or the window on the second floor...

"We don't find any old fossils of modern-day animals" -- but when you do find a coelacanth, MOST IMPORTANT PRESERVE SKELETON AND GILLS ;-)

@SteveJessop, All right, there are some current species that have changed little in recent evolutionary history and so we do find fossils of them. I was trying to describe the general trend.

@Cephalopod  Not sure what you mean. I meant "we don't know" in the sense that the scientific method (within Karl Popper's paradigm) does not prove hypotheses, it only disproves. Those hypotheses that are still not disproven after lots and lots of testing are accepted as theories. Like evolution, for example.

Nitpick: why couldn't it have been that the common ancestor of humans and chimps had 23 chromosomes, but in the chimp lineage, one of them split?

@zwol, Very good point! I didn't mention it, but we know the chromosome did not split because human chromosome 2 has an extra centromere, derived from the other ancestral chromosome. This centromere is no longer functional in humans, but clearly recognizable from sequence data. So there must have been a chromosome fusion event.

But we didn't know this before, did we? So we didn't have to find "exactly this arrangement". Could have been any number of fusions and splits of chromosomes. Also, I don't see why our last common ancestor needs to have had 24 chromosomes.

@BlindKungFuMaster, If you consider additional fusions/splits, they would have to happen independently in the same way in both the homo and pan lineages to generate two genomes that look like they are just separated by a single fusion event. That's very unlikely to occur by chance. So by far the most likely hypothesis is a fusion in the homo lineage, which implies the ancestor must have had 24 chromosomes.

@Roland you haven't explained why we would expect to find a fusion in homo rather than a split in pan, without already having looked

In your answer you derive the prediction based on the number of chromosomes alone. To me the numbers would only imply that the difference between fusion and split events in the homo lineage is one higher than in the pan lineage. If more information went into the prediction, like "the look" of chromosomes, maybe you could expand on that.

"Note that 'god made everything' is not a falsifiable hypothesis, since it makes no testable predictions, and therefore not an option." What do you mean by "not an option"? I'm confident you're not saying it is necessarily untrue, but I could easily see someone unfamiliar with the logic misunderstanding what you mean here.

@OrangeDog I guess a split chromosome in pan is a possibility a priori. Although it would somehow have to duplicate the centrosome, I'm not sure if that possible. But regardless, the observation of a fusion chromosome (with an extra centromere) is vastly more likely under the evolution hypothesis than under any alternative that I know of.

@jmpc  I mean that "god made everything" is by definition not a scientific hypothesis since it is not falsifiable. You may still choose to believe it, of course, but it's outside the realm of science.

One alternative, falsifiable, false hypothesis is that multiple species evolved in niches so narrow that there was no alternative which could lead to survival. Of course, that didn't happen (and would require an implausible transfer of this restriction from phen. to gen.; also environmental conservation of "junk", which you DON'T see in cases like convergent evolution of eyes). But it's interesting as an academic recreation to think of such things. On a small scale, though, you do get SNPs which multiply arise with no common ancestor (eg adult human lactose tolerance without common ancestry).

To be fair, the bible and religion in general provides plenty of falsifiable hypotheses. It's just that believers keep moving the goal posts and if that doesn't work anymore, they do the intellectual equivalent of sticking fingers in their ears and shouting "lalala" at the top of their lungs.

Coming back to this question after years, there’s a simpler way to look at evolution: It’s a model

If you look at a scatter plot and roughly see a line, you might deduce a linear relationship. This relationship could easily not be linear (or even not exist) but given the data in front of you, a linear relationship is the simplest explanation, and by Occam’s razor, the best.

It is vanishingly unlikely that when DNA sequences which are thousands and thousands of bases long are identical between two creatures, that those sequences have no common origin.
That's like saying, "Your Honor, I didn't pirate that Justin Bieber track; I generated random 16 bit audio samples which just happen to match!"
That is less likely than the proposition that Melania Trump's speech wasn't plagiarized from Michelle Obama's, which already sits at a laugh-inducingly low probability level.
It's not a question of what we know, but of eliminating vanishingly improbable, time-wasting hypotheses.
Not only do we have the statistical argument that even a vast number of monkeys typing on typewriters are not going to reproduce the text of Macbeth, but there is the observable fact that DNA replicates.  We can almost literally see identical pieces of DNA being reproduced from a common origin.  The replication from a common origin hypothesis to explain sameness is overwhelmingly probable, whereas independent origin is vastly improbable.
It's not a question of how do we know, but rather what is the most plausible hypothesis from among those that are consistent with our observations.
Knowing is reserved for pure facts, like consistency between logical and mathematical propositions. We can know that some theorem in mathematics proceeds from some axioms. We can also "know" the content of an observation, in some sense. We cannot know whether an explanation for it is true.
We can know when an explanation is false and we can gradually repair our understanding by identifying these failing situations and improving the explanations.
A final remark. Just because two creatures have some common DNA doesn't mean that those creatures got that DNA from a common ancestor at the time when they diverged. DNA can be introduced by vectors such as viruses. So that is to say, two creatures that diverged, say, a hundred million years ago could have some common DNA that they acquired more recently, like a million years ago. It is practically certain, though, that this same DNA itself has a common origin.
Unless you regard viruses as your ancestors, then some common strand of DNA is in fact not necessarily evidence of common ancestry per se.

It is like finding crap in your backyard and thinking about what animal must have laid it. You don’t have a camera in your backyard, but you do have reason to believe it’s your dog.

You didn’t find any other animal footprints and the DNA test matches your dog’s DNA with DNA found on the crap.
So either some animal snuck into your backyard without leaving a trace and took a crap that was then painted with your dog’s DNA, or the crap was your dog’s.

I think one very fundamental fact that you are overlooking, which we pretty much take for granted, is that DNA is the mechanism of inheritance of traits.
What I mean is that my DNA is very similar to my parents' and siblings. It's also similar, but slightly less so, to my grandparents, my cousins, aunts and uncles, etc. The further you go from my known relatives, the less similar our DNA becomes.
This is also true for all living organisms. For everything from bacteria, to plants, to flies, we can look at their DNA, and that of their relatives, and the more closely related (in the familial sense, as in parents, siblings, etc., not in the evolutionary sense, although I'll speak to that in a moment), the more similar the DNA.
So that is demonstrably true for every living thing we can observe today. But what about the past? Well, if this theory of DNA and familial relationship is true, then we can predict that, for instance, my DNA is more similar to the DNA of present-day people in the countries where my ancestors came from than from other countries, even though we have no historical/genealogical evidence of relationship. And this bears out-- a commercial DNA ancestry test shows I share genes with the general populations of the countries my recent ancestors are documented to have immigrated from.
This idea that familial relationship are biological relationship should seem at once obvious but also surprisingly insightful. If I am related to my human cousins because of the mechanism of DNA inheritance and the sharing of a common ancestor (our common grandparents), then it also stands to reason that chimpanzees are literally our familial cousins, very distant, from a common ancestor a long long time ago. Biological relatedness is in fact the same thing as familial relatedness.
If you don't buy that, then you have to explain why it's true that all observable organisms today share familial relatedness through DNA, but for some reason, this isn't true going back into the far past. What changed in the past? When did this start happening?
The only reason we get tripped up in this line of reasoning is because chimpanzees look very different from humans, and we cannot mate. In the past, people thought this was because different species were fundamentally different types of beings. But biological insights, specifically the understanding of DNA, shows that we are all fundamentally the same type of creature, with reproductive incompatibilities developing over time. The tree of life is literally a family tree.
Also, from biochemical understanding, we know generally how long mutations take to arise. Combined with fossil evidence, we can create a pretty good model of how far back divergences arose.

"Also, from biochemical understanding, we know generally how long mutations take to arise. Combined with fossil evidence, we can create a pretty good model of how far back divergences arose." I am not sure about how good those models are, given the opaque nature of mutation rates ... ;) Good answer, though!

There are some good answers here already but they mostly focus on whether similarities in the DNA sequence of organisms imply common ancestry. This misses something much more fundamental that is very strong evidence for this particular question: we all use essentially the same configuration of machinery to store genetic information and turn it into proteins.

All organisms on Earth use nucleic acids with a ribose/deoxyribose backbone and not other chemistries like XNA, PNA or other alternatives.

"There is nothing Goldilocks about DNA and RNA," Holliger told
  Science. "There is no overwhelming functional imperative for genetic
  systems or biology to be based on these two nucleic acids."

All organisms on Earth use the same nucleobases (G, C, A, T, U), even though alternatives exist that can apparently replicate perfectly well.
All organisms on Earth use the same genetic code for protein synthesis (with a few slight variations) even though the matches between codons and amino acids are probably largely arbitrary.

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What type of fish is this and why is it so big?

This is a screenshot from a youtube video that you can watch here:
https://www.youtube.com/watch?v=zcdJNPYkIE0

Some sort of grouper?

