text:
Inbreeding of selfing and outcrossing plant
I am reading John H. Gillespie's Population Genetics A Concise Guide Section 4.3 Inbreeding. I do not understand these two paragraphs quoted below concerning selfing and outcrossing.

The first paragraph states that an outcrosser individual leaves behind on average two gametes one in an ovule and the other in a pollen.

The second paragraph states that a mutant selfer will leave behind three gametes for every two of the outcrossing plants, with two in its selfed offspring and one in its outcrossed offspring.

What are the effect of the ovules and pollen here? How are these two statistical conclusions drawn? I would like to have a very detailed explanation.

Some interesting evolutionary questions arise with species that are capable
of both selfing and outcrossing. For example, in many plant species there is
an intrinsic advantage to selfing, which leads to the evolutionary conundrum:
Why don't all plant species self? The situation is illustrated in Figure 4.4. The
outcrossing pedigree on the right represents a typical individual in an outcrossing population of constant size. This individual leaves behind, on average, two gametes, one carried in an ovule and the other in a pollen grain. These gametes appear as filled circles in the figure.

Figure 4.4: The gametes produced by a selfer and an outcrosser. The p to the right of
an arrow indicates that the parent’s contribution came from pollen; an o indicates it
came from an ovule. The filled circles represent gametes from the illustrated parents;
the open circles represent gametes chosen at random from the gamete pool.
Suppose a mutant appears that self-fertilizes all of its ovules, M illustrated
on the left side of the figure. Suppose also that there is enough pollen in each
individual of this species that the few grains needed for self-pollination by the
mutant represent a small fraction of the total pollen. As a consequence, the
selfing mutant has essentially the same quantity of pollen available for outcrossing as does a nonselfing individual. All else being equal, the selfing mutant will leave behind three gametes for every two of the outcrossing plants, as indicated by the three filled circles in the figure. Two of the gametes are in its selfed offspring; one is in its outcrossed offspring. Thus, the mutant should increase in frequency, perhaps leading to the establishment of selfing as the usual mode of reproduction.

I don't think it's a terribly rigorous statistical argument, so much as a toy model arguing that there can be a reproductive advantage to selfing in an outcrossing population. Here is the logic as I see it:

Ovule and pollen represent the female and the male reproductive gametes in a monoecious plant (monoecious means that it has both male and female reproductive organs in the same individual).
In sexual organisms that do standard sex (i.e. not a complicated variety of sex), both ovule and pollen (gametes) are necessary to generate a fertilized offspring (zygote).
In outcrossing individuals, pollen is broadcast to fertilize other individuals (1 pollen gamete) and ovules receive pollen from other individuals (1 ovule gamete). Total: 2 gametes
In selfing individuals in an outcrossing population, selfing individuals guarantee that they fertilize their own ovules. Thus, they replace the pollen of other individuals (1 pollen gamete + 1 ovule gamete).
Selfing individuals still broadcast pollen to fertilize other outcrossing individuals (+1 pollen gamete). Total: 3 gametes

The key is in looking at the figure and understanding what it's arguing.
Again, these are not really rigorous ratios, details will be determined by exact biology of any case in real life. As far as I can tell from the text, the argument is not "these are the exact ratios in all organisms", but rather that "selfing gives the advantage that a selfer contributes all of the same gametes as the outcrosser, plus the male gametes to fertilize its own male gametes".
Secondary note: this model is only true when the proportion of selfers in the outcrossing population is very small. Note that as the proportion of selfers increases, everyone is just fertilizing their own ovules, and the net contribution goes back down to 2 gametes per generation. So this does not describe an equilibrium case for population composition. [As noted in comments, it is likely the case that it is equilibrium for population size, e.g. number of individuals.]
For more theory about this, you can read about the evolution of self-(in)compatibility. Here is a somewhat recent review. Evolution of self-compatibility in plants is extremely dynamic, as you might expect from the arms-race aspect.
Update:
Pulling up some notes from the comments on the assumptions of the model:

I think that this example works when population number is at equilibrium, but population composition (e.g. selfers vs. outcrossers) might not be at equilibrium.
I think that for the amount of pollen, we have to assume that all organisms contribute an equal, infinite amount of pollen. So selfers fertilize their own, and then also dump pollen into a pool into which outcrossers also dump infinite pollen.
However, there are only a few ovules; every individual contributes one. That is, outcrossers and selfers contribute one ovule per individual.
On average, everyone's pollen will be sampled roughly once (actually a little less) if every non-selfed ovule takes one pollen from an infinite pollen pool of uniform composition.
As number of selfers in the population increases, less and less of the common pool of pollen will be sampled.
If everyone in the population is a selfer, there will obviously be no outcrossing, because everyone just fertilizes their own ovule. This is the equilibrium state, if selfing is heritable and this stated advantage to selfing holds.

It is not very clear. Each plant has one ovule and multiple pollen. What prevents a selfer outcrosser from contributing more than one pollen and a outcrosser more than two pollen? It seems to me each plant can contribute as many pollen to it offsprings as it has. I suspect it is an argument for when the population is in some kind of equilibrium. But it is not clearly stated what equilibrium this is and how it is achieved. But you say it is not an equilibrium. So it is even less clear.

@Hans I think that this example works when population number is at equilibrium, but population composition (e.g. selfers vs. outcrossers) might not be at equilibrium. I think that for the amount of pollen, we have to assume that all organisms contribute an equal, infinite amount of pollen. So selfers fertilize their own, and then also dump pollen into a pool into which outcrossers also dump infinite pollen. However, there are only a few ovules. On average, everyone's pollen will be sampled roughly once if everyone takes one pollen from an infinite pollen pool of uniform composition.

I think the key is that a selfer preserves its phenotype while an outcrosser does not. The selfers' pollen "invade" the offsprings of outcrossers. The specific numbers in gametes 2 and 3 are misleading. Also it needs further constraints to make the argument stand. I suppose we need to assume that each plant produces the same number of ovules and, as you say, the same large number of pollen. The proportion of ovules from the outcrossers pollinated by the selfers is proportional to the proportion of the selfers amongst the whole population in the last generation.

+1 for your informative answer. In case you have not noticed, I have pasted text of the quotation from the textbook to my question instead of the screenshot.

Ok, appreciated. I don't use a screen reader but it is supposed to be very helpful in general. I'll edit the answer.


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Which modern methods of antibiotic production are there?
For my seminar paper in the field of biology, I have to collect modern methods of antibiotic production. The topic is a little overwhelming, but the work should also be quite extensive (approx. 18 pages).
I've already done some research, but most of the results don't help me. I would be very grateful for a few web links and keywords that I could research for in order to break down the topic.
I will visit the university library in the next few days. It would help me a lot if someone could recommend a few good books references.

Are you interested in antibiotic production (so via chemical synthesis, metabolic engineering of microrganisms or fungi, etc..) or antibiotic R&D (compounds library screening, drug design, protein-protein interactions..) ?

I remember being told that making antibiotics against gram negative bacteria is a little bit more challenging than gram positive due to outer membrane differences. As such I'd recommend reading this paper which is great (Predictive compound accumulation rules yield a broad-spectrum antibiotic): https://www.nature.com/articles/nature22308 They dissect the efficacy of antibiotics for gram negative bacteria by outlining certain requirements, such as rigidity, globularity, presence of amine groups, and amphiphilicity. Also molecular weight, and polarity play a role.

For Penicillin production try from page 165 of:
Industrial Microbiology: An Introduction
by
Michael J. Waites
Neil L. Morgan
John S. Rockey
Gary Higton
There is also a table in that chapter listing the other antibiotics and which organisms are used to produce the basic form.
I found it very readable.

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How do Helper T cells activate Cytotoxic T cells?
Helper T  cells activate the Antigen-presenting Cells (APCs) through their secretions (the cytokines) (although the T cell in question gets activated in turn). This is typically achieved by cell-to-cell contact using  receptors on both the helper T
cell and APC.
Since Helper T cells also activate Cytotoxic T
cells, I am particularly interested in knowing whether cell-to-cell contact occurs between these two T cell subtypes (as is the case in helper T cell - APC communication).

So, are you asking about whether there's physical contact between CD4+ and CD8+ T cells?

@MattDMo Yes, that is exactly what I'm asking

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text:
Is there any ethnicity difference in average pupil size?
I have seen some articles claim African Americans have smaller average pupils than whites while Asians have larger pupils. Is it true?
link:
Y. Li, D. Huang; Pupil Size and Iris Thickness Difference Between Asians and Caucasians Measured by Optical Coherence Tomography. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5785.

if you've "seen some articles", it would be good to cite them/give links in your question ...

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 particular, we expect you to demonstrate that you have done 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 this case, I suggest finding and providing references to any primary research that supports these claims. Thanks!

Please also include the complete reference information since links can (and do) break. One 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.

Note nowhere does it say they controlled for height, which is not equally distributed. A control for different heights would be important. A comparison based on latitude for a developmental effect would also be useful.


