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Do viruses or bacteria have a flavour?
My 9 year old niece asked me this when I was explaining some stuff to her about the coronavirus. She asked "What does this virus taste like? Can I tell whether my sandwich is contaminated for example?"
That sounded like a silly question and I immediately responded by saying that they are too small to have any taste, and even if you manage to eat a whole lot of viruses it would taste like water.
The day after, I searched a bit just to make sure that I haven't fed the wrong information to the kid. As I expected, there wasn't a single page mentioning this question (except this quora post with a vague answer). Now it may sound like I am overthinking and the question is too naive and isn't worth the time, but then again, I thought what's the harm in asking?

Has there been any research on the likely taste or maybe smell of a specific virus or bacteria?

While I don't think it's the bacteria themselves that cause the taste, there are quite a number of foods - cheese is a prime example - that acquire their taste as a result of bacterial action.  And if you want to expand that a little to include microorganisms in general, there's bread, wine, beer and more.

I think this is a very good question, but from the title i had assumed it would be about the sensory organs of bacteria.

same; too few characters for a title edit: ... have [a] taste [to them]?

... have a flavour (or "flavor" according to, er, taste)

I know that mold has a taste.

As you could imagine, a systematic cataloguing of bacterial or viral flavor profiles would violate a number of biosafety protocols. However, in a laboratory setting, different bacteria definitely have distinct odors. In some cases, the odor is even included in guidelines for laboratory identification of an organism. However, that odor is typically not a result of smelling bacteria directly, as very few bacteria are aerosolized from a lab culture. More likely, the odors of bacteria are a result of volatile chemical metabolites produced by the organisms. For example, the spoiled milk smell comes from a number of odiferous compounds produced by bacteria. Sometimes these bacterial metabolites have rather colorfully descriptive names, such as putricine or cadaverine.
Viruses are different though. They don't generate new metabolites on their own (outside of an infected cell) and they are incredibly tiny, even compared to a single cell. The human sense of taste is sensitive enough to detect some compounds in the low parts per million range. To even approach that range, you'd have to cram around 100 billion virus particles into a single milliliter of water (based on back of the envelope calculation). That's about 100,000 times more virus than most COVID19 positive clinical specimens, so I don't think you'll have to worry about tasting it under most circumstance. However, some research has been done to see if dogs can sniff out viral infections (likely by detecting volatile compounds produced by the infected cells, not by detecting the virus directly). Of course, they're trying to train them to detect the novel coronavirus as well.

To add another back of the envelope calculation, assuming the virus particle to have density 1 (order of magnitude) and a diameter of 80 nm (for the solid sphere), we'd expect roughly 1e-16 g per particle, so 10⁴ - 10⁷ SARS-CoV2 particles/ml should be 1 pg/ml - 1 ng/ml. Humans odor detection threshold for geosmin in water is 6 pg/ml, so in the mass concentration range of the SARS-CoV2 samples. Of course, I picked geosmin because we (those of us who do have the receptor) are extremely sensitive for geosmin. But then, that's maybe not an accident: geosmin is produced by molds, and this warns us

of mouldy water. (Geosmin also occurs in other mixtures such as some plants and actually in substantially higher concentration and IIRC contributes to the smell/taste - but in those combinations doesn't produce the ugly/warning sensory impression we get if it is in [more-or-less pure] water)

dogos? doctor doggo? :) too small for edit

It's an okay generic answer, I hope it's not too critical to say it avoids the question a little and makes it about odorants; the questioner is asking about flavour (taste!). I mention it because it's unclear from your answer that taste is a different beast from smell. Certainly a little misleading to discuss concentration (parts per million) when there exist no chemoreceptors to even detect viruses or cells... There are <1 elephant parts per million in a gallon of water too, but I'd bet you wouldn't be able to taste whole elephants, regardless of how sensitive our noses and tongues would be!

So I think this is a more conversational kind of question. I will address some misconceptions you have, and I will try to keep it brief, considering the nature and depth of your question. One could comment on the question very deeply, so I'll stick to addressing some misconceptions.

Can I tell whether my sandwich is contaminated for example?

Usually you can taste contamination because of the (action of) metabolic products of microorganisms. You do not taste nor smell the microorganism directly; you taste their metabolites or the effect of their presence, such as products of fermentation, or oxidized molecules which are normally not present because air does not penetrate through e.g. apple skins. Take filamentous fungi, for instance; they release enzymes that act on complex carbohydrates to break them down. You cannot taste the cellulose which makes up the majority of a stalk of celery, but you may be able to taste its broken down products once a fungus has begun to digest it prior to absorbing its nutrients: sweet glucose, sucrose, trioses, some acids. It depends on the food and the extent and kind of contamination.

they are too small to have any taste and, even if you manage to eat a whole lot of viruses it would taste like water.

You can taste molecules which are far smaller than a virus. Indeed, pheromones and volatile or sticky chemicals and all that jazz are definitely much smaller than viruses. Viral particles themselves may actually be too big to taste, because your sense of gustation and olfaction depends on the interaction between tastant or odorant molecules and corresponding receptors, which are situated on the membrane of sensory neurons (nerve cells which are responsible for detecting and relaying information to the brain about the outside world). These receptors harbor ligand-binding pockets that are too small to capture entire viruses. This does not rule out the ability for you to taste broken bits of viruses, but I think this is unlikely or coincidental (i.e. the particle may bind to receptors weakly and not very well).

it would taste like water

Water is a requisite for taste and smell, things have to be dissolved in water for you to be able to detect them. Water by itself has no taste! Only impurities, oxygenation and carbonation and mineral content give water flavor. I understand that you factor in temperature and texture into the 'perception of water', but these are not gustatory phenomena and use different mechanisms of detection.

Water is a requisite for taste and smell, things have to be dissolved in water for you to be able to detect them - Why is that so?

Re "things have to be dissolved in water for you to be able to detect them", is this really the case?  Most tastes are the same as smell, and the odor molecules are generally not dissolved in water, unless you're including water that's present in body fluids at the odor receptor.

"pheromones and volatile or sticky chemicals and all that jazz" are even on the large end of the spectrum. We can taste NaCl, and it doesn't get much smaller than that!

Capsaicin can certainly be tasted, and that's negligibly soluble in water.  It's fat-soluble though; the fat isn't even miscible with water.

@ChrisH Capsaicin does not activate taste buds though, it works via TRPV1 channels and at least in humans is part of the nociceptive system via the N. trigeminus, not the olfactory system via the Nn. olfactorii. @S Pr we might actually be able to taste water in itself because of its dilution of acids and interactions with carboanhydrases

@Narusan that comes down to the semantics of "taste"; in the context of the question "taste" would certainly seem to include not just the taste buds but the olfactory system.  It's not stretching things much further to include other receptors in/near the mouth that respond to foods.

@ChrisH It's a pretty clear cut distinction.  Taste receptors are part of a well defined subset of the nervous system that processes gustatory inputs from specialized sensors.  Olfactory receptors are part of a separate system that process smells with their own specialized sensors.  Capsaicin triggers pain receptors, which are of a totally different sort.  TRPV1 is a nociceptor that forms part of the body's thermoception system.  There's no way we could consider it related to taste.

@J... biologically yes of course.  In everyday language taste is a superset of taste, olfaction, and other stuff.  Ask yourself this: how many people would say "this curry tastes hot" (referring to capsaicin) compared to how many would use another verb.   Think also of "this cake tastes of vanilla" -- purely olfaction, not strictly taste at all. The question is asked on behalf of a 9-year-old; in that context the broad colloquial meaning of "taste" can be expected to apply.

@ChrisH  True, but this is bio.SE and the target audience is academics, researchers, and students on a path thereto.  I guess I'm labouring from the perspective that the discussion here intends to adhere to standard scientific terminology and that it behoves us to dispel the misconceptions that can sometimes brew in colloquial circles.

@J... I'd be the same in physics, which is my field. Then of course there's the whole fruit/veg - tomato/rhubarb - biological/culinary definitions issue). One issue I'm familiar with is that there's often no more suitable/scientific word for the superset of scientific terms.  Can you suggest anything that encompasses taste, olfaction and capsaicin-heat (whether or not it also includes real heat/cold or mouthfeel that wouldn't be culinary "taste")? "Detect" doesn't work without quite a lot more explanation, for example

@ChrisH I don't know of such a word, specifically.  Still, I wouldn't say 'taste' is appropriate in a scientific context - no more than a hot cup of coffee 'tastes' hot.  It burns just the same whether you put it in your mouth or dump it on your skin.  To call it 'taste' simply because it happens in the mouth is misleading, I suppose.

I am anosmic with no sense of smell.  I taste things but have no olfaction.  "Things taste and smell the same" is not a valid statement, as they are different senses with non-overlapping domains of subjective experience, but it points at how people with taste and smell run them together perceptually.  A mild synesthesia maybe even.  They loosely use "taste" to mean "perception of flavor" which is some synthesis of the two disjoint inputs.

It was really hard not to accept your answer. But for some reasons, I thought the other answer could be a better fit. Thank you

@terdon: we taste H⁺

"Viral particles themselves may actually be too big to taste, because your sense of gustation and olfaction depends on the interaction between tastant or odorant molecules and corresponding receptors" -- so perhaps the process in a way resembling tasting/smelling viruses is the interaction with antibodies. This does not lead to a sensory perception, however, except indirectly for the usual symptoms of your immune system being busy. At any rate, this won't help at all "tasting" infectious material beforehand.

