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Are there epigenetic effects in the regulation of human height?
Development of human average height
Human average height has fluctuated significantly throughout history. For instance, in the last 100 years or so, it has increased sharply by about 10cm. OWID (Our World in Data) has data and figures on, among other measures, the average height over the last 18K years, average male height by country over the last 200 years, annual change in average male height, and annual change in average female height.
Regulation of human height
Already the genetics of human height seem to be complicated and to involve a large number of different genes (and hundreds of loci) according to, e.g., this article by Lettre (2011). However, since the time spans are too short for significant purely genetic effects, there must be either developmental or epigenetic effects at play or both. Developmental effects have been linked to socio-economic status, perhaps via steady and good nutrition before birth and during childhood. This paper by Komlos (2007) (without paywall here) shows data for English youths in the 1700s and 1800s by socio-economic status and finds a height gap of up to 22.6cm, his sample sizes are a couple of thousands for the lower-class group and less than that for the upper-class group.
Epigenetics human height
Carey reports in her book "The Epigenetics Revolution" (2012) that people born after the Dutch Hunger Winter would not only remain small for their entire lives but that there was still a significant difference in their children, born decades later. She does not seem to refer to height differences though (I guess?), but to differences in the risk to develop certain diseases as reported in this paper by Heijmans et al. (2008) (not sure if there's a paywall; same paper is also here). They trace this to differences in the expression of a certain gene (IGF2) because of hypomethylation of that region.
Since other phenomena are thus shown to be subject to epigenetic effects, it is possible that the regulation of human height is too. To be clear, I am not aware of any study that suggests this (or investigates this). It would certainly be very difficult to identify, so I suspect this has not been thoroughly investigated. Note that the epigenetic effects shown in Heijmans et al. (2008) could only be shown because of the very specific conditions of the Dutch Hunger Winter, a short but horribly severe famine with intact medical records. But I am hoping there is some information out there.
So my question is
Are there indications that epigenetic effects may be present in the regulation of human height and its rather interesting development in recorded history? (Or is this unlikely, e.g. because the variation is sufficiently explained by other factors or because studies have tried and failed to find epigenetic effects? Or has this not been investigated so far?)

Would you care to explain your downvote? Evidently you think that whatever is wrong with my question is so blatantly obvious that I should not have dared asking this in the first place. Is it off-topic (not biology?)? Is it trivial? Is it more than one question? Is it a duplicate? Is the question unclear? Does it not show any evidence of research? Is it that you feel I'm promoting some commercial interest/ideology/conspiracy theory/bad paper? It is more likely that I can fix it if you tell me what's wrong.

https://www.nature.com/articles/ncomms13490

@user438383 Thanks, this is very helpful. I was not aware of that paper. I should probably have searched more thoroughly. I guess, this also means that the question is indeed trivial and should be deleted. I will do that shortly.

The Hunger Winter thing worries me. First it should be realized that this is all based on statistics of gross observations. There is no mechanistic evidence of a mechanistic basis for the observations. Second, if the nutritional environment has epigenetic effects during a famine, one would expect a reversal during the glut that prevailed when the Dutch were rutting in the 60s. But it appears to have persisted. I don’t buy it.

@0range no problem. I dont think it renders the original question trivial and in need of deleting. Hopefully someone with knowledge of epigenetics can give a comprehensive answer.

@David I am not sure what problem you see with statistics of gross observations. Heijmans et al (2008) say "Clinical examination, including blood sampling, was completed for 311 exposed individuals, 311 same-sex siblings, and 349 unrelated controls." Without having done a calculation of the statistical power of their analysis (I am not sure I understand the statistical properties of their assumptions well enough for that), I would assume that the statistical basis of their methodology is probably sound.

@David Regarding your second issue, Heijmans et al (2008) seem to suggest the explanation of methylation (of this IGF2 gene) being subject to changes in the early embryonic development which could account for the lack of a reversal in the same individuals in the 1960s. Note that other studies (Veenendaal et al (2013)) do not find this epigenetic effect, but they emphasize explicitly that they nevertheless find it plausible.

My point about statistics is that it says whether an correlation is likely to be true, but nothing about its basis — i.e. whether its basis is epigenetic. And as for blood sampling — not much DNA there — what does that actually mean? Such a lynchpin of human epigenetics needs more than plausibility.


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How are random mutations in cells of an organism controlled?
Even in the most stable conditions cells undergo mutations. So in humans(an example) with millions of cells, mutations must be a common affair. But how is that we are still basically the same throughout the life, and no random mutations cause sudden disorders in us. Even if mutations are rare, they cannot be nil and how are they controlled.

A rule of thumb is one mutation per cell division. Most cellular organisms have various error proof and repair mechanisms, to reduce the number of mutations. When these accumulate, they do cause sudden disruptions, such as cancer.

I think you haven't researched on the topic. Try googling "Mutation Repair" or "DNA Repair". You'll find various articles related to the same.

There are many reasons why humans rarely experience the deleterious effects of mutations. Many mutations arise from errors in normal biological processes such as DNA replication or recombination. DNA repair mechanisms and apoptosis (programmed cell death) are some ways of 'dealing with' mutated or damaged DNA. Another reason that we rarely see deleterious effects of mutations is because of the way amino acids are encoded.
There are approx. 20 amino acids encoded by the genome, yet each amino acid can be encoded by approx. 4 different codons. For example threonine is encoded by ACU, ACC, ACA, ACG. This means a point mutation is unlikely to make any difference to the final protein product as there is a high chance that the mutation will still code for the same amino acid. This is what is called a silent mutation, and there are other types mutations that do not have deleterious effects.
https://www.nature.com/scitable/topicpage/genetic-mutation-441/

There are no amino acids in the genome — it is DNA.

Sorry about that, clearly what I mean is there are 20 amino acids encoded by the genome.  I will edit that.

source: Stack Exchange

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

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Species Identification: Liberian "kiss-meat" snail
Before my wife immigrated to the US from Liberia as a kid, she loved eating "kiss meat". It's a freshwater snail they collect from the swamp during the rainy season and eat as a delicacy, so called because you suck the meat out with a kiss.
Here's a YouTube video of this process, so you can get a good look at the snail and see its habitat (mangroves).
This is the best image from the video that I could find. They've been washed and the rear of their shell has been broken off. I can't get Stack Exchange to let me add a second picture );

I have not been able to find any other references to these snails, except under the name "kiss meat". Would anyone be able to identify these?
(Note: There seems to be a similar looking brackish snail commonly called "African Periwinkle". I don't think this is the same thing.)

Welcome to Biology.SE. It is important that your question contain all the content that will help answer it, without relying on external links like videos that may be deleted sometime in the future. It's fine (and encouraged) to reference outside sources, of course, but it shouldn't be crucial to understanding the question to visit the link.

@BryanKrause Thank you for the feedback! I'll get some pictures added.

It's Tympanotonos fuscatus from West Africa. They harbor near the roots of mangrove at low tide. Due to their tendency to bioaccumulate heavy metals, they have been used in studies of environmental presence of heavy metals, and the samples taken from markets have been found to be excessively high in cobalt and manganese.

Thank you! So it seems they are the same thing as African Periwinkle...

Yes indeed, it's them.

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Characteristics of 'true' tissue
Why are sponges not considered to have tissue level organization?
Quite a few places seem to say that sponges do not have 'true tissue' and only have specialized cells.

Unlike Protozoans, the Poriferans are multicellular. However, unlike higher metazoans, the cells that make up a sponge are not organized into tissues. Therefore, sponges lack true tissues and organs;

The Wikipedia page on sponges says -

Sponges are similar to other animals in that they are multicellular, heterotrophic, lack cell walls and produce sperm cells. Unlike other animals, they lack true tissues and organs.

I have not been able to find what defines true tissue, so I would like to understand what characteristics a group of cells must have for it to be considered proper tissue.

Can you please expand your question with at least one quote from a source that uses the term "true tissue", in order to help understand your question? When I google, the term I find is "organized tissue", which may be different than you are asking about.

@jakebeal I'm so sorry, I don't really know how you add a quote from a source. However, true tissue is what showed up on multiple pages when I googled 'Do sponges have tissues and organs?'

Is this the definition you mean https://glossary.lias.net/wiki/True_tissue ?

@ani You can edit your question and add text from one of the sources that you saw.  To indicate a quote, you can just use quotation marks or do a ">" for a blockquote.

@jakebeal thank you! I've edited the question, hope it is clearer now.


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How would a virus “evolve” if someone is infected with both the omicron and delta variants at the same time?
If someone is infected with both variants (let’s say within a day or two), what are some of the likely outcomes with respect to the virus “evolution”?

is it most likely that only 1 of the 2 variants survives?

if both survive, is it likely that the 2 strains “mix” with each other to produce a 3rd strain?  Obviously 2 viruses don’t have “sex” per se, but I read https://www.cnbc.com/2021/12/05/omicron-variant-may-have-picked-up-a-piece-of-common-cold-virus.html  that the omicron strain actually has a gene that is found in the common cold virus.

