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Why is exonuclease action an important proofreading mechanism?
My copy of the Molecular Biology of the Cell (the 5th edition, so not entirely up to date) seems to claim that exonuclease action is an important part of DNA proofreading, and that dysfunction in  this leads to an increased rate of mutation (pp 276-277).
But at the same time it specifies that exonuclease action is only useful in removing incorrect bases from DNA-primers (p. 270). That means that only the base pairs in the one primer on the leading strand would be proofread, and only a minority of the base pairs in the lagging strand (The primers are vastly more numerous, but still only a minority of base pairs will be found inside primers).
In addition, these primers are made out of RNA and are only temporary, so I can’t see why mutations in these sequences would be considered important. They are replaced with DNA-segments at the end anyway and it’s these final DNA-segments that ought to be proofread.
So how can exonuclease action be considered an important (or even vaguely relevant) proofreading mechanism?

If you could find and provide links to the corresponding sections in the fourth edition available to all at NCBI Bookshelf on line, we could check whether you are misinterpreting the text. Few of us will have a physical copy to relate to your page numbers. Otherwise decent sized quotations might help.

@David
Updated text with exerpts, this was somewhat labour intensive ^^

@David .....and those changes just disappeared somehow (different versions open in different tabs?)

You have my sympathies. Sometimes I pause in the middle of an answer or edit and... I'll have a look myself when I have a moment.

I have edited your question to change "exonucleases" to "exonuclease action". DNA polymerase has both polymerization and exonuclease action, and it is this that the section you mention is referring to. This is evident in the diagram in my answer, which is therefore confined to your main problem — confusion about the usage of the term "primer".

Without access to the 5th edition of The Molecular Biology of the Cell I am relying on the section in the 4th edition which describes proofreading, and specifically Figure 5.9, which I have reworked in a linear manner so as not to occupy too much space on the page:

If this is, indeed, the section to which the poster refers, the problem is one of misunderstanding the term primer.
The poster appears to be thinking of the priming of DNA synthesis at the replication fork by RNA — Okazaki pieces to initiate copying of the template strand. However this specific usage of primer is not that which is meant in the diagram shown. Long before Okazaki discovered RNA priming of DNA synthesis, analysis of the reaction of DNA polymerase in vitro had shown that the process required 1. A template and 2. A primer with a 3′-OH end, with which the 5′-dNTP phosphate could react. And I for one (for I am very old) taught that to students.
So what the authors are referring to is the continual extension of the DNA strand, not its initiation. And the primer is the 3′-OH end of the growing complementary strand, hydrogen bonded to the template strand.
Appendix: Historical Perspective of the usage of ‘primer’
The double-stranded structure of DNA in 1953 suggested a ‘inverse copying’ mechanism to maintain the genetic information of an organism on cell division. A DNA template was obviously assumed, but it was not anticipated that the enzymes responsible for this (DNA polymerases) would have any further requirements. It was therefore unanticipated that the DNA polymerase described by Arthur Kornberg in 1959 could only ‘copy’ a DNA template if there was already a base-paired portion of DNA on the a complementary strand with a 3′-OH end with which the dNTPs reacted. The same was true of every other DNA polymerase subsequently isolated, and contrasted with the DNA-dependant RNA polymerases, which did not have this restriction. This pre-existing DNA on the complementary strand was termed a ‘primer’, with no prejudice of length implied. For the next twenty years students were taught that the three salient features of DNA polymerase were that it required a template, a primer with a 3′-OH end, and used dNTPs. And nobody could explain how initiation occured, and more saliently, how synthesis on one of the strands occured in the 3′ to 5′ direction.
It was only in the early 1980s that the repeated generation of small stretches of complementary RNA at the replication fork provided the 3′-OH ends that DNA polymerase could extend from. The term ‘primer’ was naturally applied to these complementary RNA stretches, but (especially as the RNA was later removed) with time became associated with the fragments (Okazaki fragments) being of small size. This association was further reinforced with the advent of the polymerase chain reaction which uses small synthetic oligonucleotide primers, as do other molecular genetic techniques.
The first edition of The Molecular Biology of the Cell was published in 1983, and its authors had worked in the scientific environment of the 60s and 70s, and naturally used the terminology of that era. Perhaps writing today, they might have used a term such as “elongating strand”, rather than “primer strand”, to avoid confusing a different generation of young scientists.

Thank you for your time and effort!

Not at all. I have added a historical appendix, which puts your confusion in perspective (and makes me feel very old).


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Transplant rejection through direct allogenic antigen detection: where do the T cells come from?
I just read a chapter in Janeway's Immunology on T cell development and thought about transplant rejection. But I couldn't figure out how the t cells develop which lead to the rejection.
So in direct allogenic antigen detection antigen-presenting cells from the donor present peptides on MHCI. The T cells from the receipient then detect directly that the MHC itself is foreign. The MHC here is not digested first.
Based on what I learned about T cell development I don't understand how these t cells develop which can detect foreign MHC directly. In t cell development there is positive and negative selection. T cells which present antigens on self-MHC are selected positively and t cells which interact too strongly with self-antigen die off.
But this suggests only t cells develop which can only interact with self-MHC but not with foreign MHC. So where do these t cells come from?

