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Why does DNA synthesis require nucleoside triphosphates?
Writing the DNA sequence is done with nuclosides that have three phosphates attached to them, and two of these phosphate are thrown away back into "phosphate pool" of cell. What are main reasons triphosphate structure is used? Conformational changes in the polymerase seems like it could be one of the primary ones.

Welcome. Do you know where the 'A' in the 4-letter DNA code stands for, and what function it has in the cell? That may give you a clue.

We expect questions to be accompanied by evidence of prior research. This requirement is especially important for homework questions. Is this a homework question?

unrelated to 4 bases, question is on why chain grows from nucleoside triphosphates

It seems I'm missing what your question is. Are you asking why phosphate links are used in DNA, or why a diphosphate is released (the latter seems to be the question)?

Please finish the [Tour].  Before posting read the Help on how to ask a good question. Then search for similar previous questions, which I know exist. But from your strange statement about conformation changes I wonder whether you might benefit from reading a chapter on basic chemical thermodynamics.

@AliceD it's very clear, "why does DNA synthesis require nucleside triphosphates". if your answer to why is so self-evident and obvious that the mere question is absurd, then I apologize. if not, then nothing wrong with the question.

@David whoever you are, nothing wrong with the question. there's nothing strange about nucleoside triphosphates alosterically regulating protein conformation, very basic. that the same principles is at work when it comes to nucleoside triphosphates in DNA synthesis, seems likely to me, you can Google "polymerase conformation change nucleoside triphosphates" and read around for yourself

You still have not clarified your question. Do you understand that it takes chemical energy to make a phosphodiester bond, that the free energy change  of hydrolysis of the phosphodiester bond in dNTP is coupled to making the phosophodiester bond in DNA? Or are you asking why pyrophosphate rather than orthophosphate is released? The answer to that is discussed in an answer of mine here which also touches on biochemical energetics. Or what?

As OP suggested, was correct. From Stryer Biochemistry, https://www.ncbi.nlm.nih.gov/books/NBK22374/

"the binding of a nucleoside triphosphate (NTP) to DNA polymerase induces a
conformational change, generating a tight pocket for the base pair
consisting of the NTP and its partner on the template strand. "

Further, as Mike Serfas answer states, "Enzymatic reactions are inherently reversible. If you make an enzyme that converts XMPs (nucleoside monophosphates) into DNA, then the same enzyme can convert DNA to XMPs also. " This was also a good anwer to the question, since the OP had not considered that. The OP associates is with how the substrate for translation from RNA to proteins in ribosome is not amino acids but tRNA + amino acids.
Then, as some angry comments from some random person mentioned, and the good answer from Mike Serfas also mentioned, and, the standard explanation (but, not what OP was fishing for, OP was looking more in-depth) always focuses around, entropy etc.
There was nothing wrong with the question, no formally legitimate reason to close it. It helped the learning process of the OP, and potentially others that acesss this collaboratively generated content on this public Q&A site.

So what question does this statement answer? A change in conformation of the enzyme may be involved in binding dNTP, but the question was "What are main reasons triphosphate structure is used?". Enzymes adapt to substrates, the structure of which are determined by chemical and evolutionary factors, not the other way round.

Questions of "why" in biology are not completely proper - evolution simply happened that way, and the reasons we suggest are rationalizations that may not encompass the "real" reason.  Still...
Enzymatic reactions are inherently reversible.  If you make an enzyme that converts XMPs (nucleoside monophosphates) into DNA, then the same enzyme can convert DNA to XMPs also.  Plus, there's "entropy" to consider, which is to say, if you pop off an XMP it goes flying off into the solution, it's a lot harder to round it back up again. Last but not least -- we're talking about DNA here.  Every time DNA is degraded, even if the other strand is still intact, there is some chance that some mutation will occur with harmful effect.
All this can be set right by wasting a lot of energy every time DNA is extended.  We snip off two phosphates - a pyrophosphate which is rapidly broken down by pyrophosphatase.  The way equilibrium works, that second step pulls the reaction forward because it makes sure there is no pyrophosphate left lying around.  Even if a freak surge of thermal energy at the level of molecular vibration would allow the enzyme to reattach it, the pyrophosphate no longer exists.

"f you make an enzyme that converts XMPs (nucleoside monophosphates) into DNA, then the same enzyme can convert DNA to XMPs" good point, had not thought of that. In ribosomes transfer RNA would also fill same role I guess.


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Is there a statistical analysis test I can perform that will give me a estimate of total population from my own smaller data sets?
Doing my dissertation on the long term trends in moth populations. I am looking at the trends of specific species. Is there a method to obtain an estimate of total population from smaller samples?

Do you mean estimate of population size? From what kind of samples? Do you have genetic data? do you have capture-recapture data, ...?

The point of a statistical test is not give you an estimate, it is to test a null hypothesis.

@Remi.b I disagree with the statement that statistical tests are used only to test null hypotheses. Statistical tests can be used to estimate population parameters, of which population size is one.

@kmm IMO, one might use the statistic that the test returns when you use a given package, but per say, a test means that you want to "test" a hypothesis for the sake of testing it. If the OP is trying to estimate a parameter, (s)he does not need to make any test. If (s)he has a hypothesis he wants to test (like the population size is equal to 2000), then (s)he needs a test. Asking "Was statistical test estimate this parameter?" sounds wrong to me (it should either be "How to estimate this parameter?" or "How to test to the null that the parameter is 2000?").

Why is this "too broad"? This is a very specific question on which there is a large and relevant literature. Just because you're not familiar with the topic doesn't mean it's off topic.

@iayork I agree, this should be reopened. The Q could show more effort and background, but I dont find it too broad.

I'm assuming you're asking how to estimate population size based on numbers of individuals you capture. Yes, there are many approaches to this. The R library SPECIES-R offers a number of methods of calculating this. They are described in the manuscript SPECIES: An R Package for Species Richness Estimation. Some of the methods described are:

Chao, A. (1984), Nonparametric Estimation of the Number of Classes in a Population, Scandinavian Journal of Statistics, 11, 265-270.
Norris, J. L. I., and Pollock, K. H.(1998), Non-Parametric MLE for Poisson Species Abundance Models Allowing for Heterogeneity Between Species, Environmental and Ecological Statistics, 5, 391-402.
Chao, A., and Bunge, J. (2002), Estimating the Number of Species in a Stochastic Abundance Model, Biometrics, 58, 531-539.

and many more.

±1 for your well referenced answer. My motto still is that a good answer can make the question. Perhaps you could add a little background in the question post.

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In what stage of bacterial growth can penicillin inhibit the growth of the cellular wall?
The bacterial growth has 3 main stages: lag-phase, log-phase and stationary phase. I was wondering in which one of them penicillin can inhibit the growth of the cellular wall of bacteria and why.
I was thinking that the respons would be lag and log phase, because at these points bacteria multiply the most, while in stationary phase most of the bacteria are in adult form with a well formed bacterial wall already, but I'm not quite sure.

You may be interested in the Eagle effect. (As I understand things, penicillin has no effect on gram-positive bacteria in stationary phase growth (as the bacteria are not dividing)?) From the Wikipedia article cited: "In this instance [stationary phase growth] since no bacteria are actively replicating (presumably due to nutrient restriction) penicillin has no activity."

yes, thank you! This is very usefull.

This is a really good question that requires you to appreciate a few different details and to overcome a few implicit assumptions that you might perhaps have.

The bacterial growth stages you refer to only apply to a population of bacteria. Individual cells do not undergo these stages.
Relatedly, bacterial population growth stages are independent of the stage of bacterial cell wall growth.

You can have mature or immature bacteria at any stage of "bacterial growth", with either fully formed walls, or with none. This understanding should answer your question partially.
Here are a few more things to consider, for a more complete understanding:

Penicillins are a class of molecules, of varying efficacy and bioavailability across the body and across different kinds of walls and membranes.
Inhibiting the spread of bacteria can be achieved using two types of antibiotics... bactericidal or bacteriostatic ones. Bactericidal means the bacteria die, while bacteriostatic means their growth is slowed or stopped.
Penicillins are bactericidal agents that exert their mechanism of action by inhibition of bacterial cell wall synthesis and by inducing a bacterial autolytic effect. So even mature bacteria will die off in the later stages of outgrowth. In principle, it does not matter what growth stage the bacteria are at, the bactericidal mechanism will take place regardless.
Pencillins are more effective against Gram-positive bacteria. Gram-negative bacteria have a lipopolysaccharide and protein layer that surrounds the peptidoglygan layer of the cell wall, which acts as a barrier for the penicillin from reach its target (which is responsible for completing the synthesis of peptidoglycans, the structural component of bacterial cell wall). However, penicillin can get into Gram-negative cells, for example through channels called porins.

This is more or less very standard knowledge that is easy to look up. Wikipedia's entry on penicillin is a good place to orient yourself if you already haven't.

Penicillin is a beta lactam antibiotic that inhibits Transpeptidase enzyme ( Penicillin binding protein).
Transpeptidase is required for the cross linking of murein monomers required for cell wall synthesis.
So as Penicillin binds to Transpeptidase it does not let it involved in cross linking of murein monomers and hence cell wall synthesis can't be completed.
This is how Penicillin inhibits bacterial growth .
Now the phases ( lag ,log , stationary) you mentioned are used when a culture of bacterial colonies is grown and not used for a single bacterium .

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What is the Importance of Acid Alcohol and Sodium Bicarbonate during staining?
I've just learnt about staining during a histology class and I'm confused.
Why do we have to add acid alcohol and sodium bicarbonate to the tissue during Hematoxylin & Eosin staining? Is there any difference if we don't add them at all and just skipped to eosin instead?

Mind sharing the exact staining process that you are using?  There are slight differences and honestly I have no idea what sodium bicarbonate would be for, unless it's an attempt to get some ions back into soft water used for the experiment, but study has shown that to be a very ineffective way to go about it.