By what mechanism could that have happened?  Somehow a common cold gene got inserted into the virus, or did that just happen by random mutation?
My primary question is by what mechanism would a virus insert a snippet of RNA from another virus into its own RNA?
On further study, I found this link to an OSF preprint which talks about “template switching”.  https://osf.io/f7txy/
Here is the text:

This highly mutated Spike variant harbors a novel insertion mutation ins214EPE. Although the position 214 appears to be an insertion hotspot10the EPE insertion in Omicron appears to be novel. Previous analyses of sequences deposited in GISAID suggested that insertions in the SARS-CoV-2 genome likely arise from polymerase slippage or template switching.10,21Template switching is a normal event during RNA synthesis for coronaviruses, as this process is used to generate sub-genomic RNAs (sgRNAs).22,23In this process, also known as copy-choice recombination, the RNA-directed RNA polymerase (RdRp) and the nascent strand dissociate from the template RNA strand and reassociate with a new template (or the same template at a different position), and then RNA synthesis continues. Typically, such recombination involves templates with high sequence similarity (“homologous recombination”), although non-homologous (or “illegitimate”) recombination between dissimilar sequences can also occur.

Could someone boil down the meaning here in simpler terms?  For starters, I don’t understand how recombination applies to viruses?  Isn’t recombination a DNA process?  How does it relate to viral RNA?

Welcome to the site. Please take a [tour] and visit the [help]. In particular this SE values questions that show some prior research (and attempts to answer it themselves) and scientific backing for claims. Please provide a reference for the flu gene insertion, and demonstrate what you have found out about this topic.

how rhinovirus swap RNA is not understood but we are fairly confident they do. https://www.nih.gov/news-events/nih-research-matters/understanding-common-cold-virus

Ok.  It makes sense that we just don’t know the recombination mechanism(s) yet.  I had been reading a lot of sources that seemed to gloss over the details.  I guess we just don’t know the details.

Basically your options 1 and 2 are the the only likely outcomes from a co-infection with two SARS-CoV-2 viruses. There is a 3rd option, which is that there is a co-infection, producing some amount of both viruses.
Total competition (i.e. one being completely gone, the other 100% output, your option 1) is unlikely unless one of the co-infecting strains has low initial input (i.e small amount infected), and low replicative ability compared to the other strain. In this case, you might see that one of the viruses doesn't survive the competition. However, this would be hard to detect with current technology and hard to prove experimentally as well unless the strains had sufficient differences (i.e. not just single base mutations) and you could survey the entire viral population to look for levels of output.
One of the reasons for these difficulties is that viruses, particularly RNA viruses exist as what is known as a quasispecies, this is where there is a pool of virions with variant genomes as the output from any particular infection. This is caused by errors in replication of the genome (RNA polymerases tend to be more error prone than DNA polymerases and/or not have a proof-reading mechanism, though SARS-CoV-2 (RNA virus) does have a proof-reading RdRP1 (PDF)). Because of this, and because of the way we do most sequencing - by chopping the genetic material into small bits, then assembling a consensus sequence computationally - it can be difficult to tell if there is a population of virions that are one strain or not, as the computation methods lead to missing of the non-dominant sequences. There are methods (computational and new technological) to look at these sorts of things, so we may have a better idea soonish.
For option 2: Recombination is common where-ever there is a genome, be it DNA or RNA. RNA polymerases are particularly prone to recombination events, and this is a major driver of evolution of RNA viruses2. Indeed it seems that this is a common feature of Coronaviruses in general3. Basically what is happening here is that there are multiple strands of RNA present at replication and the RNA pol can jump from one to another, often in a sequence dependent manner (i.e. at regions of high similarity) or sometimes where there is secondary structure of the RNA that causes the polymerase to jump from one location to another based on proximity, skipping the bits in-between.
Now, there's a bit of complexity here - there are multiple different genera of coronavirus called Alphacoronavirus to Deltacoronavirus (nothing to do with the SARS-CoV-2 variants, just unfortunate naming choice from someone(s) when dealing with this virus). The different coronavirus types have the same overall RNA structure (i.e. encode the same genes), but have quite diverse sequences, so an Alphacoronavirus has a different sequence to a Gammacoronavirus, meaning that homology based recombination is less likely than within the genus. Having said that, there are still highly conserved parts of the genome within the family as a whole, so those might be sites where recombination could occur.
1: Robson et al., Molecular Cell  2020; 79(3):710-727.
2: Tackas et al., Plant Virus-Host Adaption: Molecular Approaches and Viral Evolution. 2014; 385-394 (paywalled?)
3: Kek et al., Adv Exp Med Biol. 1987; 218:99-107.

Thank you for this answer.  Interesting.  So can RNA polymerase “jump” from one strand to another at any point on the strand?  Or are there only a few well-known points where jumps can occur?

Yes they can jump. Generally this seems to be done at certain regions within the RNA and these sites are consistent across a genome type. I think it can happen at any location, just is much more likely to happen at specific places.

bob1's answer describes the general mechanisms very well.
One must not forget that the emerging recombinations still underly the pressure of evolution: They need to survive and to spread with a rate at least comparable to the original strains.
Nature has done this big experiment and now we can see several small clusters of Delta/Omicron recombinations, see pango designation issues #473, #439, #444—now assigned pango lineage XD, #445—pango lineage XF, and #446 for details.
It is interesting that the successful recombinations follow some pattern: The Spike gene is completely or at least to the greatest part from Omicron, ORF1ab is completely or partly from Delta. Most interesting is the recombination described in #444: It has just an Omicron spike in a Delta backbone.
EDIT: More than half a year later, more Delta/Omicron recombinants have shown up(XAW, XAY, XBC, and XBD), some of them with considerable spread. For an overview of the current state of affairs (27-NOV-2022) see this article by C. Roemer et al. on virological org.

If you were to speculate on how omicron has a gene found in the common cold, would you speculate that this happened by random mutation, or by actual interaction with a common cold virus?  I understand this is pure speculation, but what odds would you give?

This is a different question and should be asked as a question, not in the comment section. But any acquisition of a complete gene, i.e., something with >100 nucleotides or >33amino acids needs a cause. Since common cold viruses are still coronaviruses, and two of them even betacoronaviruses, I would say that acquisition by interaction is almost secure and random mutation is precluded. But we have not seen this in the wild upto now.

Yea it is a different question, but this site frowns on speculation (understandably).  This is why I framed my original post the way I did :)


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What is the thickness of the membrane if only alpha helixes are embedded of a transmembrane protien?

Given is the representation of a transmembrane protein. Calculate the thickness of the membrane if only alpha helixes are embedded in it. One turn = 5.4Å
Please read:
The reason I didn't submit my attempt is that, I thought because there isn't an exact and precise depiction of the protien molecule and also the question is vague so I hesitated. I counted the number of turns ie 7 but still there was a lingering doubt "what if I am wrong, I would make a fool of myself."
What I know:

Protiens basically bunch of amino acids bound by polypeptide bond.
Primary structure is the sequence of the amino acids.
The secondary structure us due to the Hydrogen Bonding between the Oxygen atoms having partial -ve charge and Hydrogen atom attached to the Nitrogen, within the backbone only. eg: alpha-helixes, beta-sheets, Turns, Loops
Tertiary Structure is due to the interaction between the different R groups in the amino acids. Like the disulphide bonds, hydrophobic interactions, H-bonds, Vanderwaal forces.
Quaternary Structure is due to the overall 3D structure which is result of the aggregation of the polypeptide subunits.

Please go easy on me, its my first time posting here and I am still a 1st year in college and 2nd Sem is gonna start next week.

Please finish the [Tour] to find out how this site works. Your question is incomprehensible without reference to external sites, which is quite unacceptable. It would also appear to be a homework question which, should you edit it so it is comprehensible by itself, requires you to show your attempt to solve it.

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. Please see our homework policy for more information.

@David Sorry, I should have included it in here too. It's my first time posting here.

The question begins by telling you that only the alpha helices are embedded in the membrane. This means that if you can calculate how long the alpha helices are, you can work out the thickness of the membrane it is embedded in.
Alpha helices look like spirals (similar to fusilli pasta shapes). These are highlighted in figure A) below.
The question also tells you that each turn of the alpha helix is 5.4 angstroms. One turn if shown in figure B) below.
Looking at the picture, it seems that each helix is about 7 turns long. As each turn is 5.4 A, the length of the helices must be approximately 7 * 5.4 A which is 37.8 A.
Therefore, using the information that the membrane must be about as thick as the helices in the transmembrane proteins are long, you can deduce that the membrane must be up to 37.8 A thick, however the membrane may not actually be this thick as the question from the paper doesn't specify how much of the alpha helices are embedded in the membrane (60%, 80%, 100%?). I guess the assumption is that the entire alpha helix section of the transmembrane protein is fully embedded within the membrane.

Are the alpha helices always straight within a membrane, or could they be bent?

From what I understand, alpha helices tend to be straight due to the strong hydrogen bonding which takes place throughout the structure, so it would be unusual for kinks to appear. However, there are structures called helix-turn-helix (common in DNA binding proteins) which form an alpha helix with a kink in it. There’s some good information on this here: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/alpha-helix and here: https://www.sciencedirect.com/science/article/pii/S0005273618300518

Please do not answer questions that do not respect the model of this site.

From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.

Thanks a lot for the answer. And yeah, the question asked is very vague. I had problems because of this vagueness.


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How to find a model organism's standard data about proteome size and genome size?
I want to know proteome size(the number of proteins not length) and genome size(length) of model organisms like Caenorhabditis elegans, Saccharomyces cerevisiae etc.
I found www.uiprot.org
and I made a table which is wrong according to my prof.

for example, I searched "Saccharomyces cerevisiae" on the site.
https://www.uniprot.org/proteomes/UP000002311

I wrote 6,049 on protein. and clicked the link "GCA_000146045.2 from ENA/EMBL" on Genome assembly and annotation.
https://www.ebi.ac.uk/ena/browser/view/GCA_000146045.2

I clicked "Assembly Statistics" on the right box and wrote the total length.
where am I wrong?
It seems there are so many samples about a species. I don't know which is standard reference for the model organism. I want data as a general knowledge like on the text book
and I found model organism database sites on wiki
https://en.wikipedia.org/wiki/Model_organism_database
I don't know how to use these sites. they give me complicated sequence browsing but I only want just proteome, genome size. what should I do?

