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Why are there two replicase proteins translated from tobacco mosaic virus RNA?
I’m trying to understand how TMV is expressed and have read (here) that there is a large and small form of the RNA-dependent RNA replicase. These are translated from the same region of the genome, the larger arising from read-through of a leaky stop codon.
Why are there two forms of the replicase? My first impression was that each might produce a sub-genomic RNA, one for the movement protein and one for the capsid protein, but can find no reports confirming this.

Many proteins are made up of multiple subunits (look at pretty much any viral capsid protein for instance).

Is it possible that the subunits may have a function different from that of the completed protein? The link I put in the question states 'the small replicase is involved in replication and acts as a suppressor of RNA silencing' - I'm not sure if 'the small replicase' refers to a small subunit or the completed replciase.

Yes and no, both together make the RdRP in full, but one will be the replicase and one have other functions such as capping of transcripts, binding etc. Both will likely have several functions that do all the combined work of the RdRP.

So they are subunits that together have RdRP function, but work independently?

I have edited your question removing all reference to subunits. Subunits occur in proteins with quaternary structure — they are constituents of a larger molecule. There is no (or little) evidence that this is the case here. Certainly the word "subunit" does not appear on the page you reference. This is relevant to their function.

@bob1 Do you have any evidence for your statement "both together make the RdRP in full"? I find none in my reading (see my answer).

@David - it is called the replicase large subunit. If you follow the link and look at the information provided it says Replicase small subunit: is a methyltransferase active in RNA capping and an RNA helicase. and provides a reference. This protein, like many RdRPs, is a heteromer, and there is quite a bit of evidence for these in many species of viruses. You are welcome to add this into your otherwise excellent answer if you like. The small subunit also does host RNA silencing suppression

@bob1 — I need a reference from a research paper, not from a database compiler who may or may not know nothing about the biology.

@David See the reference I linked at the word reference

@David also try this one.

@David for heterodimerism this one

@bob — I've updated my answer regarding this.

Short Answer
As of 2021 the rationale for the production of two proteins from the Tobacco Mosaic Virus (TMV) replicase gene is incompletely understood. The two proteins share some activities but not others, and although they appear to co-operate in the replication process there is a ten-fold excess of the smaller relative to the larger.
Longer Answer
“Why is there a 126-kDa and 183-kDa form of the TMV RNA-dependent RNA replicase?”
My answer is based mainly on the review by Buck (Phil. Trans. R. Soc. Lond. B (1999) 354, 613–627), but includes material from some later sources (e.g. Malpica-López et al. (2018)). Many relatively recent papers related to the replicase (e.g. this from 2008, and this from 2012 tend to avoid this question, confining themselves to describing the properties of the two proteins. The main points are:

Both the TMV-encoded 126-kDa and 183-kDa proteins are required for maximum efficiency of TMV RNA replication. The full-length protein is absolutely required; preventing the production of the smaller protein reduces the replication rate to 20% of normal.
The rate of read-through of the stop codon is about 10%, so that ratio of 126-kDa :183-kDa proteins is 10:1.
The read-through portion of the 183-kDa protein contains amino-acid motifs characteristic of RNA- dependent RNA polymerases (RdRps) and hence the 183-kDa protein is likely to provide the catalytic activity for the synthesis of TMV RNA from NTP substrates.
“The C-terminal domain of the TMV 126-kDa protein is helicase-like. Although helicase activity has not yet been demonstrated for the 126-kDa protein of any tobamovirus, these proteins contain six amino-acid motifs, which are highly conserved in known helicases, such as the translational initiation factor eIF-4A.”
“The TMV 126-kDa protein contains two domains. An N-terminal domain with amino-acid motifs and predicted secondary structure typical of S-adenosylmethionine binding proteins, methyltransferases and guanylyltransferases is probably required for synthesis of the 5' m7GpppG cap structure. The TMV 126-kDa protein has been shown to have guanylyltransferase activity.”
The 126-kDa protein has activity in silencing host anti-virus suppression. The 183-kDa protein lacks this activity, suggesting a difference in conformation relating to the region responsible.
There is evidence for association of two forms of replicase in the replication of membrane-bound viral RNA. However no direct structural information (e.g. X-ray crystallography, cryo-EM) is available for a complex with or without the RNA.

The only suggestion that Buck makes is that as helicase activity is required for two separate purposes — to unwind double-stranded RNA during replication, and to remove secondary structure from single-stranded RNA when this is used as a template for multiple copies of the complementary strand —  the two forms of the replicase may have a different substrate specificity in their helicase activity.
Own thoughts
It is commonplace that the constraints on eukaryotic mRNA translational initiation and the small size of viral genomes have resulted in viruses adopting different strategies for maximizing their coding potential. Read-through is not unique to this class of viruses. I imagine that the replicase preceded the readthrough, in which case one wonders whether the original enzyme was a homo-dimer, which has been superseded by a hetero-dimer with similar protein–protein interaction. The problem here is that the contemporary enzyme has only one active site. Clearly, structural information is needed to address these possibilities.
Footnote: Nomenclature
The original question and some sources (mainly in structural biology) refer to the 126-kDa and 183-kDa forms as subunits of the replicase. Most virological sources do not employ this description, which I think is misleading because it ignores 90% of  126-kDa protein which cannot be involved in replication and therefore does not function as a replicase subunit. It also suggests a level of structural analysis that does not exist. Although replicase enzymes often have several subunits, they are generally structurally distinct. The situation with TMV is different.

Thanks for clearing up the misconception - the page I linked does state 'small replicase subunit' in the genome diagram which threw me off but after reading the attached literature I agree that it's not appropriate to consider the proteins to be subunits.

Ah. Fair enough. I just read it and did a text search. The authors of the page obviously chose their words more carefully than the author of the diagram (although in a diagram one is short of space, so sometimes one does that sort of thing).

The RNA-dependent RNA polymerase of the Tobamoviruses exists as a heterodimer expressed by read-through of the RdRP portion of the genome (open reading frames 1 and 2). The products of these ORFs are two proteins of 183 kDa (large replicase subunit) and 126 kDa (small replicase subunit), with the 126 kDa being produced approximately 10x more than the 183 kDa form. The functions and sizes of the various proteins are described well in Watanabe et al., (1999):

The genome of tobacco mosaic virus (TMV) consists of a single-stranded RNA molecule of about 6,400 nucleotides in length with positive polarity, which encodes at least four polypeptides: 126- and 183-kDa proteins required for transcription and replication (hereafter referred to as the 126K and 183K proteins, respectively), a 30-kDa (30K) protein for cell-to-cell virus movement in infected plants, and an 18-kDa protein for virus coat formation. The sequence of the 126K protein is encoded by the 5′-proximal region of the viral genome and includes the methyltransferase and RNA helicase motifs, while the 183K protein is a read-through protein of the 126K open reading frame (ORF) and contains, in addition to the above two motifs, the RNA-dependent RNA polymerase motif. The RNA polymerase is considered to be involved in both transcription and replication (8). From sequence analysis, it is believed that the viral RNA polymerase contains the 183K protein as a catalytic subunit, but the precise molecular compositions of transcriptase and replicase have not yet been determined.

A common feature of RdRPs in RNA viruses is that they exist as heteromers. A very well known example of this being the RdRP of influenza virus (-ssRNA), which exists as a heterotrimer consisting of the PB1, PB2 and PA subunits produced from the eponymous genome fragments. However, (many) other examples exist in the virus world, including in another plant virus genus Potyvirus, which, in common with Tobamoviruses and 90% of plant viruses, is a positive sense single-stranded RNA virus. The features of the  Potyvirus RdRP have just been published, and to quote the linked article (and references therein):

The RdRp–RdRp self-interaction seems to be a common feature for positive-sense, single-stranded RNA viruses, including insect-, animal- and human-, and plant-infecting viruses [38,49,50,51,52,53]. The dimerization or oligomerization of RdRps may increase the stability of these enzymes and protect against degradation.

As you can see from the information provided in the top quote, the functions of the different subunits of the protein are different but complementary. The 126 kDa contains a helicase and methyltransferase motifs, while the 183 kDa functions as the polymerase as well as containing the same helicase and methyltransferase motifs. Lewandowski and Dawson (2000) found that the 183 kDa subunit was capable of performing all the functions listed above, acting as the full RdRP, but with the 126 kDa subunit those functions were performed ~10 times faster. They also found that mutating a base in the helicase domain of the 126 kDa (183 kDa supplied by a helper virus that only expresses the 183 kDa form) resulted in no replication of the RNA with the mutant 126 kDa indicating that this protein is essential to RNA replication. It should also be noted here as per comments, that the evidence for heterodimerism of the two forms is not in the form of a crystal structure, but in a 1:1 stoichiometry in immunoprecipitation as discussed in the Watanabe paper linked above. To my knowledge no-one has produced a full crystal structure of the RdRP of any Tobamovirus.
However, as you might have noticed when you looked at the information on the link you provided, that there seemed to be only about 4 ORFs, and a small number of proteins produced, and you might be thinking something along the lines of

"how does a virus manage to work when it only produces so few
proteins?"

The answer to which is viral proteins perform many functions (this feature isn't specific to viral proteins). In particular, the small subunit (126 kDa) seems to act as a suppressor of the host silencing RNA system (siRNA). siRNA systems in plants function a bit like an immune system response - they signal within the cell and extra-cellularly to induce a viral RNA degrading response, so that the virus can not easily spread or establish itself in the host. I would speculate that what better place to suppress siRNA functions than at the site of viral RNA replication itself.

It should be pointed out that influenza virus is a completely different type of RNA virus, with a segmented genome. The RNA polymerase subunits are the products of separate segments are produced in similar amounts. Their relevance to the situation in TMV therefore not escapes me.

