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Monozygotic vs Dizygotic heteropaternal superfecundation
Update: I had a wrong assumption.

After triple checking, I now see that how ordinary monozygotic twins arise is 1 sperm and 1 ovum and then later the zygote splits up.

(1.1. and that that phil and lil from rugrats are opposite sex and identical twins is actually an extremely underrated genetic miracle, possibly giving more credibility to the rugrats theory/hypothesis. There's also semi-identical twins in a song of ice and fire - though i guess not game of thrones -, Ben 10, legend of korra, KND, baka to test, and i think samurai jack, etc)

Honest to God, what i weirdly remembered was that ordinary 'monozygotic' twins arise from 2 sperm 1 ovum and then this 'zygote' or whatever of 2 sperm and 1 ovum splits up into 2 zygotes i.e. the splitting up of the 'zygote' is a natural consequence from that 2 sperm have fertilised 1 ovum. From what I weirdly remembered, it would be natural to ask what if the 2 sperm were from different males.

(2.1. Additionally, the Phil and Lil thingy is not really a genetic miracle since all you need is a 22X sperm and a 22Y sperm to fertilise 1 ovum. Damn television. i really thought opposite sex identical twins were not that rare.)

However, apparently it is possible for 2 more sperm to fertilise 1 ovum, in a case called semi-identical twins or something, but there are apparently only 2 reported cases.

New question: Okay in the unlikely event that what would be semi-identical twins would arise from sperm from different males, well, then what?

From wikipedia:

Homopaternal superfecundation refers to the fertilization of two separate ova from the same father, leading to fraternal twins;6 while heteropaternal superfecundation is referred to as a form of atypical twinning where, genetically, the twins are half siblings.

There doesn't seem to be a distinction between heteropaternal superfecundation occurring with two ova and with one ovum. How will monozygotic heteropaternal superfecundation twins look like as opposed to dizygotic heteropaternal superfecundation twins and to identical twins?

Are/Were there real life cases of monozygotic heteropaternal superfecundation?

The heteropaternal superfecundation selected cases given on wikipedia seem to be for dizygotic. I tried looking up on google, but I've found so far only dizygotic.

Have you thought about how many chromosomes your one zygote with heteropaternity would have?

@mgkrebbs No. The extent of my familiarity with genetics is what I learned in a non-elective class in secondary school. Thanks for commenting. Please enlighten me. But I do remember the 22X, 22Y stuff I guess. What's the difference if the 2 sperm are from the same father vs from a different father?

A normal singleton child is a result of the fertilization of an ovum (with 23 chromosomes) by a sperm (with 23 chromosomes). After fertilization, the cell (with 46 chromosomes) is called a zygote.  All normal human cells (other than ova and sperm) have 46 chromosomes.
Monozygotic twins (identical twins) occur when the set of cells resulting from the early divisions of a single zygote separate into two groups.  Each of these two groups of cells proceed to form a normal embryo, with resulting (if carried to term) in twins.  Since these twins came from the same zygote, they have the same 46 chromosomes and so are essentially genetically identical.
Now how could this monozygotic process occur with two fathers being involved?  Only by having two separate sperm combine with a single ovum.  This would result in the zygote having 69 (3x23) chromosomes.  This could happen, but would be an extreme case of aneuploidy (abnormal number of chromosomes). Such a genome is massively defective due to the presence of too many gene copies, and the embryo (whether singleton or twin) will be spontaneously aborted.  Only a few kinds of aneuploidy can result in a viable fetus, almost all having only a single extra chromosome (one of the smaller ones); the most common case is having 3 copies of chromosome #21, which results in Down Syndrome.
So, monozygotic heteropaternal superfecundation has not been observed because the resulting pregnancy is very unlikely to go to term. (It's just as unlikely when the two sperm are from the same man.)

thanks. i apparently remembered my biology/genetics from secondary school wrong. i updated question. follow-up 1: but your answer is still the same...right?

follow-up 2: do you really mean 'the resulting pregnancy would never go to term' rather than 'the resulting pregnancy has never in human history been recorded as having gone to term' ?

Never say "never" with biology - yes, there have been a very few reports of twins apparently resulting from two sperm entering an ovum. In the well documented 2019 report, the result was twins who were both mixtures (chimeras) of cells derived from both sperm, some XX and some XY.  They hypothesize that an initial 3-way division separated the 2x69 chromosomes into 3 cells with 46 chromosomes each. I've softened the wording in my answer above.

right i never said 'never happened' i said 'never...been recorded'....anyway thanks for answering and thanks in particular for putting up with my wrong assumption about monozygotic twins


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Asexual Reproduction Of sponges through endogenous or exogenous budding?
I was studying asexual reproduction in sponges and came across two website

Wikipedia of Gemmule and there is a line....

Only Endogenous Types of Buds develop into New Sponges.

Then as I was reading this Website Sponges there is a Section 9.1. iii) Budding, in which, there is Two Parts i.e (a) Exogenous Budding and (b) Endogenous Budding
So now, I am a bit confused..... if only Endogenous Bud can give rise to New Sponges then why there is a section of exogenous budding i.e reproducing through exogenous buds,in the reproduction section of sponges, in this website sponges ? ISN'T that Contradiction?

I would say that the quoted sentence from the Wikipedia gemmule article is wrong.  The first sentence of the containing paragraph says:

Asexual reproduction in sponges occurs via budding, either by external or internal buds.

At face value, the two sentences together imply that sponges can reproduce by external budding, but that the external budding "reproduction" does not produce "new sponges"(!). Note that the most recent edit to the article (on 10 March) was by an anonymous user who changed the sentence you quoted from "Both types" to "Only endogenous types", so this was a somewhat recent corruption.

source: Stack Exchange

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

sort: votes


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When life first formed in earth's ocean, was it salty yet?
Do we have any tangible proof, e.g. by studying fossils of primitive life forms, that during their time the ocean was already salty, and at roughly similar levels to today's, or on the contrary, that water has no or very low salinity?
Did life had to adapt to dramatic changes in sea water salinity, as it has (I believe) for changes in air composition?

I've answered your first question.  I suggest you post the second part (concerning adaptation to changing salinity) as a standalone question.

Current estimates suggest that last universal common ancestor of life on earth lived in hydrothermal vents 3.8–3.5 billion years ago.1 Petrologic examination of quartz formed near these vents during that time suggests that seawater had a higher salinity compared to current oceans 2 --

Our data are in agreement with six other data sets—from the 3.75 Ga Isua Greenstone Belt (W. Greenland), the 3.24 Ga Pilbara region (W. Australia), the ∼3.2 Ga Barberton Greenstone Belt (South Africa; 2), the ∼2.7 Ga Matagami area (Abitibi Greenstone Belt, Canada), and the Proterozoic (∼2.2 Ga) Ongeluk Formation (South Africa). The consistency of fluid inclusion data suggests that Archean and early Proterozoic seawater may have been more saline, and potentially stratified, compared to modern seawater.

Note: Ga (for gigaannum) – a unit of time equal to 109 years.

Weiss, M., Sousa, F., Mrnjavac, N. et al. The physiology and habitat of the last universal common ancestor. Nat Microbiol 1, 16116 (2016).
Weiershäuser, L., Spooner, E.T.C. Seafloor hydrothermal fluids, Ben Nevis area, Abitibi Greenstone Belt: Implications for Archean (∼2.7Ga) seawater properties. Precambrian Research, Volume 138, Issues 1–2, 2005, Pages 89-123.

It's amazing that the ocean was actually more salty than today -- my intuition couldn't have been more wrong.

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


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What is the mechanism responsible for long-lasting detectable antibody titers?
As I understand, when naive B cell encounters antigen matching its receptors and is activated by a T helper cell, it can either differentiate into 4 plasma cells, produce a lot of antibodies and commit apoptosis, or into 2 memory cells waiting to be activated the next time they encounter the antigen.
On the other hand, IgG can be detected for a long time after infection.  As antibodies decay, there must be long-term production of IgGs to keep their level constant.  What is the mechanism behind that if there is no following infections?

Great question. Maybe the answer is simply that these assays are sensitive enough to detect basal levels of IgGs that memory cells continue to produce in the absence of an infection.

@DouglasMyers-Turnbull If not activated memory cells can secret antibodies, that actually answers my question.


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Why is it difficult for germs to jump species?
If you haven't watched CGP Grey's video Americapox: The Missing Plague, I suggest you watch it. It's an excellent video.
One assertion he makes is that "germs jumping species is extraordinarily rare [...] being the patient zero of a new animal-to-human plague is winning a terrible lottery."
Why is this true? Why is it so rare for a germ to move from a cow's body to a human's? Is it because it can't travel that distance while remaining alive? Is it because the human's immune system will kill it? More details will be appreciated.

A large part or the reason, especially with viruses, is that they target very specific cell-surface proteins in order to enter a cell.  So the virus is not only limited to species, it may attack only certain types of cells: https://www.genengnews.com/news/coronavirus-picks-on-some-cells-more-than-others/

Does this answer your question? Why are diseases generally specific to a particular species

The main reason is the biochemistry of two unrelated species are different. The more closely related two species the more similar things like the hormones and signaling molecules will be and inversely the more distantly related they are the more different those things will be. Even highly constrained molecules like hemoglobin may still pick of mutation that get carried on, and things like an immune system actually favor variation evolutionary speaking. Even within the same species these things vary, and this is often cited as a possible reason sexual reproduction exists at all, to make each individual slightly different, so there is less chance of catching disease or parasites from others.
Animals have many many barriers to infection, getting pass all of them is hard and tends to only occur with organisms that evolve alongside that animal and thus have been selected to get pass that specific combination of barriers. Getting past them all if you have not been evolving along side it is incredibly unlikely, some diseases manage it be cause there are billions of them, and if you run billion upon billion of random keys through a lock some may fit just due to chance. this is also why disease transfer is more likely the more closely related species are. SIV/HIV easily jumps between great apes because they are very closely related (and the insist on eating each other) the chances of a dog catching it are astronomically unlikely because the chances of the viruses surface proteins matching receptor proteins of a dog is basically only chance as there has been no evolutionary pressure to alter it.