I think it's the pacific goliath grouper

Yeah but its a whale. this is a "fish" from the title so I didnt assume it to be huge

White Shark? Whale Shark? Tuna? There are lots of large fish species...

I'm simply going off the name of it. When someone mentions "fish" you don't really imagine the really big ones. Fish you usually imagine small. Whereas if someone mentions "shark or whale", then obviously you have a different idea on size.

Whales are mammals, not fishes - calling a large fish a whale is just wrong (and of course the confusingly named whale shark is not a whale at all). Sharks are fishes, but they are a separate category of fishes from the rest. There are both large and small sharks. The smallest ones are only ~20cm, which probably makes them smaller than what you typically think of when you think of "fish".

Why is it so big? Because it’s parents were. It’s called heredity.

@KSplitX have a look at the mola mola, tuna, sturgeon, catfish, and the largest fish species in the world, Rhincodon typus for examples of BIG fish!

That is a Queensland Grouper (common name).

to be a proper answer you need to include how you determined this.

Welcome to Stack Exchange! When you reach 50 reputation points you can leave comments on other people's posts. There's a fairly high bar for posting answers, and as the other comment mentions, adding supporting sources is always a good idea and almost always necessary here. Don't worry about the negative voting so much, but if you can explain what it is that leads you to this conclusion, that would be better.

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How long can Vibrio cholerae live in its ambiental optimal context?
How long can the Vibrio cholerae live in its ambiental optimal context?
Thank you in advance. My problem is that i can't find this information. I did some research on google, but nothing was retrieved, I even used other search engines. Thank you very much for your help.

I Found It!!!!    SURVIVAL OUTSIDE HOST: Cholera can survive in well water for 7.5 ± 1.9 days and the El Tor biotype can survive 19.3 ± 5.1 days(Footnote 21). The bacterium can survive in a wide variety of foods and drinks for 1-14 days at room temperature and 1-35 days in an ice box(Footnote 21). It has also been found on fomites at room temperature for 1-7 days(Footnote 21).
Source>>http://www.phac-aspc.gc.ca/lab-bio/res/psds-ftss/vibrio-cholerae-eng.php


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What are the predators of Glaucus atlanticus?
I'm researching the Glaucus atlanticus, also known as the blue glaucus, among various other names, but after reading quite a few articles and searching on the Internet as many different ways as I can think of, I can't find any of its predators, or any indication it has no natural predators. Everything I've read is just silent on the issue. Does anyone know what, if any, predators this has? Thanks!

While I don't really know anything about that animal, it doesn't really need a specific predator (to keep its population in check) if it has to compete with other organisms for the same food source(s).

Try out using Google Scholar to take a more scientific literature-based approach to your search.
Frick et al. (2009)1 found that about 42% of logerhead sea turtle (Caretta caretta) stomachs contained remnants of G. atlanticus.

We were able to identify G. atlanticus in the diet of loggerheads because whole or nearly intact specimens were present.

 Loggerhead turtle mouth and throat with sharp papillae. Source NCSU CMAST (Photo by Craig Harms)
Bieri (1966)2 observed G. atlanticus frequently attacking one another and biting off pieces of each other. In one case, one individual ate all but the head and trunk of a smaller specimen.

Citations:
 1, Frick, M.G., Williams, K.L., Bolten, A.B., Bjorndal, K.A. and Martins, H.R., 2009. Foraging ecology of oceanic-stage loggerhead turtles Caretta caretta. Endangered Species Research, 9(2), pp.91-97.
2. Bieri, R., 1966. Feeding preferences and rates of the snail, Ianthina prolongata, the barnacle, Lepas anserifera, the nudibranchs, Glaucus atlanticus and Fiona pinnata, and the food web in the marine neuston.

Good answer (+1), however I fail to see the function of the somewhat gross picture of the loggerhead. Note2self: stay well away from the beak of loggerheads...

RHA just for the FYI nature is cool factor.


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Can a firefly control its glow?
I've just seen this animation:

I always thought the firefly glow is ongoing slow chemical reaction, like in glowsticks though through different chemicals. As such it seems impossible to control quickly, like on this image.
Is this image real or edited? Can firefly control it's glow? If it can, how much?

Yes, fireflies control their glow patterns. Different species have different patterns. You can read about the luciferase reaction and its regulation here.


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How does the human body extract energy from ethanol?
I was talking about alcohol and obesity with a colleague. I always thought the only cause of that is the sugar that is found in most alcoholic beverages. But my colleague pointed out that ethanol itself provides calories to human body.
I checked that and it seems to be the case. What I don’t understand is how is it possible. On wikipedia I found following statement:

If catabolism of alcohol goes all the way to completion, then, we have a very exothermic event yielding some 1325 kJ/mol of energy. If the reaction stops part way through the metabolic pathways, which happens because acetic acid is excreted in the urine after drinking, then not nearly as much energy can be derived from alcohol, indeed, only 215.1 kJ/mol.

The statement relates to these reactions:
$$C_2H_6O (ethanol) → C_2H_4O (acetaldehyde) → C_2H_4O_2(acetic acid) → acetyl-CoA → 3H_2O + 2CO_2$$
Now note that the wikipedia calls the pathway "exothermic". However, I don’t think that human body can derive energy from heat. Or can it?
Since most articles claim that ethanol alone has positive caloric value, how exactly is this energy extracted and used or stored as fat?

Exothermic means that a reaction yields heat, not that the body uses it. Alcohol has 7 kilocalories per gram, which is almost twice as much as carbohydrates (4 kcal/g).

To quote from the editorial on the Wikipedia page: "This article has multiple issues. Please help improve it or discuss these issues on the talk page". Wikipedia is a product of people like you and me. Be aware of that.

Preamble
The question suggests unfamiliarity with the nature of biochemical oxidations and their relation to energy transfer in biology. The naïve reader is recommended to consult a text for a coverage of this subject: all I feel is appropriate here is a general summary followed by a brief indication of the key reactions.
General principles of energetic value of and biological oxidation of foodstuffs

The energy available from the oxidation of foodstuffs such as starch, fat and alcohol may be represented as the thermodynamic Gibbs Free Energy change (ΔG) in their complete oxidation.
This value can be determined chemically by bomb calorimetry in which the oxidation is done directly by oxygen and the energy produced is in the form of heat.
In biological oxidations the immediate oxidant is a molecule (an enzyme cofactor) such as NAD+ (or NADP+ or FAD), and part of the Gibbs Free Energy change is translated into chemical energy in formation of the reduced compound — NADH etc. Only some is lost as heat; but enough to give an overall negative ΔG, that causes the reaction to proceed.
The reduced coenzymes can be used to produce ATP by oxidative phosphorylation (involving oxidation by oxygen) or in reductive processes such as the synthesis of fatty acids, depending on the organism’s energy requirements.
Likewise, the molecular intermediates produced in the course of the biological oxidation (e.g. acetate) can be oxidized completely by oxygen (the terminal electron acceptor of the electron transport chain) to carbon dioxide and water (with production of more NADH in the tricarboxylic acid cycle, and hence more ATP), or can be converted to other metabolic intermediates or used as the precursors of other molecules, including storage molecules.
If the organism has a sufficient supply of energy (ATP) already, surplus intake of foodstuffs will lead to the deposition of energy reserves.

The case of ethanol
The question rightly states that ethanol is converted to acetaldehyde and then to acetic acid, but fails to include the oxidant, NAD+, which is an essential participant in the biological reactions:

[ADH: alcohol dehydrogenase; ALDH: aldehyde dehydrogenase ]
Thus, two molecules of NADH are produced, providing either ATP or reducing power.
The question assumes that after conversion of the acetate to acetyl-CoA it will be oxidized in the tricarboxylic acid cycle*. However in a fed subject with sufficient energy the cycle is suppressed and the acetyl-CoA will be converted to malonyl-CoA, the precursor of fatty acid synthesis. These processes require both reducing power (NADPH, which can be obtained from NADH) and ATP (ditto):

*The quotation states that “acetic acid is excreted in the urine…”. I have no knowledge of what proportion of ethanol is disposed of in this way, but I would imagine it is small — certainly not enough to prevent beer belly. However this is not the main reason why “catabolism of alcohol” does not “go(es) all the way to completion”.
Postscript
The biochemistry above is covered in Section 30.5 of Berg et al., entitled “Ethanol alters energy metabolism in the liver”. This was formerly freely available to read online, but unfortunately this is no longer the case. However copies of this edition can be picked up very cheaply on eBay, for example, and the student can rely on its coverage of basic biochemistry.


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Are gene conversions and expansion/contraction of repetitive (satellite) DNA examples of directional, non-random mutations?
Are gene conversions and expansion/contraction of repetitive (satellite) DNA examples of directional, non-random mutations? For some context, it was brought to mind as a result of reading the following;
"Within the broad category of gene mutations we should consider not only the classical, purportedly random changes, but also the internally directed changes that are called gene conversion and duplicative transposition (collectively constituting molecular drive) (see Dover et al., 1981)." (From 'A Botanical Critique of Cladism', pp 14-15)

Please include your question in the question. A title is a title. This will also make you explain more fully and clearly.