Janeway's does not seem to explicitely answer your question:
A. "T cells that cannot recognize the body's own MHC molecules  (...) this process of positive selection  (...)"
B. "Lymphocytes whose receptors bind strongly to self antigens, on the other hand, receive signals that lead to their death; this is termed negative selection."
Your question refers to T cells that recognize foreign MHC.  In fact,  Janeway's does not seem to cover that situation relevant for transplantation of "allografts".
This suggests that general principles do apply:
A. Lymphocytes that do not recognize self MHC may still recognize foreign MHC.
Janeway's quote "T cells that cannot recognize the body's own MHC molecules"  - does not exclude that there are T cells reacting to foreign MHC. They would not enter the process of selection and would not be "sorted out". Your question, literally, "where do they come from" thus seems a rhetoric way to wonder a. how their existence can be taken for granted (in literature) and/or b. how it can possibly be that they have not been sorted out and died of neglect because of non binding to self MHC.
Two quotes to a. above:
From Trends in Immunology, 2016:
"Alloreactive T cells include those that recognize intact donor MHC molecules on the surface of donor cells – referred to in transplantation as the direct pathway of allorecognition – and of peptides derived from polymorphic regions of the allogeneic MHC molecules or of non-MHC proteins presented by self-MHC molecules, which is known as the indirect pathway."
Marino et al., "Allospecific T cells become activated through interaction of their T cell receptors with intact allogeneic major histocompatibility complex (MHC) molecules on donor cells (direct pathway) and/or donor peptides presented by self-MHC molecules on recipient antigen-presenting cells (APCs) (indirect pathway)".
There is no need of "presentation" on APC cell's MHC in "direct pathway". It seems consistent with the definitions quoted above to assume the existence of  allo-aggressive T cells (derived from regular lymphogenic stem cells) not binding to self MHC, thus not entering any process of "death by neglect". Put more bluntly: no fostering needed for those to remain.
Random google found this:
J J Ryan et al.(Recognition and response to alloantigens in vivo. I. Negative and positive selection ...):
"This finding may implicate other sites such as the liver where unprimed host alloreactive clones are trapped."
In that passage, if you read "unprimed" as "never got acquaninted with antigen", that quote will appear supporting the view that allo-MHC-binding T cells exist and have not been sorted out, and needed no fostering.
See also Distler et al.  "Alloreactive and leukemia-reactive T cells are preferentially derived from naïve precursors in healthy donors..." Title of paper  seems to respond to your formulation "...where do they come from?"
See also  "Between 0.1% and 10% of naive T cells within an individual are estimated to be reactive with any unique allogeneic MHC haplotype." with further reference, Brehm et al., Rapid quantification of naive alloreactive T cells...
Emphasis in quote to be set  on "naive", which might misleadingly be understood as:  not having undergone positive or negative selection. I refer on my elaboration on distinguishing "selection" and "presentation"(priming) in the very last part of my answer (more learnt then). In any case, those T cells exist and have not died.
The fact that there is "direct pathway" lays proof that, conversely, any "fostering" (survival signal) is not needed for allo-aggressive lymphocytes becoming "activated through interaction of their T cell receptors with intact allogeneic major histocompatibility complex (MHC) molecules", see quote above.
B. Refering to the "indirect pathway" and  "negative selection" (this is even more intricate, to my mind...), the sorting  out of  T-cells  which react to their specific antigen on self MHC seems to eliminate any cell reacting to that same specific antigen presented on foreign MHC by transplant cells. This is a fallacy.
Indeed, there cannot be any presentation of foreign antigen (of transplant cells)  on self APCs if, by negative selection, those specific T cells  have been sorted out. Those T cells do not exist any more.
However, the specifity of the T cell receptor is defined by a duality of signals, by the combination of MHC and antigen. The term "MHC restriction" might be misleading in that context. "Restriction" means that there need to be two signals, not just one or the other. Then,second,  specifity of the T cell receptor has been found being defined by the duality of those two signals. There is only one T-cell receptor, no two
(There is some related question at stackexchange concering "super antigens": certain antigens on certain MHC alleles - however, question of "super antigens" does not refer to the difference between iso- and allo- (transplant) antigen.)
Thus,  T cells that bind to the combination of self MHC plus antigen (possibility to immunize against transplant by presentation on self APC's MHC) may also, at the same time, react to  foreign MHC presenting that same antigen. "MHC restriction" does not rule out "homology" of T cell receptor specifity (for better understanding: antigen, not iso-/allo-MHC "determines")
To sum up, applying general principles,
a. there may be t cells recognizing foreign, not self MHC, which in lack of any binding have not received any "death signal" (cp. quote Janeway's above) and have not been sorted out by positive selection ("direct pathway").
b. negative selection does not eliminate t cells that bind  antigen presented on foreign MHC, which is consistent with duality of signal specifity of T cell receptor thus defined by a combination of MHC and antigen ("indirect pathway").
By the way, you say: "T cells which present antigens on self-MHC are selected positively..."
That should read: "T cells that react to antigens being presented on self-MHC (by APC, not t cells)..."
There is a some other question on stackexchange very much related to yours:
Understanding transplant rejection - how does the cellular, adaptive, response get underway
This question shows that it is not at all trivial to assume the existence of T cells taking foreign MHC as foreign antigen. See  quote at the very end of my answer.
Your question is a valid, my answer very much a personal one,
compare e.g.:
"Alloreactivity, defined as a strong primary T cell response against allelic variants of major histocompatibility complex (MHC) molecules in the species, has been a long-standing puzzle in immunology with some of its details remaining unclear up to now" (Nagy 2012)
Counterintuitively, "positive" selection, more than negative, might be the big exception to some rule that prohibits autoagressive killing of self MHC cells.  Conversely, to  attack cells carrying foreign MHC might be the "general principle" that needs no explanation (Interestingly, T cells are said to - in some cases - be activated by cytokines alone (interferon); interestingly, to find foreign MHC in the blood is no natural situation for human t cells - in that way, transplantation seems to imitate evolution).
Finally, here is some lengthy quote:
"Paradoxically, while T cells that obtain too strong signals from self-pMHC are removed, those T cells that survive and complete their developmental program require a productive, weaker, signal from interaction with self-pMHC to do so. T cells incapable of such signaling die by ‘neglect’ and this requirement for a survival signal from TCR recognition of self-pMHC is known as positive selection. While the experimental evidence for positive selection is overwhelming, just what this process contributes to a useful T cell repertoire has been hard to establish.", Vrisekoop et al. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4152861/
Your question seems to pertain to "death by neglect" of T cells able to respond to foreign MHC (of transplants). "Neglect" might denote nothing more than lack of survival signals; conversely only those lymphocytes able to become cytotoxic, i.e. autoaggressive,  "contribute to a useful T cell repertoire", as any anergic  T cell is no (self-!)cytotoxic killer cell which is the needed function. On the other hand, quote, "T cells that obtain too strong signals from self-pMHC are removed..." speaks in favour of MHC being recognized by lymphocytes basically as some antigen like any other: as there are T cells that attack foreign MHC there do exist - counterpart - T cells that react to self MHC even when there is no presentation of antigen. These cells, in my understanding,  "obtain too strong signals from self-pMHC" and "are removed". Negative selection discards T cells that react to self MHC if there is antigen presentation. This process does not imply the sorting out of T cells reacting to foreign MHC alone.
Cp. answer to another related question here on Stackexchange: "Why do physicians try to match HLA complexes for organ transplant?" (...)
To quote one answer: "In short, if a T cell does not find its corresponding MHC 1 complex on a particular cell, its default behavior will be to attack it." There is no contradiction to this statement assuming that foreign, non self MHC1 is the antigen the allo-aggressive T cell is "specific"; MHC1 is to be considered "antigen" (it is known that peptide parts of foreign MHC are presented on host MHC - "imagine" MHC presented on MHC...).
See comment to quote  by  User inf3rno:
"Regular T-cells (without NK receptor) seem(...) like having the same ability by not compatible MHC1, but I am not sure yet about the mechanism. I think I'll need a (week)  more to read all articles I opened and come to a conclusion about how the immune response works in this case."
Let me add one last quote I came across doing further research:
"...the closer the foreign MHC molecule is related to the T cell's MHC, the higher is the proportion of peptide-specific, alloreactive (“allorestricted”) T cells versus T cells recognizing the foreign MHC molecule without regard to the peptide in the groove. Thus, the peptide repertoire of alloreactive T cells must be influenced by self-MHC molecules during positive or negative thymic selection or peripheral survival, much like the repertoire of the self-restricted T cells. In consequence, allorestricted, peptide-specific T cells (that are of interest for clinical applications) are easier to obtain if T cells and target cells express related MHC molecules.", Obst et al.,  The Role of Peptides in T Cell Alloreactivity Is Determined by Self–Major Histocompatibility Complex Molecules
First, the formulation "T cells express MHC" bears similarity to the  wording of your question "T cells presenting antigen on their MHC" which I denounced as incorrect up above, "by the way..."
Second, I find this quotation consistent with my summing up my answer as follows:
There are a. naive T cells derived from regular stem cells that are solely allo-MHC-reactive and thus have not entered any selection process (they "just survive", direct pathway), there are b. (more intricate, indirect pathway) T cells prone to self MHC having survived selection/tolerization process that not only bind self, but also bind foreign MHC presenting antigen which there has been no tolerization for.
Let me add one quote that speaks against my answer, point A, concerning the existence of allo-aggressive T cells (for illustration's sake: "in peripheral niches")  that have not bound to self MHC and thus have not been sorted out:
"Crossreactivity seems to be an intrinsic property of the TCR required, because a single TCR must possess the ability to interact with both self-MHC during positive selection and at least one combination of foreign antigenic peptide presented by self-MHC. Recognition of allogeneic MHC molecules is an inadvertent consequence of the need for TCR crossreactivity." quoted from:  The structural basis of T-cell allorecognition, A Whitelegg 1, L D Barber, 2004
This refers to any T cell  in need of "survival signals". My answer, point A., argues that during positive selection non- (to modify my answer: too weakly) binding lymphocytes remain non fostered which does not lead to their vanishing (only non tolerant lymphocytes to  receive "death signals").
On the other hand, this quote speaks in favour of point B ("more intricate", see above): T cells that tolerate self antigen might, by "cross-reactiviy",  become cytotoxic when presented same antigen on foreign, non self MHC of allograft.
Your question - there are related ones on Stackexchange - turnes out to be some exiting one. Point A, above, is basis for debate. Here is some empirical study, corroborating my point of view: it is "not natural" for T cells to attack cells of their "own body" (self MHC). The point of "positive" selection, i.e. "nurtering" is, to find auto-aggressive T cells, or even T cells that bind to self MHC. Thus, it becomes natural that T cells that bind - aggressively - to foreign MHC survive non binding self MHC. Positive selection searches for auto-immunity (self MHC cells infected by virus, cancer cells shall be bound to); there is no natural counterpart in the negative.
Here's the quote:
"These findings suggested that the clones recognized determinants on H-2Kb that were independent of peptide.", P A Smith, Brunmarck, Potter, Peptide-independent recognition by alloreactive cytotoxic T lymphocytes (CTL), 1997
This was from 97. More and more as time goes by, from 2017, encore:
"NKT cells—originally defined as cells that co-express key natural killer (NK) cell surface markers and a conserved αβ TCR repertoire—are thymus-derived, innate-like T lymphocytes. The functions of NKT cells are controlled by self and non-self-lipid agonists presented by CD1d molecules.." from: Natural Killer T Cells: An Ecological Evolutionary Developmental Biology Perspective, Amrendra Kumar et al.
Some  reference that speaks against subsets of T cells acting like NK cells would be  Uzhachenko an Shanker (e.g.) say:
"By contrast, NK cells lack antigen-specific receptors but express (...) inhibitory and activating receptors that bind various ligands including MHC and like molecules. A highly calibrated maturation enables NK cells to eliminate target cells with lowered or absent MHC-I or induced MHC-I-related molecules while maintaining their tolerance toward self-MHC
It seems some open question if there is a full spectrum that fills the gap between T cells that undergo positve, negative selection and Natural Killer cells that just do not (but need maturation). As I  understand quote from 1997 above  those T cells may need  presentation of MHC antigen to become alloaggressive. Now, trying to  explain in a fast,  illustrative way: Corresponding to presentation  of foreign MHC peptide on self MHC there should be foreign MHC peptide presented on foreign MHC of the allograft cells to attract the activated Tc cells.  However, presentation of graft MHC as antigen on foreign graft MHC just does not exist,     does not seem to  make sense. Why should the allograft cell present its own MHC on its own MHC? How do host T cells "come on" then?
So the "priming" in that case of "transplants" very much appears as a process of clone expansion. I think it is very surprising to see the "fostering by non neglect" in "positive selection" as a very early priming (not even sure, it's seldom heard I guess to speak of "priming" when dendrite present antigen as APC in lymph nodes) of sought of "rare" - according to my view - potentially self-aggressive self T cells. It's coherent with literature to assume that there are T cells entering "late positive selection" which is nothing else than being presented with foreign MHC peptides - in that case of transplants - by self APCs (or foreign APCs, by the way, no difference).
One more quote to this, from 1991:
"The high determinant hypothesis emphasized the implication of direct contact between the T cell receptor and the MHC molecule; the multiple binary complex hypothesis envisages that alloreactive T cells are specific for self peptide bound by the foreign MHC molecule." From: The molecular basis of allorecognition of major histocompatibility complex molecules by T lymphocytes, G Lombardi 1, R Lechler
It's a possibility that  - according to a basic underlying principle - there are groups of T cells that react cytotoxically to foreign MHC cells without those presenting any peptide - as they bind to foreign, not self, MHC. No sorting out for  "NK T cells" (as NK cells).
To end up I'd like to illustrate: a memo square in "Immunology for dummies", German version, states: for graft rejection to occur  there must be antigen presenting cells  of the host, and this needed no explanation. How could cells presenting on host MHC even contact graft lymphocytes if graft's presenting cell had eliminated any lymphycyte that "does not recognize graft's MHC" in the sense: hence, recognizes any future host's MHC? This is paraphrasing your question and showing why it is a valid one.
To sum up my answer:
In positve selection, there is presentation of antigen; lymphocytes with low affinity to self MHC ("MHC restriction" must not be taken for "restriction to self MHC, it means combined, dual signal) will not be fostered.
In negative selection, there is presentation of self antigen (paralleled: not only antigen, as in positive selection there is not only MHC); lymphcytes with low affinity to self-antigen - are not killed (reverse parallel: in positive selection lymphocytes with low affinity to self-MHC are not killed; this is difficult to find reference, see above).
My hint from a learner's perspective:
Basis is "cross-reactivity" made possible by "MHC restriction" which does not mean restriction to self MHC, but does mean "homology" of dual signals.
When reading about positive selection try to "catch the eye": is there antigen presentation (or "showing self-MHC" and sorting out only, misleading).
When reading about negative selection have an eye on lymphocytes surviving because of their "low affinity" to: antigen (or is there sorting out only of antigen avid lymphocytes, misleading).