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Fate of antigen-presenting cells after antigen presentation to Helper T cells
In many texts, the Antigen-presenting cells (APCs) that initiate helper T cell responses are often "forgotten" after their antigen presentation function is discussed.
I have been wondering how the antigens in these cells are destroyed since they are complexed to MHC II protein (not MHC I).
Yes, the macrophages can receive additional signals from already activated helper T cells to destroy the pathogens harboured in their cytosol, but what about B cells and Dendritic cells which lack such abilities?

In Janeway it's being said without further explanation (I will edit and add reference)   that B-cells and macrophages "become targets" of cytotoxic T-cells after these killer cells have become activated, have been primed. However, this answers your question only if presentation on MHCII (not I) implies that presentation on MHCI has occurred as well. Only then APCs that present to T helper will be targeted by cytotoxic T cells and die. According to my basic knowledge that is the case with Dendritic cells and Macrophages. According to the explanatory text of your question Macrophages only receive signals to kill pathogens they include. Your inference may be correct that they cannot become target of T-cytotoxic cells. It is beyond your question to ask if Macrophages always do get that signal. If no that puts them into the same category as Dendritic APCs.
Understanding that there exists a signal to survive (destruction of phagocytoses pathogens) leads the way to understanding that there is cell death without killing by Tc cells:  cells that present antigens to T helper cells will "apoptotically" die because they have been infected, if not killed by immune cells to prevent the production and shedding of virions. According to my basic knowledge it is coherent  that a cell presenting is a cell sentenced to apoptosis. Killing by T cells is killing at an earlier stage only.
However, I found no reference that explicitly confirms that - maybe with very few exceptions -  that B cells do present on MHCI, to the contrary I found reference - I promise to add this one link quite soon - that explicitly states that B cells only endocytose debris, "protein" (in the sense of protein vaccination) i.e. isolated antigen, not whole virous. Thus, any antigen they present would be on MHC II, not I, as the antigen is not "endogeneous", not produced by the B cell as it has not become infected. This inference from basic textbook knowledge is supported, in this context, by the fact that B cells, just as T cells - which they are thought of as of one and the same category, the Lymphcytes - should not be killed after presentation (whereas T8, cytotoxic T cells do not present at all) as parallel to killing of T cells they still have their job to do: presentation activates the B cells which start to divide and produce antibody.
Consequently, it matters if a B cell not presenting on MHCI, thus not being killed by Tc cells, is sentenced to apoptosis and cell death because it has engulfed the antigen. In my opinion B cells - and I will add any reference to the contrary - not even need, as Macrophages, a signal to survive, as they cope with antigen alone and there is no interference with their regular by viral infection. (However cells hosting active HIV produce protein for viral ends for a long time before they finally die, but this is different.)
To sum up:

Dendritic cells present on MHCII and I, hence killed  by Tc cells or dying by apoptosis

Macrophages present on MHII and I, but according to textbook different to Dendritic cells have the option or are programmed to receive a survival signal to consume the pathogens they harbour

B cells present on MHCII and, according to my understanding: maybe, on MHCI, which would put them too in category 1: same fate as Dendritic cells, however basic knowledge coherently applied speaks in favor for B cells regularly not presenting on MHCI, not getting killed by Tc cells and not undergoing apoptosis as not "infected" by whole virus

So my own personal answer on B cells based on basic textbook knowledge and lack of explicit statements to the contrary might be very different from the answer regarding dendritic cells (and macrophages, see explanatory text of your question).
The B cells do not die after presenting to T Helper cells.


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Would an enrichment of pyrimidine runs of two of more nucleotides be an early indicator of DNA to be damaged?
I am analysing two categories of protein coding genes comparing their relative characteristics. What I am observing is that one of these, in comparison to the other, is enriched in pyrimidine runs (two ore more consecutive pyrimidines). I have counted the number of these runs (I do not call them dimers because I have no data underlining a cross-link between two or more pyrimidine bases) per protein coding-gene performing then a Mann Whitney test that indicates that one of these two group of genes is enriched with respect to the other. I am hypothesising that this enrichment could be an early indicator of DNA to undergo local conformation changes. By your experience, could this hypothesis be reliable or I am totally misleading what I am observing?

I find it difficult to understand your question. You talk about comparing proteins but refer to the nucleic acid base pyrimidine. Are you talking about the DNA sequences of their genes? If so, two consecutive pyrimidines are extremely common as they occur in 24 of the 64 codons. And when you say “categories” of proteins quite what do you mean by categories? The same protein in different organisms, protein kinases v. Immunoglobulins, or what? And you suddenly mention clusters — of what? You need to be much clearer if anyone is going to help you.

I edit my question you are right

Basically, I am comparing protein coding genes with and without tandem repeats investigating why we have in some these repetitions (at amino acid level) and why not in others. You pointed an important detail about codon usage that already helped me.


text:
Next Generation Sequencing False Negative
In Variant Detection, RNA-sequencing, and ChIP-sequencing, we showed how we matching, or aligning, short NGS reads to the genome, and then make inference using the reads which aggregate or "pile up" at a given region: either to find a SNP, to quantify the amount of mRNA, or the quantify the amount of a protein which is bound to DNA. Define a "true positive" as detecting a SNP, detecting mRNA expression, or detecting a protein which is bound to DNA. Which of the following (you can pick more than one) could possibly lead to a false negative, e.g. we do not detect a true SNP, mRNA expression, or a bound protein at a location/region?
which one is the correct answer? why? (we can pick more than one)
1.The region we care about is not in the reference genome
2.The region we care about occurs 1000s of times in the genome, and we are ignoring reads which align to so many places
3.For the region we care about, the organism's genome is so different to the reference genome that the aligning program can't find a match
4.There are never false positives

Homework questions are received well when the asker shows an attempt to answer and explains their confusion.  Which answer(s) do you think is (are) correct, and why?

I think that the second and third ones are correct. because when the region occurs 1000s of times, the amount of aligning reads to each part results in decreasing numbers of possible aligning reads to only one specific region. and in addition, when the organism's genome is so different from the reference genome it could lead to a false conclusion of the alignments of the reads. I am not sure what is the difference between the first and third options!!? could you please help me with that? if my answers are incorrect ?

An example of 1) might be if you were looking for a mutation on the Y chromosome, but your reference sequence had only autosomes.
Read #2 a bit more carefully.  If there is a region repeated 1000 times in the genome, a lot of aligners are just throwing those reads away, on the grounds that you can't learn anything useful from them, and they will uselessly bloat the output files.  Diluting the coverage by splitting the read coverage will happen with some aligners if there are just a few places for the read to go, but not 1000.
Edit.  Let me try and make a better example.
You have a sample of an antibiotic resistant strain of some nasty bacteria.  This bacteria has some genes located on a plasmid.  Some other lab sequenced this bacteria and its plasmid; that's your reference.
You align your reads to your reference strain of bacteria, but oops, you accidently omitted the plasmid.  So your variant caller spotted no differences located in the plasmid.  If you were hasty and didn't check to see read coverage on the plasmid, you might assume that your sample's plasmid matched the reference, but you accidently didn't check that.
Next you get another antibiotic resistant sample.  You align it to your reference, and see no variants.  Okay, then, that's that...except that the reason you see no variants is because the people who gave you the sample misclassified it; it's really a different sub-species, and some regions of your reference are too different from your sample for the reads to align.
In general, you just have to remember that if your variant caller says there's no variant somewhere...that could also means there are no reads there.  In real life, people will do some QC on the read alignments stats to try and catch that.

so in your opinion, the first and the second one are the correct answers?

would you please explain about the third one? I cannot recognize the difference between this and the first one.

The first three choices can and do occur in genomics. For examples of each: genomes of cancerous cells involve translocations, which can create regions of the genome which do not occur in the reference genome. There are regions which occur 1000s of times in a genome, called transposons. Many software pipelines discard reads which map to many locations, and then true biology (e.g. a bound protein) which can occur at those regions is ignored. Also, in sequencing RNA or DNA from cancer cells, there can be so many mutations that the aligning programs have difficulty finding the match in the reference genome. Or, this can happen if we align reads from one species to the genome of another species (which does not yet have a reference genome constructed).


text:
What degree of influence do SNPs have on activity of ligands at receptors?
I know that generally, evolution tends to evolve towards having some wiggle room in respect to effect of polymorphisms on binding of endogenous ligands, but with synthetic ligands, especially modern structurally-unrelated molecules, does the same continue to hold true?
I've been particularly wondering about this in respect to biased agonists with selective functionality for some pathways activated by a receptor over others - wouldn't activity of that degree of selectivity be particularly vulnerable to disruptions by SNPs?
Hypothetically, would a ligand preferentially activating therapeutic pathway A but not a highly hazardous pathway B of an ABC receptor be a viable drug at all? Or would it be prime "expect it to kill somebody sooner or later" material?

Can you please define what you mean by "effector"? It's not standard terminology. At first I thought you meant receptors, but you mention receptors in your last paragraph, so I have no idea what you're talking about.

@MattDMo Sorry, I'm still catching up to speed on biology - I'm thinking about the components of the signaling cascade that are responsible for activating the different separate effects that a receptor's activation induces with e.g. functionally selective ligands. I must have misinterpreted something along the way, as I thought the component was called an effector.

So basically, effector == signaling pathway?