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Why is the 5′ end of DNA a monophosphate?
According to my textbook:

While the 5′ end of a DNA strand is typically a monophosphate, the 5′
end of an RNA molecule is typically a triphosphate.

Source: Biology: How Life Works, 3rd Edition
How do we know the 5′ end of DNA a monophosphate? I understand that...

DNA and RNA synthesis cleaves nucleoside triphosphates into nucleoside monophosphates to form the sugar-phosphate backbone.
Necessarily, the first nucleotide will have three phosphates intact.

What I don't understand is why DNA doesn't have a triphosphate on the 5′ end like RNA. How does that happen?

Related but the answer states the opposite is true and has not been accepted by the asker: https://biology.stackexchange.com/questions/81656/how-many-phosphates-are-in-the-5-end-of-a-dna-strand

My comment serves to show that I did my work by searching for an answer in a few places.
I didn't understand the linked answer, it was too specific of a response to a general question. Secondly, there was too little activity in the linked question so I couldn't trust its accuracy. Lastly, the answer contradicted the textbook, so I thought it was appropriate to ask a new question.

@David ...He is the original poster and I find your comment quite rude..

@Andrew — The original poster of the post the poster of this post referenced. I was explaining why if that post was a duplicate of this it made no difference whether an answer had been accepted or not. Indeed it makes no difference whether it has been answered or not. If you or someone managed to persuade a mod that was rude I can only shake my head in disbelief

The deleted comment: "Whether or not the poster has accepted an answer here is irrelevant. He didn’t know in the first place so he has no authority. It works better on the original computing site Stack Overflow, where the problem is generally practical, and one accepts the solution that works. The answer to the other question actually shows a table of different genomes, so is based on experimental evidence. Have you read it? Do you understand it. Perhaps like the original poster you didn’t realize the true complexity that your probably deficient text ignored. – David 2 hours ago"

This problem wouldn't arise in bacterial chromosomes, plasmids and other circular DNA molecules, for a circle has no ends. :P As far as eukaryotic chromosomes are concerned, they have telomeres. I think reading about telomeres and the associated replication machinery from http://www.hammiverse.com/lectures/16/4.html should answer your question.

I only saw your post by chance. To draw someone's attention to a post other than the poster of a question or answer you need to preface their handle by @ . The question of reviving duplicates — answered or unanswered, accepted or unaccepted belongs on Meta. As I guessed, you didn't understand the linked answer because — from the nature of your text you are study biology, rather than molecular biology — and you would be unlikely to know about the detailed chemistry of the initiation of RNA and DNA synthesis. To say so is hardly rude.

...However the important thing for you is to help you understand your book, and for anyone who wishes to help you they need to know the context of what appears a strange statement in a book published recently. So can you perhaps give an indication of the title of the section this appears in and what follows this statement. The reason one finds this strange is that "a typical DNA strand" is unclear. I would take it to mean the ends of a chromosome — as does the linked reference. Likewise the end of an RNA molecule depends on whether it is mature and what type of RNA it is. Can you clarify?

The quoted text is from chapter 3 (nucleic acids & transcription) section 2 (DNA structure) a sentence or two after describing the nucleotides used in RNA, but before any description of transcription. It doesn't assume eukaryote/prokaryote either. I think typical may mean lacking edge cases, but I recognize biology is full of them. I interpret the text as meaning if you follow such a typical strand to its 5' end you will encounter a monophosphate and then no more nucleotides. My confusion is why this isn't a triphosphate.


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How can viruses spread so fast in a plaque assay?
I understand the basic idea of viral plaque assay, but I don't understand how the virus spreads so quickly in the culture.
For example, at 1:30 in an educational video about the subject, you can see various viral plaques all growing from single infection points and then multiplying to cover a circular area as the new virions spread outwards.
However, if you think about it, we know the virus cannot move, so when the new virions bud they can only infect adjacent cells (or bacteria). So the spread is limited to whatever cells are immediately adjacent to the infected cell(s).
So, let's say a virus is 100nm in diameter and replicates every 8 hours. In 4 weeks there would be 30 days or 90 replication cycles. Let's imagine that a virus can "reach" things 5 times its body diameter when it buds, so that is things 5 x 100nm = 500nm away. If we have 90 replication cycles then the total radius of the viral plaque could be at most 500nm * 90 = 45,000nm or 45 micrometers, which is a speck invisible to the naked eye.
However, when we look at the plaques in the video we can see they are 5-7mm in diameter and are very visible to the naked eye. So, how could the virus be traveling this far?

As Bryan pointed out in the comments, viruses infect cells, where they replicate and then spread from those cells. They do not bud off from existing virions. Cultured human cells might be roughly 200 to 500x larger in diameter (20 - 50µm) than your hypothetical virus. The virus does spread only to adjacent cells, but it does so in all directions, increasing plaque diameter by roughly 2x the cell diameter with each replication cycle.
So, to estimate plaque diameter D from cell diameter d and number of replication cycles r, in a perfecly confluent monolayer, a more accurate equation might be something like: D = d + 2dr
If you plug in your theoretical 90 replication cycles and a cell diameter of 25µm, you'd get 25 + (2 x 25 x 90) = 4,525µm or 4.5mm.
In case it's not already understood, cells in a monolayer will vary in both size and shape, and replication times will vary between different viruses, environmental conditions, and cell types. So, it's not a perfect calculation, more of a back of the envelope to show that plaques can reach visible sizes in a reasonable number of replication cycles.


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How T-Cell recognizes a cell infected by a virus?
According to few articles I read (like BBC about The people with hidden immunity against Covid-19 ):

starting out about four or five days after infection, you begin to see T cells getting activated, and indications they are specifically recognising cells infected with the virus,” says Hayday. These unlucky cells are then dispatched quickly and brutally – either directly by the T cells themselves, or by other parts of the immune system they recruit to do the unpleasant task for them – before the virus has a chance to turn them into factories that churn out more copies of itself.

When virus just entered a cell, but had no chance to churn more copies: Is surface of the cell any different? How T-cell can distinguish infected cell from non-infected?
I am no biologist, but I am fascinated about biology now, and curious to learn more. Sorry if I am not using proper terminology.
I found How do T-cells determine which cells they've already inspected? , but T-cell activation is mentioned only in the context of dendritic cells and lymph nodes. IIUC, T-cells should attack lungs cells to eliminate cells infected by covid-19 there.

Otherwise the coronavirus spike has a signal peptide and a transmembrane domain making it  secreted and anchored onto the cell's surface

All cells chew up internal proteins all the time - it's part of the normal activity of cells to recycle those proteins into amino acids to be rebuilt into other proteins. The first step is chopping up the protein into peptides by the proteasome.
When a virus infects a cell, one key thing it needs to do to replicate is to have the cell start making viral proteins. However, some of these get chewed up, too.
Some of the peptide fragments get bound to major histocompatibility complex class 1 (MHC-1) molecules. These are then transported to the cell surface. This is the cell advertising "hey, this is what I've found in the trash lately."
Sort of like antibodies, T-cells only bind certain antigens, and during development the immune system learns which antigens are self versus foreign by process of elimination: if you detect it during development, it must be yours. Everything else is fair game to attack. When a killer T-cell binds strongly to the MHC-1:peptide complex, it recognizes that this is a foreign peptide and the cell presenting it must be infected or damaged in some way, and this starts a cascade that leads to apoptosis of the infected cell.


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What factors have led to selection for intelligence in crows and rooks?
The Corvidae family could include some of the smartest species after primates. What could be the factors that differentiate them from other species of birds that have determined their potential for intelligence? The only explanation I found mentions their "juvenile gangs" but many other birds are more social and less intelligent.

@John Comments should not be used for partial answers.

@com.prehensible Comments should not be used for partial answers.

This article posits that a lot of the reasons for primates to have evolved to be more intelligent (i.e. a costly and unpredictable environment, which requires complex thinking and problem-solving skills) could also apply to corvids.  So environmental complexity might be a potential reason for these birds to have become so smart.
As far as why other birds aren't as smart, I think it's hard to say. From an anatomical stand point, smarter birds have more densely packed neurons. It's unclear based on this article why some birds would evolve more complex brains than others, but one can assume it's out of necessity based on the environment and other factors. If a species can get by with a less complex brain, it most likely will. I hope this helps somewhat.


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The significance of haplotype blocks
I looked up haplotype blocks in Google Scholar, and the results returned seemed to show that almost all the relevant articles were published between 2001 and 2009, with almost nothing since 2010.
Why has interest in haplotype blocks apparently waned over the last decade? Has the concept been discredited?

Please check out this post at academia stackexchange and maybe edit your question to include representative trend.
The top most articles found by google scholar search are not a random sample of all articles found. I don't know exact google algorithm but my guess is it puts highly cited articles near the top. Older articles had more time to accumulate citations.

can you confirm that the language hasn't just changed? i believe that many people will just write "haplotypes" these days and may omit the word "blocks". Has there been a meaningful decrease in the word "haplotypes"?

also, just posting screenshots of unsorted google scholar hits is not convincing that what you say is true. can you actually quantify the usage of the relevant terms in a time-sorted fashion?

@David yes, I actually would like to ask if the concept of haplotype blocks (or as someone likes to call it, haplotypes) has been discredited

I have edited your question, taking the emphasis away from the Google Scholar Search and towards the validity of the concept. As your inference from the search is clearly wrong, I cut two of your graphics which I hope you will agree are displensible.

Has interest in haplotype blocks waned over the decade?
No.
You can set a time range on Google Scholar, which the screenshot shows was not done. I did that and:

A search for ‘haplotype block’ from 2000 to 2009 gives 22,000 hits.