While there does seem to be evidence that both the smaller and larger proteins are part of the replication complex (e.g. co-immunoprecipitation), I don't see any direct evidence here that "The RNA-dependent RNA polymerase of the Tobamoviruses exists as a heterodimer ..."  It certainly may, but the wording "subunit" to me implies obligatory binding to perform its function. The smaller protein also seems to be synthesized in 10x greater amount than the larger protein.  It makes sense to me that the smaller protein could function on its own and may also bind to the larger protein.

@Armand well, those that study the protein themselves call it a heterodimer. It does have 1:1 stoichiometry in the IP, which is pretty strong evidence that it is existing as a heterodimer. It is called the subunit as it is transcribed from the same ORF unit on the TMV genome I suspect. No-one knows why 10x amount produced. It is definitely the large product that contains the RdRP bit.

@David I did point that out -ssRNA tells about the form of the genome (negative sense single stranded RNA), agreed it doesn't tell about the host(s), but I think most people recognize that flu doesn't infect plants. TMV and related viruses are in their own family, so there isn't anything exactly similar. If you like I can provide examples from +ssRNA, and dsRNA and non-segmented genomes too. The idea was that heteromerism is a common feature of RdRPs. I'll edit that to explain more clearly.

Re: "They also found that mutating a base in the helicase domain of the 126 kDa (183 kDa supplied by a helper virus that only expresses the 183 kDa form) resulted in no replication of the RNA with the mutant 126 kDa indicating that this protein is essential to RNA replication."  I think their inference was that the 126kDa acted on the RNA strand it was synthesized from ("in cis") so that the defective 126kDa was blocking replication of "its" RNA. The other experiment showed replication even without the 126kDa (at 10x reduced level), indicating the 126kDa was not "essential" to RNA replication.


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How to express total eradication of bacteria (inhibition zone) when placed into a table
I am a grade 9 student studying the inhibition zones of several different essential oils by comparison to Tetracycline to prove there is merit to treatment of bacterial infection (investigation is being conducted evaluating efficacy against S. epidermidis). I am analysing it by measuring the efficacy of 100% essential oil, in addition to MIC and 10x MIC.
One of the essential oils totally eradicated the bacteria. How would I express that in a table?

Please specify in which method bacteria were eradicated.

It would probably help if you included a cell-phone picture of what you mean by "totally eradicated," and something that would not fit that description, for comparison.

The real piece of information that you need to supply is what measurement in what units is in the column in your table that you are worried about. If it is "diameter", as I believe is normal in this sort of semi-quantitative assay, what is your problem? Perhaps you are worried that the reader will not realize that 10cm (or whatever) is the diameter of your petri dish, and the limit of your ability to assay high doses. If this the case, perhaps the solution is not to use cm but % of total diameter, so complete eradication is 100%. (You might even use simple geometry to find % eradication.)

And, of course, there is the question whether you should be putting the results in a table or plotting them as a graph. That might make it obvious that you have reached a saturating dose of your magic potion.

Sorry I haven't been able to  respond, I've been super busy all week with World Scholars Cup... sadly, i dont have access to cell phone images as of now, however I can answer some of the other questions. The bacteria was inoculated onto a petri dish with agar. Then, right after the bacteria was introduced, 3 filter paper discs (that had been soaked in the essential oils) were introduced to the petri dish.

In terms of David's question, the problem i face is that there are multiple discs on each petri dish, meaning that i wouldn't be able to work out a percentage eradication? Correct me if i am wrong.

Then what do you mean by "totally eradicated"?  What did you actually see?  Are you saying (I'm guessing here) that all the bacteria in the dish died off, leaving you unable to tell which disc did it?  In that case, I'd say you should re-do your experiment.  If not, what was it?  (I suppose this difficulty in explaining to us what happened is proof that you do need a better way of explaining it in your paper!  Pity you can't send a picture!  I take it you can't send a sketch either?)

Ok, so by totally eradicated, I meant that there was no visible bacteria on the dish, while on my control dish (no antimicrobials) there was evident bacterial growth. Don't worry anymore, however, as I got a chance to consult with my teacher who provided me with a way of expressing this. Thanks for all the help!

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Is this a bed bug??? Small insect with tail thing found in bed

Couldn’t find any other ones, no bites, is very very very small like almost fruit fly size

Nah, not a bedbug, those are round and weirdly flat, as shown in the photos in the posting Tyersome linked.  What you have there is a beetle of some sort.  You can tell by the hard shell divided into two halves along the back - only beetles have those.  The wings are folded up underneath there.  I couldn't say what species of beetle exactly, there are many kinds of tiny brown beetle and the photo is fuzzy.  It's harmless, anyway, whatever it is.
Beetles have no tails.  Looking at the photo, I think what you thought was a tail is actually the end of its wing poking out from under its shell.  I often see that.
Update: I found this, which has photos that look a lot like yours.  One of the photos of one of the beetles even has a nub which looks a bit like a tail.
UK Natural History Museum forum: Is this a biscuit beetle or furniture beetle?
The rest of the above is from memory from reading wildlife books, but I was asked to provide some references so here are some websites that confirm the beetle facts I mentioned.
https://www.woodlandtrust.org.uk/blog/2017/11/common-uk-insect-identification/
http://www.oum.ox.ac.uk/thezone/insects/instant/index.htm
https://www.coleoptera.org.uk/beetle-morphology
https://www.coleoptera.org.uk/what-are-beetles

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Why is the antibody light chain essential for function?
Humans and most other mammals produce antibodies consisting of two heavy chains, each linked to a light chain. Both heavy and light chain contribute to the variable region, and thus the antigen specificity of the antibody.
In contrast, cartilaginous fish and camelids have been found to produce heavy-chain-only antibodies, and thanks to their small size and ease of synthesis, camelid antibodies (nanobodies) are predicted to revolutionize antibody therapeutics.
This makes me wonder: why is this not possible with human (genetically engineered) antibodies? Apart from the fact that removing the light chain would alter antigen specificity, what hinders a heavy-chain-only human antibody from being functional? What is so fundamentally different between the camelids heavy chain (and their variable region) and the human equivalent?

It is possible with genetically engineered human antibodies. scAbs and related scFvs (single-chain fragment, variable), which are even smaller, have been around for at least a couple of decades.

This was the kind of answer I was looking for. I realize my question doesn't reflect that. Thanks!

In case someone else finds this: https://www.nature.com/articles/d41586-021-01721-5

I suspect it has to do with the fact that since the camelid scAbs are expressed in vivo, they undergo the normal recombination and affinity maturation process there as individual variable regions.  Thus, one can easily isolate high-affinity scAb mRNAs from the blood of a suitably-immunized camelid and proceed with cloning and production.
Human heavy chains undergo affinity selection while paired with light chains and so in vivo processes wouldn't work to generate heavy chains that on their own bind well to the given antigen. I suppose one might generate a display library with only heavy chain genes, but at a typical library complexity of 10^7 you wouldn't be able to cover as much of the "conformation space" as with an in vivo single chain affinity maturation process.
PS - the bit about "revolutionizing antibody therapeutics" seems like marketing hype for a 20+ year old idea.

Thanks. I guess I assumed that in vitro selection would be relatively straightforward with today's technology. But perhaps you're right about the library complexity not being large enough. And yeah, "revolutionizing" might be an exaggeration, but camelid antibody keep popping up every so often, so I really thought it was a newer discovery than 20+.


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Is alternative splicing possible in the same cell?
I know alternative splicing is possible in different cell types of an organism, or within the same cell at different developmental stages. There are several examples like this. But are there any instances of alternative splicing within the same cell at the same time? Perhaps some melanin variants producing shades of different color for example. Normal cells, not cancerous.

In complex eukaryotes like humans, alternative splicing is the rule, rather than the exception.
Eukaryotic splicing is managed by a complex regulatory system, including more than 100 different elements, some of which are enhancers and regulators.
Thus, while one form will often be dominant, one should generally expect at least some alternatives to be present in a cell.
While the amount of work on population-level heterogeneity is still much larger than that on variation within single cells, studies of splicing heterogeneity have identified that multiple forms are often present simultaneously within a single cell. For example, in this recent study, Figure 2 shows that although the distribution between two splicing alternatives is bimodal, single cells exist with the full range of fractional mixes between the two forms.

Provirus of HIV makes a 9kb pre-mRNA which can go under alternative splicing to produce a variety of different mRNAs. Therefore alternative splicing in this infected cell can happen at the same time.

I do not recall any cases of such behaviour for normal cells, off the top of my head but it must exist. Probably, alternative splicing in the same normal cell can happen in early embryo differentiation or in the case of protein localization of a specific peptide in different compartments of a cell.

What you write is correct, but the question clearly relates to cellular, not viral transcripts.


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What does "Pandercetes" (genus of spiders) mean?
"Pandercetes" is a taxonomic genus, and refers to certain Huntsman spiders (found in Australia/Asia).
It was named by Koch, a German entomologist, in 1875.
What does the name itself mean or connote? What are the defining characteristics of this genus?
I could not get a clue as to what roots the word is made of .. pander + cetes? pan + dercetes? My understanding leads nowhere this far.

Koch did write a book describing these and other species:
Die Arachniden Australiens nach der Natur beschrieben und abgebildet By Koch, Ludwig, 1825-1908 Nürnberg :Verlag von Bauer & Raspe,1871-1890.
Harvard apparently has scanned volumes: https://www.biodiversitylibrary.org/bibliography/121660
Perhaps the reasoning will be found there - should be fun hunt!

Cetus or cete means "whale" in Latin, and is the root of the English word "cetacean". Don't know how that refers to huntsman spiders, though...

biodiversitylibrary mentions highlight this genus' eyes "the eye area strongly raised in all directions" (as translated from Koch's German writings) .. and ..
Dercetes of Phyle is a character in Aristophanes' writings, whose name Dercetes itself means "looker", who ruins his eyes sobbing for his oxen.
Putting this together, I might conclude that Pandercetes can be broken into pan + dercetes, or "everywhere-looking" or simply "one with raised eye sockets in all directions"


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Tiny orange yellow bug in raspberries? What is it?
There's a tiny orange yellow bug in raspberries:

What is it? The fruit was sitting in the fridge for 3 days

What country do you live in?  That might help to narrow it down.