This is described with better detail (and better prose) in John Baker's classic description at StainsFile, but to summarize:  The procedure you're describing is a regressive hematoxylin stain with Harris hematoxylin.  To start off with, let's bear in mind that hematoxylin, a compound from the wood of the logwood tree, is actually used as hematein, by oxidizing it with sodium iodate.  (The colorless hematoxylin would naturally "ripen", oxidize over 4-10 weeks in the presence of air, even without that step, but this is more controllable)  Additionally, aluminum ions are added as a mordant, creating hemalum by binding =O and -OH on the hematein.  The Al atom is what actually binds to something in the nucleus (I found reference to lysine side chains of histone proteins and the phosphate of the DNA - I haven't sorted this part out yet).
When acid is added, it competes with aluminum, which can be thought of as Al3+.  The real bonding may be more covalent than that, but that point is considered controversial.  For whatever reasons, the H+ interferes with the Al3+ mediated attachment of stain to tissue, especially at sites of background attachment (differentiation).  The hematoxylin washes away somewhat, leaving lighter, more specific staining.  (this tactic is called a regressive stain, and is certainly not needed to do the procedure.  This is very much more art than science at this point...)
But ... the acidic hematoxylin has a reddish color, and it isn't as blue as it can be unless it is neutralized to around pH 8 - hence the second step with bicarbonate, though often plain tap water can be used.  That is an ordinary instance of a dye changing color with pH, and can be called "bluing the hematoxylin".

I'm just going to answer for the acid alcohol since I'm unaware of any purpose for using a sodium bicarbonate solution, unless you're referring to its use as a component in the eosin dye.

The acid alcohol is used between the hematoxylin staining and the eosin staining.  It's purpose is essentially to remove any non-specific hematoxylin stain (reference). Hematoxylin is acidophilic (hence its capacity to bind nuclear components such as ribonucleic acids & deoxyribonucleic acids), so if you wash the slide with a weak acid, the hematoxylin which is just "sitting around" unbound to an acidic cellular component will be washed away, making the colouration much cleaner since only the acidophilic cellular componenets will still have the blue stain on them.
On a more technical tack, it also keeps you from getting large quantities of hematoxylin in your eosin stain, thus allowing you to use your eosin stain for more slides before it no longer stains as well.

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How does expansion of the skin via mitosis influence the density of its specialised nerve endings
I found a reddit question Do nerves & nerve endings expand with skin or does skin expansion causes loss of nerve density where a user references the study Assessment of Epidermal Nerve Fibers: A New Diagnostic and Predictive Tool for Peripheral Neuropathies which states that intraepidermal nerves fiber density is not dependent on weight

No significant relationship of race, height, or weight on IENF density has been reported

Reasoning that if additional nerves are not generated in response to expansion of the skin, then one should expect a negative relationship between nerve density and weight.
My question is, upon expansion via mitosis, will sensitive skin rich in specialised nerve endings such as the Meissners corpuscles generate more of this same type of nerve endings?
Specifically i’m curious about the inner foreskin and innervation of new tissue created under foreskin restoration if that makes a difference

Foreskin restoration is the process of expanding the skin on the penis
to reconstruct an organ similar to the foreskin, which has been
removed by circumcision or injury. Foreskin restoration is primarily
accomplished by stretching the residual skin of the penis


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How is the renal osmotic gradient maintained even though the blood osmolarity changes?
I am a high school student and I am a little confused in 2 things related to our urinary system:

We know in our kidneys a countercurrent mechanism exists due to which there is a steep gradient of osmolarity is observed as we go deep inside the medulla and due to which water gets reabsorbed from the descending limb of Henle's loop into the ascending limb of vasa recta but due to the countercurrent of vasa recta osmolarity of blood doesn't changes but as collecting duct descends deep into the medulla it also loses water. Where does this water get drained? Does it get absorbed into a blood vessel? I don't think so because if the blood  is also moving down with the collecting duct then it should also lose water as osmolarity increases as we go down.

We know that ADH increases the water reabsorption from the distal parts of nephron via aquaporins but if more aquaporins are there the collecting duct should pass urine of 1200mosml osmolarity, shouldn't it? and in that case will the concentration gradient in the medulla be maintained? if yes then how?  I am not able to imagine how our kidney would behave if blood of increased osmolarity get into it.

The water doesn't get drained.  As blood flows down a vas rectum, in any given section of the arteriole the tonicity is slightly higher outside the arteriole vs inside the arteriole.  This results in a small amount of water flowing out of the arteriole to attempt to equilibrate the osmolarity.  But before this has even finished happening, the blood has flowed down another quarter of a millimeter (or whatever) where the tonicity is even higher outside the arteriole.  In other words, down the entire vas rectum the water is flowing out.  But when the vas rectum comes back up, the situation is reversed, so the same quantity of water ends up diffusing back into the blood vessel.  Thus the osmolarity at any given level of the medulla remains constant.

Correct, the maximum osmolarity of urine is 1,200 mosm/L.  The concentration gradient in the medulla will change very slightly (temporarily), but don't forget that even as the urine in the collecting tubule is being concentrated to that maximum concentration, the whole process of creating the concentration gradient is actively happening in loops of Henle all around the collecting duct.  So even if the initial effect of having a bit more water in the medulla from the collecting tubule would be to slightly lower the extracellular osmolarity, in the grand scheme of things it changes nothing since the rest of the nephron is still actively creating an effective osmolarity gradient.

References

Any physiology textbook... for instance (among others), I have Human Physiology, from Cells to Systems - in the First Canadian Edition it's pp. 553-63.

I want to know that if urine is already getting maximum concentrated {1200mosml/lit} then how the hell ADH works? what's the point of adding more aquaporins into the collecting duct and DCT if urine is already getting maximum concentrated by absorbing water? I think urine will get 1200 mosml/lit concentration only if ADH acts on it , i.e collecting duct is not so permeable for water i.e it doesn't allow water to get maximally reabsorbed on its own, it only does it when ADH acts on it? but if that's the case then osmolarity inside medulla shouldn't be maintained because pumps are actively

continuing- pumping out Na+ ions even when the collecting duct is not allowing water to reabsorb so, the concentration should increase inside the medulla ? 1200mosml/lit is the maximum concentration in medulla only when water is getting reabsorbed from collecting duct , but when its not being done then it should increase?

@ArunBhardwaj ADH is what allows the urine to be concentrated to that extent.  In the absence of ADH, the aquoporins are endocytosed, so that water is no longer able to flow down its osmolarity gradient, and the urine is consequently much more dilute.  In other words, ADH is not a water-removing mechanism so much as a control mechanism - the nephron is designed such that the urine will become concentrated by default - if it can escape the tubule.  The presence of ADH allows it to escape, the absence of ADH prevents its escape (via presence/absence of aquaporins).

but in the absence of ADH , the Na+ pumps in the ascending limb of henle's loop should also decrease or work slowly .otherwise the concentration inside medulla would increase much higher than 1200mosml/lit ,isn't it? because now no water is coming out through collecting duct it is only coming out through descending limb of henle's loop.


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How many copies of RNA per cell are usually reached through overexpression in human cell-lines? (any technique)
After 8 hours of online-research I was unable to find any info at all..
I was able to get some concrete copy numbers of DNA (e.g. plasmid) per cell after transfection of diverse transfection techniques, but I was unable to get any concrete copy numbers of RNAs that correspond to the transgene (of any overexpression technique).
My main interest would be the hek293T overexpression RNA levels using the viral plasmid, but concrete RNA copy numbers from any possible overexpression technique would be of interest. (for human cells like Hela, Hek, HepG2..)
Ideally I would need a reputable source, but 'gut-feeling comments' are welcomed as well.
In the end I would like to compare overexpressed RNA concentrations to naturally extremely high concentrated endogenous RNAs. Are these levels comparable, or are the (viral) transgene promoters that much more effective?
EDIT: Please also mind that the nucleus is a strong barrier to foreign DNA. Might complicate this answer.


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What is the ratio of pre-mRNA to mRNA?
What is the ratio of spliced to unspliced introns in a cell? I found, that the median half-life of a human mRNA is roughly 10h [1], while transcription and splicing each take around half a minute  [2, 3]. Based on this 1200x time-ratio, my default assumption is that the ratio between pre-mRNA and mRNA of the same genes follows a similar ratio.
Does this estimate seem reasonable? Are there any more direct experiments, that address this?
The context is crosslinking immunoprecipitation (CLIP), where some fragmented (and poly-(T) purified) RNA-reads might be only uniquely mapped if limiting mapping to the the pool of spliced mRNAs, while the same read may show up in introns. Knowing the ratio between introns and exons can help to evaluate the associated risk of such a simplification and to find suitable cut-offs.

Does this answer your question? What percentage of introns are spliced in polyadenylated mRNAs?

I see that you previously asked a very similar question. I think it is a duplicate, if not then it would be helpful to know in what ways it differs, or to have a single edited question.

I agree that it could make sense to ask these questions next to each other, but IMO those are dichotomous questions, requiring entirely different knowledge to be answered: One question asks about the ratio between pre-mRNAs and mRNAs, which is a question of life-times, while the other question asks about the ratio of spliced to non-spliced introns within polyadenylated mRNAs, ignoring the fraction of non-polydaenylated mRNAs.


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What is the relevance of the constant in the clearance equation?
I have seen the equation for drug half lives described variously as (0.7xVd)/Cl, (0.693xVd)/Cl, and (ln2xVd)/Cl.
What is the origin of this numerical constant in the numerator? What does it signify?

Does this answer your question? Derivation for drug half life

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). At a minimum please search on this site for similar questions that have already been asked such as the one suggested by @rotaredom. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!


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What is the name of this brown fly?
They started mating each other and there are lots of them in our hous. I saw them attached together from their bottom.

They have 6 legs and 2 antennae. They have brown wings. i live in iran, tehran. they are about size of fingertip (or smaller)

Welcomo to Biology SE. I know you are veteran from S overflow, but you should take a look how you should ask at first place. You know, ID questions can be really well  accept but you have to add some information, which somebody can start with. Like, where did you see those bugs, parametr of it and you might get answer. Anyway good luck and enjoy your time on Biology SE.

