text:
Are $DCX^{-}PSA-NCAM^{+}$ neurons the result of adult neurogenesis in human being?
A recent study by Sorrells et al. (2018) has stirred a debate whether human being really do have adult neurogenesis in hippocampus or not.
In a following paper- Adult hippocampal neurogenesis: a coming-of-age story, HG Kuhn, T Toda, FH Gage have criticized the original study by stating that

while Sorrells et al. did count $DCX^{+}PSA-NCAM^{+}$ cells as
  adult-born neurons; they did not count $DCX^{-}PSA-NCAM^{+}$ as the
  same, claiming that the latter exhibited more mature morphological
  features based on their criteria. However, the developmental time
  course of adult-born neurons in the human dentate gyrus has not been
  clearly characterized, and neurons in higher mammals take at least six
  months to fully mature (Kohler et al., 2011).

My Question is- are the $DCX^{-}PSA-NCAM^{+}$ neurons really the result of adult neurogenesis, as claimed in the second paper? Or are Sorrells et al. correct in calling only those neurons adult born that respond to both the markers (DCX,PSA-NCAM).

What answer are you looking for beyond what's in those papers? I.e., why do you think they've overlooked something that is decided in the field rather than there being disagreement? One of them is advocating a more stringent criterion, that's it.

@bryankrause the authors of the two papers are making contradictory claims, and supporting their claims with reason. One of them claims that the markers can give false positive results by identifying glia cells as new born neurons. The others claim otherwise. I need opinion of others on this disagreement, some arguments, facts and perhaps link to some sources, so that this can help me understand the situation more clearly.

Right, which is the purpose of the commentary by Kuhn et al: they note that Sorrells is being more conservative than previous work in their definitions and that "the developmental time course of adult-born neurons in the human dentate gyrus has not been clearly characterized" - in other words, if Sorrells et al criteria is right, their conclusion is right, if their criteria is wrong, their conclusion is wrong. It's hard to do these studies because there aren't many human brains available to chop up.

Kuhn isn't claiming "otherwise" they are claiming "unclear"; similarly Sorrells isn't claiming "does give false positive" they are claiming "could" - uncertainty is normal on the edges of knowledge, if it wasn't then those wouldn't be the edges.


text:
Can macrophages phagocytose viruses directly?
I've been reading that Macrophages, members of the innate immune system, can actively track bacteria and protozoa to devour and destroy them. In the same way, can macrophages devour free viruses, in blood for example, 'actively'? I can understand that random phagosomal uptake might contain virus particles, but by 'active' uptake, I mean the process by which it tracks bacteria to engulf them.
I guess not, but I need an answer. Would be grateful if a source, like a textbook, is provided as well!
Thanks in advance.

Welcome to the site. Please take a [tour] and visit the [help] for more information on this site and what we do here. In particular note that there is a homework policy that requires an attempt from the OP to answer the question for themselves. On that note - what do you know about the immune system and how it works to label foreign bodies?

If the viruses have been opsonized, macrophages will phagocytose them. I suspect that direct phagocytosis of non-opsonized viruses would depend on the type of virus and the surface molecules it expresses.

@MattDMo thanks for the response! Any example of viruses macrophages phagocytosing non-opsonized viruses?

source: Stack Exchange

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

sort: votes


text:
Exhaustion of 'memory' CD8 T cells
I've been reading literature on the exhaustion of cytotoxic CD8 T cells. In many of the papers I read, the authors aim to delineate molecular mechanisms that differ between exhausted and memory phenotypes; one such review on this field is the following from Prof. John Wherry's group.
But unfortunately, I could not find any paper that discusses the possibility of recalled memory cells being prone to exhaustion. If I'm not wrong, exhaustion markers like PD-L1, Tim-3, etc. are present on memory cells at lower levels than exhausted cells. But in response to antigenic stimulation (recall response), do such 'recalled' memory cells also start accumulating exhaustion markers like short-lived effector cells? Can someone help me out, please?

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


text:
Are DRB3 DRB4 and DRB5 different genes or different version of the same gene
From what I understand, an individual can hold up to two HLA-DRB345 alleles (but can be less) that can each be HLA-DRB3, HLA-DRB4 or HLA-DRB5.
However, since HLA-DQB1 and HLA-DQB2 are entirely different genes and we have two alleles for each of those two genes necessarily, I'm struggling to understand if HLA-DRB3/4/5 are three different genes or three different "version" of the same gene.
Similarly:

Are HLA-DRB3/4/5 located at the same place on the chromosome?
What about the people that have neither HLA-DRB3 nor HLA-DRB4 nor HLA-DRB5? Is there no genetic code at the place where other people have it?
Why is there only DRB3 on the "maps" of chromosomes like this one (http://www.biorigami.com/wp-content/uploads/2014/11/MHC1.png) and never the three of them (I wanted to know what "orders" they were in).

Finally, wikipedia states:
DRB1 is expressed at a level five times higher than its paralogues DRB3, DRB4 and DRB5 but doesn't provide a source. Would someone know about a scientific article or an entry proving this?

The reference to DRB3, DRB4, and DRB5 as paralogues of DRB1 indicates that these are different genes. However, as paralogues they share essentially the same structure, having presumably originated from a gene duplication at some point in the past.
From Wikipedia:

DRB1 is present in all individuals. Allelic variants of DRB1 are linked with either none or one of the genes DRB3, DRB4 and DRB5.

Particular alleles ("versions") of DRB1 are linked with one of the other DRB genes, or none of them. Linked genes are often located near each other on a chromosome, such that recombination rarely breaks the linkage between them. DRB1 and the other DRB genes are found on human chromosome 6 within several kilobases of each other. (Unfortunately, that link will only be valid for 90 days; a screenshot is below.)

So, for this region of chromosome 6, some alleles carry a particular version of DRB1 and a copy of one of the other paralogues, and other alleles for this region carry a different version of DRB1 without another paralogue. Since we all carry two copies of chromosome 6 we all carry two copies of DRB1, plus 0, 1, or 2 copies selected from the other paralogues.
Are HLA-DRB3/4/5 located at the same place on the chromosome?
They are located nearby DRB1, and each of them are "upstream" by about the same distance.
What about the people that have neither HLA-DRB3 nor HLA-DRB4 nor HLA-DRB5? Is there no genetic code at the place where other people have it?
Correct, they carry a deletion relative to chomosomes with one of the paralogues.
Why is there only DRB3 on the "maps" of chromosomes and never the three of them?
DRB3, DRB4, and DRB5 do not occur together on a chromosome. They are essentially different alleles, except they're alleles of a chromosomal region and not of just a gene.

Thank you so much, I have two follow up questions though: 1/ about your link, why can we only see DRB3? Is it because the person which was sequenced only has DRB3? When I  search for DRB4 I see the same (DRB4 and DRB1 but neither DRB3 nor DRB5) https://i.imgur.com/XoIRVjf.png? 2/ when you say "Correct, they carry a deletion relative to chomosomes with one of the paralogues.", does that mean that some people have literally thousands of nucleotides less than others? I thought the deletions were always very small like 1 or 2 nucleotides, but I guess I was mistaken.

Also, the "3800K", etc .. of HLA-DRB1 don't map between my screenshot and yours, is this because alleles are not always at the same "place" depending on the individual sequenced?

You can only see DRB3 because the chromosome shown (NT_167248.2) only carries DRB1 and DRB3, the one you show (NM_021983.5) only carries DRB1 and DRB4. As far as I can tell DRB3/4/5 don't occur together on the same chromosome, they just happen to be in the roughly the same place relative to DRB1. My hypothesis is that something like DRB1 existed prior to the other DRBs, but at one point got duplicated so there were two DRB1s adjacent to each other. This pair persisted in the population and the new DRB eventually differentiated somewhat from DRB1 becoming, say, DRB3.

[hypothesis continued] At a later time or in another part of the population a similar duplication occurred, but now the new DRB differentiated in a different way to become maybe DRB4. Since the new DRB3 and DRB4 appeared independently, they're not together on a chromosome. For that to happen there would first need to be someone carrying both DRB3 and DRB4, and then recombination would have to occur in just the right way for their offspring to get a chromosome with DRB1, DRB3, and DRB4.

Yes, different people can differ in their genetics by thousands of nucleotides. Either insertion/deletions (indels) or changes in the order or placement of genes. Once the differences are large enough they usually aren't referred to as just indels anymore, but a broader category of "structural variants". Capturing the diversity of structural variants is a major goal/challenge for the human genome project.

I understand! Lastly, just to be sure, the chromosomes identifiers (NM_021983.5, NT_167248.2) are basically sequences from actual humans for which we sequenced the whole chromosome?

Yes, or at least a large chunk of a chromosome.


text:
convert bright field images to phase contrast or dic microscopy images (one of those three to any of those three)
Are there neural networks or other methods (machine learning-related I would assume) to convert bright field images to phase contrast or dic microscopy (one of those three to any of those three, ideally any of those transformations would be supported).
This would most likely involve doing different type of microscopy on exactly the same cells and then training a machine learning model so I don’t know if it has ever been done or if it even exists.

I highly doubt it; those are imaging techniques that result from the way light interacts with an object.
Faking it wouldn't be useful in the context of science as conversion won't tell you anything about the object (i.e, you can't get more information from an object than is already present in the image - this is a basic tenet of information science) and ethics would suggest that you need to declare the manipulation in any publication, so the value is low for any purpose other than entertainment.


text:
Monoclonal Antibodies
In this paper, the authors say:

We demonstrate that for a considerable number of eplets, the
antibody-verified status is solely based on polyclonal serum
reactivity of multiparous women or on reactivity of murine mAbs.
Furthermore, we noted that a substantial proportion of patient sera
analyses and human mAb data presented in the HLA Epitope Registry
Database has never been published in a peer-reviewed journal.
Therefore, we tested several unpublished human HLA-specific mAbs by
luminex single antigen beads assay to analyze their HLA reactivity for
eplet antibody verification. Although the majority of analyzed mAbs
indeed verified their assigned eplets, this was not the case for a
number of eplets.