EDIT.
professor didn't tell us about strains. he just gave the table at the top of this post with data about E.coli by red text as a example.

this is what professor showed on his next lecture, which is other student's answer.
professor didn't mention which is correct or wrong, he asked if the student is sure about the source(Yu Nie) and if the source is reliable.
anyway, comparing this to my table, Mus musculus and Drosophila have significant difference.
Mus musculus other: 39,412, mine: 55,474
Drosophila other: 30,443, mine: 22,117
I searched again about these.

Mus musculus have only two result, it seems I should have chosen standard rather than close to standard.

but about drosphila, they have no standard. (I chose random one)
https://www.uniprot.org/proteomes/?query=drosophila+melanogaster&sort=busco&desc=no
where can I find about Drosophila?

when your professor asks about proteome size, do they mean number of proteins or length of proteins? usually the second is what is meant.

@Maximilian Press number of proteins.

I see nothing wrong with your method -- uniprot is a good resource. If your professor expects statistics for specific species / strains, they should supply unique identifiers or accession numbers for those organisms, at least. Did they give more information about which numbers in your table are wrong, specifically? Can you quote the wording of the assignment?

@acvill I added what you asked.


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What volume of elution buffer for plasmid-containing filter paper?
I am attempting to elute a 9kb plasmid from a square of filter paper sent to me to be transformed into DH5a E. coli (photo below). Each filter paper square has been spotted with 1ug of plasmid DNA.

I have two questions:

AddGene's protocol states to elute the DNA using 30ul of TE (I'm using H20 as that's all I have atm). Using a similarly sized piece of filter paper to test, I added it + 30ul of h20 to a 1.5ml tube with a quick 4k spin down and have observed that the 30ul is completely absorbed by the paper as shown in the photo. How should I resolve this? Add an additional 30ul? I also tried to use a pipette tip to shove the paper down and squeeze out the water but you can see it didn't work.

What volume should I use for transformation knowing that the filter paper contains 1ug and I need to use additional elution volume? Most protocols I've read call for 1-5ul of DNA and AddGene calls for 2ul assuming 30ul elution volume.

Thank you.

Are you using the same kind of filter paper (thickness matters)? Did you follow their directions, which say to use 1/2 the piece of filter paper (because they send you a two spots) and to use 30 µL (not the 3 µL you wrote)?

My sample isn't from AddGene. And I can only estimate it's the same thickness. It seems to be the same based on close inspection. The spot on the paper isn't marked and so I wouldn't know exactly the boundaries to cut out of the paper. The 3ul is an error - I'll fix that now. I used 30ul.

1 ug is a LOT of plasmid, so your elution doesn't have to be very efficient. I would figure out how much water your test piece of filter paper can absorb by adding more and spinning down until you start to see free liquid. I would then use double that volume to elute your actual sample, take 30ul and proceed with your transformation.  If your centrifuge is a benchtop eppendorf-style, I'd use the max speed rather than just 4k.

The answer to this is... some.
You only need a tiny amount of plasmid DNA to transform bacteria like DH5$\alpha$, typically in the 1-10 ng range, but much less, as low as about 10 pg (10 picograms) may still work. If you can get even 0.2 ul of the liquid out of that tube, try using that in the transformation.
Things you can try;

remove the paper, spin the tube down and see if you can recover even a tiny amount of liquid.
Add a bit more liquid - another 30 ul will be fine
Snap the tube lid closed on the paper to hold it in place, then spin the liquid out of the paper - this is quite difficult to do.

Note - even with 10% DNA recovery (very low for this method), with 30 ul you will still have 100 ng of DNA, or about 3.3 ng/ul.

These are all excellent suggestions, especially using the lid to spin out the paper. Thank you!

FYI, I was able to use a total of 60ul of TBE to elute the plasmid on filter paper, using 1ul for my transformation with success.

Good, so you probably transformed a few ng. In my experience smaller amounts <5 ng work better than higher amounts anyway.

Indeed. I did 16 experiments with varying volumes ranging from 1ul to 10ul and the lowest volumes performed best. It was a ~10kb plasmid. I actually posted most of my diy transformation protocol here.


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Identifying Promoters in Non-homologous Sequences within the Same Organism
In this paper, the authors cloned a GPD promoter for use in driving a GFP gene from Lentinula edodes using a set of provided primers. The primers were derived from the following accession GQ457137.1 containing the GPD gene for this organism.
In fact, there are three accessions in GenBank containing gpd promoter sequences for Lentinula edodes, each of varied size and homology to the aforementioned sequence used in the paper.
I am working on defining a transformation protocol for Psilocybe cubensis (of which there are no published transformations) and I would like to design some primers as done in the paper above in order to clone the GPD promoter for this organism from its DNA; however, just as with L. edodes, there are multiple accessions of GPD in psilocybe cubensis: KM273235.1 and KT067727.1
In my case; however, there is no literature referencing either of these accessions and so I don't know which of these accession I could or should use to design my primers.
I have the following questions:

Why does the same promoter within the same organism have such varied sequences?
If the promoter sequence varies even within the same organism, the how can anyone extract the promoter with certainty since the organism may carry a different sequence for the promoter?
Generally, I'm trying to find the GPD promoter for P. cubensis (or any strong promoter) and clone it for use in my plasmid for transformation. I'm stuck as to how to go about finding a suitable candidate.

Thank you.

Why does the same promoter within the same organism have such varied sequences?

While there may be other reasons, the fact that the same species has several genes encoding GPD proteins is an indication that this enzymatic activity is important for different mechanisms, times or conditions. For example, I mentioned in a comment to one of your previous questions that the three GPD-encoding genes in budding yeast (TDH1, TDH2 and TDH3) are expressed during different growth phases. Therefore, although the proteins encoded by these genes might share both sequence homology and function, their promoter regions most likely will not. We even expect their promoters to be different, to allow for such differential expression. Put differently: if the three TDH promoters were all highly similar, we would expect them to also be active at the same times, effectively rendering the three genes redundant.
There is therefore no reason for assuming that promoters driving the expression of two different genes will share any homology, just because the encoded proteins happen to share function.

If the promoter sequence varies even within the same organism, the how can anyone extract the promoter with certainty since the organism may carry a different sequence for the promoter?

The only way of knowing exactly what region upstream of a gene that regulates it's expression (i.e., what functional elements that defines its promoter) is to characterize the promoter region. This is way beyond the scope of your work. What we tend to do in budding yeast when we clone an uncharacterized promoter, is to simply take 1000 bp upstream of a gene's start codon, and assume that this includes all elements necessary for proper regulation of the gene in question (e.g. possible transcription factor binding sites (TFBSs), transcriptional start site (TSS), etc). 1000 bp is a relatively safe length in budding yeast, since the distance between genes rarely exceeds this, and we tend to assume that promoter regions don't overlap neighboring genes' coding regions. But this might be different in your species. Also, if you know the location your gene's TSS, this would be a safer reference point than the start codon.

Generally, I'm trying to find the GPD promoter for P. cubensis (or any strong promoter) and clone it for use in my plasmid for transformation. I'm stuck as to how to go about finding a suitable candidate.

My guess is that the authors that cloned the GPD promoter from Lentinula edodes either already knew that this specific gene is highly expressed and therefore selected its promoter; alternatively they might have cloned all GPD promoter variants, and then simply published the one that they saw worked best.
If you don't have any information about the expression of the GPD-encoding genes from your species, any decision as to which promoter to choose will inevitably be more or less guesswork. It seems to me that the evolutionary distance between Lentinula edodes and Psilocybe cubensis is way too large to make any direct inferences. Nevertheless, with the lack of better options here is what I suggest:

Try to identify which of Psilocybe cubensis's GPD proteins is most similar (in terms of sequence homology) to the protein the authors chose for their Lentinula edodes GPD promoter. This might indicate that these are direct orthologs, and with a bit of luck may also share similar relative expression patterns and/or levels. You could also do a similar matching with the Tdh3 protein from budding yeast, since TDH3 is indeed a very strong promoter (article behind paywall, but easy to find elsewhere). If you still don't know which of the promoters to choose, proceed with both candidates and see which one works best (although that means doubled cost and effort).

Once you have identified your candidate GPD gene, you define an appropriate region upstream of your gene’s coding region as the promoter region. This can be arbitrarily picking 1000 bp, or the entire intergenic region, as @Cholpisit suggests.

Design your primers for cloning this region into your target vector, upstream of GFP.

I really appreciate your effort to help, but I can't help but feel like you aren't quite understanding what I'm asking even though I've taken a best effort to elucidate it as clearly as possible. Furthermore, I'm asking these questions specifically to learn and reconcile my ignorance before actually designing the primers or running the experiment - you're first sentence seems to presume otherwise. This conversation format doesn't really accommodates a proper discussion where some of the miscommunication could probably be resolved in a few quick back/forth in a chat.

Anywho, I will digest the info further and see if I can think of a way to progress the conversation forward. I am sincerely grateful for your efforts.