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What is the name of this mosquito-like insect?
While I was studying, this insect fell down from the ceiling. It was alone and not in a swarm. It looked much like a mosquito but is quite larger compared to a mosquito..
I live in the Indian subcontinent (India).

Can anyone identify it??

It is a Crane fly (Tipulidae), which is a large, cosmopolitan family of flies in the order Diptera (true flies). There are about 15,000 species according to Wikipedia and some 500-odd genera.
The crane flies are sometimes known as "daddy longlegs" though this name is more commonly associated with arachnids in the order Opiliones. Both the harvestmen and the crane flies have long, jointed legs. Crane fly legs fall off fairly easily, so if you brush one off a curtain or your clothes, you are often left with a loose leg.
They are harmless, despite appearing like a giant mosquito. They like damp environments, but can be found almost anywhere there is pasture or forest nearby. They typically need a fresh water source or moisture for the larvae to mature.

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What species is this fly? Look like mosquito with unusually long legs
I found this in Bangalore, India. It looks exactly like a mosquito but with extremely long legs, first I confused it with long legged spider (which are common here) but it's not, Can someone tell me what it is?

Welcome to the site, the insect is too small and blurry in the picture to make out. For ID we ideally need several high quality photos of the organism of interest. Having said that, looks like it might be a crane fly.

Crane flies look like larger, long-legged cousins of mosquitoes, but are beneficial insects, and harmless to humans. Look for pictures of crane flies in your region and see if it resembles te critter you saw before it became...smooshed.


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How is it determined whether a chromosome is maternal or paternal for imprinting?
For imprinting, how does the cell determine which chromosome is maternal and which is paternal? For example, in the parental imprinting of insulin-like growth factor 2 (Igf2) on chr7 (autosome), how is it determined which is paternal and to be imprinted?

Imprinting occurs via DNA methylation in gametes. Different parts of the genome are methylated in either eggs or sperm, and this then marks those genes throughout the lifespan of the organism, inherited epigenetically across cell divisions. See:
Wood, A. J., & Oakey, R. J. (2006). Genomic imprinting in mammals: emerging themes and established theories. PLoS genetics, 2(11), e147.


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Tribes outside humanity
All humans are a group with common ancestry but some humans distinct themselves into sub-groups by "distinctive ancestry" and tend to ask other humans "where are you originally from" as to get a satisfying answer about the other side's "distinctive ancestry".
Asking for a precise meaning of this vague question might bring different "exact" versions such as "where were you born?" (some people were born in a ship or an airplane) or "What is your country"? (some people don't affiliate themselves with any country / "stateless") but in the end it generally boils down to "distinctive ancestry".
Is this tendency of many humans to classify other humans into these groups of two or more families with a "distinctive ancestry" (but not by the general group of humanity and not by nuclear family) exist in animals (of course, not by asking "where are you originally from" but with much more simple or "primitive" ways of communication)?
Do cows/lizards/sheep/squirrels/cats, etc. have a similar classification mechanism?

Do you mean as wolves do?

Welcome to Biology.SE. As written essentially any animal with even the most rudimentary social structure (e.g. anything that forms pair bonds for a breeding season) would fit your criteria. Questions on this site are expected to be focused, clear, and demonstrate evidence of prior research (see [tour], [ask], and other [help] for details). In addition, questions that would seem trivial to biology professionals (such as this) are considered "homework" — please read the rules for such questions and [edit] or delete your question accordingly.

Question broadly edited.

Any of the ungulates, felidae, canids, most schooling fish and social insects still fit the description as I read it.

@bob1 I know that wolves and birds pack themselves into groups / migrate but I don't know if this must be based on some "middleground ancestry".

Also, human "tribes" are often not about shared ancestry, but shared beliefs: religion, fans of sports teams, being a supporter of a certain former US President...

@jamesqf 100% but these are not "at minimum" or at least don't bring a question such as "where are you originally from".

@al-harumi-jidan - but to the best of our knowledge neither do animals, other than recognizing a "foreigner" by scent or sight, AFAIK most animals don't have the mental abilities to think more than "us" and "not us"

@al-harumi-jidan: Because "Where are you originally from?" is not usually relevant to those kinds of tribes.

It seems like your underlying question may be more psychological/social than biological. If you want to know why some people seem obsessed with labelling  people who don't look like them that really doesn't belong on this site. To make this a biological question, you probably need to find a word that doesn't carry the connotations that "tribe" has. For example, are you interested in the question if you replace tribe with something like extended family group? If you are then do some reading based on the multiple hints above and rewrite accordingly. If not please delete it.

@tyersome My question is about biology; I have described a phenomenon common between humans and want to know if there is anything near to it with animals. I think you would need to excuse me from not knowing which term to use instead tribe (which is obviously the nearest thing I could come with). Non registered users can't delete questions and I would not have deleted the question even if could !

Historically distinct human ancestry was to a large extent due to limited mobility (although also some assortative mating) - this has been changing obly in the last few decades, and mostly in developed countries.

Your problem is questions like "were were you born?" require adaptations and concepts that to do not appear outside humans in extant animals. The very idea of a question is a human thing. you may however be interested in the tribal behavior of chimpanzees. https://scholar.harvard.edu/files/glowacki/files/wrangham_glowacki_2012_warfare_hunter_gatherers.pdf


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How do non-ionic polymers help precipitate proteins?
Some non-ionic polymers (e.g. chitosan and polyethylene glycol) are also commonly used as protein precipitating agents. What is the principle of protein precipitation resulting from the addition of these polymers? Is this type of precipitation reaction a reversible or non-reversible precipitation?

Perhaps a bit too technical, but would this answer your question? At least in part?

Two interpretations of such precipitation events have been proposeda while ago according to the paper above: attractive depletion (Asakura & Oosawa, 1958) and excluded volume (Iverius and Laurent, 1967, Polson, 1977). These are discussed there too!

Protein precipitation by these non-ionic polymer is based on the principle of steric hindrance. These polymers compete with proteins (Mahadevan, 1992) for space in the solvent. Congestion caused by the physical presence of surrounding polymers force the proteins to exclude from region occupied by the polymers and concentrate together until their solubility is exceeded (Atha & Ingham, 1981). In this case, protein precipitation occurs.

"Steric hindrance" is usually invoked in the context of molecular shape as it relates to chemical or enzymatic reactions, i.e. how the relative organization of atoms in a molecule constrains the shape space of that molecule. I'm not sure if it's the right term to use in discussion of this system, but I'm open to differing opinions.

Moreover, your answer could be improved by replacing some of your terms with more concrete explanations of the physical interactions. Re: what electrostatic phenomena underlie polymers competing with proteins and congesting the solvent space? There is also a minor logical jump from exceeding solubility to protein precipitation that could be addressed.

@acvill - yeah, this is mechanism is molecular crowding, not steric hindrance


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Transpiration and Water Uptake
I know that water moves into the root hair cells from the soil via Osmosis down the water potential gradient and then this water travels through diffusion and osmosis through the symplast pathway reaching the base of the xylem vessels. But there isn't any movement of water through the apoplast pathway. So I am thinking that the water also moves in between the cell walls of root hair cells without crossing the cell membrane and hence by diffusion and then takes up the apoplast pathway. Am I correct? Because in my book, it is mentioned that water goes in by osmosis and nothing is mentioned regarding diffusion. Someone please clarify this.
Thank you

Investigate tight junctions...

water goes in by osmosis and nothing is mentioned regarding diffusion. Someone, please clarify this.

You'll need a good understanding of the difference between osmosis and diffusion for this.
Osmosis is a special kind of diffusion.
The only difference between the two is the molecules that are carried. Diffusion is used to transport solute molecules, whereas osmosis is used to transport solvent molecules (in most cases water). In both situations, until equilibrium is reached, the movement is from a higher concentration gradient to a lower concentration gradient.

Regarding the movement of water through the various pathways.

I'm quoting this directly from the Plant Physiology book (Taiz and Zeigner). Please refer to the same for more information.

In the soil, water is transported predominantly by bulk flow.
However, when water comes in contact with the root surface,
the nature of water transport becomes more complex.
From the epidermis to the endodermis of the root, there are
three pathways through which water can flow:
the apoplast, transmembrane, and symplast pathways.
In the apoplast pathway, water moves exclusively
through the cell wall without crossing any membranes.
The apoplast is the continuous system of cell
walls and intercellular air spaces in plant tissues.
The transmembrane pathway is the route followed
by water that sequentially enters a cell on one side,
exits the cell on the other side, enters the next in the
series, and so on. In this pathway, water crosses at
least two membranes for each cell in its path (the
plasma membrane on entering and on exiting).
Transport across the tonoplast may also be involved.
In the symplast pathway, water travels from one cell
to the next via the plasmodesmata. The symplast consists of the entire network of cell cytoplasm interconnected by plasmodesmata.

Please follow the three pathways in the image to get the insights.

Thank you so much!!


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Does using the human genome as a reference influence the chimpanzee genome's similarity to the human genome?
It is often stated that human and chimp genomes are 98% similar, e.g. this is included in an article on the American Museum of Natural History website.
I also see in the release notes for the NCBI chimp genome:

Contigs were assembled using the human genome as a guide, and are therefore "humanized" in their construction. This is an important distinction, as some sequences, such as insertions, deletions, and gene duplications, may not be accurately represented by the current chimpanzee assembly.

So, does building the chimp genome using the human genome as a scaffold affect the figure of 98% similarity? If so, do we know how much?
(A previous question on this list mentioned a 2018 assembly independent of a human scaffold. Has this resulted in any revision of the figure?)

@David I fixed the link, chopped an 's' off the end.  Perhaps the question I linked to has the answer I am looking for, but the technical language is beyond what I know.  I cannot derive a 'yes' or 'no' from the answer to that question, nor understand if 'yes' to what degree.

