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Do all monoclonal antibodies have a blocking effect?
I find a mAb targeting protein A, which has beed validated to work in wb/IHC/IP or antibody conjugating drugs. I'm wondering if this mAb could be used for blocking the protein A from binding with other proteins? This mAb is the only one antibody which could be bought without having to make it myself, so the answer is really important for me. Looking forward for your responses.

No. Not all monoclonal antibodies block binding of other proteins. This depends entirely on the antibody and its epitope though. Most monoclonal antibodies target a small epitope, somewhere between 7 and 11 amino acid residues in length. Where this epitope sits on the protein will alter whether the antibody is capable of blocking binding of another protein.
If the epitope is at an interaction site, then it is entirely possible that it will be a blocking antibody, but if it sits somewhere else, then it may or may not block depending on proximity and size of binding site of both the antibody and the interacting protein. In this second case non-direct blocking is known as steric hindrance or steric blocking and is due to molecular size.

Thansks for your really helpful reply! I wonna take this mAb in a vivo experiment. So does this mean I have to verify the blocking effect between protein A and other Abs before using? If so, wether just taking a flow cytometry staining is enough to verify the blocking effect. Is there any other experiments I have to do?

@jinyuhuang You can verify blocking using Flow and potentially by microscopy (e.g. fluorescence using tagged antibodies). You could also do it by native western (i.e. non-denaturing) for simulation of what might happen in-vivo. You do need appropriate controls in each case to ensure that the effect seen is due to blocking and not some off-target effect or secondary antibody effect for example. Look up "antibody validation" for more information about how to validate your antibody; don't assume, just because it is monoclonal, that it can't have off-target interactions.

Thanks for your suggestion again! This mAb had been used for antibody conjugating drugs which was approved by FDA. So, I guess there should be a extremely small chance of off-target interactions. I would like to investigate literature about flow cytometry, microscopy , and native western experiments as you suggest.


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How to compare basal expression of a gene in two tissues using qPCR techniques?
I have two tissues and they are not treated; I would like just to compare the basal level of expression of the gene of interest (goi) in these two types of tissue (tissue1 and tissue2). After qPCR, I have the following result:

I wonder how am I supposed to make a decision. Will in this case goi be more expressed in tissue2 ?  ctrl - is a housekeeping gene that we use for our types of tissue. Marked in yellow are just mean values. The last column is mean goi_value - mean ctrl_value qPCR quality is not great.

You normalized the data to the control and obtained the
normalized ct-values. Let's call it Δct.
Now you need to find the relative difference between them. In order to do that, the first step is that
you calculate the ΔΔct -> condition_1_normalized - condition_2_normalized.
Calculate the actual difference: condition1/condition2 = 2^-ΔΔct

In your case the answer would be: tissue1/tissue2 = 2^-2.4 = 0.19
The expression of tissue 1 is 0.19 of that in tissue 2. In other words the expression is about 5.2x higher in tissue 2 than in tissue 1.

thank you, but it's not exactly what I need. I am not looking for a fold change, but just a bare data to put it on a dotplot, for example. Say tissue1 must have some value and tissue2 as well. Not that tissue1 is a "control" and considered as "1" or zero. But it must have some value. Both of them.

also how did you calculate that 5.2x ?

I see. If I understand correctly, you want some kind of absolute value for your gene of interest for each of the tissues. Unfortunately, with the data you provided, that is not possible. You can only calculate the relative difference. For absolute quantification you need to run a standard with DNA of known quantity.

The 5.2x is simply the inverse of 0.19 -> 1/0.19
Then instead of tissue1/tissue2 you get tissue2/tissue1.

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Does anybody know what kind of creepy-crawly this is?
My son found this caterpillar in our garden in the UK. Have asked multiple people with more knowledge in this area who have been unable to identify it. looking for any help?
Having looked online the closest I have found are moth caterpillars, but not found anything like this one. I hope you can see from the images it has 'whiskers' around its head and around 1/4 of its body but no further, a yellow squishy looking head and quite muted green and black body.
It's the 'whiskers' (not sure of the proper term for them) not extending to its full length that I think is the most identifiable feature and that is what I have been unable to find when looking online.

Have you identified the plant it was found on, if possible?

We think it was a persicaria, it seems to be eating those leaves in the tank anyway.

It looks to my eye like some variety of tent caterpillar (though I've never seen that exact pattern before), have you noticed any silky structures in any nearby trees or shrubs? Also, if you still have it can we get a picture of its lovely face?

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What is a good expression vector for Salmonella enterica subsp. enterica serovar typhimurium
I am interested in expressing custom proteins in a Salmonella strain, however I am facing difficulties in finding the appropriate expression vector for it. It seems that most of the resources provide for E. coli expression. Does anyone have any recommendations?
Thanks in advance.

Is there a reason why you have to do this in Salmonella?

I assume that you want to e.g. express fluorescent proteins for doing some kind of experimental study of Salmonella, as opposed to industrial protein production.
I would suggest looking into prior work that uses Salmonella as a model. For example, I found this paper somewhat at random that uses several vectors in Salmonella to do experiments. Here is another. And here is another. Several of these appear to share authors, I don't know if that's Google SEO or a small research community.


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What is the approx. diameter of a completely "folded up" human DNA molecule, in inches?
The human DNA molecule would be about 6ft if stretched out to a straight line.
I'm curious what the diameter of the DNA molecule normally is when it is "all scrunched up" or "bundled" up, inside the nucleus of a human cell.
(I heard it was 30 billionths of an inch.)

Are you after the diameter of the double helix or the diameter of a chromosome? both are easily searchable.

We don't use inches in science. If you are a "student of biology" you need to get used to the metric system. If you need to convert to space shuttle disaster units, there are resources on the internet.

here measure it yourself, the scale bar is 1 um https://www.researchgate.net/figure/Metaphase-chromosome-plates-and-karyotypes-of-male-A-and-female-B-Phayres-flying_fig9_278095129

Can you cite some sources for your "6ft" fact and your "30 billionths of an inch" claim?

That's flying squirrels John.

As phrased the question is a bit confusing. In the most literal sense the diameter of a DNA molecule doesn't change much. Also, there isn't much bare DNA in the nucleus. It's largely wrapped around little spools made of protein called nucleosomes. The chains of nucleosomes are wrapped together to form chromatin fibers which make up the chromosomes. The chromosomes pull together into multiple 3-d blobs in the nucleus. Is it the diameter of those blobs that you are looking for?

Based on this picture, Chromosomes range from 2 to 12 micro-meters μm.
1μm is nearly 1/25400's of an inch
The 10-base system is more popular for science, and inches are not standard for science, but if they were, your answer would be 3/25400's to 1/2540 range.
For reference, standard writing paper and standard copy paper is about 100 μm, 0.1mm, 1/254's.


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When to clean out a bee house?
I have a bee house which seems to be very popular...

I have noticed that a hole can become vacant and then filled again within half a day. Now, it's been up a few years and I don't necessarily pay that much attention to it. I suspect that some of the holes contain failed bees, so I would like to clean them out for new occupants, but I do not want to harm any that might be in there. The holes range in size from 2.5–6 mm in diameter.
How can I mark occupied holes without using anything that could be harmful? For example, I thought of using a marker pen on the material used to cap the holes, but might the solvent, even though it'd be a tiny amount, hurt the larvae?

I suspect that your best bet will be something non-toxic.
I would make a mark that is removable and not directly on the hole. Possibly something like beeswax to mark a circle around the hole or maybe even a pencil  mark might work. In the case of a pencil I would use graphite, not coloured unless specifically non-toxic. You might also be able to use a non-toxic water based paint-pen, such as is used by beekeepers to mark the queen.
I wouldn't put anything directly on the cap as you might put damaging pressure on the developing larva underneath or possibly occlude air-flow and cause death of the larva. Marking the cap could also transfer disease from one hole to another, which you obviously don't want to do.
Please take this advice with a grain of salt, I'm not an expert on this or even own a bee-house (though about to take up beekeeping as a family) and ask your local wildlife experts - seeing as you are in the UK, the Wildlife Trust might be a good place to start.

The idea with marking the cap itself was that when the bee emerges it will remove it, so if I see a mark still there after, say, three months, I would know to clean that particular hole. But a soft graphite pencil seems like a good idea—they appear to be using sand this year rather than the darker mud that's been used in previous years.


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Overlapping annotated regions among repetitive families of human genome
I am studying the repetitive elements in the human genome and I have come to know that some genomic locations are not uniquely described by a single repeat family. What's behind this uncertainty? Does it account, for example, for the variability among individuals? or is it a fact deriving from the limitations of our current technology?
The reason behind this question is a practical issue. My team is analysing the composition of some sequencing data and is mostly interested in the repetitive elements of human DNA. I can use the repeat masks that I download from UCSC database and count their abundance. My problem is that some repeat masks overlap at specific locations in the annotation track.

Welcome to Stack Exchange Biology. Please finish reading the [Tour] and then consult the Help on Asking Questions. I think that your question desperately needs clarification with an example. When you present your example be sure to provide a link. Without this I am not sure what you are talking about.

Can you give some motivation of why regions would be covered by a single annotation? For example, a coding portion of a gene is annotated as a gene, a transcript, an exon, and a CDS. That's 4 distinct annotations! If it's a transposase, it will also be annotated as a transposon, for 5 annotations. Having overlapping annotations is to be expected. I supposed you might mean repeat family annotations, but similar logic applies. Recombination of repeats etc. is rampant: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3242629/, https://www.biorxiv.org/content/10.1101/2020.07.02.163816v1.full

Yes @Maxilimiam, I meant repeat_family_annotations. If I understand it correctly, you are alluding to the fact that some repeat families are associated to transposons elements and, as consequence of that, they are 'mobile' elements of the genome so it makes sense if some genomic locations can have multiple annotations.

@David, thank you for the clarification!

