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What are some examples of interbreeding between species that are separated by 5 million years or more?
Interbreeding is constrained with that the offspring shares the gene pool of the parents. What are some examples of interbreeding that has occurred, where the two species were separated by 5 million years or more?

Consider many cases of horizontal gene transfer. Are you interested in a given lineage in particular?

Animal kingdom, vertebrates, mammals

Years are not really the appropriate measure here, I think.  A horse for instance might have 5 years between birth & sexual maturity (thus 1 million generations in those years), while many birds grow to sexual maturity in a single year, so would have 5 million generations of divergence in the same time.

I depends a little bit about what you mean by interbreeding. In any case, my answer won't be fully satisfactory.
Horizontal gene transfer
If you are referring to any exchange of genetic materials than, you can have a look at Salzberg et al. (2001) who report 40 genes that were horizontally transferred from bacteria.
Elysia chlorotica is sea slug which is able of photosynthesis thanks to a horizontal gene transfer (Schwartz et al., 2014)
Typical interbreeding
If you are thinking about some kind of more common type of inbreeding, then you might want to consider
mule who is the hybrid between a male donkey and a female horse. Donkey and horse share a common ancestor that is about 4.5 millions years old (according to Live Science). Mules are often sterile but some of them have been fertile (Rong et al. 1988; see also this article from the Denver post; thanks @iayork)
Platanus × acerifolia is a hybrid between Platanus orientalis and Platanus occidentalis. Platanus are a rather old genera with fossils of 115 millions years old found (from wiki). However, I don't know how old is the common ancestor between P. orientalis and P. occidentalis
There are plenty of other examples in wikipedia > hybrid but I failed to find good estimate of common ancestry for those who may have had a common ancestor older than 5 millions years but it probably exist given that the mule example is already 4.5 millions years old.

Mules (and hinnies) are not always sterile; see here, here, and many other cases.

Here's some research about a fern hybrid converging after 60 million years:
http://www.iflscience.com/plants-and-animals/distant-species-produce-hybrid-60-million-years-after-their-split/
Some yeasts in a brewery apparently after 10-20 million years:
http://www.iflscience.com/plants-and-animals/distant-species-produce-hybrid-60-million-years-after-their-split/
a Goat Sheep Geep after 7 million years: https://whyevolutionistrue.wordpress.com/2014/08/03/a-new-geep-a-sheepgoat-hybrid/
for timing evolution
http://www.timetree.org/


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Why do you get an increase in bicarbonate ions after vomiting?
Why do you get an increase in bicarbonate ions after vomiting?

Welcome. Any prior research you can share with us? Importantly, where did you find your statement that vomiting increases HCO3- and where is it increased? In the blood? Saliva? Stomach?.

Although you need to show some effort , but I wanted to give you a hint - after vomiting quite a good amount of $H^+$ ions are lost (that’s because HCl is lost) now think what would happen to extracellular fluid to balance this change :)

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Is it possible for a human to live forever if he/she didn't catch any diseases?
Aging is not a disease, but it's the gradual weakening of the body, as the body gets weaker it gets more prone to diseases. So one doesn't die from aging but from diseases. So if one didn't catch any diseases, would it possible for him/her to live forever? Or just longer than the maximum life span?

A lot of deaths are mechanical, and ageing would eventually tire the muscles so much that the heart stops when the person can't even lift their arm up any more at 150 or something, heart attacks are probably eventually due to heart muscle being unfit. The nerve cells also age and dont grow new cells, the rest of the cells grow back old... avoiding blood clots in the brain requires that the person's blood flow remains pure and clean for 140 years, while in actual fact it develops kindof mechanical problems. The skin would end up so fragile at 250 years that it would be like wet paper.

just as the skin loses elasticitty, the veins do too, the person would slowly turn to mush.

Have you tried to answer why there is "... gradual weakening of the body ...".The answer is:aging manifests itself in the form of weakening type diseases termed as age related diseases and a aged human may not necessarily die of infectious diseases (if that is what you mean in the question).The weakening type diseases are inevitable because they involve mass changes at metabolic,cellular and physiological levels.