I have edited your question so that it appears as a valid independent question, not starting with an oblique reference to another question. I have included that at the end. I have also tidied up the presentation of the links so that the text is more readable.

The similarity IS high
The main thrust of the question is the high similarity (98–99%) between human and chimpanzee genomes. The concern is that the use of the human genome as a scaffold for assembling part of the chimp sequences in the whole  chimp genome project, published in 2005, is a possible source of error in this figure so that the similarity is actually signficantly less.
The answer is an unequivocal NO because:

The high similarity was known before the chimp genome project was published.

The figure refers to comparable portions of the two genomes, excluding insertions and deletions. The use of the human genome as a scaffold only introduces uncertainty into the latter, not the former, as will be explained in the next section

Thus, even before DNA sequencing, DNA hybridization methods indicated an approximately 98.5% similarity of single-copy DNA. As one would imagine, before the technology for whole genome sequencing was developed many individual chimpanzee genes were sequenced using ‘traditional methodology’ that depends on mapping and constructing overlaps, and only subsequently comparing the sequences with the corresponding human genes. This methodology also revealed insertions/deletions of the genomes relative to one another, and led Britten to estimate on overall similarity of 95%, with 1.4% divergence due to base substitution and 3.4% difference due to insertions and deletions. Furthermore the whole of chimp chromosome 22 was determined without reference to the human genome. Finally, in the whole genome sequencing project, part of the sequence was determined assembling the shotgun fragments both with and without use of a human scaffold in order to validate the former approach.
The use of the human scaffold does NOT prejudice the base reads
Comments to my initial answer on this point and my assertions in reply appear not to have been understood. I have therefore constructed a diagram (below) to explain this more clearly.

The left-hand side of the diagram shows a much simplified schematic of steps in ‘traditional’ directed sequencing. This can start with a focus on a particular gene or region of the genome from which large clones (BACs or bacterial artificial chromosomes were used for chromosome 22) and, after mapping, smaller overlapping fragments were generated, sequenced, partially assembled and further overlapping fragments generated and sequenced. In this way the assembled sequence is gradually extended. When complete (it may be joined by overlap to other large fragments) it is compared with the corresponding region of the human genome and base differences, insertions or deletions noted catalogued.
The second approach, using a human genome scaffold, relies on, and is justified by, the prior knowledge of the very high similarity between the two genomes. The approach here is to generate and sequence millions of random fragments, but as they are small the overlap tends to be small and not unique in the way that they are in the directed approach. Thus the second step is to arrange these small fragments in groups by their similarity to the human genome. I emphasize that this is done — as it must — after the chimp fragments have been sequenced. What this step does is place the fragments at co-ordinates on the human genome so that they can be located relative to one another. That’s it for the human genome — the method doesn’t need it any more. The placed fragments are then stitched together computationally into an assembly on the basis of small overlaps that would not have been meaningful without the initial alignment. Because of chimpanzee polymorphism there will be redundancies at particular positions. I read in the supplementary data to the paper that if this was greater than two, the situation would be reviewed for artifacts and dealt with.
As the disclaimer the poster quotes makes clear, the use of a human scaffold can miss duplications, but it cannot and does not change the chimp base calls. One of the key reasons for sequencing other primate genomes is to have a precise knowledge of how they differ from ours. It would have negated the whole purpose of the project (not to mention being unethical) to choose between two possibilities on the basis of which was the same as the human (as the poster suggested might occur). This was not done. Problems with the data were subject to rigorous critical review. If the sequence of a region was uncertain it was marked as such.
And, of course, having this initial sequence allowed the uncertainties regarding insertions, deletions and duplications to be specifically addressed in subsequent work.
Appendix: The 2005 report in context
The paper describing the “Initial sequence of the chimpanzee genome and comparison with the human genome” was published in 2005. It is 18 pages long (plus appendices) and contains no sequence data and was the work of a consortium of about 70 highly skilled workers at 24 different institutions with a spectrum of different skills, including informatics and statistics. There is no mention in the abstract of the overall percentage similarity, which was already known. This work was preceded by other work on this topic over a number of years (as mentioned) and was not intended as an end in itself — it was intended to lay the foundations of further work to find the effects of the differences between chimp and human genome of the type discussed in the more recent paper mentioned in the question. Work of this type has been assisted by the vast technological advances that have occurred over the last 16 years. This is the way contemporary science works.

I have now revised my answer completely. I have therefore deleted all my responses to your previous comments. This should suffice.

Thank you very much! I probably need to rework my question to make it clear where I see a specific technical problem as I'm afraid I still don't understand from your answer how they avoid the source of bias I pointed out in my previous responses.

To elaborate, in the arrangement step, they start with a bunch of very small pieces, many of which have errors.  An error that matches the human genome will produce a better alignment score than a piece without that particular error.  Since they don't know beforehand which pieces have the errors, how do they make sure they are only aligning error free segments?  If they cannot say which pieces are error free, then I fail to see how the alignment step avoids the bias problem I point out.

A second, related, issue is that with many small pieces, even without errors, there is the possibility that pieces from entirely unrelated portions of the chimp genome are aligned to the human genome because they get better matches.  I am also curious how they avoid this source of bias.

@yters 1. The fragments selected from the BLAST alignment will have a cut-off that allows for the human-chimp divergence, e.g. 95% identity, so WILL also include fragments with random errors in whatever direction. No chimp fragments will be excluded. The assembly is done after the fragments have been positioned. Because of the multifold (e.g. 10X) coverage, random errors will show up as e.g. 1/10 and be discarded, regardless of their relationship to the human genome. 2. Pieces from other regions of the genome that BLAST matches will represent duplications, for which bias is a admitted.

So it sounds like there could be a bit of bias at the nucleotide level from using human scaffolding, but I suppose you are claiming it is not significant enough to affect the similarity score.  I understand there are alternate ways the similarity has been calculated, which also show a very high similarity, but I'm interested in focusing just on the nucleotide to nucleotide comparison.  Has anyone attempted to calculate how much bias could be introduced by the errors and duplication?

@yters — Error frequency is generally estimated and quoted in such papers. For details you would need to check the original — which, incidentally I highly recommend, even if you don't understand the details. As I mentioned, the differences between the human and chimp caused by duplication etc was estimated by Britten. But, as I keep saying, the percent difference between chimp and human is known independently of the whole genome project paper which did not even report it and any numerical changes from subsequent correction of mistakes are minuscule and of little interest.

Thanks, I really appreciate the time you put into this question and researching it.

I see in the 2005 paper it says "About 98% of the chimpanzee genome sequence has quality scores of at least 40 (Q40), corresponding to an error rate of ≤10-4." So, I think that answers my question about whether base errors can create bias.  If each read is 100 bases long, and each read is duplicated 10 times, then the Q40 number means the expected number of errors is 0.1 per section read, if I am understanding correctly, which means adding only 0.1% bias in the worst case scenario.  That does seem insignificant.  Please correct me if I am misunderstanding.

You can look at the sequence similarity between homologues yourself.  Here's just one example.
http://uswest.ensembl.org/Homo_sapiens/Gene/Compara_Ortholog/Alignment?db=core;g=ENSG00000138650;g1=ENSPTRG00000016444;hom_id=55568071;r=4:133149294-133208606;seq=cDNA
Those sequences are 99% similar, and that's not because they used human reference a assembly guides.  It's because the sequences really are that alike.

Are you saying this chimpanzee sequence was not assembled using a human reference?

The base by base alignment of that those homologous genes is not affected by the use of any reference-guided assembly which might have been used to stitch larger pieces together.

The chimp genome is 3 billion bases long, so there are 6 to 30 million pieces in that case.  Additionally, my understanding is there is a fair bit of error in the piece generation.  In that scenario, it isn't obvious to me using a human reference won't bias piece selection.


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How do farmers tell if their fruits are sweet without eating them?
A relative of mine tells me that when she goes to buy fruits, she asks the vendor if the fruits are sweet. Surprisingly, the vendor is able to tell (the vendor is apparently willing to divulge this information because my relative is a long-time customer of the vendor). In turn the vendor gets the information from the farmer.
How can the farmer tell if their fruits are sweet without eating them? The only thing I can think of is they eat a very small batch, e.g. if they produce 100 apples then they eat one and use that to infer if the remaining 99 apples are sweet - but can we say with certainty that if one apple on a tree is sweet, then all the other apples on the tree (or on the farm, even) must also be sweet? If we can, what is the biological basis for this inference?
If this is not the method farmers use, how else can the farmer tell if their fruits are sweet without eating them?

What exactly do you mean by "sweet"?  Are you using it as a synonym for ripe?  There are many ways to tell if fruit is ripe - color, whether it's hard or soft to the touch, how it smells, and so on, and these vary by the type of fruit.  It's simply a matter of practice.  If you mean sweet, that will also depend on the type of fruit: a good number aren't - quince, for instance, or cornelian cherries. (Making a batch of jam at the moment, and you have to add quite a bit of sugar to make it palatable.)

@jamesqf "sweet" is not ripe; it means one of the five basic taste sensations. If you are concerned about how some types of fruits might not be sweet, then narrow the question and consider only apples.

In the case of apples, you know the sweetness (and other characteristics) primarily by variety - cooking apples will be less sweet than eating apples, and crabapples are distinctly tart.  Another factor is ripeness, which for apples you usually judge by the skin color, and somewhat by the season.  As a grower, you have learned that for instance your Red Delicious apples are ripe in October.

A relative of mine tells me that when she goes to buy fruits, she asks the vendor if the fruits are sweet. Surprisingly, the vendor is able to tell (the vendor is apparently willing to divulge this information because my relative is a long-time customer of the vendor). In turn the vendor gets the information from the farmer.

Whether a fruit is sweet is not a classified information: a good groceries store would typically offer several types of the same species of fruit, depending on their sweetness, crunchiness, how long they can be conserved, etc. This is in order to suit the tastes of the customers (not everyone likes extremely sweet apples that desintegrate in your mouth), their purposes (eating raw, making jam, cooking purée for a baby), etc.
How do they know? The varieties of fruits with different tastes are a result of breeding, just like different varieties of cows, dogs, etc. It is not uncommon to see charts like this one.