If you don't feel my response answer your question(s) you can wait with accepting it and see if someone else addresses it better :)

My intent was not to insinuate that you are not trying to understand, I just think that if you don't understand why homology between promoters of paralogous genes is unlikely, you will probably want to understand that before you go about with your endeavor. But explaining why this is the case is a completely different question. In any case, I will edit that comment out from my answer. Also, if you can point out exactly what parts you didn't get answered, you might get better answer from me or from others.

I accepted it to ensure my comments didn't take away from the effort you put into the response! Duly noted re: the other parts.

I have rewritten parts of my answer, hope it's clearer now. If not, we might be able to continue the discussion in the chat, but I'm not sure how that works.

Let us continue this discussion in chat.

Left you some messages in the chat. We're in diff timezones so might be tough to hop on at the same time.

I'm not well-verse in fungal transcriptional system but I did some digging in bacteria before, so not entirely sure this perspective will help.
The promoter region of any gene should be upstream of the transcriptional unit and usually remains in the intergenic region, not being part of the CDS of interest and the adjacent gene. If we're digging a promoter of an essential gene, probably constitutively express with decent strength, ones might be able to chop the whole intergenic region and the part of the adjacent genes (in case they contribute to the transcriptional control). A well-annotated genome would be required for this approach.
Considering the different promoter/gene annotations available in the database. It might be hard to pinpoint if they're the same strain/substrain or not and that may affect the genetic variation to a certain level.

The doubting 3 GPD promoters of Lentinula edodes you mentioned are from unpublished sources from 2 teams. Do we know if they're exactly the same strain? As for those two sequences from the same team, they share sequence similarity to a certain level, GQ457137      is part of GQ457138 according to the alignment.
As for the P. cubensis GPD promoter, you can try chopping the intergenic sequence upstream of the coding sequence as gaspanic mentioned above. The GPD accessions KM273235 and KT067727 might be referring to different strains as well. Depending on the strain you're working on, you may prefer the sequence submitted as that strain. However, you'll have to look for more information since those deposited sequences refer to partial CDS, not the promoter itself like in the case of Lentinula edodes.


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What determines the physical appearance of a tangible amount of bacteria or viruses?
As in the title, I was wondering how would feel an amount of one type of bacteria or virus, big enough to have a tangible size of the sample. What color, state (liquid, solid), textures, smell ecc. of the sample would be.
Ideally I would consider only the bacteria or virus, and none of their possible byproducts, and without any medium where they normally live in. Just the organisms in a tangible amount.
Therefore: why a set of bacteria will look like that? Why, for example, some are fluffly molds, others looks like a dough and so on. Is this representative of the physical structure of the bacteria?

Lab-grown E. coli is kind of a light-medium brown color, and smells like... E. coli. I don't know how to describe it. It's kind of squishy if you play with it, which I wouldn't recommend because you just used a lot of media to grow that much. I imagine it would get hard(er) if you dry it out, but I've never fully dried a pellet that big, just used it for protein purification.

It's going to ultimately depend on just how much you have. I'm not really seeing the practical reasoning behind this question, though. Can you explain what is directly motivating your question, and perhaps narrow it down substantially?

It has absolutely nothing practical. It is more philosophical. I've read somewhere that the total amount of covid-19 in the world is estimated to be some hundreds of grams, and I wondered how that would look like if all gathered. Question is then extended to bacteria as well. In other words, is exactly in line with the "what-if" questions.

@BryanKrause I thought you were going to refer to this xkcd, which is even more on-point.

@jakebeal Ah, had forgotten that one, nice!

@jakebeal there is always a relevant xkcd.

I was expecting a scientific answer. But I've got an equally valid xkcd link. Amazing! If that is true, if they look like that, I wonder if viruses are actually wet, or the "wettiness" is just how physically look like just the sheer amount of them. After all, water is not wet, if you take a bunch of molecule at a time. Actually, the concept of wet it would not even exist at that scale. Like a pool full of small balls: they look wet if you are big enough compared to the balls. Who knows if this applies here too. Should I move to stackexchange chemistry? :D

Is this really a question about a problem in biology at the standard of a site for professionals and serious students of biology? Or is it just idle curiosity about an unnatural situation to elicit a “fancy that!” response. Are you going to apply the information in any way? Do move the question to SE Chemistry — I imagine they will tell you what to do with it.

@David it is just idle curiosity. Moving to a place to know what to do with it, it would not help, as there is no practical reason behind. I am more active on electronics stackexchange, afaik over there humble curiosity for the sake of it is appreciated - when there is an effort shown. in this case, I did not know how to prove such effort, being illiterate in biology myself. for sure, I did not wanted to let anyone lose their time. my apologies if that was the case, although very unintended!

I am afraid that Electronics, Biology and, one would imagine, any other SE have the same statement in the Help on questions not to ask "You should only ask practical, answerable questions based on actual problems that you face. Chatty, open-ended questions diminish the usefulness of our site and push other questions off the front page." There is also the injunction "inspire answers that explain “why” and “how”" — describing the appearance and feel of something is not it. Try dried yeast in the supermarket or wet yeast in a baker's.

@David I understand now. I think the edit is more representative and more meaningful of the original question. If necessary, I will ask a new one.

There is no one answer to this question, any more than there is a single answer to the question of what color, texture, or size a mammal is.
To get a sense of some of the diversity out there, the American Society for Microbiology has a nice gallery of bacterial colony morphology, showing that in most cases, you end up with basically variously colored and shaped blobs of snot-like substance. At a larger scale, some microbial mats are formed of bacteria, and can form more fibrous mats bound together by extracellular substrate.

As mentioned in another comment, I wonder if when the sample looks "wet", is just an effect of the amount of the bacteria, or they are actually wet. Again, because the concept of wet would not exist if taking water molecules individually, maybe with bacteria is the same. I think all depends on the extracellular substrate here mentioned.

I'm not sure how meaningful it is to attempt to separate an organism from the context in which it normally lives in this manner. Consider the fate of deep sea creatures brought to the surface.

Meaningful not quite. I thought more from a physical point of view. I began to work with e-ink displays which are using very small spheres. That made me think over different type of simple particles how result at a bigger scale, just with those particles. Then the curiosity was steered toward complex, not obvious structures, like bacteria, cells or viruses. To keep the same analogy, the thought was considering just the living creature, but in neutral atmosphere - therefore is a pure hypothetical situation, where a physics can answer, but physics are unaware of living creature dynamics.

Indeed the example of the fish makes sense, it cannot be considered out of the deep sea, neither the concept of (perceived) consistency of an object might look the same in such extreme pressure. Nice catch! But I think hypothetically bacteria have a theorized "consistency" at our pressures, so I thought it would be possible to imagine it (like in the xkcd comic) - hence why I asked biologists, not chemists.


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Using PCR to add the overhangs to gBlocks for NEB HiFi
Does adding the overhangs to gBlocks for NEB Hifi using PCR pose a big problem? The IDT website suggests that one should design the gBlocks with the overhangs. However, if I did not do this, will it be a problem?
Edit: I intent to use Q5 High-Fidelity Polymerase and the gBlocks range from 500-2200 bp in size. It's not necessary for the exact sequence to be present.

Welcome to Biology.SE. Please [edit] your question to provide more details such as: the error rate of the polymerase you intend to use, the size of the gBlock, and how critical it is to you that the exact sequence be present for your application. You may also benefit from taking the [tour] and consulting the [help] starting with [ask]. This will familiarize you with how this site works and what the expectations are for questions. Thanks.

You could add the overhangs with PCR, then gel purify or PCR purify. I don't think it will pose a big problem as I've done it before and all of the colonies I screened were correct.

Welcome to Biology.SE. We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. In particular, you are ignoring a potentially significant problem with this approach — the error rate of the DNA polymerase being used. I've posted a comment to the OP asking them to give us more detail, but please also edit your answer to be more complete. Please see the [tour] and [help] starting with [answer] questions effectively for details about site expectations. Thanks!

Error rate here of Q5 polymerase is 5.3 x 10^-7 [1].  One would have to be remarkably unlucky for error to propagate into your final clone.  [1]  Paulo Cseri Ricardo, Elaine Françoso & Maria Cristina Arias (2020) Fidelity of DNA polymerases in the detection of intraindividual variation of mitochondrial DNA, Mitochondrial DNA Part B, 5:1, 108-112, DOI: 10.1080/23802359.2019.1697188


text:
Are there complexity requirements on potential hosts to be susceptible to parasites?
Are there lower bounds to complexity for hosts and how are these described or modeled? In other words, one would expect an organism to have a certain amount of "surplus tissue" in order for parasites to be able to feed on it, at least without killing the host too soon for the parasites to thrive.  For example, humans have surplus blood (we can draw a lot of blood and survive), making it possible to live with a few leeches, ticks, etc. Is this supposition really true? That is, do we know that "very simple" organisms cannot have parasites? If so, how do we characterize what is "too simple to be a host" and does it have anything to do with having "surplus tissue"? (I assume "surplus" is not the term used in parasitology because I haven't seen it in the books...)

yes it most at least have cells otherwise it does not qualify as a host.

"Complexity" is a difficult term to operate with in biology; most people that use it don't have an idea of how they'd like to operationally define it, and without an operational definition it isn't meaningful.
Phages are effectively parasites of bacteria - one could bicker that a virus can't be a parasite because it's not "alive", but I think this is just a semantic argument about what it means to be alive, and many of the definitions that exclude viruses are problematic because they those same terms exclude animal parasites.
Not all parasites are of the "feed on the host just a little bit" variety, either. Parasitoid wasps, for example, typically consume the entire target host, sometimes paralyzing it at the same time an egg is laid. Cordyceps is another fun group of (mostly) parasites, whose targets include other fungi and insects.
The only limit seems to be that the host must somehow be of use to the parasite. It must also be complex enough to be considered a living organism in its own right: you can't have a parasite of something that's already dead, for example, since that has a different meaning. I think these meanings are rather tautological, rather than interesting, though, so I'd answer your title question to say "no, not in any meaningful, non-tautological way".