@cbeleitesunhappywithSX oh wow, that's what we detect as "sour"! I had no idea, thanks!

Hi all, I arrive to see a nice comment section, good points too! They are a case in point why I included a disclaimer on brevity at the beginning, the conversation gets deep quick, since it's a well studied branch of neuroscience :) @J... the term which encompases reception of taste/smell/capsaicin would be chemosensation, even though capsaicin works via the noci- or thermo-ception pathways. I am aware some detectable (and delectable!) compounds are immiscible in water and thus may need to be fat soluble - as long as they are free to bind with our 'repertoire' of receptors.

@jamesqf Even odor molecules must become dissolved in the watery mucus at the olfactory epithelium to be detected; odorant receptors are not air-exposed. Even in invertebrates such as worms and insects, odors enter into specialized structures called sensilla through nanopores, whereby they dissolve into an aqueous lymph where sensory neurons project into. Never a bad time to remember how water-based all life is, even terrestrial life ;)

@S Pr: Yes, that's the distinction I was trying to make.

Already 2 good answers (MikeyC and S PRr), but one point missing:
We are very good at detecting the presence of some bacteria and fungi in our food in unhealty amount. We detect (by smell or taste) the products of these microorganisms as "food gone bad".
That's how we survived when the food didn't have expiry term labels mandated by the government.
We are also very good at avoiding places and things that smell bad. Bad smell is an indirect indication of an unhealthy thing, probably having bad viruses and bacteria ready to get us.
Then again, most microorganisms that make us ill actually don't eat much of our food. They hide in the food (or elsewhere) in order to eat us. That's why we cannot detect most of them. They don't leave much of a chemical trace.
Viruses are even harder - they do nothing outside of the host and there is too little of them in order to sense them directly.

We detect (by smell or taste) the products of these microorganisms as "food gone bad". isn't that because of bacterial products instead of bacteria themselves? Since OP asked specifically about the taste of microbes, the other answers didn't talk much about their products (but still touched upon it). Not saying that your answer is bad, but it sure needs some references ;)

@another'Homosapien' a lot of taste and smell sensation comes not from the main substance or object one smells and tastes, but from the product of the object interactions with the environment and/or degradation/decomposition of the substance or object, and/or some by-product from the object/substance creation. We say "smell of rotten eggs" and not "smell of the substance that rotten eggs evaporate".

Yup, I get that. But my point was that OP specifically asked about the taste of microbes, not their products (maybe I'm being pedantic here). There's nothing about your answer that is wrong or I don't understand, it's just that it doesn't answer the exact question. Also, the answer lacks the much-required references :P


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Can intracellular protein initiate strong immune response?
Some autoantibodies escape immune tolerance and can cause autoimmune disease. In order to cause harm to the tissues by these autoantibodies, do the antigen need to be extracellular or membrane bound, so that they are exposed to the immune system?
What happens if the target protein of the autoantibody is intracellular? Does the cellular localization of the target antigen plays any role?

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

Labeled

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

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

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

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

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

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

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Metrics to analyze branch lengths in phylogenetic trees
I'm interested know about some basic metrics that could be used to discriminate trees based on their branch lengths. I know of branch length unaware topological/tree shape-based methods such as Colless and Sackin's indices and am curious whether there are similar metrics that utilize branch length to discriminate. For example, the two trees below have an identical topology but are very different.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, this question seems like it might be a better fit for [Bioinformatics.SE]. (Note: please don't repost your question to that site — instead request migration). Thanks!

Thanks @tyersome! This similar post elsewhere on this site brought me here.

You're welcome! Bioinformatics.SE didn't exist 4 years ago, so that isn't really a good indicator of what is currently a good fit for this site ...

Are you essentially asking how to interpret the difference in the two phylo trees(that is,given the tree,what do you conclude),or are you asking which tree to produce for your data(that is,given the items,which tree to produce)?The horizontal length gives you a sense that two things are very separate or not.Looking at the second tree,you could say that right at the beginning of time,d,e,f differentiated but a,b,c remained identical until some much later date when they finally split and differentiated.The horizontal distance doesn't have to be time-any measure that measures similarity will do.

There are a variety of measures of tree similarity implemented in the TreeDist R package. (Your phylogenies appear to be from the R ape package, so hopefully you are somewhat familiar with R.)
Other tools include treedist from Joe Felsenstein, which computes Robinson-Foulds and the Branch Score Distance (which sounds closely related to your interests, described in this paper). You can see that software page for a lot more information.
For a practical description of the different tree comparison metrics you can see this article.
I would suggest taking a look at the manual and the multiple vignettes associated with the TreeDist package to learn more about how exactly those metrics work. There appear to be a wide variety of metrics in there that I have never heard of, such as clustering entropy or split entropy or Nye similarity.
This package also includes tools for making visualizations of differences, such as that shown below:

I don't know whether this is actually used in phylogeny, but if you restrict the problem to cases where the topologies are the same, each tree can be described as a point in a n-dimensional space where n is the number of branches, and each axis represents the (possibly normalized) length of one of the branches.
You can then compute distances between points (i.e. trees) in that space.


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Does the human eye’s field of view shrink when focusing on far away objects?
It seems like the lenses of the eye is like a fisheye lens that flattens out to a normal lens when looking at far away objects. Does that also mean that the field of view gets narrowed down as well? Or is that not how light works?

It's not quite as simple as a plain camera lens.  For instance, the different types of photoreceptors aren't evenly distributed on the retina: https://www.ncbi.nlm.nih.gov/books/NBK10848/  Then the brain does a lot of image processing, so while the optical field of view might stay the same, the field of attention will change.

The lens does flatten when contracted to look at far objects. This is however still a regular cylindrical lens. It's not perfect (even when corrected), but close to it. Straight lines project to straight lines on the image plane (for your eye the retina).
A fisheye lens is different because it creates strong geometrical distortions. A straight line will appear curved on the image plane. You can see that on the images taken below (from some random source). Left is a regular lens, right is a fisheye lens.

The human eye actually introduces some so-called barrel distortions (so it's a little bit like a fisheye lens). You can demonstrate that by looking at this checkerboard pattern (from Helmholtz's treatise on physiological optics). If your eye is close enough you'll see the checkerboard straight, because the barrel distortion introduced by your eye will "straightens" the distorted checkerboard.

Focusing at different distances will make objects appear sharp. Because all light rays coming from this object will project at the same point on your retina. Objects at a different distance will appear blurred because light rays will project at different points causing a "spread" (defocus blur, see image from wikipedia "circle of confusion" article). This is however totally independent from the field of view. Test it yourself: take a pen, place it close to your eye. Pay attention to an object far in your periphery, nearly outside your field of view. Now focus to the sky behind the pen (~infinite focus distance), then your pen. In both cases you can still see the object in periphery because your fov hasn't changed.


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About what percent of mutations are not adaptive?
Many popular texts that discuss evolution and natural selection often mention that many (or most) mutations are bad (not adaptive).
Have there been any studies on what the rough percentages are? (E.g. Is it 90%? 99%? 99.9%? If this number varies by species, an answer could just focus on one particular species.)

It would depend dramatically on where the starting point is on the fitness landscape.  If it's on a peak, all mutations that aren't neutral are bad.  If it's at a low point on the fitness landscape, more mutations will be adaptive than, e.g., mutations  when the starting point is relatively high up the slope of a fithess "hill".

As suggested by the McGrew comment, this is dramatically dependent on the shape of the fitness landscape. It will vary quite a bit from situation to situation.
More precisely, you are interested in the distribution of fitness effects (DFE) of mutations, and the upper tail specifically.
Wikipedia has a section on this. In there, they note one study of a virus that suggests that ~4% of mutations are beneficial. That may be an overestimate, and many of those are probably only very slightly beneficial. Probably the number is lower in non-viral organisms.
For a review on the DFE of new mutations, see here. They write in their section "Advantageous mutations":

As expected, relatively few of the mutations that are not
effectively neutral are advantageous.In three mutagenesis
experiments, the proportion of advantageous mutations was 4% in the RNA virus vesicular stomatitis virus (VSV)15 (FIG. 1), 0% in Escherichia coli(14), 0–15% in the bacteriophage φX174 (REF. 40), 0% in φ6 (REF. 13) and 6% in Saccharomyces cerevisiae (16).

It is necessary to distinguish mutations from substitutions: assuming for simplicity that a mutation can happen at any place in the genetic sequence, most mutations are bound to result in non-functional genomes. Substitutions, on the other hand, are mutations that resulted in viable organisms - they can still have negative fitness effect, but not outright deleterious.
Note also that non-adaptive mutations are not necessarily bad - the neutral theory of evolution tells us that, due to randomness effects, substitutions may fix in the population without having a direct fitness advantage.
In viruses the quantity of substitutions can be very high - tens of percents, to the point that one has to introduce ad-hoc thresholds to distinguish viral strains, e.g., viruses that differ by 30% of their genetic content. How much of this is adaptive depends on the shape of the fitness landscape, as noted by @MaximilianPress. E.g., for HIV it has been found that up to a third of the sequence changes tend to revert to the ancestral HIV sequence, i.e., constitute host-specific adaptation.
Clarification
In view of the discussion that followed, I would like to add some precisions to my answer:

My distinction between mutations and substitutions is essentially distinction between the actual and the observed mutations. This is different from the more common usage, where substitution means point mutation, with mutation being a more general term.
Since I mentioned the neutral theory, it is necessary to remark that the entirety of its claims is not generally accepted and/or supported by data. Moreover, its validity depends on the organisms in question. My use of the neutral theory is therefore limited to the fact that being adaptive/non-adaptive is not the only factor that determines that a mutation fixes in the population.