Does this mean that all apples of a specific kind (like "Ginger Gold") will taste the same? If so that's certainly something I never noticed, will pay more attention next time.

@Allure they will not all taste exactly the same, and on occasion one may encounter a bad batch. However, in comparison with other varieties, the taste remains more or less uniform.


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What morphological traits can be used to diagnose members of the Eucalypteae?
I read the Wikipedia article on Eucalypteae and it doesn't actually say what these plants have in common.
(I am now reading through https://bsapubs.onlinelibrary.wiley.com/doi/pdf/10.3732/ajb.1200025 and I think I've found the answer to this question.)

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

In particular, what all taxonomic groupings have in common is an ancestor — however, this definitely falls under the category of "trivial to biology professionals" and so is a "homework" question. If that isn't the question you are trying to ask, please [edit] to clarify what you do want to know and to demonstrate your prior research effort.

Wouldn't that be all clades? With taxonomic groupings also being on the basis of traits?

Well, I'd say it is more a matter of inference  — what we care about is the evolutionary history. If we were to find that one group of eucalypts had a different ancestor, then those plants would be moved into a new group. The traits (now primarily based on DNA sequences) are the evidence used to determine relatedness — my understanding is morphological traits are now primarily field marks for diagnosing to what group an organism belongs. ——— At any rate, it seems your question is more about common traits, so I think it would be helpful to edit your question's title and body to emphasize that.

I've edited your title to something that seems clearer to me — please make additional changes if I'm still not understanding you correctly, or if you prefer a different wording.

If you're reading now the article that you link to in your question and you think it answers your question, then perhaps you might consider accepting my answer which linked to and quoted the same article (before you edited it into your link).

Couldn't find the place to click it. Much appreciated.

Have you had a look at the APG website ? http://www.mobot.org/mobot/research/APweb/orders/myrtalesweb2.htm#Eucalypteae it may give some interesting information ...

It's a slightly tough question that can't be answered with a simple "they share X characteristic in common". It's more that some of them share a characteristic, and some of those share a characteristic with another load of species within the same sub-clade, and some of the characteristics they have are shared with some more... etc.
The American Journal of Botany puts it:
(Synapomorphy: a shared trait believed to have been present in a common ancestor.)

Currently, no unambiguous morphological synapomorphies have been confidently  identified as defining the Eucalypteae in comparison to other
Myrtaceae (however, see Wilson et al., 2001 , for some possibilities).
Within the Eucalypteae, however, subclades are defined by
synapomorphies. For instance, Angophora Cav., Corymbia , and
Eucalyptus share several possible synapomorphies, such as presence of
oil glands that protrude above the surface of the epidermis (“emergent
oil glands” of Ladiges, 1984 ).

These are modified into distinctive
bristle glands in Angophora and Corymbia ( Johnson, 1972 ; Ladiges,
1984 ), which are a unique synapomorphy for the Angophora - Corymbia
clade ( Ladiges et al., 1995 ; Wilson et al., 2001 ). Angophora ,
Corymbia , and Eucalyptus are also characterized by having compound
petals and, in Eucalyptus, a portion of the compound petal is usually
modified into a staminophore, or stamen-bearing tissue ( Drinnan and
Ladiges, 1988 , 1989a , b ,  1991a ).

Other characters are apomorphic
but are likely homoplasious, having arisen more than once within
Eucalypteae. For example, some Corymbia and Eucalyptus species are
characterized by the presence of calycine and/or corolline opercula,
or cap-like perianth whorls that are deciduous from the flower at or
prior to anthesis (e.g., Johnson, 1972 ; Hill and Johnson, 1995 ;
Boland et al., 2006 ). Opercula likely have separate origins in these
genera ( Ladiges et al., 1995 ; Parra-O. et al., 2009 ). A caducous
calyx that usually leaves a scar on the flower bud (see Johnson, 1972
; Boland et al., 2006 ) is also an apomorphic but homoplastic
character within Eucalypteae, being a synapomorphy for a clade within
Corymbia ( Ladiges et al., 1995 ;  Parra-O. et al., 2009 ) and having
arisen at least once on the stem of Eucalyptus subgenus Symphyomyrtus
( Fig. 1B ).


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COVID-19 exposure risk from passing joggers versus walkers
What is the COVID exposure risk from passing close by someone who is jogging relative to passing close by someone who is walking?
The reason I ask is with regard to going out for exercise, or to run errands: going out early in the morning means passing fewer people, but a larger percentage will be joggers. I'm trying to figure out whether there is an overall risk reduction, whether early morning is safer than the middle of the day.
I have only been able to find answers to adjacent questions:
'Either way, the risk is low outdoors versus indoors.'
Right. But what's the relative risk between these two low-risk outdoor events?
'Ideally, you should keep 4.5m separation from joggers.'
Ideally yes, but as it turns out, sidewalks are not 4.5m wide.
'We don't have enough data to be sure.'
Right. But decisions have to be made based on the best currently available guess. What's the best currently available guess for this? 1.1x? 2x? 5x? 20x?

This is a well-worded question, but I imagine there is no research that will give you the precise answer you seek. There are a multitude of variables, each of which is hard to control and provides minimal useful insight: relative viral shedding of a runner v. a walker due to different rates of respiration, the differences in turbulent airflow caused by running v. walking, etc. Moreover, the applicability of results obtained from such a study would be constrained to situations where environmental variables are similar: temperature, humidity, wind, inter-individual variability in viral load

I agree with @acvill, you might see papers looking at 1 of the variables each, but it would be very hard to do it all in one study.

Questions relating to medical advice are off-topic on biology. You might get an answer on SE Medical Sciences, but there are many reputable sources of information on this topic on the Internet (see the Meta article).

@acvill Sure, I'm aware there is no precise answer, like I said, I don't seek one, just a best guess to an order of magnitude.

@David This is not medical advice, and there are plenty of not purely theoretical questions on covid on biology. As I said, I have searched the Internet, and found nothing that addresses this question, only the adjacent questions I mentioned. Which Meta article are you talking about? The ones showing in 'featured on meta' in the top right, are on completely different topics.

The Meta article is here and was a response to the "plenty…questions" that on covid which were imho not on topic here, and for which this  forum is not a place to get the most informed information on a topic for which answers intrinsically constitute medical advice.


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What is the dynamic range under initial conditions?
could someone help me to understand the following sentence better?
It's from the book "A Practical Guide to Assay Development and High-Throughput Screening in Drug Discovery".
And it's about fluorophors used in FRET-assays, for screening of protease inhibitors.
"In contrast to many other FRET dye pairs, both EDANS & DABCYL and Mca/Dnp generate a dynamic range between cleaved an uncleaved substrate, sufficent for the application of such protease assays in HTS and high-throughput compound profiling under initial conditions. "
I'm confused about the last part of the quote "under initial conditions".
What does that mean?
the question summarized "What is the dynamic range under initial conditions? "

I think that they mean initial profiling as the profiling/screening is the subject of the clause.
In this case it would mean that FRET with these compounds has enough difference between cleaved and uncleaved that you can use this difference to tell if it has inhibited or promoted a reaction between your target and its substrate or not in a quick/high-throughput assay for mass screening of potential inhibitors/promoters.

I've read that its common to do HTS screening first with an easy and cheap assay.
Afterwards more complex assays follow, which sort out more substances.
So "initial" in this case would mean, something like: "the first assay to screen for substances?"

@Mourinho_1 that's how I read it.

thanks a lot. I did not consider that it could mean something like this. I would say that this sounds plausible


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Can mrna spike protein block other proteins entering cells?
When vaccinated with pfizer a mrna is injected which eventually creates spike proteins. These will bind to cells. Now there is a rumour that when these spike protein binds to cells it can block other important proteins from binding to that cell. Is this true? Can someone debunk this.

I’m voting to close this question because this site doesn’t exist to debunk rumours about things that do not happen, but to answer questions on biological problems about things that do happen.

Skeptics.SE exists for just this sort of question. As with any SE site, search for a similar question before asking.