I've often seen something very similar to this, only reddish-brown.  (Not particularly on fruit.)  Shiny, about 2-3 mm long.  That's in the UK.  So I'd like to know the answer, too!

chances are it is an "aphid"
https://influentialpoints.com/Gallery/Amphorophora_idaei_Large_raspberry_aphid.htm
take a look here
https://www.rhs.org.uk/advice/profile?pid=883
here,
https://www.extension.iastate.edu/news/yard-and-garden-insect-pests-raspberry-fruit
Raspberry's are yummy and there is a lot of competition!

body shape and size are wrong. I'm guessing it's a mite of some kind.

Welcome to Biology.SE. You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. Also note that answers must be self-contained (must not require following links). ——— You may also wish to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you.


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Why do we have two kidneys but one liver?
Both the liver and the kidneys are involved in "cleaning" our blood. But why we have one liver and two kidneys? I can just as well imagine that we have two livers and one kidney. Is this just a coincidence?

Most "why" questions are super vague, they need to be narrowed to some level of analysis to be meaningfully answerable, otherwise you're likely to get answers that don't really approach what you are thinking about at all, and that's frustrating for everyone.

In addition to being unclear and likely to answered with opinions, this is a duplicate of at least these two other questions. As part of the expected prior research you should search on this site for similar questions before posting.

All your organs come in pairs, with one major exception, the digestive tract and the outgrowths from it (liver included) are singular. The real questions is why do you have two lungs. its the only organs that breaks the rules.

@BryanKrause asking why some organs are pair and others are not a fairly straightforward question, I don't see how it being a why question makes it vague, any more than asking why male deer have antlers.

@John Do you mean that lungs break the rule because we have one mouth?

The liver can change in size and adapt based on what you throw at it, the kidney not quite so much. This at least partly explains why you don't need two livers but why it's nice to have redundancy wrt the kidney.

Your organs can be grouped into two categories.
The digestive tract organs, which are singular.
These form from the endoderm.
The liver and pancreases are all direct outgrowths from the digestive tract which is again singular.
Everything else which comes in pairs.
These form from the mesoderm or ectoderm.
Even the brain and heart are paired organs, the heart starts as two organs and fused during embryonic development. The whole circulatory system starts perfectly paired, (embryonically and evolutionarily) but then specific parts close off to create the complex circulatory system of "higher" animals so we can have a high pressure section and low pressure section.
The spine is also sort of singular but is basically the the line splitting the left from right half of the body. Everything that branches off the spine does so in pairs.
The real questions is why you have two lungs and one spleen. They are the only organs that breaks the rules. The lungs are an outgrowth of the digestive tract and the endoderm, but is paired. The spleen is part of the circulatory system, but singular. Now the most primitive lungs are singular, it split later likely as animals got larger and needed more lung capacity and also needed a tight connection with circulatory system (paired). The spleen is the weird one, and likely harkens all the way back to before vertebrates existed, it predates the closed circulatory system, and develops on the midline of the body just like the spine and digestive organs. Just like how the spine is the midline dividing the nervous system into pairs the spleen divides the circulatory system into pairs.
https://www.researchgate.net/figure/Embryology-of-the-gallbladder-A-In-the-early-embryo-liver-specification-occurs-in-the_fig1_303959093
https://embryology.med.unsw.edu.au/embryology/index.php?title=Cardiovascular_System_-_Spleen_Development
https://embryology.med.unsw.edu.au/embryology/index.php/Gastrointestinal_Tract_Development#Germ_Layer_Contributions

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Although most people have two kidneys, some have only one kidney. We can live with only one kidney. Infact, there are some animals still only have one kidney such as single-kidney rats. Many people are born with only one and we don't need two kidneys. One healthy kidney can work as well as two.
A pair of Kidneys evolved in humans as bilateral symmetry in vertebrates by evolutionary modifications of the nephridia. During embryological development, the organs are that fall outside the bilateral symmetry are singular (which includes the digestive tract organs as mentioned by @John).  But if you notice, liver also has two lobes.

But why hasn't the liver evolved symmetrically into two livers?


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Do Scrubjays weigh peanuts by picking them up?
I have been feeding scrubjays where I live (Monterey, California) with peanuts in the shell.
Something interesting I've noticed them do is, after I've laid out a selection of peanuts for them, they pick them up in their beaks and seem to be determining which one they want to fly off with. I have seen them first eye them all for a couple of seconds, then pick one up, shake it in their beak as if listening or "weighing" it, then picking up another one, or even three, and then going back to one of the previous ones and flying off with it.
What are they doing? Weighing them? "Counting" how many nuts are in the shell? Listening for something?
Here is one "in the act":

I doubt anyone knows the answer to which aspect of variation jays are considering when sampling nuts (although my guess would be mass). Langen (1999) did do experiments that explored the sampling behaviour you've noticed — they offered jays samples of peanuts with ranges as wide as 1 g (i.e. over a range from 1 to 2 g). The analysis mostly focused on when jays would be choosy (lots of nuts vs few nuts available; low vs high variability; competitive vs non-competitive scenarios; subordinate vs. dominant individuals; etc.)
Jays were reasonably accurate at visual assessment (the first nuts they sampled were statistically significantly heavier than a random sample of the available nuts), and their subsequent sampling behaviour (what you're observing) further improves their success in selecting heavier-than-average nuts:

Jays improve their accuracy at selecting a high-quality peanut via the initial visual scan and the subsequent sampling behavior. Peanut sampling (using the beak to handle several  peanuts  in  succession)  results  in  a  higher  rate  of food  storage  than  is  attainable  by  simple  visual  inspection, at least when options are not too similar.

In order to figure out what aspect of the nuts birds are actually assessing, you'd have to do experiments where you found a way to independently vary the number of nuts, mass, sound of the nut when shaken, etc., and see what happened.
Jablonski et al. (2015) actually did experiments with Mexican jays (Aphelocoma ultramarina) to evaluate proximal mechanisms of nut choice, and suggested that they do use auditory cues — but the authors don't actually show any tests of auditory cues:

(abstract) Jays evaluated each peanut by performing fast movements of the head combined with additional fast movements of the beak, which may open and subsequently close producing sound at the moment of hitting the shell. These movements seemed to provide Jays with additional sensory information that led to a more strict discrimination against non-preferred peanuts. ...
(discussion) We are now analyzing a series of experiments that seem to indicate that sound is indeed taken into account by Jays handling the peanuts and that it may be more important than the perception of heaviness ...

If these subsequent analyses were ever published, I haven't been able to find them online ... if you were really interested you could contact the authors and ask them ...
For what it's worth, there is also a paper titled "New Caledonian crows infer the weight of objects from observing their movements in a breeze" ...
Again, my guess would that the jays are 'weighing' the nuts. Mass should be pretty easy for them to assess, and closely related to the energetic/nutritional reward given by a particular nut.

Langen, Tom A. “How Western Scrub-Jays (Aphelocoma californica) Select a Nut: Effects of the Number of Options, Variation in Nut Size, and Social Competition among Foragers.” Animal Cognition 2, no. 4 (December 3, 1999): 223–33. https://doi.org/10.1007/s100710050043.
Jablonski, Piotr G., Sang-im Lee, Elzbieta Fuszara, Maciej Fuszara, Choongwon Jeong, and Won Young Lee. “Proximate Mechanisms of Detecting Nut Properties in a Wild Population of Mexican Jays (Aphelocoma ultramarina).” Journal of Ornithology 156, no. 1 (December 1, 2015): 163–72. https://doi.org/10.1007/s10336-015-1193-6.


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Sansevieria falling back to the wild form via leaf cuttings but not via micropropagation
I have heard that when you propagate Sansevieria via leaf cuttings, you get the wild form again. But if you use only meristem tissue, you can propagate the multicolored cultivated forms. What would be a possible explanation for this phenomenon?

This might be a better fit for [gardening.se].

A source for the claim would be a big help.


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Cell location co-ordinates
I have just had the nails on both my big toes removed.  I am much happier.  But it got me to thinking, as there is no 'root structure' from which the nail grows, is there an x,y,z, type co-ordinate system in the genome which says the nail cell structure starts from here or what is the determining factor which says these skin related cells stop forming here and now nail cells start forming but only in this narrow band.

Why do you say there's no 'root structure' from which the nail grows? Have you read anything about the anatomy of nail growth which leads you to believe there's no root structure?


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Do sharks possess a more hydrodynamical shape than dolphins?
I do not study biology at all. Is it known if sharks who evolved over milion of years have more hydrodynamical shape than say e.g. dolphins who evolved for much shorter time. It probably depends on many factors e.g. how fast on average a predator swims, strategy of hunting etc. I think marlin have quite hydrodynamical shape. Generality of this question (which I do not want answer) is how fast evolution produce certain quality. It probably is not a gradual process, I think.
To sum it up: my question is about hydrodynamical shape of body of two species (sharks, dolphins). And second part is: if time of evolution of given species plays a role in hydrodynamical shape?

You really need to do some physics to determine whether sharks are in fact more hydrodynamically efficient than dolphins.  Then you need to consider that hydrodynamic efficiency is not the only factor at work.  Sharks have evolved many variations over the ages, e.g. https://www.fieldmuseum.org/blog/four-fossil-sharks-are-cooler-megalodon  And is the modern hammerhead shark all that hydrodynamically efficient?

Try SE Engineering for questions on hydrodynamics. A separate straight question on evolutionary timescales in relation to trait development would be appropriate here. And if you want to post on scientific sites you need to remember the English you were taught at school. Interrogatives by inversion in the present tense went out several centuries ago except in poetry and didactics. It’s “Do…” (See my correction of the title.)

@David: OP may have English as a second language, or may have other language problems (and not be lazy/forgetful). Editing to correct grammar seems fine; giving questioners a hard time about grammar seems inappropriate.