According to whose definition?! It’s neither a very common nor a particularly useful definition. It’s much more common that “mutation” refers to any change of genetic sequence, and “substitution” refers to the exchange of a single nucleotide (it’s a type of mutation, same as e.g. indels or rearrangements). Neither terms say anything about the change’s effect on fitness.

@KonradRudolph Indeed, there are no unique agreed upon definitions for either term. Which is why I explicitly explained what I mean.

Hmm I disagree with the substance of that. There are widely agreed definitions, and they are different from the ones you are using, which needlessly causes confusion. And the distinction you introduce doesn’t help answer OP’s question, it’s completely irrelevant here. — Another problem with this answer is that the neutral theory of evolution is extremely controversial and, to put it bluntly, probably untrue (or, if it happens to be true in some extremely narrow sense, it makes no useful predictions).

@KonradRudolph The difference is between actual and observed mutations. Indeed, the subject is not widely covered in standard textbooks, but familiar to anyone dealing with phylogenies. The statement that neutral theory is controversial should be made in a qualified manner, just like neutral theory does not mean that Darwin was totally wrong.

Oh, I agree that that distinction is indeed important for answering OP’s question, I didn’t get that this is what you’re referring to from your answer. — And regarding my statement of “controversial”, I was being diplomatic. There is effectively zero evidence in favour of the hypothesis, and modern statistical evidence is pretty one-sidedly against it. The way the hypothesis is nowadays “defended” is by diluting it so far that it makes no predictions.

@KonradRudolph You mean that the claim that most mutations are neutral is disputable. But we do agree that neutral or even slightly deleterious mutations can fix in the population? I have to say that my experience is mainly with viruses - I think the validity of the neutral theory claims depends very much on the type of organisms that we discuss.

@KonradRudolph I added clarifications to accomodate your comments.


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Why is selection less effective in small populations than in larger?
I can understand that the genetic drift has a higher impact on smaller populations, but what does it mean for the selection to be less effective in small populations than higher?

Hi Gljiva, could you please specify what kind of selection you are talking about, as well as the context to better understand what "effective" means?

@F16Falcon e.g. this sentence on Wikipedia "In small populations, selection is less effective, and the relative importance of genetic drift is higher because deleterious alleles can become more frequent and 'fixed' in a population due to chance." https://en.m.wikipedia.org/wiki/Small_population_size

This question seems to be about negative/purifying selection, judging by the wikipedia quote. Positive selection can often (but not always) occur more slowly in smaller populations, but 'efficiency/effectiveness' of selection generally means the rate at which deleterious variants are purged from the population, so I'll skip out taking about positive selection (unless you did mean that).
First, genetic drift: Genetic drift is the stochastic change in allele frequencies caused by random differences in the survival of different individuals. For example, a mouse might get struck by lightning and not transmit any of its genes to the next generation. Whether or not it was struck by lightning probably wasn't related to its fitness, it was just 'bad luck'. As population size increases, genetic drift becomes weaker because the larger the population, the smaller the proportional impact of each random event that concerns just one individual
Negative selection tends to be less effective in smaller populations because random fluctuations in allele frequency (drift) may lead to deleterious alleles reaching higher frequency. The rate at which deleterious alleles are removed from a population depends on mutation, dominance, linkage, and demography and can vary across populations. Therefore, the average fitness over time may become reduced. Kimura in 1963 was one of the first people to show this.
In reality, 'low efficiency of selection' and 'strong drift' in small populations are the same thing.


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Examining antibody - target interactions in PyMOL
I'm a student currently looking at antibody responses against a viral target protein of interest.
I have my own, annotated PyMOL session of my protein and I also have .pdbs of crystallised antibody structures that bind to this protein and rougly know whereabouts it binds. I would like to know if it is possible to combine these two structures into a single session to observe or at least overlay the two structures together. Many thanks!

You might find a PyMol expert on this list. If not try SE Bioinformatics or even Chemistry.

I don't think PyMOL has built-in functions for that; you might have to use a docking software like AutoDock. I'd also recommend asking on Bioinformatics SE as David suggested

Multiple structures may be read into a given session using the following for each pdb:
File -> Open

In the narrative below, the reference antibody has the name AAA and the second antibody has the name BBB. The heavy and light chains have pdb chain IDs A and B, respectively. Adjust those as needed.
Whole molecule overlay
Make visible the reference and the moving molecules.
From the menu item next to the BBB molecule name (right panel), select:
A -> align -> to molecule (*/CA) -> Object: AAA

Antibody's variable domain overlay
I think it may be more helpful to align the variable domains than the whole antibodies or Fabs. Typing the following on the command line is a temporarily adequate way to align proteins:
align BBB and chain A+B and res 1:109, AAA and chain A+BL and res 1:109


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What is this insect in Southern Colorado?
We have found this insect in a bit of a swarm on a concrete pad and on some insulation next to and around our greenhouse in which we have tomato plants.
The insect is about 2mm wide at its widest, and 4mm long at its longest.
What is it?


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Can plants break down cellulose for energy?
I know humans and other animals start using their own proteins as food when starving. This made me wonder if a plant that is deprived of sunlight, after using up its sugar reserves and other carbs, could break down parts of its own woody structure in order to feed the rest of itself.
Googling yielded no useful results, which leads me to think the answer is no. I've never heard of plants themselves possessing cellulase, only certain animals.
Additionally, I would imagine that cellulose is not easy to transport, so it would have to be decomposed by the region of tissue surrounding it - which obviously couldn't last for long before that region died due to cannibalizing itself.

Then deciduous trees would absorb back their leaves rather than losing them in autumn. I think that plants can take back most things from leaves except cellulose.

breaking down cellulose is very different than breaking it down FOR energy, which are you looking for> it would not surprise me if there are plants that can break down cellulose but do so at a net loss.

Plants do not produce extra cellulase to break down cellulose for an energy boost when they are grown in dark conditions (that I know of). But remember, cell walls are the structures maintaining turgor pressure in the cells, so breaking them down would be very costly to plant survival. A couple notes: plant cell walls have more components than just cellulose, and they ARE dynamic. In dark-grown conditions, plants elongate (etiolation) during which time, enzymes (expansions) break down cell wall bonds to allow the cells to elongate the stems of the plants. Elongation is an evolutionary advantage to find light when things get shady.
To read more about what the cell wall is made of, and the function it provides to the cell, try watching the Khan Acadamy video about cell walls. Light signaling is an entire field in Plant Biology (example). Read more, if you are interested in how immobile plants handle shading from other plants or periods of darkness. Plants do break down proteins for reuse! Read more about plant vacuoles if you're interested in how they recycle and break down some molecules and proteins when needed (related to your question's parallel to animal cells; although, not cellulose breakdown to replace photosynthetic sugar output).

This is a good answer, but it is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, the most directly relevant part of your answer is indistinguishable from opinion and someone with no plant biology background will be unable to judge your assertions. ——— Note that links often break, so we prefer that you also include citation information. This is a good example of how to format references. Thank you!

Plants do not break down cellulose for energy, although it does store energy. Plants store their energy in the form of starch, which is broken down into glucose for the plant to use for energy. Most plants do not survive once the starch is utilized (but they do not breakdown cellulose).
Because cellulose molecules bond strongly to each other, breakdown of cellulose is relatively difficult compared to the breakdown of starch. High temperature is required for breakdown of cellulose, which plants cannot breakdown.


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How many of the four meiotic daughter chromosomes of a homologous pair can be recombinant via crossover?
In graphics I've seen, crossing over occurs between the "inner" two chromatids in a side-by-side arrangement of two duplicated chromosomes:
This suggests that only two of the four meiotic daughter chromosomes of a homologous pair can be recombinant via crossingover. Is this true? Or can you have more complex patterns, like the one below, in which all four daughters are recombinant? Does the X-shaped geometry of the doubled chromosomes play a role in models of crossover phenomena?

ps. Sorry if my terminology is strange. I'm a beginner! Experts: Edits to improve clarity welcome!

You appear to be assuming that your organism only has one chromosome. Since that is a highly unusual situation and may not be what you meant I encourage you to [edit] your question to make it clearer what you are trying to ask. One possibility is that you didn't mean gamete and you are actually trying to ask about chromosomes .... ———— Please also specify an organism or at least group of organisms — there are many variations on meiosis including some where no crossing over takes place!

Thanks for the advice, @tyersome! I hope it makes more sense now. I'm focusing on one pair of homologous chromosomes in a cell undergoing meiosis. I have drosophila in mind because that's what I've been reading about.