For Repetitive Sequences:
Duplications of repetitive DNA (as in replication-slippage) are not "as random" as radioactivity, but still, there is no genetic mechanism that intentionally triggers the duplication of a gene. Also, during replication slippage the site of DNA-pol re-association is random, causing duplications of different lengths. So I'd still call it a change that's both "random" (in terms of sequence) and "non directed" (as in "lacks a direct purpose").
Together, I'd prefer the term "duplication" over "mutation" for the expansion of repetitive/satellite DNA, (while "duplication" is a type of "mutation")
For Transposons:
Your reference cites 'duplicative transposition', and a lot of repetitive DNA originate from transposons (Belyayev 2020). For jumping genes, I would prefer the term „recombination“ instead of "mutation".
The appearance/exchange of specific large sequences is called Recombination.
From Harret & Sherrat 1997:

In bacteria, two categories of specialised recombination promote a variety of DNA rearrangements. Transposition is the process by which genetic elements move between different locations of the genome, whereas site-specific recombination is a reaction in which DNA strands are broken and exchanged at precise positions of two target DNA loci to achieve determined biological function. Both types of recombination are represented by diverse genetic systems which generally encode their own recombination enzymes. These enzymes, generically called transposases and site-specific recombinases […].

Furthermore, so it‘s incorrect to categorize transposons as „non-random“, since they insert mostly at random sites and can cause random DNA-damage next to the excision/insertion site Wicker et al. 2016.

Indeed, the 3,000 bp flanking the excised transposons can contain over 10 times more mutations than the genome-wide average. Since DNA transposons preferably insert near genes, this is correlated with increases in mutation rates in coding sequences and regulatory regions.

In my eyes, a better example of "directed"/"intended" (but random in sense of sequence) mutagenesis would be AID, an enzyme that increases antibody binding variability by intentionally introducing point mutations at very specific and isolated sites inside one gene.

I can see how AID increases genome-wide mutation rates, but the individual mutations are still 'random' in the sense that there's no bias towards a specific sequence appearing at any site in the genome. On the other hand, it would appear to me that slippage at repetitive sites, and gene conversions (transpositions too though I didn't mention them), bias the appearances of specific sequences in the genome.

AID does not act genome wide. It‘s directed towards the variable region of immunoglobulin genes where it introduces random mutations in an isolated section in a controlled manner. You are mistaken, Transposons are not specific. They can even insert inside genes an inactivate them, and if too many transposons are active, they will destabilize the genome  (see piRNAs and infertility). In general, when talking about mutation, geneticists don‘t immediatley think about transposons. A far better term for large sequences changing location would be „recombination“

Understood for immunoglobin genes although the same point applies, the 'gene-wide' mutation rate doesn't bias the appearance of specific sequences or nucleotides (or does it?). I was not saying transposon insertion sites is non-random: what's non-random is the appearance of sequences specifically corresponding to the transposon sequence.

Yes, but the appearance of specific large sequences is better described with the term „recombination“ than with „mutation“. Yes, the term mutation is associated with transposons, BUT the mutation from transposon is due to random errors that come with sloppy deletion/integration of the transposon and subsequent DNA-repair (and not due to appearance of large specific sequences) Wicker et al. 2016.

Yeah, it makes sense to better describe it as recombination. What about expansion/contraction of repetitive DNA and gene conversions? Do you agree that this is directional mutation when it comes to appearance of specific sequences or do you think this is still, technically, random?

I'd say gene conversion is more recombination than mutation. I don't know about the expansion/contraction of repetitive DNA, isn't repetitive DNA just tons of inactive Transposons?

Not really. When repetitive DNA is being replicated, the nature of the repetitive region results in the slippage of the replication machinery, which can wind it backwards (thus re-replicating the same repeats, resulting in more repeats) or forwards (thus shortening the number of repeats). The actual repetitive sequences make it more likely that this kind of slippage happens during replication, thus biasing the appearance of more of the same repetitive DNA.

I see. This mechanism is not recombination then, obviously. I’d call this simply „(Gene) duplication“, when talking about this mechanism. Using the term „mutation“ isn‘t really incorrect, but still much to general or abstract compared to „Duplication“

Well ... i dont know if it's 'gene' duplication if you're not duplicating a gene, although short short repetitive sequences can be duplicated. From ScienceDirect: 'In replication slippage, a long stretch of repeat sequences in the DNA folds back and pairs on itself, forming an internal hairpin or stem–loop structure, during replication.' This seems to me to be a simple replication error, and therefore can be called a mutation. Of course you can be more specific in describing any kind of mutation.

Exactly, "mutation" is just too broad. It's good practice to specify the type of mutation, if you know it. If one says "cancer mutates" that can mean anything from chromosome breaks (aneuploidy) to point mutations. However, if one says "gene mutates", most people think that of (functional or non functional) point mutation(s).

Let us continue this discussion in chat.


text:
Why is linkage disequilibrium high on either side of a beneficial mutation, but not between sites across the mutation, during a selective sweep?
I was reading the paper "A survey of methods and tools to detect recent and strong positive selection" (2017) and came across this:

Upon fixation of the beneficial mutation, elevated levels of LD emerge
on each side of the selected site, whereas a decreased LD level is
observed between sites found on different sides of the selected site.
The high LD levels on the different sides of the selected locus are
due to the fact that a single recombination event allows existing
polymorphisms on the same side of the sweep to escape the sweep. On
the other hand, polymorphisms that reside on different sides of the
selected locus need a minimum of two recombination events in order to
escape the sweep. Given that recombination events are independent, the
level of LD between SNPs that are located on different sides of the
positively selected mutation decreases.

I am having trouble understanding how this works. If I am understanding this correctly, if you took two sites on the left side of the beneficial mutation during a selective sweep, you would see high LD between them. The same goes for taking two sites on the right side of the beneficial mutation. (Provided they are close enough to the mutation site of course.) However, if you took one site 300 bp to the left of the mutation, and another 300 bp to the right of it, you may not see the same rise in LD. I am not sure why this would be the case: wouldn't the entire region linked to the beneficial mutation, regardless of which side of the mutation it occurs to, be co-inherited and thus display similar high LD across the board, provided it is overall close enough to the site of beneficial mutation?

High-level answer
Obviously, if the positively selected site occurs on a single haplotype, then all the polymorphisms on that haplotype "win" due to hitchhiking and will have some degree of LD, regardless of whether they are left or right. All that this scenario is asserting is that the left and right flanks have a higher degree of within-flank dependence in their fate than they have inter-flank dependence.
In other words, the right flank will be preserved by recombinations left of the selected site, and the left flank will be preserved by recombinations right of the selected site. The flank blocks' interests are to some degree independent or antagonistic, whereas the polymorphisms within each flank have a common interest.
More detail
For the purpose of discussion, I think it is worthwhile to include the figure that they show here (Figure 2 in the paper):

It is less that there is no LD across the site, but rather that the LD is less marked than between sites on either side and the focal positively selected site (in black, in this figure). Negative selection is removing left or right flank polymorphisms separated from the selected site by recombination. As your quote notes, you would need a compensatory recombination to preserve LD across the site, which is relatively rare. So negative selection is not acting to preserve LD from the left to the right flank.
Everyone on the left is co-inherited due to the selection against recombination in that window. Everyone on the right is co-inherited similarly. However right and left are not co-inherited.
Note: since all polymorphisms on the haplotype are hitchhiking along with the selected site, when I say "selection against" what I mean is that recombination will mean that sites on the other side of the recombination event from the selected site cannot hitchhike at the same time. That hitchhiking is (as expected) the ultimate source of this pattern. And all of these LD blocks will decay with distance as expected.
Omega calculation clarifies within-flank dependence
If you go on to look at the equation 2 that immediately follows in the paper, this becomes maybe a little clearer:

\begin{aligned} \omega = \frac{\left({l \atopwithdelims ()2} + {W-l \atopwithdelims ()2}\right)^{-1}\left(\sum _{i,j\in L}r_{ij}^2 + \sum _{i,j\in R}r_{ij}^2\right)}{\left(l(W-l)\right)^{-1}\sum _{i\in L, j\in R}r_{ij}^2}. \end{aligned}

$\omega$ is looking for two flanks of fairly high intra-flank LD within themselves that have relatively low inter-flank LD with each other.

Thank you, studying your answer I feel like I largely understand this now. May I ask you to clarify your ‘Note: ‘ paragraph?

done. that passage was trying yet another way (possibly superfluously) to express that hitchhiking on the haplotype is still the only relevant selection happening in these flanking polymorphisms (for a strong canonical strong sweep). Hitchhiking on a single site plus recombination should equal this pattern.

Thank you. Btw, I think your second "Everyone on the left ..." meant to be "Everyone on the right ..."