@BenBolker I have lived or worked in France, Germany, Italy and The Netherlands. The worst possible thing is when people do not help you improve your language by not correcting you. You do not learn, and the implication is that they do not think you are worth the effort of teaching. Have you ever been in that position? Of course the questioner is not a native speaker. I have pointed out to him the specific grammatical details (present tense — "have you seen" works) and literature ("See ye not?"). I have supervised non-native speakers' theses.  I am helping him. (And some people need kicking.)

The question has 3-4 related questions which are all different and very broad, and some mistakes like calling sharks and dolphins species. The fastest sharks are faster than the fastest dolphins, while using less energy, 70kph vs 56kph, while a slow shark is the Greenland shark, top speed at 2.6kmh in cold water, it can live 500 years in deep seas. I can give a good answer to this but not on this forum, consider asking on reddit askbiology/askscience for the leisurely questions.

@David I wasn't suggesting not making the corrections, or even not pointing them out. I was suggesting a slight moderation of tone (which is admittedly tricky).


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Can Monsanto's (in)famous hybrid seed crops be cloned/grafted? If not, is there a technical or legal reason?
I understand that the seeds of a crop made from modern-day super hybrids will not, usually, produce the same quality plants in the next generation. Therefore, farmers have to buy new hybrid seeds each year (or season) from the original company. But, what if a farmer tried to clone his extremely productive plants?
Is there a scientific reason why modern hybrid varieties cannot be 'grafted', to create next season's high-quality crop, or is it due to a contract agreement signed by the farmers with their seed company? I am very curious as to why modern 'hybrid' crops cannot be propagated in this way.

Yes, it's stipulated very clearly in the contracts that any such efforts are strictly prohibited. Besides, would you want to graft an entire corn field?

I last worked on maize a mumble decades ago, but as far as I know grafting in grain producing grasses isn't practical. Please look for evidence that this is possible or if you meant some other type of plant please be specific. ——— Also note that the legal aspects of your question are off-topic for this site.

One needs to take into account how much work and research would go in cloning these productive plants - this is a task that Monsanto could handle, but probably not a single farmer. Also note the underlying misconception about how the capitalism works: if there was a way to to make these crops more productive, Monsanto would have already done  so and would charge a higher price for them. And if they tried to hide this knowledge in order to keep selling more lower quality crops, they would be quickly bypassed by their competitors or the farmers cloning the crops illegally.

You’re not even allowed to replant the seeds from the crop you harvested the year before.

@canadianer If the crop was a hybrid, there's not much point to replanting with the seeds, as they will all be different genetically.

My understanding is that at least some of it is due to F1 genetics, the F(n) generations will be different


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Are IgE antibodies capable of binding water molecules?
I learned in med school, that they are too small to trigger the IgE reaction that causes the release of histamine. However, I came across reports of this condition;
https://en.wikipedia.org/wiki/Aquagenic_urticaria
Some people with this cannot drink plain water without experiencing symptoms in their mouths and throats. In some cases, they report anaphylaxis if they drink a sip of water. The drug 'Xolair' blocks IgE and is effective in people with this condition.
But, I thought the water molecule is too small to bind to IgE antibodies? At least, that was what I learned in med school. Now I'm kind of confused. Aren't IgE antibodies literally dissolved in/surrounded by water on a constant basis? Wouldn't the water in the liquid these cells are always in be triggering a 24/7 reaction in their skin and their throats? Not just when they drink some water or take a shower. The epidermis is just dead cells, the mast cells in the skin have to be submerged in a mostly water medium to survive.
These people rely on milk and orange juice to drink, as it does not elicit the internal allergy reactions.
https://rarediseases.info.nih.gov/diseases/10901/aquagenic-urticaria
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276800/
https://pubmed.ncbi.nlm.nih.gov/32940373/
https://www.businessinsider.com/toddler-allergic-to-water-aquagenic-urticaria-2018-2?op=1

Welcome to Biology.SE. For the reasons you mention it seems clear that this can not be a reaction to water molecules. (However, note that anything in aqueous solution will have many interactions with water molecules.) Please [edit] your post to include more reliable background information — I suggest you look at other sources in addition to Wikipedia (it's a fine place to start, but the quality of the information can be highly variable). Please see the [tour] and  [help] pages starting with [Ask] questions effectively for details of what is expected in posts on this site. Thanks!

It is as you suggest: IgE antibodies are incapable of binding to water.
The immunogenicity of water is not explainable that simply. It is also important to know that it is a variant of physical urticaria, which presents the same symptoms but via different provocation, such as pressure, cold, heat, or exercise and sweating (cholinergic urticaria). There is some discussion on the topic here.
Some competing explanations in the links you provide are:

water reacts with something on the body, and the product of the reaction is immunogenic, or water solubilizes a surface antigen that penetrates the skin, and
contaminants or impurities in the water elicit the immune response.

First, I will offer my amateur thoughts on the matter, and then provide you with transcripts of what doctors who have had experience with treating this have come to understand. Do note that this is still an incompletely understood (rare) disease and that there exists no definitive mechanistic understanding, though histopathological examination has been performed, and it does indeed seem like the presence of water induces an immune reaction. It also seems immunologic due to the fact that patients respond well to antihistamines and related treatments that suppress the immune system.
As you can guess, this is a very rare disorder and it is difficult to rule out things such as an uncommon reaction to (perhaps) improperly cleaned or cleared water. However, some studies have been done to rule out impurities in water by the use of a water provocation test, or "water challenge test", where source of the water has been shown to not matter, thereby likely ruling out the impurities hypothesis. Patients also have similar responses to rain, tap water and swimming pool water. It too may be that the preparation, processing or chemistry of milk or orange juice renders an aqueous medium as incapable of eliciting a reaction on the skin, perhaps due to the presence of molecules or simply by virtue of things like pH being different than that of water. Reportedly, pH and temperature do need seem to play a role. It is also possible, though unlikely, that the immune response to water is psychogenic, and seems to occur more predominantly in females around puberty, and has been anecdotally reported to co-occur with some diseases like Bernard-Soulier syndrome, polymorphic light eruption, familial lactose intolerance and papillary carcinoma of the thyroid.
Anyway, I doubt anyone here at this SE can do a better job than the summaries I have here below.
A discussion of the cases and literature from 2011 can be found here:

The pathogenesis of AU is not fully known; however, several mechanisms have been proposed. Interaction with water with a component in or on the stratum corneum or sebum, generating a toxic compound, has been suggested. Absorption of this substance would exert an effect of perifollicular mast cell degranulation with release of histamine. A study by Sibbald et al. demonstrated that complete removal of the stratum corneum appeared to worsen the reaction, rather than prevent urticaria. These authors also demonstrated that pretreatment with organic solvents enhances wheal formation in contact with water. They suggested that enhancement of the ability of water to penetrate the stratum corneum increases wheal formation. Czarnetzki et al. hypothesized the existence of a water-soluble antigen at the epidermal layer. The antigen diffuses into the dermis by water and then causes release of histamine from mast cells. Tkach hypothesized that hypotonic water sources could lead to osmotic pressure changes, resulting in indirect provocation of urticaria. Others have recently stated that 5% saline was more effective than distilled water for eliciting the wheal-and-flare reaction. They hypothesized that the salt concentration and/or water osmolarity may influence the pathogenic process of AU, possibly by enhancing solubilization and penetration of a hypothetical epidermal antigen, in the same way as has been postulated for enhancement of organic solvents. Another proposed chemical mediator in AU is acetylcholine because of the ability of the acetylcholine antagonist scopolamine to suppress wheal formation when applied to the skin before water contact. However, another study failed to reproduce this finding when pretreatment with atropine did not result in suppression of subsequent wheal formation. Methacholine injection testing is negative in patients with AU; however, it is often positive in cholinergic urticaria. Serum histamine levels are variable from patient to patient. Antihistamines have been used to treat AU; however, the therapeutic effect and prognosis vary. In some cases, complete control of symptoms with antihistamine has been reported, whereas in other cases, there is a failure to adequately control symptoms. Refractory cases have been treated with ultraviolet (UV) radiation (both psoralen plus UVA therapy and UVB), either alone or in combination with antihistamines. It is hypothesized that the effect of ultraviolet therapy is mediated by thickening of the epidermis, which may prevent water penetration, interaction with dendritic cells, and immunosuppression or a decreased mast cell response. Barrier methods involving application of oil-in-water emulsion creams on the skin for water protection are effective. AU responds to stanazolol treatment in human immunodeficiency virus-positive patients.

Another discussion, from a paper from 2017:

Many of these histopathologic findings are the same as those of acute
urticaria, in which interstitial dermal edema, dilated venules,
endothelial swelling, and sparse infiltration of inflammatory cells
have been described. Mast cells are concentrated around the blood
vessels of normal dermis, with one to three cells per cross-sectional
vessel profile, but in this patient there were slightly increased
numbers of mast cells around blood vessels.
Antihistamines are the first line treatment for aquagenic urticaria.
In recalcitrant cases, the dose can be increased by as much as
four-fold the conventional dose. Phototherapy and barrier cream are
alternative or additional treatments if antihistamines fail to prevent
recurrence. The efficacy of phototherapy is related to its induction
of both immunosuppression, including a decreased mast cell response,
and epidermal thickening, which disturbs the penetration of water and
thus also inhibits mast cell stimulation. Barrier cream prevents
the penetration of water into the dermis. However, the various
emollients and water-resistant creams investigated have not yielded
conspicuous success, except in a few cases in which a
petrolatum-containing ointment was applied before water exposure.
Anticholinergics such as scopolamine may also offer relief. Most of
the patients were successfully controlled with antihistamines,
although some of them changed treatment modalities because of
drowsiness.