@AVO on the order of 50% of the human genome is repeats. Of that, >80% of the repetitive contents are mobile genetic elements (MGEs; see Table 1 of linked paper). So yes, when you talk about "repetitive DNA" you are generally speaking talking about MGEs. But the logic is actually that depending on what you mean by "annotation", you might have the same element annotated as a LINE, a SINE, an Alu, etc. (all MGE types), because these are sometimes chimeric or recombinant.


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Plants taxonomy: priority of names published in the same year
Article 11.3 of the International Code of Nomenclature for algae, fungi, and plants states that the earliest valid name with the same rank has the priority.
The question is: if two names (or more...) of the same species have been validly published exactly in the same year and, apparently, it seems impossible to ascertain which one was published earlier, how to decide which one is the name which has the priority?
Thanks

Is this a hypothetical? Because I can't see this actually happening unless it's a new species identified separately by two individuals unaware of the other's discovery.

Not hypothetical. It is something that happens.
It is a case of two binomials (referring to two distinct plants) but that are exactly homonymous and have been published exactly in the same year. So, I have the need to decide if one or another has the priority.
Unfortunately old works did not show the month of publication, so at the moment I cannot uscertain which one was published earlier in that year.

As you state, it's not just the year but any point earlier in time. Even though the publications may not indicate themselves exactly when they were published, I think this still holds. I know there are cases where folks have done a lot of extra research to establish when, or likely when, certain manuscripts were published in order to clear up questions like this.

@David, nomenclature is essential for talking about anything in biology, and the taxonomists who craft the various Codes are working biologists, so they may indeed frequent this site and know the answer. It's true that this question isn't about biological processes, but this site is "for biology researchers, academics, and students," and specifically covers "questions about techniques in a biological or biochemical laboratory," which I think pretty squarely includes taxonomic techniques.

@Darlingtonia - I could not agree more that this question, though it may not have an answer, belongs on this site. To the OP, is it possible to contact the publisher(s) for the date of publication? If you must write about it, you can give both names. For a good while after orexin/hypocretin was discovered by two separate groups pretty much simultaneously, it was referred to as "orexin/hypocretin". Now it's usually referred to as "[one], also known as [the other]". I have no idea when this will be resolved.

Please supply details of the case and provide a link to the International Code of Nomenclature.


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Migration of cut vs. non-cut plasmid on gel
As you might know there are 3 common forms of a plasmid:

ccc-form (CCC), being supercoiled.
oc-form (OC), being nicked and therefore relaxed.
linearized form (L), being cut on both strands and linear.

In theory the fastest migration should be the CCC, then L and the slowest is the OC-form.
Source: https://www.sciencedirect.com/science/article/abs/pii/0147619X81900123
So I have a plasmid with 7631 bp from a Midiprep. I cut this plasmid with NotI and put both versions on a gel, to check for the quality of the Midiprep.
I expected my plasmid to have the CCC form and therefore be faster (lower) than the cut L-form.
I ran the gel and the result is the opposite. My plasmid runs slower (higher) than the cut version.
Why is that? Do I have a misunderstanding somewhere? Is my plasmid ok?

For clarification: NotI- means that the plasmid is not cut. NotI+ means that the plasmid is cut (and therefore linear).

What organism are you propagating your plasmids in? What kind of gel / buffer are you using?

E. Coli (DH5-alpha).
This is a 1% agarose gel with 1x TAE.
Digest was done with NEB enzymes and CutSmart-Buffer according to protocol. Non-cut plasmid was treated the same, but without enzyme.

What kind of plasmid prep are you using? I remember having rarely seen the ccc form. If all three where present, it was usually the weakest band.

What do you mean with plasmid "pred"? The kit is from Qiagen. The plasmid itself is a vector for lentiviral transduction. I'm just confused because only the oc-form would be slower than linear. But I don't believe that all my plasmid is nicked.

@FelixH. Pred -> prep. If you are new at this game, you probably won't see much supercoiled, mostly circular or nicked circular. Supercoiled can also run in quite a few positions depending on the state and if you overloaded or not.  I'm assuming that the NotI+ is running at the correct size (only 1 cut site)? If so, don't worry about how the uncut is running too much. That looks like 1kb plus ladder; if so, size is right.

It should have been "prep", a simple typo. Otherwise I agree with @bob1

@bob1 Thank you for the reply! I'm not particularly new at these things, but once in a while I try to ask myself questions that are considered "basic" or "easy" but most (even advanced) scientists around me do not seem to have an explanation for. A good midiprep should be mostly supercoiled. bitesizebio.com/13524/… pubmed.ncbi.nlm.nih.gov/22693686
It also does not seem to be overloaded, since its roughly 200 ng/µL (diluted midi).
The cut is the correct size and yes NotI cuts one time in my plasmid.
The ladder is 1kb+.

Just for clarification, I know that the midiprep is probably fine, but I experience so often that people around me tell me "that's just the way it is", instead of trying to find proper explanations. I'm just curious why my results do not fit with the standard theory/papers of plasmid migration.

@FelixH. always good to challenge the paradigm! I agree your midiprep looks good.  In my experience, supercoiled can run in a number of positions relative to cut; I can't recall exactly the reasons I was taught many years ago, but I think residual protein contamination, entangling of the ccc form with others, and overloading/underloading all play a role.

@bob1 Thanks for your reply. Entangling sounds like a reasonable explanation - I think I have even read that somewhere recently, when I was trying to find an answer.


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Can multi-cellular organisms transform into single-cellular organisms and conversely?
If we have a multicellular organism A, can it transform into an organism B in its lifespan, so that B is single-cellular?
And conversely given a single-cellular organism B, can it become a multi-cellular organism C?
Does any organism which satisfies both of those properties in some way exist?
I don't have background in biology and this question was mostly curiosity, so this might be a bit vague.

All "higher" animals and plants (i'd have to review other types, but pretty sure mosses, ferns etc also) go from single cell to multicellular in their life cycle. Fertilized egg/ovum ->  adult. You might want to check out sponges, which can reproduce by fragmentation, but I don't recall if they need more than one cell type for this.

A model for the evolution of single-multicellularity is choanoflagellates. Here is a video lecture. They are super cool.

The unicellular protists called choanoflagellates, ichthyosporeans and filastereans are the sister groups of metazoa (animals). They are single-celled but can live in multicellular versions. Either through aggregates (genetically different cells coming together) or by clonal division (like an animal - cells are genetically identical). So right now this is a huge field of research, in which scientists try to understand the evolution of multicellularity in respect to animals (multicellularity also arose multiple times in other species, e.g., fungi, plants etc.).
Sponges are very basal animals and have very unstable cell states. Meaning, many cells can differentiate into other cell types and if you fragment a sponge (into single cells) given that a few specific cell types are present, it can simply regenerate. But as far as I know, a single cell alone can not regenerate a sponge.
So to your questions:

If you talk about reproductive scenarios then a multicellular organism does convert itself into a single-celled organism (think about sperm, oocytes or about spores etc.).
As explained before, many unicellular organisms have multicellular states (mostly triggered by some kind of stress response, e.g., starvation).
The organisms I described before switch between these states, but they are not as complex as typical animals.


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Do Glycosides in plant seeds serve some other function than protecting the seeds?
Many plants have toxins like glycosides in the seeds and I think other parts of the plant and the accepted reason for this I believe is to discourage animals that ingest the seeds from digesting theses seeds -- the goal is for the animals to eat the fruit and disperse the seeds where they can subsequently grow. (The seed has not just toxins but also very tough shells often as in stone fruit like cherries and peaches.)
My question is whether these toxins when the plant begins to grow have some other biological function?

There are a lot of different glycosides with many functions. you may need to be more specific.

@John -- i am asking if any toxic compound in the seed has some function beyond protecting the seed from being eaten.


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What do alleles look like visually on linear DNA strands?
I've seen many textbook images of alleles on homologous chromosomes with the gene loci identified but how could this be visualised on linear DNA sequences with the bases written out? Is it that you would have one DNA strand with its nucleotides and then another adjacent DNA strand with nucleotides at the same locus but different in sequence? Any visual representations would be helpful
Edit:
This picture below shows how alleles can be seen on the chromosomes but it's not clear about where the change in sequence would be on the nucleotide bases. The typical diagrams show the homologous pairs but they don't usually show the change of base sequences on a small scale.

Unclear exactly what you mean. An allele is a variant. It's like having 1st edition vs. second edition of a book, where a typo was fixed on page 32. In a cell of a diploid organism, you might have 2 1st editions, 2 2nd editions, or one of each. But each of them is just a long string of characters. But there isn't a "right" way to visualize this because it's too small to see, all of these are metaphors to help us understand what's happening at the single molecule level.

An allele of a gene is a segment of DNA so its diagram will be like any DNA helix with a unique nucleotide sequence. A chromosome is a single molecule of double stranded DNA with histones. So two alleles will be two extremely similar DNA segments. Or as @MaximilianPress said two editions of a book. I guess you asked for a diagrammatic representation?

@MaximilianPress Could also be a truncated version that ends on page 100 out of 500 original pages, or arguably even one that doesn't exist at all.

I've posted an answer and I would be interested to know if it answers your question. However can I ask two things of you. 1. Please finish reading the [Tour] — we know you haven't because you don't have the badge for doing so, and it will help you learn how this site works. 2. When you ask a question related to something you have read, please post a link to it, or even a copy of a typical image in this case. And did you search for such pictures? I found the one I modified Googling for images related to Sickle Cell Allele.

Thanks for the response David, will do the tour now and see if I can attach said pictures I was referring to

I think I may understand the point of difficulty the poster is encountering, and have produced the diagram below (adapted from an internet source) in the hope that it may help.

This diagram shows the allele for the mutation in β-haemoglobin that causes sickle disease. The key points are:

There are two copies of the chromosome in diploid cells, either of which may be normal or mutated.
Each chromosome contains double-stranded DNA, so the mutation affects both of the two complementary strands. Thus the stated expectation of the poster to see “one DNA strand with its nucleotides and then another adjacent DNA strand with nucleotides at the same locus but different in sequence” is incorrect.