No that is not possible ever. There is something called telomere which is present in the chromosomes of cell .These Telomere triggers the action of ageging and leads body towards death. When we are in growing age the amount of telemere is very less but as we get older and older the amount of telemere get increases .
The rate of increase of telemere increases with each succesive cell disivision. Hence death is sure no matter what ever you do.

The diseases are only a part of it. Aging is also accidents and such. Cancer would still be prevalent as would accidental deaths. Even a perfect body would eventually fail because individual cell death would lead to organ failure and then death. This cellular death would come from cells failing to commit to apoptosis or from mutations. It won't be possible to live forever, but by using science and medicine, we can greatly lengthen our lives.

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Multiplication of bacillus subtilis
I have a supplement for use in horticulture.  It is a powder that contains mostly subtilis with smaller amounts of a few other strains.
Prior to horticultural application I would like to "multiply" them so as to get to most out of the product.
Is water and a drop of molasses sufficient? (that seems to be accepted in cannabis culture)
How fast do these guys replicate? Without high tech lab equipment is there anyway I can tell that they are in fact multiplying?

You need to add some protein to your media. Use yeast extract if it is available or just boiled commercial baking yeast.

I am basing my answer on this document issued by one of the departments of the Ludwig Maximilian University of Munich.
Bacillus subtilis:

Doubling time: 30 minutes
Incubation temperature: 37°C
Growth conditions: strictly aerobe

Recommended media:

Luria-Bertani (LB) broth/plates - (for everyday use)
Difco Sporulation    Medium (DSM) - (for long-term storage)

You can find the formulations for the aforementioned media by following the link above.
With regards to the latter part of your question, the easiest way to tell (and doesn't require any "high-tech" lab equipment) whether your cells are multiplying or not is to inoculate a broth and see whether there is turbidity after a certain time of incubation. However, please be aware that you may have cross-contaminated your broth so unless you do further testing you cannot know for certain if it is Bacillus subtilis in your broth.


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Does the number of base pairs between the end of one gene and the start of the next gene have to be a multiple of 3?
I'm working on a project for a Coursera course where I need to scan a string of base pairs and identify possible genes, but there's something about real DNA that I need to know to design the algorithm correctly.  My question is best illustrated by example.
Suppose we have a strand of DNA like this : ATGxxxyyyzzzTAAqqATGrsssATGuuTAAvpppTAG
The lower case letters just stand for general base pairs that are not in the sequences "ATG", "TAA", "TAG", or "TGA".
"ATGxxxyyyzzzTAA" constitutes a gene for the purposes of the assignment, and my program does correctly identify that string of base pairs as a gene. What I want to know focuses on what happens after that first gene is found. Let's consider the last portion of the string:
"qqATGrsssATGuuTAAvpppTAG"
My current gene-finding program would identify "ATGrsssATGuuTAA" as a gene, but notice that this strand starts after only two base-pairs ("qq") have been searched through. Does that matter? I.e., would this happen in real DNA, or should the second valid gene be identified as "ATGuuTAAvpppTAG"?

without providing sources or getting into reading frames, I would say that bc DNA is sometimes damaged and not always cleaved at the end of a codon when digested for analysis, sometimes you can get 1 or 2 base pairs that are irrelevant for your purposes. Short answer: it's fine to ignore the "qq" like you've been doing.

I question the value of the course you are doing if it describes open reading frames (ORFs) as genes. This is biologically incorrect, so you can only be expected to follow the precise mathematical specifications given you. Thus the correct biological answer Remi gave you is less relevant than the actual spec, which you don't give. There are other pitfalls that relate to the two strands of the DNA (note that your lower case letters represent the bases of nucleotides — not base pairs), their directionality, and the possibility of overlapping ORFs. Have you considered these?

It’s a programming course, not a genetics course. The actual focus of the exercise is string manipulation, where the input is supposedly a block of base pairs read in an actual gene, like Axl2p. My intent is really more to refine an algorithm to solve a vastly oversimplified problem based on something that computer scientists would actually do on a genomics project.