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Why can't H3O+ ions pass through aquaporins?
Aquaporins are proteins that facilitate the movement of water (and related molecules) through cell membranes. (Also, these transport proteins are very specific about what they transport.) Interestingly, aquaporins can facilitate the passage of glycerol but not H3O+ ions. This is difficult to comprehend as the structure of glycerol is quite dissimilar to H2O while H3O+ is quite similar to H2O.
What is the reason behind this?

This question has been directly addressed by the paper The Mechanism of Proton Exclusion in the Aquaporin-1 Water Channel. I think it's a pretty good one too! I paste the abstract below:

Aquaporins are efficient, yet strictly selective water channels.
Remarkably, proton permeation is fully blocked, in contrast to most
other water-filled pores which are known to conduct protons well.
Blocking of protons by aquaporins is essential to maintain the
electrochemical gradient across cellular and subcellular membranes. We
studied the mechanism of proton exclusion in aquaporin-1 by multiple
non-equilibrium molecular dynamics simulations that also allow proton
transfer reactions. From the simulations, an effective free energy
profile for the proton motion along the channel was determined with a
maximum-likelihood approach. The results indicate that the main
barrier is not, as had previously been speculated, caused by the
interruption of the hydrogen-bonded water chain, but rather by an
electrostatic field centered around the fingerprint Asn-Pro-Ala (NPA)
motif. Hydrogen bond interruption only forms a secondary barrier
located at the ar/R constriction region. The calculated main barrier
height of 25-30 kJ mol(-1) matches the barrier height for the passage
of protons across pure lipid bilayers and, therefore, suffices to
prevent major leakage of protons through aquaporins. Conventional
molecular dynamics simulations additionally showed that negatively
charged hydroxide ions are prevented from being trapped within the NPA
region by two adjacent electrostatic barriers of opposite polarity.

The difference between glycerol and and a protonated ion such as H3O+ is charge, and many ion channels are selective based on charge too. Of course, other properties play a role, such as size and steric shape, but charge is a very important one and this applies to a great many channels beyond aquaporin!


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Which cells do mRNA vaccines target?
mRNA vaccines instruct cells to produce spike protein that will trigger an immune response. But which types of cells will it work on? and which cells will it not work on?

I’m assuming the question refers to the Pfizer/BioNTech and Moderna vaccines in which Lipid NanoParticles (LNP) are used and to the injection to be intramuscular (i.m.). According to a blog by Derek Lowe [1], the parts of your body producing the coronavirus Sprike protein antigen are:

the muscle tissue at the site of injection, the lymphatic tissue downstream in your armpit on that side, your spleen, and (for the first day or two) your liver.

In other words, it is not only your muscle cells that become the antigen factory.

[1] Lowe, Derek (2021) “mRNA Vaccines: What happens”, Science Translational Medicine, AAAS, https://blogs.sciencemag.org/pipeline/archives/2021/01/21/mrna-vaccines-what-happens .

You might make it clear that the liponanoparticles do not contain any components that target specific cells. The site of injection and the propensity of cells to take up liposomes are the only factors involved. It would seem that the latter point is most relevant to the question. Do cells differ in this respect?

According to this paper written by Emily Bettini and Michela Locci, mRNA-LNPs and locally produced antigens are taken up by dendritic cells via endocytosis [1]. Within the cell, mRNA is translated into the antigenic protein. These locally produced antigens are either degraded by proteasome in the cytoplasm or secreted from the host cell, leading to 2 different immune response activation pathways [2].
When antigenic proteins undergone degradation by proteasome, the generated antigenic peptide epitopes are loaded onto MHC class I molecules within the endoplasm reticulum, then transported to and expressed at the plasma membrane [2]. When dendritic cells transfer to the lymph nodes, these loaded MHC class I peptide epitope complexes are recognized by CD8+ T cells. This pathway induces the formation of cytotoxic T cells which are capable of directly killing the infected cells [1].

Figure 1. Immune responses elicited by SARS-CoV-2 mRNA vaccines [1]
When antigenic proteins are secreted from the host cell, they are recognized and taken up by dendritic cells again. They are then degraded in endosome, loaded onto MHC class II molecules, followed by expression at the cell surface [2]. At the lymph nodes, these loaded MHC class II peptide epitope complexes are recognized by CD4+ T cells. This pathway induces the formation of memory B cells (MBCs) and the antibody-secreting long-lived plasma cells (LLPCs) [1].
Resources
1)Bettini E, Locci M. SARS-CoV-2 mRNA Vaccines: Immunological Mechanism and Beyond. Vaccines (Basel). 2021;9(2):147. Published 2021 Feb 12. doi:10.3390/vaccines9020147
2)Wadhwa A, Aljabbari A, Lokras A, Foged C, Thakur A. Opportunities and Challenges in the Delivery of mRNA-Based Vaccines. Pharmaceutics. 2020; 12(2):102. https://doi.org/10.3390/pharmaceutics12020102

"and locally produced antigens are taken up by dendritic cells via"  That's how the immune system processes them, but are those the only cells that take them up?  Or they are taken up by every other cell, too?

This is highly speculative, I don't think we know yet for CoV2 mRNA vaccines which cells produce the most spikes, the most MHC-I and where most (dendritic cells) MHC-II come from. The spike is not quite secreted, it is anchored onto the membrane.


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Is this a hornet?
I live on the 2nd floor of an old apartment building in Vancouver BC (Canada). A couple of years ago we had an issue with a hornets nest that was difficult to remove because of its location. They managed to find a way into the actual apartment despite window screens etc. We thought the issue had been resolved, but today I saw this flying around outside my window:

The main body was maybe 2-3 inches, but it had a very long "tail" or I guess what might be stinger. Never seen anything that large before. This insect was much larger than the hornets from previous years (which were at most 1 inch in length)
What type of insect is this, and should I be concerned?

This is not a hornet, this is an Ichneumonidea wasp, which is a superfamily of parasitoid wasps with about 100,000 species. I would go so far as to think it is within the Ichneumonidae family and think that it is probably Rhyssa lineolata, though I am certainly no entomologist of any sort. Note that because there are so many species, it might be quite hard to identify, though this is a large one, and has the very long ovipositor so that should narrow it down for someone more skilled at ID than me. Most Ichneumonid wasps are much smaller and lack the long ovipositor.
All parasitoid wasps lay eggs on or inside another species of insect or arachnid, where the egg hatches and uses the host species as food for its larval development. These sorts of wasps usually parasitise larvae of wood-burrowing species, so they use the long ovipositor to drill into the wood and deposit their egg(s). There's some footage and images of this for a Rhyssa species on Wikipedia
I don't think this species will sting as the ovipositor is too fragile and long to be easily manipulated to sting someone. These sorts of ichneumonids usually are looking for dead wood with grubs in it, so it could potentially indicate that you have some grubs in wood in/around your house, but it is much more likely that there is a tree with a dead branch nearby.  Apparently they are also attracted to fresh sawdust (thanks to comment from @polypipewrangler)
As far as I know, these are solitary wasps - they don't build nests, so you won't see more than 1 or 2 at a time.

They are also attracted to the smell of fresh sawdust.

That makes a lot of sense given 1) right outside my window is a whole bunch of trees and 2) theres been some construction outside as well. Thanks!

@PolypipeWrangler I didn't know that. I will edit it in. I wonder if this is because the burrowing larvae are putting out "sawdust" as they burrow.


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Herbivore digestive System
Why do Herbivores have many different types of digestive Systems? for example a Rabbit has a mono-gastric Digestive system and a hippopotamus has a pseudo ruminant digestive system but they are both Herbivores.

Rabbits and hippos are separated by ~95 Mya of evolutionary time: http://www.timetree.org/

This is kind of like asking why animals have so many different ways of moving quickly (dogs run, birds fly, kangaroos jump...)  There is a problem, and evolution has solved the problem in different ways.
In the case of herbivores (and in particular leaf and grass-eating herbivores) the problem is that their food is low in nutrients and high in indigestible cellulose. The particular solution depends on other evolutionary pressures.  For many leaf-and-grass eaters the solution is to become big, with complex many-chambered digestive systems that allow for long slow processing of the food. Horses, hippos and ruminants all tend to be large. This means that the animal can eat a lot and hold the food in themselves for a long time, allowing enzymes and gut bacteria time to work.
Rabbits, as burrowing creatures, can't evolve a large size, so depend on a range of gut bacteria and coprophagia to pass food through their intestines twice.
Grasshoppers can produce their own cellulase to break down cellulose without microbial assistance.
There's more than one way to do it and as a rule, in evolution, for every possible solution, some animal will be using it.

there are plenty of other factors as well, like grazers having to deal with highly abrasive food that browsers don't have to deal with.

Another factor is that there's not a strict divide between herbivores, omnivores, and carnivores.  Examples of each can be found on many branches of the mammalian evolutionary tree, implying that digestive systems must have undergone frequent modification.

"for every possible solution, some animal will be using it." is inaccurate - evolution has to discover a possible solution, and nothing guarantees that it will discover them all in finite time.


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Why does warfarin decrease biological activity of protein C?
Warfarin inhibits VKOR. Hence it disrupts vitamin K dependent $\gamma$-carboxylation of Fc- II, VII, IX, X.
But what exactly it does to Protein C and Protein S? How does it also affect anticoagulant system?
[Ref. Kim, Yesel, and Oh Young Bang. “Paradoxical Procoagulant Effect of Early Doses of Warfarin: Possible Role of Non-Vitamin K Oral Anticoagulant in Patients with Atrial Fibrillation-Related Stroke.” Journal of stroke vol. 17,2 (2015): 216-8. doi:10.5853/jos.2015.17.2.216
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4460341/]
I couldn't find an article regarding the mechanism of this inhibition. Any help will be appreciated.


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Ticks hitching a ride on a fly?
Recently, my brother has been bothered by some particularly aggressive houseflies.
According to him, when these flies are squished, there is often a clacking noise, and then small arachnids come crawling off or out of the body (it's unclear which).
He recently managed to take pictures (see hereunder) where two of the things are in view, and I tentatively recognized them as ticks.