I don't understand how did they have access to the monoclonal antibodies that were published but not in peer-reviewed journal. Surely those authors of non peer-reviewed journals did not ship the antibodies to the authors of this article, right?
Is there something I'm not understanding?

This is not a question about biology but speculation about the provenance of material described in a paper — a question that nobody can answer other than by further speculation.

@David I think this is a reasonable question covering techniques in a biological laboratory. It's very helpful that OP provides enough source material to help answer the question, including a reference to a specific paper. You don't have to answer it.

@BryanKrause I will. It is completely trivial and the only methodology involved would be seem to be navigating a database and sending an email . The poster seems to labour under the misaprehension that it is only possible to obtain antibodies when they are described in a publication. The database is too specialized for me to check, but I imagine that anyone can submit, publication or no, and there are details for each eplet (whatever that may be) deposited by the depositors, including names and institutional addresses, regardless of publication. Protein and Gene databanks work that way.

I believe the eplets are the target of the antibodies (the variable region of the epitope) so whilst we have their sequence I'm afraid we do not have the sequence of the antibodies themselves. But there could be a way that the authors skimmed through the articles of the non-peer reviewed articles in which there might have been description of how to get the antibodies (maybe they could be ordered commercially?).

Update
It was pointed out by OP in a comment that the sequences/structures provided in the db are not antibody but antigen sequences, which I overlooked. Therefore, no clear sequences of the antibodies are provided directly in the db.
Original answer
Your confusion is warranted, given that the authors of the paper simply do not describe how they obtained the antibodies (as far as I can tell, though I only skimmed a few sections).
However, I'll note that many researchers would respond to reasonable request for reagents- specifically if it were publicly reported in a database somewhere, which is not too different from publication (peer review not being necessarily any particular mark of distinction; and presumably there is some minimal vetting before database inclusion).
Furthermore, it does appear that for at least many of the antibodies in that database, either full sequence information is available, or the antibodies can be directly ordered commercially.
In such cases, obtaining antibodies would not be an obstacle (though possibly expensive).

For the "sequence information is available", I'm afraid that's the sequence of the protein targeted. I don't think that's the sequence of the antibody.

@FluidMechanicsPotentialFlows ah I see, sorry I misunderstood the db and assumed that the provided structures were antibodies. I would probably remove your "answered" thing if possible, if not I'll delete the answer.


text:
How do fish transport egg to, and out of, coelom?
How do gametes get into coelom, and, later out of it? Excretion can be under quite heavy pressure, see https://www.youtube.com/watch?v=1OsRbuEINXI

As question has not received answer, will answer to best of my ability. Eggs are plopped off from ovary, into coelom. Duct out of coelom is the oviduct that opens into it. The fish must apply pressure to the whole of the coelom, I guess, to push it out. That part is a bit of a mystery to me, an expert answer would be better.


text:
Why viruses "die" outside the host?
Why viruses "die" outside the host after sufficient time? I want to know the biological process behind it. What role being exposed to air plays in virus destruction? What role sunlight plays in the same?
Now there might be many biological processes behind this phenomenon, please mention the same and explain about any specific virus.

Answers on that post doesn't explain the biological process involved.

But the question covers your point. Sorry, the message is autogenerated to be polite, but in doing so misses the point that SE Biology doesn't do duplicate questions as the idea (at least in principle) is to amass a definitive collection of questions.

@fghjkl: Virus "death" isn't really a biological process, it's a chemical one.  Think of viruses as complex chemicals, and those chemicals degrading in the presence of UV light & oxygen, or just drying up because they aren't in a liquid environment.

Viruses are metabolically inactive outside the host cell. They bind to the specific receptor to be activated. They cannot replicate without a host.
For example, in case of HIV, the protein envelope of the virus binds to CD4 receptor fo T helper cells and thus supressing the immune system gradually.These viruses are only active when it binds to CD4 receptor and not any other receptor.


text:
Why does insertion of transmembrane domains occur in the rough ER?
To elaborate on that question, why in the secretory pathway does the insertion of transmembrane domains into the membrane occur in the rough ER as the protein is translated and threaded across the ER membrane? This is the answer to a problem from a science textbook. I thought that integral proteins are first produced in the rough ER, modified in the Golgi apparatus, and then shipped in vesicles that fuse with the cell membrane. If that's the case, wouldn't insertion of the entire protein into the membrane happen when the vesicle fuses with the cell membrane?

Why do you think transmembrane domains are integrated into a membrane as translation proceeds?  Can you quote something saying that?

Sure, the exact question and answer. "At which point in the secretory pathway would the insertion of transmembrane domains into the membrane occur? Answer: It occurs in the rough ER as the protein is translated and threaded across the ER membrane."


text:
How are different sensations of tiredness/exhaustion biologically different?
Last weekend I did some very vigorous work in the garden - fun, but I overdid it. I noticed I had several different types of tiredness/exhaustion, or at least different subjective sensations, and I'm interested how they are different physiologically.
(1) Saturday I left lunch too late and felt tired before eating, though just fine afterwards. Is this "only" blood sugar?
(2) On Sunday evening I felt pretty much literally too tired to think. I had a good night's sleep of my normal length and woke feeling good and alert as normal (of course tired).
(3) Monday and Tuesday I've continued feeling tired - not toxically tired, just the usual tiredness you'd expect after doing too much gardening, but without the foggy add-on that (2) seemed to have.
What is the body doing diferently in recovering from each of these three things? And can (2) and (3) indeed be different?

You're asking about something very subjective (fatigue), a condition that would require a fair number of questions to evaluate. This puts the question in the "medical advice" category. I'm voting to close for that reason.

I'm having trouble thinking of a way that someone would answer this question that does not become either a medical advice answer (as anongoodnurse is concerned with) or an overbroad introduction to fatigue. That sort of broad overview is not a good fit for the Stack Exchange format, this is one of the reasons we have a requirement for "prior research" to narrow down a question asked. I might suggest you start with https://en.wikipedia.org/wiki/Fatigue - Wikipedia is often a good starting point for general information on a topic - and see if you have a specific, answerable question afterwards.

In particular, see the section "Classification".

@BryanKrause - Although I agree with you that Wikipedia is as good a starting place as almost any for a layperson, that section is sub-par (?), and unsupported by the cited reference. Maybe this is a better short answer that explains how complex fatigue is?

If this is not the right place to ask, OK. I'm asking about everyday experiences out of pure curiosity. There is clearly some difference between feeling tired but revived after eating; routinely tired after eg going to the gym; and gosh-I-overdid-it-in-the-garden (or HIIT, or marathon) that takes longer to bounce back from. These are the everyday experiences I'm asking about. The sharp difference between too tired to think but fine after a normal sleep, is doubtless uncommon but caught my attention. I guess mentioning it caused confusion, and it is maybe purely idiosyncratic.

@AndrewWhite - This isn't the wrong place to ask. It's just not answerable. Loads of people think of complex things in simple terms ("Clearly..." x is the same in the terms x and 4x.) Did you revive because you had a meal,  b/c you rested while eating, b/c you were looking forward to getting back, or all/none? There's no confusion. One school of thought is that fatigue unrelated to illness is just one thing but different in severity; then there's the complexity in the abstract, and lots of things in between. And fyi, dizziness and fatigue are extremely common complaints in medicine.


text:
Spider identification: Nesticodes rufipes or Loxosceles gaucho? (South of Brazil)
I need help identifying a spider species frequently encountered in my apartment in Porto Alegre, southern Brazil.

Habitat: Found indoors on ceiling/wall corners, door frames, and behind paintings.
Web pattern: No discernible regular web pattern observed.
Size: Body length approximately 5mm, excluding legs.
Geographic location: Porto Alegre, Rio Grande do Sul, Brazil.
Behaviour and other notes: I've found them on any season, any time of day, and not hidden at all (ceiling/wall corners). They are usually standing still, and when prodded with a stick either curl up into a ball or very quickly draw a string of web and descend. I've seen much smaller ones (spiderlings?) whose body length is 1mm or less.

I think might be either of these:

Nesticodes rufipes
Loxosceles gaucho

I took some photos to the best of my ability/equipment, all of them are the same specimen but under different lighting and angles:

I've contacted Instituto Butantan (main producer of antivenoms and antitoxins in Brazil), inquired about this specimen and forwarded these photos.
They have confirmed it is Nesticodes rufipes.


text:
How it is determined that a particular gene or set of genes is responsible for a trait?
How it is determined that a particular gene or set of genes is responsible for a trait? Is it just a statistical analysis of people showing and not showing the trait and the genes they have (or don't have) and their variants (alleles)? Or, there is something more.

The classic procedure was to establish an association, typically by observation, statistics, or reasoning. Then, you start doing the molecular genetics. First, knock out the gene(s) and observe the phenotypic effect. Second, express the gene(s) in a mutant knockout organism and see if the phenotype come back. Attaching the gene to an inducible promoter makes this pretty simple to do. However, this basic procedure has had to get much more complicated and nuanced over the years, as we've expanded the repertoire of genes that we want to study.

This "knock out the gene(s) and observe the phenotypic effect" is for animals right?

@AmitMaurya You can knock-out gene to any living creature; procaryote or eukaryote (incl. plants, fungi, animals, and others) and even viruses. The only theoretical restriction has to do with ethics. It is typically not allowed to make such experience on humans.

Yes, I was refering to ethical considerations.

Then how mechanism is established in humans?