There absolutely is not a rule saying that all genes on a strand should be in the same frame.
Your program is looking for ORFs (open reading frames) and it should identify all of them, in every frame.  If you were being very thorough, you should generate the reverse complement of your sequence, and search that for ORFs too.  But I guess if you were given this sequence, presuambly the professor gave you the sequence in the desired orientation.


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Is the barcode COI sequence the sense or antisense strand of DNA?
Is the COI sequence commonly used for DNA barcoding the sense or the antisense strand of DNA?

You could use either with the same results. I imagine researchers would refer to the sense strand.

When the barcode sequence is generated by Sanger sequencing, it is sequenced in both strands, and presented in sense strand.

Thank you very much for your answer, which I will accept. But it raises two further questions:

Is it always the case (at least for phylogenetics) that the sequence reported for a gene is the sense strand?
(i.e. the strand which reads the same as the mRNA).

I was a bit confused when you said that both strands are sequenced in Sanger sequencing. I thought that just one of the complementary strands was sequenced?

Careful workers ALWAYS sequence both strands, because some nucleotides are hard to read. Especially at the beginning and the end (the first 35 nucleotides or so, and anything out past 500 from the primers). So you sequence both strands so that one confirms the other. As one strand extends out past the easy to read "sweet spot", between 35 and 300 nucleotides from the primer, the other strand picks up with higher quality reads. Then you put the two together, carefully edit, and report the sense stand to GenBank.


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Why do some yeast flocculate on top an other at bottom?
When fermenting beer normally after the fermentation has completed the yeast flocculate and drop to the bottom. However occationally they form a foamy layer on top of the beer.
The difference is maybe strain dependent. But exactly what is it that makes the yeast drop to the bottom or raise to the top of the beer?


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When can we know if one develops immunity (to SARS-CoV-2)?
I've been thinking for this for a while. It seems there's no ethical experiment to perform to check if immunity is actually developed (the obvious experiment would be to expose someone that have recovered from the infection, but that's unethical).
My idea is that lack of immunity would eventually result in observation of reinfected subjects and one should be able to estimate the likelyhood of that. An experiment would for example be that if we study a set of subjects over time and at one time 1% are infected and later when these have recovered we at a later time find that 1% are infected then perhaps 1% of these would be expected to be among those that were infected the first time (unless immunity has developed).
How did we realize that we get immune to measles, chickenpox and mumps for example?

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Why there is replication of DNA before meiosis?
It seems to me that, even without replication of DNA before meiosis, the homologous pairs can still do crossover, and then be pulled to opposite poles, directly forming 2 haploid gametes.


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Sound produced by muscle tightening
If you are at some quiet place, you will hear some mild noise when you tighten your jaw. Why is this? Is this sound produced by face/jaw muscle?

You can do something similar with your ears as well What causes “ear rumbling”? and What is official term for contraction induced muscle “vibration”?

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Species richness corrected for area -- should area be log-transformed?
I am doing a study to compare plant species richness (total number of species per site) to a bunch of environmental factors of sites at which these plants were surveyed. Because these sites are different in size, I have converted species richness to a species density measurement by dividing by the log of site area (species density = species richness/log[area]).
I log-transformed area, because the relationship between species richness and area at my sites is linear on a semi-log scale. Now that I have calculated species density in this way, I am having a hard time convincing myself that calculating density with log(area) was the correct approach. Does anyone have some insight on this? My community ecology background is not strong and I am getting bogged down in the literature.
Thanks!

related: Can I compare Shannon-Wiener diversity indices between plots of different sizes (area)?

Let me offer my answer even though I have not worked in ecology.
You are asking two questions if I understand you correctly:

Should you normalize to the area sampled?

The answer to that depends on whether the area sampled is a nuisance variable or not. Is it the case that you just happened to sample from areas with (largely) different sizes? Or do you rather expect or are interested in whether it may display some interaction with the environmental factors that you study? In the first case, normalize with clear conscience. On the latter, you should probably include the area sampled in your model. The reason for this is that by normalizing, you are assuming that the relationship between the response variable (number of species) and the predictor (area sampled) is fixed and has a slope of 1 irrespective of the variation of the rest of the variables included in your model. If that is not the case, you want to explicitly add the area sampled as a fixed factor in your model.