Thanks for the reply. I saw them in my house. I think they have 6 legs. I dont really know anything about flies. I was just wondering what species are these. Also they fly like a butterfly.

They have solid brown wings

Please edit the question to include the details in your comments. You should also note your location as different countries have different species.

@Michael_A Ive tried to provide information as much as i could.

They look more like moths than flies.


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Why does the number of mutations per individuals follow a Poisson distribution?
I was reading this review. On page 11, left column, first paragraph, one can read:

[..] there is a Poisson distribution of the equilibrium number of mutations per individual, if fitness effects are multiplicative.

with no further explanations. In other words, let the variable $X$ be the number of (deleterious) mutations found in one individual (irrespectively to whether the mutation occurred in the parents gonads or is older back in the lineage). The variable $X$ is Poisson distributed.
Why is this statement true? I suppose that the statement also assumes that all mutations have the same effect on fitness, is that true?

It might be worth reading the paper that is cited there, Kimura & Matuyama (1966). They seem to justify it via the process of free recombination (see page 2, though the derivation starts at the bottom of page 1).

Oh I missed this part where he first talk about it and accompany the statement with a reference. Ok. I'll read that then. The question still hold though. Thank you

A Poisson process follows these postulates:

$\lim\limits_{h\to0+}\frac{P(N_h=1)}h=\lambda$  i.e. the probability of occurrence one event in a very small interval of time is equal to the macroscopic rate or intensity ($\lambda\,$).
$P(N_h\geqslant2)=o(h)$ i.e. the probability of occurrence of more than one events in an infinitesimal interval is essentially zero.
Events are independent.

If you consider a single individual (for simplicity assume a single cell), then the DNA will undergo mutations at some fixed rate (which we assume to be uniform for all loci). Now each mutation event is independent of the previous event and in a very small interval of time the chance of two or more mutations is negligible. Considering all these facts and assumptions, it can be said that mutation in a single cell would behave like a Poisson process.
From the Poisson postulates you can derive the expression for the Poisson distribution which describes the probability of $k$ number of events in a given time interval, $t$. Hence, the number of mutations in an individual for a fixed time window ($t\,$) follows a Poisson distribution.
$$P(N=k)=\frac{(\lambda t)^k e^{-\lambda t}}{k!}$$
You can find the derivation of Poisson distribution from the postulates from many sources. I referred to this book:
Hogg, Robert V., and Allen T. Craig. Introduction to mathematical statistics. New York: Macmillan, 1978.
EDIT
The effect of deleterious mutations, in the mentioned section of the linked paper talks about Muller's ratchet that describes the accumulation of deleterious mutations and its effect on the population (i.e. extinction). Like any mutation event, accumulation of deleterious mutations will also follow Poisson distribution. Muller's ratchet just says that beyond a tolerance limit, deleterious mutations will cause extinction of asexually reproducing organisms. Perhaps if each deleterious mutation had a strong effect on the fitness, then sampling from the population may lead to non-Poissonian estimates.

Sorry, I think there is a missunderstanding. I was a bit unclear. The question is not why the number of new mutations per reproduction event is a Poisson distribution but why the number of deleterious mutations per individual follows a Poisson distribution. Thank you though for your answer, I'll try to clarify the question.

@Remi.b probability of any mutation will have a Poisson distribution. Not specific to deleterious mutations. In fact for deleterious mutations there can be non Poisson observation when you sample the population because they may be selected out.

I talk about deleterious because they assume multiplicative fitness effects. But what they say is that the number of mutations/segregating loci in any single individual is Poisson distributed. Of course the number of new mutations transmitted to the offspring is also Poisson distributed (and I understand why) but I don't understand why the number of mutations/segregating loci is Poisson distributed. Do I missunderstand something?

Sorry, I will just repeat what I said above. I think you are not answering to my question here. I am NOT asking why does the number of new mutations per reproduction event follows a Poisson distribution. I am asking why does the number of segregating sites per individual follow a Poisson distribution.

@Remi.b I did not say anything about reproduction. I also do not know what is a segregating site. I am just saying how the process of accumulation of mutations in the DNA will have a Poisson distribution.

Ha ha seems like we have some communication issue my friend! A segregating site is a polymorphic site, a site for which more than one allele exists in the population (at a given instant of course).

Let us continue this discussion in chat.

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Count colonies in the right way
I use Rose bengal agar cloramfenicol for search yeast and molds for inclusion in petri plat. Which is the method correct for count? I'm not sure if i count everything or only the bigger one?

Yes, you have to count every individual colony.
However, in practice the question is more, what is deemed a countable plate and how important is it. In many laboratories you will find that technicians and scientists won't bother to count each and every colony on the plate if you have a visibly high number of colonies. They will for example simply say (with a bit of experience), the count for this plate is greater than 300 (write >300).
Nevertheless, you will of course still need a count, so it is common practice to do one of the following:

Split your plate into sectors of equal size (you can draw lines on the bottom of the plate), count all colonies in one sector and then multiply this number by the number of sectors you have divided in. So, say, you have split your plate into 4 sectors (quadrants) by drawing a big cross on it, you would count the colonies in one quadrant and then multiply by 4. This is obviously an extrapolation.
The other option, is to dilute your sample until you get it within countable range. So you could do a serial dilution, put it onto plates and then once your organisms have grown you can count the entire plate and then multiply by the dilution factor. So, say, for example you have your sample in an enrichment broth and do two 1/10 dilutions (1/100) and then plate out 0.1mL (counts as 1/10), you have a final dilution factor of 1000. So you would need to multiply the count that you get on this imaginary plate by 1000.

In your sample you obviously have a variety of different organisms. It is probably advisable to check official methods for what they recommend. Here is an excerpt from the official BAM method for Yeasts, Molds and Mycotoxins:

Count plates after 5 days of incubation. If there is no growth at 5 days, re-incubate for another 48 h. Do not count colonies before the end of the incubation period because handling of plates could result in secondary growth from dislodged spores, making final counts invalid. Count plates containing 10-150 colonies. If mainly yeasts are present, plates with 150 colonies are usually countable. However, if substantial amounts of mold are present, depending on the type of mold, the upper countable limit may have to be lowered at the discretion of the analyst. Report results in colony forming units (CFU)/g or CFU/ml based on average count of triplicate set. Round off counts to two significant figures. If third digit is 6 or above, round off to digit above (e.g., 456 = 460); if 4 or below, round off to digit below (e.g., 454 = 450). If third digit is 5, round off to digit below if first 2 digits are an even number (e.g., 445 = 440); round off to digit above if first 2 digits are an odd number (e.g., 455 = 460). When plates from all dilutions have no colonies, report mold and yeast counts (MYC) as less than 1 times the lowest dilution used. Isolate individual colonies on PDA or MA, if further analysis and species identification is necessary.

Please see link here.


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Why does the slope of parent-offspring regression equals the heritability in the narrow sense?
Background
---- Notations and assumptions ----
let $W_{ij}$ be the fitness associated to the genotype $AiAj$. $x$ is the frequency of the allele $A1$ in the population. The frequency of the allele $A2$ is $1-x$ because we'll consider only the case of a bi-allelic locus. Also, we consider that only one locus influence the random variable $W$ (the fitness). We will assume that the environment does not influence the fitness. We also assume random mating in order to use hardy-Weinberg equilibrium.
---- calculations ----
The mean fitness is:
$$\bar W = x^2W_{11} + 2x(1-x)W_{12} + (1-x)^2W_{22}$$
The variance of fitness is:
$$\sigma^2 = x^2(W_{11}-\bar W)^2 + 2x(1-x)(W_{12}-\bar W)^2 + (1-x)^2(W_{22}-\bar W)^2$$
We then want to calculate the covariance between father and son with respect to fitness.
Suppose first that the father is $A_1A_1$ Then the son will be $A_1A_1$ if the mother transmits an $A_1$ gene to him, an event with probability x. Similarly the son will be $A_1A_2$ with probability $1-x$. The father himself will be $A_1A_1$ with probability $x^2$. Continuing this wa it is possible to draw up a table of the probabilities of the various father-son combinations in genotype and hence fitness.
Therefore, assuming no change in frequency of $A1$ between the two generations, the covariance father-son is:
$$cov = x^3W_{11}^2 + 2x^2(1-x)W_{11}W_{12} + x(1-x)W_{12}^2 + 2x(1-x)^2W_{12}W_{22} + (1-x)^3W_{22}^2-\bar W^2$$
which also equals
$$cov = x(1-x)(xW_{11} + (1-2x)W_{12} - (1-x)W_{22})^2$$
The correlation between the two fitnesses is found by dividing the co-variance by the variance (since the variance of sons is the same as that for fathers):
$$cor = \frac{x(1-x)(xW_{11} + (1-2x)W_{12} - (1-x)W_{22})^2}{\sigma ^2}$$
We then define dominance and additive variance:
$$\sigma_D^2 = x^2(1-x)^2(2*W_{12} - W_{11} - W_{22})^2$$
$$\sigma_A^2 = 2x(1-x)(xW_{11}+(1-2x)W_{12} - (1-x)W_{22})^2$$
such as
$$\sigma_D^2 + \sigma_A^2  = \sigma$$
My question
The slope of a parent-offspring regression equals the heritability in the narrow sense $h^2_N$.
Heritability in the narrow sense is defined as $h_N^2 = \frac{\sigma_A^2}{\sigma}$ (see Why is a heritability coefficient not an index of how “genetic” something is?).
We defined above that the correlation between parents and offspring is $cor = \frac{cov}{\sigma}$. So I'd expect the slope of the parent-offsprings regression to equal $cor = \frac{cov}{\sigma}$ and not $h_N^2 = \frac{\sigma_A^2}{\sigma}$
What am I missing? Is there a mistake in my background calculations? Is there a mistake in the way I defined some concepts? The answer might be much simpler than it looks like!

Man, your questions always scare me :).

Well, I think I found the very simple mistake I made…
Looking again in my equations, I realize that (for some reason) $cor = 2 \cdot \frac{\sigma_A^2}{\sigma}$
And looking at this website, I see that the slope of the parent-offspring regression is $\frac{h_N^2}{2} = slope$
Here was my mistake!