Apparently the clacking noise is produced when the arachnids are squished.
Are these actually ticks ? And is this normal behaviour ? I haven't managed to find anything about ticks hitching a ride on flies, but I don't have any other ideas.
If it helps, he lives in Brittany, in western France.
Edit : For scale, the fly in the pictures was a little below 1cm long

Viewer discretion advised: The image above contains blood and violence ;) Jokes aside, I haven't heard of ticks riding on flies, but I read that they can carry parasites such as pinworms, roundworms, hookworms and tapeworms.. Here is some more info

There are mites that ride on bumble bees.  https://www.bumblebeeconservation.org/bee-faqs/bumblebee-mites/

Do you have a scale on how big those are? Most mites are <1 mm across.

@bob1 the fly was a bit under 1cm, i'll edit the question to add this

@NinDjak - great, that makes these <1 mm, so they are likely to be mites.

What about seed ticks? They are very tiny as well. I am thinking flies can carry them.

These are not ticks. They're parasitic mites

Without a close up examination of the subjects, which would require microscope images or a decent macro image it is impossible to identify these creatures with any certainty to the level of species. With that in mind I will give an attempt at an answer.
These creatures are not ticks, they are almost certainly mites. Mites are of the subclass Acari within the Arachnida (spiders and scorpions also belong to this class). Ticks also belong in the Acari, so they are closely related to mites and quite similar morpholgically.
Mites are quite diverse, but generally less than 1 mm (0.039 inches) in length and are very diverse in what they feed on, ranging from being decomposers in the soil, to grazing algae in water, to feeding on plants and parasitising animals. As humans we have a particularly odd one (to me at least) called Demodex that lives in hair follicles, eating the sebaceous (oily) secretions and dead skin cells from around the hair.
For insects I believe (with no certainty, experts please weigh in) that the majority of mites are parasitic, feeding on the insects hemolymph (blood equivalent for insects) by puncturing the seals at the joints in the exoskeleton. Incidentally, you can see some mites feeding on the legs of the crane-fly in this SE Biology post.
In the case of the OP we are likely looking at a parasitic mite of the common house fly (Musca domestica, which have left the now dead insect as their food source is no longer supplying food.
Flies do have a common mite species Macrocheles muscaedomesticae, which is a mite that feeds on the eggs, and to some extent the larvae of the house fly and several other species of fly, and may also be associated with a range of other insects (see Biology Ecology sections here). The mite is found world-wide and is believed to be distributed on the adult flies. It is uncertain if the mite actually attaches to the adult fly while it is being carried.
There are several species in the Macrocheles genus, which all parasitise in a similar manner to M muscaedomesticae. There are also a few other species of mites that seem to parasitise house flies, including Poecilochirus species, but these are less species-specific as far as I can tell.

A very thorough answer, thank you ! Since your mention of mites in the comments i've also found references to mites being used for house fly control in livestock farms , so this definitely checks out.
I doubt there's much more to add, and the question's been open for a few days, so I'll mark this as accepted answer.


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What Old World fish produces "white gems" in its brain?
In his ancient list of "white gems," Isidore of Seville mentions the "cinaedia," which he describes as follows:

Cinaedia is found in the brain of a fish with the same name; it is
white and oblong. People say that with it they predict calm or storm
at sea (Etymologies 16.10.8)

This seems to match the description of a lucky stone, except that freshwater drums (Aplodinotus grunniens) would hardly have been endemic to Isidore's (Old World) setting. What fish could Isidore have been referring to?

Otoliths are common (if not ubiquitous) among fish. I think the solution is to figure out what fish would have been called Cinaedia, which isn't so much a biology question as a Spanish language or etymology question.

@kmm It would be a Latin question, not Spanish but I think you're right and this is not really on topic. I posted an answer since I did find a reference, but I'll also vote to close.

I’m voting to close this question as off topic because it isn't really about Biology but about what a specific Latin name for a fish meant.

Turns out there's a paper that has looked into this:  Christopher John Duffin (2007). Fish Otoliths and Folklore: A Survey. Folklore, 118(1), 78–90.         doi:10.2307/30035398. The paper investigates the history and folklore associated with fish otoliths, and includes the following note:

Claudius Aelianus (On the Characteristics of Animals IX. 7; see Aelian 1959) (c. 175-235) suggested that
"Cinaedius" might be the Bass, and thus synonymous with Lupus.

So, based on my (very) cursory reading of the paper, it looks like it isn't entirely clear what fish was referred to by the name Cinaedius in Latin, but Bass is a contender.

Seems that leaves the question "which bass", especially given the diversity of species that carry that label, though at least it's more narrow than "fish".


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Identify species of snake in India
image

Is this snake poisonous, found wrapped around a tree in middle of hot summer of 40 degrees celcius, in himachal, Northern INDIA, Himalayan foothills?

This appears to be a bronzeback tree snake, which is a common species of tree snake in India. It is a slender snake with characteristic bronze body and a pale stripe down the sides. It usually has a white spot on top of its head, which I think you can see in the second picture. It should also have blue inter-scale areas if you pull the scales apart.
It is non-venomous, but like all snakes may bite if attacked.


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Are the kind of mutations different in an antibiotic setting than they are in a non antibiotic setting?
Hy everyone!
I'm looking for experiments that deal with the kind of mutations that arise in antibiotic environment, as opposed to non antibiotic environment. As far as I understand, AB (anti biotic) doesn't change the kind of mutations that arise, it only gives advantage to the lineage that's already resistant. However I cant find an experiment that deals with this directly. What google brings up is only the Lederman experiment, however I can't find an experiment that deals with the aftermath.
What I'm imagining is this:

we create a replica from bacteria and put one of them in AB environment (or preferably many replicas from both groups
at every generation (or at least at certain times) we check the genetical makeup of bacteria in both of the AB and non-AB populations

Will the groups of bacteria at the same place (the "same" lineages) have almost the same genetical makeup with a comparable genetic drift? Or will there some specific mutations arise repeatedly in the AB group as opposed a non selective environment? I understand this can only be tested up to a few generations because after a while we are only testing selection and not mutation itself. However Im curious if there is such an experiment out there and if there isn't, why?
Thanks in advance!

This is essentially the same as the Luria-Delbrück experiment. They were interested more in phage resistance than antibiotics, but there is no theoretical difference. (https://en.wikipedia.org/wiki/Luria%E2%80%93Delbr%C3%BCck_experiment) Similar work has been done in antibiotics, even earlier it seems, though not so famous. A recent theoretical treatment with many relevant citations is here: https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1007930

Thank you for the answer, sorry for responding so late. Maybe I'm misunderstanding but it seems to me that the Luria Delbruck experiment deals with preexisting variations, before they are introduced to the virus. What I'm curious about is whether once a line of bacteria is introduced to the environment with the virus and it survives, will it start to develop a different group of mutations compared to a line that wasn't introduced to the virus? Maybe it is a pointless test, as the underlying mechanism is supposed to be the same as the L-D experiment, but I'm curious if it has been carried out.


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mRNA vaccine and cell mitosis
What happens with the injected mRNA when cells are in the different stages of the mitosis process? Does the mRNA enter the cell and behaves normally throughout the mitosis phases?

I'd be interested in some reference. What made you think about the relationship of  m-RNA and cell cycle? (This reminds of some current issue: activation of LINE1 (LINE-1) retrotranscriptase, i.e. transcription of viral mRNA to DNA, depending on cell dividing or not).

According to this paper written by Abishek Wadhwa and his colleagues,  the vaccine mRNA will exert its function independent on active cell division because it is not integrated into the host genome [1].
Interestingly, I also found this paper which indicates that there is a possibility that the mRNA can enter the nucleus during cell division. During the prophase of mitosis, the nuclear membrane is dissolved, allowing mRNA to passively diffuse into and be included within the nucleus later during telophase. In addition, if endogenous reverse transcriptase is present, the mRNA can end up being integrated into the host genome [2].
Resources:

Wadhwa A, Aljabbari A, Lokras A, Foged C, Thakur A. Opportunities and Challenges in the Delivery of mRNA-based Vaccines. Pharmaceutics. 2020;12(2):102. Published 2020 Jan 28. doi:10.3390/pharmaceutics12020102

Sousa A, José M.M., Velilla A. Z.mRNA, Nanolipid Particles and PEG: A Triad Never Used in Clinical Vaccines is Going to Be Tested on Hundreds of Millions of People. Biomedical. 2021;34(1):2574. Published 2021 Feb 22. doi:10.26717/BJSTR.2021.34.005501

Please note that the first of these articles was accepted nine days after submission. This suggests it was not properly reviewed. In addition, the publisher of "Pharmaceutics" is "MDPI" — a publisher with a history of poor behavior and minimal peer-review. I would tend to treat articles published in such journals as highly suspect.

Predatory journals are a huge problem — you can learn more and see lists of predatory journals including the original Beall's List.

The second article, by Sousa et al., was published in the "Biomedical Journal of Scientific & Technical Research" which is not peer reviewed and seems to accept any paper if the fees are paid.  Among the gems it has published are "The Expression of the Proper-Name Effect Reinforces the Disarticulation ofCommunicative Rationality" and "Nietzsche and the Big Health. The Art as Culture’s Therapy".

@mgkrebbs I can't even hazard a guess at the content of the second paper.

@tyersome The 1st article was accepted about a month after submission (Received 2019 Dec 28; Accepted 2020 Jan 26), and it's a review. The timing does not seem to be an issue, although the publisher certainly may be.

@Armand — Interesting, I may of screwed that up, but I wonder if they've changed that info (nine days doesn't fit any of the currently listed publication related intervals) . At any rate this is a suspect journal and is being used to support an answer that makes dubious claims.


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GHK Equation and Action potential
Can GHK equation be used to predict the membrane potential even if the cell is not at resting state?
To say it again, can we use GHK equation at every moment during Action potential?
I'm confused because GHK equation is derived at the situation with total ionic current is zero, but is that true also during AP?