Now this may be a slip of the typewriter fingers on the part of the poster, but it may also be confusion because of there being two copies of the same chromosome. Anyway, the diagram seems to me to give an example of what was requested. It can be amended if necessary
Of corse the allele may extend over more base pairs if the mutation is a deletion, but let’s walk before we try to run.

This illustration could mislead some, as the left-hand part illustrates a chromosome form that is not typical in the life of a cell, but is a form that occurs during meiosis.  That special form of chromosome has two chromatids with the chromatids having different alleles.  (The normal form of chromosome has only one chromatid, and hence only one allele form.)

@mgkrebbs — Yes, that was a point of concern to me also, although I'm not an expert on chromosomes, just graphics. Is the replacement OK? The combination of 2D and 3D jars, but then, nobody is paying me for this.

Yes, that is a definite improvement, as it shows two homologous chromosomes as normally exist in a cell.

Hi David, thanks for your response - this is more what I was looking for with the visual representation as a lot of the textbook diagrams show a more zoomed out version of the chromosome which made it hard for me to visualise how the nucleotide bases looked.
Just to clarify are alleles comparing the variation of genes on the different chromosome then? As opposed to an allele being the variation of genes on one chromosome on its own?

For example is the change of sequence (on small scale terms) going to be on one antisense strand whereas the sense strand has the typical reference sequence? Or is it comparing the differences of sequences on the other homologue as opposed to a single change in sequence on one chromosome? Apologies for the long winded question. I'm just trying to visualise this for a short sequence (e.g. 10 bases) not a large scale one as usual.
Also, I think what tripped me up with the textbook diagram is that I thought the chromosomes shown only had one singular strand instead of the double stranded form.

@mydearestpotato — 1, Yes, if you take the NIH definition of allele: "An allele is one of two or more versions of DNA sequence (a single base or a segment of bases) at a given genomic location." each version, is and has to be, on a different chromosome. 2. There is no possibility of the different strands being informationally different in the double-stranded DNA of an individual chromosome in a diploid cell. This is because they have to form complementary base pairs. (Only at the point when a mutation occurs can it be on one strand, unti the DNA replicates and daughter dsDNAs are formed.)

Thank you for these explanations and the diagram, it's been really helpful


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Triangulation Number of Icosahedral Capsids: Formula Variable Definitions
I'm trying to understand the definition of the Triangulation Number for Icosahedral Virus Capsids: In Alan J. Cann's "Principles of Molecular Virology 5th Edition", it is defined as

$T=f^2\times P$ where $f$ is the number of subdivisions of each side of
the triangular face, and $f^2$ is the number of subtriangles on each
face; $P=h^2+hk+k^2$, where $h$ and $k$ are any distinct, nonnegative
integers

I have also seen the Triangulation Number defined as

The number of structural units that creates each [triangular] side

in Chapter 2 of Jennifer Louten's "Essential Human Virology". I have redrawn part of a diagram I am confused about:

Only one face shows the relevant subdivision, with sides drawn in yellow. Blue marks edge subdivision points, and red marks triangular face subdivisions. To my eye, the $T=1$ icosahedron has 1 edge subdivision per side, again marked by the blue dots. If $h$ and $k$ are $1$ and $0$, then it makes sense as to how that icosahedron has $T=1$, and similarly there is only one shape repeated 3 times comprising the triangular face, so Louten's stipulation makes sense to me so far (I don't understand where the 1 subtriangle for $f^2$ is, maybe its considering the whole face as a subtriangle). For the $T=3$ icosahedron though, it appears to me that there are two subdivisions per edge, and there's no $h$ and $k$ such that $3=4\times P$. Further, in "Principles of Molecular Virology", the $h$ and $k$ for $T=3$ are listed as $(1, 1)$, unless I'm misreading; How are those values distinct per the original definition?
My raw questions coalesce to this list:

What is being counted in the "number of subdivisions of each side of the triangular face"?
What does "distinct" mean when referring to $h$ and $k$?
How is a "structural subunit" defined? For example, in "Essential Human Virology" Figure 2.8, why is the (A) $T=1$ tiling considered a single structural subunit while the $T=4$ tiling is not? The distinction of what is and is not a "structural subunit" seems nebulous to me. I could see it being the largest average number of non-overlapping triangular units excluding non-triangular subfaces, but I can't tell if that's just me grasping at straws

I don't have Cann's virology on hand here, can you provide their figure that shows subdivisions? Or another redraw for that one? I suspect their use of the the terms "subunit" and "subdivision" is at least slightly different from Louten's.

The above diagrams are from Cann's, I can redraw the other capsid on the diagram too if that's what you're referring to (I think its T=4), in the originals the subdivisions are drawn on every triangular face but in my redraw I only drew the subdivision for the face facing the observer, to reduce visual clutter and because I am lazy; They repeat on each face in Cann's. I'd post the diagram itself but I'm worried about copyright. I can do another redraw once I'm back home at my drawing tablet, I just want to ensure I'm including the parts you're mentioning.

I'm not familiar with the $T = f^2 * P$ formulation. In Caspar + Klug (1962) $T$ itself is equal to $h^2+h*k+k^2$, so I guess $f$ is assumed to always =1. So I don't really know the answer to your first two points.
As for the last point, "structural subunit" basically means an individual copy of the protein that makes up the viral shell. Icosahedral symmetry means there must be 60 identical "asymmetric units", regardless of the $T$ number. In these diagrams its usually presented as the 20 faces of an icosahedron, which are equilateral triangles and therefore can be divided into 3 identical parts, so $3 * 20 = 60$. (I find it more helpful to focus on the 12 vertices, where 5 faces come together, so $12 * 5 = 60$) The $T$ number for a particular icosahedral virus tells you how many copies of its protein are needed for its asymmetric unit. So in fig. 2.8 of Essential Human Virology, the structural subunits are the trapezoids, not the tiling of three of them in a face.
One of the important results from this theory is that only certain T numbers can exist. For example, you can't make an icosahedral shell out of 120 subunits ($T=2$).

Thanks for your answer! Could you wager a guess as to why the T=3 Cann diagram splits the face into 4 unequal parts instead of 3 identical parts then? And defined like that can't you just take the average number of proteins on a face and divide it by 3 to get the triangulation number instead of the whole $T=f^2×P$ formulation?

Yes, the large hexagon in the center of the T=3 diagram should be composed of 6 triangles identical to the ones at the corners. so 9 identical parts.

Generally you can't tell where one protein ends and another begins until you have a very good 3D reconstruction of a virus, while general symmetry features like T number can be determined from very low-resolution data. I assume the T=f^2×P formulation is useful in some situations, but I don't know what those are.


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Can I reuse agar in Petri dishes?
Can I simply re-melt agar in a contaminated Petri dish to use it again? I've tried searching for the answer on the Internet, but I was only able to find information about reusing Petri dishes themselves, not the agar in them.

reuse for what?, plant food, sure, for an experiment, no, spores are things.

@John Microwaving does not destroy the spores?

No, not just heating it enough to melt, many spores need prolonged heating to be destroyed  and some spores can survive anything short of incineration. Your not just talking about human dangerous spores, a plate can be contaminated by all kinds of spores.

Depends on what the dish is made of - plastic ones might well melt.

Is it a broth agar or other with some nutrients in it? If so, once used some (a small fraction or more depending on how heavy the growth was) will have been used up, and there will be an accumulation of metabolic byproducts, so newly plated growth may be affected. You also run the risk of not eliminating all microbial contaminants. If you're a hobbiest, it might not matter to you (eventually the agar will be useless), but if you're serious, the answer is to stick to accepted protocols.


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Why were vegetation coverages not assumed to be affected by precipitation, humidity or temperature?
I am trying to understand the graph topology of the structural equation model (SEM) given in Figure 1 of Bisset et al 2023. It is stated in the paper that it reflects an a priori causal structure.

I am trying to understand why the SEM assumes that climate variables do not affect the vegetation coverage variables. It seems like basic plant biology that they are affected by precipitation, humidity and temperature. Did I miss something about the nature of the coverage estimates?
Why would vegetation coverage not be assumed to be caused (in part at least) by climate these climate variables?

EC: electric conductivity
OC: organic carbon

Probably mostly because people misuse these sorts of models all the time.

The title of the article is (my emphasis):

Linking niche size and phylogenetic signals to predict future soil microbial relative abundances.

To look at bacterial abundance, they generated models that look at factors that affect bacterial abundance. In this case, this is a mathematical model that is used to describe the effect (emphasis mine):

Whereas a number of multivariate methods are largely descriptive and more appropriate for exploratory analyses, SEM is able to test a network of causal hypotheses and is recommended for evaluation of multivariate hypotheses (Grace, 2006; Grace et al., 2012). Specifically, we used SEM because it allows the evaluation of simultaneous influences...
...The method is thus appropriate for establishing probable causality at the system (for example, climate-vegetation-soil-bacteria), rather than the individual level (for example, climate–bacteria).

So, they are generating a model that looks specifically at establishing a causal model for bacterial abundance only. This model does not seek to establish causality for other factors, such as vegetation cover, even though this might be related to some of the factors being investigated. In fact the models explain mathematically only the significant factors for bacterial abundance, and factors that are left out of the model have no effect in the system being described - basically Occam's razor being applied.
You could indeed examine vegetation cover using a variables used in this system, but you would need to establish a whole new mathematical model to do so, and you might well find that the variables are different or need other factors not shown in this model.

I disagree with you and the authors on how to proceed with causal inference (see Pearl 2009 for an introduction), but your answer clarifies why the authors might have thought to exclude this relation between climate and vegetation.