In the below list of technics, I am assuming we are talking about haploid individuals (to avoid discussion about dominance relationship) and assuming no epistasis but the technics can 'easily' be extended to include these cases. I also assume we are talking about coding regions.
Note that I am more of a biostatistician / population geneticist than a molecular geneticist, so I am pretty sure I will unwillingly bias my list toward what I know most. There is a lot to say about every single technic but of course, this cannot be covered in a single StackExchange post.
Technics

Statistical association (observational study) with existing variance in natural population. Do carrier of a given allele have another trait value than the carrier of the other allele. Possible confounding variables include population structure and linkage disequilibrium.

Population structure: To deal with this confounding variable, we can make a genetic PCA and include the first two axes as covariate in a type I sum of squares regression. We can also use tools such as STRUCTURE to infer the population structure and then use the inferred groups as a nominal covariate.
Linkage disequilibrium: We typically consider a number of marker that we try to associate to a specific phenotypic trait. It is impossible to tell whether the observed association is directly caused by the marker we observe or by a tightly linked marker. For further investigations below technics must be considered.

Statistical association (experimental study). It is possible to create the treatment groups by knocking out (or other technics such as the now popular CRISPR technic) specific gene in out in some individuals and look for a statistical association. The advantage of such manipulation is that we can create the optimal level of genetic variance we need to increase our statistical power.
Transcriptome analysis. Making sure the coding region is being expressed in the tissue of interest. E.g. if you expect a given gene to affect myosin tertiary structure, you might want to make sure the coding region is indeed expressed in the muscles and not only in the brain!
Protein action. It is also possible to study the specific action of the protein coded by the coding region of interest. Such studies typically require the study of an entire biological pathway and is often demanding and quite expensive. Here the methodology are diverse but they're discussion is both outside the scope of the question and outside the scope of my knowledge.

Example - Genetic Basis of Color Adaptation in mice
In a comment, you asked

Is there any research paper, review paper or blog which covers entire details how the association and mechanism was established for any of those discoveries?

In most study cases, not all of the above steps are being considered. Also, even if it is the case, such study will be covered by several peer-reviewed papers and not a single one. I don't know of any peer-review paper that explains the whole process for a particular case but those probably exist.
There are documents that explain such process for layman. For example From Darwin to DNA: The Genetic Basis of Color Adaptations by Hoekstra is a standard reading for undergraduate that will interest you. It is easy and pleasant to read. Quoting from this article

In this essay, we will take a journey — into the laboratory and the field — to understand the genetic basis of adaptation in natural populations of mice, and the phenotype we will focus on is the color of their fur.

The gene of interest in this paper is melanocortin-1 receptor (Mc1r). Depending on what level of understanding you want to reach, the article might be a bit too introductory but it refers to some good peer review papers that will allow you to further your knowledge.

First two methods establish the association, and fourth one establish the mechanism. Is that correct inference?

Yes. First two are pure staitstial association. 3 ensures that the association seems to make sense. 4 goes into the detail mechanism of why such association exists

There must be traits controlled by a single gene. Is there any research paper, review paper or blog which covers entire details how the association and mechanism was established for any of those  discoveries?

@AmitMaurya See edit! I hope that helps

I think WCGNA is a fascinating method of unsupervised gene-trait relationship determination, and they have very nice tutorials on how one might carry out such an analysis (ref). The only issue with unsupervised methods, of course, is we often use them when we have no other information about a system but they're also prone to inaccuracies. A good starting point, however.

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


text:
Do bisexuals have any evolutionary advantage over straights and gays?
Do bisexuals have  any evolutionary advantage over straights and gays? Bonobos exhibit bisexuality extensively. Why so?

Welcome to Biology.SE. You should have a look at Is homosexuality an adaptation in humans? and How can homosexuality evolve despite natural selection?. If insights from these posts don't answer your question, can you please elaborate on why they don't.

those questions are about homosexuality vs heterosexuality, mine is bisexuality vs homosexuality/heterosexuality.

@AmitMaurya Can you point out what elements of the answers of those questions do not apply to your question?

@BryanKrause you tell me which element is applicable? is it established that bisexuality and homosexuality caused by same gene(s)?

The genetic basis of either is not well established. The research cited also doesn't look at all at particular genes, it looks at reproductive rates among relatives. It also doesn't look at purely binary genders or sexual preferences and actually groups people into "heterosexuals" and "non-heterosexuals", the latter clearly including bisexuality. Please at least make an effort to read the answers and citations, like this one.

Also bonobo sexuality is interesting but I would be careful to overly anthropomorphize bonobos, despite their similarities to humans. It isn't right to consider bonobos bisexual without considering all of bonobo sexuality. Actions that humans interpret as sexual in bonobos are a major way that they interact with each other: you might as well ask why bonobos socialize with both sexes rather than why they interact sexually with both sexes.

so  are  you saying the behaviours observed in bonobos and interpreted as sexual by us may not be sexual at all for bonobos?

Like many things, whether bisexuality is advantageous for an individual's reproductive success or not depends on the environment. The fact that a wide variety of sexual systems and behavior exists in the animal kingdom suggests that. Also, "advantageous for an individual's reproductive success" doesn't necessarily imply "will spread via the processes of evolution"; for a trait to spread via natural selection+random mutation you need the trait to promote the individual's reproductive success, and for it to be reliably passed down to its offspring. And as the causes of sexual orientation in humans aren't well understood there is always the possibility it isn't strongly or genetically inherited.
As far as bonobos go, I am given to understand they use sex as a social tool, much more so than we do. In that context it does seem like bisexuality would be advantageous; it's silly to only be able to use your most powerful tool for conflict-resolution and social bonding on half of your community. This particular advantage won't be true, or will be much reduced, in species that don't use sex in the same way, i.e. all or most other species that we know of.

are you saying bonobos' bisexuality is because of social learning rather than being genetically determined which is naturally selected?

"Like many things, whether bisexuality is advantageous for an individual's reproductive success or not depends on the environment"  so what environmental characteristics  make bisexuality advantageous in bonobos but not other animals?

@AmitMaurya I'm not saying that no; I don't know why Bonobos are bisexual. I certainly think it's plausible that bisexuality is subject to natural selection, and that it was naturally selected in Bonobos because of their social use of sex, but I don't know whether those things are true or not and I don't think research has demonstrated anything on the subject.

@AmitMaurya "so what environmental characteristics make bisexuality advantageous in bonobos but not other animals?" I described them in my answer; things like "other organisms of the species", "the social structure of a social species", etc are part of the environment.

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


text:
What causes cellular differentiation?
Each cell in our body contains identical dna. And, yet some cells become liver cells, some become brain cells etc. How this happens , when all of them has same dna? Is it because of epigenetic control of gene expression?

This is a very broad question. Please start reading a textbook on this topic.

You can start with Wikipedia's cellular differentiation article.


text:
Microarray with n channels
Recently we've been learning about Microarrays, and the typical method seems to be to run a two channel microarray where your RNA from each cell is labelled with a different fluorescent marker, and then the relative intensity of the fluorescent label can be used to identify a ratio of relative gene expression.
I was wondering if it would be possible to use a larger quantity of DNA sequences on the array and then run a number of sets of RNA fragments - for example, say you extract RNA from cells from a cell culture at constant time intervals, then you label them with fluorescent markers which are orders, and then scan the fluorescent labels to find out how the expression varies over time?
Why wouldn't this work?
Thanks!


text:
Where does new blood comes from when penis get erected?
In Humans, During sexual arousal in males, his penis will get erected with blood.
Where does this new blood coming to fill his penis which is required for erection ?

There are areas in our body which act as reservoir for blood , so when a body part needs excess of it can be diverted to it. ex: lungs.

see this : http://biology.stackexchange.com/questions/20174/where-does-extra-blood-come-from-to-fill-your-muscles-during-exercise?noredirect=1&lq=1


text:
Why does scraped knee hurt more in hot water than cold water.
I was asked this question by my 5year old son. I do not know how to explain to him .

Cold decreases nerve ending firing. It's like a burn; ice feels good (but is not recommended!); warm water would make it hurt more.

The nociceptors i.e. the nerve cells that relay pain due to injury (mechanical), noxious heat and noxious chemical burns, get sensitized upon stimulus. I guess the injury sensitizes the nociceptors and hence they also become sensitive to heat (I am not finding a valid reference for this, at the moment). What @anongoodnurse says also makes sense but I am not sure if that is true. Extreme cold also elicits painful stimulus. Have a look at this post too.

I also suggest that you add some more content in the question body. The body does not convey any question. The title should be a one line summary of the body. If you do not have a lot of details to add then you can still restate the title content a bit more elaborately. We also appreciate some basic attempt from the side of the asked.

as objects heat up they vibrate more at the molecular level which accentuates interactions ... in your case raw nerve endings receive greater agitation ... cold reduces the frequency of this vibratory movement

2 reasons. The first (as anongoodnurse mentioned) is that cold temperatures temporarily knock out dermal surface nerves (in the winter you can verify that your face goes numb after a while outside).
The other reason is that a knee scrape produces inflammation (swelling and increased temperature). Cold water (or anything cold) counters these: stopping the inflammation temperature increase, then freezing out enzymes and proteins needed for inflammation and causing them to slow down or malfunction.


text:
In Vitro Meat Initial Production
I've gotten interested in the science behind in vitro meat, and I was wondering what would be necessary to create it. Would you initially need a primary culture, or an immortalized cell line? And how would you go about creating such a culture that differentiates properly?
The closest analog to this, I think, would be tissue regeneration but I'm finding it hard to figure out the answers to these questions.
Thanks so much!


text:
Can there be medium height(neither tall nor short) pea plants in Mendel's experiment?
Can there be medium height(neither tall nor short) pea plants in Mendel's experiment?
All textbooks I have read seem to imply that pea plants have to be either tall or short, nothing in between.