I thought the range of heritability is between 0 and 1.  But values of parent-offspring regression times 2 calculated this way can certainly be higher than 1.  Am I wrong about heritability?

@sterid Parents share 50% of their genetics with their offspring. So we need to multiply by 2. See: https://biology.stackexchange.com/questions/112552/is-heritability-just-slope


text:
Nerve endings on the skin
We can perceive sensation of pain if we are poked on any part of the skin.  Does this mean there is a nerve ending at every point on the skin?
Does this also mean that each of these nerves go all the way to the brain as single strands so that the brain can distinguish between the touch at any two distinct locations?

Could you? I don't believe you can. Try blindfolding yourself, have a friend poke you with a sharp pencil, then you try and mark the exact spot (after the pencil has been removed) with an ink pen or Sharpie, then have the friend tell you how close you were, or take an image before the pencil indentation fades.

Testing this is a common experiment given to public-school children; described here for example.  As that link shows, threshold distances vary widely over the body, with few regions being remotely as sensitive as the question asks.  Since the premise of the question is shaky, you may want to revise it to focus on the question you want answered.

@MattDMo - Hope the question is now valid


text:
The falsifiability of natural selection
I was wondering if we could think about experiments to falsify natural selection . According to this wiki : we could invalidate natural selection

“...if it could be shown that selection or environmental pressures do not
  favor the reproductive success of better adapted individuals”.

So, to test this hypothesis we would have to:

Have different individuals that are defined as more or less adapted to a given environment
Put them in that environment
See if the better adapted individuals have a better reproductive success. (I will avoid the word fitness because one can consider it already contains the principle of natural selection)

But is it possible to define a priori that an individual is more or less adapted? Of course, we could suppose a priori that because of some or other trait (higher longevity, higher stress tolerance, or whatever), an individual carrying that trait will be more adapted. But if we find out this individual does not have a better reproductive success in that environment, we could conclude it was just not the right trait to be better adapted and it would not invalidate natural selection.
Isn’t it, on the contrary, the fact that some individuals have a better reproductive success which allows defining them as better adapted a posteriori? There would then be some kind of a vicious circle.
Ok, so one could say that we do not need to define a priori better or less adapted individuals. We could just put individuals in an environment and see if at least some have a better reproductive success. That would mean that they are better adapted –and so that natural selection occurs-. But suppose we find no significant differences in individuals reproductive success: that could indeed mean that natural selection does not exist. But, well, that could also just mean that there was no selection pressure in that environment.
So if we want to test natural selection existence, we need either to get individuals that are a 100% sure better adapted than others; or environmental conditions that 100% sure exert selection pressures on organisms ; and we need to know this a priori. But, it seems to me that considering an individual as “adapted” or an environment as “selective” can only be done a posteriori if we already accept the idea of natural selection.
That’s why, to me, it is difficult to think of an experiment that would falsify natural selection. Is natural selection falsifiable ?

Short comment... Why do you think we have multi resistent bacteria? Let me tell you why... we are selecting those few in a group with higher resistance everytime we expose the group to an antibiotic.

Okay, sorry for that I'll edit my post. Just to be clear however : I never implied that anything sucked and I never doubted about natural selection's validity. This was just a serious question about its epistemological status.

What is natural selection?
Natural Selection (NS) is an evolutionary process causing a directional change in both a phenotypic trait and the allele frequencies associated with particular values of this phenotypic trait whenever there is a trait that

Has a non-zero narrow-sense heritability $h_N^2$

See this post for the definition of heritability
Note that if $h_N^2 ≠ 0$, then it necessarily implies that the trait is variable in the population.

Correlate with fitness variance in the population

See this wikipedia article for the definition of correlation

You may want to have a look at this post (maybe in particular Lewontin's recipe explained in this answer) or have a look at an intro course to evolution such as Understanding Evolution by UC Berkeley if this is unclear to you.
You may also want to have a look at the post How is “selection” best defined?
Note about the environment
Note that the genotype - fitness covariance does not necessarily need to be dependent or correlated with a specific environmental variable. Many selection pressures are indeed independent of the environment. If one specific genotype is associated to heart failure, then the environment may matter little. This genotype will always be associated with lower fitness.
In other words, you do not need environmental change, or environment specific adaptations in mind to test NS.
Would evidence that what is needed for natural selection to happen does not exist falsify NS?
Mutations
I don't think that an evidence that mutations do not occur would falsify NS because while NS needs genetic variation (fuelled by mutations), the process per say does not refer to the creation of new genetic variance via mutations. Showing that mutation do not occur would not per say falsify NS (I think) but it would make the point that NS cannot happen. A bit like, the absence of energy would not falsify the theory of gravity but it would prevents any gravity to ever happen.
The theory of evolution as whole would be falsified if one were to show mutations never occur (or occur at a much lower or much higher rate than currently observed) though.
Heritability
Similarly, if one could show that $h_N^2 = 0$ for all traits (nothing is heritable), then this would also prevent any NS to ever happen
Fitness variance
Similarly, if one could show that there is no fitness variance in population or even that fitness is always independent of the gentic variance (in other words, fitness itself is not heritable), then NS would never happen.
How to falsify natural selection?
You could show that for a phenotypic trait $h_N^2 > 0$ and show that genetic variance correlates with fitness variance (fitness can be measured as the number of offsprings) and yet repeatedly fail to see any change in the phenotypic trait values (or frequency of the loci explaining variance for this trait) over time. Such observations would falsify NS.

I think my difficulty comes from the fact that it is hard to think a situation in which a heritable trait which provides fitness benefits would not bring to a change in genotypic or phenotypic frequency associated to this trait over time. I wonder if theoretical models have shown this possible.

Well, no, I don't think a theoretical model has shown the opposite possible. But it is not because a cause to consequence is too easy to grasp that it makes its formulation unfalsifiable. All our models have been developed following some logical cause-consequence relationships. Some are hard to get an intuition from. NS has the advantage to be a fairly simple mechanism, easy to understand even for a layman.

I also wonder about something you said: can environnent really be independent on the genotype-fitness covariance ? If you put a terrestrial mammal with a heart failure gene and one without it at the bottom of the sea, they'll both have null fitness. Put them both in a futuristic world where every disease is cured before birth, they will have the same positive fitness.

The genotype-fitness covariance is measured on an existing population. You cannot observe the effect of extreme environments not explored by the species range. But I agree this can be misleading. Of course, genotype-fitness covariance would necessarily be dependent upon the environment but not necessarily upon the experienced environment.

@Remi.b This is a good definition, but where in this definition is an ability to distinguish between natural selection and genetic drift?

@Remi.b Depending upon how you define "directional", there can be genetic drift responsible for "a directional change in both a phenotypic trait and the allele frequencies associated with particular values of this phenotypic trait" with the trait having non-zero heritability and being correlated with fitness variance.

@Remi.b Do I not have comment-editing privileges?  To clarify what I mean when I say that there can be genetic drift responsible for a directional change in both a phenotypic trait and the allele frequencies associated with particular values of this phenotypic trait" with the trait having non-zero heritability and being correlated with fitness variance. If you determine that evolution by drift is responsible for a trait (or a modification of the fixated trait), this is consistent with: directional change in both trait & allele, non-zero heritability, and a correlation with fitness variance.

Genetic drift is a stochastic process. So, yes at any given instance the change goes in a certain direction but if you were to replicate the process, then if genetic drift alone is considered, you should have on average no effect on the phenotype and allele frequency.

I don't know why I wasn't notified of this reply.  So, I think what you are saying is that selection comes with an expectation that there is a change in frequency, such that the population is better able to manage the selective pressure in the future than it was before the selection.

The change brought by selection are a change in allele frequency. NS does not necessarily increase the survival probability of the lineage (or whatever you mean by the population is better able to manage the selective pressure in the future).

@Remi.b, why does it not necessarily increase the survival probability of the lineage?  (Hold aside sexual selection and I mean increase the survival probability in comparison to if the selection had not occurred, so hold aside Van Valen's red queen representation.)

I can't answer all your questions in comments (here and on other posts). This last question takes quite a bit of time to address and more text that can fit in a reasonable number of comments anyway. Please ask your questions in new posts.

@Remi.b OK, thank you.  I will ask that question.

@Kjian That is just evidence that NS is the correct interpretation, it is like saying under what conditions gravity could be shown not to be true, the conditions only need to be hypothetical but recognizable and testable. That is the difference between falsifiability and falsification.

@John Yeah that was my question actually - are there testable conditions that could show it not to be true - I don't think it would actually, I was just wondering if such conditions could exist.

@Kjian yes for instance if you could show all population's gene pool never changed across all generations, even if conditions were changed in many many different ways.


text:
What butterfly species is represented on this painting?
I am wondering if the butterflies represented on this painting correspond to a real species.
Do you know if this is the case and if yes, what species they belong to? Or at least, what species could have inspired the author?
I think the flowers that butterflies land on are probably poppies.
The painting is from the book "Ehon mushi erami" (Picture Book of Crawling Creatures) by Kitagawa Utamaro, a Japanese painter (the book was published in 1788).

If this were in the US, I'd say this was a cabbage butterfly (Pieris rapae), which is white save a black or gray spot or two on each wing. But it's not in the US; it's in Japan.
Being interested in most things natural, I Googled "all-white butterfly Japan".
I think you've come across a partial depiction of a story, not an attempt to paint an actual, realistic butterfly. Googling "all-white butterfly Japan", there were many hits with the same theme: the soul is like the white butterfly and love is the power that transforms.
From another site:

In Japanese folklore, the white butterfly symbolizes selfless love stronger than death, as told in an ancient tale of lovers named Takahama and Akiko. In modern-day Japan, the moral of the myth has been retained, and a white butterfly sighting continues to hold special significance.