In addition to the other great answer, I would like to revisit my question because I came across a stellar explanation in another paper I am now reading that also answers the question very succinctly and which I share here:

The LD within both flanking regions of the selected site is compared
with the LD between flanking regions. Selective sweeps lead to high LD
within but not between the flanking regions.
...
Selective sweeps generate a very specific LD pattern at sites
neighbouring the beneficial allele, which can be captured by the ω
statistic (Kim & Nielsen, 2004). Owing to the fast increase in
frequency of the beneficial allele, genetic variation in the region
under selection is only maintained by recombination during the
selective sweep. When conceptually regarding a chromosome as two
flanking regions adjacent to the selected site, a recombination event
divides the chromosome into two parts: (1) the original genetic
background of the selected site including one flanking region, the
selected site and the second flanking region until the recombination
breakpoint; and (2) the alternative genetic background, starting from
the recombination breakpoint at the second flanking region. Hence,
recombination will always affect only one side of the genomic region
separated by the selected site per recombination event, leading to
independent recombination patterns at both flanking sites. Therefore,
LD should be high when comparing sites within one flanking region but
low when comparing sites between the two flanking regions.
https://doi.org/10.1093/zoolinnean/zly007


text:
Complementarity of cDNA
Strictly speaking, what is the definition of cDNA?  This confuses me, since usually it is said to refer to DNA that is complementary to mRNA.  Is this correct?  Is it restricted to mature mRNA?
I also find directionality very confusing.  As I understand it, mRNA has a sequence equivalent (less introns, after splicing) to the so-called 'coding strand' of DNA.  Does this mean that cDNA made from mRNA, at least before treated with a DNA polymerase, is also complementary to the original genomic DNA?  Is this the better definition (I have seen this used as well, though the first definition seems far more common).
Lastly, as I understand it each chromosome has a forward and reverse strand, defined by convention, but that the 'coding' strand of a given gene is random.  This seems counter-intuitive... is it just because both strands are equivalent?  Does it introduce complications in terms of the cell 'knowing' which strand is the coding strand for a gene?
The most upvoted reply to this question (http://www.biostars.org/p/3423/) confused me even further.  I feel the same way as 'Onefishtwofish' does, in the replies.  Can anyone clarify?

It's a good question and has confused me as well.
A standard definition of cDNA is that it is a double stranded (ds) product of mature mRNA. I suppose it is possible to get a nascent RNA strand copied into cDNA, but I've never heard of that being done.
Because cDNA is dsDNA, the original strand is made from your mRNA as the complementary strand, but then you dispose of the RNA and make the second strand to get a stable, reproducable molecule. The total dsDNA molecule is what we refer to as cDNA (not a single strand of this material).
consider this simplified DNA molecule:
ATG-INTRON-CTCTAG
TAC-INTRON-GAGATC
this could be transcribed into the following mRNA (corresponding to Met-INTRON-Leu-Stop):
AUG-INTRON-CUCUAG
before nuclear export the intron is removed, making mature mRNA:
AUGCUCUAG
you make cDNA from this:
ATGCTCTAG
TACGAGATC
So, you have both a coding and a complementary strand in your cDNA.
As for directionality on the chromosome, genes can be in either direction (meaning that they can use either strand as the coding strand), but remember that the forces that contribute to transcription are just locally determined (assembly of transcription factors, etc) and pay no heed to what direction they're going or strand they are on relative to any other gene. The strands are labeled as positive and negative, but that's just a reference for orientation. A good place to browse the human (or other species) genome is the NIH's map viewer. Click on a chromosome to see the genes mapped to it. Note the column labeled 'O' is for orientation.


text:
Can kit foxes and red foxes produce offspring?
Can a kit fox (Vulpes macrotis) and a red fox (Vulpes vulpes) together produce offspring?
Would such a hybrid be fertile?

Red foxes will kill kit foxes in the wild, so presumably this would be a pretty big barrier to producing offspring.

I realize that it does not occur in the wild, but I was interested in whether they were genetically compatible enough.

Yes, a red fox and a kit fox could produce hybrid offspring, but it would be sterile.
Sterile red fox / arctic fox (V. lagopus) hybrids have been bred for the fur trade for decades (source).
Arctic foxes are quite closely related to kit foxes, and both species are equally distantly related to red foxes, so since one can produce hybrids then the other should be able to as well. Here's a screenshot from onezoom.org showing their relation. (Arctic fox = Vulpes lagopus)

Red fox / kit fox hybrids have not been observed in the wild, and kit foxes are not widely kept in captivity except in zoos, so I am not aware of any record of such hybrids. It would likely take intentional effort on the part of a fox breeder to produce them.


text:
Can mutation rate be increased for instance by mutagenesis targeting the DNA polymerase?
I am studying a non-cultivable bacterium living in an insect host, and I would like to generate some random mutants of this bacteria while preserving the insect.
I am wondering if one way to do so might be to use directed mutagenesis directed towards the bacterial polymerase, which would leads it to increase the error rate.

Does any one has already seen a study with this kind of approach?
Does any one knows or guess another way to obtain some random mutants of the bacteria while preserving the host insect?


text:
How does the negative charge on endothelium prevent blood coagulation?
I was reading about the factors that keep the blood inside the body in fluid state and came across a line in my book which states that, "Smoothness of the endothelium, its negative charge and its normal health are among the important factors"
Does the vascular endothelium have negative charge on it, and if it does, how does it prevent coagulation of blood or keep it in fluid state?


text:
If a human is stranded with beer but no water, should they drink it?
TL;DR: At what percent (if any) will alcohol dehydrate you more/faster than drinking nothing?
Let's contrive a situation for dramatic effect...
A human goes out on a boat for a nice sail in the sea. But oh, the sea was angry that day, my friends. The weather turns, and the sailboat is tossed asunder. Luckily, our survivor grabs hold of some debris and is washed onto a deserted island.
Lo and behold, the debris that floated with the survivor to the island is a cooler, and it is filled with beer! There are no other food or water sources on the island. What should our survivor do in regards to the beer to stay alive for as long as possible?
The crux of the situation and my question: will drinking the beer help hydrate the human, keeping them alive longer? Or would the effect of the alcohol as a diuretic actually dehydrate them, causing an earlier demise?
Details and follow up questions:
Let's assume this is an average beer ~4% alcohol. However, I know there must be a breaking point. Some kombucha or ginger beer with .5% alcohol should surely be imbibed. But should this beer still be drunk? What if instead it was a 7% IPA? Or a 14% quadruple IPA like I have in my fridge? What about wine, whiskey, or gin?
How would the situation change for a caffeinated beverage like coffee? Or what if the cooler was filled with energy drinks?
I look forward to your answers!
EDIT: The linked question, while similar, does not answer my question. It links to one 1996 study that talks about the effect of alcohol on rehydration, but not the specifics of yes, probably ok to drink at about this percent ABV, and no don't drink at above this percent. It also doesn't discuss rate of intake, changes based on body weight, etc. which are all things I would surmise have an impact on this. I understand there isn't going to be a hard and fast STOP percent level, but I would like to understand more about the underlying mechanisms and factors that change things.

This is way too many questions. Focus on one or two beverages, please, or just alcohol, plain and simple.

There is one main question, at what percent alcohol is drinking nothing better than drinking the alcohol for survival. A possible follow up would expand this to caffeine.

If you read The Ghost Map, you will find that the people who survived a particular cholera epidemic that erupted around them in London, were workers in a brewery who were paid in part with the fruits of their labor, and drank beer and not the water from the local pump.

Let's hope the beer is chilled ;)

There is quite a lot of misunderstanding about alcohol (and caffeine) as a diuretic. It's not nearly as cut and dry as you're presenting.
There is no answer to your question. Sodium and water are very tightly regulated, and a lot has to go wrong before they fail. If alcohol could easily derail water regulation, there would be far, far fewer alcoholics in the world.
Alcohol is primarily a toxin, not primarily a diuretic. The diuretic effect of alcohol depends partly on your hydration status. If you're fully hydrated, you'll produce slightly more urine on drinking an alcoholic (>2%) beverage than when you drink water. If you're dehydrated, your body will conserve the water more. The more alcohol in the drink, the less value it has as a rehydrating solution.
You won't find good studies because it's not a scenario truly worth studying. The toxic effects of alcohol are already known and bad enough. It would be unkind to conduct a study where higher concentrations of alcohol were the sole fluid available and length of survival on animals, let alone humans.
N.B. There have been lots of studies with acute alcohol intoxication and diuresis because that is a scenario that occurs, and which can be mitigated.
Effects of a moderate intake of beer on markers of hydration after exercise in the heat: a crossover study
Hydration Status and the Diuretic Action of a Small Dose of Alcohol

Why do you say that alcohol is a toxin? It is common metabolite in many species and unlike methanol, ethanol is not considered toxic.

@WYSIWYG Alcohol is most definitely a toxin. Your assertion is absurd.