Should you log-transform the area sampled?

If the answer to the first question is that the area sampled is a nuisance variable then it does not matter whether you log-transform or not as now you are interested in a new measurement, species density. Hence, you may work with the untransformed variable which would simplify the interpretation of the results by a tiny bit. If the answer to the first question is that you want to investigate the interaction of the variable 'area sampled' with your other predictor variables, then you do not need to log-transform your variable as this is rarely needed, even if you use parametric inference. To summarize, you do not need to transform the variable 'area sampled'.

If the relation between species richness and area is linear on a semi-log scale (as the question states), wouldn't it be best to include log[area] in your model ?

Assuming that you will use a model with a linearity assumption, you don't need to transform the predictor variable. It's only a matter of taste for the interpretation of the results. The most common variable to transform is the response variable, if needed. But I am assuming that this follows a discrete distribution like poisson. So you wouldn't perform a linear regression but a poisson regression. We would need more details about the analysis to say more.

If you choose to study species density, which will follow a log-normal distribution as I understand, then you will probably need to transform the species density response variable, or use a GLM with a log-link.

I think that the latter will be the case. However, I am beginning to wonder if this question shouldn't be migrated to stats.exchange...

The important factor of the question on whether to normalize or not is a biological question (see my point 1). Regarding log-transformation of a predictor variable you will find many (potentially duplicate) posts in stats.exchage, including the one I linked.


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Is there a way to measure the handicap principle?
The handicap principle is used as an explanation for some genetic traits, such as bright tails in male peacocks. However, it seems that this principle could be used to justify sexual selection of almost any trait. Consider the following examples justifying selection of two opposite traits:

Assuming everything else equal, an individual with a larger body has higher nutritional requirements, which are harder to meet. Therefore individuals with larger body sizes were selected because that signals higher fitness.

Assuming everything else equal, an individual with a smaller body can't protect itself as effectively. Therefore individuals with smaller body sizes were selected because that signals higher fitness.

Does this discredit individual applications of the handicap principle? Or is there a way to measure the extent to which the handicap principle has affected selection of any given trait?

I don't have any expertise in this realm, but I will agree that your example does indicate that at the least, one should be rather careful applying this kind of theory to real data, due to the risk of building a just-so story. I think that a more nuanced view of the principle could argue against your second case, considering e.g. conspicuous consumption, so a strong case would need to engage with that IMO (just as one example).

@MaximilianPress This is more about how one would support the idea that the trait has evolved due to the handicap principle and not something else. Would that require an exhaustive argument considering all possible alternatives?

@rus9384 Yes, more or less. None of these principles occur in isolation so to get the full picture, you need to consider all the relevant factors. Compare "island gigantism" with "island dwarfism" for examples; both are things observed in animal populations on islands - why one way and not the other?

@rus9384 I agree with bob1. If you are arguing for or against a specific instance, you need to include detail from natural history, consider alternate hypotheses, and evaluate each argument in light of available data. The kinds of statements in your question are very difficult to evaluate when isolated from data; there isn't a purely logical solution. You could probably write down some fancy differential equations arguing either way with equal elegance.

@MaximilianPress It's more so that even if, say, handicap principle explains peacock tails, it's not clear if it explains it 100% or maybe there are other factors. So, the expanded question would be "Is there a way to estimate how big of a factor the handicap principle is for a given selected trait?"

@rus9384 Oof, quantitative causal inference in evolutionary reasoning is extremely tricky. In no case will it be 100% one factor. Peacock tails couldn't happen outside of the context of birds, or of having tails, or of feathers, or of pigment biosynthetic pathways. Your best bet would likely be something like comparative method: in the bird lineage, how often did peacock tails arise (or be lost), and can you find correlations with other features indicating "handicap principle"? For one-off cases, it's very hard to make robust arguments.

One recent phylogenetic methods pub: https://academic.oup.com/sysbio/article/67/6/1091/4985805

@bob1 Island dwarfism - usually large animals, such as elephants, getting smaller, Island dwarfism -usually small animals, such as hares, getting larger. Each one for different reasons as on Flores Indonesia.