I don't know how true this is, as I do not much trust everything I read on the Internet. But it appears, as here, often on searches varying the words.
If it were meant to be an actual white butterfly, cabbages are also common in Japan, as seen on this stamp:

If someone could read the writing on the painting, it might help a lot.


text:
Strand representation in the DNA version of the Genetic Code
A Wikipedia entry entitled DNA Codon Table states that the codons presented in the table are on the ‘sense strand of the DNA’. But what is the purpose of this, if the sense strand doesn’t code for anything? It stated that it is used a lot in computational biology, what exactly is the use of it in that field?

@David https://en.wikipedia.org/wiki/DNA_codon_table

@Remi.b your answer would have been fine with a minor edit

Thanks for the ref. You will see that I have suggested better terminology in my own answer. Also I have modified your title to make it more informative and less adversorial. Questions that say "what is the point of" tend to antagonize people.

Mind you, I would not object to the phrasing "What is the point of a Wikipedia entry" for something which is just the standard Genetic code with U changed to T. Almost everyone analysing data will be using a computer program and any computer program for DNA analysis will have it — and variants — encoded in a suitable format. Marginally useful for somebody somewhere, but a Wikipedia entry — really?

The genetic code was a seminal discovery in the field of molecular biology. The experiments leading to the results in this table have lead to the existence of the field as we know it today. It's been important reference material for interpreting mutations in disease and evolutionary biology for decades. Asking why there is a page for this is misunderstanding it's importance in biology, there is a wikipedia page for it for the same reason there is a Wikipedia page the atom and periodic table. It's fundamental knowledge in Genetics.

The sense strand has the same sequence as the transcribed RNA. The antisense strand is read in the other direction. For a particular gene, the sense strand is the genetic code, the other strand is the complementary template used to transcribe the RNA from it. The resultant pre-mRNA molecule (before introns are spliced our) will be single-stranded in the 5’ to 3’ direction with exactly the same sequence as the coding sequence (except for U instead of T). As such, the sense strand is the coding sequence of a gene (as it corresponds directly to the transcribed RNA sequence).
It is important to distinguish the direction of a DNA sequence. Genes can overlap in opposite directions. DNA and RNA molecules can only be synthesised by enzymes in one direction. This is important for DNA synthesis in vivo  (e.g., Okazaki fragments) and molecular biology experiments in vitro (e.g., PCR and NGS). Antisense RNAs are also expressed and are important in regulating cellular functions: this includes enhancers which sometimes express bi-directional RNA and short RNAs involved in RNA interference, microRNA, and CRISPR-Cas).
In molecular, cellular, and computational biology, the sense strand encodes the coding sequence (gene or other transcript). This is the sequence of any resulting RNA. Hence we define a codon as the nucleotide triplet that corresponds to a resulting amino acid. The antisense DNA strand and the tRNAs are complementary to this. Therefore there is an agreed upon convention to determine which strand is “coding” and it is straightforward to derive the resulting amino acid sequence of the encoded peptide given a coding sequence and a start codon (AUG). The antisense strand is the reverse compliment sequence which can also be computed. It is not necessary to store the sequence of both strands of a gene since the coding sequence can be used to infer the sequence of both strands.

See Figure 6-7. Molecular Biology of the Cell. 4th edition. Alberts B, Johnson A, Lewis J, et al. New York: Garland Science; 2002. excerpt online

You say "It is important to distinguish the direction of a DNA sequence. ... DNA and RNA molecules can only be synthesised by enzymes in one direction." - That could be a great start-up for learners. Does RNA-polymerase (that does the m-RNA read only from 3'to5'? -  Rarely will I find "negative RNA" in humans declared in that context, thank you!

Generally no, RNA and DNA polymerases both synthesize a new strand from a template strand in the same direction. It is possible there are exceptions in prokaryotes. Anti-sense RNA is usually transcribed independently (not in the opposite direction) by using different primers or promoters on the opposite strand of DNA. Long non-coding RNAs are regulated and expressed separately, they are not simply genes in reverse.

The Problem is in the Terminology
There have been several variants of questions of this type relating to the DNA strands in genes. In my opinion the reason that this is a common problem for students first encountering the topic is poor or ambiguous terminology.

In science loose expression reflects and/or encourages loose thinking.

This answer attempts not only to answer the question, but to encourage both the inexperienced and experienced to communicate with more clarity and less ambiguity.
It is the Genetic Code, not the DNA code
If the genetic code is related to any particular nucleic acid it is to mRNA. It is a table indicating which amino acids correspond to (are inserted in protein in response to) mRNA codons made up of triplets of the ribonucleotides corresponding to the bases, A, U, G and C. It does not include the DNA base thymidine.
The Genetic Code was established using artificial mRNAs and triplet oligonucleotides. Not DNA was used. It was further confirmed using translatable RNAs from the genomes of bacteriophages and eukaryotic viruses the genetic material of which is RNA, not DNA. Not only is there no reason to mention DNA when discussing the genetic code, but for the majority of scientists who believe that RNA preceded DNA, DNA was not even present when the genetic code emerged. Indeed, the title of a 1965 paper by Nirenberg et. al. (who were major contributors to deciphering the genetic code) was:

“RNA codewords and protein synthesis, VII. On the general nature of
  the RNA code”

Another reason for not referring to the “DNA Code” is that genomic DNA contains encoded other information (e.g. transcription start sites) besides the sequence of amino acids.
DNA sequencing and the presentation of genetic information
What, then, is the table presented in the question which — containing T, instead of U — clearly relates to DNA? It is a reflection of the fact that about ten years after the genetic code was deciphered it became possible to sequence DNA with much greater ease than RNA, so that the sequences of fragments of the genome were determined, annotated, and deposited in databases. When users researched and retrieved such sequences, they obviously wanted them presented in a manner that most clearly communicated those annotated features that related to the function of the genomic fragment (or later, whole genome). One of the most important features for users was obviously the sequence of the protein which the gene specified. In addition, because of the complementarily of the two strands of double-stranded DNA genomes, it was not necessary to present both strands, and presenting one strand would increase clarity. Therefore, the databanks adopted the following policies:

Only a single strand of the DNA was presented (in the 5ʹ to 3ʹ direction, as the convention for chemical abbreviation assumes).
Where the DNA fragment contained a single gene, the strand presented was that which could be interpreted by the scientist as if he were reading a strand of mRNA, but with U replaced by T.

To aid such interpretation (or for human or computer analysis — the latter mentioned in the question — of both strands of DNA to identify potential protein-coding regions) tables of the type in the question are produced. They are perhaps best referred to as ‘DNA versions of the genetic code’ or the like.
How to refer to the two DNA strands?
When referring to a segment of DNA containing a single gene, I think the most unequivocal way to refer to the two strands is:

The transcribed strand, and the non-transcribed strand.

This relates to the actual event — transcription — that produces the mRNA. I would advise its use by those teaching and writing on the subject.
Alternatives to the term non-transcribed strand
Unfortunately the strand presented in sequences of genes retrieved from the databases, as described above, is the non-transcribed strand. Perhaps from a reluctance to give a word with negative connotations to something of semantic importance, this term is very rarely used and is never likely to be generally adopted. Instead the following are often employed for the non-transcribed strand — the name of the transcribed strand is given in parentheses.

coding (non-coding)
non-template (template)
plus (minus) or positive (negative)
sense (anti-sense)

I have already discussed the problems with these terms in more detail in answer to a related question, where I explained why I discourage the use of  any of these other than sense/anti-sense — the sense strand conveys the sense of information of the mRNA. Coding/non-coding causes confusion because the naïve student may well assume that the transcribed strand holds the genetic information and feel that the term ‘coding’ should apply to it. (In fact both strands hold the information, as the existence of single-stranded negative-strand (here the terminology is correct) viruses attests.
RNA polymerase-recognition sites
A related problem has been the source of a question as to why CAAT boxes — recognized by RNA polymerase — are named for the non-transcribed strand. The answer is that having developed a convention to represent the strand of a gene that allows us to discern the protein product and the features of mRNA and mRNA precursor, the main concern of the scientist is to see the transcription features in relation to this, rather than to another strand, with A/T, G/C and 3ʹ/5ʹ mental conversions.
Remaining Problems
As discussed in the answer to another question, the use of any description — even non-transcribed — with the unqualified noun strand is a problem because it suggests that the genome as a whole has one transcribed and one untranscribed strand, whereas almost always there are genes with both orientations, and hence transcribed from different strands. It is perhaps better, therefore, to refer to the strands of a gene, except in those cases (generally bacteria or viruses) where two genes overlap in opposite directions. But Biology is not Physics, and sometimes nomenclature has to be descriptive rather than definitive.

This is incorrect. The sense strand is coding and the antisense stand is the template. Non-coding does not refer to DNA strands, it refers to RNAs (which are transcribed) that are not translated into proteins. The “transcribed strand” is not terminology used in this field, learning it is unhelpful and counterproductive.

@TomKelly It should be clear that I am not advocating anyone learn the term transcribed because there is no need for anyone to learn it. Once a student understands DNA replication, transcription and translation, the term is descriptive of one of the strands of a gene in an unambiguous definitive manner, which all other designations are not. Even if you have never heard it used before you know which strand I mean. Hence it can be used as a reference point for explaning the meaning of terms that are in use, but are not self-explanatory. It would be helpful for explaining template.

@TomKelly Thank you for pointing out that the transcribed strand is sometimes referred to as the template strand, a most ambiguous term because the DNA strands are both templates in replication and I would reserver template for mRNA. I have corrected my answer accordingly. I would never use coding or non-coding for DNA strands (I am familiar with its uses in relation to RNA), but the Wikipedia entry for Coding Strand in which the use of template strand is explained uses both coding and non-coding. I am only listing the terms in use.

Since the terminology has been corrected, this should cause less confusion. The terms themselves make sense to me but I have am very familiar with them as a Geneticist (some are used more often than others). Still to avoid any misunderstanding, we frequently use diagrams to show this sort of thing.

Since I started to assume (skipping the Okazaki-part) that RNA-polymerase knows only one "direction" (see above) I feel better,  further assuming "negative"  is synonym to "transcribing", and "negative" is from '3 to '5.  Indeed, I came across "coding strand" not being used according to convention.  - Also, negative RNA (not DNA) does exist und must be coded. - Moreover, I believe in "coding" refering to DNA, by convention. "Transcribing" instead of non-coding is a helpful idea, but it needed to become convention,  isn't it ironic.