@Galen I agree, it doesn't make sense to a me either, but this is how the mathematical models work, for better or worse. The factors that they show in the model are explicitly the ones that affect the thing being looked at and explicitly exclude those that don't, even though from a logical sense it might make sense to include them. Basically aiming for a minimal component model.

I have substantial disagreements with you, but I don't think it will be productive to clarify and argue here. It just isn't a great venue for it. There is a rigorous approach to thinking about statistical models in conjunction with causality. The book I cited is a detailed account, but if you don't have the time/money for it you might find Science Before Statistics: Causal Inference to be a feasible investment at least to get the general idea.

@Galen I'm not a modeler or anything of the sort, but thanks for the link. I agree this isn't the right place for discussion of your point. I've had similar arguments with modelers in the past, with me in your position, so I totally understand where you are coming from.


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What exactly is "Whole-genome sequencing"?
Newbie question: For few years I have seen news like “Whole-genome sequencing” is now under $1000 etc. I believed that this means all the base pairs of all chromatids in a single cell are identified and stored in a digital format in the original sequence. Just checked this Wikipedia article as well, which seem to align with my understanding.
Today I saw many news articles saying that Y-chromosome was fully sequenced for the first time. For example this article, which also mention that other chromosomes were fully sequenced only early this year.
What am I missing? Perhaps "Whole" is not "whole"?

So in short, the human genome project (HGP) and Greg Venter with his companies (fascinating story, I recommend to read into it) were unable to sequence many heterochromatic regions (with lots of repeats). Why? Because for repeats you need long-read sequencing methods (e.g., Nanopore, PacBio) that only became available in recent years. So apparently the HGP and subsequent attempts left out about 8% of the genome (https://www.science.org/doi/10.1126/science.abj6987), which simply consisted of some repeats and as the believe at that time was anyway that all these repeats are "junk" and the genes (about 2-3% of the genome) are the important stuff, they could argue that they sequenced the "whole" genome. Now of course we know that also repeats can be important for disease, gene novelty (evolution) etc.
Hope that helps.


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Why is it that once mould is growing, and it releases spores, it can grow in or on materials that are not damp?
My home had some flooding recently (from a burst hose connected to a tap, but I'm not sure that's relevant), and in the process of rectifying the situation, a few things were told to me. I'd like some clarification around these statements, and maybe have some misunderstanding on my part cleared up.

If the carpet's underlay, and the subfloor are not dried correctly, in a timely manner, there is a risk of mould growing.
If mould grows in the carpet, spores will be released, and the mould will start growing everywhere, even in places that are not damp. Even if the underlay is dried too late, mould will still grow.

I feel like this leads to a contradiction. I've got a couple of ideas in my head.

The mould grows in the carpet when it is damp, because there are already mould spores in the carpet, and the moisture "activates" them. But this would imply that the spores still would not grow in other places that are not damp, which contradicts what I was told. I'd also be curious as to how the spores got there in the first place.
Mould can grow spontaneously in damp places, without mould spores. This sounds quite ludicrous to me, unless perhaps dampness somehow attracts spores, or small animals and insects that carry spores and deposit them. Then once the mould grows in the damp place, spores are released, and because of their proximity, they then grow on other surfaces, despite the lack of moisture. But it requires the dampness to bring the spores in the first place.

Its not that there is no moisture, there is just less and it changes day to day. once mold has stated to grow it saturates the surrounds with spores which means as soon as conditions allow it they grow, whereas normally you need the coincidence of spores happening to be land in the right conditions.
think of it like a fireworks factory, why are they dangerous. Why are fireworks factories, absolutely insane about fire safety. Being in a factory does not make fireworks more flammable, but it does mean any spark has a much better chance of landing on a firework. there is not more sources of fire in a fireworks factory but the factory is "saturated" with something that is highly flammable.
the sheer amount of spores makes it more likely they will find the right conditions at some time during the year. A normal home is someplace mold can grow part of the time but getting those conditions at the same time a spore happens to float in is rare, most spores that make it in will not find the right conditions. Up until you have a lot of moisture, then any spore that floats in finds the right condition, and we go from saturation of moisture to saturation of spores.


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Why do V_Na and V_K stay unchanged in Hodgkin-Huxley model?
In the Hodgkin-Huxley model, ionic current $i_\mathrm{Na}$ and $i_\mathrm{K}$ are given by
$$
i_\mathrm{Na}=g_\mathrm{Na}(V_\mathrm{m}-V_\mathrm{Na})\\
i_\mathrm{K}=g_\mathrm{K}(V_\mathrm{m}-V_\mathrm{K}),
$$
where $V_\mathrm{Na}$ and $V_\mathrm{K}$ are the equilibrium potential, and are kept the same during the burst of action potential:
$$
V_\mathrm{Na}=\frac{RT}{F}\ln\mathrm{\frac{[Na^+]_o}{[Na^+]_i}}=35~\mathrm{mV},\\ V_\mathrm{K}=\frac{RT}{F}\ln\mathrm{\frac{[K^+]_o}{[K^+]_i}}=-85~\mathrm{mV}
$$
This means $\mathrm{[Na^+]_o,~[Na^+]_i,~[K^+]_o,~[K^+]_i}$ are all constants, which is really confusing. In my opinion, the inward/outward current of sodium/potassium ions should definitely change the concentrations of Na+ and K+.
Well, it makes sense that $\mathrm{[Na^+]_o}$ and $\mathrm{[K^+]_i}$ can hardly change because they are large enough compared with the lost ions into the regions with fewer ion concentrations. Then what about $\mathrm{[Na^+]_i}$ and $\mathrm{[K^+]_o}$? They are so small that even very a few ions added to them can change them a lot.
For example, $\mathrm{[K^+]_i}=90~\mathrm{mM}$ and $\mathrm{[K^+]_i}=3~\mathrm{mM}$. If the potassium current leads to a change of $\mathrm{1~mM~[K^+]}$, now $\mathrm{[K^+]_i}=89~\mathrm{mM}$ and $\mathrm{[K^+]_i}=4~\mathrm{mM}$. $\mathrm{[K^+]_i}$ changes by 1.1% which can be neglected, but $\mathrm{[K^+]_o}$ changes by 33.3%, which cannot be neglected. Also, the equilibrium potential of potassium now becomes 25*ln(4/89)=-78 mV! This really changes a lot. How can we ignore it?
Moreover, in the Quantitative Model of Gastric Smooth Muscle Cellular Activation of Corrias and Buist (Annals of Biomedical Engineering, Vol. 35, No. 9, 2007), both $V_\mathrm{Ca}$ and $\mathrm{[Ca^{2+}]_i}$ does change during the burst of action potential as follows:
$$
\frac{d[\mathrm{Ca}]_i}{d t}=-\frac{I_{\mathrm{caL}}+I_{\mathrm{caT}}}{2 * F * V_c}-I_{\mathrm{CaExt}}.
$$
But they also ignored the change of $\mathrm{[Na^+]_i}$ and $\mathrm{[K^+]_o}$. Hmmm, really confsuing.

As you've figured out, the reversal potentials don't change because they're assuming the concentrations don't change. Even relative to $\mathrm{[Na^+]_o}$ and $\mathrm{[K^+]_i}$ the number of ions that move is small (e.g., see this previous Q&A: Ambiguity about the relation between membrane potential and concentration gradient in neuron cells - the squid giant axon isn't quite as efficient as a mammalian neuron but it's not so bad, either): 1/100,000th of the internal potassium is still on the order of 1/10,000th to 1/1,000th relative to the outside. Changing the concentrations by 0.1% isn't going to appreciably change the reversal potential. The example you give of a 1 mM change is far, far greater than what occurs with typical neuronal activity.
Of course, over a longer time scale there would be changes in concentrations, but those changes aren't observed as long as the sodium-potassium pump is active. The pump is working all the time to maintain the concentration gradients observed in neurons, and if you were to disable it the concentrations would eventually equalize across the membrane.
Calcium is in much lower concentrations than either sodium or potassium. It's also buffered heavily intracellularly so that the "observed" calcium concentration is absolutely miniscule: free calcium ions are important in signaling, but they are very quickly bound strongly by various chelating molecules inside the cell. Inside the cell, just a few hundred or thousand calcium ions make a big difference.
There's a bit of a famous quote/aphorism by statistician George Box and others that goes something like "All models are wrong, but some are useful" - so, that's what you're seeing here. Is the HH model absolutely complete to cover all aspects of neuronal function? No, of course not, but if it were it would be missing way more than just the changes in concentration of the ions involved. For the data that HH were fitting, and for many other circumstances involving neurotransmission, this model does well enough. It certainly does well enough for learning, describing, and teaching the basic mechanisms that are critical to neurophysiology. Including more of the total system would require many more free parameters without much improvement to the model.
In some other circumstances, such as hypoxia where the sodium-potassium pump does not function well, or seizures where the level of activity is extremely high and the extracellular space can get flooded with potassium, it may become more important to account for changing sodium and potassium concentrations. For more typical cases, they can usually be ignored and assumed to be held near enough to constant both inside and out thanks to the sodium-potassium pump.


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Asymmetric sequencing | Can you sequence 250 bases on Illumina Novaseq S4 (read 2)?
I would like to sequence 250 bases on Illumina Novaseq S4 on read 2.

Kits of illumina come in the following sizes: https://emea.illumina.com/systems/sequencing-platforms/novaseq/specifications.html

You can setup the sequencer for asymmetric sequencing, so that from a standard paired-end 2*100bp kit reads 150 bases from R1, and only 50 of the R2 (or vice versa).

On SP kit they now support 2 x 250 bp, but not on S4.

On the largest S4 kit it would be theoretically possible to sequence 250 + 50.

The read quality at 150 bases is excellent, so I expect at least 200 useful bases.

Did anyone try this, or could point me to relevant information?
Can you even specify such strong asymmetry in the software?
Very importantly: Are there any risk of losing the lane?
Are there any other risks (other than quality issues beyond 150 bases, which i assume I can easily trim away)?

ps.: Cross posted on seqanswers for a possibly more appropriate audience.