@Rich Yes I am aware of what each is (there are even cases of small things getting even smaller), but I think you missed the point of my comment (read the one above it I am addressing). The reasons you mention are the context of the evolutionary history for each case, so to argue for the handicap principle would require a contextual argument that excludes other causes such as nutrition, etc and credits a "handicap" for a feature. Which is what I was trying to get across in my comment.

Let me give two separate answers.
First, for your example specifically, you could design a test to see whether body size has any selective effect from your proposed mechanisms.  There are 4 tests, you'd need to do to establish the hypothesis. First you have to test whether the opposite sex finds your proposed trait attractive.  For example, inject half the animals with growth hormone so they become large and see if the opposite sex prefers them or not.  Second, stunt the growth of half the animals so they become small and again test to see whether the opposite sex actually finds them attractive or not. It's possible the opposite sex won't even notice the difference much less make mating choices based on them.  You need two more experiments to establish the cost of the trait in natural selection.  Test whether larger animals have more trouble surviving harsh winter by measuring the amount of food they each eat and seeing if animals that eat less food actually suffer health consequences.  Maybe they just hibernate an extra week and everything is fine.  Similarly with the small animals, test to see if small animals really do get caught and eaten by predators more often.  Only once you have shown that the trait of interest has a negative effect on the animal's survival but a positive effect on its mating chances, does the handicap principle come into consideration as a possibility.
Unfortunately, before you can come close to concluding that's the reason, you have to look at all the other possibilities.  For example, maybe the reason larger animals have better mating success isn't because they signal being healthy enough to compensate for their size disadvantage.  Instead, if animals grow large BECAUSE they eat lot's of food, then perhaps the opposite sex will select them for mating because the animal sends a signal that they are good at finding food and thus will find a lot of food for the children they have together.  There is often a strong incentive to find a mate that can find enough food for your children.  There could also be genetic linkage between traits that control size and traits that control some other gene of interest.  For example, if the size genes are next to the genes for pheromone emissions, then maybe it's completely by luck that the larger animals also have genes that emit more mating pheromones to attract mates, and actually the opposite sex is selecting on that.  There could also be linkage between the gene for body size and gene for mate preference.  I don't want to write  a super long explanation, so look up "runaway sexual selection."  And of course, there are many, many other possibilities.  For example, the sexy sons hypothesis posits that females will select sexy males not because they find the males attractive, but because other females do.  And they want their own male offspring to be found attractive, so therefore they decide to mate with a male that is considered handsome so that her sons which carry her genes will be able to mate a lot.  And there's a lot of complexity with any specific real world example.
So this brings me to my second answer which is that while it's fun to think about these concepts, and its certainly useful to study these things in terms of being able to explain the natural world. That is, find evidence for the hypotheses, try to find examples, etc.  At the end of the day, I wouldn't put too much stock into these types of considerations.  It takes a lot of work than can actually be done in most cases to prove one specific reason is why a species has its mating habits, and once you do prove it, so what?  It was all just random to begin with, and other times, other random things will happen, so its not too impressive to say "hey, this time the random thing that happened is the handicap principle because of all these interesting reasons, circumstances, and coincidences."  Biology is a very unsophisticated science, and evolution (my area of expertise) is probably the least sophisticated of all the fields within biology, so as long as you don't buy into these theories hook line and sinker, you can have a lot of fun bullshitting about what might or might not be and even trying to actually test these things when possible (which it usually isn't; I mean who's cruel enough to inject animals with growth hormone just to see if the opposite sex finds them more attractive?)

Does this discredit individual applications of the handicap
principle?

Both support the handicap principle.

Or is there a way to measure the extent to which the handicap
principle has affected selection of any given trait?

No, there is not a good way to do this yet.


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Do breasts size depend solely on fat amounts?
I've read the first answer here on quora and it suggests that (not during pregnancy and breastfeeding) breasts differ in size only due to the amount of fats. However, there can be firm or soft breasts of the same size and this is somewhat disputing the claim. Also, women with firm breasts can find it painful when their breasts are squeezed while those with soft breasts are less likely to have the same experiences.
So, what makes breasts firm or soft given the same size?