Medium height (like in people) and other traits that seem like a mixture of two extremes are often a result of incomplete dominance. For example, a red and white flower are bred to produce an offspring with pink petals.
Mendelian genetics does not include incomplete dominance (which is classified as, surprisingly, non-Mendelian genetics).
Basically, Mendel got very lucky with his choice of plant. Pea plant height is strictly dominant, meaning one dominant allele results in tall plants, regardless of the identity of the second inherited allele. This is a consequence of the genetic makeup of pea plants. Had he tried a similar experiment with snapdragon flower color, he would be very confused.
(See https://www.ndsu.edu/pubweb/~mcclean/plsc431/mendel/mendel2.htm for snapdragon incomplete dominance example.)

I don't think Mendel got lucky; I think he worked with these plants and on these traits specifically because he noticed the patterns in them.

Because of law of dominance
Because dominant gene Express themselves and suppress effect of other gene . In case of pea  tall(t) is dominant and overrides effect of other recessive allele and does not even produces any intermediate trait.

Welcome. We require answers to be accompanied by suitable, credible answers. A little more detail and elaboration will help a lot too. It's more of a comment than an answer now.

I believe  AliceD was meaning to type: "accompanied by suitable, credible references".


text:
Why does the inside of ear smell nice?
You can judge my habits later, but sometimes I stick my finger in my ear and smell my finger. When doing this, I get a pleasant smell for some reason. I haven't use hair lotion for a long time cause I have like no hair. I suspect it has to do with my headphones since I wear them often, but i have them for more than a year.

Welcome to Biology SE. You could visit the tour-page for basic informations, the help-page for more detailed informations about what could be asked or could not be. For formatting tasks in command prompt, visit this help sub-page. Thanks.

Did anyone else stick their finger in their ear and smell it?


text:
Can conventional PCR amplify DNA from different organisms from a specimen in a single step?
I've understood so far that in conventional PCR, the most abundant DNA/genotype present in the speciment at the beginning of the reaction is selected and esponentially amplified. So that cPCR are likely to miss mixed infections.
But I had 1 case in which when I sequenced the PCR product I got in BLAST 100% similarity for 3 different species at the same time. Is this suggestive of a mixed infection?

If you had a 100% BLAST hit for 3 species from a single amplicon sequence then it only means that region of DNA is conserved in the three species so you have at least one of those species present not necessarily all three.
If you had three different amplicon sequences and each one matched one species to a total of three, then you have all three species present.

I see. Is it correct to say that: 1) it is possible that one PCR product contains more than 1 organism's DNA, for example if your primers are quite generic and you got several unspecific bands. 2) the readable sequence corresponds to only one organism, even if this sequence is equally conserved in more species ?Thanks

You have have more then one species PCR product in the same band. If you get multiple bands then they by definition have differing sequences. That doesn't mean it's two species, it could be one species with two different amplicons in it's genome. And 2) No, if the sequence is equally conserved in more species you can't say which or how many species are present.


text:
Why are synthetic Auxins capable of killing dicots such as weeds at high concentration but do not cause damage to monocots?
I read that synthetic auxins like 2,4-D and 2,4,5-T can be used as herbicides against dicots but they don't affect monocots. Can someone explain how they damage dicots and not damage monocots


text:
What is the main difference in chromatin fiber and chromonema?
What I understand is both are coiled version of DNA along with histone but are termed different based on their degree of condensation. My question is when do we call it chromonema and when chromatin fiber? Do we consider 30nm fiber as chromatin and 10nm fiber as chromonema or something else?

10nm fibres are seen only by electron microscopy,while chromonema fibres refer to chromatin fibres visible by light microscopy. See this paper. 10nm or 30nm fibres are thus much, much smaller than chromenema fibres. There are likely several layers of organization (like 100nm and 200nm fibres) before you get all the way up to chromenema fibres.


text:
What is the terminal electron acceptor in methanogenesis?
I learnt that methanogenesis is a type of anaerobic respiration that utilizes carbon compounds such as CO2 or acetic acid as their terminal electron acceptor in their electron transport chain rather than using oxygen. However, when I went through my textbook, I found out that conversion of CO2 to CH4 is not one step reaction but many other compounds are synthesized in between and methyl-SCoM is converted to methane.In one article I read that Com-SH is the terminal acceptor When I tried searching in google for the same I came across a lot of diagrams of mechanism but some of them did not match with each other. I have no idea what's going on. It would be really helpful if you can help me out here.


text:
Why can't plain water be used in dialysis? Why is buffer used?
I read that buffer is used in dialysis because usage of water could cause precipitation of proteins but I don't really understand why and how water can cause precipitation of proteins and buffer cannot.

I read that buffer is used in dialysis - where did you read this? The context of a direct quote would be helpful.

In my teacher's learning materials.


text:
Could a vaccine injecting B cells theoretically work?
So I was in the car riding to school today when I was struck with genius. Each B cell is attuned to a different pathogen, am I correct? By that logic, would a vaccine injecting a dose of B cells attuned to the pathogen you're trying to protect against work?

Yes, take the cells out, purify, multiply them with the right stimulus and reinject.
You have been struck with genius, but I think some other people with the same idea got prizes already. Good to see you thinking, dont stop!
A review of just one application of this is here.
"Cancer Immunotherapy"
by
Wennhold K.a · Shimabukuro-Vornhagen A.b · von Bergwelt-Baildon M.
https://www.karger.com/Article/Fulltext/496166
permanent ref is http://doi.org/10.1159/000496166


text:
Explanation of "differential transcript usage" (DTU)
This paper describes differential transcript usage as

Differential transcript usage (DTU) is a special case of alternative splicing in which a gene’s relative transcript abundance (RTA) profile, the proportion of total gene-level expression that arises from each of the gene’s transcript isoforms, differs between conditions (Soneson et al., 2016). [...] An example of DTU may be illustrated by the scenario where the total gene expression is the same between conditions A and B, but transcript isoform 1 is the predominantly expressed transcript in condition A while transcript isoform 2 is the predominantly expressed transcript in condition B.

My question is: is differential transcript usage essentially the same as the usage levels of particular codons? If not, what is the difference? I am unsure of what "transcript isoforms" are, so I'm not sure whether it's talking about codons here or something entirely different.

No, it is a completely different thing, which has to do with splicing and alternative splicing.
I refer you to some genetics text for details on splicing and alternative splicing, but I will give here a very brief and incomplete explanation fo what they are and how they fint into DTU.
Genes are composed of introns and exons. Exons are the only parts of genes that are usually composing the mature transcript (intron retention is possible, but we are not interested in that).
Splicing is the mechanism by which in a eukaryotic gene, introns are removed, and the mature transcript is assembled only using exons.
During splicing, not all exons are necessarily retained. Imagine a gene with exons 1, 2 and 3. It is possible that the main form (called isoform) is the one consisting of exons 1, 2 and 3. Let's call that Isoform 1. However, due to a phenomenon called alternative splicing, other isoforms, can be generated, for example one isoform composed by exons 1 and 3. Let's call that Isoform 2.
On average, we may imagin that the abundance of Isoform 1 compared to Isoform 2 is rather constant. However, some treatments or some changes in environmental stimuli, can give rise to a Differential Transcript Usage by which the relative abundance of the two isoforms changes.

Thanks, but doesn't codon usage bias directly affect splicing, which directly impacts differential transcript usage due to evolutionary selection/pressure for certain isoforms over others?  Would it be possible to update your answer relative to what's written in the "Patterns across a gene" section of https://www.nature.com/articles/nrg2899, specifically the first paragraph part that ends with "...in shaping codon usage near intron–exon boundaries".  There seems to be a lot more nuance here than first meets the eye.

I would say it's true codon usage could affect splicing, but that's mostly for comparing across species. In the same species, the codon is the same for a given gene, therefore it has nothing to do regulating alternative splicing. Differential transcript usage under different conditions should be regulated by other factors.


text:
If split peas are good for health, why didn't evolution favour humans liking split peas?
Split peas, being legumes, are a source of food unanimously considered as healthy. My question is why didn't evolution favour humans that liked the taste of split peas? And/or maybe that could eat split peas raw without cooking them? Those humans would be favoured since they wouldn't have to cook them and/or would be favoured because they would eat plenty of this healthy food since they like it?
Forgive me if that's already been answered but sometimes I have those questions which I don't find answers to and it puzzles me.
EDIT: I'm not saying that split peas taste bad, but for most people, it does not taste as good as nuts, which are healthy too, for example (no source but I think most would agree)

Remember the prior-research requirement, see lectins.

Don't mistake evolutionary solutions for optimal ones. You need selective pressures, pre-existing mechanisms to work with, and luck.

I love split peas. I love lima beans more, and would happily eat brussel sprouts every day. I don't like apples. I like a few kinds of nuts but nowhere near as much as brussel sprouts. Yet I am an end product of evolution. Did I "devolve"? Or is your opinion only that: someone's opinion?

In the ~500 million year evolutionary history of taste buds, or even in the ~2 million year evolutionary history of humans, how long have we been eating domesticated peas? Maybe like 10,000 years. And by that point we were probably manipulating their evolution through agriculture. So the question should be, why didn't we select for peas to taste better?

@MikeyC or the question could be, Why did split peas/legumes evolve to taste bad? or perhaps Why are most legumes not edible raw? There I can see selection pressures..