There can be and often is more than one crossover per chromosome in meiosis, but how many crossovers occur can depend on the species, sex, age, environment, and which particular chromosome is involved1,2,3. For example, humans typically show 2-3 crossovers per chromosome, but females often show higher recombination rates than males.
However, the structure you drew seems unlikely due to a phenomenon known as crossover interference, which suppresses the occurrence of closely spaced crossovers4,5. See also this historical introduction from Nature.
In Drosophila melanogaster, males do not make any crossovers6. In contrast, females show an average of around 1.2 crossovers per chromosome7. This means that most tetrads have just one crossover, but some will have more and this second crossover can occur between any pair of chromatids. Thus, there can be from two to four  recombinant chromosomes, but most commonly there will be two.
(Note that this last reference (7) is a 2018 review article on this subject and could be a good place for you to start learning more once you've mastered the basics of this subject — figure 1 in particular seems directly relevant to your question.)
References:

Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Meiosis. Available from: https://www.ncbi.nlm.nih.gov/books/NBK26840/
Fledel-Alon, A., Wilson, D. J., Broman, K., Wen, X., Ober, C., Coop, G., & Przeworski, M. (2009). Broad-scale recombination patterns underlying proper disjunction in humans. PLoS genetics, 5(9).
Wang, Z., Shen, B., Jiang, J., Li, J., & Ma, L. (2016). Effect of sex, age and genetics on crossover interference in cattle. Scientific reports, 6, 37698.
Berchowitz, L. E., & Copenhaver, G. P. (2010). Genetic interference: don't stand so close to me. Current genomics, 11(2), 91-102.
Otto, S. P., & Payseur, B. A. (2019). Crossover Interference: Shedding Light on the Evolution of Recombination. Annual review of genetics, 53, 19-44.
John, A., Vinayan, K., & Varghese, J. (2016). Achiasmy: male fruit flies are not ready to mix. Frontiers in cell and developmental biology, 4, 75.
Hughes, S. E., Miller, D. E., Miller, A. L., & Hawley, R. S. (2018). Female meiosis: synapsis, recombination, and segregation in Drosophila melanogaster. Genetics, 208(3), 875-908.


text:
If Melatonin is anti-gonadal, why is it associated with early sexual maturity in congenitally blind girls?
If melatonin is anti-gonadal, that is, it delays sexual maturity, then shouldn’t it delay sexual maturity in congenitally blind girls rather than helping them attain sexual maturity at an early age?

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melatonin released from pineal gland and and its one of the function is that it delays sexual maturity. but there are also a point to remember that pineal gland is activated at that time when light stimulate the retina but in the case of blind person activation of pineal gland is not occurs. that's why hr. like melatonin is not secreted and sexual maturity come before time. it come 2-4 years before the normal age.

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i read this from books so you may find this at : 1. ncert - biology - xii   or 2. allen module-8 chapter 2

Isn’t melatonin secreted during the scotopic phase? That would mean that in blind girls melatonin levels should be higher compared to serotonin (secreted during daytime). Therefore, blind girls should have a delayed sexual maturity rather than early sexual maturity.


text:
Are children's ears more vulnerable to loud noise than adults?
I am interested , what are child's ear development stages?
Do newborns' have already developed (defensed) ear like adults have and there is no much difference with regard being vulnerable toward sudden burst noise, which we (adults) bear easier (i.e. popper burst within 1 meter range)?

I would suggest that this type of question, not relating to specific biological processes, might be more appropriate on SE Medical Sciences.

@David sorry, but there is no chance such question to be accepted on medicals.se. I have experience there. my question is formed to be non-medical and it is about ear-development stages.


text:
On stochastic Lotka-Volterra predator-prey model
I am currently working (as a mathematician) on some estimations involving an stochastic predator-prey type model in which some of the coefficients have been perturbed by a Brownian Motion yielding to a system of stochastic differential equations.
The basic formulation of this problem can be found for instance in this article.
We have the following model
\begin{equation}\label{0}
    \begin{cases}
    dX(t)=X(t)\left(a-bX(t)-\frac{sY(t)}{\beta+Y(t)}\right)dt\\
    X(0)=x>0,\\
    dY(t)=Y(t)\left(\frac{h X(t)}{\beta+Y(t)}-c-fY(t)\right)dt\\
    Y(0)=y>0.
\end{cases}
\end{equation}
where we use Holling II response function.
In the literature (mostly mathematics literature) the authors propose to perturb the birth rate of the preys $a\mapsto a+\dot{B}_1(t)$ and the mortality rate of predators $c\mapsto c+\dot{B}_2(t)$.
This yields to the following (stochastic) system
\begin{equation}\label{1}
    \begin{cases}
    dX(t)=X(t)\left(a-bX(t)-\frac{sY(t)}{\beta+Y(t)}\right)dt+\sigma_1 X(t)dB_1(t),\\
    X(0)=x>0,\\
    dY(t)=Y(t)\left(\frac{h X(t)}{\beta+Y(t)}-c-fY(t)\right)dt+\sigma_2 Y(t)dB_2(t),\\
    Y(0)=y>0
\end{cases}
\end{equation}
I know nothing about biology but I am concerned about a couple of things regarding this particular formulation:

If we assume that the Brownian motions are perturbing the birth/mortality rates, how can I interpret the fact that this new "perturbed" rates can become negative (due to the effect of the BM). Does it have any sense (in the framework of this particular model) to talk about "negative birth rate" or "negative mortality rate"?
What if the "perturbed" mortality rate goes beyond $100 \%$? Mathematically nothing "wrong" will happen, but what about the interpretation?

Notice that the "noise"  and the model as a whole can be interpreted differently (ignoring the fact that we are actually modelling the dynamics of two species) but my main issue is that if I(together with many authors) am stating that we perturb a certain parameter I believe that we must respect the basic assumptions of the model!
I hope everything's clear and I thank you all in advance, any opinion or suggestion will be welcome!

Have you considered to change how the noise scales with the population sizes? If done properly, this avoids negative population sizes and other unrealistic results and may be more realistic anyway. More specifically, if the noise is bounded by the square root of the abundance (for small abundances), everything should be fine. A typical example for a model that does this is the minimal market model.

To interpret $a$ and $c$ as a birth and mortality rates is somewhat inaccurate, as $a$ and $c$, as written are density-independent rates that grow or shrink populations exponentially. If $a$ were negative, the prey population would shrink and most people would find a problem like that unexciting unless it was, say, a sink population maintained by immigration from another population. This is true of $c$ being negative, where the predator population would grow independent of the prey population. More accurately, $a$ can be interpreted as the difference between birth, $b$, and deaths, $\delta$; i.e., $a = b - \delta$. In this case, depending on the kinds of stochasticity being added to the model, negative $a$ is not just normal, but expected. The same is true for $c$. Ultimately, a perturbations like the white noise in this equation is simultaneously perturbing the difference between birth and death rates, which explains the negative difference.
The value of the rates seem to have the same interpretation if they are constant or are perturbed to an arbitrary magnitude.

I hope this helps!

thank you very much, now it's clear that my understanding about the true meaning of the parameters was actually wrong.  In case you care I leave you the link to the preprint of the article I mentioned in the question https://arxiv.org/abs/2009.14516

You're welcome. It seems to be inconsequential to your work and tends to be prevalent in the mathematical literature, so it's not a big deal. The work looks interesting and I will study it later. Since you are working in 2D, I also wanted to pass along a method that is of growing interest to find the quasi-potential of the system to study stability and first-passage time: Nolting and Abbott 2015. (The supplemental material is where all the math is hidden.)

Ey Chris thanks for the reference, the approach seems very interesting and uses some techniques that I've never seen! I'll be reading it in detail since my idea was that of further studying the two dimensional case!


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Do person with strong immune system have less chance of surviving SARS-COV-2 attack?
In most of the cases dealing with SARS-COV-2 disease, the major mortality cause is due to cytokine storm in response to Corona-virus that also attack healthy organs causing multiple organ failure.

leading to inflammation and fluid buildup in the lungs.(7) Certain kinds of cytokines trigger cell death. When you have many cells doing this at the same time, a lot of tissue can die. In COVID-19, that tissue is mostly in the lung.(5)

Among the many mysteries of Covid-19 is why relatively healthy young people suddenly become critically ill — or die.Many otherwise robust patients were experiencing cytokine storms. One key sign of that was the body’s levels of ferritin, a protein in the body that binds to iron. This massive over-reaction, known as a cytokine storm, is believed to be a major reason that a growing number of exceedingly fit people find themselves fighting for their lives.(7)

Assuming healthy people having a strong immune system have greater cytokine storm against SARS-COV-2, isn't coronavirus naturally selecting people with "weaker" immune response?
However an interesting case has been observed within Haemodialytic patient(not-healthy):

HD patients with COVID-19 even displayed more remarkable reduction of serum inflammatory cytokines than other COVID-19 patients. Epidemiological, clinical, and immunological features of a cluster of COVID-19 contracted hemodialysis patients

References:

https://scroll.in/article/962574/what-is-a-cytokine-storm-and-why-is-its-prevention-key-to-treating-covid-19
https://www.sciencedaily.com/releases/2020/05/200521165706.htm
https://www.sciencedirect.com/science/article/pii/S1359610120300927
The cytokine storm in COVID-19: An overview of the involvement of the chemokine/chemokine-receptor system
Cytokine Storms May Be Fueling Some COVID Deaths
Why Some COVID-19 Patients Crash: The Body's Immune System Might Be To Blame
He ran marathons and was fit. So why did Covid-19 almost kill him?

Is this a question or a blog post? The answer (if it is really meant as a question) may be yes (or no) but before anyone can attempt to answer it they would need to know what “a strong immune system” is (as well as its relationship to athleticism etc.). Is this something that can and has been measured, or is it something purveyed by the media and other charlatans? Perhaps you could provide references to this, or ask a separate question on this specific point (preferably to SE Medical Sciences).