Thank you this is very interesting! I guess I asked the  question a bit wrong: I meant specifically hosts that are multicell organisms and specifically parasites that feed on a host for an extended period (as opposed to consuming it or killing it entirely). In these restricted senses, one would expect (although I am asking because I'm not sure) that the host must have "surplus tissue" to be able to yield to the parasite without dying. I guess I am interested in this from an evolutionary perspective: do we see the entry of parasites as correlated to the development of "surplus tissue"?

@Antoshka I don't think you'll be able to do anything mathematical here in order to develop any "rule", just to look at examples, and biology is pretty good at coming up with exceptions to any rule you think you found. It's certainly not true that parasites of the type you describe only feed on "surplus" tissue: tick infestations can be fatal to deer, weakening them to the point they cannot recover.


text:
Ferns: How big can a circular sorus be?
I looked at some small ferns under the microscope. The circular sori of the ferns I looked at were less than 2 mm in diameter. The microscope I used had rather weak magnification, so I didn't get to see lots of detail. Later, I came across an image of large sori Wikipedia:

Image source. License: public domain.
I am surprised by the size of the circular sori in the image. If I could obtain large sori such as these, I would probably be able to see more detail under weak magnification. I'm wondering:

How big in terms of diameter can circular sori be?

What are some species of ferns with large sori?

Try members of the Asplenium genus, particularly the widespread Asplenium trichomanes or Maidenhair fern.
Without a location in the world, it will be difficult to give you a more specific answer.
Sori can be a few millimetres across, I would hazard a guess at about 5 mm diameter in my experience, but I have no scientific backing for that as a maximum dimension, and I'm only really familiar with plants in my country so can't make assumptions about other locations.


text:
Is the swimming pool water harmful to frogs who jump in? If so, how?
Here is an odd question:
Frogs have permeable skin. Indeed, via capillary action, frogs absorb water through their skin.
Chlorine is in principle a harmful substance. I am sure what percentage of chlorine is in swimming pools usually, but the pH level is kept to around 7.4. This is the desired pH level, as a pH of 7.4 is the pH-level in human eyes and mucous membranes.
One of the "common wisdoms" I had growing up was that if a leopard frog (i.e. The Northern Leopard Frog, rana pipiens) jumps into a swimming pool, it must die soon, because the chlorine would kill it. However, I now doubt this is true.
So, do frogs die from swimming pool water? If so, why? What exactly is killing them? Chlorine poisoning?
PS: I am having difficulty finding the correct tags for this question. Any help is appreciated.

Have you considered why they add chlorine to swimming pools? If it inhibits the growth of a broad spectrum of microorganisms perhaps it also has detrimental effects on metazoans, including amphibians? If you had some water from a swimming pool and some frogs then you could test this directly. Barring that situation you could try searching for relevant studies in PubMed.

@mdperry That would be cruel, and not really answer my question. I would need a statistically very large sample of frogs, roughly the same age.

The chlorine concentration in pools is +- 0,5 mg/L.

+

0.002 mg/L will fatally damage the sensitive skin on tadpoles, frogs, salamanders and other amphibians.

another source:

Free chlorine (Cl2) is a greenish gas that is well known for its
  highly toxic properties as can be attested to by the thousands of
  soldiers that died and were severely injured from chlorine exposure
  during World War I. In water, chlorine is the most toxic substance
  that we will discuss. Ironically for the amphibian keeper, it is this
  toxic nature of chlorine and its ability to denature proteins, which
  makes its encounter inevitable. Chlorine is generally used as an
  antibacterial agent in municipal water supplies and may be present in
  concentrations of over 9 mg/1 in some tap water (measured in Houston,
  Texas as an example, although levels were generally lower). The
  concentration of chlorine in municipal water supplies can vary greatly
  from day to day, or even hour to hour, depending on conditions at the
  water treatment facilities. Concentrations as low as 0.0034 mg/1 have
  been noted to reduce reproduction in fathead minnows with 72 hour
  LC100 (lethal concentration for 100% kill) at 0.15 mg/1 (Arthur and
  Eaton,1971). LC50 (96 hour) for the shiners (Notemigonus chrysoleucas)
  was as low as 0.19 mg/1 (Esvelt et al., 1971). The concentrations
  found in municipal water supplies are many times greater than the
  minimum lethal concentrations for many aquatic life forms.

Thus, the well being of the frog in the water of the swimming pool depends on the time the frog spends in the water. Eventually, with extended exposure the chlorine concentration will exceed the one compatible will life and the frog will die. This time is multifactorial variable, thus cannot be assessed easily - the weight and the skin surface area and skin permeability will affect the frog survival in a great degree.

So what exactly kills the frog?

@the high concentration of Chlorine is toxic and causes oxidative damage to cells.

Frogs die in minutes in our subdivision pool. Usually tree frogs . I pull out about one a week ( I go first thing in the morning). Toads survive, I pull out one of them from time to time.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Does acuity of a re-mapped region of cortex depend on the need of the animal to resolve between two closely related stimuli?
From my informal research so far, I've learned that cortical magnification is evident in at least the visual cortex and the somatosensory cortex.
My question is the following:
If there were a hypothetical experiment to be done where the one area of the cortex, say the visual cortex, were to be re-mapped to a different sensory modality like touch, would the acuity or "resolving power" of the re-mapped region depend on the extent to which the animal needed to distinguish between closely related touch stimuli? In other words, has anyone tried an experiment that results in a re-mapped and magnified cortical portion in one go?

Interesting question. I doubt an experiment like this would survive an Institutional Review Board (IRB) review, though, so my guess would be that this hasn't been tried (if it is possible from a surgical perspective).


text:
To which thing does "two-thirds" refer here?
Life and Letters of Charles Darwin, volume 2 includes the following letter from Darwin to Hooker, about a examining a plant that absorbs ammonia:-

Reflect how little ammonia a plant can get growing on poor soil—yet it is nourished. The really surprising part seems to me that the effect should be visible, and not under very high power; for after trying a high power, I thought it would be safer not to consider any effect which was not plainly visible under a two-thirds object glass and middle eye-piece.

To which thing does "two-thirds" refer here, i.e the size or magnification or something else?

For future reference, it looks to me like this type of question would be more appropriate on [HSM.SE].

The use here of "object glass" is equivalent to our current usage of "objective lens" on a microscope. In this case Darwin used a 2/3 lens and the "middle eye-piece" from a particular microscope. I think (but can't find confirmation) that the 2/3 refers to the width of the field of view in inches.
The letter you quote is to Edward Cresy Jr. on the 2nd November 1860. I can't find much on Darwin's microscopes, other than in the Whipple Museum, where they have 2 microscopes of Darwin's. One of these purchased in 1847 is a microscope with exchangeable lenses. This microscope was a Smith and Beck compound microscope. You can find examples of these for sale in antiques collections and a similar one is probably this one, which comes with a number of objectives and a 3 magnifications of eye-pieces (~1/2 way down page). The magnification of a 2/3 objective looks to me to be about 10-20x (confirmed in this review as ~15x (about 2/3 way down page)).
As for the middle eye-piece, based on the same  Microscopy UK page linked above, it is probably a #2 eye-piece of about 8.5x, so a total magnification of about 125x (127.5x, if the numbers are accurate).


text:
Is it possible for a brown cat to birth an orange kitten?
I have a brown (cinnamon) cat, I assume her alleles would be b’b’ and oo. She was bred with either a black male (B_ o) or an orange male (__ O), or both if it’s possible for her to have carried the black cat’s sperm with her for a while until she met the orange cat. I can’t remember how long, I was eight or nine when this happened. She had five kittens, an orange female, an orange male, two black males, and a cinnamon male. From my understanding, it shouldn’t have been possible for her to have two orange kittens, let alone for one of them to be female, with either male. However, I have only taken two genetics classes! So, how could this have happened?

Edit: cat coat color genes:
Primary coat color alleles: B- black, b- chocolate, and b’- cinnamon. B is dominant to b is dominant to b’.
Orange coat color alleles: O- orange, o- not orange. These alleles are carried only on the X chromosome. If the cat has OO or OY, they will be orange. If the cat has Oo, they will be tortieshell. If they have oo or o, the primary coat color will be displayed.
If my cat (b’b’ oo) mated with the black cat (B_ oY), the kittens should have been 50% black and 50% dependent on the second allele of the male, either black, chocolate, or cinnamon. None should have been orange.
If my cat mated with the orange cat (_ _ OY), the kittens should have been 50% non-orange males and 50% tortie females. None should have been orange.
I’m unsure about the black cats’ statuses as tabbies, as it can be hard to tell, and the black cat was a stray that we don’t have photos of to even try to check, but the brown cats and orange cats were all tabbies. None were dilute, none had white patches, etc.
It is possible for cats to be intersex and for this to affect their coloration (XXY is how we get male calicos and torties), so perhaps the male orange kitten was OoY, but that would have made him a tortie. For there to have been an orange female or orange XXY male they would need two ‘O’s, which would not have been available to them. Or perhaps the female was just O? But I feel like the odds of there being two intersex kittens in the same litter must be very low. Plus, she had no other physical anomalies (she went thru a series of tests including ultrasounds, x-rays, and a CAT scan to diagnose a well-hidden tumor later in life and nothing strange came up internally either). The orange tom could not have been XXY, as this causes cats to be sterile. Also, the only mutations I have found that causes oo kittens to be orange also tend to cause a shift in coat color during kitten-hood, which none of the kittens experienced.
My cat:

My cat with the orange female and short-haired black male:

The orange female grown up:

The orange male grown up:

One of the black males:

Here is that same black male grown up, he’s the only one of the family with long fur!