Short answer: No.
What I am going to do here is some back-of-the-envelope style calculations and a bit of explaining, so bear with me...
The way that these vaccines work is by causing the mRNA to enter the cell, where it is translated into the encoded protein sequence. This is then translocated to the surface of the cell and in some cases into the extracellular space (ref 1; see figure 2).
This means that some of the protein produced is floating around and could bind to a cognate receptor on another cell (or even on the surface of the cell it came from, in which case it won't go any further). However, in the case of the spike protein, this receptor is the Angiotensin converting enzyme-2 (ACE2) protein, which is a receptor for Angiotensin II. In a natural infection it is thought that the levels of spike protein (ref 2) produced by the replicating virus are high enough that it prevents the normal function of ACE2 and enhances damage and further infection.
We (by that I mean I, myself) don't know what proportion of the expressed protein is released from the cell into the extracellular space, but based on my experience in the lab using similar methods for DNA transfection, it will only be a small proportion of the protein produced. It may be that this information is known or it may be proprietary, but I would be willing to bet it is less than 50%, and maybe much lower.
We do know the sequence of the mRNA in the vaccine and can make at least some order-of-magnitude estimates of the number of RNA molecules in a dose (30 micrograms for Pfizer, or about 0.5 ug/kg body weight, assuming 60 kg average body weight per person). Not all of these molecules will be fully functional - some will have manufacturing errors that terminate the protein early, some won't be packaged properly, some will be degraded during preparation, some won't make it into a cell, etc.. However, we can assume about 1-10 trillion (1-10 x 1012) molecules, which as it turns out, is about the 10-100 times the number of viral genome copies that your lungs produce at peak infection (ref 3; see fig 1). Now, if we assume that each produces a single protein before being degraded, we have a corresponding 1-10 trillion protein molecules.
This sounds like a lot, but rest assured that this number is tiny in terms of what we are looking at - there's about 1021 sugar molecules in a teaspoon of sugar (4.2 g/teaspoon, molar mass sucrose = 342.3 g/mol).
Now, back to the virions. If we assume that each one of these genomes produces a virion (whether functional and infectious or not), and that each virion contains 24 spike trimers (ref 4), or 72 individual spike proteins (24 trimers x 3 spikes per trimer), then we have roughly the same number of spike proteins produced by the virions as by the vaccine, and we know that the virus can do some damage via this route (see ref 2). So, in theory, we could produce enough protein to effect some damage to your cells.
The other major variable here is the amount of ACE2 in a cell - I don't think this can be quantified easily. It is known that some cell types have more than others, but in terms of molecules per cell, it is unlikely to be static and would be very very hard to determine. This means that maybe there are only 10 (very unlikely, it is an important molecule) or maybe there are millions of molecules per cell (also unlikely). If we take a number somewhere between the two - lets say 100,000/cell (105/cell) - that means we would need 107 (10 million) cells to mop it all up. There are about 4-6 million cells in a ml of blood, so we would need about 2 ml of blood to cope with that. I can also say, just to give you some sense of scale, if you clumped the cells together, 10 million cells is about the size of a large drop of water while it is hanging.
However, it's not that simple in any biological system, these sorts of things have kinetics of production, so we wouldn't produce all that protein in one big hit. Here's some known kinetics (ref 5; see fig 3) for a test of these sorts of vaccines, which shows that about (I estimate) 50% of that protein is produced within a few hours and then tails off over the next day or so.  Indeed these people (ref 6) showed for their experimental spike vaccine version, that the vaccine peaked at 12 hours and was gone 48 h post injection. Spreading the production out means that the body has time to produce more ACE2, minimizing the affect of the spike production. Some (as I mentioned before) won't make it out of the cell or won't be released into the extracellular fluid. The vaccine particles are also spread via the blood, so the effect is not localized and any effects somewhat diluted because of that.
Whatever actually happens, we know that this type of vaccine has almost no short-term serious side effects, and is very unlikely to have longer term effects too. The vast majority of people experience a sore arm for a day or so and maybe some other symptoms (aches, tiredness, fever), almost all of which can be attributed directly to activation of the immune system.
So, the (very) long and short of it is - while it is plausible that this vaccine could IN THEORY produce enough protein to block the normal function of ACE2 in some cells, we don't see this happening in real life for a huge number of reasons.
References:

Park et al. Int J Biol Sci. 2021 17(6):1446.
Sriram and Insel. Br J Pharmacol. 2020 Nov;177(21):4825-4844
Sender et al. PNAS.  2021 Jun 22; 118(25): e2024815118
Ke et al., Nature. 2020 588:498–502
Pardi et al., J Control Release. 2015 Nov 10; 217: 345–351.
Zhang et al., Cell. 2020 Sep 3; 182(5): 1271–1283.e16


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Electrodes in non-conducting fluid? Are they neutral? Electrolysis, Electrophoresis
I'm a moleculary biology student and have to do a detailed presentation about SDS-PAGE for my next lab.
So I was currently trying to understand the physics of electrophoresis and electrolysis. Since I was never very good at physics I wanted to make sure I understand it correctly:
Am I right in saying, that if I have two electrodes in a non-conducting fluid, that no current will flow and that thus the electrodes are not actually charged but neutral? Since if you have a normal current with a metal wire, current also does not flow, if you have a gap in the wire. The electrones are not "waiting" and the ends of the wire, if you know what I mean.
So the electrodes are uncharged, right? But if I would take salt water as the fluid, the charge can be balanced by ions, and the electrodes themselves will get charged, if we assume that no Redox reaction occurs. So that there is e.g. the cathode with an excess of electrons, and sodium ions moving towards it and then surrounding it. And the more electrons flow over time, the more sodium ions gather there. Am I picturing this correct? But since water is present, electrolysis could occur and the electrons in the cathode would get less (and more in the anode). But why can it still attract proteins and nucleic acids in electrophoresis, if the electrodes are constantly held neutral? Is it because there are constantly electrones flowing and thus the electrodes are never actually neutral?
I must say, trying to understand things in detail is very confusing, especially in physics. I hope someone can help and/or maybe recommend a book or other source where this is explained. Most books and videos only explain it superficially and jump right to equations. Thanks :))

I’m voting to close this question because it concerns electrochemistry and is therefore better suited to a chemistry or physics forum. The application of electrophoresis to the separation of biological molecules is tangential to the core of this question, which concerns the charge of the electrodes.

Electrodes are neutral, but they are held at different potential. This is similar to the current flow in a wire: although current flows, the wire remains neutral, i.e., no charge is accumulated (unless we have a capacitance somewhere in the circuit).
Analogy: flow of water
A good analogy to current flow is a flow of water in a river. The water itself is charge, while difference in height corresponds to the potential difference. It is clear that water will flow from higher ground to lower ground, but the density of water at a particular place is not changing, because, as water flows, more water is supplied from the source, while the excess water at lower ground does not stagnate, but moves further towards the sea.
Electrolysis
In electrolysis cathode supplies electrons, while the anode collects them. They are held at different potentials, so, if ions are present in the liquid, the negative ions will drift towards the anode, whereas the positive ions drift towards the cathode.
When the negative ions reach the anode, they give it their excess electrons, contributing to the current flow. The ions themselves transform in neutral molecules and condense on the anode. Similarly, when the positively charge ions reach the cathode, they take come electrons and become neutral. As long as there are ions that can come and take/give electrons from the two electrodes, the current will flow. The excess electrons are supplied and taken back by the buttery that supplies the potential difference. Buttery is akin to evaporation in the water cycle in the nature in the above analogy, which takes water from the sea and back to the river source.

Thank you for the quick reply. Just to be sure: Let's say the power source is a capacitator (so just seperated charge, which creates a potential difference). Would that mean, that if the fluid is not conducting, that no electrons flow from the capacitator to the electrode? Or wait, do electrons even "flow"? And since you said the electrode is always neutral - why are positvely or negatively charged ions attracted to them?

If the fluid is non-conducting, the current will not flow. Note however, that a capacitor is not a buttery - if a current flows, it gets discharged, i.e., the potential difference will decrease and the current would eventually stop. The gravitational potential that make a river flow is very similar (even mathematically) to the electric potential - why does water in a river flow, even though there is no empty space ahead?

Yes, that makes sense.
Can you have a current without electrolysis?


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Ordering Primers: When to choose wet vs dry delivery format?
Whenever ordering primers, I'm always asked to specify which delivery matrix I prefer to have the oligos delivered in: wet (in water or some kind of TE buffer) vs. dry.
My understanding is that when stored dry, the primers can last up to 24 months in the freezer. However, for the primers to be useable, one needs to rehydrate them into the appropriate concentration.
So I'm wondering, what are the pros/cons of having primers shipped wet vs dry?

Pros of wet:

No need to rehydrate to use.
For e.g. 96-well plates, this can be a big deal as it's a pain to do this for large numbers of samples.
More accurate concentrations (oligo manufactureres are better at rehydrating oligos with e.g. accurate volumes than most people).

Pros of dry:

last longer (until rehydrated)
cheaper

This is great summary of the pros/cons. Thanks!


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How does the blood flow in the glomerulus when everything except plasma is drained out?
So I learned that in the glomerulus, everything smaller than the RBCs is filtered out, but I had learned previously that - Blood needs plasma, water medium to flow. So if its drained out into the Bowman's Capsule, how does the blood leave the efferent arteriole.
Could anyone please clarify,
Thank you.

Welcome to Biology.SE. I'm almost certain that you are misreading (or reading from a source that is in error). Please check this 'fact' with additional sources and then (if this astounding claim is true) update your question to include supporting references to reliable sources (preferably primary literature, but textbooks are acceptable if they are available online). If this is based on someone's misunderstanding/miswriting then please delete your post.

If it were true (and this is but one small example in the scheme of things) protein, lipids/lipoproteins, and glucose in the urine would be of absolutely no concern.

Pardon me for my ignorance. So what actually happens? It wasn't explained clearly in my textbooks or on the internet.


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Can offspring be less genetically similar to the parent than more distant relatives?
I'd be interested in answers about any sexually reproducing species, but for simplicity I'm going to focus on humans in this question.
If the parents are very genetically different (i.e. the number of alleles they share is much less than the average number of alleles shared by 2 people in a population), is it possible for, say, the father to be less genetically similar to his offspring than he is genetically similar to, say, his cousin? If so, what about an even more distant relative?
Of course anything is "possible", so really I'm asking if it's reasonably likely and if so, how likely is it? If, for example, a genetically east Asian person and a genetically south African person had a child, would that child likely be less similar to either parent than the parents are to their respective cousins or even non-relatives from the same area?
If there are any false assumptions I'm making in the question feel free to point them out, but please provide references.

Provided that a significant percentage of fathers are not biological fathers of their children... ;) More seriously: what is meant by similarity here? Genetic similarity or phenotype? I think clarifying this would already suggest the answer.

I think it's pretty clear I'm talking about genes. Genes determine phenotypes so the questions would have the same answer but the nice thing about genes is theyre quantifiable. You can count the number of alleles.

Gene are not the only thing determining the phenotype. Moreover, one can easily resemble one parent, despite having 50% of the genes inherited from the other.


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Are there traits exhibiting avoidance of the mean?
Sometimes if two organisms with an unusually large value of a continuous trait mate their offspring on average will not have a value as large as one might naively expect. Regression toward the mean is the name for this phenomenon.
If I understand correctly for it to happen it is essential that the trait is controlled by recessive genes.
However if there was a continuous trait controlled by dominant genes or genes with heterozygote advantage we would instead observe avoidance of the mean right? Is there a real-world example of this?

Welcome to Biology.SE. What is a "recessive gene" (you almost certainly mean allele) and why do you think dominance/recessiveness is associated with regression to the mean? Please [edit] your post to address the above issues and include support (preferably including references to peer-reviewed sources) for the multiple assumptions you are making. You might also benefit from thinking about the genetics behind a "continuous" trait. Finally, please clarify why you think "dominant genes" would show "avoidance of the mean" — it may be that by working through the logic you will answer this yourself.