@David By Strong immune system, I meant adequate immune response generated by the patient to quench the effects of pathogenic diseases. Although I didn't find any journal paper that would answer the question given in the title, I welcome any comment that would provide some key insights


text:
What is this Kenyan insect?

This insect was seen in Nairobi, Kenya. Underside is striped black and white. What is it?

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Perhaps a bug (Hemiptera) that is mimicing the cotton stainer bug. Might be an assassin bug.


text:
Why is cannibalism not an evolutionary stable situation?
In the 'the selfish gene' Dawkins writes (page 109):
"The reason lions do not hunt lions is that it would not be an ESS (evolutionary stable situation) for them to do so. A cannibal strategy would be unstable for the same reason as the hawk strategy in the earlier example."
To quickly summarise this: we consider an interaction between two animals where one possibly stands something to gain. Dawkins then defines 'hawk' behaviour as attacking behaviour, whilst 'dove' is described as peaceful and retreating behaviour. He then argues that a population of purely hawk or purely dove is unstable, since in either of the situations the other kind of behaviour is more favourable. As it turns out, the stable situation is 7:5 for hawk:dove.
Turning to cannibalism, we can regard the hawk behaviour as 'engaging in cannibalism' and dove to be the refraining party. Why, then, don't we see similar behaviour when considering cannibalism, i.e. why don't we see a reasonably large amount of lions engaging in cannibalism whilst the others refrain from it? If I am not mistaken we see in fact the situation more closely described by completely dove?
Any insights are appreciated!

Cannibalism is incredibly common in nature. There are more species that eat their own kind than do not. Chimps eat other chimps. Lions eat other lions. Wolves eat other wolves. Prairie dogs go into the burrows of other prairie dogs and eat their babies to get the protein-rich meals needed to produce milk for their own litter. The only animals that don't regularly engage in cannibalism are some birds, and that is more because they physically cannot fit other members of their species down their throat than any moral qualms.
However, cannibalism is typically a bad evolutionary strategy, long term. For several reasons...

in a dioecious species (i.e., one with two sexes), cannibalism means a 50% chance of eating a potential mate and losing the opportunity to pass on your genes
diseases are more likely to transfer between species the more closely related they are. If you are a cannibal you are eating a species with a 99% similarity to you and are more likely to get diseases or parasites. Like kuru/mad cow/chronic wasting disease.
it precludes social behavior and all its benefits. Why engage in mutually profitable behavior when you can just eat those around you? This is thought to be one reason why pack-hunting is rare in some groups of vertebrates like monitor lizards.
on a broad-scale evolutionary perspective, cannibalism means removing members of your own population from the gene pool. It may be good for the individual but it's bad for the species as whole
cannibalism means you are feeding on an animal that is potentially your own size. That's a bad strategy in general. Most cannibalism in nature tends to be adults eating infants or adults scavenging carrion of their own species. By contrast predators are normally larger than their prey, with a few exceptions like pack-hunting wolves and lions.

Perhaps one also needs to distinguish occasional cannibalism and a situation where cannibalism is the main source of food. In this latter case the birth rate is always behind the rate of the population decrease due to the cannibalism. It is obvious for lions, but I think the argument could be made general for all species, based on energy considerations.

Further WRT point #5, if you are to be a successful carnivore, you really don't want to be hunting prey that can fight back, since that sort of prey can either kill you (making you an unsuccessful carnivore :-)), or injure you badly enough that you can no longer hunt, with much the same result.  So you would expect intra-species cannibalism to only involve eating weak members of the species - young, or moribund adults.


text:
Why does an autoclave need to pressurize steam?
I've looked this up on other sites and they say that an autoclave needs high pressure in order to raise the boiling point of water so that you can achieve steam of a higher temperature.
If you look at this diagram though, it seems to me as if it would be much simpler to further heat the steam at the ambient pressure of the autoclave room. Does the pressure of the chamber play some role that I am unaware of? Thanks in advance for clearing this up!

An autoclave can sterilize both solids and liquids, whereas an oven with no pressure control is typically not suitable to sterilize liquids.
Not only do you need to heat the chamber to 121°C, but you also need to make sure that the things you are trying to sterilize are not degraded by the treatment.
For dry objects (e.g. glassware) you could heat the chamber up to 121°C at ambient pressure. In that case, the instrument you're using is called a "dry heat sterilizer" rather than an "autoclave" (REF)
So why use an autoclave at all, and not just a dry heat sterilizer? Quite often the things you would put in an autoclave are water-based solutions (for example, LB broth or buffers).
If you do not increase the pressure and try to heat to 121°C, the liquid in your bottles will first boil around 100°C until all the aqueous solvent is in the gas state (i.e. your solutions are going to evaporate) and then the temperature will increase to 121°C. However if the pressure is raised to stay at the liquid-gas phase transition, then the gas and the liquid are in equilibrium, therefore you neither lose or gain any volume in your solution.
So in theory, if you autoclave 1L of medium, then you get 1L back at the end. Note that in real life, the temperature and pressure of the autoclave are set based on the diagram for water, but for concentrated solutions these settings may be slightly off, meaning that the volume in the bottle at the end of the cycle is sometimes a little different from what you put in there at the beginning. See this illustrative diagram of how a solution behaves differently from the pure solvent:

(Copyright: Lumen Learning)

Thanks for the answer! Looking back, it feels kind of ridiculous that I didn't think of that

it would be much simpler to further heat the steam at the ambient pressure of the autoclave room

You cannot do that, physically. If you put water in a closed (water-vapor-tight) container, then heat it, the vapor "wants" to expand with growing temperature. But as it cannot expand your metal container (autoclave), the pressure goes up instead. It happens automatically, that's how molecules function in a gas (don't ask me to remember the name of that law please).
You could, I guess, try constructing an elastic autoclave where the pressure stays the same and the volume changes. But that would be mechanically challenging - what material are you going to use that is elastic, won't tire with time, won't deform on you during use, won't burn at the heat source, will conduct warmth well, etc.? Also, you will lose your convenient way of ensuring that you are at a target temperature. Since a certain pressure always equals a certain temperature (at constant volume), you can construct a weighted valve to keep a constant pressure in your autoclave - this is cheap, easily doable with 19th century tech, and more accurate and failsafe than creating a cybernetic control loop with a measuring device such as a thermometer or a manometer.
I don't know if there are also biological reasons to prefer it with with a higher pressure - the number of bacterial species which can withstand high temperature is higher or equal to the number of species which can withstand high temperature combined with high pressure - but I doubt that this was a driving factor in the design and adoption of autoclaves.
The standard autoclave is easy to invent, does its job, does it well, and is cheap and unfussy (when compared to a hypothetical room-pressure-wet-autoclave). The pressure is more of a side effect nobody sees the need to remove - on this site, I'm tempted to call it a spandrel.

https://en.wikipedia.org/wiki/Ideal_gas_law

Once the middle is dried, the steam can be overheated at constant pressure, the excess of steam is just released by a pressure relief valve.

As you say it is possible to increase the temperature of the steam over the saturation pressure. And with overheated steam, the instrument would reach the desired temperature as is the case in an autoclave.
But the difference is how many time it would take to heat the sterilized instruments. And the difference is actually huge, we are talking of order of magnitude. The reason is that the heat transfer inside an autoclave is evaporation-condensation. But if the autoclave were not pressurized, there would be a first efficient phase of evaporation-condensation followed by an extremely slow natural convection phase.
Let's try to explain it in few lines.
On the difference between the heat transfer by evaporation-condensation and heat transfer by condenstation
Evaporation - condensation is the most effective way to transfer heat. Just consider the fact that uranium is used in nuclear power plant to boil water.
Transfer of heat by natural convection of gas is very slow.
The difference is many order of magnitude, heat transfer by evaporation is typically of the order of 1'000'000 W/m² (1MW/m²). Heat transfer by natural convection it is of the order of 100 W/m².
What is happening when the autocalve steam is saturated.
Liquid water inside the autoclave boils. Its temperature is the saturation temperature that is a function of the autoclave pressure. The vapor moves and condenses on the surface of the instruments that are being sterilized. The temperature of the liquid film that is formed by condensation on the instrument surface is the boiling temperature. The heat transferred by this evaporation-condensation is huge, in few seconds the surface of the sterilized instruments get close to the saturation temperature and in few minute instruments are homogeneously heated.
What would happen if the steam was overheated without pressurization.
Liquid water boils at 100°C and then a heater in the gaz phase overheat this vapor. The steam reach the instrument and condense. But the temperature of the liquid film that is formed on the instrument is still the saturation temperature: 100°C, not more. So in few seconds the instrument surface reaches 100°C. After a few minutes, the instrument reach an homogeneous temperature of 100°C. Then start a second and slow phase: the condensed liquid films dries, then the instrument get heated by the overheated steam through natural convection, and this is very slow. It would take hours for the instrument to reach the steam temperature.


text:
in order to align genome multi-fasta files, do you ignore the chromosome sections?
I want to test my implementation of Needleman-Wunsch on two fasta files downloaded from https://hgdownload.soe.ucsc.edu/.
However, fasta files on this site are multi-fasta and therefore are split into sections each one belonging to a chromosome.
If I want to align the entire genomes in these files:

do I just ignore the chromosomal separation inside these files? thus do I stitch the chromosomes of each file into one big chunk?
or do I align combinations of these chromosomes?