Here is the other black male, you can see the stripes on their legs a bit as babies, not so much grown up:

The brown male:

And lastly, here is my cat and her brother as kittens, you can see he also had faint stripes. All of the kittens in their litter looked like either one of them and their mom was brown as well:

I don’t have pictures of either toms, one was a stray and the other was a farm cat. I do have a picture of my cat's mom and her litter if anyone is interested in that.

What breed of cat did you have?

@classy_BLINK Sorry, she’s an American shorthair! All three of them should be/have been American shorthairs.

It would be very helpful if you also add her picture in question.

Welcome to Biology.SE. I think you will get a better response if you elaborate on what lead you to your conclusions about your cats genotype (and what alternative genotypes you have considered). As someone with a genetics background, but who isn't current on the genetics of cat coat color (and no time to read up on that) I would personally find it helpful if you laid out the logic of why you think orange kittens are impossible.

@tyersome Thank you! I added in some more clarification.

@classy_BLINK I had to go searching, but I got pictures of momma and all the kittens!

Cat coat color is controlled by many genes not just two and at least partially environmentally developmentally triggered. so its not entirely genetic on top of being genetically complex. worse some genes are unknown and some other genes are sex linked so will not express in some sexes.

If Momma cat is photos 1 and 2 then what you have there is a tabby cat - these have agouti hairs and the Agouti colour alleles. Agouti means that they have bands of colour on the hairs. I don't know if this means that they also carry other colour alleles.
In addition, I believe that cats are superfecundators (fertilization of multiple eggs from separate acts of sexual intercourse), which means that if they mate with more than one male during the fertile period, then they can have multiple fathers for one litter, as is discussed in this article.
So - yes, it is possible that there are more than one father associated with this litter, and that there are some underlying genetics that can also result in this.


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How many MAOA alleles are there?
The question is about the human gene MAOA.
I've seen MAOA-H and MAOA-L mentioned in papers.
The page https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000189221;r=X:43654907-43746824 does not describe the gene alleles as far as I can tell.
There is a base sequence of exons provided at https://www.ensembl.org/Homo_sapiens/Gene/Sequence?db=core;g=ENSG00000189221;r=X:43654907-43746824 however since all the nucleotides are already written in I don't understand which base pairs can vary and which are always the same.
So is there a reference that describes in detail all the known MAOA alleles and which base sequences they have?

I recommend searching a resource such as dbVar that is targeted towards human genomic variation, rather than serving up slices of the human reference genome.
The human reference genome is a single sequence that, as you say, does not try to represent genetic variation. It is merely a reasonably good representation of what a single haploid human genome copy might be expected to look like.
I searched MAOA on dbVar and found 426 different variants (alleles observed via DNA sequencing) that have been described. A minority of these have been annotated as either pathogenic or benign (see "Clinical Assertion" column), but for the most part we don't know what effect these alleles have, if any.
For richer information about specific disorders related to MAOA mutations (alleles), you might also consider looking at OMIM. However this will only include instances of alleles thought to affect phenotypes.


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If brine salt percentage is between 1 and 2 percent, can Clostridium botulinum growth prevail over Lactobacillus acidophilus?
After searching in various websites, I found mostly that Clostridium botulinum doesn't grow easily in a salty environment, and that it needs a pH from 4.6 to up;
as I am lactic fermenting some bell peppers, I searched and found that their pH is between 5.5 to 6.5;
I applied a salt concentration of 1 - 2 % on the solution (brine);
I didn't find a clear answer to whether or not the bacteria can grow in those conditions, only that it isn't likely, and most websites make similar statements, therefore looking for clarification
In an environment of about 20 degrees Celsius, salinity of 1-2%, and pH between 5.5 to 6.5 (bell pepper),
is it possible that Clostridium botulinum could grow and compete with Lactobacillus acidophilus?

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details. ——— You may find this webpage helpful.

Also note that a "colony" is the form seen on growth media — I think what you want to know is do they grow? In addition, there are standards for naming of species (including bacteria). 1) The genus (first part of the binomial) is written out in full (the first time it is used) and is always capitalized. 2) The whole name should be italicized. I have fixed these problems, but please do some reading and revise your question accordingly as soon as possible to avoid receiving downvotes — if your question is closed editing your post will also allow you to request it be reopened.


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Do cheetahs compete with lions?
Do cheetahs compete with lions for the same prey?
A quick Google search says the answer is no:

Lions hunt big animals such as buffalo, giraffe, wildebeest, and zebra. What prey do cheetahs hunt? Cheetahs hunt small animals such as gazelles, hares, and impalas.

Such videos I have seen of the two species hunting, appear to confirm the above.
But I've also heard and seen multiple accounts of lions killing cheetah cubs. Why would they do that, if there is no competition? If another predator eats different herbivore species than you do, their existence is good for you, not bad; by reducing the number of their prey species, they reduce the herbivore competition, thereby increasing the number of your prey species.
A bit more searching found this paper: https://journals.co.za/doi/pdf/10.10520/EJC117300

Based on
actual diet, lions exhibited the least amount of
overlap with wild dogs (31.6%), leopards (39.1%)
and cheetahs (42.5%; Table 2)...  Lions exhibited
the least amount of overlap of preferred prey with
wild dogs (41.0%), cheetahs (43.7%) and leopards
(48.3%).

'Least amount' notwithstanding, that claims more than 40% overlap, in other words a very high degree of competition between lions and cheetahs, in direct contradiction to the story I had previously understood.
Which of these claims is true? And if the two species do compete, how does that work? Which prey species do they both eat?

Yes, cheetahs do compete with lions. Cheetahs can share the same habitat with lions; however, they actively avoid lions (and also hyenas and leopards). They are smaller carnivores/predators than their competitors and they are non-confrontational in nature. They would avoid unnecessary injuries at all costs because they rely on speed to hunt and survive. An injury that can slow them down is potentially life threatening.

Cheetahs have been reported to suffer from intraguild competition by lions Panthera leo, spotted hyenas Crocuta crocuta and occasionally leopards Panthera pardus. These larger predators represent a threat to the smaller-bodied cheetahs as they can affect their food intake by limiting access to high resource areas or kleptoparasitism (e.g. 10–12% of kills are kleptoparasitized in Serengeti National Park (SNP)), and reduce population sizes via increased cub mortality (e.g. 73% of cub mortality was due to predation in the SNP). In response, cheetahs often demonstrate avoidance behavior to minimize interactions with dominant carnivores , with spatial and temporal partitioning regarded as the principal behavioral mechanisms by which this is achieved. Accordingly, cheetahs have been described as a refugial species that seeks competition refuges within the landscape with low densities of lions and spotted hyenas.
Rostro-García S, Kamler JF, Hunter LT. To kill, stay or flee: the effects of lions and landscape factors on habitat and kill site selection of cheetahs in South Africa. PLoS One. 2015;10(2):e0117743. Published 2015 Feb 18. doi:10.1371/journal.pone.0117743

 (removed the citations)
The definition of the terms used in the above citation:

Intraguild predation, or IGP, is the killing and sometimes eating of a potential competitor of a different species. This interaction represents a combination of predation and competition, because both species rely on the same prey resources and also benefit from preying upon one another. - Wikipedia
Kleptoparasitism, literally meaning parasitism by theft, is a form of resource acquisition where one animal takes resources from another. Although kleptoparasitism of food (i.e., kleptoparasitic foraging) is the best known example, the stolen resources may be food or another resource such as nesting materials. - Sciencedirect.com

One of the prey species that cheetahs and lions both eat is Thomson's gazelle (Eudorcas thomsonii). Thomson's gazelle is the primary prey of cheetahs. Probably, the most amount of overlap in their diet comes from eating this prey. However, lions would hunt them less or just steal them from cheetahs.

The prey species included buffalo (Syncerus caffer), wildebeest (Connochaetes taurinus), and Thomson's gazelle (Eudorcas thomsonii) as the three main prey species of Serengeti lions, hyenas, and cheetahs, respectively (Schaller, 1972; Sinclair & Norton‐Griffiths, 1979).
Swanson A, Arnold T, Kosmala M, Forester J, Packer C. In the absence of a "landscape of fear": How lions, hyenas, and cheetahs coexist. Ecol Evol. 2016;6(23):8534-8545. Published 2016 Nov 6. doi:10.1002/ece3.2569

The same paper (cited above) talks about the coexistence of lions, hyenas and cheetahs in Serengeti National Park, Tanzania and provides analysis on the avoidance behavior among the predators. It has the conclusion that despite cheetahs avoid lions, they are not displaced from their habitats and they don't lose access to their prey. In contrast, African wild dogs are displaced from their habitats by lions.

Competition describes where two species have negative effects on each others fitness. But what is sounds like is described here is amensalism, where one species has a negative effect and one has no effect on the other. If cheetahs don't have a negative fitness effect on lions, then the ecological and evolutionary consequences are different for this case amensalism compared with competition.