Can you cite a valid reference where alcohol is classified as a "toxin"? By your logic even oxygen would be primarily a toxin.

@WYSIWYG - by your logic, tetrodotoxin (made naturally by puffer fish), though it does get someone high, is not toxic. Enough.

Please refrain from making unprofessional expressions. If I do not understand what you are saying then I have the right to ask. Alcohol is an end product of fermentation and is not a product specially synthesized to cause harm to other species. It is like lactic acid (which can also cause metabolic acidosis at high concentration). Comparing TTX with alcohol is too far fetched.

@WYSIWYG- as I said, I'm done with this. Surely you can look it up yourself. You didn't so much ask a question as make an absurd statement.

I can look it up. But being a member of the community I have the right to ask for a referenced answer. Your claim can mislead others. And I do not really understand the "absurdity" in my comment. Would you please care to enlighten me?

Ethanol poisoning https://www.cdc.gov/niosh/idlh/64175.html


text:
Are humans capable of both anaerobic respiration, and lactic acid fermentation?
Are humans capable of both anaerobic respiration, and lactic acid fermentation?
And if so, when do they do each?
I understand that the difference between respiration and fermentation is that respiration takes place in the electron transport chain. I understand that aerobic respiration uses oxygen in the electron transport chain, and anaerobic respiration uses some other molecule in the electron transport chain instead of oxygen, like nitrate. Whereas fermentation doesn't use the electron transport chain at all.
I know humans have an anaerobic metabolic process that produces lactic acid, but I'm not clear whether it's respiration or fermentation, or whether it could be either, in which case when it is which?
added
some further discussion w roland at  the chat link / https://pastebin.com/raw/mkxckeqA / http://archive.is/CwCRL   and on this q at chat link here / https://pastebin.com/raw/9sV38LnQ / http://archive.is/HJVVe     and example of conflicting definitions available https://pastebin.com/raw/3EKGmEb6 / http://archive.is/9sAlY

lactic acid fermentation produces lactate not lactic acid(it's named after the bacteria that do it).see https://biology.stackexchange.com/questions/61315/does-glycolysis-produce-lactate-or-pyruvate where a post mentions the bacteria.Like dna is a misnomer,it does stand for ...acid, but the actual substance is really deoxyribonucleotide.   There r 2 types of lactic acid fermentation,humans do homolactic fermentation that produces lactate and no ethanol, as opposed to heterolactic fermentation that produces lactate and ethanol http://onlinebiologynotes.com/different-fermentation-pathway-bacteria

Humans have no anaerobic respiration, if we define this as oxidation of a substrate with an external electron acceptor other than oxygen. In humans, the terminal electron acceptor in respiration is always oxygen, which is reduced at complex IV in the respiratory chain. Alternative electron acceptors are mostly found in bacteria and archaea.
I would call the anaerobic metabolism of glucose to lactate in humans a fermentation process. It consists of glycolysis, which converts glucose to pyruvate, which in turn is converted to lactate by lactate dehydrogenase. There is no terminal electron acceptor in this case; instead, energy is extracted from glucose by rearranging the molecular structure of the sugar into a more favorable ("low energy") configuration, without any net donation of electrons.

Note: this is how I use the terms, and I believe this is the most common usage in biochemistry today. But I am sure you can find other sources that define them differently. This is rather common in biology and biochemistry, and these terms are very old and fraught with all sorts of historical connotations. But names are not crucial; understanding the biochemical processes is. The important distinction here is that conversion of glucose to lactate does not oxidize the substrate and therefore needs no external electron acceptor; in this way it is fundamentally different from oxidative metabolism.

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

and just in case they try to delete the chat link, it's also here https://pastebin.com/raw/mkxckeqA

Muscle tissue is a good example of anaerobic fermentation. Lactic Acid is fermented and builds up in this tissue when we do large amounts of exercise. We use the Pyruvate molecule and LDH to produce Lactate when required but it is only for short bursts of energy in specific tissues.
Try a google image search for the glycolytic pathway. Usually Aerobic and Anaerobic paths are listed after the Pyruvate molecule is formed at the end of this pathway.

When you say muscle cells do fermentation, are you saying it's not respiration?

you write "Lactic Acid is fermented "     <-- From what I understand, the term lactic acid fermentation is named after the bacteria (lactic acid bacteria) that do the process. But lactic acid is not produced. And when you say "s fermented"  I suppose you mean is produced by (that) fermentation, So you mean Lactate is produced by the fermentation, not lactic acid. see https://biology.stackexchange.com/questions/61315/does-glycolysis-produce-lactate-or-pyruvate where a post there mentions that and lactic acid bacteria

specifically humans do homolactic fermentation that produces lactate and no ethanol, as opposed to heterolactic fermentation that produces lactate and ethanol  https://www.onlinebiologynotes.com/different-fermentation-pathway-bacteria/

I mentioned in comment quite early "apparently humans don't do anaerobic respiration at all. They only do a)aerobic respiration and b)fermentation. Humans can't use nitrate or sulfite as acceptors in the electron transport chain"
I'll expand on that a bit.. https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/variations-on-cellular-respiration/a/fermentation-and-anaerobic-respiration
"Anaerobic cellular respiration is similar to aerobic cellular respiration in that electrons extracted from a fuel molecule are passed through an electron transport chain, driving ATP synthesis. Some organisms use sulfate as the final electron acceptor at the end of the transport chain, while others use nitrate, sulfur, or one of a variety of other molecules..
What kinds of organisms use anaerobic cellular respiration? Some prokaryotes—bacteria and archaea—that live in low-oxygen environments rely on anaerobic respiration to break down fuels."  (i.e. not humans)
and "Fermentation is a widespread pathway, but it is not the only way to get energy from fuels anaerobically (in the absence of oxygen). Some living systems instead use an inorganic molecule other than O2, such as sulfate, as a final electron acceptor for an electron transport chain. This process, called anaerobic cellular respiration, is performed by some bacteria and archaea."
Humans aren't able to use sulfate or nitrate(or any inorganic molecule other than o2) in the electron transport chain. So they can't do anaerobic respiration.
That is certainly the point made by khanacademy, and made by another microbiologist I spoke to, and echoed by Roland's answer.
Note- as of writing, Roland has undermined his answer somewhat.. Since the first sentence of his answer says "Humans have no anaerobic respiration" But a comment he made, says "I think these terms are defined somewhat differently depending on who you ask, and I agree with @David that it's not very interesting to argue over definitions. But my own preference would be to use the term "anaerobic respiration" only for oxidation of substrates that delivers electrons to a terminal electron acceptor other than O2, and "fermentation" to mean a process that does not result in any net oxidation. This is a major biochemical difference, so it motivates different terms, imho. With these definitions, muscle does not do anaerobic respiration"
i.e. he's saying the definition is only his preference. And that while it has good reason behind it, it's just still his preference. And so it's a question of some peoples' preferred definitions, over others.
I have spoken to a microbiologist who says all the advanced scientific texts use that definition (introductory texts aside, and human biology tests aside), i.e. it's not just some peoples' preference.  I have added further re that -  And what I have found strong evidence/proof that supports that there is a strict distinction made, in the non-introductory microbiology texts. He is probably correct that scientific journals such as PNAS, Nature and Science, make the distinction too.
Added
The microbiologist that I spoke to said that often biology 101 texts get it wrong so e.g. that boundless biology textbook, even the title gives away that it's a very intro level book.  So no surprise that it gets it wrong.  He said often introductory undergraduate books get it wrong.  And books on human biology, since they don't need to distinguish between types of anaerobic metabolising, can get it wrong sometimes, because they don't need as much clarity as they aren't needing to distinguish between anaerobic processes.  But the science journals such as PNAS, Science, Nature. And the advanced microbiology texts get it right.  Sure it's possible for a person to use a very general definition of respiration and then to ask whether the electron transport chain is used, but the microbiology texts have no need for that question to even be asked, since they define their terms to make that distinction.
If one goes to google books and searches microbiology,  I see he is correct.
For example, googling in google books for microbiology fermentation respiration
The first result is introductory so I won't look at it.
The second result is Microbiology & Plant Pathology by Dr. P.D. Sharma
"heterotrophs exhibit two basic strategies the fermentation and respiration"
"In contrast to fermentation, respiration requires an external electron acceptor"
agrees
The third result    distinguishes but is by the same author so i'll skip it.
agrees
The fourth result   - Principles of Microbiology - Page 530
"A comparison of aerobic respiration, anaerobic respiration, and fermentation"
And it distinguishes

agrees
The fifth result   "Microbiology: A Clinical Approach, Second Edition: - Page 39"   here
has a diagram that distinguishes