@MattDMo Is that the proper term, then? If so then yes.


text:
Parts of Brain Active for Dreams | Right Hemisphere or Cortex
I found a research that states cortex is responsible for the contents of the dream. Contents could be people, place, objects etc.

The cortex is responsible for the content of dreams, including the monsters we flee from, the people we meet, or the experience of flying. Since we are highly visual animals the visual cortex, right at the back of the brain, is especially active, but so are many other parts of the cortex.

While the other says right hemisphere is responsible  to create the dream.

The right hemisphere of the brain actually creates and displays the dream

And another source

the dream contents have their source in memories and impressions stored within the right half of the brain.

While there is another research that states posterior cortical hot zone that are responsible for our dreams.
Question: So what part of the brain is it? I know a coordination of various parts of the brain makes dreams possible but what part of the brain is responsible for main contents of the dream or major contributor to the dream?

Search this on google scholar- you will get a well sourced answer. Three of your sources are unreliable.


text:
Difference between Processing and Preprocessing
In the wikipedia article of emotion lateralization it is mentioned:

The right hemisphere is important for processing primary emotions such as fear while the left hemisphere is important for preprocessing social emotions

So I am wondering what exactly processing and preprocessing mean? What happens in preprocessing that they use this distinct word instead of mere processing?

They cite a source for that sentence, you'd have to go there. They probably talk about some later step that they think of as "true" processing, but there is no standard neuroscience answer to your question.

@BryanKrause you mention that they "think", so is it not well established?

I take it to be purely their opinion and narrative description. It does not have other meaning unless they define it.


text:
What is the common ancestor of humans and trilobites?
I have always been immensely fascinated by trilobites. What is the single common ancestor of humans and trilobites? Do we know? Do we have a name for it? Have we identified it?

Welcome to Biology.SE! 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). I suggest you start with the wikipedia page for trilobites and pay particular attention to the "Scientific classification" panel. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

try searching common ancestor of arthropods and vertebrates.

Thanks guys :) I have always been fascinated by science. I look forward to spending more time here on this wiki.


text:
Is the coronavirus getting less dangerous?
Please note

This question is based on data from the UK government's web site (data from the ONS). I am not taking this data as accurate, but am using this as it is the only source of data I can find, and is what (presumably) the government themselves use when deciding what to do. My question is about trends, not the accuracy of the government's data.

I'm also not asking about the wisdom of government policy, that is a political issue, and I'm only interested in biology and statistics here.

Finally, I realise that my analysis is all quite rough and ready, as there are many indeterminate factors involved. Again, I'm interested in an overall picture, so a rough analysis is probably reasonably informative.

Here in the UK, the data on new virus cases seems to imply we have a serious problem...

This was plotted using data from the government's web site, and shows that the number of new cases has risen dramatically since the beginning of September. I used a 5-day average to smooth the line (same for the other graphs below)
However, if you look at the number of deaths, it seems that the increase is nothing like as rapid...

Whilst there has been an increase since the beginning of September, it is very much more modest, and not necessarily indicative of a serious problem.
Now, I'm not a medical expert in any way, but it seems to me that the fact that the number of deaths is growing more so much more slowly than the number of new cases indicates that things may be not actually be getting worse, but may be getting better. Sure, more people are getting the virus, but the percentage of those who are dying (which I would have thought is the most important issue we need to consider) is not increasing.
To check this, I divided the number of deaths by the number of new cases, and it showed a very different picture...

As you can see, there isn't a noticeable increase since the beginning of September. To examine this more closely, you can zoom in on the past 8 weeks or so...

Whilst there was a jump in the middle of Sept, it hasn't really increased since then, and may even be decreasing.
So, is my analysis wrong, or is the virus actually becoming less of a problem in the UK?

One obvious problem with your graph is that people don't die immediately after diagnosis.  Many people diagnosed in September will die in October, but you aren't counting them.  You can see possibly the beginning of an October death spike in what data you do have.

@swbarnes2 That would also make the beginning of a good answer.

@AvrohomYisroel, The UK's coronavirus stistics are some of the least thorough and systematic, because of their lack of a pandemic preparation and free test centers. S. Korea and Germany give better data and wildly different data than the UK.

This would be improved by cutting out some of the rhetoric, e.g. "winding people up into a panic", which suggests that you already have an answer in mind.  You might also consider that (if the UK was like the US) many of the early deaths were among extremely vulnerable populations such as older people in nursing homes.  Those people having been killed off already, so they aren't a factor in ongoing statistics.

@jamesqf I agree with the first part of your comment, but definitely not with the second. There are still plenty of very vulnerable people around (at least in the US) that avoided being infected during the first round, but are still quite susceptible to disease should they be exposed to it. Round I was certainly not a clear-cutting operation among the sick and elderly by any stretch of the imagination.

@jamesqf I tried to edit that part out, but it got rejected for some reason. I'm keen on cutting out any kind of political or emotive language in these kind of discussions,

I have voted to close this as it is not a question about biology in terms of SE Biology but an analysis of a public health situation in one country at one time presented to start a discussion or as a “I think this, try to refute it?” shot.

@swbarnes2 Good point, I hadn't thought of that.

@jamesqf You're right, I did have an answer in mind, but was trying to ask objectively, as I'm quite prepared to be proven wrong. I've edited the answer to remove the comment you mentioned.

@MattDMo: I have no data beyond news reports (e.g. mass deaths in nursing homes &c), but I think we might be talking about different degrees of vulnerability.  I didn't actually intend to imply that it was a clear-cutting, as you put it, but rather a thinning, which reduces later mortality.

The issue is using the number of positive tests as a measure for the total number of active cases at a given time. At least in the U.K., the early testing capacity was much lower than it was now:
Because of this, many people who were infected were not being tested and so weren't included in the total number of infections. Therefore, the total number of infections in April/May time was likely a large underestimate. It's been estimated that there was something in the range of 150,000-200,000 new cases per day in that time period.
On the other hand, testing capacity in the U.K. at the moment is much higher and will catch a much higher proportion of the total cases.
Therefore, your crude calculation of 'death rate' = deaths / cases is skewed by the error in the estimated number of cases, making it appear the 'death rate' is going down because we underestimated the total number of cases early in the pandemic.
The other thing to note is that the 'death rate' is dependent upon demographic factors, most obviously age. Early in the pandemic in the U.K., a large number of cases occurred in care homes, where the residents were particularly vulnerable. On the other hand, cases are high in students at the moment, who are a low-risk group. If the age distribution of cases is relatively skewed towards older people, then the 'death rate' will appear higher than vice versa, even though nothing may have biologically changed with the virus.
Note: Sorry, I don't have citations for a lot of this. I will try and find them and add them at a later point.

Thanks for that, very informative answer. My only comment would be that while everything you say makes sense when comparing data from the spring to now, but if you only consider data from (say) the beginning of Sept, as I did in my question, your points wouldn't make such a big difference. Or would they? I would be interested to hear what you think. Thanks again

Just by looking at the data, I would say that those deviations could well be within the margin of error (i.e. confidence intervals) of the numbers of cases and deaths recorded. Of course, there is a large amount of error in the estimation of the number of cases, so I expect those confidence intervals to be quite large. IN that case, the deviations we see may well just be 'random noise' that don't correspond to anything meaningful.

Fair comment, thanks

Schools opened
What happens in the beginning of September. Something that would expose a large number of people to the virus, particularly people young and healthy enough to have a low risk of death due to virus but who still have decent chance to catch the virus.

Excellent observation, never thought if that. I wonder if there is any data showing deaths by age, as that would help confirm or contradict your suggestion.

@AvrohomYisroel you also have to keep in mind that the death rate amongst young people is a lot lower than for older folks, but young people can pick up the virus and spread it to older people they come in contact with, while not necessarily getting very sick or dying themselves. I think one lesson out of this is that there are all sorts of variables at play here, and you can't necessarily draw universal conclusions just out of the data you've analyzed so far.

@MattDMo Agreed, very valid observation. I said right from the start that my analysis was rough and ready, I'm now seeing quite how rough it was!


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Specific mechanism behind lethality of yellow coat color in mice
Our high school genetics chapter has some extra information about L.Cuenot. It only covered his research, and the fact that mice homozygous for yellow coat color would die before birth. It was an example of a lethal allele.
We have learned about sickle cell anemia, thalassemia, and hemophilia. All of them had a specific reason/mechanism which caused damage. For example, it's not the shape of the red blood cell in itself which is problematic, it is the fact that it can't carry enough oxygen. Therefore the cell will die off much quicker than normal cells.
I asked few of the biology teachers why the yellow coat color was lethal, but they couldn't provide any answer.
My question is, what causes the mice to die before birth?
Links to relevant articles or excerpts from them are highly appreciated.

Good question!  Minor quibble: the shape of red blood cells is very problematic because it can cause sickle cell crisis, the prevention of which is, unhelpfully, "live a life free of physical and mental stressors, have perfect hydration habits, and don't exercise in non-ideal conditions"

@Punintended Wow! I didn't know about this angle of the clogging of small blood vessels due to their shape. I guess there's only so much they teach you in high school.