Although the bulk of the explanation is done in the other answer, my answer will focus on the observations in Serengeti national park and the studies made.
Lions in fact kills cheetah cubs. In the 1990s, a researcher documented lions attacking and killing up to 57% of cheetah cubs (kleptoparasitism) in Serengeti National Park but they rarely ate the cubs completely; the cheetah mothers often consumed the remains of their offspring after the lions had left. However, the increasing lion population has not triggered a drop in cheetah numbers. They have remained stable, despite losing many of their cubs. They are apparently able to compensate for the loss of their cubs because females become fertile within 2 weeks of losing their offspring.
Cheetahs also adopted different strategies to deal with threats from lions. Cheetah females were found to set up their dens precisely where there are the most lions. Researchers says it is counterintuitive but their study offers a plausible mechanism for this and they called it "fine scale behavioral avoidance of the lions, a sort of carnivorous ballet". Male cheetahs and single females eat their prey as quickly as possible. Mothers with cubs, on the other hand, watch out for possible threats while their young are eating in order to give them enough time to eat their fill. Cheetahs do not have the strength to haul their kills up trees to keep them safe from scavengers as a leopard does, nor can they physically defend themselves against a lion. They therefore tend to hunt when larger predators are away or less active and eat their prey as quickly as possible before it can be snatched away from them.
References

https://www.science.org/content/article/carnivorous-ballet-helps-cheetahs-coexist-lions
https://www.springer.com/gp/about-springer/media/research-news/all-english-research-news/how-cheetahs-outsmart-lions-and-hyenas/15602738


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Why does the Puma Concolor live mostly near the mountain range in Argentina and not in other places of it, when in other countries lives everywhere?
I was watching the Puma Concolor habitat in Argentina, and it lives mostly in the mountain range with a small part in the North and in the middle,
Puma Area
when in other countries with different geographies it covers all the territory, for example it lives in the whole Brazil, Bolivia, Paraguay, Colombia, Mexico, the whole central America, etc.
Why does the Puma Concolor live mostly near the mountain range in Argentina and not in other places of it, when in other countries lives everywhere?

Note that the distribution map you provided is 2d and doesn't showcase differences in altitude etc. so it misleads you to think that the puma concolor (cougar) doesn't live in mountainous regions in other countries as well.
In Argentina, cougars mostly stick to the Andes and Sierras because these spots have the dense vegetation and rugged terrain they like, plus plenty of prey like deer and guanacos. The central and eastern parts of the country are pretty urbanised and used for farming, which means less habitat, fewer prey, and more run-ins with humans, so cougars get pushed out. The mountains also have national parks and reserves that protect them from hunting. In places like Brazil and Bolivia, there are huge, continuous forests with less human activity, so cougars can live almost everywhere. Plus, there's less competition from other big predators like jaguars in those areas.


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Do ethnic groups differ in non-coding DNA?
There are services (23andme, AncestryDNA) that will associate an ethnic group to you from your spit. Could non-coding DNA in theory be useful for this goal i.e. are there statistically meaningful differences in non-coding DNA between different ethnic groups?

We only deal with one question per post. The first would be about the standards applied in a test by a commercial service - this would likely be off-topic here as it could be seen as promotion of that service. The second might be on-topic , but you would need to show what researches you'd done on the topic and where you'd gotten stuck. (Personally I'm interested in the answer should it be different from expected heritable differences by a significant amount). You should take our [tour] and refer to the [help] for guidance to our ways - then [edit] the question to show your workings.

This answer links to the site of 23andme https://biology.stackexchange.com/a/7295/68099

Well then, perhaps it would be on-topic - but beware, that's from 2013 and the site-rules have significantly tightened since then - I'll let those with greater familiarity with this site on the stack tell you the current policy. (A cursory search of our meta didn't enlighten me on the subject). You would still need to show your researches into the remaining topic.

Personally I see nothing wrong with discussing particular direct to consumer genetic testing companies.

Not only 'in theory', but it is used for ancestry testing.
Coding DNA (exonic regions) tend to be more highly conserved between individuals, as changes to the sequence are more likely to have a deleterious effect on an important phenotype (think a mutation which makes someone only have a single arm). Non-coding DNA is less constrained by selection and varies more between individuals / ethnic groups. This makes it more useful for identifying variants specific to different ethnicities, which makes the basis of ancestry testing. Typically in ancestry testing SNPs which show evidence of being under some kind of functional selection (i.e. are out of Hardy-Weinberg equilibrium) are excluded from the analysis. Neutrally evolving SNPs (which are more likely to be found in non-coding regions) are more likely to reflect the true population phylogeny.
I'll try and update this post with some references.

But when people try to determine someone's ethnicity by looking at them they are relying on information (eyes, cheekbones, skin color, fat level, lip size, height etc.) primarily shaped by coding DNA right?

@fielanb The differences that you note between people of different ancestry groups are largely red herrings. They give a superficial impression of difference (which in some cases does not have a clear genetic basis), relative to overwhelming similarity in functional regions of DNA (https://nyti.ms/3CxBxcj, https://www.nature.com/articles/ng1456). Noncoding regions on the other hand tend to yield a reasonable historical record of population differentiation, because they are not functionally constrained, and mutations in regions without functions are therefore more likely to be passed on.

user438383's answer is correct. Non-coding DNA is much more useful for ancestral research, especially of ancient ancestry, because it preserves mistakes or changes that would damage a person if they occurred in coding DNA. For this reason people have SNP's in their DNA that date back thousands of years. By comparing and contrasting SNPs it can be determined absolutely how different people are related to each other. We are all related to each other, the only question is how far back you have to go to find the relation.
Concerning physical characteristics like eye and hair color, those are indeed determined by coding DNA, but are what are called "expressed traits" which means that how they get expressed is complex and depends on random factors. For example, I have seen a clone of a cat where the original was completely black, but the clone had a white patch on its chest. However, a littermate of the original did have the same patch. So, you see the gene codes for black, but when the organism grows in the environment, random differences can occur. Part of this is due to a process called "methylation". When a zygote is developed, the egg's genetic material is methylated and this inactivates or activates genes randomly (see "Methylation dynamics during the maternal-to-zygotic genome transition in dioecious species" Willian T. A. F. Silva for more information), thereby causing differences in physical makeup of the organism. Note that a person has many different copies of the same gene which can differ from each other, so which particular gene gets activated will affect the final form of the organism.
Physical characteristics can be a clue to a genetic heritage, but it is important to realize that for every gene that gets expressed many more are latent and go unused, perhaps to surface in a later generation.

The classic reference for reaction norms (gene x environment interaction) would be Lewontin 1974 (here is a republished version that is easy to access: https://pubmed.ncbi.nlm.nih.gov/16645033/).


text:
How have some cancers "evolved" to be so aggressive and treatment-resistant?
[In this post, I may ascribe agency to processes, inanimate objects or microorganisms: this is rhetorical, I know they don't "intend" anything. I will also use "evolution" in a fairly loose sense of "learning" (again, rhetorical agency) to overcome obstacles to survival].
Assumptions:
Cancers are caused by mutations of cells, and "successful" cancers are caused by mutations that result in a, sometimes literally, killer combination of

Suppression of their own apoptosis
Invisibility to the immune system or resistance to immune attack
Ability to co-opt biological resources such as bloody supply so they don't starve

The various "types" of cancer that we know and give names to are the end-points of available "mutation pathways" that cells can take to get to such a "successful cancer" state. Because lots of mutations result in cancers that don't "work" for some reason (e.g. immediately shut down by an immune response), they just don't result in a noticeable tumor. Therefore, we end up with a discrete set of "familiar" cancers, each representing a different path, and their frequency related to how likely it is that path is hit (i.e. how many mutations needed, etc).
Some cancers, the malignant ones, happen also to spread very effectively, though this is not specifically required by the above success criteria, so we also see benign tumors which don't spread but still can be said to "succeed" in that the cells survive.
Once mutated, cancers are presumably fairly genetically static within a single case, otherwise we'd see a storm of cancer variants developing within patients over a relatively short period as an evolutionary arms-race took place, much like the race between antibiotics and bacteria.
However:

Some cancers have quite "advanced" mechanisms for spreading1
Some cancers are extremely resistant to human treatment

The question:
How did these "dangerous" cancers becomes so dangerous?  A dangerous cancer seems to be "fully capable" of effective spread in the first instance, rather than undergoing a complex evolutionary battle with the host's own anti-cancer abilities or some exogenous treatment.
Furthermore, even cancers that "succeed" can't effectively propagate themselves like bacteria, because they're always in the same body2. If anything, cancers that do not kill the host should be selected for, since people with genes "near" dangerous mutation opportunities would be less likely to reproduce effectively3. So (naively, since it's clearly not the case), if people do evolve such that they can get cancer4, cancers would tend towards being both benign and generally non-life threatening.
Even if they do somehow "evolve" to spread and threaten the host (as they indeed evidently have), why are they then also often so good at evading non-host treatment?
It seems like two warring armies (host vs. cancer) that have evolved together using hand weapons, evenly matched for centuries. The cancer invents the crossbow (mutates) and starts to win the war. Then, aliens (doctors) suddenly turn up with UAV surveillance and cruise missiles (imaging and treatment) and side with the host, but the cancer still wins much of the time, even though they're facing an Outside Context Problem that by rights they have no innate ability to counter.
So what results in these cancers being so adept at spreading themselves without some adversarial evolutionary process (à la bacteria vs. antibiotics)? Furthermore, how are they so often also resistant to human-directed treatment? Is it just because the human treatment is crude (i.e. not so much aliens but a large but unruly peasant milita that often doesn't really help that much)? Is there more "evolution" going on within a single cancer patient than I imagine?
Expansion in response to comments: if my assumption that the cancer cells are not usually "evolving" once formed is indeed incorrect: is that evolution then usually the cause of treatment escape? And does that mean that treatment-escaping cancers are freely evolving, in that they could take a number of case-dependent paths to escape (as opposed to the original recognizable cancer "type" which took one of a limited number of available mutation pathways through the fairly static environment of human biochemistry to become that cancer in the first place)?