I have done this on MiSeq and NextSeq though it was several years now. It is possible to specify cycle numbers in the GUI input (page 54) in theory, unless they changed things (though they only mention up to 151 cycles).
I previously emailed Illumina technical support about this (the docs for the NextSeq also said "up to 151 cycles") and they said this:

The reason the MiSeq 300 cycle kit supports for 250x50 is because the MiSeq chemistry has been tested at those long run lengths and the same chemistry is implemented in the 500 cycle kit that allows for 2x250. In the case of the NextSeq, there is no 500 cycle kit and it has not been tested for run lengths beyond 151. That said, there should not be anything in the software that prevents you from running a 250x50 on a NextSeq 300 cycle kit, but the quality for any cycles past 150 may be low.

It might be worth following up with them to make sure that it would still work.
For our application, the quality was sufficiently good that we were able to use the data (from a capture panel). Admittedly, we were using a somewhat bespoke alignment strategy rather than e.g. traditional variant calling.

Thank you so mcu!  We also used asymmetry in other setups,  without problems, but at the end we went with standard settings here - it was too expensive to risk anything going wrong!


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I have a fruit fly problem
I've add fruit flies raising a garden every year I am very familiar with them and how to kill them. But twice now I have killed one by smashing it and upon doing so two little tiny bugs or crawling on me after I smashed the fruit fly and wiped it off of my hand. I am curious of what these little tiny bugs are that are living on the fruit fly. Can you help me identify them[![

Unfortunately the picture is too blurry, so I can only talk from experience : They might be parasitic mites. Insects often carry parasitic mites around.
Look at this article for example :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10317784/
It seems like Drosophila is no exception.
Moreover in this article :
https://www.jneurosci.org/content/36/44/11275
you can see that Drosophila has evolved a defense mechanism against such mites.
Parasitic mites of insects breach the cuticle and suck the hemolymph (equivalent of the blood + lymph of insects) out of their host.


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Is this part of a claw to a Dinosaur?
Agitzed claw 1 large and 1 smaller  underneath.  What I found is about 4" long and about 3/4" in diameter which gets smaller towards the tip. Underneath it appears to be another small claw tip about 11/4" long and appears 1/4" in diameter. They look like stone or aeget.

There are  many fossil id forums where specialists often know the latin name of 150 types of ammonites and they know a lot about tdino claws too.

What's the rock matrix - typically fossils are only found in sedimentary rocks...

Where is this from geographically? What formation?

I discovered it in the Pacific Northwest on one of the beaches off vashon

without knowing the rock type or higher quality images it could be coral or crinoid, or a dozen other aquatic animal fossils. dinosaur fossil is very porous so its unlikely.


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How to empirically differentiate social interaction from self-awareness in the mirror test?
When placed in front of a mirror, manta rays are more active (e.g. expose their ventral side to the mirror) and present more frequent and repetitive movements (e.g.  furling and unfurling their cephalic lobes) relative to being placed in front of a white board. Such behavior has been interpreted as self-awareness by some scientists, and as social behavior (i.e. the manta believes its reflection is a different individual) by others.
What test, if any, could be performed so as to distinguish which of these cases, self-awareness or social interaction, is causing the mantas to behave in such way?

I think this one would need to be answered by oceanographers who are very familiar with manta behavior in nature. I think the response to your first link (i.e. the second link) is much more convincing than the first link you provide. The further away from mammals one gets, the harder it is to determine if the animal is self aware. See the related question in the sidebar.


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Do African wild dogs have sharper teeth than domesticated dogs?
When I see African wild dogs hunting it appears easy for them to tear open their prey, whereas when a dog like a pitbull terrier bites a wild animal it looks like more of a just bite crush or puncture wound.  Do wild dogs have some sort of teeth that can tear their prey open?


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Transfecting cocoon or chrysalis
Do you know whether anybody tried to transfect insects during their cocoon/chrysalis stage, and if so do you have a link to such studies?
I was thinking it would be easier to do given that it's a more macroscopic manipulation than during initial development, and that — given that the organism dissolves itself — one could obtain (almost?) organism-wide coverage via a simple injection.

I'm not sure I understand. How much material are you thinking? I'll confess right off the bat that I know very little about transfection, but what method would you use (viral? Chemical, e.g. cationic lipids/ other?)? What do you want to introduce into the cell(s)? A small amount might infect (sorry, transfer genetic material) into a few cells, but how do you know how much might harm/kill the organism, or does that not matter? Sorry for all the questions, but it might be better if you clarify re. intent. You may very well know far more about this than I do.

What do you want to introduce into the cell(s)?
Either DNA or RNA. As for the rest of the questions regarding methodology, I think that's what an answer would contain.


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How does positional memory in fibroblast cells work?
I have a question regarding how positional memory in fibroblasts work, specifically, where the memory comes from/how its made.
For example, the Salamander & other amphibians are able to regenerate almost perfect copies of decapitated limbs, but lets say we have a female Salamander who is effectively given hormone therapy to “masculinise” them, if a limb was severed, would it grow back according to the hormone profile? So essentially a bit smaller since males are typically smaller?
I’m very interested in the possibility of sex change through genetics, especially after bones have fused, effectively a reversal. It seems as though this may be a way forward though I am unsure.
Thank you for reading!

I don't have in depth knowledge about how amphibians are regenerate their limbs but in embryonic development all tissue's cells differentiate and come from stem cells according to tissue they inhibit or enhance the transcription of which genes that defines the attributes of tissue. Connective tissue such as fibroblasts differentiated from mesenchymal stem cells. So, in theory if you want to regnerate or in this case replace the "Feminine" muscle and bone alignment with "masculine" we need Embryonic STEM cells to generate it but also we need to broke down former ones. So just we need to utilize apoptosis and use gene therapy to do that. There is risks involved currently with recent gene theraphy techniques and also concentrations and conditions in vitro are affecting the differentiation process when using ste cells. In short every tissues fate decided by STEM cells. Ah I checked stem cells, I just googled sex change by stem cells and find some articles
Click first!  "They produce male and female stem cells from same person that have mosaicism"
And also second!"Tissue Engineering Neovagina for Vaginoplasty in Mayer–Rokitansky–Küster–Hauser Syndrome and Gender Dysphoria Patients: A Systematic Review"
And lastly!"Biotechnologies that empower transgender persons to self-actualize as individuals, partners, spouses, and parents are defining new ways to conceive a child: psychological considerations and ethical issues"

Thanks for the response! In the case of an adult having their muscular skeletal structure changed from feminine to masculine & vice versa, would the cells have to at least have the memory to create the post-pubescent human structures? So perhaps growing subject tissue under a sex hormone & transferring the relevant genetic information over to the main subject?


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Gene Name Finding
X8HS20 - please help, I am not able to find the proper name or function of this gene in any database - can someone kindly help to figure out what it is ? I hypothesize that it is some gene of mitochondrial importance on the X chromosome- but I am not sure. Thank you :)

Can you give more information on where you found this name and why do you think it exists? You must have some source?

Thank you, but I can't disclose it - I think I managed to find an answer though, will check in with the organization which I derived the data from much later on, thank you :)

Ok I just found a possible match - it could be the V-Set Pre-B Cell Surrogate Light Chain 3 gene - called 8HS20. Derived from KEGG - will have to check in with more research papers to see why a X is placed before the 8HS20. Definitely not a clerical mistake on my side though.


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Why is mean systemic filling pressure used to calculate pressure differential for venous return?
I'm really struggling to understand venous return curves and their relationship to mean systemic filling pressure.
I understand mean systemic pressure is the pressure that would be measured throughout the cardiovascular system if the heart stopped beating and hence pressure would be the same throughout the body and no blood flow because there is no pressure difference.
I'm very confused about the effect of gravity on this, surely if you are standing up the pressure of the blood pooled in your extremities is greater, so is this value just a mean of all the pressures? And I don't understand the usefulness of this parameter, this occurs when the heart has stopped functioning so why do we relate MSP to be a part of the pressure differential driving venous return in the equation:
Vr = (MSFP - PRA)/venous resistance
Maybe my confusion would be resolved if this graph was explained better:

One might notice that during this entire process, somewhere in the circulatory system there is a points which remains at a stable pressure (which happens to be the MCFP),  irrespective of the catastrophic events reverberating through the rest of the organism. Rothe (1993) thought that this probably happens in small venules (less than 1mm diameter), and that it is not constant - present at different points of different organs, and changing constantly depending on prevailing conditions.

I think this means that MSFP might be the high starting pressure in the venules that drives flow towards the right atria and so the MSFP being equilibrated pressure if a heart fails is just that. But I find that arbitrary and entirely confusing.

I think the words tripping you up are "mean" and "systemic". Specifically, it sounds like your intuition is that you should be thinking about an average (mean) across space, across all the systemic circulation, and hydrostatic pressures are dominating your thinking. Probably this is the fault of the person who strung these particular words together, but more generally I'd urge when learning terminology in biology and medicine to not let yourself get fooled by etymology and the meanings of specific words, but rather to treat terminology as terminology.
Instead, I'd think about this as it's usually measured, which is as a pressure at the venous return with the heart stopped. For "mean", I would not think of this as an actual average in the typical sense, but rather just as a steady-state, when there is no pressure differential between veins and arteries, rather than no pressure differential between head and foot.
Physically, MSFP represents the pressure of the compliance of the vasculature. Blood vessels are not hard plastic or metal pipes, they are flexible and muscular, and they push on the blood inside to create a pressure even without any pumping or anything. That's what MSFP is trying to measure. Don't forget that in physiology we are nearly always talking about relative pressures rather than absolute; we don't think of the approximately 760 mmHg of atmospheric pressure when we measure blood pressures in the range of 10 to 200 mmHg, there's always a reference point, usually the immediate vicinity outside the vessels/outside the body. That would also be a good approximate reference to the pressure in an "empty" heart, so if you measure the pressure right outside the heart at a steady state, it gives you an idea of on average how much tendency there will be for blood to flow into the heart if it were empty.
I hope that's helpful, you might try to read more from other sources if your textbook isn't quite clicking:
https://en.wikipedia.org/wiki/Mean_systemic_pressure
https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04024-x
As far as hydrostatic pressures, I think you're not seeing them discussed in this context because they just aren't that relevant to this particular static model of what is happening to blood at the level of the heart due to passive tension and blood volume in the vasculature. I'd set it aside and learn separately about how blood flow overcomes hydrostatic pressures particularly in the legs through valves and pressure generated by surrounding tissues.