Really interesting question: The lethal yellow mutation (also abbreviated Ay) affects the agouti signalling protein which plays a major role in pigmentation. Heterozygous expression of it leads to the dominant expression of pheomelanin (which is yellow), causing the mice to express this color (among other effects). To understand why it is homozygous embryonic lethal, we need to take a further look at the gene and its organisation.
Agouti is located on chromosome 2 of the mouse genome and downstream of a gene called "Raly" (synonymous also MERC)(Image from NCBI Genes)

The Ay mutation now deletes a large chunk of DNA, removing about 170kb between these genes. This removes parts of the coding sequence of the Raly gene and the complete promoter and (non-coding) exon1 of the Agouti gene and results in a fusion protein in which the agouti gene is put under the control of the Raly promoter. This leads to the expression of Agouti every time when Raly should be turned on.
Schematically, this looks like this (figure 4 from reference 2):

Raly is an RNA binding protein, which is highly expressed in embryonic tissues. The mutation leads to the expressing of Agouti there instead. According to reference 3 this leads to embryos which do not develop further than the blastocyst stage leading to premature death of the embryo.
So in short, the deletion removes the expression of Raly, a protein important for embryonic development. Im homozygous mice this is embryonical lethal, in heterozygous mice this can obviously be compensated. However, these mice tend to be obese and are more susceptible for certain tumors (reference 4).
References:

The embryonic lethality of homozygous lethal yellow mice (Ay/Ay) is
associated with the disruption of a novel RNA-binding protein
A molecular model for the genetic and phenotypic characteristics of
the mouse lethal yellow (Ay) mutation.
Pleiotropic effects of the mouse lethal yellow (Ay) mutation
explained by deletion of a maternally expressed gene and the
simultaneous production of agouti fusion RNAs
The molecular basis for dominant yellow agouti coat color mutations

It looks like Eif2s2 on the opposite strand would also be deleted in Ay mice. Do you know if this has any effect on the phenotype? It would be interesting to see if researchers knocked in Eif2s2 somewhere else and looked to see if there were any confounding effects.

@MattDMo I don't know, but I'll have a look into it tomorrow when I have access to journals again.

In other words, the yellow color is just one obvious manifestation of a more significant syndrome, which under 2 copies becomes massively worse and causes complete failure of the organism?


text:
Proinsulin is an 84 residue polypeptide with six cysteines. How many different disulfide combinations are possible?
Generally cysteine residues form disulfide linkages - so how many combinations are possible out of (say) six residues. Also can cysteine form bonds with all the residues?

I suggested some minor changes to the text of the question, but did not want to alter the second sentence : do you mean something like "can all these disulphide links be created"?

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

yes, actually i wanted to ask can all disulfide links be created?

The short answer is that you need to use the binomial coefficient ("n choose k")
$$ \binom{n}{k} = \frac{n!}{k!(n-k)!} = \frac{6!}{2!(6 - 2)!} = 15$$

This is a mathematical problem rather than biological.
see this
the refined question would be this :
we have 6 items and we want to pack them in 3 groups of 2.(We assume that all six cysteines do form a disulfide bond with each other and none of them are ungrouped or left out.Let me know if you have the question about the latter situation.) How many different sorting are possible?
Disclaimer: I am terrible at these types of mathematics . but I believe I have found the right answer.
Method A :
Write all of them!
six items are called A,B,C,D,E,F respectively
Fix A.
AB/CD/EF
AB/CE/DF
AB/CF/DE
AC/BD/EF
AC/BE/DF
AC/BF/DE
AD/BC/EF
AD/BE/CF
AD/BF/CE
AE/BC/DF
AE/BD/CF
AE/DC/BF
AF/BC/DE
AF/BE/DC
AF/BD/CE
THE ANSWER IS 15
Method B:
you could also use C(n,r) function for better understanding but I'm going with this:
we have 6 items. Split them into 3 groups of 2. Group 1 ,group 2 , group 3.
calculate number of different combinations.
group 1 : 6 * 5 /2 = 15
(you can reverse the order of the first 2 objects and the group would still remain the same)
group 2 : 4 * 3 /2 =6
(you can reverse the order of the first 2 objects and the group would still remain the same)
(Two of the items are used in the previous group)
group 3 : 2 * 1 /2 =1
(you can reverse the order of the first 2 objects and the group would still remain the same)
(Four of the items are used in the previous groups)
You have to multiply these numbers . But do not forget that combination between group 1,2,3 does not matter(you can call any of them 1 , any of them 2 ,etc and the result would NOT change. It is just naming.)
3!=6
we have 6 repetitious/same groups counted in each unique combination . Therefore devide the whole amount by 6
15 * 6 * 1 / 6 = 15
About the second question the answer is no. Cysteine form disulfide bonds only with itself as far as I know

If the question is mathematical it is probably off-topic as it bears no relationship to the reality of biology. Even assuming a random chain finding different combinations, rather than the chain folding in a manner governed by the amino acid sequence) the possibility of a second disulphide bond forming after one has formed would depend on their relative location. In fact the protein probably forms first and then oxidation occurs. So the answer is 1.

the nascent protein translocates into the ER then it is oxidized to form S-S bonds. Suppose our protein has 6 cysteines. A biochemical procedure occurs by Ero1 and DPI which oxidizes the sulfurs exactly one after another ( i.e. cys1 is bound to cys2 and cys 3 to cys4 and cys 5 to cys 6) . This intermediate might be thermodynamically-instable . So here comes PDI again to REARRANGE the incorrect disulfide bonds , Literally testing each combination of S-S until it gets the most stable combination/conformation.  So in theory there might be all different combinations of disulfide bonds......

The less stable combinations are later degraded . Here's the references: Molecular Cell Biology Lodish et al 8th ed chapter 13  figure 13-19 . Also take a look at  M. M. Lyles and H. F. Gilbert, 1991, Biochemistry 30:619.


text:
Does glycerol in E.coli culture media somehow inhibit the lac-operon?
I have have been taught that one should induce protein expression with IPTG at an OD of about 1.0 - 2.0 when E.coli grows it TB media (terrific broth). As a reference point, one typically induces protein expression at an OD of about 0.5 in the commonly used LB media (Lysogeny/Miller broth). IPTG is a lactose analogue that will induce the expression of proteins encoded in the lac-operon. I have been told that it is important to have a high OD before induction, because the added glycerol in the TB media (5%) will somehow inhibit expression of protein in the lac operon if it is not 'used up' before induction. However, glycerol itself should not inhibit the lac-operon from being transcribed (?).
I have several speculations about this: Could it simply be that TB-media has a very long exponential phase (rumoured to support an OD up towards 16.0, personally I routinely reached an OD of 10), and it is therefore not wise to induce protein expression too early (and thus has nothing to do with using up up the glycerol)? Another rational explanation that I came across is that glycerol might induce carbon catabolite repression, meaning that glycerol might inhibit the uptake of IPTG (or down regulate cAMP levels) and thus indirectly inhibit expression of protein from the lac-operon, but I found it a bit difficult to get a straight answer about this in literature.
Does anyone have some good references for these speculations?

You can induce as soon as cells go into exponential phase. It is during the lag phase where you should avoid burdening the cells.

Yes, I was however wondering about the use of glycerol and TB media, i.e. why 'everyone' says to wait for an OD of 1 or more before induction? Are you saying that this is a myth, and it simply does not matter as long as one is in the exponential phase? Or that it simply takes longer to get to the exponential phase in TB media, and thus the recommendation of inducing at a higher OD? I actually haven't document the growth curve in TB-media, I have simply used or modified protokolls, which has worked well for me.

I cannot provide a conclusive answer here but how soon you induce depends on the load of protein expression. It would vary for different kinds of media. I haven't used TB media, so I can't say much about it. A long-lived protein will reach 90% of steady state concentration within 4 divisions. Based on these factors, you can decide when to do the induction to minimize stress and maximize protein concentration.


text:
Can ants distinguish individual ants in the colony?
I am aware that ants have the ability to distinguish which female is the queen and which ones aren't. However, can ants also uniquely distinguish other individual ants in the colony? Is the differentiation between the classes only (worker-ant, queen, non-queen) or is it within the classes as well like hey its bob?

I edited for clarity and conciseness, but please check to make sure I have preserved your intent. Also note that 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). Starting with wikipedia is often a good bet. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

@tyersome, thanks for the edit. Yes, the intent is preserved and I shall add references later. +1


text:
How can Chronic myeloid Leukaemic drugs reduce the production of the Philadelphia genotype?
How can Chronic Myeloid Leukaemic drugs (Tyrosine kinase inhibitors, e.g. imatinib, etc.) that act by inhibiting bind of ATP to the active site of the BCR-ABL1 protein actually reduce the prevalence of the Philadelphia chromosome? (For example, optimal response to TKIs in 3 months would be Ph+ <35% and/or BCR-ABL1 <10%.) What I am actually asking is how a drug that targets the result of the oncogene (the BCR-ABL1 protein) can have an effect on the source (ie. genotype of the cells), as CML is a clonal haematopoietic stem cell disorder?
An example Reference paper: Apperley JF. Chronic myeloid leukaemia. Lancet. 2015 Apr 11;385(9976):1447-59. doi: 10.1016/S0140-6736(13)62120-0. Epub 2014 Dec 5. PMID: 25484026.