For example, the use of matrix metalloproteases to escape into the bloodstream, the use of cytoskeletal locomotion and various other highly specialized mechanisms that I would normally associate with a long and involved adversarial evolutionary arms race on a far longer timescale than one patient's cancer progression
Certain transmissible cancers like in Tasmanian devils notwithstanding
The obvious mechanism for this is they die or become critically disabled before having children, but it could also be disadvantageous for elders to die too early, especially for humans, when they assist in rearing their own descendants
Perhaps as a by-product of some otherwise-advantageous genetics, like sickle-cell anaemia and malaria resistance, where the occasional lethal downside of in a certain percentage of people is outweighed by the statistical benefits.

"Once mutated, cancers are presumably fairly genetically static within a single case" this is not always the case, and varies from tumor to tumor. The reason cancer is cancer in the first place is because of genetic instability (mutations) that either overcomes normal regulatory processes like DNA repair and cell-cycle checkpoint pathways to grow uncontrollably, or constitutively activates tumor promoters like growth factor receptors, thereby forming a tumor (in solid tissue cancers - blood cancers often don't form tumors). Once those negative regulatory pathways like DNA damage repair [...]

[...] are compromised, mutations continue to accumulate, which leads to further genetic instability and more mutations. This can lead to both metastasis and escape from previously (mostly) successful treatments, but it can also lead to complete dysfunction inside individual cells and cell death.

Here's an interesting and potentially relevant paper that I saw presented at a journal club recently: Cycling cancer persister cells arise from lineages with distinct programs. Tumor heterogeneity at the metabolic level accounts for some cancer cells' ability to withstand treatment and proliferate. Great question, btw

Cancer being 'dangerous'
I define 'dangerous' as reduces survival of patient significantly. In my experience, cancers become dangerous, if one can't remove the tumor. This happens if it starts spreading (metastasize) or start infiltrating surrounding tissue. In order to do so, cancer has to 'digest' extracellular matrix (e.g. the stuff that holds cells together as connected tissue).
Each cancer has its own mechanisms, allow me to illustrate this in one example, multiple myeloma:
Multiple myeloma degrades surrounding tissue (bone), because doing so directly yields a massive survival benefit. Bone is a huge storage for TGFβ, a growth factor, so myeloma cells get a huge growth boost from mining away bone tissue. To do so, myeloma cells upregulate metalloproteases (MMPs, enzymes that shred proteins). They can do that, since myeloma cells have a mutated form of the NF-κB, a transcription factor that can upregulate a shit-ton of genes (including MMPs, and also growth and survival genes).
So you see, all these mechanisms are focused on maximizing the expression of survival and growth genes. Becoming untreatable in the process (and hence 'dangerous') is simply a "side-effect".
Other cancer types infiltrate surrounding tissue, since their fast increase in size has made them starve for oxygen (hypoxia & angiogenesis). They secrete signals for blood vessels to grow into the tumor and provide oxygen. This can also make a tumor "untreatable" since they cannot be removed, without risking irrepairable blood loss. But you see, this is also just a "side effect" of the tumor maximizing survival.
My point is, the "danger" of a tumor is not a direct consequence of the evolutionary armsrace towards huge growth and survival. It just happens as a side effect, since cells are stupid and can ignore the needs of surrounding tissues.
About Tumor spreading
I got two disagreements.
These spreading mechanisms do not have to be "advanced". Sometimes one requires just one dysregulated transcription factor (NF-κB) to induce MMP expression (ref1, ref2). And given their rapid mutation rate, cancer cells populations are very heterogenous and hence provide for a huge functional plasticity, so even 'advanced' mechanisms are possible.
Degrading surrounding tissue does provide a success criterium, like I said, myeloma benefit from mining growth factors (TGFβ) from bone, or from degrading surrounding tissue to provide room for blood supply.

Cancers that do not kill the host should be selected for

Sadly, this is incorrect. Most humans get cancer after the reproductive age. In other words: Cancer happens when you're old and already had children, so it did not prevent you from having children. That's why cancer is not that much of a selective pressure today. It would be, if e.g. a large proportion of teenagers/young adults would get cancer, but that's simply not the case.
About Cancer Resistancy
Cancer resistance to treatment often times is a side-effect of them upregulating survival factors and downregulating apoptosis factors. In other words, the drug is damaging the cancer-cell, but the cancer cell simply doesn't know how to die.
Of course, the treatment kills a lot of cancer cells, but resistant ones remain (e.g. using ABC-transporters to pump the drug right out of the cell). And I gotta say: Most classic chemotherapeutics out there are simply very very ineffective.
I hope that I could answer your question somehow. I am sorry for not providing references for each point. If you want some sources on specific points, I can look through my papers and see if I can provide something.


text:
What are the types of human intersexuality?
Every genetically-male human has a female-like sex organ until about the seventh week of pregnancy1, then, in general, due to male chromosomes' effect → androgens would be produced and cause that organ to change into male sexual organs1.
Such a course may be "biased" (for lack of a better term) towards intersexuality, in each of these contexts:

True hermaphoriditism
Androgen insensitivity, partial or complete
Non androgen insensitivity "feminization" in at least one aspect (for example gender dysphoria in the apparently genetically-male)

What are the types of human intersexuality (are these the only types)?

I suggest adding here clear definitions of what you mean by "sex", "gender", "gender identity", etc. - otehrwise yoru last sentence may be misinterpreted. While the identity and phenotipical features may vary, the genotype is usually unambiguous (unless we account for trisomy).

it is not clear what your question is. SE communities focus on asking and answering questions - you cannot simply have a discussion on the subject here (not that I would be personally against learning more on the subject).

@RogerVadim would you say that the question is clearer now?

Isn't this a bit too general? What do you expect as an answer? - more precisely, can an answer fit into one page?

@RogerVadim I expect a similar list of a few (I would guess 5, probably not more than 10); I am certain that an answer can fit into one page.

in other words, you expect a review from an expert rather than an answer to a specific question. I suggest that you do a bit of research (i.e., googling) on your own and pose a more specific question. It will simply increase yoru chances of getting an answer.

@RogerVadim what you wrote is untrue, I have done a lot of prior research in a that topic and actually asked about what I have found so far which I think is more than enough for asking a question here; I am not looking for a higher chance than there is now.

Besides, there is nothing wrong in asking in expert's review if the question is useful for general audience and the longevity of the post is plausible.

you have nothing to prove to me... let's hope that somebody takes time to write a kind fo review that you ask for.

Hopefully someone here would clear the comment section.

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [Ask] effectively on this site and [edit] or delete your question accordingly. In particular, your question is a duplicate and lacks sufficient evidence of prior research — this site has many related posts and wikipedia resources include articles on the Quigley scale and intersex, which includes a relevant list.

Does this answer your question? Is sex a spectrum?


text:
Why does distention of the veins not decrease their resistance in the first case but decrease it in the second?
Here are two quotes from Guyton and Hall Textbook of Medical Physiology, Chapter 20 (emphasis mine):

Why is venous resistance so important in determining the resistance to venous return? The answer is that when the resistance in the veins increases, blood begins to be dammed up, mainly in the veins themselves. However, the venous pressure rises very little because the veins are highly distensible. Therefore, this rise in venous pressure is not very effective in overcoming the resistance, and blood flow into the right atrium decreases drastically.

A sudden increase in blood volume of about 20% increases the cardiac output to about 2.5 to 3 times normal. An analysis of this effect is shown in Figure 20-15. Immediately on infusing the large quantity of extra blood, the increased filling of the system causes the Psf to increase to 16 mm Hg, which shifts the venous return curve to the right. At the same time, the increased blood volume distends the blood vessels, reducing their resistance and thereby reducing the resistance to venous return, which rotates the curve upward. As a result of these two effects, the venous return curve of Figure 20-15 is shifted to the right. This new curve equates with the cardiac output curve at point B, showing that the cardiac output and venous return increase 2.5 to 3 times and that the right atrial pressure rises to about +8 mm Hg.

The quotes are from different sections of the chapter, so I believe they are unrelated. It seems that the distensibility of the veins doesn't cause their resistance to decrease in the first case, but does in the second case. Why?

Resistance clearly changes in the first case, as the paragraph is describing what happens specifically when resistance increases, which in turn leads to changes in venous volume. The second case is completely different, it is describing what happens when volume increases. Please think about it a bit and clarify your question.

@BryanKrause I've changed the title to make it better correspond to the question in the body of the post.

It still doesn't make sense, though. In the first case the scenario is that the resistance is increased. You seem to be asking "Why doesn't resistance decrease when resistance increases?"

@BryanKrause I'm asking why it doesn't decrease despite the high distensibility of the veins. Look at the second quote: the increased blood volume distends the blood vessels, reducing their resistance. I assume the blood also distends the veins in the first case, but why doesn't that cause the resistance to decrease, as in the second case?

Because the scenario there is that the resistance is increased... that's your given. Think if you were solving an electricity problem using I = V/R - if I said "R is increased" you'd know that either I must decrease or V must increase for the equation to hold. If you were then told that also "I is unchanged" you would then know that V must have increased; you would not ask "why isn't R decreased" when that happens.