agrees
The sixth result  Alcamo's Fundamentals of Microbiology - Page 183
"a different inorganic molecule as a final electron acceptor"
note- can't be pyruvate as final one, as pyruvate contains carbon so is organic.
He then gives the examples of a species of bacteria that uses nitrate and a species that uses sulfate
agrees
It is indeed the case that fermentation doesn't involve an electron transport chain, but also, fermentation does involve a final electron acceptor, just it's pyruvate or a pyruvate derivative.
Microbiology By Cynthia Nau Cornelissen, Richard A. Harvey, Bruce D. Fisher here
"the terminal electron acceptor in fermentation, is pyruvate or a pyruvate derivative"
And as the microbiologist I spoke to said, it's more a question of whether the final electron acceptor is internal/endogenous (i.e. produced by the organism itself), or whether it's external. (rather than whether it's organic/inorganic)
One thing boundless biology says (using the strict definition of fermentation and respiration), and consistent with that.   https://www.boundless.com/microbiology/textbooks/boundless-microbiology-textbook/microbial-metabolism-5/anaerobic-respiration-49/electron-donors-and-acceptors-in-anaerobic-respiration-313-8023/
" Both inorganic and organic compounds may be used as electron acceptors in anaerobic respiration. Inorganic compounds include sulfate (SO42-), nitrate (NO3-), and ferric iron (Fe3+). Organic compounds include DMSO."
(DMSO for example is organic/carbon based, but it's an external electron acceptor, thus, still respiration when it's used)
related chat- https://web.archive.org/web/20210507000853/https://pastebin.com/raw/mkxckeqA
Conclusion-
That  and all those definitions clearly distinguish respiration and fermentation, with the same strict definition, that confirms that humans do not do anaerobic respiration, they do fermentation, which is not a form of respiration.
Nevertheless, despite that, it's clearly the case that outside of advanced microbiology texts.. (And I suppose outside of scientific journals), so in introductory biology texts, and in human biology texts, and high school texts.. and among many on this website who clearly have a deep interest in biology, that general definition of respiration is still around. And in such a situation, it makes sense to pay less attention to the term but to ask regarding specific features e.g. "Does it involve the electron transport chain" / Does it use an inorganic compound such as nitrate or sulfate as an alternative to O2?  if one wants to know if it's respiration, Or if one doesn't care what the term is and just wants to know what the features are so may ask that and further questions like "Does it use oxygen", or features that aren't even relevant to the term,  such as what interested in commenter in how they think of the terms - "Is it being done by an animal, or not(so directly from the environment to the cell)".
Further conclusion
further clarification on the distinction..
When I asked this question to the microbiologist-
I understand respiration is usually done with an inorganic substance (O2) as terminal electron acceptor, but that it can be done with an organic substance DMSO. So, is there still an enormous chemical difference between respiration and fermentation, when respiration is done with DMSO?  I don't see how the final electron acceptor being internal vs being external, would cause a major different in the chemistry.
I got a very good answer-
He said - Fermentation doesn't use a proton gradient and chemiosmotic force to generate ATP.  Oxidative phosphorylation vs substrate-level phosphorylation
Looking further..  I see Glycolysis produces ATP via substrate-level phosphorylation. Looking at the distinct parts of respiration and fermentation i.e. after glycolysis. (some define respiration and fermentation as excluding glycolysis anyway). Then, (after glycolysis),  Respiration uses oxidative phosphorylation.   Fermentation, if it produces ATP (which it usually does), then it is done via substrate-level phosphorylation.
(Physiology and Biochemstiry of Prokaryotes   https://i.sstatic.net/PkRw9.png    Taking pyruvate to acetate gets you oATP.  Taking pyruvate to propionate does not.  It's Fermentation either way. If it produces ATP it's substrate level phosphorylation, and if it doesn't then there's no phosphorylation)
Many sources online explain how a)those two types of phosphorylation are very different chemical processes  and b)oxidative phosphorylation uses the electron transport chain whereas substrate level phosphorylation doesn't.  So that explains the significance/relevance/reason of the distinction between fermentation and respiration.
Added important note
An exception to this is oxidative fermentation, which does use the electron transport chain. Apparently part of the metabolic pathway doesn't use the ETC and part of it does, in such a way that it's in some way a mixture of respiration and fermentation and they decided to call it fermentation. Also see Do acetic acid bacteria use the electron transport chain when converting ethanol to acetic acid?


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Does Glycolysis produce lactate, or pyruvate?
EDIT- Somebody suggested that this is the same question as this, it isn't. This one is asking about the definition of glycolysis. That one was asking about the definition of fermentation.
Does Glycolysis produce lactate, or pyruvate?
I'm aware that ultimately in the human body, after sugar is converted into pyruvate, then if fermentation happens it will be converted into lactate, or if aerobic respiration happens then it won't.
My question is on the term Glycolysis
I notice that most sources seem to say glycolysis ends with pyruvate
e.g.
Glycolysis.. is the metabolic pathway that converts glucose.. into pyruvate
The only time lactate comes into it is After glycolysis.
(so in this wikipedia page on Glycolysis, in the Post Glycolysis part it mentions this)
https://en.wikipedia.org/wiki/Glycolysis#Post-glycolysis_processes
"pyruvate is converted to lactate "
However, on the other hand, I see some sources, even another wikipedia article titled "anaerobic glycolysis", which the page says isn't well sourced, it has glycolysis as ending in lactate.
https://en.wikipedia.org/wiki/Anaerobic_glycolysis
"Anaerobic glycolysis is the transformation of glucose to lactate when limited amounts of oxygen (O2) are available"
Also here
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4343186/
"we contend that La− is always the end product of glycolysis"
(putting aside their controversial claim that it is always the end product, i'm interested here in the idea of theirs that it is ever an end product, so, their use of the term glycolysis)
So it seems that there are those two positions
For the purposes of this question i'll call one position the lactate position and the other position the pyruvate position.
One position, call it the lactate position, which is those sources that place lactate,  as the end product of glycolysis.. thus counting not just sugar->pyruvate, but sugar->pyruvate + the whole fermentation process, as glycolysis.
While others, call this the Pyruvate position,  count purely sugar->pyruvate those sources count just that, as Glycolysis.
I'm wondering if both definitions are correct.. / both usages are valid.. Or if one of those e.g. if the lactate one, is an odd one out and if most academic texts wouldn't use that definition, and would use the pyruvate position for their definition of Glycolysis.
Note- I had written that glycolysis ends with pyruvate {or pyruvic acid which dissociates into pyruvate}, and the lactic acid fermentation ends in lactate {or lactic acid which dissociates into lactate}. But what is in those curly braces there is wrong and I have been corrected on that one. Glycolysis produces pyruvate, and Lactic Acid Fermentation produces lactate.  The reason (answerer David explains), why Lactic acid fermentation bears that name, is it is named after what are called "lactic acid bacteria" "Lactic acid bacteria are named for their effect on the medium in which such bacteria grow, not for the ionization state of lactic acid in the cell and when bound to enzymes (about which the namers could have had no knowledge)." and they do that type of fermentation that produces lactate.  There are two types of "lactic acid fermentation", https://en.wikipedia.org/wiki/Lactic_acid_fermentation  homolactic fermentation, and heretolactic fermentation. Humans do homolactic fermentation that produces lactate and no ethanol, as opposed to heterolactic fermentation that produces lactate and ethanol https://www.onlinebiologynotes.com/different-fermentation-pathway-bacteria/
Also, note that Muscle cells do what is called "lactic acid fermentation", but the idea that they produce lactic acid is a myth that has been commonly propagated in sports science(I guess perhaps partly as a result of what I think is biology's poor nomenclature, the fact that the process is called lactic acid fermentation). Muscles don't produce lactic acid, in fact, it's not lactic acid and they don't produce it. Muscle cells use lactate, they don't produce lactic acid. This is verifiable from googling humans produce lactate not lactic acid eg the first line here mentions that myth and calls it out as a myth.  The  body of the following question and its answers here are related and very interesting.

Possible duplicate of Is glycolysis the beginning part of fermentation, or does fermentation follow glycolysis?

@bpedit No it isn't. That question you linked to is asking about the definition of fermentation. This is asking about the definition of glycolysis. I shall edit my question and make that point

"or pyruvic acid which dissociates into pyruvate" No. Pyruvic acid is not the product of pyruvate kinase reaction. The substrate (PEP) is ionized at cellular pH and I imagine the enzyme will bind its negative charges. That part of the molecule is not changed.

@David ok is this similar statement correct? "or lactic acid which dissociates into lactate"

No. It's lactate. The pKa is ca. 3.9.

Yea. Pyruvate is formed.. No chance of formation of lactate
... Thats glycolysis. The synthesis of glucose into pyruvate by the use of several enzymes

@David So why is that fermentation sometimes called lactic acid fermentation  and not a name like lactate fermentation https://en.wikipedia.org/wiki/Lactic_acid_fermentation  (i'm assuming lactic acid fermentation is the same fermentation that produces lactate?)