If the fasta really are chromosomes, there will be one per chomosome. Check this in case the multi-fasta you have is an incomplete sequencing of an organism. There is a bioinformatics site on Stackexchange now at https://bioinformatics.stackexchange.com

Chromosomes do not form one continuous genome, so I would suggest creating a separate alignment for each chromosome.

If the fasta really are chromosomes, there will be one per chomosome. Check this in case the multi-fasta you have is an incomplete sequencing of an organism. If incomplete there will be many more fasta. There is a bioinformatics site on Stackexchange now at https://bioinformatics.stackexchange.com .You would get better answers there.


text:
How are proteins containing other elements encoded?
If I understand correctly, proteins are formed by associating each three-letter DNA sequence  to a certain amino acid. Yet there seem to be proteins which contain elements such as copper, which isn't present in any of the amino acids. How are these encoded?

Those are called cofactors and they are not coded for.

Thanks! What causes the cofactors to attach to the protein, though? Is it a certain sequence of amino acids that chemically reacts with them to bond them to the protein?

Essentially yes, though their need not be a chemical reaction. Molecules can bind one another through various intermolecular interactions. It’s also not so much the sequence of amino acids that is important but rather their spatial organization (which, albeit, does depend in large part on the sequence).

Let's use an example, a case in point: the best known and plentiful one would be hemoglobin. It is a protein formed through the association of alpha- and beta-globin peptides into dimers or tetramers. The shape is largely a result of the sequence (peptide folding is reproducible, especially with the help of chaperones which may aid the correct folding process) and they fulfill their function by making use of an iron atom which they capture allow for their oxygen-carrying capacity. The iron is not encoded (since it's not an amino acid) but the sequence certainly determines the ability for globins to come together and sequester iron. If you wish, you could mutate the sequence to produce globins which would have reduced (or a complete inability) to use iron at their cores! The organism would be anemic, and depending on the extent of the effect, would be impaired or die.
Quoting the beta-globin gene page:

More than 10 mutations in the HBB gene have been found to cause
methemoglobinemia, beta-globin type, which is a condition that alters
the hemoglobin within red blood cells. These mutations often affect
the region of the protein that binds to heme [iron].

Lastly, a quick note on exactly how iron fits into the picture... inorganic iron can't simply be sequestered by the hemoglobin protein. The iron atom must first be covalently bound to form an organic compound called a heme group (see picture 1 below) which then acts as a 'prosthetic group' for the hemoglobin protein. When both enzymatic protein and prosthetic group come together, we jointly call them a holoenzyme, the complete unit which performs the oxygen capturing, carrying and releasing function inside red blood cells (see picture 2 below).

I think it would be helpful to clarify that it is the iron containing heme complex that is captured by the hemoglobin protein. Iron is not directly bound to the polypeptide ...

I've expanded based on your suggestion @tyersome.

Great! (+1) I would, however, encourage you to add credits for the diagrams ...

One can look at this in a wider context, however. Where does the Fe come from to associate with Fe-containing proteins? Is it present/available in all cells? Is there any special mechanism to get it to reticulocytes or their precursors? Never mind the proteins encoded by the urease operons in bacteria for importing nickel (if I remember correctly).


text:
Does epigenetics suggest there is at least some element of truth to Lamarckism?
I am not a biologist. But googling "epigenetics lamarck", I find many different opinions:

For: Lamarck rises from his grave, Epigenetics: Lamarck’s Revenge?, Darwin’s theory ... is incomplete without input from evolution’s anti-hero: Lamarck;
Against: One more time: no, epigenetics is not Lamarckism, Why epigenetics is not a vindication of Lamarckism.

This is highly confusing to laypersons such as myself and I'm hoping an expert here can explain to me why there seem to be such vehement disagreements on this matter.
Here's my simplistic layperson understanding of the matter:

Lamarck: Variations transmitted from parent to child can be influenced by the experiences of the parent.
Darwin: Lamarck is wrong, variations transmitted from parent to child are purely random and cannot be influenced by the experiences of the parent.

Based on my above simplistic understanding (correct me if I've made any errors), it seems to me that epigenetics suggests that there is at least some element of truth to Lamarckism. Am I mistaken?

This post is similar to [https://biology.stackexchange.com/questions/3789/can-epigenetic-changes-affect-reproductive-success].

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text:
How far up a limb can a severed artery retract?
This is about the application of tourniquets. I was taught a hand width above wound, but recently I read severd arteries can in some cases retract higher than that which would then bleed into the arm.
Doesn't matter if cut or tear, and if the limb is torn off or just the artery cut through, but on arms and legs, how far up can it retract?

Welcome to SE Biology! You may consider posting this question to SE Medical Sciences instead (https://medicalsciences.stackexchange.com/), where it would be more appropriate and you will likely get better answers.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. I’m voting to close this question because it seems more appropriate for [MedicalSciences.SE] (please don't repost — instead request migration). Thanks!


text:
Delta G and Temperature
I'm now designing primers for PCR. I use Oligo analyzer to check the primer secondary structures.
Ex: Delta G:  -4.16 kcal/mole  Base Pairs: 4
5'        GCCGTCTAGCAGCACATAATG
            :  ||||  :
3' GTAATACACGACGATCTGCCG

So my question is with delta G = -4.16, how do I know how much temperature degree can break these bonds?


text:
What is this red orange insect with black dots found in Japan?
I searched with picture to Google, and they suggest it might be

Fire-coloured beetle

I also went through the list of insects from this page, http://www7a.biglobe.ne.jp/~yabuyama/koucyuumoku.html, it is in Japanese. The bug that looked like the one in picture the most was a ベニカミキリ (latin name: Purpuricenus temminckii), but it did not have the black dots, and it seems too small.
The insect was found near a pond in a Japanese garden in Fukuoka, Kyushu in June. I do not recall the size of it, but I think it was somewhere between 1cm and 3cm long.

I was able to find it in an insect lexicon. It is all in Japanese, but the description fits the image. The insect is in fact a カミキリ、a ホシべ二カミキリto be exact. And the binomial name is Eupromus ruber

Here is also some more information https://www.insects.jp/kon-kamihosibeni.htm
And a Wiki page in english https://en.m.wikipedia.org/wiki/Eupromus_ruber


text:
Are there animals that have evolved a resistance to human activity or encroachment?
There are countless sources, both peer-reviewed and popular, explaining how overuse and misuse of antibiotics is breeding a new generation of antibiotic-resistant "superbugs" such as MRSA (Methicillin-resistant Staphylococcus aureus) and MDR-TB (multidrug-resistant Tuberculosis). Over in the animal kingdom, the opposite seems to be happening - species after species is becoming endangered and/or extinct as humans destroy or alter their habitat through increased hunting, farming, construction, etc.
Are there any non-human animals that have been found to have evolved resistance to human encroachment into or alteration of their habitat in a way analogous to how bacteria have evolved resistance to human attempts to get rid of them? For example, this could consist of:

an animal that has adapted stronger bones to better survive collisions with vehicles
an animal that has significantly increased its blood coagulation rate to survive gunshot wounds from hunters
an animal that has developed better vision to see in urban environments
an animal that has evolved a skin pigment change that enables them to not take as much damage when they are sprayed with agricultural pesticides

One answer that came to mind is domestic animals - the horse and dog in prehistory, the cat in ancient Egypt, etc. That seems too obvious on one hand, and on the other hand may not really be an answer, as there seems to be no indication that pre-domestic animals were endangered by humans in any meaningful way. Are there animals that have significantly adapted themselves to surviving as wild animals in human-influenced environments?

Welcome to Biology.SE! Is there any reason to exclude the numerous "pest" species (e.g.s: cockroaches, mice, rats) that often "share" our homes?

"Evolved" is rather tricky, but there are a number of species that live happily in places densely populated by humans: pigeons, the urban peregrine falcons that nest on skyscrapere & prey on them, urban coyotes, bears that feed on trash, even the occasional mountain lion that comes into town to visit the casinos: https://www.kcra.com/article/a-mountain-lion-in-a-casino-don-t-roulette-out/6398674#

@tyersome thanks, and not really. An example of cockroach or rat evolution could be an answer, but I'm looking for cases in which the organism has clearly developed a notable adaptation that it didn't have (or that at least was rare) before, rather than cases of animals that have more or less always been pests. For example, if there is a paper showing that certain varieties of cockroaches in North America developed bleach resistance between 1830 and 1870 as a result of its use as a pesticide, that would be an answer.

By excluding cats, you're excluding what is possibly the clearest example.  Cats don't fit the normal profile of domesticated animals -- you can't tame a cat the way you can tame a dog or a horse.  One explanation for this is that cats weren't domesticated.  Instead, they evolved to fit into an agrarian society.

An example given in "Guns, Germs and Steel" is the simple observation that megafauna extinctions were near total anywhere humans first arrived as fully evolved homo sapiens, but significantly less extreme anywhere humans had been co-evolving with the local megafauna (in particular Africa, to a lesser extent across Eurasia). We can't say precisely what attributes and behaviors African/Eurasian megafauna evolved that American/Australian megafauna did not, but the historical evidence suggests that simply having time to co-evolve to deal with humans helped a lot. "Fear of humans" seems likely.

There are some good examples of behavioural adaptations to urban environments listed here: https://www.independent.co.uk/news/science/why-did-the-hedgehog-not-cross-the-road-because-it-had-adapted-its-behaviour-in-order-to-thrive-in-a-8527825.html

Does "becoming cuter so humans will protect you instead of hunt you" count?