What is a “continuous trait”? What is a “mean right”? I’m afraid that if you come from a numerical discipline and ask questions on a biological site, they need to be expressed in a language we can understand.

By "recessive genes" I guess you mean genes such that the recessive phenotype has a larger value of the trait?

Then the reasoning from Wikipedia applies - The phenomenon is better understood if we assume that the inherited trait (e.g., height) is controlled by a large number of recessive genes. Exceptionally tall individuals must be homozygous for increased height mutations at a large proportion of these loci. But the loci which carry these mutations are not necessarily shared between two tall individuals, and if these individuals mate, their offspring will be on average homozygous for "tall" mutations on fewer loci than either of their parents.


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How does slowed action potential propagation in the optic nerve cause blurred vision?
Multiple sclerosis is accompanied by optic neuritis, and there is demyelination of the optic nerve, causing the action potential to be propagated more slowly along axons. But how does this lead to blurred vision?

Demyelination per se is not the whole story behind the blurring of vision seen in MS patients.
MS results in an inflammation of the optic nerve (optic neuritis) and demyelination of the optic nerve fibers. It is commonly seen in MS, and is associated with blurred vision, basically because the signals are not sent properly along the optic nerve. Blurred vision in MS can have several reasons. These include:

On the one hand blurring of vision is caused by the swelling and loss of optic nerve fibers due to the inflammatory effects accompanying optic neuritis.
The demyelination of the optic nerve fibers associated with optic neuritis caused by MS disrupts signal transmission especially in the central eye field, leading to blurry parts in the center of focus due to impaired neurotransmission.
Another symptom of MS is double vision, this is caused by demyelination of neurons in the brainstem that coordinate the control of the muscles that control eye movement. If the eye muscles are not working properly, and especially if one side of the brain is affected more than the other, it will cause blurred vision, because both eyes do not move in a synchronized fashion anymore.


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Saving a Maize Landrace from Inbreeding Depression
I have 10 seeds of a rare corn landrace. I probably won't be able to acquire more and the cultigen's long term fate is unknown. So, I want to do my best to preserve it for future generations.
Corn is largely out-breeding and used to growing in very large populations, so it's very susceptible to inbreeding depression. The seed I got came from a small but reasonably heterozygous, healthy population with a modest/good amount of diversity.
If I want to preserve the corn without crossing it to anything else, what should I do?
My thoughts are that I have to ensure that it does not breed true for maladaptive recessive alleles. So, I plan to increase seed stock until I have enough genetic material to grow out thousands of individuals and cull any sick plants over several generations, while trying to keep the population contributing to the next generation large. In other words, purging the poor genetics.
I also thought it might be a good idea to breed a few lines from the initial stock to ensure even more diversity.
Is my plan viable? What are my chances of success? Are there any better protocols?
Thanks.

I don't suppose you have the space for rudimentary cloning tech handy? Just a thought, but keeping some of the original plants handy in slow-growth mode might help with later crosses.

@ARogueAnt. As a matter of fact, I do. That is a very good idea. Thanks.

After planting the 10 seeds, manually cross-pollinate the plants with each other to ensure that (1) there's no self pollination, (2) every seed contributes equally to the gene pool, and (3) no foreign pollen contaminates your gene pool.
Cross plant 1 with plant 2, plant 2 with plant 3, plant 3 with plant 4, plant 4 with plant 5, ... and plant 10 with plant 1. Then you can pick an equal number of seeds from each cob to build a population from which you can start eliminating weak or off-type plants.
(A second round of controlled cross-pollination to ensure that seeds from the same cob don't cross pollinate may not be a bad idea: cross plant 1x2 with plant 3x4, 2x3 with 4x5, 3x4 with 5x6, ... and 9x10 with 1x2)
Controlled crossing ensures that no "good genes" from the initial set of seeds are lost by accident.


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Is this a Box Tree Moth?
This moth has been hanging about near my house recently (South London area, October 2021) - I have seen it 2/3 times in the last fortnight. I have never seen anything this colour before which is why it caught my eye.
Its wingspan is about 30mm and this photo was taken from the inside of a window it had landed on.

Basic google searches lead me to believe it is a Box Tree Moth - am I correct?

What a beauty, do you have a picture of the back?

@CoDa Unfortunately not, it flew off before I could get one


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Genetic evolution without crossover
Can someone please point me to the origin of the system of coupled differential equations (1) in Section 2 of Shahshahani's book$^\star$?
$$ \dot{x}_i = x_i \sum_{j=1}^n m_{ij} \frac{x_j}{|x|} $$
Shahshahani claims this equation is well known as a simple consequence of random mating and cites Crow, J. F., Kimura, M., et al. (1970). An introduction to population genetics theory, but I have not been able to find the equation there.

This is a dynamical system with $x \in \mathbb{R}^n_{>0}$, and $m$ is a symmetric matrix with constant coefficients. The equation models the evolution of a genetic system subject to selection in population genetics.  The variables represent

$n \in \mathbb{N}$ number of types of gametes in a diploid population
$i \in \{1, \dots, n\}$ labels the types of gametes
$x_i \in \mathbb{R}_{>0}$ number of gametes of type $i$
the unordered pair $\{i,j\}$ represents the genotype determined by the gametes $i$ and $j$
$m$ is the selection matrix and $m_{ij}=m_{ji}$ is the selective advantage of the genotype $\{i,j\}$
$|x| := x_1 + \dots + x_n$

$\star$ S. Shahshahani, A new mathematical framework for the study of linkage and selection, Memoirs of the American Mathematical Society, Volume 17, Number 211, 1979.

Can you please provide enough information in your question so that it can be understood without reading external references? What is the meaning of the variables in the equation?

$m_{ij}$ is the mean number of descendants at the next generation from a single individual carrying $i,j$, so $m_{ij}$ has to be multiplied by the number of individuals carrying $i,j$ at the current generation. $ x_i  \frac{x_j}{|x|}$ is supposed to be that number of individuals. This is a very simplified model assuming perfect mixing between individuals carrying $x_i$ and those carrying $x_j$ and I'm not sure the "unordered" is taken in account correctly. But anyway it gives you a rough idea of what this equation says and how useless/simplified it is.


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Why do bacteriophages look like tiny little robots?
I get it, evolution is funny and works in mysterious ways. But come on. You can't tell me this thing doesn't look like a nanobot.
Why do bacteriophages look this way? With their cylindrical heads and multiple "feet"?

Welcome to the site! Personally I think the question is reversed; the discovery bacteriophages pre-dated the design of nanobots; hence the question ought to be "why do nanobots look like bacteriophages?" and as such it's not really a biology question.  For it to be a good fit for the site, you'll have to show clear biological links rather than visual links with modern technology.

Why do they look like that? Because they do - there's not some deeper reason why they might look similar other than because people might have designed nanobots to look like bacteriophages (or maybe they didn't), especially given 'nanobot' doesn't have a strictly defined shape.

Honestly, that only looks like a functional bacteriophage to me, so, yes, I can tell you that doesn't look like a nanobot to me. Then again, I studied bacteriophages, but never nanobots. I wouldn't recognize a nanobot if I was shown a photograph of one.

Many things on nanoscale look like small crystals or several small crystals put together - i.e., they adopt a limited number of symmetric shapes allowed for packing identical objects in three dimensions (see, e.g., the shapes given here). Viral capsids, composed of many identical proteins (capsomers) is an example of such crystal structures.

The reason they look like that is because they have very small genomes so they have to build themselves out of multiple copies of a few building blocks. This leads to a high degree of symmetry in the component pieces; in particular icosahedral symmetry in the genome storage capsid (made of 235 copies in the smallest phage, 3115 copies in G-phage, as described by Caspar Klug theory) and helical symmetry in the tail. (made of an arbitrary number of copies, depending on the length.)
Industrial manufacturing also relies on efficient use of standardized mass-produced parts, so it's not surprising that you'd see similarities.
Also due to various differences between bacterial and eukaryotic cells, bacteriophage rely on their own complex protein machinery to physically breach their hosts, rather than tricking the host into using its own membrane machinery to import the virus.


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Why are IMAC and gel filtration combined?
In a practical course I used an Biorad Profina system to purify a protein with a histidine tag.
The device uses a column for IMAC and one for gel filtration. Why are these two devices combined in one? Why is there a need for gel filtration?
I missed my chance to ask this in the practical training, thats why I ask here!
Thanks for your help!

What is IMAC? Please do not use non-standard abbreviations in questions or include thanks.

Immobilized metal chelat affinity chromatography

Then spell it out! (And get chelat spelt properly when you edit your question.)  And do some research and provide some detail if you post here.

Without knowing your specific protocol, it is common to use more than one purification method for a single protein. Given the broad similarities that all proteins and even most biomolecules share, it is impossible to completely purify a protein in a single step. The strategy therefore must be to purify via as many properties unique to the target protein as possible until the purity of the sample is sufficient for the desired application. These properties can include most commonly affinity (eg immobilized metal), charge (ion exchange), hydrophobicity (reverse phase) and size (gel filtration).
In a perfect world, a protein could be purified in a single step affinity-based protocol. In the real world, however, non-target proteins can bind the column nonspecifically (for example, binding to the positively charged nickel column or to the agarose matrix itself). Nucleic acids may elute with your target protein or your target may form large, undesirable aggregates. The list of potential problems is long and this is why multiple different rounds a purification can more effectively discriminate between the target protein and other contaminants in the mixture. As an example, let’s say there there is a contaminant binding the Ni-NTA matrix by charge. Using gel filtration afterwards, which separates by size and not charge, allows removal of the contaminant from the target protein.
A major benefit of gel filtration as a final polishing step is that it can also be used as a desalting column. Besides further purifying contaminants from your target protein, gel filtration allows removal of unwanted small molecules (eg imidazole from IMAC) and elution in a buffer desired for downstream applications.
I looked for some further reading in case your interested and found this protein purification handbook which talks about developing purification strategies.

thanks a lot! Not all heros wear capes, some wear lab coats!