Here is the entry in ensembl for the human transferrin gene.  In real life, people look at cDNA sequences, not RNA sequence, and don't see the U's, just T's
http://uswest.ensembl.org/Homo_sapiens/Transcript/Exons?db=core;g=ENSG00000091513;r=3:133745956-133796640;t=ENST00000402696
Look at that first exon, which starts 5'-GGGCTTTGCCTGTCATT.  Look at the DNA sequence in that region.  It's the same.  The template stand for this gene runs reverse, which makes the strand itself look just like the DNA sequence in the forward direction.

The link you gave doesn't seem to bring up exons. - Can it be true that the template for the non-template has got the same row of nucleic acids? It's got to be complementary, not just the other way round.


text:
Are redundant codons used in translation?
I am learning about redundancy in genetics and I came across this statement in my textbook:

more than one codon for an amino acid means that some codons are redundant - the process of protein synthesis could function without them.

I understand that codons are used to make specific amino acids. Does the statement from my textbook mean that if there are two codons which code for the same amino acid that only one of the codons code for an amino acid and not both? I know the term reduntant means that in some cases - more than one codon can code for the same amino acid - but does it also mean that some codons are not used because another codon codes for the same amino acid?
Thanks

The textbook is asserting that translation could function without redundant codons, not that it does. In reality, all possible codons are used.
See this answer on the interchangeability of codons.

The term ‘redundant’ is not ideal in this respect, as that implies a redundancy in reality rather than theory, as @canadianer points out.
Redundancy and Degeneracy
However I would mention that there is another term more usually applied to the fact that certain amino acids are encoded by more than one codon — degeneracy.
There is a Wikipedia entry on Codon Degeneracy:

Degeneracy of codons is the redundancy of the genetic code, exhibited as the multiplicity of three-base pair codon combinations that specify an amino acid. The degeneracy of the genetic code is what accounts for the existence of synonymous mutations.

Although this definition may appear circular in that it refers to redundancy, I am fairly sure that historically degeneracy was one of the attributes listed for the genetic code (e.g. by Crick):
specific
non-overlapping
comma-less
degenerate
universal (no longer true)
I perceive the traces of this  in the Nature Scitable entry for the genetic code.
Synonymous Codon Usage
Codons that code for the same amino acid are termed ‘synonymous’. An obvious follow-up to the question and answer in this post is on the lines of “Does it matter which synonymous codon is used? Are all used equally and is it the same in all organisms and genes?”. The answer is that synonymous codon usage is non-random in various different circumstances. This is a broad area, but the Wikipedia entry on Codon Usage Bias is one place to start. There is also a question on this topic on this list.
“Does it also mean that some codons are not used?”
Answering this specific question here (documented in the references above) even where there is extreme bias in the codon usage in a genome, generally all possible codons are employed. This may be for regulatory reasons (if the tRNAs for these codons are rare, and hence this would be a way of slowing down translation for proteins only needed in small quantities), structural reasons (to allow a particular secondary structure for the mRNA) or some other less obvious reason.


text:
How do PARPs counteract coronaviruses?
I read that

[SARS-CoV-2 has] a nonstructural protein called NSP3, a component of which blocks the host’s efforts to fight off the virus. In particular, this protein shuts down host enzymes called PARPs, which prevent viruses from replicating, and interferes with cellular calls for the release of virus-fighting immune proteins called interferons.

I'm somewhat acquainted with interferons, but I'm trying to better understand the part about PARPs. Alas the Wikipedia page on these does not mention an anti-viral-[replication] function. So, how do PARPs stop viruses from replicating? (Is it by triggering cell death?)

Nsp3 is the other protease and it is also characterized as 'inducing with nsp4 & nsp6 the formation of double membrane vesicles' (where the replicase complex (nsp7 to 15) comes anchoring and doing the genome and mRNA synthesis)

I think this is an interesting question, but I have altered your title to make it less specific to mechanism (replication). Although the quotation mentions this, there is no evidence that replication is specifically targeted by PARPs in coronavirus infection (just as there is nothing I have read to support the contention that nsp3 "shuts down" PARPs). Better, I think, just to say "counteracts" and let the evidence do the talking about mechanism.

Summary
The poster’s answer to his own question focuses on the end results of the anti-viral action of poly- and mono- ADP-ribosyl transferases — PARPs. The references he provided stimulated me to read about the molecular aspects of this topic, which is where my own interests lie. The ‘answer’ emerging from this reading is somewhat extensive, but can be summarized as:

The molecular details of the way in which PARPs act as anti-virals against
  coronaviruses, and in particular whether and how they antagonize viral
  protein NSP3, are still unknown. There is indirect evidence to
  implicate PARP9, PARP14 and PARP15, which — like NSP3 — share a
  structural feature known as a macrodomain, although their mode of
  action is complicated by the fact that PARP9 does not catalyse
  ADP-ribosylation. The viral NSP3 protein has the ability to remove
  ADP-ribose from proteins in vitro, but whether this is its mode of
  action in the cell is yet to be established.

The role of PARPs in the cell (1)
The name PARP is an acronym for poly-ADP-ribosyl transferase, although the 17 human PARPs are defined, not by this catalytic activity, but by the possession of a domain homologous the catalytic domain of the founder member, PARP1 (2). On the basis of assaying the cloned, expressed proteins for self-ribosylation activity most of these (eleven) have only mono-ADP-ribosyl transferase activity, and two (PARP1 and PARP13) are inactive — a conclusion consistent with the substitution of a key catalytic residue at the active site (3).
   One can consider three stages in the involvement of catalytically active PARPs in cellular metabolism: activation, catalytic action and effect.

A common feature of activation seems to be the response to some stress signal, which may result in increased transcription of PARP genes or activation of an inactive form, for example by combination with an accessory protein (4).
   Catalytically active PARPs covalently attach one or more ADP-ribose groups most commonly to specific glutamate residues (less frequently to asp, arg, or ser residues) of target proteins (or in some cases themselves) using NAD+ as a donor:

For those PARPs that catalyse poly-ADP ribosylation (PARP1, -2, -5a and -5b)) linear or branched chains are formed by glycosidic bonds between the 2′ and 1″ positions of ribose rings.
   Although all PARPs — by definition — contain the PARP domain, they vary considerably in the other domains they possess, and this would be expected to be the basis for different substrate specificities. However for many PARPs these substrates have not been identified — only the processes they affect, the main processes (other than anti-viral action) appearing to be DNA integrity, telomere homeostasis, RNA transcription, regulation of mRNA translation by cytoplasmic stress granules and degradation of proteins through the ubiquitin pathway. Most effort has been directed at the substrates of PARP1, which include histones H1 and H2B and  the chromatin insulator binding protein, CTCF (in response to DNA strand breakage) and the transcription factors NELF and C/EBPβ.
   The effect of modification of the substrate protein may be a change in its activity (as exemplified by the inhibition of translation EF-2 by diphtheria toxin) or more generally interaction with some other protein that recognizes the ADP-ribose moiety. One feature of this recognition — particularly significant in the context of virus–host interaction — is that it often involves a specific domain called the macrodomain (5), named after the C-terminal domain of the histone H2A variant, MacroH2A.

Macrodomain from Archaeoglobus fulgidus protein AF1521 showing binding of ADP-ribose (red)
The macrodomain is found in certain classes of enzyme responsible for the turnover of the reversible modification of proteins by ADP-ribose. These include the polyADP-ribose glycohydrolases — which cleave ribose–ribose glycosidic bonds — and MacroD1 and MacroD2 — which hydrolyse the ester bond between the amino acid and the terminal ribose.
   Also of interest is the fact that, several macrodomains are found in three PARPs: PARP9, PARP14 and PARP15.
PARPs in cellular anti-viral responses and viral anti-PARP proteins (6)
   In different classes of viruses PARPs can act in a pro-viral or anti-viral manner. In coronaviruses (human SARS-CoV has been the subject of most study) they exert an anti-viral effect, as indicated by the effect of inhibitors of PARPs. Furthermore certain PARPs (-9, -12, -13 and -14) are induced in response to interferon, itself a consequence of viral infection. As mentioned by the poster, PARP13 binds directly to viral RNA resulting in its eventual destruction. However in most cases it is unclear which PARPs are involved, what their targets are, and whether their anti-viral action is a result of their catalytic activity — clearly not in the cases of PARP9 and PARP13. This is an important proviso to what follows.
   A study of the evolutionary conservation of the all 17 PARPs in different primate species showed that five of these underwent rapid evolution, typical of proteins involved in host–viral conflict (7).
   One of these was the catalytically inactive PARP13, which before its assignment to the PARP family had been shown to have anti-retroviral properties and was termed ‘ZAP’ (Zinc-finger Antiviral Protein).  The zinc-finger domain binds directly to a long stretch of viral RNA (8), but the details of the recognition and how binding leads to the destruction of the viral RNA (is the PARP domain involved?) remain to be elucidated.
   More relevant to coronaviruses, perhaps, is the positive selection of PARP9, PARP14 and PARP15, which all contain the ADP-ribose binding macrodomain. In contrast to PARP13, the mutations in these PARPs are found throughout the proteins, including the macrodomain, where they are found distributed in surface patches, rather than in the ADP-ribose pocket. The relevance of this to anti-viral action is that there is a virulence protein, NSP3, in SARS-CoV which posses three macrodomains, one of which (MAC1) is structurally homologous to the macrodomain of the PARPs. (This macrodomain is also found in the virulence protein of hepeviruses and togaviruses.)