Very interesting question! Could you cite a paper too? thanks

@EvanP Just added. Thanks!

The key is that TKIs, such as Imatinib, are a therapy rather than a cure
Per Wikipedia, Imatinib acts as a competitive inhibitor of the otherwise constitutively-active BCR-ABL fusion protein, rather than the fusion gene.  By binding the kinase domain, BCR-ABL is unable to phosphorylate downstream effectors that result in unchecked proliferation.  As long as a patient continues to take Imatinib, BCR-ABL activity should be blocked.

In the past few years (i.e, long after imatinib's discovery) there has been a lot of research into exactly how hematopoetic stem cells, which reside in the marrow and create leukemic blasts, work. Most HSCs remain in a quiescent state, but it's not particularly well-known how frequently they turn over.  Recent CML studies have shown that after ~5 years, a large portion of CML patients can safely taper the the drug.  Presumably this is related to HSC turnover, but frankly as a leukemia molecular biologist rather than a physician, I'm not the best font of clinical knowledge.


text:
Why do mosquitoes appear to be repelled by magnets?
A few days ago, I was playing with magnets and thought of placing one near a live mosquito (I had it held between my two fingers so it had no chance of escaping). When near the magnet, it twitched and flew away! I tried the same with semi-alive mosquitoes, but nothing really happened.
I googled about this and learnt that mosquitoes have got to do something with magnets, but I'm still confused. Could anyone tell me why mosquitoes get repelled by magnetic fields?
PS. I'm no biology student, so please go easy on me, thank you ahead of time!
Source (PDF)
EDIT: Strickman et. al. (2000) says:

we found that some specimens had a significant magnetic remanence
Could this possibly be the reason why mosquitoes may get repelled by magnetic fields?

That paper also states:

the mosquitoes were able to detect the magnetic fields but sensed a magnetic pattern that was impossible in nature.

Reference:
Strickman, D., Timberlake, B., Estrada-Franco, J., Weissman, M., Fenimore, P. W., & Novak, R. J. (2000). Effects of magnetic fields on mosquitoes. Journal of the American Mosquito Control Association-Mosquito News, 16(2), 131-137.

According to the research cited by the OP (Strickman et al. 2000), mosquitoes alter their behavior in the presence of a magnetic field, and the measured changes in behavior are statistically significant. The authors of the study found that the external surfaces of mosquitoes attract ferromagnetic particles from the air. They speculate that changing their orientation to the earth's magnetic field helps mosquitoes navigate while approaching a potential host.
Reference Cited
Strickman, D., Timberlake, B., Estrada-Franco, J, Weissman, M, Fenimore, PW, and R.J. Novak. 2000. Effects of magnetic fields on mosquitoes. Journal of the American Mosquito Control Association 16(2):131-137.

This seems far-fetched...kind of like Magneto's escape during X-men 2.

Answers on this site are expected to be fact based not speculative. Your answers is thus much more likely to receive a favorable response if you [edit] it to include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and would be more appropriate as a comment. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit or delete your answer accordingly. Thanks!

@tyresome, I apologize for making a speculative suggestion on Stack Biology. I have updated my answer which now cites the primary literature and describes the conclusions of the cited study. I hope the OP will benefit.


text:
What changes do ants make to the soil they use for building ant hills
I live in South India ,and among the many species of ants in and around our house, some of them except the weaver ants build the typical small ant hills in the garden.

I have examined the coarse sand like grains on the top of the ant hill. They are somehow modified and don't mix with normal soil or disintegrate in water.The region I live in has red soil.
A quick search on ant hills brings up information from here

The ant hill is a byproduct of ants building their colony. As ants dig their long and winding tunnels beneath the ground, the excess dirt and debris is carried out and placed near the colony entrance, creating the ant hill. At the top of the hill, there will be a small hole that serves as the entrance and exit to the colony.
Typically, an ant hill will be made from a combination of dirt, small rocks, pine needles, and whatever other materials were left over after the ants have dug their colony.

Other sites also state same facts on the composition of ant hills, but nowhere I can find any secretion or something which changes the properties of the ant hill soil.

So do they secrete enzymes or something or mix the soil with plant
debris to change the size of grains?
Does doing this confer some added protection to the ant colony living underground ?


text:
What is a metabolite?
I am a mathematician and work on metabolic networks as networks. But I could not find a proper definition for a metabolite? Are they organic molecules? can a gene or a protein also be a metabolite?

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

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If you go by meaning that "organic"  means made in the organism by biological processes ,then in vitro metabolites are surely organic ,if the reactions are occurring in-vitro.https://en.wikipedia.org/wiki/Metabolism

Thank you, indeed I meant in general because in a paper I found it is an organic molecule, but from the below comment I found it depends on the context.

Why was this question closed? It seems to be relevant to biology and helpful to a general audience to investigate a solid definition of "metabolite".

yeah, I think many people who are not a biologist they might have these kinds of questions.

This definition of Metabolism is similar to most I've seen in biology textbooks.

Metabolism: the sum of the chemical reactions that take place within each cell of a living organism and that provide energy for vital processes and for synthesizing new organic material.

The broadest definition I would give for "metabolite" is any molecule that's part of or a product of a metabolic reaction. They are molecules, but not necessarily organic molecules (in the traditional sense). For example, any metabolically active cell is going to constantly generate inorganic phosphate as a metabolite of ATP hydrolysis.

can a gene or a protein also be a metabolite?

I suppose A protein could be considered a metabolite, but it would depend on the context. most people probably would not be talking about proteins when making reference to "metabolites" in general way. For example, an enzyme acting as a catalyst in a biochemical reaction would probably not be considered a metabolite of that specific reaction (since it's not chemically changed in the process). But in a metabolic model involving protein degradation, it would have to be included in some way. However, amino acids (the monomer building blocks of proteins), are often incorporated into metabolomic analyses, and could be considered important metabolites in many different cellular reactions.
A gene is not a metabolite by any reasonable definition. A gene is not a biological molecule, but a unit of hereditary information. One could argue that the nucleic acid molecules (DNA or RNA) encoding a gene sequence are metabolites, but as with proteins, it would really be context dependent. Also similar to proteins, the structural subunits of nucleic acid polymers (nucleosides and nucleotides) are often important metabolites involved in a great number of cellular functions.
Is all of that about as clear as mud?

Thank you MikeyC, now many things are more clear for me.


text:
What keeps mitochondria from multiplying out of control?
What keeps mitochondria from multiplying out of control and killing the cell?
According to endosymbiotic theory, mitochondria were once free-living bacteria that got ingested but not metabolized by the host cell. What prevents mitochondria from replicating out of control and overpowering the host cell? The question was inspired by this brainstorming session about engineered endosymbiosis.

Could you please add some more details or show some sign of research on your own? E.g. any citations on mitochondrial replication?

It seems like a pretty straightforward and self-sufficient question. What would be the purpose of adding such a paragraph? I'm not against it, I'm just trying to understand the rationale

well, as your accepted answer begins, "I'm guessing at the motivation of your question..." I think jamesqf does a good job of rephrasing the question into something that's a lot easier to answer.

err. i mean acvill. those are more answerable questions. Additionally, you should have provided your brainstorming link in the first place if that was where you were coming from.

I hope this fixes it

I'm guessing at the motivation for your question -- In the evolutionary history of eukaryotic cells, mitochondria were once free-living bacteria.  What prevents them from acting as intracellular pathogens and replicating out-of-control?
Yes, by endosymbiotic theory 1, mitochondria were once free-living prokaryotic organisms.  This is evident because they have their own DNA, undergo replication by fission, and have characteristics similar to proteobacteria.
However, some of the genes required for mitochondrial replication have been moved to the nuclear genome.  This means that, while mitochondrial replication is not necessarily tied to cell replication, factors encoded in the nucleus are necessary for mitochondrial replication.2

https://en.wikipedia.org/wiki/Symbiogenesis
Ali, et al. Nuclear genetic regulation of the human mitochondrial transcriptome. eLife 2019;8:e41927.

That's all I needed to hear:) The question was actually motivated by this brainstorming session about engineered endosymbiosis https://brainstorming.com/r/s164

I think we might have to go back further than the present situation.  A bacterium couldn't become a successful endosymbiont if it multiplied out of control and killed its host, and it would seem that this non-lethal behavior must have existed long before evolution moved the genes around.

Good point. I will set the question as not answered to see if we can come up with something that accounts for this. Dirigible did solve the question I had in mind, but now that you mention this plot twist, I would love to know:)

jamesqf's point is a good one.  However, the original question was "What keeps mitochondria from multiplying out of control and killing the cell?", not "What factors contributed to the intracellular symbiosis that led to mitochondria?" Post a new question (with preliminary research / thoughts) if you want a new answer. It's poor etiquette to post a question, accept an answer, add more questions, and remove your accept.

understood. will fix it

@RetardiGrade Thank you. Of course, if someone provides a better answer to your original question, feel free to accept that answer. https://meta.stackexchange.com/a/93970/722486.  I encourage you to ask you "sub-question" as a new question, as it will likely generate interest.