@Mourinho_1 Haha you’re welcome.


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Number of membrane proteins of a particular type per cell
Is it possible (or meaningful) to count how many proteins (protein copy number?) of a certain type a given cell has on its surface?
For instance, say there is some membrane integral protein X. Is it possible to take a population of cells, and arrive at a number (say 100) that reflects the average number of X per cell in the population?
I'm trying to look for publications that have done something along these lines, and I've had no luck so far. This made me wonder if this is even a meaningful idea at all, so I decided to see clarification here. (Apologies if this is a trivial question.)

The dimensions of every cell are different. So, The number will definitely be different for integral membrane proteins, and other cell constituents.  Mass-spectroscopy can be used to calculate cellular protein fractions. I'm not sure specifically for integral membrane proteins.

Nobody is going to publish a paper where the main result is the number of proteins of a particular type in a cell. It’s not what modern science is about. Any protein for which there is a quantitative assay would allow one to deduce this in the usual simple arithmetic manner. I used to drive my students mad making them do this sort of sanity check. Welcome to the club.

@David I think you're mistaken, unless I am misunderstanding your comment. In the time since I posted this question, I've managed to find a few papers that have addressed this topic (albeit, admittedly, not perfectly, and at a general level). See, for example, Ho et al. 2018 (https://www.cell.com/cell-systems/fulltext/S2405-4712(17)30546-X).

For the budding yeast pheromone receptor Ste2 this has been done long ago: https://pubmed.ncbi.nlm.nih.gov/3023832/
There is also later work that used fluorescently labeled ligands, allowing for these analyses on a single-cell basis to study cell-to-cell variability.

If you know the stoichiometry of a particular ion channel and do something like patch-clamp, where you know the surface area being clamped, then you can measure the ion-flux per unit time and from that infer number of the channels in that area. From this you can make some inference as to the number of ion channels on that particular surface of the cell.
However, this doesn't equate to the total number at all, as the different surfaces of cells have different numbers depending on their functions. For instance tight-junctions might have a different number from apical surfaces which will have a different number to basolateral surfaces.


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New ORFs occurring in SARS-CoV-2 due to mutations
Are there examples of new ORFs in SARS-CoV-2 created by mutations?
The ORFs should not be present in the reference virus, but they should occur in a lineage occurring in the wild (at best, being part of the definition of the lineage). Of course those ORFs will somehow overlap with the well-known ORFs of the virus, potentially frame-shifted.
Bonus: Is there evidence that a protein is produced from the newly emerged ORF?

Not a new ORF but new or increased occurence of non-canonical subgenomic mRNA https://virological.org/t/genomic-gymnastics-in-the-nucleocapsid-gene-of-sars-cov-2-during-transmission-in-humans-transposition-of-acgaac-and-creation-of-the-novel-n2-gene/715 confirmed in raw sequencing data https://www.biorxiv.org/content/10.1101/2021.03.02.433156v2

There is surely better but

A few sequences have G881T which extends MKIFKKTGTLNIAVVLPVNSCVSLTEGHTLAMSITTSVALMATLLSALKTF
to  MKIFKKTGTLNIAVVLPVNSCVSLTEGHTLAMSITTSVALMATLLSALKTFYHVLVKLHALCPNNWTLLTLRGVYTAAVNMSMKLLGTRNVLKRAMNCRHLLKLNWQRNLTPSMGNVQILYFP in frame -1 at the beginning of ORF1a.

A few sequences sequences have A2182G which extends MKNSNPSLIGLKRSLRKV to MKNSNPSLIGLKRSLRKVWSFLETVGKLLNLSQPVLVKLSVDKLSPVQRKLRRVFRHSLSL in frame +1 in ORF1a

An so on, in fact most "stop codons" in alternative frames seem to be mutated in some sequences. Of course most of those "new ORF" are probably not detectably translated. Introduction of new TRS has more chance to produce new subgenomic mRNA whence translation of new proteins.

If you only consider the consensus sequence of each pango lineage then you'll probably won't find much convincing event of this kind, except for the introduction of TRS in N which did happen in B.1.1, P.1, B.1.1.7,
as well as a deletion causing the merging of ORF7b and ORF8 in B.1.1.318

The answer to this is both yes and no.
The reason I say yes and no is that SARS-CoV-2 exists as what is known as a quasispecies. Quasispecies are the population of virions that exist in an infection, with each separate virion containing a genome with its own mutations as a result of natural error rate of the RNA dependent RNA polymerase. When we sequence a virus and call the result its genome, what we are actually looking at is a consensus sequence, not the individual sequence of each virion that went into the sample from which the genome was derived.
Now, the problem with a quasispecies is that not all the virions produced in an infection are actually viable and can go on to produce more virions. In some cases there will be defective genomes, some more will have defective capsids or defective packaging of the genome and so on. These together make up a series of defective particles with a range of different terms depending on how they behave in an infectious process.
In many cases there are defective interfering particles, which miss parts of the genome or have genomes that are otherwise defective but are capable of infecting cells, but not capable of producing infectious particles themselves, and can compete with functional particles for infection (hence the interfering part).
In some of these described particles and within the sphere of the quasispecies will be virions that contain new ORFs. How those ORFs behave in an infection is very difficult to say as they are very hard to study. In most cases these new ORFs will cause a failure of some other (already) critical function and produce non-viable virions, but without examining any potential new ORF functionally in a lab we can't be certain that a potential new ORF does anything or indeed what the product might do.
For an estimate of the coding capacity of SARS-CoV-2, you can look at this study (1), published in Nature, which revealed that there probably are unknown ORFs within the virus. However, I suspect that these were there already and are not newly evolved as such, just newly identified.

Finkel et al., Nature  589, pages 125–130 (2021)

I don't really see how it is related to the question. Please take a look at the ORF8 deletions in SARS, in particular the 29nt deletion present in the main epidemic strain but not in some earlier strains, causing a much shorter ORF8 protein, named ORF8a, and a new ORF8b ORF overlapping the end of ORF8a in a different frame. In the early strain https://www.ncbi.nlm.nih.gov/nuccore/AY390556.1 the long ORF8 is called ORF10-11 and in the epidemic strain https://www.ncbi.nlm.nih.gov/nuccore/NC_004718.3?report=genbank there is ORF8a and ORF8b

@reuns - Why don't you post that as an answer yourself. The reason I posted this is because they genuinely do produce new putative ORFs all the time because of the quasispecies thing. However, a new ORF does not necessarily produce a functional protein or may alter the function (e.g. decrease expression) of a functional ORF, so you end up with non-functional or less functional particles that don't lead to anywhere in evolution terms.

@reuns ORF8a/b was identified in SARS-CoV (the original one) so I don't think this is a new thing at all for CoV-2, which is what the question was about.

I appreciate this answer although I hadn't really asked for it, because it broadens my view on the virus genome of SARS-CoV-2. I am still interested in more answers, describing situations for SARS-CoV-2 like the one exemplified by @reuns' comment for the original SARS virus.

Right now, there is a new preprint by Harriet Mears et al. on biorXiv with interesting new ORFs in SARS-CoV2 opened by some mutations.

The mutation N:R203K N:G204R found in pango lineage B.1.1 creates a transcription regulatory sequence (TRS-B) that triggers the expression of a proteine starting with N:M210 to the end of N. This proteine acts as an interferon antagonist. This ORF is named N:iORF3 by the authors.

Other mutations create new ORFs in nsp16 (coded by ORF1ab) and in the Spike gene.


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Is it advised to calculate QED parameters for salts?
QED (quantitative estimation of drug-likeness) is a score which helps you to predict if a small molecule is desirable as an orally absorbed drug, described in the Quantifying the chemical beauty of drugs article.
Its calculation is based on well defined chemical properties such the number of hydrogen bond donors and acceptors, aromatic rings, rotable bonds, octanol-water partition coefficient etc...
All of this properties can be derived from the structure of the molecule. One can use for example the QED module of RDKit
I develop a compound database for drug discovery. Some compounds are salts where one ion is the organic molecule and other is common inorganic ion such as $\ce{Na+}$, $\ce{Ca2+}$, $\ce{Cl-}$, etc...
When I load the salts into the database I derive their non-salt form, just the organic molecule.
My guess is that I should only calculate the QED score and its associated parameters, or any chemical parameters for ADME  for the organic molecule, but not for the original salt compound.
My logic is, when we apply a drug as a salt orally it will dissociate into ions, so the organic bio-active molecules will be separated from the inorganic ions. Of course the inorganic ions will be present in the gastrointestinal fluid, but in such a small quantity compared to the other inorganic ions (often the same type) that they will have no significant effect.

QED is quantum electrodynamics: https://en.m.wikipedia.org/wiki/QED_(play) ;)

I found the answer when I was reading about InChi in more detail.

For example, to a bioscientist “glutamic acid” and “glutamate” are the
same thing, but to a computational chemist the loss of a proton, or
its variable site of attachment is critical.

So the guess in the question is OK in a bioscientist perspective, but not for the computational chemist perspective, and since this is biology oriented computational chemistry question both the ionic and neutralized form must be considered.
To test this I calculated the Quantitative Estimation of Druglikeness (QED) for in a simple case for , sodium acetate, acetate (just the organic anion) and acetaldehyde. Their mean QED:
sodium acetate: 0.2777
acetate: 0.3498
acetaldehyde: 0.4298
The ionic forms (sodium acetate, and just the acetate anion) are less likely drugs since ions, since ions has an extremely low chance to pass biological membranes passively. The sodium acetate has lower likelihood then acetate, because it contains 2 ions and the QED algorithm has now way to tell which should be the drug and assumes that both ions must pass the membranes which is a great penalty.
In conclusions the QED parameters should be calculated both form the neutralized and organic ionic forms. The in-vivo relevance of the two forms will heavily depend on the chemical environment, since they will be in a dynamic equilibrium, which mostly depends on the PH of the micro environment. The QED parameters should not be calculated from the salt form, since we are not interested in the QED of the inorganic ion, further many more inorganic ions will be present next to that.