A search for ‘haplotype block’ from 2000 to 2009 gives 25,700 hits.

(The term haploblock is now often used as an abbreviation, but it turns out that haplotype block is still much more frequent.)
So I have to conclude there must have been something wrong with the approach adopted by the poster. It is worth mentioning, however, that a Google Books ngram analysis of haplotype block shows first usage in 2000, a peak at 2007 dropping to a approx. 30% of the maximum in 2019. This may just reflect an rush to publish books on a new topic that has subsided, although the rate of publication in journals has been more constant.
What are haplotype blocks, why are they interesting, and how do they differ from haplotypes?
This is illustrated by an interesting paper in a recent (2020) issue of Nature that comes from the work of a large consortium addressing the  question of the adaptation of sunflowers to different ecological niches. This involves the evolution of so-called ecotypes, differing in properties such as flowering time and ability to grow on sand dunes.
The problem is that these adaptations involve many different genes (and hence alleles) which means they involve different haplotypes, according to the definition in Wikipedia:

A haplotype (haploid genotype) is a group of alleles in an organism
that are inherited together from a single parent.

However these different sunflower ecotypes are not physically separated from others, so that one would expect hybridization between them to occur, resulting in the loss of the haplotype and the adaptation. As the paper points out, this problem is actually a reformulation of criticisms of Darwin’s theories by his contemporaries:
Romanes, G. J. “Physiological selection; an additional suggestion on the origin of species.” Zool. J. Linn. Soc. 19, 337–411 (1886).
(although I must admit not to have read the original.)
The fact that this does not happen is because the alleles constituting the haplotype exist in non-recombing blocks — haplotype blocks.

A haplotype block is a region of an organism’s genome in which there
is little evidence of a history of genetic recombination, and which
contain only a small number of distinct haplotypes.

What prevents the recombination of such blocks? It appears that the most come explanation is that rearrangement of the regions containing the haplotype blocks occurs, preventing recombination. One of the easiest rearrangement to understand is simple inversion, two large blocks of which were found on chromosome 5.
The studies in the paper started with two haplotype blocks which had been shown to be involved in the ecotypes shown, and which were found to contain genes previously implicated in these processes, such as FLOWERING LOCUS T and HEAT-INTOLERANT 1. By genome-wide association studies they identified a total of 37 haplotype blocks on the basis of linkage disequilibrium. A diagram of some of these blocks in different sunflower species may wet the reader’s appetite:

So, in answer to the poster’s specific query: The concept of haplotype blocks is very much alive!


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Finding total concentration of enzymes
Sorry if my question is very basic for biology majors because I am not. I am trying to build a mathematical model of a particular pathway using systems of differential equations and in order to reduce the number of parameters, I need to know the total concentration of multiple enzymes. How are enzyme concentrations usually reported in the literature so I can google it? Also, this does not seem to me to be a straightforward measurement for professional biologists, so how are enzyme concentrations actually measured or approximated? Thanks in advance!
I am interested in the following pathway:

I wonder whether you could clarify whether your equations deal with concentration in term of physical amount of enzyme (mg/ml) or (functional) activity (enzyme units per ml). The reason I ask is the latter is what I would think determines the operation of the pathway. But perhaps I misunderstand what your mathematics is modelling. Presumably you are trying to quantify the effect following some stimulus — can you elaborate. Oh, and in what tissue in what organism do you wish the concentrations?

@David: I am interested in the physical amount of enzyme, because I intend to use an oversimplified relational equation: $E_T=E_f + ES$ where $E_T$, $E_f$, and $ES$ stands for total enzyme (physical) concentration, "free"-enzyme, and enzyme-substrate complex, respectively. I think this would be a way to approximate a model of inhibition where $S$ is an inhibitor of the enzyme $E$, since the inhibitor would "eat up" the amount of free-enzymes. Ideally, I am interested in human fibroblast or endothelial cells. However, if data is too scarce for human cells, then mice would be fine.

@David: Also, by functional enzyme, did you mean an active enzyme?

Yes. I was trying to use layman's terms (not very helpful). I'll think about your approach and see if I have anything useful to contribute.

Hi again TheLast Cipher,
Enzymes in a cell are usually semi-quantified by the: Western Blot technique.
But there are lesser known techniques.
E.g. For a Western Blot the unit of measurement is the color intensity of the enzyme band on the blot membrane.
If I were you I would look for journal articles covering your pathway of interest.
E.g. https://iubmb.onlinelibrary.wiley.com/doi/abs/10.1002/biof.5520320129
Covers the electron transport chain (Co-enzyme Q10)
If you can get through the pay-wall & read their results and you will find:

"Western blot analysis of membrane protein isolated from keratinocytes derived from one young and old donor. A representative picture out of five experiments is displayed."

Also they used and I quote:

"Arbitrary Units"

Maybe you could comment on which pathway and I can find some assisting material.

Thank you very much, Andrew! I've uploaded an oversimplified version of the pathway as a rough sketch of what I am working on. So there are kinases in between the interactions and I'm interested in their concentrations (e.g. PIP2, PRAS40, TSC2, Rheb-GDP, Rheb-GTP, as found on figure 3 of https://pubmed.ncbi.nlm.nih.gov/28069808/).

Your attachment is unfortunately RNA concentrations. I'll see what I can find.

The BioNumbers site (https://bionumbers.hms.harvard.edu/search.aspx) is often useful for these types of questions, if you're interested in an order of magnitude. However, if you want precise concentration ratios (i.e. something like "is there twice as much Ras as ERK, or more like half as much"), you are unlikely to get a definitive answer.
These may be cell type-dependent and even vary from cell to cell due to noise. You probably want to simulate your network with a variety of absolute concentration, and then the most interesting behaviors are those that are reasonably robust to the exact numbers used (results that depend on, e.g., having almost exactly the same number of molecules of Ras as ERK are likely irrelevant as they would be too "brittle" inside a living cell). Once you find out what the necessary limits are for a given behavior that you find interesting, you could think about checking whether values reported by the literature indeed tend to fall within those bounds.

Hey, thank you very much for this. This looks like a great resource!


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Identify a small spider from southern Poland / eastern Europe
Can anyone identify this spider that I have just found in my home?

Details:

location: Katowice, Upper Silesia, southern Poland, eastern Europe (46.42 N, 17.78 E),
size: ~3-3.5 cm (from tip of one leg to tip of opposite leg) / < 1 cm (corpse lenght),
date: July 23th, 2020 (summer, approx. 10:30 am).

Are those ice crystals in the photo? I'm curious as to what surface the spider is on, seems almost like the windshield of a car.

No, it can't be ice, because it is a middle of summer here, in Poland right now. I found this spider in one of my rooms, captured it gently to some plastic pot and then move it to a windowsill beyond one of my windows, where it was released. These marks you spotted are microfractures in the windowsill itself. It seems, it was painted with using a fairly cheap paint, since in went into this condition in less then 10 years of a moderate weather conditions, we have here.

It is a Barn Funnel Weaver (Tegenaria domestica), In Europe it is known as the domestic house spider.
Here's some photos of this species to prove the similarities:

What caught my eye in particular that made it more clear that it was this species was the color patterns on the abdomen and cephalothorax, the size you mentioned, the shape of the feelers as well as the location.
The slight difference in shade of color may be due to being a different variety of the species or simply because of the weather and habitat that the spider is in.

Thank you! As for the other differences you mention, I can't say anything specific as I am not a arachnology expert by no means. As for the size, I can be completely wrong, because when I came back to measure it, the spider was simply gone. But, I can see at Wikipedia: "Their body/legs ratio is typically 50–60%, which accounts for a body size of 7.5–11.5 mm" whic means, if I am not mistaken, that it has 2 cm at max. The one that I was observing certainly wasn't that small. I think it was more closer to 3 cm.

barn funnel weavers tend to have banded (striped) legs, while the specimen in question doesn't have banding and so it is likely Eratigena (a genus offshoot of Tegenaria) especially considering the leg length ratios. This is likely a 'giant house spider,' one of the Eratigena species.

@JimN You raise a fair point, I suggest you make a detailed answer.

Your spider is one of the Giant House Spiders. (Eratigena atrica complex). There are three species in this complex in Europe: E.atrica, E.duellica, E.saeva.
With the lack of banding in legs, it is not a barn funnel weaver as suggested in the other answer. ("Tegenaria spp. have banded legs, Eratigena spp. have plain legs" - https://www.naturespot.org.uk/species/giant-house-spider#:~:text=The%20former%20genus%20Tegenaria%20has,the%20genitals%20of%20mature%20specimens. )
Some sources will equate the Eratigena and Tegenaria genuses with each other, while most separate them with a notable recent change of the hobo spider which used to be Tegenaria agrestis and now considered Eratigena agrestis. Taxonomy is ever-changing. A hobo spider would have two dark stripes running lengthwise on the carapace like the barn funnel weaver, which your specimen does not have. The Carapace marking of giant house spiders can have two dark stripes or a other patterns that look like radial lines emanating from the centre of the carapace.
Here is a photo of a giant house spider:

They darken in colour as they grow in their shell/exoskeleton, and after molting, they are very light coloured (and vulnerable).
This second photo is one believed to be E. saeva:


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DNA damage theory of aging and sex
If aging is due to accumulation of damages in DNA, then shouldn't the DNA in gametes also be damaged and so the next generation should be borne old! How does gametes avoid this DNA damage accumulation?

I've answered a related question, which was wondering why older people get more cancer from accumulated DNA damage and yet their children aren't immediately susceptible to it, here:
https://medicalsciences.stackexchange.com/questions/19915/why-do-age-related-dna-transcription-errors-not-manifest-in-children-as-readily/
Quoting from my answer there:

...a parent does not pass on all their mutations in all their cells, they pass on just one, which need not have any deleterious mutations at all, even if the parent has cancer themselves in some other part of the body.