Because our modern nutritional needs are different than the ones we evolved with. Also cooking.
For a lot of our evolution, food was a limiting factor. Our ancestors regularly died of starvation, and sustaining sufficient calorie input was really difficult.
Part of the evolutionary "fix" for this is a preference for calorie dense foods - like nuts, or sweet tasting things, or, say, fatty cuts of meat (mmm, bacon). This is reflected in types of taste receptors (sweet, protein rich, and salty all trigger different receptors), and our brain wiring to perceive these as good.
The second part - why do they taste bad? Well, our taste receptors are relatively crude, but have inbuilt warnings - bitter is often "this food is off" but can also be "there are toxins in this" - Our receptors are relatively indiscriminate in the flavours they pick up on.
The third part is that humans, fundamentally, are weird. We like powerful chemical irritants (chilies, peppercorns), signals of decaying food (cheese, alcohol), and a whole range of other things that animals with less curiosity would have treated as the dangerous substances they deserve to be. So our tastes are built up from some hard wired stuff (mmm, sugar) and some social or learned stuff (mmm, moldy, solidifed cow's milk)
When we also throw cooking into the mix, humans eat a wide range of things our bodies are not well adapted to eat. But, the wiring for taste receptors remains pretty similar to before cooking, so they throw up false warnings - this bean is indigestible, and contains a bunch of bitter things that might be poison. This round, bitter bit of brassica has few calories, but a bunch of minor toxins, so we reject it. Eating enough of them raw will upset our stomachs, at the very least.
But, we can learn to like things - and some of that is us forming good associations with the food we're eating, and some of it is a dampening down of the warning signals - eat something bitter regularly, and your brain stops going "shit, you're trying to poison us" and instead starts realising it doesn't get sick from this particular food

There are a fair number of questionable statements here, making this answer very much just opinion (which isn't a good fit for a science site.) If you could provide references to back up your points, it would be very helpful. Thanks.

all very fair - I think I've not got time to dig through for the sources, and it was a bit of generalization, pitched at the level the question was being asked at - think it's better to delete or leave it?


text:
Why can't protein pumps reuse phosphate groups?
I am currently in AP Bio, and our textbook has a diagram of a sodium-potassium pump:

If I am understanding correctly, every time this cycle occurs, an ATP is hydrolyzed in step 2 to produce a new phosphate group. Why can't the pump reuse the phosphate group it released in step 4 from the previous cycle?

The phosphate group must be detached from the protein to cause a change in conformation. The lost phosphate group is drifting in the cytoplasm and cannot be reused without reattachment to ADP (creating ATP), since attachment of phosphate to the protein requires energy.


text:
Pee Shiver: Any reliable research about this phenomenon?
I came across 2 webpages about the science of pee shiver.
Link 1
Link 2
I wonder if there any reliable scientific research about this phenomenon. The 2 webpages I have hyperlinked attribute this to ANS(Automatic Nervous System) or sudden decrease of temperature in exposed body part while peeing.
But these 2 are just hypotheses, not proved reseach. Is there any?

Sadly, nobody really knows why this happens. Interestingly, those 2 links are the only 2 major theories about this :P

@another 'Homo sapien' I think the hypothesis of relating pee shiver to autonomous nervous system is more realistic.
What do you think?

Yeah, that temperature one does not seem much satisfactory. However, I did not study either of them in detail, so I can't approve any right now...maybe somebody would also like to share opinion ;)

@Always Confused Yes, there is. I frequently perceive it.

It's been found that many people don't notice this phenomenon with themselves.

@Always Confused Perhaps you should try drinking too much water, then holding your bladder for too long, then pee. you might perceive it. And speaking of hot climate, I live in a tropical climate. Yet, I perceive it


text:
What is the replacement period of gastrolithes in doves?
Gastrolithes are common in doves and pigeons. Do they keep ingested stones for ever? If not, how often are they to be replaced?


text:
Why X-chromosome linked diseases happen due to recessive gene?
All the X -chromosome linked genetic disease I have studied (Color-blindness, Haemophilia, Muscular dystrophy) happen due to a recessive gene.
At first, I thought it was because there could be a 'good' copy of that gene on the other X chromosome (in case of females). So that's why these genes are recessive. But this is a bogus reasoning, I soon realised.
So, why X-linked genetic diseases happen due to a recessive gene? Maybe not all. But why some are recessive?

You might be interested in this

First of all, most observed mutations are recessive (see the answer to this question; in brief: homozygous carriers are strongly selected against, heterozygous carriers are not affected only if the allele is recessive). So you wouldn't be surprised to find the same pattern on the sex chromosomes.
A good way to think about the specialty of recessive alleles on the X chromosome, is to think about why these diseases are most often visible in males (and you are on the right track there) ... Most alleles causing heavy disease - be it a mutation on the autosomes or the sex chromosomes - are rare (it is for the same reason they are recessive which is described in more detail in the answer linked above; it is due homozygous carriers being affected by purifying selection again) and therefore female carriers are most likely heterozygous and therefore healthy. In males, however, a carrier is always affected by the disease because the carrier is hemizygous.


text:
Is hair made of protein or dead cells or both?
Some sources say hair is made of dead cells:

it's mentioned in many titles of Google searches, so I'm linking the Google search search

Other sources say hair is a protein filament:

Protein filament that grows from follicles found in the dermis, or skin

I don't think protein and dead cells are the same thing. Where am I mistaken?

I found the answer while trying to write the question. Hopefully this helps others

We usually say that hair is “made” of a protein called keratin—that’s a bit of a simplification. As hairs become part of the shaft, they undergo a process called keratinization, in which they become filled with keratin. So, technically, instead of being made up of pure keratin, hair is made up of dead cells that are filled with and surrounded by keratin.

Source
I'd say some visualisation would be helpful, please add a new answer or propose edits to this answer


text:
Should I consider [H+] as substrate in MCT transport equation?
I'm trying to model the transport of lactate in cells (in both direction via Monocarboxylate transporters):
[Lactate]intra + [H+] <----> [Lactate]extra + [H+]
I found some data on kinetics of Lactate itself (Km and Vmax) but I don't find anything on [H+].
My initial thought was to consider [H+] as a substrate, and model the transport as a sequential ordered Bi-Bi reversible reaction (from this paper: Poole & Halestrap (1993). Transport of lactate and other monocarboxylates across mammalian plasma membranes. doi:10.1152/ajpcell.1993.264.4.c761)
But it require a lot of parameters (Ki, Km, Vmax) for each substrate involved (especially H+).
So my question is: Should I consider [H+] as a substrate or just as an external parameter that impact the direction of the flux ?
Thanks everyone
(first question on Stackexchange)

To include or exclude the H+ basically depends on the scope of your model. The H+ can be used as external parameters if you assume that both sides of the membrane are well buffered and the pH will not change. If you want to simulate a condition during which the pH changes, like for example strong exercise in muscle or ischemia, then you would need separate H+ for each side of the membrane.

Thank you for your answer. Yes the pH will change at each side of the membrane (I simulate cancer cells with high glycolytic activity). But if I consider H+ as a substrate like lactate, should it follow a michaelis-menten kinetic (or derivatives) ? If so do you have any idea of where I can find this information about H+ ? I didn't find any paper measuring such parameters for H+.

I think this article can give you some kinetic data on proton symporters with different pH. There is a lot published on the subject but it is difficult to find the best search term... perhaps this paper or this paper may also give some usefull parameters.

Thank you ! I already downloaded the second article but didn't saw Km values for H+, a second read is usefull :) The cell's paper seems really promising, I'm going to read this right away.


text:
About genomic imprinting
In the context of genomic imprinting, how does a human cell "know" whether a chromosome is paternal or maternal(out of a homologous pair), in order to silence genes?

What precisely are you referring to by “gene silencing”?  The only thing it means to me is ensuring the X chromosome of females (in man) only expresses genes to the same extent as in males. As far as I am aware this silencing of one gene copy occurs at random, without any reference to the parental origin of the chromosome. And please do not use the anthropomorphic “know” in questions.  You can phrase them in the passive voice, e.g. “how is it determined”. Sloppy phraseology leads to sloppy thinking.

@MaximilianPress. Once again. The question talks about gene silencing in a chromosome copy-specific manner. This is not equivalent to genomic imprinting, which is not mentioned in the question.

Deleting the answer-to-comment and my other comments as they seem to be problematic.


text:
Is this basic gene diagram correctly labeled?
I keep seeing this gene diagram, and I am not sure how to interpret it. I don't know what this diagram is called or where it was first depicted, but in the second picture, I have labeled it with what I think are the correct regions.
Unlabeled

Labeled

If the labels are correct, does this mean that an open reading frame (and consequently, the CDS) does not have to begin at exon 1?
If the labels are not correct, could you make some suggestions on how to fix the mistakes or point me towards some resource for interpreting this diagram?

I'm finding there are lots of ways to label genome fragments, and a thin/thick block doesn't always mean the same thing, so just want to make sure I'm learning things the right way. Thanks!

Welcome to SE Biology. We would encourage you to provide a link to things you "keep seeing". That way we can check them out ourselves. As to one of your questions: "does this mean that an open reading frame (and consequently, the CDS) does not have to begin at exon 1?" Does the ORF have to (or ever) begin at the start of the mRNA transcript? If it doesn't, why would you expect the ORF to have to start in the first exon?

I'm seeing them in coursework, the diagrams are a notation used in this class but I'm not able to find out where they came from (I only see this kind of diagram in the class).

To your second question, I don't know, that's precisely the question I'm asking. I could deduce it if I knew my interpretation of the diagram were correct

My professor got back to me and said my diagram is correct -- and that allows me to answer my second question: an ORF does not have to begin in the first exon.
(The UCSC Genome Browser uses a similar format to display genes.)


text:
What does it take to start producing(cultivating) probiotics?
Is there a DIY way?
Is it possible to make a bacteria strain from scratch based on an existing one ? (for example lactobacillus reuteri).

have you looked elsewhere for potential ways?

Is "probiotic" a scientifically meaningful term?

you are right @jamesqf but I don't know the correct english word to refer to this commercial name...

@VanceLAlbaugh yes I looked online but I didn't found nothing useful..