@RetardiGrade I think you should look up retrograde signalling between the Nucleus and mitochondria if you would like to know the molecular mechanism regulating mitochondrial numbers.


text:
Plating 96-well bacterial transformations
I need to clone 96 different inserts into the same backbone in arrayed format. I am planning to perform Gibson assembly reactions in a 96 well plate, and then do chemical transformations in a 96 well format.
However, I am not sure how to plate 96 well transformations in the most efficient way. I could just plate them one by one onto petri dishes, dividing each petri dish into 4 sectors. However, I suppose there could be a better way of doing it. Any suggestions?

You could plate them in 6-well or 12-well plates, so you don't have to juggle all the Petri dishes.

If you want to plate them as usual you can use glass beads instead of a spreader to spread them.

I think your approach very much depends on how essential it is that you get discrete single colonies, and if this is a one off or a regular process. To preface, similar to what Maximilian Press said, using a single welled plate like a nunc omnitray would be your best bet.
The main consideration you need to take into account for high-throughput transformations is the transformation efficiency (TrE). Naturally in a big petri dish, 100 µL of a single 1:10 or 1:100 dilution of your recovery culture can bring out nice discrete colonies. When you start reducing surface area and volumes, the chance of discrete colonies obviously diminish.
The best way I've found is to do a test transformation using the backbone of your choice and gauge the average TrE over a few runs to hone in on a 'one size fits all' dilution/volume, then apply that to your full high-throughput run. Assuming your inserts are of similar size, you should see a relatively similar TrE between them (bar edge cases). Another option would be set up three 96-well plates and do three separate dilutions, 1:10, 1:100 and 1:200 at 100 µL a pop so you at least get some fudge factor.
In terms of the chemical transformation itself, doing them in a 96 well plate format will guarantee lower TrE simply due to the characteristics of the plate itself. Thicker plastic and sub-optimal heating (if you aren't using a thermocycler and PCR plate) requires a slightly longer heat shock, and recovery in media requires much more vigorous shaking due to the mixing characteristics within the wells.
If you don't care about plating out in 96 well plates, like Maximillian Press said, use a single welled plate and format it in a 96/48 well fashion. Will save a massive headache when pouring. Just make sure you leave it to dry to prevent any running culture.
In terms of actually growing the colonies in a 96 well plate, if you're making the agar yourself I'd recommend adding an extra 0.5% agarose to thicken it up (I doubt you'll be using one, but make sure your plate is non-tissue culture treated). Wait for it to cool just above its solidifying temperature (around 45 °C in my experience) and then transfer out using a pipette or low volume serological pipette to reduce the meniscus formation. If the agar forms a high angled meniscus, your colonies may form smears and will not be discrete. Leave the plate out to dry as well, colonies may also smear from the agar being moist.

TBC, I was talking about plating on a flat plate, not 96-wells! It has the same shape and size as a 96-well plate but is otherwise a flat bottomed plate. The similar format makes it easier to organize and avoid errors, but pouring 96 wells sounds like a huge headache.

Ahh yes I was agreeing with you, just mix up in what I was calling them!  I agree, using actual 96 wells is a real pain.

gotcha, cool, seems like we're on the same page.

I would suggest pouring solid media selection plates of something like this, that have the same shape and size as the 96-well plate. You can then directly spot your transformations from their wells onto this plate, which has a similar format. You will not be able to pick colonies per se (you will just have a confluent spot of cells that can grow on the selection), but if you are just interested in the constructs it would save a lot of labor and potential confusion.

An alternative to the confluent spot could be to do spot plating from dilutions as it is done in survival experiment. This would allow the recovery of individual colonies.

@GaelC a good point, though I worry about transformation efficiency being high enough to reliably recover colonies from dilutions. Maybe do a 1:10 dilution series and plate each dilution, to account for variation between reactions?

Yes, for the first time I would do that and see if 2 or 3 dilutions points could be enough for the next time.


text:
Why do Oak Processionary caterpillars form processions?
Firstly ,I don't live in Europe. I live in South India, and my garden has a Night Flowering Jasmine tree.
And these trees are quite popular, but notorious for their caterpillars. In our region ,there are no specific names or identification these caterpillars and the thick mat they form on the tree trunks.

And one day, I was looking through images of caterpillars online ,when one seemed similar. It was called Oak Processionary.I am not sure if the caterpillars found in my area are the same species or something else entirely, but their behavior is similar .  As per as Wikipedia and some other websites, they are usually found head to tail moving together.
My question is

Do they have some chemical signaling agent like pheromones ,or like ants when they follow each other?
Why do they form such processions in the first place? Wouldn't having such a large ,conspicuous gathering make it easier for predators to spot them from afar?

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

Would it be to their advantage to look like a snake?

@PolypipeWrangler they don't look much like a snake, rather a kind spiky doormat.:)

Here's a paper that gives the distances traveled, the directions, phototactic strategy of the leading caterpillar (away from shade). He doesn't state a reason, it's presumably a variety of protective reasons, because they burrow and cocoon in trees socially, and because of birds/crows/lizards https://movementecologyjournal.biomedcentral.com/articles/10.1186/s40462-020-0189-x


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Advice on type of database and software for research on genetic diversity of crops
for a research project I am evaluating the potential of Robusta coffee genetic resources in the tropic region of Africa. Different ex-situ genetic lines will be mapped as well as chemical, morphological and organoleptic analysis of the coffee beans.
I am looking for a type of database and software that would be well suited for this type of dataset. Are there any genetic database programs out there that allow you to merge other datasets (like plant descriptors or cupping profiles)? Or should I look the other way around and use a database that easily links with genetic fingerprint software?
Thank you,
Robrecht

This question is more likely to be considered on-topic in SE Bioinformatics as it seems mainly about the choice of software. I suggest deleting and reposting, but in your repost you should specify what you think a database program is — i.e. what data you wish to store and what processing of the data you are hoping external programs to do. Your computation skills will also be of relevance. You need to be more concrete.

ok thank you David, I will do that.

I don't know whether this is relevant for you, but I see here an example of tropical crops database that says it is made using the generalist mySQL system: https://tropgenedb.cirad.fr/tropgene/JSP/presentation.jsp

Also, much coffee research is published in Portuguese

Thank you for the advice.


text:
Why do diseases in the tap water of developing countries affect people from developed countries more?
My siblings and I went abroad to a country that doesn't have drinkable tap water, but we did not know this at the time as the people who lived there used to drink it all the time with no issues.
One day, we all decided to drink a glass of water from the tap and we all ended up in a hospital and were really ill (I'm unsure of what we had as it was a while ago). We were told it was due to the tap water and were advised to only drink bottled water in the future as the tap water is unsafe.
My question is, why did the tap water only affect us but was fine to drink for the residents there? Is it maybe because our bodies are used to clean tap water?

The locals develop immunity to whatever is in the water, so they can drink it with no (or relatively few) problems. Since you didn't have this pre-existing immunity, you got sick.

So does this mean that certain pathogens in the water could in fact kill me but not others who are immune to them? Also does this mean that they did in fact get ill but a long time ago and then became immune after that? Also does this mean that I could be immune as I had the water and healed but with the help of some fluids that were injected into me. If certain pathogens in water kill humans how could someone become immune to it if they die when they have it? Sorry for the thousands of questions I just find it hard to understand. Thank you for your comment :)

Just to add to the other answer, people in those countries do still get sick on occasion and you don’t build up immunity to all possible pathogens. Getting sick now and then is just fact of life. I spent 5 years in SE Asia and locals would get the runs just as well. They just tend to blame it on other things like ‘spicy food’.

@James: Many different things at work, here. You can become immune to pathogens. You can develop a tolerance (which isn't the same thing). Or you can be smart enough to filter and / or boil the water before drinking it...

@AndrewT. Singaporeans had a higher chance compared to whom?

You can expect that someone drinking from a water source regularly will develop immunity to the pathogens in that water source by being repeatedly exposed to them.
However, it's not quite right to say that poor quality drinking water impacts mostly tourists. It mostly impacts the people drinking that water, especially children. Immunity comes at a cost. Some example statistics from Wikipedia:

Between 2000 and 2003, 769,000 children under five years old in sub-Saharan Africa died each year from diarrheal diseases

In South Asia, 683,000 children under five years old died each year from diarrheal disease from 2000 to 2003. During the same period, in developed countries, 700 children under five years old died from diarrheal disease.

And from WHO:

Contaminated water can transmit diseases such diarrhoea, cholera, dysentery, typhoid, and polio. Contaminated drinking water is estimated to cause 485 000 diarrhoeal deaths each year.

These statistics conflict a bit, and I won't go too far into the reasons why or try to identify the correct number. I think they are all sufficient to identify this as a substantial issue in the world.
Responses to disease vary between individuals for all sorts of reasons, including genetics, overall health at the time (for example, someone well-nourished versus poorly nourished), and access to medical care and treatment. Some you could also add up as effectively "luck". In a hypothetical scenario, you could expose 100 people to a pathogen, and of those 100, many may get very sick and a few die. The survivors may then have future immunity to the same pathogen, but it would be wrong to say the population as a whole is not affected by it, you're just looking at the people who survived.

Assuming that contaminated drinking water is the cause of ~25% diarrheal deaths (the majority stemming from contaminated food perhaps), the statistics need not be in conflict.