Structure of SARS-CoV genome and domains in gene nsp3 (from (6))
This macrodomain has been shown to bind ADP-ribose, and mutations in the macrodomain of nsp3 have been generated at key residues at the binding site. Using these mutants it has been established first, that such mutants have reduced virulence compared with the wild-type virus, but that this difference is abolished when infection was in cells with knockdowns in the gene for macrodomain-containing PARP14  (although also in PARP12 knockdowns) (9).
   It has been demonstrated that NSP3 can remove ADP-ribose from proteins in vitro, suggesting that this catalytic activity may be the basis of its virulence (6). However evidence for such action during infection is lacking.
   If indeed the continual mutation of the macrodomain of PARP9, -14 and -15 is part of an “evolutionary arms race” with NSP3, the nature of the postulated interaction or antagonism between these proteins remains to be determined.
References
   1. Gupte et al. (2020) Genes & Development 31, 101–126.
   2. Schreiber et al. (2006) Nature Reviews: Molecular Cell Biology 7, 517-528.
   3. Vyas et al. (2014) Nature Communications 5, 1–13
   4. Suskiewicz et al. (2020) Nature 579, 598–605
   5. Leung et al. (2018) PLOS Pathogens 14(3): e1006864
   6. Fehr et al. (2018) Trends in Microbiology 26 598–610
   7. Daugherty et al. (2014) PLoS Genetics 10(5): e1004403
   8. Guo et al. (2004) Journal of Virology 78, 12781-12787
   9. Grunewald et al. (2019) PLoS Pathogens 15 (5): e1007756.

From one of the review papers of the author/prof (mentioned in that article) it looks like (table 1) PARP12 and 13 have direct anti-viral activity at least against some viruses; PARP12 was shown to have some activity against the Zika virus by binding the viral RNA and blocking translation, while PARP13 binds and degrades some influenza proteins like PB2 and PA.
There are quite a few paper cited in that review, which probably have a lot more details.
Basically type I interferon is not directly an anti-viral compound but rather activates/enhances a series of downstream mechanisms (interferon-stimulated genes) which translate into anti-viral compounds that regulate translation initiation and elongation... and among these are some PARPs (12 and 13, the latter actually seems to have two splice variants.)

the best-characterized antiviral protein is PARP13 or zinc finger antiviral protein (ZAP), which is encoded by the zinc finger CCCH-type, antiviral 1 (ZC3HAV1) gene. [...] ZAP is transcriptionally upregulated by type I IFN signaling and directly induced by phosphorylated IRF3 in virus-infected cells. [...] ZAP was first discovered as a potent antiviral factor against the retrovirus Moloney murine leukemia virus (MLV) in a cDNA library screen. Since then, it has been shown to inhibit a broad range of RNA and DNA viruses, including other retroviruses, alphaviruses, filoviruses, and hepatitis B virus. It is not understood what determines the broad yet specific antiviral activity of ZAP. It binds viral RNA via its N-terminal zinc fingers, and ZAP-responsive sequence elements in MLV and Sindbis virus have been mapped. ZAP recruits the exosome to target retroviral and specific host mRNAs for degradation but also acts to block viral genome translation. ZAP dramatically reduces Sindbis virus production, and experiments utilizing temperature-sensitive Sindbis virus mutants that are unable to replicate the RNA genome at nonpermissive temperatures support a mechanism in which ZAP represses translation of the incoming viral genome. [...]
In addition to ZAP, other members of the PARP family are upregulated by IFN and have also been shown to inhibit alphaviruses. Murine PARP7, PARP10, and the long isoform of PARP12 (mPARP12L) block cellular translation and inhibit replication of Venezuelan equine encephalitis virus (VEEV), another member of the alphavirus genus 20, 21. mPARP12L also blocks infection of a variety of RNA viruses from other families, such as vesicular stomatitis virus (VSV), encephalomyocarditis virus (EMCV), and Rift Valley fever virus (RVFV). Similar to ZAP, mPARP12L affects protein translation, and the tethering of mPARP12L to a renilla luciferase reporter mRNA inhibits its translation. Furthermore, mass spectrometry identified ribosomal proteins and proteins involved in translation as interacting partners of mPARP12L. mPARP12L interacts with ribosomes in the polysome-containing fractions at 4 hours post-infection (pi) with VEEV but facilitates disassembly of polysomes at later times of infection (12 h pi), which is dependent on its RNA-binding and PARP catalytic activities.

Weirdly enough Wikipedia has a page on antiviral protein which discusses ZAP, but fails to identify it as PARP13...
And a 2019 paper found that there are four ZAP isoforms, with varying degrees of effectiveness against different viruses.

Regarding the lack of mention in the Wikipedia article that ZAP is PARP13: the "weirdness"  reflects the scientific history and the way Wikipedia works. The history is that ZAP was discovered — and the article written — before it had been shown to have a PARP homology domain (and which is catalytically inactive). Anyone can write an article for Wikipedia, and presumably the original author was interested in anti-viral proteins in general, made a general survey, wrote a short piece on each, but has not bothered to update it since. Anyone can update it, so I probably will. Caveat emptor.

I've just edited the Wikipedia page on anti-viral proteins, so, assuming that my edit is not removed, your comment about Wikipedia needs removing or updating. In fact that particular page is of quite low quality in general. Someone had the idea of grouping anti-viral proteins together and started a few entries for examples he was familiar with, hoping others would expand it (you can see that in the Talk section). However that section hasn't been touched for ages. I see some of the PARPs have their own Wikipedia entries, but not PARP-13. Only those of known protein structures.


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Are pseudogene counted as a subtype of long non-coding RNA genes?
Are pseudogenes regarded as a subtype of the genes for long non-coding RNAs?
I could not find the answer to this question in an internet search.

A note on nomenclature in modern biology
As it stands, this question seems to assume there is some legal commission, Académie française, or the like that is devoted to continually determining scientific nomenclature, and that those in the field obediently follow it. While organizations like IUPAC — The International Union of Pure and Applied Chemistry — do exist for standardization, they move very slowly, and only come out when the dust has settled (so to speak). So if I write an article about genes I can classify them as suits my purpose. I may wish to distinguish just between coding or non-coding; or between structural, informational, regulatory and junk etc. etc. Nobody is going to throw me in gaol if they disagree.
Is it scientific to classify pseudogenes in this way?
By this, I mean do the genes (for that is what we can compare) for long non-coding RNAs (ncRNAs or lncRNAs) have enough general features shared by pseudogenes that it would be useful to sub-type pseudogenes in this way. In my opinion, No. Pseudogenes are generally regarded as non-functional — remnants of unsuccessful or uncompleted gene duplication, or of reverse transcription of mature mRNAs into the germ-line DNA. In many cases they are not even transcribed.  There may not be a single function for those gene-products termed lncRNAs but in general they are transcribed and thought to have functions concerned with gene regulation. There are no structural similarities with pseudogenes, so that all the genes have in common is that they are, well, long, so to that idea I would say “So long!”
How do the genome annotators regard this?
The people that make the rules, de facto — and revise them as science advances — are the ones with the job of annotating sequenced genomes. I haven’t made a general survey of genomes, and am restricting myself to the genome of the fruit fly, Drosophila melanogaster, with which I am familiar. The distinct Biotypes for genes in the data at FlyBase are currently (2019) as follows:

ncRNA (aka lncRNA)
protein coding
pseudogene
snRNA
tRNA
rRNA
snoRNA
pre miRNA

I suspect that this is standard among the large genome databases, and it can be seen that pseudogene and ncRNA are regarded as distinct categories.
Of course, one can argue with this classification — where are the SINES and LINES and Drosophila-specific mobile elements, for example? But that just illustrates what I have written above.

Thank you @David for your comprehensive response.


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What physical traits are derived from the Neanderthal DNA in human DNA?
Some researches had found that Human DNA has a bit of Neanderthal DNA. So they suggested there would have been crossing between Homo sapiens and Neanderthals.
Now the Neanderthal looked a bit different from Homo sapiens, so is there something in human that has some neanderthal looks?
And is it only found in European people or also in Asian or African people. Could it be be possible that a larger hairiness of European man is due to Neanderthal DNA?

Adding to @David's answer, there has been some recent work looking at Neanderthal DNA in the context of Denisovan and modern human populations.
David Reich's group [Sankararaman et al. Nature 2014] found Neanderthal-derived alleles in genes that affect skin and hair (specifically keratin filaments), as well as some that confer risk of disease. Another cool finding:

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

A pair of papers from the groups of Joshua Akey [Vernot and Akey. Science 2016] and Tony Capra [Simonti et al. Science 2016] found associations between Neanderthal alleles and various phenotypes including depression, hypercoagulation, and tobacco use. These results are nicely summarized here.

There was a very readable piece on this topic by Chris Stringer in Nature in 2012. At that time his general conclusion was:

It is not yet clear whether the archaic DNA many of us carry is tied to any visible traits.

Although he added:

More controversially, some of the known differences in coding DNA
  between Neanderthals and recent humans are associated with brain
  development and function

quoting the paper in Science (2010) in which the Neanderthal sequence was published. There may be more recent information of which I am not aware.
As to your question about Neanderthal DNA in different populations, it is not present in people of African origin, but is present in those of Europeans and Asian origin.

Some more recent work has also linked Neanderthal-derived alleles with a plethora of phenotypes. See Sankararaman et al. Nature 2014, Vernot and Akey. Science 2016, and Simonti et al. Science 20160. Also a nice summary: Our hidden Neandertal DNA may increase risk of allergies, depression

Thanks. I suspected there was more recent stuff. You should add it as your own  answer.


text:
How is it known that Homo sapiens and Homo neanderthalensis interbred?
Many recent articles maintain that a small percentages of Neanderthal genes (up to 2%) are found in modern non-African people. (I believe that currently there is insufficient genetic material from older hominids, such as H. erectus, to decode a genome).
My question is: how is it known the “Neanderthal genes” found in modern humans got there by way of interbreeding? What distinguishes those genes from genes that both species inherited from a common ancestor? After all, Neanderthals and H. Sapiens are over 99% genetically identical. How is it determined that gene A is found in both because it was from H. erectus, from which both evolved; but gene B was not already present in H. sapiens, so it must have arisen through interbreeding?

Good question +1. About the claim Neanderthals and H. Sapiens are over 99% genetically identical (and the similar claim about the chimpanzee and human comparison), you should read the post “Same” DNA vs genes

@Remi.b Read that question. It left me very confused. I kind of understand it, but not fully

You will not have found a value of 40% in any reputable source, and it implies that you have not properly researched your question to mention it without citation. I have edited your question using 2% as the upper limit, consistent with reputable studies, such as the one I cite in my answer.