Probiotic prebiotic and synbiotic, are used to indicating health promoting bacteria, compounds that stimulate growth of probiotic bacteria relative to other bacteria and a mixture of both respectively.

@Alessandro Carrese: Don't feel bad.  I'm a native English speaker (and I think a fairly well educated one), yet I really have no idea what "probiotic" means beyond being a marketing term in the health food industry.

I did a master's thesis involving enzymes from a probiotic bacteria. Many of the known probiotics were cultivated from faeces but others have also been isolated from breastmilk. Many of the probiotic bacteria are strict anaerobes and can only be succesfully cultivated in modified atmosphere. You may need to use selective plating with various prebiotic compounds such as Galactooligosaccharides or similar compounds in order to control bacterial growth. I recommend incubating at 37°C or slightly below depending on how well controlled your incubator is.

Thanks for correcting my spelling mistakes. I have a question about references... Is it allowed to self reference a peer reviewed article?


text:
Technologies that rely on evolution
It's possible that this is offtopic here; if so, please let me know.
I'm wondering what technologies exist that rely on evolution being a correct model; I'd like to be able to offer examples of that to people who find it to be "just a theory". As an example, I can point out lots of technologies for which our models of electromagnetism have to be correct to an immense accuracy for them to work - computers, any electrical wiring, electrical motors, light bulbs, electrical ovens, etc. etc.
The best I could find as examples of technologies that require our models of evolution to be fundamentally correct are things like pharmaceutics that work against germs that have developed a resistance against other pharmaceutics.
What are some good examples of technologies that require our models of evolution to be fundamentally correct for those technologies to work?

I think this is probably too open-ended and discussion-based to make a good SE Q&A, but I'll reserve my close hammer for now. "All of molecular and cellular biology and almost all modern medicine" would be a start of an answer. Ultimately, though, I think this is probably a poor strategy for argument: people who have decided to believe evolution is false have not done so based on fact, so additional facts are unlikely to persuade them.

@BryanKrause I realize that it's probably a bit wide of a question, thought I'd give it a shot anyway; maybe "all of molecular and cellular biology" could be narrowed done to a handful of striking examples? As for whether it's a good strategy for argument, I'm optimistic it helps. Many people have been argued out of all kinds of denialisms and cherished irrationalities, and even people who don't rule out creationism come in flavors of being less convinced than card-carrying religious fundamentalists. I've found it's relatively effective to have something concrete, specific to talk about.

Not a technology, but a biotechnological product. The enzymes required to fermentate milk and make yoghurt will ( and gonna ) mutate. So, you can genetically modify and setup bacterial lines with a fixed sequence that ensure the production of enough and functional enzymes. Also, the creation of clonning vectors is a technique developed with evolution in mind. Sometimes you want evolution, and sometimes you dont need it.

Vaccines, and nearly anything else based on epidemiology. Most of modern agriculture is based on artificially selected organisms. If evolution did not work, hens would only lay a few eggs a year and an ear of corn would still be as small as a head of wheat, and tomatoes would still be the size of grapes.  basically all forms of animal testing, including much of genetics, rely on common ancestry.

This site does not exist to supply people with debating material on evolution. If you cannot marshal the arguments yourself you are never going to convince anyone else. Certainly not in this case where you are using a false premise because you don't understand that evolution is an explanation of something that happened with no predictive power, unlike the laws of physics, for example. In any case you are reckoning with people who will not be convinced by rational argument because their position is based on irrational religious beliefs. Don't waste your time.

This is an excellent Idea which is actually a tool used in everyday Molecular biology if you look at it with the right perspective.
Evolution, if broken down into its basic components has been with us and created many technologies to date.  This is probably not all encompassing, but lets look at diversity and selection which are principal components of Darwin's fundamental theory.  Darwin distinguished between 'Natural Selection' and 'artificial selection'. That's a great place to start.  Artificial selection is a means people have used for millenia to get desirable traits for products.  Beef (well all of our meat), wheat, textiles from wool and cotton, pets, fruit and vegetables are all the product of selection where the farmer/flock owner will save individuals with desirable traits and breed them for the next crop.  This is one of the principle evidence for Darwin's work: He extended the case of Artificial Selection to understand how it works in the natural world.
In more more recent decades we have come to use Artificial selection with genes and pieces of DNA, changing them, adding them.  Molecular biology uses a selection technique where genetic changes of interest are accompanied by a resistance to an antibiotic.  Now we are changing how well the genes work and using them to say make better insulin for diabetics.
Artificial Selection can look very much like Natural Selection since the definition of 'Artificial' is simply that people did it; by definition there never will be a technology that comes completely from Natural Selection.
There have been more sophisticated versions of Artificial selection where artificial selection have used diverse genetic backgrounds to find individuals with amazing abilities.  One of my favorites is an experiment where they simply were looking for yeast cells that floated.  They created an environment where the floaters were carried on for further experiments for i think it was about a month.  In the end they found some yeast that tend to stick together and form colonies - a trait that was on the edge of multicellular life.

Evolution is not the type of theory that is mainly directed towards technological applications, as opposed to many physical theories. It is a principle to understand living systems, from the simplest to the most complex. So it mainly gives understanding, not 'solutions' to particular problems.
That being said, evolutionary principles can be applied to many 'practical' problems.
For one, all of the technologies that rely on sequence alignment and phylogenetic inference use models of substitution based on evolutionary principles, in which you have hypotheses based on the probability that some evolutionary changes occur (these changes can be at the nucleotide level or at the organismal level), and then you infer which hypotheses are the most plausible given the evolutionary and ecological context of the problem. A 'practical' side of this, for instance, would be to infer the evolutionary trajectory of the COVID-19 epidemic, or the study of the geographic spread of the virus given the sequences of the virus at different locations/time. A lot of modern molecular biology is based on a comparison of sequences.
Another 'application' is that of designing enzymes or other molecules, that have a desired function or feature. In fact, a recent Nobel prize was awarded to Frances Arnold for harnessing the power of evolution in her research on molecular design.
Some other applications besides the ones people have mentioned in the comments above are medical applications. It is well known that cancer lineages evolve, so the principles from evolution can be used to better treat cancer progression, for instance by adjusting the evolutionary outcomes of a particular treatment (you can read a fascinating example here). In fact, the understanding of cancer itself, besides therapeutic interventions, has used evolutionary principles for some years now (see a nice example of evolutionary dynamics in metastases here).
I also want to mention an important example from microbiology. It is a pressing issue of public health the fact that no novel antibiotics have been developed in the last few years, and that the existing ones are less and less effective given to the evolution of antibiotic resistance. What if we could make "evolution-proof" antibiotics? That's a fascinating question that some people are starting to explore, for instance by combining classical antibiotic treatments with phage therapy or molecules different than the traditional antibiotics (a cool paper here).
Finally, I want to mention that these applications of evolutionary principles do not "rely" on evolution being "fundamentally correct". Evolution is a process for which we have a lot of evidence, so at this point (and for a long time) evolution is an uncontroversial fact to the scientific community. This is similar, for instance, to the fact that we have lots of evidence for the phenomenon of gravity; so what scientists are doing at the moment is figuring out the mechanisms by which evolutionary processes occur (just as physicists are looking for gravitons). Another addendum is that evolution seems to be an open-ended process. This means that many of the mechanisms we can find in evolution will be, to a high degree, statistical in nature, because there are just so many possibilities that we cannot account for all possible outcomes. This is a fundamental difference to many theories in, say, physics, where there are clear "solutions" to a problem (in the form of an equation, for instance). I say this because people keep coming up with examples that "disprove" evolution, but they just don't consider that evolution is a statistical process, which allows for "outliers". In fact, the outliers are quite informative for evolutionary theory, not at all undesirable (consider for instance the origins of life, or the emergence of consciousness, these are unique 'events' for which we have no mechanism to explain why did they emerge).

These are all interesting examples, thank you for that. While I don't think they fit what I'm looking for, your last paragraph does a great job at explaining why what I'm looking for might not be easy to come by, or exist at all; especially the statistical nature of evolution probably prevents this.

Two types of technologies come to mind. The first involves techniques that improve the traits of strains used in biotechnology. For example if you are using genetically modified yeast in wine making or for making a commodity chemical and want to improve quality or production rate of that compound you can generate yeast mutants that meet your goals. One easy way to do this is to subject the yeast to UV radiation and look for good mutants. Someone who has no understanding of genetics and molecular biology would not understand why subjecting yeast to harmful radiation will help make them better. The reason is that UV radiation creates DNA damage and innacurate repair of that damage leads to diversity in traits, which may enhance or worsen the trait you are after.
One could say "you don't really depend on evolution for that to work because if you try it once and it works then it will work for another trait". But why should we believe that because mutagenizing yeast with UV radiation helped make wine better it will help make more acetic acid? The reason is because the mechanism is the same. And how do we know that we aren't just wasting our time and some traits can't be improved. The reason is because all the diverse life around us developed from a common ancestor through the same principles.
The other technology is ancestry analysis through genome sequencing. We know that we don't need to look at all the billions of DNA bases that make up our DNA to see if we are related to someone or some group. We only need to look at a smaller subset like single nucleotide polymorphisms (SNPs). And using this information we can track the migration of human populations over long periods of time. Again looking at DNA sequencing data could be doubted as just a coincidence or that other explanations or possible. Maybe contrary what the genomics data tells us, population A didn't migrate from population B, but it arose at the same time? But the theory of evolution assures us that our conclusions are the most reasonable.
I should also add that if evolution wasn't true then both of these technologies would be nonexistent and we might not even have any alternatives to answer the questions that these technologies are employed for. If organisms don't adapt how can we make yeast produce more ethanol without dying to it? If humans don't have common ancestors why does random variation exist even among our progeny and how do we explain archaeological data?


text:
Are there evolutionary advantages for the bee sting to kill the bee?
The question title says it all: are there advantages for the sting of a bee to kill the bee? It seems to me getting rid of this would have only advantages, and might've been selected for if a mutation like that occurred.