Looked at another way: Later repeated exposures to some source of pathogens are less likely to affect you than early exposures, since you’re more likely to be immune. So later exposures will bring your lifetime average risk-per-exposure gradually down (and your “recent average” more so), but will continue to add to your lifetime total risk.  So tourists have significantly higher marginal risk per-exposure than local adults; moderately higher liftime risk-per-exposure; and much lower lifetime total risk.

"will develop immunity to the pathogens in that water source by being repeatedly exposed to them." Either that, or they stay ill almost constantly and/or eventually die. Death by unclean water is still a common problem in third-world countries.


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what is this centipede like creature?
They are very big. About the size of my hand in length and I've seen two now. My cat brought one in from the Texas border region.

giant centipede. Probably a Common Desert Centipede (Scolopendra polymorpha)

Yes ,surely a centipede.Looks similar to the ones on https://extensionentomology.tamu.edu/insects/centipede/.

dark bands between segments and long tails match:

Distribution matches:

I’m fairly sure it is a centipede. However, the picture is too fuzzy to make out the exact species.
You can try comparing with the many recorded observations of centipedes around Texas: https://www.inaturalist.org/observations?place_id=18&taxon_id=49556


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Do bees from different continents have different "taste"?
This question was already asked by me at Gardening Stack Exchange, but I was advised to ask it here instead. I see there is already a closely related question: Do animals have different taste preferences within the same species? . However, I would like some bee-specific clarification or study material, if possible.
I live in Europe, and planted several supposedly bee-attracting, but non-native (originate from Americas) perennials, most notably:

echinaceas
hellenuims
rudbeckias

For all species, I chose several cultivars, for the sake of experimenting.
Although all three species are listed as bee-attractive, bees at my place like only echinaceas and hellenuims. They totally ignore rudbeckias! Is there any plausible explanation for this?
Can it be that european bees are just not used to rudbekias, or simply don't like it, while american bees do?

Did you check the YT channel where he gives bees different types of water and nectar and checks which they go for?

No, but would definitely love to see that video, any link perhaps? Many thanks for idea/suggestion! @aliential

Probably bees communicate which flowers have the "most" amount of nectar, whereas the chemical makeup of it is a complex topic and probably a secondary choice option, they are picky about water though... https://www.youtube.com/watch?v=fVuxhp4TWNs&t=2s  bee dieting: https://now.tufts.edu/news-releases/bees-adjust-seasons-nutrients-flowers-and-dirty-water

I'm writing as a comment b/c I'm hypothesizing without examining the life cycles (are they even all flowering at same time?) or pollination syndromes of these specific plants. Bees, like all animals, need multiple nutrients (carbs, fats, proteins, etc), and their sources of each may differ. 1 flower may have  nectar richest in carbs and another maybe has a pollen richest in protein. Local surrounding plants might also provide better sources than your plants. The sources for each nutrient may also change throughout the year. In fact, the bees' actual needs may change throughout the year.

In other words, it's much more complex than simply planting bee-attracting plants.


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RNA vaccination and Autoimmune Reactions
To my knowledge we do not have any robust experience with RNA vaccination. Most likely this will change in the near future as RNA vaccines against COVID are in the pipeline. The rationale behind this method: Viral mRNA is injected (I guess in a muscle), the mRNA is translated (in muscle cells, for instance), the protein is exposed on the cell surface to cause a response of the immune system. As we know proteins tend to interact and build complexes. I speculate that this could easily lead to an immune response against cellular protein structures.
Is there any knowledge or speculation concerning an autoimmune disease in succession of RNA vaccination?

I would imagine the proteins are secreted instead of being cell-bound, just for this very reason.

Welcome to SE Biology. I think it is important to realize certain things about this site. First, this is a question and answer site, not a discussion site — answers that are mere speculation or opinions are generally off-limits. Second it is a site concerned with specific aspects of Biology (see the [Tour]) rather than medicine — for which there is a sister site SE Medical Sciences. In my opinion your question should have been submitted there, if at all. I say, if at all, as there are recent authoritative articles which I would try first. E.g. Go to nature.com and search for covid vaccine.


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Question About Molecular Weight
In Lehninger's Principle of Biochemistry Pg. $14$, this is the definition for molecular weight (relative molecular mass):

The molecular weight of a substance is defined as the ratio of the
mass of a molecule of that substance to one-twelfth the mass of
carbon- $12$ ($12$C). Since $M_r$ is a ratio, it is dimensionless—it
has no associated units.

What I do not understand is how we find the mass of the molecule in the beginning. What unit would we use?

@user1136 The phrase "molecular weight" may be frowned on, but I doubt it's ever going to go away unless all the reagent makers get on board. I don't think I've ever seen a protein standard marketed as a "molecular mass marker"...

@user1136 I agree with you that the most precise term should be used, I just wanted to make the point that there is a lot of historical weight (so to speak) on the term "molecular weight", and I don't think its usage will decrease until reagent makers get on board.

I voted to close this question as off-topic as it is a general chemistry question.

The mass of a biological molecule is evaluated by the process of Mass Spectrometry (specifically MS/MS or MALDI-TOF). These are an improved version of Mass Spectrometry(MS) and results from the works of physical chemists.In a nutshell, you can ionize the molecule. It dissociates into several ionized particles. Then subject them to a magnetic field and an electrical field at the same time.
The ionized particles take a curved route while moving , and the amount of curve depends on m/q of molecule ( mass of particle (in kg) and charge of it)
see
https://en.wikipedia.org/wiki/Mass_spectrometry
Molecular weight is dimensionless indeed. However one may add Dalton/amu/u "False" physical units for better understanding.
The best other example in physics is radians. Angles are defined in radians in physics. But they are dimensionless.
In Circular motion , we have these formula :
$ v = \omega \times r$
$\theta = \omega \times t$
see:
this
unit of $v$ is (meter per second) and unit of $r$ is (meter). therefore the unit of $\omega$  is  $s^{-1}$ .
unit of $\omega$ is $s^{-1} $ while the unit of $t$ is $s$.
So $\theta$ is dimensionless although we describe it as radians for better understanding


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What is the evolutionary advantage of breathing and heart beats syncing between partners?
I recently read that partners who are close to one another usually when touching have their heart beats and breathing in sync. Why does this occur? What is the benefit of it occurring? How does this occur?
The study linked below states that this phenomenon may reduce pain. Is it possible that is the evolutionary advantage? How is it that 2 peoples bodies sync their heart rates without knowing the other persons heart rate or being able to see the other persons heart beat?
Goldstein, Pavel, Irit Weissman-Fogel, and Simone G. Shamay-Tsoory. "The role of touch in regulating inter-partner physiological coupling during empathy for pain." Scientific reports 7.1 (2017): 1-12. APA

I think you need to make your question a bit more focussed. The proximal reason (how - i.e. the causal physiological mechanism) is very different to the ultimate reason (the 'evolutionary advantage') - but you seem to have asked both. I suspect that the former question could be answered - but question involving the 'evolutionary reasons' of such a trait are often impossible to answer without speculating, since we can't go back in time to investigate the different selection pressures which may have driven it.

That's a pretty weird study. If you had posted graphs from the study it would be a much better question. The graphs that they researchers drew do not demonstrate very amazing measurements at all.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6421336/


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Animals with very high bite pressures
When media, such as this site wants to explain just how dangerous large animals are, they often quote bite-forces as pounds per square inch (psi).
However, it appears that they mixed up the units, as the numbers they give are the total force in pounds.
But what animals have the strongest bite force per unit area? There is no obvious scaling law here: scale up an animal 2 fold and the cross-sections of both the muscles and the teeth and jaws both quadruple. This puts tiny insect mandibles are on a level playing field with our largest beasts.
Instead, bite-pressure will be niche-dependent as well as the details of the animal's anatomy (such as mechanics of the jaws). It may be somewhat hard to define contact area given the complex shape of teeth and mouthparts in general; maybe one could measure the indented area in a tough material that the animal chomps down on.
Given that our strongest biomaterial found yet is microscopic teeth and that microscopic materials tend to be stronger than bulk materials, it seems likely to be a small animal. Is there any data to support this?

I think the correlation between strength of materials and highest bite pressure may be misguided. You don't need an even stronger exotic material or construction if maximum bite pressures can be supported by the more mundane materials and constructions that everything else with lower bite forces already uses. Kind of like assuming strength of materials in eating utencils correlates with the weight of  food being eaten...steel is already so strong food weight is not even part of the equation.

They are not confusing total force and PSI they are giving you the force per unit area. (although the megalodon is achieved with poor methods) A T-rex is putting 10,000 pounds of pressure on a square inch of tooth surface. Muscle strength is based on cross section, larger muscles have larger cross sections producing drastically more force.

@DKNguyen: Material strength is important well beyond maximum bite pressure. Accidental ingestion of rocks or bone, eccentric loading, fatigue, etc mean you want a high "safety margin". Human teeth do break after all.

@John: Don't larger mouths have larger teeth as well, so there is more tooth area to distribute the force on?