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What is the cost of increased neural adaption for strenght?
Axiom: Physical strength is a function of muscle mass and neural adaption.
I understand that increases in muscle mass incur associated metabolic costs. What are the corresponding costs for neural adaption for strength?

not just muscle mass, muscle composition as well, chimp muscles are stronger (~1.4 times) than our at the cost of worse endurance, because they have more fast twitch fibers. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5514706/


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According to an online course, ribose and adenine can bond to make ATP. Is this true?
I recently came across this question in the MIT Open Learning Library Pre-7.01 Biology Course. It is question 2d in Problem Set 1 (archived link).
The question, as well as the correct answers and explanation from the answer key, is shown below:

The following is adenine base, which can covalently bond, through condensation reaction with ribose sugar to form a nucleotide (ATP).

Which carbon atom of the ribose sugar would covalently bond with the circled region of adenine to form Adenosine triphoshphate (ATP)?
 C1' ← correct answer
Ⓑ C2'
Ⓒ C3'
Ⓓ C4'
Ⓔ C5'
Would you classify this base as purine or pyrimidine?
 purine ← correct answer
Ⓑ pyrimidine
Explanation:
Bases bond to the 1' carbon (C1') in the formation of nucleotides. Other key carbons are the C5', which binds to the phosphate groups, and C3', where new bases are added in nucleic acid synthesis.
Purines have two rings, a hexagon and pentagon, while pyrimidines have only one (hexagonal) ring.

The question, answer, and explanation are confusing to me:

It looks like the molecule shown in the picture (labeled adenine) is actually guanine. Is this a mistake in the question?
I know that a nucleotide is formed when adenine bonds to (deoxy)ribose which bonds to a phosphate group, but the question says that adenine covalently bonds with ribose to form adenosine triphosphate, which it calls a nucleotide.

Is ATP a nucleotide?
Ribose ($\text{C}_5\text{H}_{10}\text{O}_5$) and adenine ($\text{C}_5\text{H}_{5}\text{N}_5$)—or ribose and guanine ($\text{C}_5\text{H}_{5}\text{N}_5\text{O}$)—do not contain any phosphorus atoms, so it doesn't make sense that they would be able to bond to form ATP ($\text{C}_{10}\text{H}_{16}\text{N}_5\text{O}_{13}\mathbf{\text{P}_3}$). Furthermore, the reactions would not balanced in either case without using multiple molecules. Am I missing something?

Creative Commons Attribution Notice
The image above and the text of the question discussed are licensed by the Massachusetts Institute of Technology under the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

The structure shown is indeed of guanine, not adenine.

A nucleotide is defined as being composed of a nitrogenous base, a pentose sugar and phosphate (see, e.g. the Wikipedia entry). So the simplest nucleotide based on adenine would be AMP. However ATP is also considered a nucleotide, as can be inferred from this IUPAC entry. Often we refer to it as a nucleoside triphosphate. (A nucleoside is just the base–sugar combination.)

I think you misinterpret the wording as describing the formation of these compounds. The wording — which is poor — is meant to describe the components and bonds in the chemical structures, not laboratory chemical reactions or the mechanism of the formation of the compounds in the cell (which is different, complex, but well documented). The use of bond and bind as verbs is bad, as it implies an active process. If I were writing this (and I am an educator and an author), I would write something like “In this structure there is a covalent bond between…”

If you paid for this course, I would ask for a refund. If it is free, “You get what you pay for.”

With all due respect, but if MIT out of all places is hosting this I think it's much more prudent to make them aware of the mistake so they can fix it instead of taking a "You get what you pay for" stance.

@David Thank you for the excellent response! Can you please clarify your third point? Are you referring to the question "Which carbon atom … Adenosine triphosphate (ATP)?" If so, I'm afraid that I don't understand your explanation of how you interpret the question.

If only the synthesis pathways were as simple as that text you linked makes it sound...

@IanCampbell — Metabolism is not simple. However it can be understood if it broken up appropriately, and learned in an appropriate order. If one starts learning the central pathways of metabolism (as organized in a text book) one becomes familiar with the building blocks that are available. One will learn how ribose is made in the pentose phosphate shunt, and how phosphate is present in the cell and is introduced into sugars. Finally one can consult a text to see what constituents are used to assemble the more complex purines and pyrimidines. The overall balance between these follows.

@BenZelnick — The key statements I am criticizing in point 3 are "Bases bond to the 1' carbon…" and "…C5', which binds to the phosphate groups…". I should also add that "…C3', where new bases are added in nucleic acid synthesis." All of these suggest that the actual biological synthesis of nucleotides is being described, which is clearly NOT the case. It looks as if the author was just trying to describe where the components of the structure are connected by chemical bonds, but lacked the appropriate vocabulary or was following the road to hell known as "elegant variation".

@Mast — I am judging the material as I see it. Anyone can copy and paste the structure of the wrong compound. However the ambiguous use of the verbs "bond" and "bind" indicate to me that the material is poor. If the poster wishes to make the producers of the course aware of this, that is his concern, not mine.


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Does tetrachromacy affect eye color?
The majority of people have three cones in their eyes, though there are rare cases of some people having 4 cones (tetrachromacy). There is some genetic testing to support evidence of tetrachromacy, as well as some less reliable tests, but there have only been a handful of confirmed cases. The amount of cones present in a person's eyes determines the range of colors they can see. Tetrachromacy is associated with mutations of the X chromosome.
Does the X chromosome affect eye color significantly? Do people with tetrachromacy have a higher variation in eye color on top of being able to see a more diverse range of colors?


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Is it possible to proccess human genome in a local computer?
I have some basic programming knowledge, and I would like to take a look at my genome and search for specific sequences related to mental illness and addiction.
The test costs only 1000$ in Spain and I can pay it, but I don't earn a lot of money and I would only pay for it if I could process it on my local computer with 32GB RAM.
Is human DNA too much big to process at a local computer?

What do you want to process? A sequence file is basically a text file which is not very big. You can download the reference genomes easily from the various repositories on the web.

Thx. I want to have the file and write universities to ask for some genes I am curious to know if I have. Possible so?

It all depends on what sort of analyses you want to do and what sort of information you get from the sequencing. There are a lot of open-source programs for genome alignment (often the first step in analysis) that will work perfectly well with 32 GB RAM, it might take a day or two to run the program. I suggest that you look into the analyses you want to do and then come back to this question.

I'd say probably yes, but as others point out it all depends on the data you have and the analysis you want. From what I understand, most commercial tests don't provide raw sequence data, but a list of thousands of locations that are most variable in the genome, and which variants you have at those locations. This should be a lot less memory intensive.

Did you look at all the human genomes and genomics code on GitHub, search it for you own specific tasks: https://www.google.com/search?q=human+genome+project+github

@bob1 Thanks. GPT4 explained me that. After doing the genome alingment it says it takes no time to search for example APA gen, even it has 290.000 nucleotides. I have been reading about schizofrenia gens and maybe I need to invest a year or two for this project, but even I am searching for 1000 gens in a single execution GPT4 says I could process it at my local computer buyed in 2020. I have asked and the file costs 2.000 euros in Spain. In september 2024 I finish paying my car and I will do the analysys, and will come back if I have questions and get not convinced with GPT4 explanation

@bandybabbon Thanks, I will take a look.

I don't know what you mean by "process".  Aligning to the human genome might be a strain on your computer, since it has to hold the whole index in memory, but I don't think you'll have to do that.  If you get your genome as a fasta, that's just plain text.  A vcf file with just the variants is even smaller.
Just don't expect to get much.  The truth is, scientists don't know enough to be able to look at a genome and go "oh, that's your problem!", except for a small number of really detrimental things.  You probably are not going to be able to find some "gene allele for addiction".  You are almost certainly not going to find anything clinically actionable.

As a scientist, I am genetist anyhow. DNA has 4.5 billion years while human brain has 1my. I have been reading that trash psychiatrist write.I think they are lost.I think in the next decades there will be a bit of ligth in menthal health coming from DNA.I am diagnosed of schizoaffective wich is just a kind of schizophrenia. I have read delusional disorder genes (the disorder I think I have) are of the same family of schizophrenia ones. I want just to take a look at this...

By the way I could see if I have for example Alzheimer genes. If this is possible and cost less than 1000$ I don't know why lots of people are not planing to do the same as me. For example for Alzheimer prevention is esential. They are doing blood test to try identify it soon.

How about this.  Before you spent the money, write up exactly what outputs you expect the sequencing group to give you, exactly what your plan is for "processing" it, and what actionable information you think is reasonable to expect from that processing.

@swabarnes Ok, I migth post more questions if I start the analysys, but most of them are for neurosciences site.

For instance, before I mentioned vcf files, did you know what they are? Do you know what's in them, and what you can learn from them, and where to get the information required to interpret them?

I have been reading this days and I will need to read a good DNA book, some genetic-psychiatry and some bioinformatics to know what to do. And I may not get very far in what concerns my diagnosis because delusional disorder genes are of the same family of schizofrenia ones. But I would like to check also because my mother has some Asperger behaviours. I am bussy with a football app now and if I do it I will do it in two years or so. Thanks for your time swabarnes2


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When the CD4+ gets activated and help B cells, does it have to be the same pathogen?
Does the peptide (presented by the class II HLA molecule) that activates a CD4+ T cell need to be from the same pathogen as the antigen recognized by a B cell when the CD4+ T cell promotes the activation and differentiation of that B cell?