The bees you are most likely to be stung by, do not participate in reproduction.

The ones that do participate in reproduction do not die if they sting you.

@Aron That's an interesting piece of info, if you'd like credit for it, please post it as an answer.

@Aron, I believe that bees capable of reproduction do not have stingers. Male bees either get a reproduction organ (drones) or a stinger (workers). Never both.

@Octopus Queens do not have barbed stingers. In some cases Queens (often related) will fight to the death over a hive.

@Aron, Queens also are not male.

@Octopus, firstly. Worker done bees are female. Secondly what I said was carefully chosen. I might have implied that all bees that participate in repro can sting, I never did. I merely stated that those bees who do sting you would not likely die from stinging you.

Fitness of the colony vs fitness of a single worker
Bees have a division of reproductive labour (they are eusocial). Only a queen reproduce (and the males called drones) while the workers dedicate their existence to ensure the survival of the colony. If committing suicide will be of any help to the colony then one would expect a bee to do so. What I just said is an oversimplification of the structure and mating systems of bee colonies.
You should have a look at the field of social evolution to have a better understanding of what's going on with bees!
What is the cost?
Above I argued why nobody really cares much if a single worker dies. This being said, if the bee survived to stinging, then it could eventually keep protecting the colony as it was doing before stinging. So why does it has to die? Clearly, there must have a cost to not die. It seems very plausible to me (but cannot offer an evidence for it) that there would be a strong physiological cost to create a stung that that would not kill its carrier. Such physiological cost (even if mild) can by large outweigh the cost of losing a single worker for the colony.

Re "Only a queen reproduce(s)", surely the drones play a part as well, no?  But I think the key here is looking at the survival/fitness of the hive, not individual bees.

Well sure. The drones aren't really part of the colony though and they are just fed as larvae and then fly away (although it may vary among species). In some species (of ants at least), workers sometimes take over colonies or reproduce secretly. I'll fix the eventual confusion but we'll keep my answer as simple as it currently is. Thanks for your comment.

"Clearly, there must have a cost to not die" I disagree. Evolution is not about optimization. Its about "good enough". A barbed stinger increased the effectiveness of the stinger at the cost of the bee's life. Losing the bee is "good enough".

My answer is an oversimplification as I did not want to dig into the details of kin selection theory for such a simple question. I don't understand how your metaphors of "what evolution is about" mean. If there was no cost to being able to stung without dying than one would expect variants that do not die to increase frequency. Sure, it is possible that there is a phylogenetic constraint or something similar going on.


text:
Would BMP7 introduced to a Petri dish with cartilage cause chondrocytes to replicate?
Chondrocytes are the cells that make up cartilage. As I understand it, the best growth factor that signals replication of chondrocytes is Bone morphogenetic protein 7.
If supplied with a sufficient source of nutrients and a growth factor, would those chondrocytes begin to replicate?
If you prepare a Petri dish full of blood and cartilage and add BMP7, would the cartilage start to grow? Are those two questions the same?

Hello and welcome Delaney Fitzpatrick.
BMP7 - Bone morphogenetic protein 7 - Plays a role in cartilage homeostasis.
Chondrocytes - A cell which has secreted the matrix of cartilage and become embedded in it.
Chondrocytes therefore make cartilage. Cartilage unfortunately has a poor regeneration capacity.
BMP7 stimulates Chondrocyte division
Naturally the question then becomes, does BMP7 also increase cartilage production?
A paper from 2009 - Chondrocytes that expressed increased levels of BMP7 in defected rabbit knees showed statistically significant repair when compared to controls.
Although an early study, it does suggest that BMP7 may improve cartilage repair.


text:
In the female reproductive system, is the labia minora / labia majora / labia as a whole the female counterpart of the scrotum in male?
I am confused about which labia is the counterpart of the male scrotum. Any help would be appreciated. My first question so pls try being more lenient with downvotes.

We have an expectation here, as is common across StackExchange, that questions contain evidence of prior research. An example here might be quoting from (and citing) a textbook or other source like Wikipedia that states this homology but is unclear about the details you request. We also ask that questions be free from "meta" information like that it's your "first question": we're building a repository of Q&A here, so ultimately who asks a question isn't supposed to matter, just the content itself; other text is just noise for the next person who finds this Q&A via Google or elsewhere.

https://www.kenhub.com/en/library/anatomy/homology-of-the-male-and-female-genitalia


text:
Would muscles still twitch if the applied potential is reversed?
In Galvani's experiment with frog legs, he applies an electric potential across the muscles of a frog which causes the leg muscles to contract. What would happen if the polarity was reversed (I do not know the polarity he had originally used). Would the muscle still twitch?

Here the voltage is applied by using two different types of metals fused to each other

A nerve fiber is something like a cylindrical tube: it has walls (cell membrane) on all sides, and at rest is a bit negative inside, like this:

There are channels in the membrane that are sensitive to voltage. They are oriented with an inside-side and an outside-side, and move according to voltage such that they are closed when the inside is more negative than the outside. Most or all will be closed when the membrane potential is around -70 mV. If the voltage gets closer to equal, though, say -55 mV or more positive, the channels open, let more positive ions come in, and this current flows down the fiber depolarizing more membrane and opening more channels.
When you stimulate electrically with an external shock like in an experiment like this, the situation looks more like this:

You've added some huge voltage in some direction, here I've drawn it assuming the positive terminal is somewhere to the left and negative is somewhere to the right. For that brief time that the stimulus is on (it better be brief or you'll start cooking your tissue), you can just about ignore the little charge inside and outside the membrane that set the membrane voltage. All the membrane "sees" is your big stimulus.
For the membrane on the left, it's going to see a strongly negative voltage inside (towards the negative terminal) versus outside (towards the positive), and the voltage-gated sodium channels will stay closed. It doesn't really matter to the channels that this is extremely negative compared to normal rest: closed is closed.
For the membrane on the right, though, it doesn't have a negative voltage inside relative to outside anymore: the outside is facing the negative terminal, and the inside is facing the positive terminal. This is going to open some channels and let in some sodium ions.
A brief moment later, the external stimulus is gone, but those channels were opened and some ions were let in, making the inside less negative than it was, opening more channels, etc.
So, what if we flipped the polarity? Well, just flip the image, and apply the logic the same way. You can put the positive terminal into the page, too, and the negative outside (remember, we really have a cylinder here): as long as you make a voltage across the combined membrane of the fiber, you're going to stimulate a response. Even if your voltage source was at the top and bottom of the page, nerve fibers aren't perfectly straight, and anywhere that there is a bend will be susceptible to the shock (though not as sensitive as if the whole fiber was exposed across the potential gradient).
In practical, non-theoretical terms, sometimes the polarity you use does change the effectiveness a bit, but it's usually a subtle effect. I'll admit I'm not entirely sure what is physically behind this, but I think it has to do mostly with the electrode material and an inductance/capacitance that reduces the intensity of the voltage gradient depending on which way the stimulus is applied.
It's common in electrophysiology also to use biphasic square-wave pulses; in that case, the polarity reverses in the middle of the stimulation. This helps keep the electrodes in good shape and not depositing salts on them (the way you'd get in a battery-style chemical reaction), but it works just as well for stimulation.


text:
Does poop have protein?
Popular health advice suggests that one shouldn't consume >30g of protein at a time (without a gap of ~3 hours, or otherwise depending on the type of protein), because only so much can be digested at a time.
This seems wrong to me? Shouldn't the protein just form a backlog? Where does the protein go? And if this were true, couldn't people just lose weight by consuming all their meals in one go?
I was under the impression that poo doesn't contain any macronutrients (apart from some occassional indigestion, or fats not absorbed on a high-fiber diet), just fibre and water. Perhaps it has to do something with protein synthesis, and the amino acids get excreted in urine?

Trivially, feces contains cells and cell waste, which necessarily have proteins. You may want to narrow your title and question to discuss the persistence of dietary protein in the human GI tract.

I wouldn't start with popular health advice as a basis for understanding anything.

perhaps try some before your exercise sessions and see if your gain weight? were you thinking of starting a line of poop protein supplements for gyms?

Human stool, on average is about 25% solids and 75% water. Up to 54% of the dried solids consist of bacterial biomass, of which protein comprises up to 50% (1). This is pretty consistent with other research that stool contains up to 25% protein (dry weight) (2), although there is still debate over how much of that is attributable to undigested protein and how much is bacterial biomass.
Basically all dietary protein is absorbed in the duodenum and proximal jejunum (3), so, pretty much just the first half of the small intestine. And, since the food you eat only spends a finite amount of time in this region of the gut, protein uptake is likely limited by transporter density and also by the kinetics of gastric and pancreatic enzymes that break down large dietary proteins into small, absorbable peptides and amino acids.
Lastly, when your body does uptake more protein than it needs (or can utilize) at a given time, it doesn't just backlog (there is no storage form of protein in humans). Instead, it's catabolized and used to generate glucose or ketone bodies, which can eventually be stored as glycogen or fat. These processed also generate a significant amount of ammonium waste, which is converted to urea in the liver and excreted in the urine, putting extra strain on the kidneys.
References:

Rose C, Parker A, Jefferson B, Cartmell E. The Characterization of
Feces and Urine: A Review of the Literature to Inform Advanced
Treatment Technology. Crit Rev Environ Sci Technol. 2015 Sep
2;45(17):1827-1879. doi: 10.1080/10643389.2014.1000761.

Volk T, Rummel JD. Mass balances for a biological life support
system simulation model. Adv Space Res. 1987;7(4):141-8. doi:
10.1016/0273-1177(87)90045-7.