If that one cell is defective in some way, it is less likely to be involved in creation of a successful pregnancy, and may lead to miscarriage. Therefore, the probabilistic process of reproduction tends to result in offspring from selection of healthier gametes.

There are in fact mutations that accumulate in gametes, but if any of those mutations are very serious, they are unlikely to support development of an entire new organism, and they are also relatively few. The burden of age on the genome is spread over all the cells in a body, and worst in types of cells that divide the most, when errors are most likely to occur.

Yes and no. Your concept about DNA damage causing aging is good. But aging is caused by DNA damage that causes the biologic / signaling pathways to not work as well as they once did. Think of biophysics and interactions among the plethora of proteins, molecules, etc. in your cells and tissues and all of the interactions therewith where even the electronic charge + vs -  and quantity of molecules (charged or not) in a vicinity influences the effectiveness of a biological pathway etc. This is aging. Basically, if you have learned about development biology at the molecular and cellular levels, you would know that much of that is not yet developed at the gamete stage. Therefore, there's not a whole lot of aging that can be had at the gamete stage because there's frankly nothing going on just DNA damage. Granted the DNA damage can influence on a grander scale as Bryan points out above - life or death (rather non-life) or the imposition of birth defects and other serious issues - but this is not how we define aging even if they are somewhat conceptually related. In short, aging is caused by the inefficiency and impairment of otherwise optimal (at birth) biological processes that slowly decay over time (silent mutations, environmental impositions, etc. that cause biophysics-based alterations at the smallest scale that impact exponentially as magnified over multiples of molecular interactions across a grand array of biological pathways and other molecular/cellular interactions).


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Why are monarch butterflies attracted to particular flowers but not others?
I have a "Purple Emperor Butterfly Bush" (Buddleia davidii 'Purple Emperor') and sure enough it does attract butterflies.
I have seen monarch butterflies using it, which confuses me, because I thought that monarch butterflies only fed from milkweed.
What makes this type of bush a substitute for the milk weed, but not other flowers?

It's the Monarch caterpillars that only feed on milkweed. Adult Monarchs, like many butterflies, feed on the nectar from flowers. https://www.fs.fed.us/wildflowers/pollinators/Monarch_Butterfly/habitat/index.shtml


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At small axon diameters (<1 µm), why does myelination not increase neuronal conduction velocity?
As per the diagram below (and other graphs available online), why do unmyelinated fibres have a higher conduction velocity than myelinated fibres when the axon diameter is less than around 1 µm?

Graphs like these are based on a complete cross-sectional area. Myelination adds thickness, so if you want to add myelin outside and keep the same diameter, you have to have a smaller lumen inside the axon.
As you can see in the "unmyelinated" plot versus diameter, smaller fibers have lower conduction velocity. Since the benefits of cross-sectional area are most important at small diameters (because the velocity changes with the squart root of diameter), for small diameter axons you end up losing more from losing internal area than you gain from adding external insulation.
If you keep the internal diameter the same and just add myelin, you will always increase the conduction velocity, but the total diameter including the myelin won't be the same anymore.

This explains it perfectly. So going from unmyelinated to myelinated is always beneficial in terms of conduction velocity, but it may not be in terms of space-saving. Thank you!

@pincushion44 Exactly, and space is at a premium in nervous systems!

That's observed due to passive conduction. With more area of cross section resistance is decreased (ohm's law). Myelin has just function of insulation the graph showing conduction in neuron fibre varying with thickness of neuron (hereby also thickness of myelin sheath).
Conduction is ruled by multiple factors not only just thickness of insulation. check this out https://www.ncbi.nlm.nih.gov/books/NBK10921/
When the area is so less than certain level the resistance is really high and insulation provided by myelin sheath works against conduction rather than supporting it. Conduction happens superficially instead in the bulk.
Where as in non myelinated fibre the insulation of myelin is not barrier.
Straight line tells me that my reason is legible probably since current is proportional to (1/R and hence) A

Sorry, I am slightly confused as to why insulation from myelin works against conduction when the area is low (and so longitudinal resistance is high)?

will try to make answer better after studying more about it

try that citation if it helps tell me.

It might also be possible that at smaller diameter cohesive forces of myelin sheath material close the node of ranvier and reduce it in significant amount


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Are Flippase Recognition Target sites read through during transcription?
I believe it is quite straight forward, but if i have a FRT site following the last exon of a gene (with the stop codon removed), would the transcription factors read through the FRT site and transcribe whatever follows it, or would transcription be halted?

Welcome to SE Biology. One general piece of advice in communication is always to define acronyms and avoid using them in titles of questions unless they are very well known (DNA etc.). This will increase the likelihood of people looking at and understanding your question and answering it. You can edit your question. Perhaps shorten the title removing what comes after "or" (that can go in the body) and putting in the question mark.

@David thank you! And appreciate the advice, made the changes as well!


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How to produce and isolate an enzyme?
I have recently learned that one of the best ways to isolate a protein in industry is via Chromatography. What are other ways enzymes are isolated in industry? Are there other ways?

Chromatography is one of the best ways to isolate a protein, full stop. It is extremely widely used in both academia and industry.
Before we get into the details, though, a definition is in order. Chromatography is a means of separating components of a mixture using a mobile phase (liquid or gas) traveling though a stationary phase (a solid, gel, or very small beads, frequently with something attached to them). Chemical and/or physical interactions between the components of the dissolved mixture and the stationary phase cause those components to migrate at differential rates, separating them out from each other.
There is a huge variety of protein-stationary phase interactions that can be utilized in chromatography. Microscopic beads made of different substances can be used to create a matrix of pores where larger proteins will migrate more quickly than smaller ones. Epitope tags such as Myc or FLAG can be recombinantly added to a protein's sequence and purified using beads that have epitope-specific monoclonal antibodies covalently bound to them. The tagged protein is "grabbed" by the antibodies while the rest of the mixture washes through, then the binding is reversed by various chemical means that interrupt the protein-antibody interaction, such as high salt concentrations, varied pH levels, or chaotropic agents and the concentrated protein collected all at once.
Sometimes it is known that a certain class of proteins (such as antibodies, for example) will bind very specifically with another protein or protein fragment (in this case, the bacteria-derived Protein A). That protein is covalently bound to beads and used to purify and/or concentrate all antibodies in a solution, regardless of the antibody's specific target. Protein A binds to a section of an antibody known as the Fc region, so that sequence is sometimes fused to a non-antibody recombinantly-expressed protein so that it can be easily purified by this method. Antibodies that are specific for the protein of interest itself can be used for purification.
Many other chemical reactions can be harnessed to cause a protein of interest to bind to a stationary phase substrate and later eluted by reversing or inhibiting the chemical reaction. One example is purification based on electrical charge, called ion-exchange chromatography. If it is known that a protein has an overall positive charge, negatively-charged beads can be used to bind it (and all other positively-charged proteins in the mixture). Once washed, the protein(s) can then be eluted by changing the pH, hence neutralizing their overall charge and breaking the ionic bonds which bound it to the stationary phase. Positively-charged beads can also be used to purify negatively-charged proteins.
There are many other strategies besides the ones I've highlighted here – the term chromatography encompasses a huge range of possibilities for protein purification. I would say that in the majority of large-scale industrial purifications, combinations of different types of chromatography are the only methods used. There are of course other methods involved in the manufacturing of a protein therapeutic, such as cell lysis, filtration, concentration, dialysis, formulation, etc., where chromatography is not used, but for purification it's typically the only one. One reason for this is automation. Chromatography columns can be loaded, washed, eluted, cleaned, and regenerated without the need for any human interaction other than to provide the necessary buffers and materials. It can often also be scaled up quite a bit from benchtop to manufacturing suite, allowing for more material to be processed per batch. And, once everything is tweaked and optimized, you can get extremely pure material out of it.
There are some other protein purification methods, such as organic extraction, density centrifugation, and differential precipitation/solublization, but these are typically (but not always) used more in research and development than manufacturing, for various reasons. You don't want toxic organic chemicals like phenol, chloroform, ether, etc. involved in your manufacturing process if at all possible, because it takes a lot of work to prove to the FDA that all traces have been removed at the end. Centrifugation is not very scaleable, and is rather difficult to automate. One of the issues with precipitation is ensuring that re-solublization is both complete and consistent between batches. The amount of work that goes into validating manufacturing processes for injectable drugs and getting FDA approval is absolutely mind-boggling. Trust me :)
Hopefully I've answered your question! Please let me know if I missed anything or you want to know more about something.

Hi MattDMo, that answers my question very well. If I could ask another question in relation to 'manufacturing of a protein therapeutic, such as cell lysis, filtration, concentration, dialysis...' how do I find out what steps are appropriate if I only know the protein? Journal articles? Or online databases?

@Andrew Yes, those, experience, and trial and error. If you gave me a new protein to purify, I'd first check journals and look at several protein databases to get as much info as I could. What you're going to be using the protein for is another consideration - are you treating cells with it? Injecting it into mice? Doing biophysical experiments? Do you want just the natural protein, or can I epitope-tag it to ease purification? Another thing I'd check for is whether there are good antibodies available for the protein, as you can use them both for purification itself and for detection. [...]

[...] Just starting out, I'd probably epitope tag it just so I can easily purify it, detect it, and test my protein-specific antibodies on it, then go back to the natural sequence if you need it in that form. You have to be able to look at a sample or column fraction and figure out if your protein of interest is there, and check quantity and purity. Western blotting is usually the best tool for that, along with Coomassie or similar gel staining. Then, it's just a matter of trying different column types based on the protein's predicted biochemical characteristics and seeing what you can get.

You also need to remember that there's not necessarily only one "right" way to do it. I might do ion-exchange followed by nickel followed by size exclusion, whereas someone else might do three different types of ion-exchange.

Thank you for all your help. I appreciate it heaps.