This is just a guess, and hence a comment. I don't know of any mechanism preventing it being from a different pathogen/source of antigen, but since co-infection is typically quite rare, it would be rather unusual to find a B cell recognizing one pathogen while taking up a completely different other one and presenting it via Class II MHC. You also need to keep in mind that the antigen recognized by the BCR and internalized by the B cell is directed into the MHC II processing pathway for presentation to T cells.

Yes I guess that makes sense, small question though, does the peptide presented via class II MHC has to be from the pathogen the B cell recognizes? Can it not be something else? (if the B cell is infected by a virus, a peptide from that virus for example)


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Database of insect sounds
I was thinking last night as I laid listening to the loud insects at night here in Georgia, that I wanted to be able to hear the bug sounds people listen to all over the world. Could not find much online but maybe I’m bad at searching. Is there a database of insect sounds?

Not surre absolutely, but iNaturalist often has sound files, as does BugGuide.


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Explanation behind the observed chloroplasts in Elodea during Hypotonic vs Isotonic Solution
Me and my colleagues put the elodea leaf in distilled (hypotonic) and tap water (isotonic). We observed under the microscope that the elodea under the hypotonic solution became elongated and turgid, while the ones on isotonic solution was less firm in shape.
My confusion comes in the observed green like particles which I assume to be chloroplasts. They are scattered all over the place for hypotonic solution, while in the isotonic was located on the cell's plasma membrane.
Shouldn't the chloroplasts be on the side for a hypotonic solution due to the expansion of the vacuole? Similarly, shouldn't the chloroplasts be more scattered in the isotonic solution due to the vacuole not expanding that much?


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Calculating pitch of B-DNA
From this question (How pitch of a DNA Helix is 3.4 nm?), I've learnt that for counting the number of axial rise for 10 base pairs in 1 helical turn to measure the pitch of B-DNA, we have to include the space above $1^{st}$ base pair and below $10^{th}$ base pair as per this image - https://i.stack.imgur.com/cZzOj.jpg
But now I'm confused as to why we include these spaces. Why do calculations fail if we were to measure starting from the base-pairs itself? Any help is valuable!

The answer is mostly that you have to use the right denominator, as suggested by @DrRadium's comment.
The crucial mistake in the other answer was measuring 9bp and dividing by 10. That's measuring the length of 0.9bp, not 1bp.
You have chosen to measure the length of 9 base pairs and divide by 9. That works! you have shown that you get the right answer. In that case you don't need to add any space on either side.
In the other question, 9 base pairs were being measured, and then they were dividing by 10- the distance between first and tenth bp is not equal to the length of 10bp. The distance between the the $n$th and first basepair will $n-1$, or in this case $10-1 = 9$.
If you take the comment suggestion and add 1/2 on either side to your distance measurement, you are then measuring 10bp truly, so you'd better divide by 10.
So if you wanted to omit the space, you could measure the distance from the 1st to an 11th base pair. That would be 11-1=10bp long.
You may be interested in reading more about 0-based vs. 1-based indexing. This is an example of a classic "off-by-one" error that arises when you mix up the two indexing styles.


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qPCR from tissue to compare T-cell subpopulations
In the experiment, groups of mice have been intranasally immunised with different vaccine formulations. We have stored nasal tissue (basically, the front part of the skull without muscles, brain, etc.)
Hypothesis: local T-cell subpopulations differ between groups.
Problem: we don't have access to flow cytometry, therefore we would like to compare RNA expression from bulk RNA with the qPCR.
Question:

due to very small amount of T-cell RNA from nasal tissue, is it even plausible to try (anyone has done similar tissue bulk RNA processing?)
which housekeeping genes would be best candidates for further work (see Why are some housekeeping genes considered better?)(any links appreciated)


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Effects of oxygenated water on bacteria
I was curious if any of you would happen to have any experience with this but any hypotheses regarding how this would turn out would be much appreciated.
I’m wondering if water fully aerated with oxygen via pressure at a low temp could be useful in food preservation and distribution. For example if soaking meats and seafood in this water could help slow down and prevent bacterial growth.
Thanks in advance

This is just some oxygen dissolved in water. What is different for this oxygen to the one in air? It is not activated or otherwise more reactive.

We expect questions to show some evidence of prior research: what led you to asking this question? Why would you think oxygen-aerated water could be useful in food preservation?

Do you want to know about oxygen being toxic at high concentrations? If yes then I guess it could be considering anaerobes cannot survive in oxygenic conditions and high levels of oxygen will also kill aerobes. The practicality, limitations etc are unknown to me.


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Why do zygotes divide internally and not externally?
As far as I understand, two gametes fuse to create a zygote. Gametes are created via miosis, they are haploid and when they fuse they become a complete cell (diploid). And diploid cells divide via mitosis.
However, I wonder why a zygote does not become two zygotes? What is different about it that makes it divide internally?
In other words, why does a liver cell become two separate cells, yet the zygote becomes two cells inside the same shell?

Update:
Maybe this image can help:

The zygote is dividing. But what is that external package? Why do those divided cells remain in a circular sac (Sorry for this stupid terminology, I want to make myself clear)?
But in simple mitosis (the image below) divided cells are not inside a package anymore. They are 100% separate from each other.

As I have understood it, the divided cell remains in the parent tissue. A liver cell after division becomes two cells inside the liver. The container is the liver.
However, the zygote is not like that. It's internal mass divides and remains inside the same zygote. I don't know what's so hard about understanding this for your guys.
Maybe the zygote is not the outcome of the fertilization of the egg and sperm. Maybe an egg has a package and a cell inside it, and that package is not part of the cell. That's why I'm asking.

What do you mean "inside the same shell"? Zygotes divide just like liver cells...

look up monozygotic twins

It seems that I'm missing something here. Maybe a zygote is not a cell. Maybe it's a biological envelope, containing a cell, and then the inner cell divides. But the monozygotic twins images do not show that. Bot inner cells, and the envelope divide.

@BryanKrause, please look at this image for example. The inner cell (blue dot) divides, and the outer shell also divides.

What do you mean by "shell" a zygote divides into two sperate cells just like all cell divisions. Are you maybe thinking of the corona radiata, which breaks down after fertilization.

If the term zygote is a diploid cell, then when it divides there is nothing strange in the fact that it becomes two diploid cells. If the term zygote indicates its special origin, it is impossible logically for a daughter cell to have the same origin. Your expectation that the zygote would divide into two haploid gametes seems bizarre. The “magic” thing would seem to me to be meiosis and fusion. Once you have a zygote it’s not quite back to normal because the cell must differentiate, but mitosis is the default cellular behaviour.

If you don't understand the parts of an illustration you should probably ask about that before guessing and asking a confusing question based on your guess.

@John, then please clarify my misunderstanding instead of criticising me. Thank you.

@SaeedNeamati its not criticism its how questions work, the site is for answering specific questions

@John, is the image I have shown up not clear? What can not be understood from that image?

You have half  dozen questions here, I will answer one, that outer membrane is called the zona pellucida. it exists to control fertilization. https://study.com/learn/lesson/early-embryonic-development-human-stages-formation-mechanisms.html

@John, so I was right. The egg is not a cell. It's a cell inside a package. The Zona Pellucida is not part of the normal cell that divides. It acts as the container for the fetus and placenta.

No it breaks open long before either is formed, again research don't guess.

@John, please don't be harsh. Either help or leave this question for others to answer. I have watched dozens of videos regarding this. I have done my research to ask this question. And you just complicate things. So either help or please leave.

I'm complicating it by trying to lead you to asking a coherent question instead of just voting to close for asking several separate questions. Or at least figure out where your confusion is coming from.  there is no difference between liver cells and zygote cell division. a liver cell divides into 2 separate liver cells and a zygote divides into 2 separate zygote cells. A dividing liver cell does not become 2 livers why would a dividing zygote cell become 2 zygotes? if you want to know about the function of the Zona Pellucida ask that as a question. You could also look into cell adhesion.

this may help you https://www.twins.org.au/how-to-determine-zygosity/89-placenta and https://twinstudies.org/zygosity-and-chorionicity-of-twins/


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How to disambiguate between chromosome and chromosome pair?

Our genetic information is stored in 23 pairs of chromosomes that vary widely in size and shape. Chromosome 1 is the largest and is over three times bigger than chromosome 22.
Source: https://www.ncbi.nlm.nih.gov/books/NBK22266/

There are 23 pairs of chromosomes. But the article is using the phrase "chromosome 1" and "chromosome 22" to refer to "chromosome pairs".
What is the correct term here?
Is there a term referring to a chromosome class or type or something similar?