APUS: An Introduction to Nutrition 1st Edition (Byerley); Chapter 5.4: Protein Digestion, Absorption and Metabolism. https://med.libretexts.org/Courses/American_Public_University/APUS%3A_An_Introduction_to_Nutrition_(Byerley)

Interesting. So where does the bacterial biomass protein come from? Does bacteria convert fiber into protein?


text:
Identification of a Tettigonia specimen
At least I think it is a Tettigonia sp. but I have problems identifying it exactly because it is still a nymph. OK, it is a female, that is hard to overlook, but is it T. cantans (my guess) or T. viridissima or am I completely misled?
Found in western Germany (quite rural, Lower Rhine region, north of Dinslaken) in mid-june 2014 on a tomato plant.

The tomato plant is a mini cocktail tomato plant and its leaves are a bit smaller, so here is an example of one with a metric measure tape aside for metrological purposes.


text:
How many cells need to be damaged before a human can feel it as pain?
I'm guessing the answer to this question is rather large. Skin cells die all the time, it seems, and that never registers as painful. But suppose you rupture or otherwise destroy a group of cells, say in the dermis or something, which enough precision to be able to specify the exact count. How many would you have to destroy before it would be perceptible? What if you add a delay between the destruction of each cell in the group? If it was staggered in time, would that make it imperceptible again?

Although any number estimation would be inaccurate, I can think on two factors that can influence the count.

Cells location: Pain is trigger when specialize cells (Nociceptors) fires action potentials. The density of those nociceptors is greater in the tip of your finger than in your back. So the number of cell damage that trigger the pain would be different in those areas too.
Cell death rate: The delay that you mention is a key factor. Slow death like the normal on skin is done by a regulated mechanism (Apoptosis), in this process the cellular components are recycled. In fast cell death, the cellular components are released causing inflammation, which increases the nociceptors sensitivity.

Would it still be true that "any number estimation would be inaccurate" if we hold the cell location constant? Surely this could be studied empirically? Not that it would necessarily be a good idea to do that.

Have in mind that pain is felt when nociceptors are activated. If you have a method clean enough to kill cells without activate nociceptors directly, then the debris of the death cells can cause nociceptors activation because of the inflammatory process.

@bxw the location matters a mot, for instance you could destroy most of the brain without pain, since it has few pain receptors.

There is no specific number of dead cells to be honest that serves as the threshold for pain, it is the molecules that are responsible for decreasing or increasing the threshold of pain either peripherally (at the site of nociceptors) or centrally (endogenous opioids). Here is a diagram that kind of summarizes pain pathophysiology at nociceptor level.

For example, sunburn produces temporary sensitization of the affected area. As a result normally innocuous stimuli, such as light touch or warmth, are perceived as painful (a phenomenon referred to as allodynia), or normally painful stimuli elicit pain of greater intensity (referred to as hyperalgesia)
As correctly stated in the previous answer, Apoptosis would never initiate pain since it doesn't involve any inflammation.

Reference-  Basbaum AI, Bautista DM, Scherrer G, Julius D. Cellular and molecular mechanisms of pain. Cell. 2009;139(2):267-284.
doi:10.1016/j.cell.2009.09.028
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2852643/


text:
Will wiping a phone down with isopropyl alcohol daily breed bacteria resistant to disinfectants?
The title says it all. If you disinfect something more regularly, aren't you just selecting for bacteria which are most robust to that method of disinfection? I've heard it said about some medications that they "can't cause antibacterial resistance". In particular I've read that this is claimed about topical benzoyl peroxide in the context of skincare. Do these claims have any weight to them?

Does this answer your question? Why can bacteria resist topical antibiotics, but not compounds like Benzoyl Peroxide?

It is possible to select bacteria in vitro, with some help, to withstand 50 g/L (5% v/v) of isopropanol.   According to this paper, bacteria at hospitals in Peru have a variable but increased resistance to isopropanol.  (That study was preliminary, however)  Since bacteria can produce isopropanol themselves, some degree of resistance is very plausible.  Even so, the fundamental nature of 70% isopropanol's attack on the membrane makes it hard to defeat.  Anything is possible in biology, but the more proper the application of disinfectant in terms of exposure time and concentration, the less plausible the selection of resistant species or strains from the bacterial community will become.


text:
Chromosome Deletion Notation in Cancers
The cancer literature often refers to the deletion of certain sections of a chromosome (e.g. "17p del" or "Del(17p)" for the deletion of chromosome 17's p-arm.)
Does this mean both alleles of the chromosome were deleted for the specified cytoband (i.e., copy number analysis would show zero in this case)? Or does it mean one of the alleles was deleted, and thus one remains (copy number analysis would show a copy number of 1 in this case)?
Thanks


text:
Can we decode memories?

Premise: I don't have a strong background in neuroscience or human biology, so I would ask you to answer like you would at a 5 years old child. I have done a couple of research on the web, as well as here on StackExchange, but the answers that I have found are either pretty old or difficult to understand for me.
I have read that memories are not stored in a unique place in our brain.

If you knew the region where the particular memory you are looking for is, would you be able to decode it?

Example: Let's say that someone said to you something you perfectly remember even after a few years. Since you remember the exact words, I suppose that those words are stored in our brain somehow. Is it possible to retrieve what those words were?
To summarize my question, what do we know (and don't know) about how we encode memories?
Thank you all.

Given recent advances in AI related neuroscience, I can easily imagine a future where it is possible to decode thoughts and impressions. In fact, we are already nearly there.
It seems like the limitation is not the decoding of memories, but their detection or measurement: While you are seeing an image and the brain actively is working on it its perception, causing your neurons to fire in certain patterns that can physically be measured with fMRI, there is the possibility to decode some information out of these signals. Same if you remember a scene in your memory.
However, I don't see any theoretical potential to read memories out of inactive/dead brains. So I hardly can imagine that any machines can read anything that's not currently happening in the brain. Maybe your brain can be stimulated somehow and its response can be read, but in the end you need physical measurements.


text:
How quickly are plants able to sense changes in light intensity?
Evidently due to the process of photosynthesis, plants are able to "sense" light (as demonstrated by the phototropic response). My question is, how quickly are plants able to perceive changes in light intensity?
I.e. if there is a strong light shining on a plant, and at t=0 the light is switched off, is there some delay τd before the plant exhibits a response to the change in light intensity?

Hi, welcome to StackExchange Biology. While this is an interesting question, it could benefit from a look at these points: 1. 'Evidently due to the process of photosynthesis, plants are able to "sense" light (as demonstrated by the phototropic response)' This statement needs modification as photosynthesis and phototropism are very different processes. (Though one could argue that phototropism evolved to increase the efficiency of photosynthesis.) 2. It would also be nice to include (in the question body) efforts you made to answer the question: what books/sites you read, what you found out.

Hi. As a preface let me apologize for my lack of clarity / background knowledge. Biology is not my field of study, but I have been curious about this question for a while. To address your concerns: 1) By this I mainly meant to indicate that plants evidently do have some pathway for sensing the intensity of light. Phototropism is evidence of this, as it shows that plants have some "awareness" of the location of a light source. 2) I have searched for research relating to the response times of photoreceptors in plants, but have only been able to find information such as absorption patterns.

I should add that some of my confusion comes from not understand the difference between animal and plant photoreceptors. If they are very similar, then it could be inferred that a plant's response time would be very similar to that of a human. However, I imagine there is very little evolutionary advantage for plants to have a fast response time to changes in light when compared to animals.

Thanks for the clarification. Please edit your question body and incorporate your comments into it (in a concise manner). This will improve your question and increase the chances of getting a useful answer.

The delay for UVR8 photoactivation seems to be in the range of picoseconds depending on the wavelength:

Global analysis in terms of a model of parallel decaying
components indicated four lifetimes of 14.7 ps, 370 ps, 1.9 ns,
and 5.9 ns.

The photodynamics of the Trp ensemble in UVR8 can be summarized as
illustrated in Figure 5B. We observe excited state decay in the
few-hundred- picoseconds to nanoseconds time domain to the triplet
intermediate U460.

For a better understanding of photoactivation mechanism times, you can read the following article:
Proton-Coupled Electron Transfer Constitutes the Photoactivation Mechanism of the Plant Photoreceptor UVR8
Journal of the American Chemical Society 137(25) · May 2015


text:
How is knowledge about farming transfered between generations in farming ants
There are some varieties of ants capable of "agriculture", e.g. dairing ants farming aphids and leaf-cutting ants farming fungus.
How is the knowledge about the techniques involved passed between generations (in the case of dairing aphids I mean e.g. milking the the aphids to get honeydew, and protecting the aphids)? In short, is it more "genetic" (so that lab-cloned ants are capable of it) or is it more part of "culture", i.e. younger ants mimicking the older ones? I'd be mostly interested in answers with references to relevant experimental research.

Knowledge and technique are probably the wrong words for what is essentially instinctual behavior.

knowledge, technique, intuition, etc. are all not well-defined terms, which is why I'd favour references to experimental research. If you have a particular definition in mind of "essentially instinctual", and there are research papers which use that definition, and which indicate that the behaviour of the farming and dairing ants is of this kind, I'd be glad to see some details. All else is an opinion.

If you're interested in opinions here's one: there exist slave-making ants which "teach" ants of other species to work "for them", and perhaps one could imagine that "farming slave-making" ants could exist, in which case farming could hardly be considered purely "instinctive". For another opinion, I consider it  more likely that instinct is involved on a higher level, imprinting the ants to e.g. "follow other workers which are successful in bringing in food etc.", whereas the particular strategies of particular species  are "learned" by means of such an instinct.

Have you searched? If so what did you find? So people don’t waste time with repeats..

I haven't searched outside of wikipedia and links there (for example to the discussion in Origin of Species about slave-making ants).