”Microscopic agarose beads can be used to create a matrix of pores where smaller proteins will migrate more quickly than larger ones.” Perhaps I am mistaken, but this sounds like you are describing gel filtration. If that’s the case, however, it is larger proteins which elute more quickly than smaller ones.

@canadianer good catch. For some reason I was thinking of electrophoresis, where smaller goes faster.


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Do Termites and Silverfish metabolize cellulose the same way?
I am fascinated with silverfish and would like to understand more about their metabolism.
I learned that they can survive on a diet of cotton which is nearly pure cellulose. Do they metabolize cellulose in the same way as termites?  Or do some insects have different metabolic pathways for cellulose?

It has been known for 40 years or more that some insects such as termites digest cellulose by synthesizing their own cellulases, whereas others have a symbiotic relationship with gut micro-organisms that perform this digestion (see Martin, Comp. Biochem. Physiol. (1983) 75A 313-324  — requires subscription — or this short popular science article).
What is the situation for silverfish — Lepisma saccharina? Today the evidence that generally determines whether an insect can digest cellulose itself is the presence of the genes for the cellulase enzymes in its genome. There is a relatively recent review of this in Annu. Rev. Entomol. (2010) 55 609–32 — again requiring subscription for access — in which the species in which these genes have been detected are listed. I know nothing about organismal biology or taxonomy, and can only summarize the species represented there for others to comment on:

Orthoptera
Blattaria
Phthiraptera
Hemiptera
Coleoptera
Hymenoptera

This doesn’t seem to me to include Lepismatidae (which Wikipedia tells me is the family), but what do I know. (I only know the genes aren’t present in fruit flies.) However some earlier indirect experiments studying the effects of antibiotics on insect cellulase levels suggest that Lepismatidae may have their own cellulase.


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Different Mutations Leading to Same Allele?
Can different mutations lead to the same allele? In my genetics books, I always see alleles referenced as, eg. Aa where A = dominant and a = recessive, but are these strictly binary phenotypes? Since there are an infinite number of mutations that could theoretically take place, wouldn't there be an infinite number of alleles? Eg (not an actual biological phenomenon but just as an example) A1C on chomosome 3 leads to allele a1, A1T leads to allele a2, etc.

You are looking at high school biology books. if that.  I'd be shocked if a high school text didn't mention blood group genes, for instance.
The simple genetics that Mendel elucidated only applies to a very small number of situations.
In real life, very few situations are explained by the interactions of only two different alleles, one of which is classically dominant to the other, within a single gene.
So sure, you could have many alleles which break a gene, but where the presence of one working allele is enough to be functionally indistinguishable from having two working copies.  You could also have slight sequence differences that are functionally identical.
Here's a random example; all the variants ensembl knows about for a random gene.  Note that these are only variants which have been found, obviously private individuals and families might have their own variants that are not documented
http://uswest.ensembl.org/Homo_sapiens/Gene/Variation_Gene/Table?db=core;g=ENSG00000280165;r=13:61409685-61415522;t=ENST00000409204
Most of these are in the 3' UnTranslated Region, and likely have no functional significance.


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What are the physiological effects of retinal exposure to 380–400nm light?
There are two categories of sunglasses: UV380 sunglasses block all light with wavelength 380nm or lower, while UV400 sunglasses block all light with wavelength 400nm or lower.
This made me wonder, what are the physiological effects of retinal exposure to the 380–400nm band of light, which is not covered by UV380 sunglasses?
Also, assuming that the 380–400nm UV light does cause eye damage, does any potential pupil dilation caused by the dark tint of such glasses have an effect on the amount of damage caused?

I suggest editing your question to remove all references to possible health effects and just focus on the scientific question of the physiological effects of retinal exposure to 380-400nm light. Make it a science question, not a personal health one.

@MattDMo Thanks for the suggestion, I tried to do just that.

Looks much better.

dunno but long term exposure would increase the risk of cateracts later on, just getting a milky zone on the iris. I think that's one of the main things that sunglasses protect from.

Answering my own question after thorough research:
Definitions
First, I noticed that there is no consensus on where the UV spectrum ends and the blue portion of the visible light spectrum begins.
According to the WHO, as well as to most other sources, the UV spectrum covers the wavelength range 100–400nm (1). However, a few other sources, notably the SCENIHR, define visible light as starting at 380nm (2), hence UV light would be 100–380nm.
Another source, the ICNIRP, directly mentions that the boundary is not clear-cut, “the band 315 to 380–400 nm is designated as UVA” (3) . At least one source refers to the 385–405nm band as the “UV/Visible Radiation Boundary Region” (4).
Tinted Lenses
To address the part about the dark tint of lenses causing pupil dilation, it is first worth noting that not all lenses that filter out UV light have a dark tint.
In fact, clear lenses can actually offer up to UV400 protection (5). There is even some research specifically on UV protection by clear lenses (6).
Back reflection of UV light
UV380 and UV400 are not the only eyeglass specifications relevant to UV protection. There is also eye-sun protection factor (E-SPF®), which was introduced in order to also account for back reflection of UV light from eyeglass lenses to the eyes (7). Therefore, this back reflection should also be taken into account when examining the effects of 380–400nm light exposure on the eye.
The 380–400nm Band
Now let’s get to answering the question.
According to the Texas Technical University Health Sciences Center, 40% of the radiation harmful to our eyes falls within 380–400nm, which they call the “UV protection gap” (8). Another source states that, while 100–380nm light is “very harmful”, 400–460nm blue light can still cause retinal damage and macular degeneration (9). The American Optometric Association also states that blue light, which they define as the range 380–500nm, may cause eye damage (10).
An article by ZEISS Vision Care explains that the UV380 standard was a “pragmatic choice” by the ophthalmic industry, and does not reflect “biomedical realities” (11). The article refers to the 380–400nm spectrum as the “most intense portion of solar UVR on Earth”. I assume the author is referring to the physical definition of intensity of radiant energy, which is the power transferred per unit area, however I am not 100% sure that this is the intended meaning of “most intense”.
I also found an article claiming that the WHO recommends UV protection up to 400nm (12), which again implies that 380–400nm does cause significant retinal damage. However, I couldn’t find the actual WHO publication stating the recommendation.

Hello and welcome hb20007,
I would like to introduce the types of Ultraviolet light to you first.

Ultraviolet A - UVA - 400–315 nanometers
Ultraviolet B - UVB - 315–280 nanometers
Ultraviolet C - UVC - 280–100 nanometers

UV380 sunglasses block all light with a wavelength < 380nm. Blocking most UVA, UVB & UVC.
UV400 sunglasses block all light with a wavelength < 400nm. Blocking all UVA, UVB & UVC.
The first article you attached is poorly written. It states that quality control is at fault by some sunglasses manufacturers. Meaning some sunglasses aren't made right because they do not meet appropriate manufacturing standards. Therefore they are damaging to eyes. Which is true.
The second article is also true.
UV380 sunglasses are fine for UV eye protection, if you would like greater protection from ultraviolet light (all of UVA), then buy UV400 sunglasses.
I talk more about ultraviolet (UV) light and it's cancerous consequences here.
Wikipedia has well-written free scientific information that I would highly recommend.

You did not address the apparent trade-off where wearing UV380 sunglasses dilates pupils but does not fully block UV light. I would like to have more information regarding this point. All I could find was this, which mentions pupil dilation and goes on to say that 100% UV protection is important.

In the original first article you reference, it is the 'Dark lenses' they are talking about that cause dilates pupils. Not the UV380 sunglasses, hope that is helpful.

True, but UV380 sunglasses will also cause dilation while not offering full UV protection. I'm interested to see if there is any research on the effects of the 380nm-400nm UV band on the eyes.

There is no evidence that UV380 sunglasses causes pupil dilation. As for your other question, nothing came up when I searched it on google scholar. It may not be ethical for animal models, and it is definitely not ethical for humans to be exposed to UV light of an exact band. Unfortunately I don't believe this is an area this we as humans know much about.

UV380 sunglasses, as well as any other form of sunglasses, would cause pupil dilation because of their dark tint.

Correct, the dark tint is what causes the pupil dilation. The dark tint the sunglasses they are referring to in that article is from faulty manufacturing - not from their ability to protect UV light < UV380.


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Limits of gene editing
I was reading some articles about CRISPR and the world of gene editing, but then a lot of questions for which I couldn't find any answer online came into my mind. Those are all about how far can we edit an organism. So here is the general question, followed by some other to narrow down a little bit this broad subject:
What are the limits of gene edition?

Can one edit the genes in its entire body? (as a human, or a multicellular organism)
What are the risks? I heard that some people who did try gene therapy ended up having some of their modified cells turned into cancer. Was is because of gene incompatibility  or because of error during the gene editing process?
Can we go as far as adding some chromosomes or changing an entire chromosome? For example, if a male human would like to change their sex, could they switch all their Y to an X?

EDIT: I decided to accept the answer from @MattDMo. However, I'm still interested in some development (clues with other technologies...)

Your question is very broad, but I'll try to address each of your points briefly.

It would be nearly impossible to edit the genes in every cell of a human being or other complex organism simply due to the number (and accessibility) of cells. A full-grown human has in the neighborhood of 30 trillion cells - 30,000,000,000,000. Cells in locations such as the brain and central nervous system are protected by the blood-brain barrier, which would keep most gene therapy vectors from accessing those cells. There are other reasons why editing each cell in the body is virtually impossible, such as vectors accumulating in the liver, but this is one of the main ones.

Cancer is indeed a risk from gene therapy in general, although DNA editing technologies like CRISPR in particular have a lower risk due to thTe circumstances surround exactly how the therapy is delivered to the nucleus of the cell where DNA resides. Other risks include potentially serious or fatal systemic inflammation due to an immune reaction to the viral vector which carries the CRISPR "machinery". Off-target effects can occur due to the wrong cells being targeted (although this risk is generally lower with CRISPR). Additionally, there is the very small but non-zero chance that the genetically-engineered vector could somehow regain its native infectious capability. Newer generations of gene therapy have significantly reduced this chance, however.