@David As far as the 40% goes, I'm mostly reading layperson articles because either I don't have access to the scientific ones, or they're just way above my pay scale. I'll look for the one that had that number later, but I think it was not saying that 40% of our genome is Neanderthal, but that 40% of the Neanderthal genome can be found in various modern humans. So I mis-stated that. I'll leave your edit. I just wanted to indicate that I spent days worth of reading online trying to figure this out.

OK. The three papers I cite are all available in free-to-view format, although in some cases it is as manuscript versions.

@David Thank you for those links. Reading the Green paper right now. Just as an aside, I think part of the problem with academic papers is that they often have such generic titles (i.e. “A Draft Sequence of the Neandertal Genome”) that search engines do not find them, or if they do show up in the search queue it doesn’t look to the user (i.e. me) like they will be useful. Academic writers should put a bit of thought into how their titles look in a search queue. If someone is researching a topic they often only see the title to determine if it is relevant.

Given your question, it makes sense to recommend David Reich's recently published book Who We Are and How We Got Here. Reich has been one of the principal people working on genetics of archaic peoples. In his book he goes into further detail on the methods used to detect interbreeding.

Although this question makes some false assumptions, it is fundamentally interesting as the methodology used is neither simple or easy to understand. It is not my area, but I have found it especially interesting to read the long 2010 Science paper by Green et al.. One really needs to read it for oneself (it is free view), but it is not a trivial undertaking.
False assumptions / misconceptions in the question
The main misconception in the question are:

That it is necessary to know anything about the genome of H. erectus to make these conclusions. The methods used do not require this. (Although comparison with chimpanzee is sometimes used to give an indication of whether a genetic change occured in humans or Neanderthals.)
That the similarities and differences under discussion relate to differences in complete genes — “but gene B was not already present in H. sapiens…”. They do not, which makes the analysis more complex to follow.

Towards an explanation
Let me start by addressing the question “What distinguishes those genes (purported to have been acquired by H. sapiens from Neanderthals) from genes that both species inherited from a common ancestor?”. The answer relates to the absence of such genes from modern humans of African origin, and the fact that we know the general evolutionary relationship between neanderthals and modern humans (African and non-African) from a wealth of non-sequence paleontological evidence. This is shown in the diagram below, modified from a recent and recommended review by Nielsen et al. in Nature (2017).

Clearly any gene present in the common ancestor to humans and Neanderthals should be present in both African and European populations, unless it had been lost from the African population.
So if the analysis is not done by detecting gain/loss of individual genes, how is it done? Certainly not by overall percentage sequence similarity, because of the high overall similarity and the population variation. It is done by studying SNPs — single nucleotide polymorphisms — in particular genes.
For example, consider a gene that has only a single haplotype in Neanderthals, and originally had a single but different haplotype in humans. (This might determine something like eye colour, although this is not an actual example.)  If the other haplotype were acquired by humans as a result of interbreeding, then the modern human population would contain both alleles. When you compared the relationship of the SNPs for this gene between different humans and between humans and Neanderthals you would find different results from those for a gene the variant of which had not been acquired by interbreeding. The acquired gene in humans would be more related to that in Neanderthals than non-acquired genes, but less related to that  in other humans (because of its more recent appearance in the population and time for homogenization, I believe).
The African/non-African aspect is explained in the Science paper cited in my introduction, but there is a good visual diagram in a 2014 Nature paper by Sankararaman et al., the manuscript of which can be viewed freely in PMC through the US HHS.

(1) Sites where a panel of sub-Saharan Africans carries the ancestral allele and where the sequenced Neanderthal and the test haplotype (marked non-African) carry the derived allele are likely to be derived from Neanderthal gene flow; (2) Haplotype divergence patterns. Genomic segments where the divergence of the test haplotype to the sequenced Neanderthal is low while the divergence to a panel of sub-Saharan Africans is high are likely to be introgressed.
These papers contain a wide range of controls, including comparisons of different non-African population groups, and detailed discussion of alternative possibilities.
A final point of interest is that Sankararaman et al. examined some of the genes in which these SNPS suggest Neanderthal origin. They write:

“…genes involved in keratin filament formation and some other
  biological pathways are significantly enriched in Neanderthal
  ancestry in European populations, east-Asian populations, or both
  …. Thus,
  Neanderthal alleles that affect skin and hair may have helped modern
  humans to adapt to non-African environments.”

Coda
It would be scientifically dishonest not to mention some oddities. One is that the Green et al. paper suggested that gene flow had been uni-directional: from Neanderthals to humans, which is apparently unusual in interbreeding. However a more recent study (Kuhlwilm et al., 2016) shows some human gene flow into Eastern Neanderthals, although not into European Neanderthals. (Thanks to @iayork for pointing this out.). The other is that modern Asians appear to have more Neanderthal DNA than modern Europeans. (This is discussed in the paper already mentioned by Green et al.)

+1 This makes much sense now. I'm confused about relate to differences in complete genes. Are you talking about the fact that the genes are there, but different alleles of those genes? Because that I understand. I maybe should have said "alleles" in my question. Or are you referring to something different?

I mean the same genes are there, but there are alleles in Neanderthals that are were not present in the  human population before mixing. I had been thinking I could clarify my answer and will do so now.

One is that gene flow appears to have been uni-directional: from Neanderthals to humans. Ancient gene flow from early modern humans into Eastern Neanderthals

@iayork — Thanks for pointing that out. I have ammended my answer accordingly. Do raise any other points you feel I have not addressed correctly or clearly enough. I find the question interesting, but it is not my area of expertise.


text:
ATP and Muscle Contraction
I have a question regarding how molecular interactions manifest in physical actions - such as hanging from a bar. To the best of my understanding, when it comes to the contraction of muscles, ATP is required for myosin to detach from actin - terminating contraction.
So, what I'm wondering is when we are hanging from our bar, utilizing our grip strength, we are in a constant state of contraction. However, eventually, our muscles fatigue and we let go. I presume this is because we are running out of energy, but isn't energy (ATP) what was necessary to terminate contraction? Why do we eventually let go of the bar and how is this represented on the scale of muscle fibres?


text:
Can stress and arousal be independent?
I'm trying to figure out if it's possible to have a stress response without being initially, or simultaneously aroused. I'm defining stress to be physiological stress (ie. release of cortisol) and arousal to be activation of the sympathetic nervous system.
Every example I can think of, these two are not independent. In the case of "fight-or-flight," one initially activates the sympathetic nervous system, which is then followed by the release of cortisol. Or in individuals with major depressive disorder, their sympathetic nervous systems are constantly activated while cortisol is being secreted.
So, is it possible to experience cortisol release without activation of the sympathetic nervous system?

Stress response has 2 main components:

Quick response, within minutes, is by the Sympathomedullary Pathway (SAM): hypothalamus > sympathetic nervous system > release of adrenaline and noradrenaline from the adrenal medulla > stimulation of the heart, dilation of the muscle arteries, constriction of the gut and skin arteries, glcogenolysis (the breakdown of glycogen into glucose) > more glucose available as a fuel
Delayed response, within hours, is by the The Hypothalamic Pituitary-Adrenal (HPA) System: hypothalamus > pituitary gland > ACTH > release of cortisol from the adrenal cortex > gluconeogenesis (formation of glucose in the body from other substances) > more glucose available as a fuel

Cortisol secretion from the adrenal cortex can be stimulated by things other than stress, for example, hypoglycemia, but hypoglycemia will simultaneously activate the sympathetic nervous system, which will trigger the release of adrenaline (Neuroendocrine Response to Hypoglycemia).
Some cortisol is also secreted along with aldosterone in response to hyperkalemia or hyponatremia (Vivo.colostate.edu), for example in SIADH (A Case of Transient Hypercortisolism Simultaneously Occurring With the Syndrome of Inappropriate Antidiuretic Hormone Secretion Induced by Olanzapine).
Cortisol can be also increased without stimulation of the sympathetic system in Cushing syndrome due to a pituitary adenoma or, rarely, other tumors that secrete ACTH or in adrenal adenoma, which secretes cortisol.


text:
What’s the name of this tree?
I’m trying to find information about this tree that I didn’t plant. Looking for information in terms of pruning, etc.

It had white flowers on it this spring, but is now flower less and has very few young berry-esque type fruits growing on it. They’re very small still, but it seems they’re going from green to a red. This in Michigan.
Additional pictures:

Thanks to Bryan Hanson for the answer! Found a picture online of it with flowers:

Where is this plant located?

Could you please add close-ups of the leaves, flowers and fruits?

@Chris Michigan. Sorry I should have included that in OP. I will upload closer pictures sometime today when I return home.

@Taskle please [edit] your own post to include your location as well as additional close-up images of the leaves and fruit. The more detail the better!

I've added additional pictures, with closeups on the leaves as well as one of the fruits. I can really only count 2-3 fruits growing as of right now on it.

Revised Answer
The additional pictures point to something in the genus Prunus.  Note that there are extrafloral nectaries at the base of the leaves, and feathery stipules are visible (see here for annotated picture of a different species).  Since it has a weeping habit, and doubly toothed leaves, I think what you have there might be a Japanese Weeping Cherry Prunus subhirtella var. pendula (but other names seem to be in use).  Some info here which seems consistent with your specimen.
Original Incorrect Answer
I think you are probably looking at Ulmus glabra "Camperdownii" or a similar cultivar.  This is a "weeping" elm variety that is produced by grafting; all plants are descendants of a single tree. Wikipedia gives the full background.  Your specimen has somewhat more pointy leaves than many of the images for Camperdown Elm I found online, but apparently there can be some variation.
EDIT: The fruit picture (added after my answer) clearly rules out my answer!  Also looks like there are nectaries at the base of the leaves.

The Japanese Weeping Cherry is definitely it. I found some pictures online and the “snow” colored flowers are a perfect match as to what it looked like back in April.