Normally it takes many generations for genetic adaptation. But I realized through your question, that by removal (e.g. hunting) of a specific phenotype encoded with one dominant gene allele, that allele is removed as well. Unless one knows how a phenotype is encoded genetically, it is not possible to conclude that it was an evolutionary human encroachment with wildlife, i.e. whether the genome was changed or not.

An excellent example of physical adaptation is the American Cliff Swallow which appears to be evolving a shorter wingspan, enabling them to be more agile in traffic. I'd post this as an answer but bio.SE doesn't love me :(

@vsz yes, I think it does.

@RobertColumbia : they I guess cats will count...

Note: This is an answer to the last line of your question.
A classical example of animals adapting to the influence of humans on their environment is the adaption of the Peppered Moth.
Here is a brief summary:
The peppered moth was originally a mostly unpigmented animal (<1800). During the industrial revolution in the southern parts of the UK a lot of coal was burned. This led to soot blackening the countryside. Soon afterwards, a fully pigmented variety was first observed. Only a hundred years later, in 1895, this pigmented variety almost completely displaced the unpigmented variety.
It has been shown that the pigmentation is under strong selective pressure as birds hunt these moths. Since birds rely on their visual system to detect their prey, the variety that blends in with its environment (=camouflage) has a selective advantage over the variety that stands out.
As pointed out by Tim in the comments, since the 1970s there has been a rapid reversal with unpigmented animals being more abundant. As far as I understand, it is accepted that this reversal is due to a decrease in human induced air pollution leading to less sooty barks on trees which makes the unpigmented variety harder to prey upon.
Addendum: genetic basis of adaption
In a beautiful recent study, the causal mutation for the pigmented, or melanic, variety was identified: A ~9kb transposon insertion in the first intron of the gene cortex. The authors calculate that this mutation happened in the year 1819, a few years after the industrial revolution was in full swing. The interpretation is that due to sooty tree bark this mutation, causing pigmented moth, was under strong selection.

This is a famous example of observed evolution. The early research had a couple of hiccups, but plenty of other research has verified it. +1

This is a famous example of natural selection.  One should take care about equating that with evolution, which includes genetic mutation as an essential component.  As far as I am aware, the peppered moth case has not been shown to have involved introduction of new or variant genes, but rather just environmental factors favoring a previously rare phenotype.

@JohnBollinger, the authors of this recent paper (https://www.nature.com/articles/nature17951) find that a transposable element in the 'cortex' gene is causal for the pigmented moth variety. They calculate that the insertion happened around 1819 when the industrial revolution was well underway. I don't want to overload the answer - do you think it would make sense adding to the answer as an addendum?

That's (obviously) news to me, @dtadres. In any case, I was primarily responding to your first comment, not directly to the answer, which presently does a smooth job of avoiding the question of how to label the phenomenon it describes.  I think it's doubtful that the OP cares much about the distinction, so I think the answer is fine as it is, but if you want to add an addendum referring to the paper then I don't think it would be overbearing.

Many insects (as well as some other animals) have documented resistance to pesticides.
For example, the German cockroach (Blattella germanica) can be resistant to multiple insecticides1. In addition, some populations of this cockroach are now repelled by glucose, which leads to them avoiding traps2.
References:
1: Fardisi, M., Gondhalekar, A. D., Ashbrook, A. R., & Scharf, M. E. (2019). Rapid evolutionary responses to insecticide resistance management interventions by the German cockroach (Blattella germanica L.). Scientific reports, 9(1), 8292.
2: Wada-Katsumata, A., Silverman, J., & Schal, C. (2013). Changes in taste neurons support the emergence of an adaptive behavior in cockroaches. Science, 340(6135), 972-975.

Bighorn sheep are developing smaller horns and elephants are becoming tuskless in Africa:

The horns of some bighorn sheep are getting smaller, because hunters are picking off the most impressive rams before they reach their breeding peak
Elephant poaching, for example, is thought to have led to an increase in the number of tuskless animals in Africa.

Source

Though it's an interesting question whether these statistical adaptations represent survival benefit for the populations.

Rattlesnakes in the southwest US are learning to stay quiet around humans so they don't get shot.

Nightingales have adapted to city noises by singing louder. Given that one function of singing is finding a mate there must indeed be a high, direct selection pressure to make oneself heard. Other birds have adapted in a similar fashion, e.g. by singing in a higher pitch, or at different times.

Not so much physical changes, but changes in behavior caused by human activity has numerous examples.
Foxes, pigeons, sea-gulls adapt very well to city life. Some species nowadays have larger  numbers in cities than in the country side.
Polar bears are another good example. Disappearing sea-ice and increased human activity in the Artic has turned many polar bears into pre-dominantly garbage scavengers in stead of hunters/carrion-eaters.

Is the polar bear adaptation really due to evolution? Have there really been enough generations to allow this to happen? I suspect they're just naturally flexible enough that they've been able to alter their behavior. Kind of like how human society has suddenly adapted to Coronavirus.

@Barmar That’s the question isn’t it. Polar bears are opportunistic scavengers, but in what degree this is evolution? It’s probably too recent to say for sure. Another thing about polar bears: they are moving South and come in ranges where regular brown bears live. Hybrids are becoming ever more common. These hybrids are apparently fertile with polar and brown bears leading to the question if polar bears are actually a separate species or just a local color variant of the brown bear. Biologists can’t agree on that one.


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How much heat for how long to Kill RHDV?
Rabbit hemorrhagic disease is caused by the Virus RHDV.  There are two verisions V1 & V2.
It is extremely devastating to both pet and wild rabbits.  With fatality rates reports of 75%+.
It is currently devastating rabbit populations in the US. There are a number of vaccines but non-are approved for use in the US.
I have been reading up about it and found this claim in a few places.

RHDV is also reported to survive exposure to pH 3.0, heat of 50°C (122°F) for an hour Source

.

It survives heat of 122F for one hour. source & source

My question is: How much heat for how long will kill RHDV?

Often, in studies of viral infection, heat-inactivated viral stocks are used as a non-infectious control.  See Matthaei et al. 2014 1 for an explanation of how such a stock was prepared for RHDV:

Heat-inactivated RHDV stock was generated by incubating the virus preparation in 2 ml screw cap tubes for 180 s at 85°C in a water bath to ensure a drop in infectious virus of more than 99.9%

The methods section for that paper cites a study by Duizer et al. 2 on the inactivation of caliciviruses (which include RHDV).  Therein, the authors tested the heat inactivation of canine calicivirus no. 48 (CaCV) and feline calicivirus F9 (FeCV) at 4, 20, 27, 37, 56, 63, 71.3, and 100°C for time periods varying from weeks (4°C) to seconds (71.3 and 100°C):

Times required at different temperatures to achieve a 3 log10 reduction in viable virus titer (TCID50) in DMEM (3 to 4 μg of protein/ml).

Note that, in both studies, viral heat inactivation is carried out in liquid culture, where it is easy to obtain a uniform temperature by mixing.  For heat inactivation of RHDV on food/hay, rate and uniformity of heating will be different.
Citations

Matthaei M, Kerr PJ, Read AJ, et al. Comparative quantitative monitoring of rabbit haemorrhagic disease viruses in rabbit kittens. Virol J. 2014;11:109.
Duizer E, Bijkerk P, Rockx B, De Groot A, Twisk F, Koopmans M. Inactivation of caliciviruses. Appl Environ Microbiol. 2004;70(8):4538-4543.


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What kind of snakes are in this photo?
What is the name of these snakes? I saw them in the street and I don't know if they are dangerous for people? Photo is taken near to Tbilisi, Georgia.

Welcome to Biology.SE! Identifications questions should include: 1) the species-identification tag; 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information; and 4) an estimate of the size of the organism. Please [edit] your post to include this information as it can be essential for a proper identification. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

@tyersome why do you keep downvoting me? What kind of information are you looking for? The OP only provided a photo and a location. That means identification must rely on appearance and location and can be easily verified by examining other photos of the putative species.

Based on the species description in Speybroeck et al. 2016 and pattern of stripes (one central stripe with stripes on each side), and the lack of a distinct neck, the specimen in the top left appears to be an Eastern slow worm (Anguis colchica). That species is known to occur in Tbilisi.
Based on the species description in Speybroeck et al. 2016 a smooth snake (Coronella austriaca), also known from Tbilisi. The reddish color, two rows of dark spots, and the markings on the head are typical of this species. Also it can be seen that the anal scales are divided, which is a characteristic of this species.
Cited
Speybroeck et al. 2016. Field Guide to the Amphibians and Reptiles of Britain and Europe. Bloomsbury Natural History (publ).

I haven't downvoted this answer! I may have downvoted other posts by you, but I almost always post a comment before I downvote. ——— This answer looks OK to me, but please make sure that you credit image sources. Another improvement would be to include complete reference information — an easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references.

Also note that it costs reputation to downvote answers, so if you are getting a lot of downvotes on answers that suggests that you might also want to revisit some of your other posts and see if they also can be improved. The [tour] and [help] pages such as [Answer] should provide guidance and you can also consult on [meta]. ——— Note that moderators put up the banners; therefore at least one has felt your post lacked sufficient references, but I think that was before your recent edits. Hope this helps!

Does Stack Biology fancy itself a kind of scientific journal, where people publish the results of research and provide references to back up claims? Or is it simply a public forum where knowledgeable people can share their knowledge with less experienced people in an open informal exchange? I thought it was the latter but it seems to have become the former.