Very briefly, no. DNA is made up of "letters" (A, T, C, and G) called bases or base pairs, and typical CRISPR constructs only operate on 10-20 bases at the most — usually it's just one or a couple that are changed. A typical human chromosome has millions of base pairs encompassing hundreds to thousands of genes, so editing, adding, or removing an entire chromosome is simply out of the realm of possibility with this technology.

Thanks for your answer that was the one I was looking for. However, what are the vectors you're talking about? Retroviruses? Moreover, without using CRISPR specifically, what prevent us from just removing an entire chromosome "by hands" and then injecting a new one in one cell?

@MiKiDe As far as I know, you wouldn't want to use a retrovirus as a CRISPR vector, although they can be appropriate for other types of gene therapy. As far as removing a chromosome, you need to remember that most of the time, chromosomes are in a "relaxed" state and not tightly wound up into a single particle that could be picked up or manipulated. They need to loosen so transcription factors can get at active genes and transcribe them into mRNA. Condensed chromosomes are also extremely small, so manipulating them would just mechanically be very difficult.

Check out this and this for a brief and much more in-depth look, respectively, at how gene therapy works, including different types of vectors.


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Is this a bed bug skin?
I found this bug skin on my friend’s couch. Is it a bed bug? Could it be any other bug?

Here is a photo.


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Na+ / K+ ATPase: How does it restore resting membrane potential?
Could not find any sources talking about this (in a clear manner). If the Na+ / K+ ATPase pumps 3 Na+ out for every 2 K+ it pumps in, thus making the cell more negative, why is the Na+ / K+ ATPase used to restore resting membrane potential following hyperpolarization? Wouldn't that must make the cell more negative, which is the opposite of what we want?

The Na+ / K+ ATPase is not "used to restore resting membrane potential following hyperpolarization", it is used to maintain the concentration gradient of sodium and potassium.

@BryanKrause: How are the concentrations of Na+ and K+ outside / inside the cell rebalanced after hyperpolarization then?

Try also https://biology.stackexchange.com/questions/76166/ambiguity-about-the-relation-between-membrane-potential-and-concentration-gradie/76167#76167 https://biology.stackexchange.com/questions/57064/why-is-it-possible-to-calculate-the-equilibrium-potential-of-an-ion-using-the-ne/57066#57066 https://biology.stackexchange.com/questions/66166/are-cells-electrically-neutral-or-charged-to-setup-the-membrane-potential-across/66174#66174 in addition to the marked duplicate https://biology.stackexchange.com/questions/77919/why-does-resting-potential-not-become-continually-more-negative

The sodium-potassium pump does keep the concentrations of Na+ and K+ constant in the long term, but that's not necessary for transient changes like you get from receptor activation or action potentials, those are governed by opening and closing of passive ion channels.


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What is the difference among these compounds?
I'll preface this question by making clear that I'm not not well versed in biology.
Anyway, within the context of biocides/antimicrobial products using them as active substances, what is the difference among these three quaternary ammonium compounds:
benzyl-C12-16-alkyldimethyl, chlorides (CAS number - 68424-85-1)
benzyl-C8-18-alkyldimethyl, chlorides (CAS number - 63449-41-2)
dimethyloctadecyl[3-(trimethoxysilyl)propyl]ammonium chloride (CAS number - 27668-52-6)
How does one's antimicrobial properties differ from the other? And which is more hazardous? And which is least hazardous?

At a glance, they all seem potentially hazardous. The relative risk from using them will vary more with how and where they are used, in what forms, who's using them, how are disposed of, etc. It would be helpful if you included some context for their intended use in your question.

As you point out, these are all quaternary ammonium compounds that are likely to work in a similar way (membrane disruption) and are very broad spectrum. Any differences in efficacy against a given pathogen would need to be established by empirical testing on that particular organism, as these kind of things are highly idiosyncratic--it's not like an enzyme inhibitor where you can ask whether the organism has the relevant enzyme or not. The first two are even not pure compounds, they're mixtures whose precise composition is not known a priori.
As for hazards, these kind of quaternary ammonium compounds are frequently used in topical disinfectants for use on human skin, and even in low concentration in things like eye drops that go in the eye. Obviously as with anything, the dose makes the poison, and a concentration you would use to scrub your bathroom sink is not safe to put on a mucous membrane on your body.


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Red flower with yellow star in center with fig-like leaves
This plant has red flowers with a yellow star in the center and has fig-like leaves.

Location: Toronto
Size: 4ft tall by 3ft wide
Date: July 25th, 2020

What is it?

They are common hollyhocks, they come in many colors. As a little kid from Chicago , I was impressed by flowers taller than me when visiting rural Wisconsin . Then the standard for hiding/decoration outhouses.


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What are these small, indoor bugs?
I live in Switzerland and have noticed these small bugs appear in my bedroom, either slowly crawling on the parquet flooring, lazily buzzing around or dead on my windowsill (as pictured):

I'm not sure if these bugs are currently appearing more often – or if I just notice them more because of the fact that I'm spending a lot of time in my bedroom due to Corona lockdown.
The only hint I've got is a friend saying that they live in wooden floors. No idea if that's correct.
Thanks for any help or hints!

I doubt you'll get a positive ID from that photo. It might be some woodboring beetle, maybe genus Anobium or Hedobia. FTR, if they are chewing on your wooden floors, you might be able to hear them if you listen carefully.
I suggest you collect some, maybe even living, in a small tube and ask a specialist. My first idea would be someone at a nearby university or natural history museum working in entomology, and specifically on Coleoptera if possible.

I think this is a species of Varied Carpet Beetles. The varied carpet beetle (Anthrenus verbasci) is a 3 mm-long beetle belonging to the family Dermestidae. They are a common species, often considered a pest of domestic houses and, particularly, natural history museums, where the larvae may damage natural fibers and can damage carpets, furniture, clothing, and insect collections.
Source: Varied Carpet Beetle

This is incorrect

This is what I could find closest to those shown in the image. I might be wrong.


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What is the meaning of deep winter mixing?
I was reading a paper about eutrophication and there was a term "deep winter mixing" in which an abundant supply of phosphorus is released to the surface waters. I searched a lot but nowhere I could find a definition for that.

The winter mixing of stratified layers in lakes and seas due to temperature changes can vary in depth, so scientists sometimes say "deeper winter mixing" and "deep winter mixing". Scientists measure the water arising from 300 or from 800 meters depending on the year, so the deeper winter mixing is a relative term. i.e.:
1992, associated with more stormy weather and higher precipitation than usual. This anomaly was the cause for the deeper winter mixing in the Cyprus Eddy (>500 m) than the typical 350 to 400 m reported by Brenner et al. (1991). Exceptionally deep vertical mixing (>850 m) was reported that winter also in the Gulf of Aqaba https://www.int-res.com/articles/meps/167/m167p047.pdf
Here is basic description of winter mixing:
https://teara.govt.nz/en/diagram/11817/water-circulation-in-a-lake

and here is a science paper:
https://www.jstor.org/stable/2259960?seq=1
A wiki page on lake stratification:
https://en.wikipedia.org/wiki/Lake_stratification


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Partial pressures of different gas in human blood and how they are calculated?
In Respiratory Physiology, we use the $P_x{O_2}$ and $P_x{CO_2}$ in blood at different regions of the peripheral circulation. From my Chemistry knowledge I know that $P_x$ of a gas in a solution is the fraction of total pressure caused due to the gas dissolved. But in blood $O_2$ is present mostly as $OxyHb$ and $CO_2$ is also present as $CarbaminoHb$ & $HCO_3^-$. In blood their dissolved state fraction is very low. Now my question is how do we measure the $P_x$ of any gas ($O_2$ or $CO_2$) in blood and what is the logic here? [x means either arterial blood or venous blood]
Here is the data I'm talking about.(https://i.stack.imgur.com/lA1M5.jpg)

As a notation note, I never seen your $P_a{O_2}$ notation used except for referring to arterial partial pressure ($P_v{O_2}$ would be venous). Generically, partial pressures are usually noted as, for example, $P_{O_2}$.
When we talk about partial pressures in biology, we literally mean the partial pressures: that caused by dissolved gas.
Hemoglobin-bound oxygen is not the same as gaseous oxygen, nor is carbonic acid the same as carbon dioxide. Neither contribute to the partial pressure. They do relate to the total oxygen/carbon dioxide carrying capacity of blood, but this cannot be measured directly through partial pressures.
See this Q&A for a situation this comes up: Why is arterial pO2 normal in carbon monoxide poisoning?
In medicine, it is common to use oxygen saturation as an alternative measure of blood oxygen concentration; this refers to the percentage of oxygen binding sites of Hb that are saturated.
It is important to realize that the partial pressures of dissolved gases will eventually reach equilibrium with the surrounding atmosphere; the lungs are a great gas exchange organ (that's their entire job), so blood leaving the lungs should have partial pressures that approximate those inspired air (in practice, there is some discrepancy because the lungs are very humid and also are constantly refilled with $CO_2$ from blood, so water vapor and carbon dioxide contribute a substantial gas pressure that pushes out other gases: see the similarity between arterial blood and alveolar gas in your data table and the differences between atmospheric gas and alveolar gas).
Clinically/in a lab, we measure these things with a machine that just magically gives the numbers. I looked for a simple description of how these machines actually function, and found https://acutecaretesting.org/en/articles/understanding-the-principles-behind-blood-gas-sensor-technology to be useful. In summary, $CO_2$is measured by exposing a captive solution to the gas and measuring the pH, giving an indirect (but accurate) measure of $CO_2$. $O_2$ is measured with a reducing current. It's also possible to measure concentrations of arbitrary compounds more directly with gas chromatography - colleagues of mine have used this for anesthetic gases, for example.