@KevinKostlan no more tooth area means a larger total force for the calculations given. Keep in mind we are given the PSI. If you were calculating from the total force then yes more area would mean less PSI. Teeth in general is a way to increase the PSI of a bite, pointed teeth spread force across a smaller area.


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Mammalian advantage at filling large-animal niches after the KT extinction?
Larger animals are more prone to extinction due in part to smaller numbers. The asteroid that impacted 65 million years ago killed off the larger mammals and dinosaurs but spared some of the smaller ones. The smaller niches were refilled by both mammals and Theropods (as birds), but there is a paucity of large bird species. Is there a reason mammals were better at refilling these large-animal niches?

Just a guess, but most birds fly.  Evolving a large size means they can no longer fly, so there's a complex evolutionary path, probably first becoming a small flightless bird (as e.g. the kiwi), then increasing in size.  Mammals just had to become bigger.

Also, there is an additional evolutionary barrier in that birds wings might need a lot of evolution to become limbs again - so the mammals have a head start on being quadrepeds.

@Polypipe Wrangler: Quadrupeds, yes, but we have a number of examples of large flightles birds that are bipedal, with vestigal wings - the ostrich, emu, rhea, and the extinct phorusrhacids (AKA "terror birds"): https://en.wikipedia.org/wiki/Phorusrhacidae

Birds have to feed and guard there eggs for 30-40 days, against the elements and against predators, whereas mammals can bear larger offspring in exposed environments. That's especially an advantage for swimming mammal megafauna, because the birds can't lay eggs in water, and also for predator-intensive environments and for forests.
Birds lack hands and teeth and four sets of claws for manipulating leaves and prey and defense. Birds can only have a hooked bill to peel up prey, and less sophisticated molars for herbivory. The sheer range of mammal teeth shapes appears to be an advantage compared to beaks.
Quadrupeds have some advantage for running and turning without falling over, whereas birds mostly have long necks which are a bit of an easy target for horns and claws and teeth.
It's interesting to think about a pack of wolves attacking an ostritch, and a pack of predator ostritches attacking a springbok... The wolves and the springbok have a wider range of attacks and defenses to use for survival.


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Can a hinge joint technically allow rotatory motion?
Let's use a hinge joint and pivot joint as examples.
When talking about the difference between them in terms of movements permitted, I see that on any websites and textbooks, the term 'rotation' is applied to pivot joint only rather than hinge joint.
For example, according to Moore Clinically Oriented Anatomy 10th edition.

Hinge joints permit flexion and extension only, movements that occur in one plane
(sagittal) around a single axis that runs transversely; thus, hinge
joints are uniaxial joints.
Pivot joints permit rotation around a central axis; thus, they are
uniaxial. In these joints, a rounded process of bone rotates within a
sleeve or ring.

I never see the word 'rotation' being used to describe hinge joints' motion, however, doesn't hinge joint technically allow rotation, just that the rotation for hinge and for pivot joints are over a different axis? For example, at the anatomical position, flexion in the elbow's hinge joint involves rotating the joint along the tranverse axis.
So my question is, can a hinge joint technically allow rotatory motion? If not, am I misunderstanding what is meant by 'rotation'/'rotatory motion'?

Do you understand the difference in between a hinge (elbow) and a pivot (hip)? Rotation just means move-round in an arc. It can be used as a general term in anatomy, to describe moving around a central point in an arc. The sense is slightly figurative if you compare it to a literal mathematical rotation, i.e. an arc of a compass. Anatomy also talkes about sinusoidal movements, and straight lines. even though they are just general descriptions. I don't understand the question though.

@aliential the hip is not a pivot joint, it is ball and socket.

You seem to understand how these joints move, so your question seems to be more about English usage in this context rather than anything fundamentally biological. If this is true then I don't think your question belongs on this site. If I'm misunderstanding your question would you please clarify?

@tyersome you're right, I think it's more about the English usage in this context. I thought it'd belong to this site as scientific terminologies and nomenclatures play a big part in biology.

It is about the movement of the bone along its major axis of movement. A hinge joint moves like a lever while a pivot joint involves rotation side to side like an axle.
It helps if you look at a example of a bone that has both types of joints. The radial head is part of both a pivot and hinge joint, with the ulna it rotates allowing the hand to pronate and is a pivot joint, while with the humerus it is a hinge allowing the arm to swing through an arc.
Keep in mind these are biological terms and not strict engineering descriptions, biology is more interested in how tissues move relative to each other. Biological terms are not interchangeable with geometry and engineering, nor are they designed to be perfectly rigorous, they are descriptive in nature. In biology rotation is a term reserved for more wheel and axle type motion where a bone is revolving around its own axis.

Find more help here.


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Is social anxiety a part of human gene pool and caused by natural selection?
I'm reading a book called 'Why Buddhism Is True' and I'm not sure I understand author's point regarding social anxiety and natural selection:

Our ancestral environment didn’t feature cocktail parties, slumber parties,  or  PowerPoint.  Our hunter-gatherer ancestors didn’t have to navigate roomfuls of people they’d never met or send their children off to sleep in homes they’d never seen, or give presentations to an audience consisting largely of people they didn’t know very well, if at all.
Just  to  be  clear  (and  at  the  risk  of  repeating  myself),  I’m  not  saying  that  social anxiety isn’t in any sense a product of natural selection. The ancestral environment—the  environment  of  our  evolution — featured  lots  of  social  interaction,  and  this interaction had great consequence for our genes. If you had low social status and few friends, that cut your chances of spreading your genes, so impressing people mattered, even if PowerPoint  wasn’t  the  thing  you  impressed  them  with.  Similarly,  if  your offspring  didn’t  thrive  socially,  that  boded  ill  for  their  reproductive  prospects,  and hence for your genes. So genes inclining us toward anxiety about our social prospectsand our progeny’s social prospects seem to have become part of the human gene pool.

So, from what I've understood, author claiming that the fact that we have social anxiety around people which we probably will never meet again is caused by the fact that in the past every social interaction mattered. Is it true from science perspective? I mean, the people who weren't social in the past would just die without passing their genes, how the social anxiety can become in the human gene pool in this case?
I always thought that social anxiety/confience it's just byproduct of all the events which happens with a child(if a child's social behaviour is positively reinforced then there would have less fear in regards to socialazing, public speaking, leadership etc).
PS: English is not my mother tongue, so I might formulate the question not clearly enough, so, it would be ideal if you can get additional context by clicking on the link and reading the chapter which the passage belongs to(6 pages). Just to be sure the answers aren't based on my interpretation of the author thoughts, but rather on the actual text of the book.

I think you are very wise to be skeptical of 'evolutionary' explanations of something like social anxiety, which could otherwise be explained by an environmental effect. In general, tread very careful around people making big claims based on evolutionary psychology - it makes hypotheses which are almost impossible to test. That statement in the book is pure speculation with absolutely no basis in evidence or theory as far as I know.

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 particular, 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). ——— The wording of your question makes me think you don't have a good grasp of genetics and the (very complex) connection between genes and phenotypes — for this reason I encourage you to check out the links I'll post below. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Short answer - Probably not.
When we talk about traits in evolution, we generally talk about things that are absolute (for example, you either have an attached earlobe or you don't). However, a psychological phenomenon as complex as social anxiety is definitely not controlled by a singular trait. Instead, a number of traits, if found, lead to the phenomenon (things such as physical appearance, susceptibility to sadness et cetera).
This is not to say that the phenomenon doesn't have its roots in genetics, some part of it might be controlled by genetics as well. But logically it's much more plausible that a psychological phenomenon such as social anxiety is dependant on environmental factors much more than genetic factors.
We hear countless stories of people who used to be socially anxious but bettered themselves by forcing themselves out of their comfort zones. This would not have been possible if the trait was genetically controlled.
One other thing to be wary of (as mentioned in a comment on your question) is the fact that many people use false claims of 'darwinism' in order to make their pseudoscience seem legitimate. There is no proof currently that proves it so, and probably never will be.

Welcome to Biology.SE! Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. ——— You make several incorrect statements for example your first sentence — many traits with a strong genetic component are quantitative (e.g. height) and thus are in now way "absolute". You also fall into the trap of assuming that traits result from either genetics or environment rather than the interaction of genes with environment. (cont)

Your answer is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. Looking up references supporting your statements will also allow you to find and correct the errors in your post. Thanks!


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What fish is it?
I bought this 2 weeks ago, but i forgot to ask the seller, what fish is it.
Currently the size is 1 inch.

it is one of the 1300 types of cichlids,i do not know what type you have in your tank other than it is definitely a cichlid.

So, its gonna be 6 in ?

It looks like albino mouthbrooder for me, actually there is a SE site that is more suited for species identification, it's Biology SE, would you mind to have this question migrated there?

Really bio site can identify fish? I dont mind though

Welcome to Biology.SE! For identification questions please [edit] your post to include the location (e.g. country and region — the more specific the better) where this creature originated. The location can be an essential clue for identifications. ——— Clear, closeup photos of the creature from multiple angles would also be helpful. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Do you have any clearer photos of it? It's pretty blurry.

An African cichlid. Because it is apparently albino you may not find an exact match.  Start looking under "apistogramma".

it is a poor picture,over exposed and out of focus so i am not sure it is an albino cichlid.