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how to culture mc38 cells
I work at a start up company in a vivarium. My boss would like me to start working with MC38 Cells. I bought all of the equipment (recommended by a colleague) and should be ready for the cells. Could anyone recommend a good place to learn how to do this fast? He has surprised me and already ordered the cells. I do have some knowledge on the subject ( from bachelors degree in Biology), but it is not enough. I need somewhere that can teach me even the little steps. I have tried looking at scientific papers, but they typically skip over much of the steps that are common knowledge (to most).

actually, this question may be a duplicate of this question: https://biology.stackexchange.com/questions/36255/textbook-lab-manual-for-mammalian-cell-culture.

Does this answer your question? Textbook/lab manual for mammalian cell culture

Edit: Similar questions have been asked before: Textbook/lab manual for mammalian cell culture
Cell culture reagent/consumables suppliers can have good step by step recommendations for how to use their products. For example Thermo has some guidelines that you may find helpful. Specifically, cell culture maintenance would seem to be helpful.
These folks also have what superficially look like good resources.
Reviewing MC38 culture requirements is also always a good idea.
Good luck!


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Is there a proton gradient across the cell membrane, just like for the mitochondrial membrane?
Mitochondria have a proton gradient, is there also a proton gradient between cells and the extracellular medium?

Welcome to Biology.SE! Please provide more detail — are you only interested in proton gradients or also other electrochemical gradients? In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, since it appears you can easily answer this using reliable sources online this question seems to fit this sites criteria for "homework". (Note this can apply to questions not assigned as homework.) Thanks!

Cell has potassium and sodium gradients obviously. I am not asking about chemical gradients in general. The question is on if there are proton gradients between cells and extracellular fluid.

That's not answered on your link there. So, you can edit your comment and remove that part.

Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Comments are ephemeral and often unread. ———— I recommend that you delete "similar gradient" from your post or otherwise make clear in the body that you only care about proton gradients. In addition, if you aren't interested in the somewhat trivial answer that many (maybe all?) bacteria (e.g. the ancestors of mitochondria) create a proton gradient you will want to specify what types of cells you do care about.

And your name is Mitchell! (At least that’s my hypothesis.) So ask yourself (or research) how the proton gradient is produced, and why. And then consider whether what you propose would be likely

@tyersome Yes, bacteria have proton gradients. Question on eukaryotic cells mainly, could have specified that but it's in some way implied since it compares "the cell" to mitochondria.


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Will ammonia continue to accumulate in an aquarium tank if a strong antibacterial or chlorine is added to the water?
I've always wondered what would happen if dead plants and fecal matter lay in chlorinated waters and/or waters treated with strong antibacterials or antibiotics.
I've heard that aquarium tanks owners warn against using strong antibiotics as it can kill nitrifying bacteria which convert toxic ammonia to a safer form of nitrate. Otherwise, ammonia levels can buildup and be toxic to the aquatic life in the tank.
However, that doesn't make sense to me. Even if the nitrifying bacteria die, wouldn't the ammonifying bacteria which produce ammonia in the first place also die? Would there be greater amounts of ammonia in the water after these agents are repeatedly used, or would ammonia levels with nitrate levels together fall significantly?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, I think you find that learning about how fish excrete nitrogen will be illuminating! Thanks!

A very large part of the bacteria and fungi will die so very few biological processes will continue in the tank if you add chlorine or antibacterial chemicals.
Ammonia will slowly outgas from the water oxygen and CO2 will reach equilibrium in the water as little oxygen is used and little CO2 is produced, it is the same with the other atmospheric gasses.
Life in the tank will simply stop until the toxins are broken down or removed,by toxins i mean chlorine and/or antibacterial chemicals.
Nitrate level will not change as little is produced and little is used, any denitrification will stop too.
Denitrification can only happen in an anaerobic environment but denitrfying bacteria too are killed by chlorine and antibacterial chemicals.


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Do viruses pickup new genetic sequences from the host cell?
Virus replication does not involve meiosis so the virus genome does not gain diversity from having two parents , so other than from mutation, do viruses obtain new genetic sequences from the host cell ?
Do virus genomes show evidence of containing base pair sequences which originated from host cell ?

look up the term "mutation" that is the source for new genetic sequences in sexual species as well.

Yes, it does seem that a virus can pick up transposable elements from the host — you may be interested in this related question: https://biology.stackexchange.com/questions/92829/do-any-known-viruses-contain-junk-or-parasitic-genomic-information

Yes.  See for example this article, which describes how some viruses can pick up bits of human DNA.  Here's a quote from the article:

...researchers have shown that a large group of viruses, including the influenza viruses and other serious pathogens, steal genetic signals from their hosts to expand their own genomes.

I really like that you gave an answer, but an appropriate quote from the article would make this answer soooo much better, earn you upvotes, and defeat the effects of a broken link.

OK, added a quote.  When I tested the link, it worked.  Is it broken from your perspective?

Nope. Perfect !

“Steal genetic signals” Obviously a case for the local constabulary.

It gets worse. The article in question reckons “they steal our genetic code”. Are you sure it isn’t a tweet from that flatulent person?


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Origins of transcription factors and RNA Polymerase
I was learning about transcription factors and RNA polymerase from Khan Academy to supplement Dr. Robert Sapolsky's lectures on Human Behavioral Biology. As I understand:

RNA Polymerase transcribes DNA to RNA
Transcription factors are proteins that help the RNA Polymerase bind or inhibit it from binding to the DNA and transcribe it to RNA
Transcription factors called activators help RNA Polymerase bind to the DNA
Transcription factors called repressors prevent RNA Polymerase from binding to the DNA

It seems like we need transcription factors and RNA Polymerase to express genes and produce their corresponding proteins. But transcription factors and RNA Polymerase are proteins themselves. Thus, they must have come from their own respective genes. This seems like a "chicken and egg" problem.
How did early organisms with genetic material get around this problem?

You might look into the transition between the RNA and DNA world: https://www.ncbi.nlm.nih.gov/books/NBK6360/

This is one of the main features of the RNA World.
What I mean by that is, RNA not only acts as a repository of genetic information, it also acts as an enzyme. This enzyme is known as Ribozyme. Ribozyme confers a self-replicating property to RNA, leading to the hypothesis that RNA might be the ancestor to the present day self-replicating genetic material.

The word ribozyme just means “RNA enzyme”. It does not define the catalytic function of the RNA. You are correct in implying that the RNA world hypothesis suggests that an RNA ur-genome might have been able to replicate itself without a protein RNA polymerase. However I am not aware of any contemporary ribozyme with this ability. Are you? Most seem to be nucleases or RNA ligases.


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What is the Icosahedral Matrices?
This website introduces the "Icosahedral Matrices".

What are the locations of the other half?

It only shows around 30 numbers of the 60 facets. So how to know the other 30 numbers on the back?

The 60 transformation matrices are shown below in the website. Are they rotational matrices? What are the exact meaning of those 9 numbers for a particular matrix? For example,

Welcome to Biology.SE! I’m voting to close this question because it is much more likely to get answered on other SE sites, like Mathematics.SE. If you want to transfer this question to another site, please request migration instead of reposting. Thanks :)

Thank you for your advice. If possible, can we wait for a few days? It is an interdisciplinary question. And I think the virologists are more likely to answer it.

Sure! Closing a question requires 5 votes; that would give plenty of time for others to see and possibly answer it.


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How to fit simulated with measured data having systematic errors?
Consider a given time series of measured data, i.e. the number of persons tested positive for COVID-19. And consider a simulation - consisting of a model, possibly fed with some parameters estimated a priori (not via the measured data) - which gives another time series.
More often than not these two time series won't fit at once. But the goal of a simulation usually is to have a fit with measured data, and finally one wants to show: "See, these two histograms do match essentially."
That they don't match may have two reasons:

the measured data are erroneous (possibly in a systematic way) and/or
the model and/or the estimated parameters are erroneous

Assuming that the model is roughly correct (i.e. an advanced SEIR model) what are acceptable ways to "explain away" the gap between measured and simulated data?
The measured data may have two sources of error that are known in principle but not quantitatively:

a reporting delay (which includes incubation and latency time, time for testing, and time for proper reporting), giving rise to a shift of data.
a dark figure (i.e. cases that were not detected, falsely attributed, or false negative or positive cases), giving rise to typically lower values of the measured data (than in reality).

What is the "right way" to reflect these sources of errors, especially when drawing diagrams?

First correct and adjust the measured histogram, assuming some estimated reporting delays and dark figures, and then compare the corrected histogram with the simulated histogram?
First adjust the simulated data in a reciprocal way (by artificially adding some fictuous estimated reporting delay and dark figures) and then compare adjusted histogram with the non-corrected histogram of measured data?

Is one of these the one and only "good practice" - or are both or none of them scientifically tenable.

This is an interesting question, though I think you're more likely to get a rigorous answer addressing your problems (time series modeling, error correction) on stats.SE, no? The bits of your question concerning COVID could be removed without changing the meaning.

Am I understanding the question correctly: to remove errors, should changes be made to the stimulated model or to the data? Wouldn't it depend on the phenomena you are trying to model, and what the sources of error are? Like here, both the mentioned errors appear to be due to the data, not the epidemic that you're modelling.

@AP2261: You are understanding correctly. And yes, you are right: both errors are due to the data, but they are only examples. Possible sources of errors of the model are countless.