Extremely sorry for using wrong notations. But $CO_2$ is more soluble in water than $O_2$. So then wouldn't that imply $P_{CO_2}>P_{O_2}$ ?

@A.N.Ψ No, it would not imply that. If you want you could ask about why that is on the Chemistry stack exchange, since it's unrelated to biology.


text:
Variation in deathstalker scorpion
I recently encountered a (probable) deathstalker scorpion in the Negev desert in Israel:

However, when trying to identify this species I found that in many/most photos of the yellow scorpion the final segment before the stinger was dark or even black (see the wiki link for examples) i.e., not yellow, as shown in the photo.
Is a black/dark pre-stinger segment an indication of some sort (perhaps venom?), or is it an indication of a separate species, or other? Clarification on this matter is most welcome.

Update - I contacted an Israeli PhD from Haifa University who wrote the following:
"...looks like Andrtoctonus amareuxi (also referred in the past as Andrtoctonus amareuxi hebraeus, Israeli fat-tailed scorpion (קטלן עברי)
the genus common name is fat-tailed scorpion... The color of the last segment of the abdomen before the stinger is not a very good sign alone for species identification, as it is variable in the population and also found in at least 2 other genera/species (in the genus Buthus and in some species of the genus Compsobuthus). Anyway for sure it is not the deathstalker which is easily identified by a marking on the prosoma, behind the central eyes, that looks like a lyre  and the ridges on the abdomen..."

The scorpion in question appears to be Buthacus leptochelys, and is not a Leiurus sp.

According to the Israeli Scorpions Field Guide, deathstalkers can have also pale metasomal segment V, so a black one isn't a sure identification sign although it is very common among deathstalkers. The characteristic of the Israeli deathstalker are 5 ridges along its back. The species of deathstalker in the Negev (and Israel) is Leiurus hebraeus.

I haven't found an official reference, just a mention that the metasomal segment V can be pale in some adults.
Perhaps after molting the colour is different?
Also, dont know if it is Leiurus quinquestriatus, L. hebraeus, or L. abdullahbayrami
I see picture with the same pale coloration at sciencedirect.com/topics/agricultural-and-biological-sciences/…


text:
Why is thoracic breathing dominant in women while abdominal breathing is dominant in men?
In human males, lateral movement of thorax constitutes 25% of breathing while abdominal movement accounts for 75% of breathing. It is exactly the opposite in the case of women.
I got this piece of information Trueman's Elementary Biology.

Welcome to the Biology community. Please improve your question by: 1. Citing sources for the information you provided (i.e. differences in respiratory movements in the sexes), and 2. Describing what efforts you made to answer this question (e.g. reading books or journals, doing your own experiments). This will invite good answers to your question. Cheers!

Some workers (https://www.karger.com/Article/Abstract/87456 and https://journals.physiology.org/doi/abs/10.1152/jappl.1975.39.4.608) have observed that respiratory movements do not differ in males and females, at least in quiet breathing. That makes it even more important to cite your sources in this question.

I think that your question will be correct if you give a reference for the percentages. it is true though, otherwise just take the percentages away and cite this paper: http://rc.rcjournal.com/content/57/9/1442.short ... Upper thoracic movement was significantly decreased with age. There was less abdominal movement in females than in males, except during quiet breathing in the supine position.

@Meercat Here is a good article that should answer your question: https://breathe.ersjournals.com/content/14/2/131. (You can read and download it for free.)

Probably an evolutionary feature to prevent pregnancy from making breathing difficult.


text:
How to build SEG in your personal environment?
I'm trying to implement SEG (Wootton & Federhen,1993) in my MATLAB and Python environment. From this oriinal article I cannot figure out what I need to build my script. Are there any related article that explains the various steps to build this algorithm (from the mathematical point of view)?

Your question seems to relate to software rather than biology. You are likely to have more luck in SE Bioinformatics.

Yes I know that it seems like that. But I do not want anyone to explain me the code. I want to know if any of the users of this blog know the related articles. From a certain point of view it could be related to the biology context since we all have to study and we all can share our experience!

That paper isn't open access, so many potential helpers (including me) can't read it...


text:
RNA polymerase Sigma subunit: transcription factor, coenzyme, or what?
Studying prokaryotic transcription, it seems that the α2ββ′ω core enzyme + the sigma (σ) subunit comprise the ‘holoenzyme’ required for prokaryotic transcription. In traditional enzyme nomenclature, this would indicate that the α2ββ′ω is the ‘apoenzyme’ and that the sigma subunit is the cofactor or coenzyme. However, I’ve not been able to find any sources that clarify whether or not the sigma factor is indeed a coenzyme (not cofactor since that has to be non-organic), and if not what it actually is and why. Any clarification would be appreciated.

No.
I don’t think anybody would call the sigma factor of bacterial RNA polymerase — or indeed any other protein — a cofactor or a coenzyme, the subset of cofactors that are organic (the original poster is wrong in his declaration about cofactors, or at least one reputable text book disagrees with him).
I could justify this statement by quoting a definition from the section linked above:

“The catalytic activity of many enzymes depends on the presence of small molecules termed cofactors, although the precise role varies with the cofactor and the enzyme.”

by saying proteins like the sigma factor are not small.
However it is more interesting to me, and more useful to the naive reader, to make some general remarks about definitions in biochemistry and molecular biology.
What are definitions good for?
Definitions of terms are useful for scientific discussion or argument to enable those involved to be sure they are talking about the same thing. They often arise at the stage of a field of science when things are crystallizing after a period of uncertainty or lack of clarity. Even so they may lack precision. Cofactor just means “something else that is needed for certain enzymes to work” — biology is not physics.
Definitions are also useful for students and their teachers. They allow students to try to build a rational picture of a subject that is new to them. They allow teachers to systematize a subject (or lazily set rote-learning type MCQs instead of asking students to explain things).
The student new to the subject might find it helpful to consult glossaries such as those in Molecular Cell Biology, Molecular Biology of the Cell and Pearson’s Biological Glossary.
What are the limits of definitions?
The problem in a fast-growing field like modern molecular biology is that the period of resolution — when old men can form committees to give names to things — seldom lasts. Biology is anarchic, and new things come along that don’t fit into the neat pigeon holes that have been so carefully assembled. Nor do the anarchists or revolutionaries care. They find new things, describe them, and then get on with the next experiment. Why spend one’s time reading yesterday’s newspaper?
But the problem for the student comes when he discovers that everything does not fit into the neat categories he’s been taught, that there is a world beyond lactate dehydrogenase and metal proteases.
Sigma factors — what’s the problem in categorizing them?
The “classic enzymes” studied in early biochemistry catalysed simple chemical reactions between small molecules. However catalysis also occurs in more complex polymerization processes like nucleic acid and protein synthesis, that have the complexity of repetition along a polymeric substrate, and the necessity of having a specific start and stop along that substrate. It turns out to do that, that rather than enzymes such as RNA polymerase being a single catalytic protein they are complexed with other proteins that are necessary for certain of these functions. In the case of proteins like the sigma factor(s), this is complicated by the fact that these accessory proteins do not remain permanently associated with the catalytic protein subunit.
The poster, in his title, asks whether the sigma factor is a transcription factor. The answer to this is yes… and no. And calling it a transcription factor doesn’t really help much. Yes, it is a transcription factor because it is necessary for transcription and different sigma factors can impart a certain specificity to bacterial transcription. No, because the term transcription factor is mainly used for the much more specific proteins in eukaryotes that work in a rather different way.
What to call it? A subunit of the enzyme, is sufficient for Berg et al.. An accessory protein might perhaps add something. But don‘t worry too much about naming it, learn how it works.
Postscript: Other fruitless terminological disputes you may wish to avoid

Why is NAD regarded as a coenzyme and ATP a co-substrate?
Why is it epidermal growth factor, not epidermal growth hormone?
Why is it called vitamin D when it’s actually a hormone?
Should the term, molecule, be applied to double-stranded DNA or the individual chains?
How long must an oligopeptide be before it is called a polypeptide or protein?

No doubt there are others that I have missed that can be found in the list archives.


text:
Evolution: Can the genotype frequencies change, but the allele frequencies remain constant?
If a population isn't evolving because it's in Hardy-Weinberg (HW) equilibrium, then I know that both genotype and allele frequencies must stay constant.
My question is, can evolution still not occur even if Hardy-Weinberg conditions aren't met? In all of my books, the conclusion seems to be that if HW conditions are met, then evolution doesn't occur. However, they don't clarify if HW conditions being met is both a necessary and sufficient condition for evolution to not occur (they only imply that it's sufficient).
Any thoughts?

Could you clarify what specially you mean by 'evolution'? Are you referring to the evolution of a morphological trait, molecular evolution, evolution as a general response to selection? I'm also a little bit confused as to how this relates to the title of the post.

That’s important because by definition, if HWE assumptions are all met then there can’t be any selection occurring.