Lactic acid bacteria are named for their effect on the medium in which such bacteria grow, not for the ionization state of lactic acid in the cell and when bound to enzymes (about which the namers could have had no knowledge). Anaerobic oxidation of glucose to lactate also produces a hydrogen ion which would cause the pH in the cell to drop if this, and the counter-ion lactate were not excreted from the bacteria (or from the mammalian muscle), Thus it is the external medium (or blood) that becomes acid.The LDH structure shows lactate bound by +ve counter-ions, as expected at this pH.

@David and to clarify, when you say " the ionization state of lactic acid in the cell and when bound to enzymes "  Do you mean that in the cell and when bound to enzymes or anywhere in the body, it's lactate, not lactic acid?

I mean when bound to enzymes or immediately on generation in a reaction. (The latter is covering my back for the remote possibility that a reaction mechanism might actually generate -COOH, e.g. by the oxidation of an aldehyde. But this certainly does not happen as the acidic residue in pyruvate and lactate is generated way back in glycolysis as 3-phosphoglycerate.) However, without wishing to patronize you, I wonder how familiar you are with the ionization properties of weak acids. Do we need a question relating to this material?

A key term in the study is "anaerobic" glycolysis, glycolysis is part of aerobic metabolism as well.

I think you will find all text books (e.g. Berg et al. Ch 16) describe glycolysis as the conversion of glucose to pyruvate, as this is how it has been defined and considered in countless biochemical papers. The subsequent reactions of pyruvate  are regarded as separate metabolic steps or pathways.
The title of the short review article you cite (“Lactate is always the end product of glycolysis”) has mislead you — it was obviously meant to be controversial. It is the ambiguous term “end product” that is the (deliberate?) cause of the problem. What the article suggest is that the product of glycolysis — pyruvate — is always, at least partially, converted to lactate in animal cells. It would have been better entitled “Lactate is always produced from the pyruvate generated in glycolysis”. Whether or not that is true (and that is not your question as I understand it), the conversion of pyruvate to lactate is not considered to be part of glycolysis any more than its conversion to acetate.
There may be ambiguity in the use of the ancient term ‘fermentation’, but not with glycolysis and other metabolic pathways established in the twentieth century.

Thanks. What is your view regarding this source I mention in my question https://en.wikipedia.org/wiki/Anaerobic_glycolysis "Anaerobic glycolysis is the transformation of glucose to lactate when limited amounts of oxygen (O2) are available"

@barlop — This entry relates to Anaerobic Glycolysis and is obviously incorrect as anaerobic glycolysis in brewer's yeast leads to the production of ethanol. You or I could edit it to correct it if we felt like it. The Wikipedia entry on Glycolysis is much more detailed and documented. The first illustration shows the conversion of glucose to pyruvate.

@David funnily enough I see that the more comprehensive Glycolysis page says https://en.wikipedia.org/wiki/Glycolysis  "Fermention of pyruvate to lactate is sometimes also called "anaerobic glycolysis", however, glycolysis ends with the production of pyruvate regardless of the presence or absence of oxygen."

@user1136 Could you give me a page ref. because I suspect your quotation is taken out of context. Figure 16.3, Table 16.3, and the separate discussion of different fates of pyruvate (Figure 16.10) all indicate that Berg et al. regard glycolysis as the conversion of glucose to pyruvate.

@user1136 I am afraid the paper you cite uses a definition of glycolysis that differs from that in general use, perhaps because the authors appear to be chemists, rather than biochemists. The Greek root of a word does not constitute a definition of its English meaning, but, in any case, glucose is split in the formation of pyruvate which is then reduced, rather than being split further, if it goes on to form lactate. Berg is careful to refer to "the pathway", not "glycolysis", and immediately goes on to say that "the fate of pyruvate is variable" and "three reactions are of prime importance".

@user1136 — I replied to your comment out of courtesy, however I now see that you have your own answer and were involved in long series of comments which was moved to chat. I was not involved in the criticism of your answer, and I really think it better if you desist from commenting on mine now. Just let the answers stand on their own for people to decide. This is not an undergraduate debate about what Berg did or did not mean.

Lactate, not pyruvate, is the end-product of glycolysis. If pyruvate was the end-product, there would be a major problem: glycolysis would stop.
I am talking here about how cells 'obtain' ATP from the splitting of glucose under strict anaerobic conditions (glycolysis).
Glycolysis is the splitting of glucose, and occurs anaerobically without any net oxidation or reduction, and the free energy sequestered in the form of ATP is derived from the splitting reaction.  In thermodynamic terms, we can envisage that entropy makes a contribution to the overall (favorable) Gibbs free energy change: splitting a molecule into two parts makes the system more disordered (to take a crude view of what entropy means). But of course the rearrangement of chemical bonds will also make a (major?) contribution.
Let's be blunt about the role of oxidation and reduction: as stated, there is no net oxidation or reduction in glycolysis.  But in this last statement lies a major paradox, and  therein is the reason why we must consider lactate  (and in alcoholic fermentation, ethanol) the end-product of glycolysis.

Although glycolyis proceeds without net oxidation or reduction, a supply of oxidied NAD (i.e., NAD+) is required in order for the process to continue.

I am of course talking about the glyceraldehyde-3-phosphate dehydrogenase (GAPdh) reaction, that ubiquitous enzyme of glycolysis.
$$ \mathrm{\text{glyceraldehyde-3-phosphate}\,+\,NAD^{+}\,+\,P_i\text{ =  }\text{1,3-bisphosphoglycerate} +\,\,NADH\,+\,H^+}$$
Pyruvate production from glucose is an oxidation - we have 'removed' a pair of electrons (strictly speaking, 2 pairs), but for glycolysis to proceed we (paradoxically) need a reduction - we must (somehow) get rid of the electrons from NADH, and one way (crazily at first sight) is to 'give' the electrons back to the carbon skeleton from whence they came - to pyruvate in the case of muscle (lactate) glycolysis.

One of the key steps to understanding glycolysis is to ask the question: how is the NADH produced in the GAPdh reaction oxidized back to NAD+?

In lactic acid fermentation and in muscle glycolysis, this it done with lactate dehydrogenase (LDH), which catalyzes the NADH -linked reduction of pyruvate to lactate, with concomitant production of NAD+, thus allowing glycolysis to continue. If we could 'knock out' the LDH gene, there would be no glycolysis (a lethal mutation), unless the cell could somehow find another method of regenerating NAD+.
The splitting of glucose into lactate may be represented stoichiometrically as follows (one glucose is split into two lactic acid molecules):
$$ \mathrm{\text{1 }C{_6}H_{12}O_6\text{ = 2 }CH_{3}\,CHOH\,COOH}$$
We may note that there is no oxidation or reduction. In aerobic respiration, glucose yields 12 pairs of electrons to the respiratory chain, and all are 'held' in either carbon-carbon or carbon-hydrogen bonds.  Each lactate acid  molecule (or more precisely, each lactate molecule) has six (C-C and C-H) bonds: they are all there, nothing has changed.
Furthermore, it is the above reaction that yields the free energy, no matter how we view the intricacies of the molecular processes that lead to it. That is, fundamentally, lactic acid fermentation (or muscle glycolysis) is a sequestration of Gibbs free energy, in the form of ATP, obtained by the splitting of glucose into two molecules of lactate.
In the case of pyruvate, we would need to write the equation (balanced in terms of electrons but not hydrogens) as follows:
$$ \mathrm{\text{1 }C{_6}H_{12}O_6\,+\,2\,NAD^{+}\text{ = 2 }CH_{3}\,(C\text{=}O)\,COOH  +\,2\,NADH}$$
If we count the number of (C-C and C-H) bonds in pyruvate, we see there are five: one pair of electrons is 'missing' and is now 'held' by the nicotinamide cofactor.
So what of alcoholic fermentation? How is NADH re-oxidized here? In this case, pyruvate is first decarboxylated to acetaldehyde and CO2 by the enzyme pyruvate decarboxylase, and  NADH is reoxidized by the enzyme alcohol dehydrogenase acting as an aldehyde reductase. That is, the NAD+ necessary for the GAPdh reaction is 'regenerated' by the reduction of acetaldehdye to ethanol. As far as anaerobic fermentation in yeast is concerned, ethanol is a 'waste' product (but very useful to us humans).
$$ \mathrm{CH_{3}CHO\,+\,NADH\,+\,H^{+}\text{ = }CH_{3}CH_{2}OH\,+\,NAD^{+}}$$
If we count the number of (C-H and C-C) bonds in acetaldehyde, there are five, but in ethanol there are six. As two molecules of ethanol are produced for each glucose, the total is twelve and we have accounted for everything: once again there is no net oxidation and reduction, and the stoichiometric splitting of glucose  in alcoholic fermentation may be written as follows (one glucose gives two molecules of ethanol and two molecules of carbon dioxide),
$$ \mathrm{\text{1 }C{_6}H_{12}O_6\text{ = 2 }CH_{3}CH_{2}OH\,+\,2\,CO_2}$$
and it is the Gibbs free energy 'released' in this reaction that is used to 'make' ATP.
NADH produced in glycolysis may also be regenerated 'aerobically', that is by reoxidation in mitochondria via the respiratory redox chain. The problem here is that the inner mitochondrial membrane is impermeable to NAD, and a  shuttle system, such as the aspartate-malate shuttle, is required to get the electrons across the inner membrane. If NADH is regenerated via mitochondrial respiration, this is of course an alternative to the LDH reaction and lactate need not be formed (but we are no longer talking about anaerobic glycolysis). This, I suspect, is where the confusion often arises.
To make one final point about lactate glycolysis in humans. A muscle cell, perhaps obtaining as much energy as possible from glycolysis during vigorous exercise, regards lactate as a waste product. But this is not true of the organism as a whole: the lactate is taken to the liver where it may be converted back to glucose (via pyruvate) as part of the Cori cycle (which is way beyond the scope of this answer).
So why the apparent paradox of NAD oxidoreduction during glycolysis? And why oxidize a carbon skeleton with NAD+ and then regenerate the oxidizing agent by reducing the carbon skeleton at a later step? I have no explanation, but this is surely a great example of what Albert Lehninger called the molecular logic of living organisms.