This is standard. For a typical human diploid cell there are two copies of chromosome 1, two copies of chromosome 2, etc; you'd have either two copies of the X chromosome or one X and one Y.
There's not really any ambiguity, the chromosome IDs are always a type or class in some sense.
See for example https://en.wikipedia.org/wiki/Karyotype

Is it because of the said ambiguity that in mitosis chromosome number remains constant till  anaphase and doubled after anaphase upto cytokinesis. Also  chromosome number is halved in meiosis 1 but DNA is  halved(again) in meiosis 2

I remember our teacher telling us that after DNA replication both sister chromatids are together called 1 chromosome but after sister chromatids separate each sister is treated as an individual chromosome


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Looking for specific alga and a recently extinct (or rare) marine animal from the same region for novel
I'm writing a novel where there is a drowned body in an inland lake. The idea is that she was drowned after a fight in a container containing sea water for smuggling a recently extinct (in the novel, supposedly extinct) or a rare marine animal, and there was also some species of alga in her lungs.
Hence, I'm looking for two species from the same ocean or sea (endemic or not), where some info on the genome is known. The best thing (or you tell me if it makes sense at all) I could come up with so far is the Great Auk (Pinguinus impennis) and brown alga of some species which I think is mostly found in the North Atlantic.
Very grateful for any info on the genome (no details necessary, just whether the DNA has been sequenced and whether it would be possibly to identify by a tissue sample), chromosome number and other info on the great auk and some Phaeophyceae alga or any other input for a fitting pair of species. My novel is set in 1994, and they identify the species by forensic PCR methods, no need for a specific match, but by a shred of skin or so I need two marine species identified (not with 100% certainty, good odds or a near-match is enough) by some forensic way, can be anything really, one of them small enough to be in the water in the lungs of a drowned body. Or a genus could be enough, the plot element is just that she drowned in a container used to transport an animal.
Sorry if it's inappropriate to ask this here, it's not a scientific question I know, but I trust I get the highest quality input here.
Actually, the alga is of secondary priority, if someone could point out a recently extinct marine animal which can be matched by its DNA, or by a tissue sample using some other method, I can even scratch the alga, but it would be a nice cherry on top.

Yes, at least some of the genome has been sequenced for the Great Auk (Pinguinis impennis): Taxonomy browser @ NIH (click on the 45 next to the Genomic Sequences title). There appear to be 45 different genomes published. All of them are mitochondrial genomes, which are relatively easy to reconstruct, as well as super abundant in any tissue. They can be used to identify samples to the species level.
I don't know of any specific algae that might match, as these tend to be very widespread (as one might expect for a marine species that is distributed by currents). You might be able to concoct one fresh-water one that comes from some remote island where the Auks are found. Perhaps a land-bound plant pollen or spore (moss, fern) in the lungs instead if she has been collecting these animals from somewhere? It doesn't have to be real after all, just believable (for example Dan Brown's Da Vinci Code theories etc.)!

You might find this Telegraph book review fun (best book review I ever read): Don’t make fun of renowned Dan Brown.

@anongoodnurse I think I have seen that before, or perhaps a similar one about another author, still gets a laugh out of me.

Hey, thanks a lot for the input! I guess the Auk will do then with your confirmation that it can be positively identified by the mDNA -- But, @anongoodnurse, just asking out of curiosity (and thanks for the funny review, or whatever it is, I assume I'm missing out on something, his constantly referring to himself as renowned I assume); is it that (a) this part of the plot sounds so far-out it reminds you of Dan Brown or (b) my grammar or style reminds you of Dan Brown or (c), heaven forbid, both?

It will be much more far-out pulp stuff than Dan Brown, but with a tiny difference: the book won't take itself seriously. Or so I hope. So heaven forbid anybody associate my grammar or style with Dan Brown, that was my point, although I'm writing the first version in German, so I'm off the hook for the time being.

@bob1, however, has this been sequenced in 1994? I understand PCR was fairly new then so you'd need a huge sample? Could they run as many cycles as they do today? Also, the genome is only 16k base pairs and 10k are identical, is that correct?
Sounds like nothing, I thought humans have several billions and the onion (I heard) has much more...? But most of it is junk anyway, or so they claim?

@FissionChips PCR is largely unchanged since the 90's, besides some advances in detection technology, mechanization and enzymes, the reaction used today is the same as Kary Mullis invented. I was doing PCR in the late 90's on machines that are still sold today. Sequencing - massive advances since the 90's. Sanger sequencing (chain termination) is still common and largely unchanged since the 90's too. Both definitely possible and quite sensitive even back then. Wouldn't have been able to do sequences off historical things back then though, ancient DNA tech has come a long way.... cont

cont... Those are mitochondrial genomes (~16k bases) and all from the same species, so about right in terms of diversity. These will be distinct from other species though, at least in the right regions, so is very useful for species ID. These were 4 mtDNA genomes generated in 1994 -see fig 2 and section "early mtDNA discoveries" for more info. Earliest were 1980's, so it isn't out of the realms of possibility to have had great auk there, it's jsut that people focussed on easy (abundant) species first.

@FissionChips I mentioned Dan Brown as an e.g. of someone who gets the details wrong, but still tells a story that is believable. Your has to stretch the tech and knowledge a bit to get Great Auk sequenced in the 90's; the ability was almost there, just people hadn't got around to it. Another e.g.: I remember reading a fiction novel in early 2000's about a person with dwarfism who modified an embryo and implanted it in a woman so that the child would carry his form of dwarfism. We weren't capable of doing that sort of thing at the time of setting, but still an interesting read.

@FissionChips - No, not at all! Actually I upvoted your question because that sounded like a fun twist. I only posted that review because Dan Brown was mentioned and it's so on-point about his writing, which is terrible. I doubt he could have written the question you wrote as well as you did. :) He has his fans, though, which is fine by me. I'm not high-falutin (sp?), though. I read The Silmarillion, but actually had to take notes to keep things straight. Could not finish Foundation, though I love Asimov. Too complicated for me.


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Do endogenous retroviruses (ERV) have a high degree of heterogeneity among people?
Endogenous retroviruses (ERV) make up 5~8% of human genome. These ERV are ancient retroviruses which infected germ cells and therefore became parts of our genomes. However, unless the ERV can increase the survival chance to its host, it wouldn’t be able to expand its frequency in our genetic pool. So there must be some mechanisms that expand the copy number of ERV. The infection of germ cells can happen more than once. Alternatively, ERV can reactivate at some point of the development of the host and make new copies in the genome. Considering that the sites of integration of retroviruses are highly random, even the same ERV can appear in different loci or different chromosomes. Have large scale genome sequencing revealed a heterogenic map of ERV?

Of the papers I reviewed to answer this,
Variation in proviral content among human genomes mediated by LTR recombination
addresses the question most directly. I recommend you read it if you have access. To summarize, most ERV in the human genome integrated before the separation of human and chimpanzee lineages, and some before the emergence of placental mammals. Among these, there is relatively little variation:

an HERV-H element on chromosome 1 (1q25.3_H3) was shown to exist as proviral and solo LTR alleles in two related individuals

"solo LTR" allele means that the viral genes have been deleted by homologous recombination of the Long Terminal Repeats (LTR) that flank the intact provirus, leaving only one LTR. These don't code for any protein, but can still be "active" by affecting the expression of nearby regions in the host genome. The paper I cited above verified four other HERV-H variations and identified 67 potential variations.

We were intrigued to discover a dimorphic element for the HERV-W family (18q21.1_W2). This element is represented as a solo LTR in the reference genome, but our data clearly show that it also occurs as a provirus segregating in South Asian populations (Fig. 3a) and likely in other diverse populations (our pipeline predicted a provirus allele in 194 out of 279 individuals surveyed, Additional file 2). To the best of our knowledge, this is the first HERV-W locus reported to show any type of dimorphism. This particular HERV-W insertion must have occurred between 18 and 25 million years ago because a provirus is found at orthologous position in all other ape genomes including gibbon, but is absent in Old and New World monkeys [67]. Our discovery illustrates the potential of LTR recombination to alter genome structure long after a proviral insertion has occurred.

The HERV-K family, however, integrated into the human germline relatively recently (estimates span 3 million - 250 thousand years ago).

Among the diverse assemblage of HERV families in our genome, a single subfamily known as HERV-K(HML2) has been reported to exhibit insertional polymorphism in humans [17, 28, 29, 36–47]. Thus far, approximately 50 HERV-K(HML2) proviral loci are known to occur as empty (pre-integration) and/or solo LTR alleles segregating in the human population [17, 43, 45, 46], but more may be expected to segregate at low frequency [39, 48]. These observations are consistent with the notion that HERV-K(HML2) is the most recently active HERV subfamily in the human genome [49–53].

The 2020 review article Human Endogenous Retrovirus K (HML-2) in Health and Disease gives a quantified overview of the variability of the HERV-K family.

It is known that there are more than 1,000 HERV-K (HML-2) loci in the human genome. Most of them reside in the genome as solo-LTRs generated by homologous recombination between the LTRs of a single HERV-K (HML-2), resulting in the deletion of the internal sequence (Hughes and Coffin, 2004). Solo-LTRs are approximately 10-fold more abundant than their full-length or nearly full-length proviral integrations (Subramanian et al., 2011). In total, there are 1098 reported loci whose insertional elements possess functional elements, including 1061 reference (hg19) insertions and 37 non-reference insertions (Subramanian et al., 2011; Lee et al., 2012; Marchi et al., 2014; Wildschutte et al., 2016; Wallace et al., 2018; Xue et al., 2020).

My summary: Most of the ERVs in the human genome are present only as remnant solo LTR alleles. Since virus reemergence is harmful, deletion by homologous recombination is likely selected for. This kind of deletion has been happening continuously along the human lineage and accounts for most of HERV differences between human genomes. Only the HERV-K family shows differences in insertions between humans. Across humans, roughly 95% of HERVs are identical for everyone, and roughly 5% are absent in some people. All of the HERV families are considered extinct. That is, there are no retroviruses circulating currently that correspond to any of the integrated HERVs.
I didn't see much discussion about smaller-scale insertions, deletions, or point mutations within HERVs, except to note that intact provirus could be dated by the amount of sequence difference in the LTRs at either end. That is, the LTRs are by definition identical when the retrovirus genome is inserted, but will accumulate mutations independently afterward, so the difference lets you estimate the number of mutations and thus how long ago integration occurred. If the LTRs of a provirus diverge enough, they will no longer be able to homologously recombine, and the virus insertion will become permanent. As a caveat, genomics is not my specialty; I may have combined information from different sources incorrectly.
some other notable references:

Identification of the distribution of human endogenous retroviruses
K (HML-2) by PCR-based target enrichment sequencing
Is the
HERV-K HML-2 Xq21.33, an endogenous retrovirus mutated by gene
conversion of chromosome X in a subset of African populations,
associated with human breast cancer?