At the risk of further confusing the issue (there are already 2 answers focusing on different aspects!!), I am going to focus on a somewhat different aspect of this question that I think we need to nail down before it can be addressed.
Going mostly off your question title, it would help to know what you mean by genotype vs. allele frequencies. These are quite different, and it's not clear how you are trying to employ them. Speaking strictly, we use alleles to talk about genetic variation within a locus, and genotype variation to also mean variation across loci as well (how alleles across loci are sorted into individuals; this is sometimes also called "gamete frequency"). Of course, people generally talk about HWE in the context of only a single locus, which means that it is easy to get tripped up here.
It is possible for us to have non-equilibrium genotypes while also having equilibrium allele frequencies, in direct response to your question title. A trivial example of this is linkage: when two loci are very close to each other on a chromosome, their alleles will be more closely correlated than genes on different chromosomes. This yields the phenomenon with the unfortunate name linkage disequilibrium (LD), which implies nothing about evolution or HWE but rather about a non-equilibrium mixing of alleles into genotypes.
For context, it is quite common to apply tests of HWE locus-by-locus in genomics, as a sort of quality control or preprocessing step. It is also common to measure LD for relevant pairs of loci, but there is not much biological relationship between these measures (even though LD can be thought of as an extension of Hardy-Weinberg to a multilocus case, for historical perspective see here.). In any realistic case, global linkage equilibrium across the genome is very unlikely, whereas HWE for most loci is very likely.
As a thought experiment, imagine that a (neutral) inversion arises, and then starts segregating. All of the alleles remain at HWE, but suddenly you have new LD (genotypic disequilibrium) that wasn't there before.
With all that out of the way, I see no reason why evolution could not happen at the level of overall genotypes even in the case that HWE is maintained statistically. This can be achieved by the evolution of e.g. sign epistasis, I am sure there are other examples as well that would yield apparent HWE while trait evolution is technically still going on.
I think that it might be fair to say that monogenic evolution isn't happening with apparent HWE, I don't think that you can say the same thing for polygenic evolution.
I'll finish by just saying that I refer specifically to the statistical phenomenon of HWE, and not to the assumptions themselves (which would be tautological; "can evolution happen if you assume there's no evolution?" as commenters point out). After all, You can violate most of the assumptions of HWE and still end up with allele frequencies that look like HWE:

Although statistical deviation from Hardy-Weinberg expectations generally indicates violation of the assumptions of the theorem, the converse is not necessarily true. Some forms of natural selection (e.g., balancing selection, which maintains multiple alleles in a population) can generate genotypic frequency distributions that conform to Hardy-Weinberg expectations. It may also be true that migration or mutation is occurring, but at such low rates as to be undetectable using available statistical methods. And, of course, all real populations are finite and thus susceptible to at least some evolution via genetic drift.

Where do you get that populations aren't evolving?
A population might be in HWE for a particular trait if there is no selection on that trait, but that doesn't mean that there is no selection or drift happening on any trait!

True but that wasn't the main purpose of my question. The more important part is regarding whether HW is necessary not just sufficient

@Ally Maybe an example of what you are thinking of would be helpful. As-is, to me this question just raises my eyebrows. I think you might have confusion somewhere but I'm having trouble pinpointing where that is.

If a trait is under selection, by definition it's not in HWE.

Yeah so reiterating the question in an if..then format might make it more clear. Right now, I'm getting that "if HW, then no evolution", which also implies "if evolution (aka if a trait is under selection), then no HW". However, from the original premise it does not necessarily follow that "if no evolution, then HW". So my question was basically asking if there was no evolution occurring, would that necessitate the population being in HW or if there was some other mechanism / set of conditions that would allow no evolution to occur

Stop talking about "evolution". It's too broad, and the idea that evolution "stops" because you try to apply some equations to a single trait is silly.  Evolution is pretty much always occurring, even if the proportions of some individual traits are stay steady.

The HW principle is not a mechanism.  They are equations that build a rather simplistic model that sometimes is applicable and useful in real life.

Let me focus on the necessary and sufficient part: such a language is suitable in mathematics, but does not really have much meaning in evolutionary/statistical context. Instead we talk about rejecting the null hypothesis, which does not mean accepting the alternative hypothesis. Equally, a failure to reject the null hypothesis does not mean that this hypothesis is true.
Hardy-Weinberg is a null model of evolution with about a dozen of assumptions. It is not a model of "no evolution", but rather a model of how evolution happens all the time (but it seems like "no evolution" in the sense that not much interesting is happening). Rejecting this null model/hypothesis means that some of its assumptions are violated. However, if the genotype frequencies do satisfy HWE, it doesn't automatically mean that the assumptions of this model are satisfied.


text:
What would sanitiser fail to do that detergent and warm water would do in cleaning glasses frame that isn't 'visibly soiled'?
Update (from comment):

It's certainly possible that the manufacturer had that in mind when making their cleaning recommendation, but I'd like to think they would specifically warn against it if it was a common issue.

For an arbitrary glasses frame, specifically the earsocks, can regular alcohol/sanitiser replace detergent and warm water? Apparently some brands of glasses frames recommend really detergent and warm water. I mean, with alcohol and sanitiser, am I perhaps killing only 99% of the germs instead of 99.9% of the germs? (If we wanted planes to be safe "with statistical significance" that is 99% confidence level we'd have between 400 and 2500 crashes a day.)
I couldn't find any videos for this on youtube. Most of what youtube gives is cleaning ears or cleaning the lenses.
Edited to add: I got the following with my new glasses.

Kind of a hassle to do the recommendation especially that I've never cleaned glasses frames in my 13 years of wearing of glasses, except when they were, to borrow a term from WHO, 'visibly soiled':

Clean your hands by rubbing them
with an alcohol-based formulation,
as the preferred mean for routine
hygienic hand antisepsis if hands
are not visibly soiled. It is faster,
more effective, and better tolerated
by your hands than washing with
soap and water.

• Wash your hands with soap and water
when hands are visibly dirty or visibly
soiled with blood or other body fluids
or after using the toilet.

Alcohol is a substitute for soap and water for hands that are not 'visibly soiled'. Is there perhaps some kind of substitute for glasses frame?

Did your recommandations specifically mention killing germs? Because glasses have special coatings that may be damaged more with one cleaning product than the other.

Are these recommendations specifically for the purpose of decontaminating or santizing your glasses, or for removing the oils and debris of everyday use? In my experience, ethanol doesn't do a great job of removing oils or drying clear. Most hand sanitizer has additional additives that may leave even more residue. Also, soap or detergent and water is effective against a much broader range of germ, as there are many on which alcohol sanitizers have little to no effect.

@Cell Thanks. Edited to add details. Kind of a hassle to do the recommendation especially that I've never cleaned glasses frames in my 13 years of wearing of glasses, except when they were 'visibly soiled'. Actually now I'll edit to add more details about 'visibly soiled'.

@MikeyC Thanks. Edited to add details. Kind of a hassle to do the recommendation especially that I've never cleaned glasses frames in my 13 years of wearing of glasses, except when they were 'visibly soiled'. Actually now I'll edit to add more details about 'visibly soiled'.

At least as I read those instructions, the purpose of cleaning is to remove accumulated dirt, dust, and natural skin oils, not to kill bacteria.  AFAIK hand sanitizer - a product I was entirely unaware of until the recent COVID-19 pandemic - is not designed for cleaning.

@jamesqf Ah so hand sanitiser(/alcohol?) would kill bacteria but wouldn't necessarily remove dirt, dust or oil?

@BCLC: Yes - or so I'd suppose from what I've read about the product.  As I said, I've never actually used it myself.

@jamesqf i mean in general with sanitiser/alcohol on hands, tables or glasses frames they kill bacteria but do not necessarily remove dirt, dust or oil?

@BCLC:  Once again, I DON'T KNOW for sure.  I've never used the stuff, and had never even heard of it before the COVID-19 panic buying caused it to become news.

Ignoring any possible impact alcohol-based solvents might have on the material or coating of frames, alcohol won't really remove anything it dissolves unless it is rinsed or at least thoroughly wiped off. When the alcohol evaporates, it will leave behind a residue containing anything that was dissolved in it. That's why your hands sometimes feel sticky after applying that gel hand sanitizer. The gelling agents don't evaporate with the alcohol, but instead remain on your skin.
But since this is the Biology stack, so I'll try to provide a more biological answer.

What would sanitizer fail to do that detergent and warm water would do in cleaning glasses frame that isn't 'visibly soiled'?

While alcohol based sanitizers are effective at killing most pathogens, it's typically on par with a soap and water scrub. However, for the purposes of sanitation (which seems to be the only reason you'd need to clean frames that are "not visibly soiled") there are several indications for which alcohol based sanitizers are considered ineffective and inferior to soap and water. This is generally because of the specific physiology or life cycle stage of certain organisms which allow them to be resistant to the biocidal effects of alcohol. Common examples include Cryptosporidium, a water-borne protozoan parasite, norovirus, a non-enveloped intestinal virus that spreads notoriously fast in hospital environments and on cruise ships, and almost all endospore-forming bacteria, like Clostridium perfringens and Clostridioides difficile. In the lab, we actually use alcohol to isolate live bacterial spores from the vegetative components of a culture. It has also been reported that alcohol based sanitizers are more likely to cause allergic reactions (e.g. contact dermatitis) from skin exposure.
Most of these statements can be referenced in this open-access article on PubMed, with links to primary sources if you're interested in following up more.
Gold NA, Mirza TM, Avva U. Alcohol Sanitizer. 2020 Jun 24. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513254/#

Thanks MikeyC! So actually alcohol or sanitiser may be harmful to the frame? ('Ignoring any possible impact alcohol-based solvents')

I only mentioned it because the possibility had been raised in some of the comments and the previous answer. It's certainly possible that the manufacturer had that in mind when making their cleaning recommendation, but I'd like to think they would specifically warn against it if it was a common issue.

MikeyC, GENIUS. thanks. i added part of your comment to an update to the question post

The earsocks on Oakley brand sunglasses are made of a proprietary hydrophilic rubber called Unobtanium 1.  From what I can find, Unobtanium is likely a styrene copolymer 2, possibly a formulation called Kraton G 3.  Polystyrene is insoluble in water, but soluble in ethanol and 2-propanol (isopropanol) 4, which are the most common alcohols used in sanitizers.
So, as suggested by @Cell, soapy water is likely recommended by the manufacturer because it is unlikely to damage the glasses, whereas alcohol-based cleaners may degrade the soft rubber components.

https://www.oakleyforum.com/threads/how-to-restore-old-unobtainium-that-has-gone-sticky.10821/
https://www.oakleyforum.com/threads/rubbers.21973/page-2
https://kraton.com/products/KRATON_G.php
https://www.bangslabs.com/common-solvents-and-non-solvents-polystyrene

Thanks Dirigible! So actually alcohol or sanitiser may be harmful to the frame? ('whereas alcohol-based cleaners may degrade the soft rubber components.')