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


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Do sulfate reducing bacteria ingest their sulfate as solid, or as dissolved in water?
Do sulfate reducing bacteria ingest their sulfate as solid, or liquid or gas?
I understand that almost all forms of sulfate are solid.. and sulfate can be dissolved in water(thus no longer solid, but liquid).
So, do sulfate reducing bacteria ingest sulfate in its solid form, or do they require it to be dissolved in water?
A similar question in fact, for nitrifying bacteria, though if that's complex I might make it a separate question.
Also, even though it's respiration(which tends to be associated either with the breathing process - in the case of physiological respiration, or with having breathed prior - in the case of cellular respiration), here it's not using a gas. So i'm curious if biologists ever use the word "breathing" for such a process.  wikipedia for example, says https://en.wikipedia.org/wiki/Sulfate-reducing_bacteria  " In a sense, these organisms "breathe" sulfate.." I wonder if biologists use the term 'breath' in such a general sense(to include consuming a substance dissolved in water), or only in a specific sense of gas or air, or if they don't use the term 'breath' at all. So, how strictly is the term breath defined in biology.

Sulfates in water would not be liquid. Their melting points are far to high. When a sulfate dissolves into sulfate ions and some cation such as potassium, we say it is solvated, not liquid. Sulfates would also not be present as gasses due to their ionic nature as well as high molecular weights. So that leaves solvated sulfate ions and solid sulfates that have not completely dissolved.
To be ingested in bulk as a solid would require endocytosis which is not performed by prokaryotes: http://faculty.ccbcmd.edu/courses/bio141/lecguide/unit1/proeu/proeu.html
Further research indicates sulfate, as ions, enters the cell through permeases: http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.532.943&rep=rep1&type=pdf
Edit: Here's some files to help with the idea of how ions and other molecules enter cells. Again, bacteria do not engulf substances whole, in the process of endocytosis, such as eukaryotes are capable of. Here is an image of a nitrate ion within a transport protein. Only a few amino acids of the protein are shown here, the actual protein is much larger and spans across the entire membrane creating a channel for the ion to enter. http://www.rcsb.org/pdb/ngl/ngl.do?pdbid=4U4W&preset=ligandInteraction&sele=[NO3]
Here's another channel, aquaporin, which allows transport of water across the membrane. http://pdb101.rcsb.org/motm/173 The top left image shows the channel in the protein leading to the interior. The third image down shows the interaction between the water and the amino acids (backbones only are shown) which facilitate the water's passage.

what about salt.. when it breaks into Na and Cl, ions, are they also still solid? also I heard that most sulfate is solid but "dihydrogen sulfate" is a liquid, is that wrong?

@barlop. No. Solids are formed when the particles have close neighbors that have fixed positions relative to one another. When in water, most ionic substances, such as table salt, have their ions pulled apart from one another by attractions to the water molecules. Sulfate ions, being negative, will be surrounded by the partial positive charges on surrounding water molecules. This allows them to be delivered one at a time to the proteins, permeases in the case, that transport them into the cell

is it the same situation with nitrifying bacteria - the bacteria can consume small amounts of solid nitrate, and larger amounts of solvated nitrate? Also in the case of a tiny bit of solid nitrate(not dissolved), does it need to be in water for the bacteria to accept it, or can it accept it dry?

@barlop. I suspect the presence of a certain amount of water is essential. Even if most of the neighboring nitrate is in solid form, the nitrate ions would have to be peeled away as solvated ions before interacting with the prpteins that transport them into the bacteria. https://www.ncbi.nlm.nih.gov/pubmed/11289303

can you comment on the use of the term breathing (see last paragraph of my question)

@barlop. The process of bringing these substances into the cell is called transport. Breathing would not seem appropriate. Cellular respiration and breathing respiration are two entirely separate processes even though the breathing variety provides oxygen and eliminates the CO2 associated with cellular respiration. The Wiki reference is a useful simile but I've never heard nor read of the term breathing actually being seriously used in this manner.

Let us continue this discussion in chat.


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C Form DNA Base Pairs Per Turn
How does C-DNA have 9.33 base pairs per turn? The number of base pairs should be quantised. How can it be a decimal?

There is no requirement that DNA should have a whole number of base pairs per turn. As a thought experiment, say you have a helix of dsDNA with 10 base pairs that completes one helical turn (ie it has 10 bp/turn). Now, twist that DNA along its axis so that it completes 1.5 turns. There is still only 10 bp and thus 6.67 bp/turn (which you should notice is a decimal).


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Names of different cyclins
Different types of cell cyclins are designated as a to y
Why are some letters like m, n, p, q.. etc. skipped?

Source: https://en.wikipedia.org/wiki/Cyclin

Biological nomenclature can be impenetrable. Almost certainly, at some point in history, there were cyclins designated with these letters. Researchers would have discovered apparently novel cyclins which were subsequently determined to be part of an existing family and renamed. For example, this paper reports the discovery of:

a new cyclin, cyclin M, which appears to be most closely related to cyclin L. Its biological function is unknown, but it is related to cyclins that regulate transcription.

It is now called cyclin L2.
I hope this answer satisfies you to some extent. I doubt anyone is going to sift through the literature and try and determine why all cyclins are are named as they are; that is certainly a losing proposition. The naming of genes/proteins is rather trivial and doesn't generally follow any specific set of rules. Outside of curiosity, the knowledge of cyclin naming doesn't have much, if any, practical relevance.


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DNA replication: How many DNA polymerase molecules work in parallel?
Background research
I am aware that DNA polymerase works in pairs, at least. This is to process both opposite stands of a given chromosome. The 3'-to-5' "leading strand", and 5'-to-3' "lagging strand" simultaneously. This two-DNA-polymerase process is beautifully shown in this TED talk by Drew Berry.
I have not checked any non-online sources but simple Google queries failed to answer my questions below.
Question
Within a single Eukaryotic cell, is the process of DNA-replication carried out by just a single pair of DNA-polymerases? Or do multiple pairs of DNA-polymerases work in parallel?

In the (beautifully rendered) video you linked to, the green molecules are DNA polymerases. So you can already see that there are more than two DNA polymerases at work!
At each replication fork, there is generally one DNA polymerase working on the leading strand, but on the lagging strand, multiple DNA polymerases may be working at the same time (as depicted in the video). Note that different types of polymerase are thought to be primarily responsible for the leading (Pol ε) and lagging (Pol δ) strands in eukaryotes (but not prokaryotes, which use Pol III for both).
Next, note that at every origin of replication, there are two replication forks working simultaneously, one in each direction. So that's double the number of polymerase molecules.
On top of that, a single eukaryotic cell has multiple chromosomes. Each one must have at least one origin of replication of its own, which can operate in parallel. In reality, each eukaryotic chromosome has up to thousands of origins of replication (prokaryotic chromosomes generally only have one). Human cells have on the order of 100,000 origins of replication. So depending on how many origins are active simultaneously, there are likely many thousands of polymerase molecules acting at once to replicate the DNA of a single eukaryotic cell.
You could probably do a rough estimate of the number of polymerase molecules active simultaneously by taking the average duration of S phase in your cell of interest and dividing by the genome size and the speed of polymerase.

Never be too trusting of pretty pictures (/videos), there being multiple DNApol in the video could have been precisely why I asked the question in the first place (to check it's accuracy)

Fair point! But after checking the math, I trust that they did get that detail right in the video.

Having another read of your answer this is awe inspiring, thanks leekainthesky!


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Are insects capable of gliding on the air with their wings spread, similar to birds?
Sometimes birds can use the air to float on with their spread wings. Now, the wings of insects are too small to see if they can do that too. So is it possible for insects to do this also, or can't they hold their wings spread or is the air drag not enough?

"Insect" is a very broad catagory.  Simplistically, some can: ever watch large butterflies?  Just as some birds, like hummingbirds, can't glide well, if at all.