The GHK voltage equation also known as just "Goldman equation" is always valid for determining the voltage at which the net current is zero, given internal/external ion concentrations and their permeabilities. This includes times during the action potential, though the result you get from GHK will be changing faster than the actual membrane potential itself, since the change in membrane potential brings about changes in permeabilities.
It's still useful to think about this equation to determine in which direction the membrane potential is changing instantaneously: it will always be changing towards the equilibrium potential. You can also qualitatively estimate the relative rate of change: if the current voltage is very far away from the equilibrium potential, the voltage will change more rapidly than if it is close to equilibrium.
However, this equation is just a steady-state equation. It doesn't tell you how quickly you will get to the new voltage or exactly which ions will move. For this, you need some other equations and other parameters, namely the actual permeabilities (rather than relative permeabilities) of the ions and the membrane capacitance.
The GHK flux equation can help: this will give you the flux of each ion at a given membrane potential (Wikipedia shows how this equation is related algebraically to the Nernst equation, which in turn is equivalent to the Goldman/GHK voltage equation for a single ion). You can also think in terms of the Hodgkin-Huxley model and the simple differential equation for current.

In summary, with respect to your question:

Can GHK equation be used to predict the membrane potential even if the cell is not at resting state?

It can predict where the membrane potential is headed, but not what it actually is or how fast it's changing, and the voltage you get from GHK will itself change as membrane potential changes affect the parameters that go into the GHK equation itself.


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How many senses do humans have?
I recall learning that humans have 5 senses, but that may have been an over-simplification to focus on the most notable ones, or simply that no others were known about at the time. Wikipedia says:

Although traditionally around five human senses were known (namely sight, smell, touch, taste, and hearing), it is now recognized that there are many more.

Is there a known, discrete number of senses (and, if so, how many are there)?
Note: If there's disagreement in the scientific community about the answer it would be interesting to learn what most biologists consider most plausible.

Downvotes? Really? Why!?

This post has 3 close votes as "opinion based" — probably be because this requires sharp distinctions among  fuzzy groups. ——— In addition, the Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may also be subject to down-voting and closure. For example, you could start with the wikipedia on senses.

@tyersome is it opinion based or just not well enough understood to have consensus yet? I presumed the latter. I did 3 things before asking: 1. Googled (lots of unreferenced articles I didn't trust), 2. Wikipedia'd it (see link above), and 3. Searched Biology SE (not previously asked here). I guess a 4th was look for an example of a nebulous biological concept (I searched for an article I read some time ago stating there were 13 different definitions of 'species', but I couldn't find the article so left that analogy out). BTW, if there's not consensus on this, that itself is an answer

This kind of question generally isn't interesting to professional biologists (in fact they are actively disliked). In part this is because even if you could answer it you wouldn't have learned anything particularly interesting (Let's say that it's 13 — so what?). This is also inherently dependent on how you define a sense and where you put the (somewhat) arbitrary boundaries among them — even within the traditional 5, smell and taste overlap. That makes it difficult (maybe impossible) to enumerate the "senses". More research could change this, but efforts aimed at counting won't get us there.

Would a brief explanation of why it doesn't work like that be a valid answer by the Biology.SE rules?  I think I could manage that myself, if nobody else wants to.  As you guessed it might be, stevec, the answer is that, like species - in fact, more so - once you know more about the details it becomes clear that different senses can't be classified neatly enough to be counted.  As tyersome said, what's usually referred to as "taste" is partly the same as "smell" and partly not, whereas "touch" is a lot of things (heat, vibration, pressure) which are actually separate systems.

@A.B. I think that would be helpful! Please include leads for what to look up for the genuinely curious if you can

@A.B. — Welcome to Biology.SE! It is unlikely that (m)any of the established users will see your question. The correct way to get that type of feedback is to post it as a question on the [meta] site with a link to this question (click where it says "Share" to get such a link). To me what you propose seems reasonable (depending on how brief and how well referenced your answer is), but I'm a relative newcomer and wouldn't want to lead you astray!

I'd like to challenge your question.
What is a sense?
Are you looking for a complex organ that integrates with the central nervous system? Or just any part of your body that can be used to determine the property of something in the outside world? For example, you can use your toenails to test whether a hot plate is of sufficient temperature to melt dead keratinous biomaterial, like your nails. This would count as an integrated sense for a specific physical chemistry.
Or do you think a sense is a thing that detects a singular property of the world? For example, do you discriminate proprioception from gravity sensing, even though it may be performed by the same organ? Historically, each classic sense is limited to one property, but this I think is outdated. For example, skin is not only capable of performing touch and texture detecting ("tactile" sense), but also heat, pain, and other things like sensing noxious poisons such as bee stings.
Also, do senses have to detect stimuli in the external world? Plenty of sensing goes on internally, both in interstitial spaces and fluids in your body, on the surface of cells, as well as within cells, and the variety of cellular and sub-cellular equipment is hugely various. Should light receptive cells only count as 'vision' or 'light receptive' when they are found in the eye, or can light-sensitive cells found deep within the body can also be classified as part of the visual sense? There are many animals and tissues in biology where light-sensitive receptors are not exclusively found in eyes.
These are only 3 things you did not consider. There are many other questions you must answer along these lines to have a clear, at least temporarily operational definition that can be used to make distinctions to answer what things can count as a separate, countable sense.
Just as a proof of concept, I can list more than five senses off the top of my head to show you that the "five senses" concept is woefully outdated in my view, and I'm sure some others would agree. I will pick some weird examples just to demonstrate the complications that the above questions illustrate.
Chemosensory systems
(considered a sense for chemistry? or a collection of senses?)

Olfaction (smell, as carried out by neurons in the nasal epithelium; e.g. smell of vanilla, and smell of bad food)
Gustation (taste, as carried out by neurons on the tongue; e.g. salt, sugar)
Antigen chemosensing (chemical sensing, as carried out by, for instance, immune antigen receptors on B cells)
Hormonal signaling chemosensing (chemical sensing of hormones such as insulin, as carried out for instance by myocytes)
Starch sensing? (amylase in saliva can be used as a test for digestable starch)

Visual system, at the retina?

Visible light (sensing electromagnetic radiation on the order of a few hundred nanometers in wavelength)
Internal methanol sensing (the visual system as a sensor for methanol, which disproportionately affects myelin surrounding the optic nerve)
Pressure sensing (see phosphenes)

The vestibular system

Gravity sensing
Balance
Coordination
Motion sensor
Head position sensor
Spatial orientation

Skin

thermosensation (touching a hot kettle!)
Nociception (pain sensing)
allergen sensing
sensor for gamma rays, X-rays and UV light (indicated by radiation burns, development of skin cancer, sunburns, etc.)

Bones and muscles?

Kinesthetic and bodily proprioception

Brain/mind/mental/social senses?

mental pain
boredom
mental or spiritual distress
sense of self and other, including friendship, power, place in social hierarchy, reputation, companionship
motivation and love (oxytocin, dopamine, etc. in limbic systems and other neural correlates)

I'm sure some would agree, and some would disagree about the specific cases I provide. Thus the definition of senses, or sensing, seems to be opinion-based or at the very least very sensitive to an agreed-upon operational definition, for which there is none.

This is better and covers more things than what I was going to say (which was much the same thing, otherwise), so I won't.


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Identification of an animal building

I live in south-west Germany and today while mowing the lawn I discovered a strange structure. It looks like a molehill on which additional branches were placed. This kind of branches are easy to find in my garden, because they were removed from the trees by a strong wind. However, I have no explanation for this accumulation of branches on a small mound of earth. I have seen an animal that looked like a rat in the last few days.... But I think a rat would not build such a building? What kind of animal lives in my garden?
Additional Picture:

I would like to edit my question to provide the additional information requested by "tyersome":
There were high winds about two days before I discovered this structure. However, what is disconcerting to me is that there is obviously soil under the branches here, and the branches are conscientiously piled up.  The other branches are widely scattered in the garden. There have often been strong winds, but a similar structure has never been created before. I have been unable to detect any other signs of animal activity associated with this structure. I have left the structure undisturbed and have not investigated it further so far, as I believe it to be an animal burrow and I do not want to cause any disturbance to the inhabitants. Thus, I have not cut the grass around this structure, but have left it standing. Animals that can be observed in my garden are for example: pigeons, squirrels, other birds, mice.
Second Edit: There are trees nearby. Could it be a bird's nest that fell out of a tree? In addition: Is it safe for any occupants if I examine the structure more closely or turn it over?
UPDATE:
Day 2: Encouraged by your valuable comments, I examined the structure more closely today. Turning it over showed that it is probably, as you suspected, a bird's nest. There was also no entrance in the ground where the structure was located. I could not find any eggs or feathers. Therefore, the species of bird that built this nest remains unknown. The nest has a total diameter of 80 cm (31 inches). The diameter of the inner ("soft") nest is about 20 cm (8 inches). I didn't expect such a big bird's nest in my garden.

The nest may have fallen from this tree:

UPDATE (10. May 2021):
Since I had to assume that additional information would be needed to determine the species, I again examined the area extremely carefully today. In doing so, I was able to find eggshells that were located near the tree. I cannot say with certainty that these eggshells are directly related to the nest, but it is likely.

Then I researched, which bird eggs might correspond to these.
Based on the appearance of the eggs, I suspect the following species: The Common Blackbird (Turdus merula), the Eurasian Magpie (Pica pica) and the Eurasian Jay (Garrulus glandarius).
I have observed each of these species in my garden:
The Common Blackbird: very often,
the Eurasian Magpie: occasionally,
the Eurasian Jay: occasionally
Wikipedia states that the eggs of the Common Blackbird (Turdus merula) are  2.9 × 2.1 centimetres (1.14 × 0.93 in) in size.
The eggs of the Eurasian Magpie (Pica pica) "measure 32.9 mm × 23 mm (1.30 in × 0.91 in)".
However, I could not find any information about the size of Eurasian Jay eggs.
I would guess that the blackbird is too small to carry the large branches that are used in the base of the nest. I have also seen a blackbird's nest in a bush in my garden: I think the eggs were smaller and the nest was also made of much finer material.
So the Eurasian Magpie, as stated by "tyersome", is a very hot candidate for me. Can this be confirmed from the eggshells?

Welcome to Biology.SE! If possible please [edit] additional information into your post. Is there any chance this fell out of a tree or bush? You refer to branches being removed due to strong winds — did you have strong winds in the day(s) before you observed this structure? Can you see any other signs of animal activity around this — e.g.s droppings, feathers, hairs, other fibers? Finally, if you moved this structure did you find a hole underneath?

I, too, thought it looked like an upside-down bird's nest. If that were the case, there's no harm in examining it more closely; the possibilities are 1) there were only eggs (now smashed), 2) dead hatchlings, or 3) it was an empty/old nest. If anything existing had survived, you'd have seen parental bird activity (at least initially). This is assuming it's a bird's nest.

Possibly the least effective hedgehog of all time?

Great updates — 20 cm is quite big so I would guess this might be a largish corvid. One example (of many) would be the Eurasian magpie — the black-billed magpie of North America has a nest of similar size and construction. If you don't get an answer here you might try contacting local birding organizations. You probably need someone with local expertise. I also encourage you to note of what birds you are seeing and hearing — the builders could still be in your area.

Firstly, I thought that it was a Dusk-footed-rat from the image of the inverted, upside down nest. But, thanks for your updated clarification, I was able to Google Lens Search the images and here's what I found:- It is nothing to worry about, as the egg shells that you found are of House Sparrow's eggs. These birds can be commonly found and they usually make bigger nests (as you found in your garden).

Google lens doesn't know correct answers. That's a terrible way to try to identify anything with accuracy

You are crrect. That's why I rechecked Sparrow nests and eggs on Wikipedia and other sites then I gave you the answer.


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Does cell culturing contribute to dangerous antibiotic resistance to the same degree as livestock?
According to the CDC, antibiotic resistance is one of the biggest public health challenges of our time. The largest incubator for antibiotic resistance is the factory farming of animals where livestock are administered large antibiotic doses often and kept in infection-prone conditions.
Another area where antibiotic use is common is in cell culturing for biological research and engineering. To what degree is this use of antibiotics contribute to the public health challenge today, and moving forward as the biotechnology sector grows?
I am curious both about the impact for yeast cell culturing, and also for the culturing of meats as a future food source. I wonder how the problem differs from the antibiotic resistance problem in the livestock industry, and how this might affect the outlook of a future filled with synthetic biologic products and lab-grown meat.
I see two differences off the bat between livestock farming and cell culturing:

animals have much more powerful immune systems than cultures
culture contamination can be much more readily monitored and responded to by operators

Antibiotics are used in very different ways in cell culture and in livestock farming.
As you note, in farming, antibiotics are used to manage infection in unsanitary conditions and also to increase animal growth. Farming is essentially an inherently non-sterile environment and so there's not really any good way to keep microbes from spreading and interchanging, potentially carrying antibiotics resistance with them.
In cell cultures, on the other hand, one is typically working with a largely sterile environment, and it has to be maintained that way in order for the cell culture to work. They are far, far more delicate than farm animals---but they also can be entirely enclosed in a sealed vessel. Getting a significant contaminant into such an environment is not a "treat the sick animal" situation but a "sterilize and purge the bad batch" situation. Antibiotics are indeed often used as part of this defense, but the potential modes of infection are very different than with animals, which rules out many classes of pathogen simply because they are adapted for respiratory or gastrointestinal transmission, and a cell culture does not have these things.
Moreover, for most current industrial cell cultures, if the product is not the cells themselves, everything alive including pathogens will generally get killed off during later stages of the process (e.g., pasteurization of wine and beer).
If the cells themselves are the target of mass-scale culturing, e.g., cultured meat, however, then there will indeed be opportunities for antibiotic resistant pathogens to be developed and spread, particularly as increasing scale of operation
offers more opportunities for sloppy operations and regulatory evasion by low-cost operators.
Bottom line: antibiotic resistance is generally far less of a concern with cell culture than with livestock, but may still be at least somewhat of an issue.


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What actually kills a plant that requires winter dormancy if it is kept indoors all year?
In bonsai practice, beginners will commonly purchase a juniper (often Juniperus procumbens 'Nana'), which is an outdoor tree, and keep it inside all year.  The tree invariably dies.  It is commonly explained to the beginners that this is because junipers are outdoor trees and require a winter dormancy.
My question is what exactly goes wrong that leads to the death of the plant?  Let's assume that the person gives the tree appropriate care, e.g. assume that desiccation or root rot or other more direct causes of death are not the reason.  (Of course, a valid answer is that it is impossible to give "appropriate care" for some specific reason.)
I have two strong hypotheses, in more detail but not in a rigorously scientifically biological detail.

The first is that the warmth and low humidity of the indoor environment cause the plant to continue to transpire water and attempt to grow or maintain foliar mass, while the reduced daylight hours signal the plant to "do something" (what, though?) that results in lower metabolic action.  And so the tree expends its stored energy (starches and sugars?).  Then in spring, the when the tree tries to put on a strong flush of growth, it has nothing left to build on.  So it struggles and eventually dies.

The second is that there is a daily metabolic cycle that is disrupted when the tree is kept in the more or less constant indoor environment.  That is, there is a cycle that depends on the daily differences in temperature and humidity the tree experiences during daytime and nighttime.  Through my own measurements, I have found, for example, that the vapor pressure deficit (VPD) reduces to near zero outdoors during the night in springtime as temperatures drop and relative humidity rises.  This, I think, means the respiration demands on the tree are near zero.  That is not the case indoors, where the VPD is more or less constant.

Is either of those at all consistent with what really happens?  And what does really happen from a biological perspective?  That is, what part of the plant's metabolism fails?  Is there something that happens during dormancy that doesn't happen when it doesn't get a cold dormant period?  Is there something detrimental that happens when it should be dormant but isn't?
If anyone has any pointers to resources where I could do further research on this question, that would be much appreciated, too, and I will update here with any further information I can find.

Here's a link with a discussion that is a step in the right direction.  http://www.omafra.gov.on.ca/english/crops/hort/news/orchnews/2016/on-0216a2.htm  Specifically, it says that there is an endodormancy period where the tree will be dormant of its own volition and will stay dormant until it has been cold long enough.  This is followed by an ecodormancy period where the tree remains dormant so long as external conditions are not favorable to growth.  It references a paper called "(Westwood, 1993)" but with no corresponding bibliographic entry.

Some plants that naturally survive frost periods outside, produce antifreeze proteins and shed any leaves to prevent actually freezing during this period. The production of antifreeze proteins requires a decent amount of energy (not sure how much i couldn't find any bio-energetic stuff) and when they are housed indoors you warm them up enough to signal that they can stop the production of these antifreeze proteins but you don't keep them at an ideal temperature all the time (such as during the night when you're asleep things cool down again and when you wake up you might put a heater on and warm them up again) and so they end up producing more antifreeze proteins. So this constant cycle of production -> loss -> production of antifreeze proteins coupled with no leaves to make more ATP starves them and kills them.
NOTE however, this is also just a theory and i have not seen/couldn't find any papers or info about experiments directly for this question and it is likely that the reason for plant death have many factors, potentially including your theories. I encourage a read of this which is all about antifreeze proteins and goes more into detail about the biology.
https://link.springer.com/chapter/10.1007/978-3-030-41929-5_7

Please better indicate which of the statements are covered by the reference.


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Understanding mRNA vaccine for COVID
As I've learned, mRNA helps us to produce virus spikes proteins to induce learning of the immune system.
But then, I remember to have read that the coronavirus has some trick to pretend to be "food" to our cells, that is it has some lipid element. So it can entry the cell easily. But this was not same part as the spike protein, right? (otherwise it would have been contradictory with the mRNA approach?)

You have it wrong. Coronaviruses are part of a family of viruses that are called "enveloped viruses". These all have an "envelope" comprised of a lipid layer derived from the host cell as the virion exits. The envelope is distinct from the spike. The spike protein is produced by the virus during replication and is not found naturally in a host cell.
This does not pretend to be "food" at all, but it can help evade host immune responses by hiding the other virion capsid proteins.

thx this was the missing bit if information


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Exploring speed of ants
I'm working on developing a model of ant foraging. To do this, I have simulated food morsels distributed randomly within an area, with the minimum distance between morsels being variable. I'm trying to get a good idea of the scale at which I should define the distances. This has to depend on ant walking speed and their usual foraging distance.
I'm not very species-specific in my approach. One study (1) shows a survey of foraging distance for different species. They found that most of the species had a maximal foraging distance of less than 1m. Some species did go upwards of 10m. I presume this distance would increase with the presence of trails, but to only focus on finding food by exploring, I can keep the distance between food morsels to be 2m-3m.
Now, I also want to figure out the time that it would take an ant to start from the nest and reach the food given its distance. This is where I'm stuck. I wasn't able to find any survey or study on walking speeds of different ant species. I need an approximate 'exploring speed' of ants, which is just time taken to reach a morsel after leaving the nest. Are there any references I could use to estimate this value for my model?
References:

Eguchi, K., Bui, T. V., & Yamane, S. (2004). A preliminary study on foraging distance and nesting sites of ants in Indo-Chinese lowland vegetation. Sociobiology, 43(3), 445-457.

I don't think it's reasonable to try to do this in a species-independent manner, since there is so much difference between ant species. Leaf-cutter ants, for example, will build trails to forage 200 meters away from their nests. Likewise, ants vary by two orders of magnitude in size and the walking speed of an ant will vary accordingly as well. Finally, I don't think that you can reasonably exclude trail-building from your simulation, since that's a key ingredient of foraging.
Bottom line: pick a species to model and look for information on its specific mobility.