You are asking two different, but related questions

Does breast size depend solely on fat amounts?

First, breasts are made up of skin, blood vessels, ducts, fibrous tissue, and fat. There is variation between individuals and within an individual the relative composition changes with age, nutrition, and hormonal status. The size of each of those elements will determine the overall size of the breasts.

What makes breasts firm or soft given the same size?

We don't know, but it's not fat. You can determine the relative amount of fat in breast tissue (fat is black, or radiolucent, other structures are white, or radio-opaque) using mammography. There is even a term for the ratio of non-fatty structures to fat (mammographic density) but physical findings by trained examiners regarding the firmness or softness of breasts do not correlate with the relative composition of a breast. This is tricky because breast density as it is defined in mammography is relative amount of non-fatty structures compared to fat, but you can't predict the mammographic breast density with physical examination of the breast.

It is interesting that biologists do not know it, since somehow men prefer firm breasts, I thought women with firm breasts were somehow more fit, than those with soft breasts (given everything else the same, including their size).

@rus9384 funding agencies don't give a lot of grants to study men's preferences in women's bodies

Okay, there even is a research, even cited on wikipedia, so, I'm correct. https://en.wikipedia.org/wiki/Physical_attractiveness#Breasts

@rus9384 you misinterpreted my comment. I meant funding agencies are not going to give a grant to study the composition of an attractive vs. unattractive breast. They will give a grant to study aspects that make it more difficult to diagnose breast cancer with a mammogram. This is why it is not surprising that we don't know what makes breasts feel firm or soft on palpation, but we do know what makes breast cancer harder to diagnose with a mammogram.

I thought it's because of lack of methods to do it (well, actual cutting breasts, of course, is a straightforward way to do it, but juridically problematic one).

Breast density reflects the amount of fibrous and glandular tissue in a woman’s breasts compared with the amount of fatty tissue in the breasts, as seen on a mammogram.
On a mammography report, breast density is assigned to one of the following four categories:

The breasts are almost entirely fatty (about 10% of women).
A few areas of dense tissue are scattered through the breasts (about 40% of women).
The breasts are evenly dense throughout (about 40% of women).
The breasts are extremely dense (about 10% of women).
Women in the first two categories are said to have low-density, non-dense, or fatty breasts. Women in the second two categories are said to have high-density or dense breasts. About half of women who are 40 years old or older have dense breasts.
This mammographic density doesn't correlate with physical density on a clinical exam. You can have mammographically dense breasts that feel soft to the touch and vice versa.


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How could one calculate the gene flow between two populations?
Imagine there are two populations X and Y, and for each population you have the genotypes of each individual in that population (e.g. Aa, AA, aa, etc.), but for multiple loci (e.g. AABb).
How could one calculate the gene flow between population X and population Y?
An answer would ideally recommend either or:

An R/Python/C++ library, or any other software tool
the breakdown of the maths, for which I would be much obliged, but not entirely necessary in the answer

Background reading

Indirect measures of gene flow and migration: FST≠$\frac{1}{4Nm+1}$

Related questions

Variance in Fst in the infinite island model (by Remi.b)

@Remi.b here's the question in case you are interested in finding out the answer (great hearing from you too by the way)

Theoretical Background
From Slatkin 1991, at equilibrium
$$F_{ST} = \frac{1}{1+4Nm\left( \frac {d}{d-1} \right) ^2}$$
, where $N$ is the per island population size, $m$ is the migration rate and $d$ is the number of islands ($d$ stands for "deme"). As $d \rightarrow \infty$, $\left( \frac {d}{d-1} \right) ^2 \rightarrow 1$ and Slatkin equation becomes the standard Wright's equation $F_{ST} = \frac{1}{1+4Nm}$.
From the above, it is easy to show that
$$m = -\frac{(d-1)^2(F_{ST}-1)}{4 d^2 F_{ST} N}$$
For 2 islands, it becomes
$$m = -\frac{9}{16} \frac{(F_{ST}-1)}{F_{ST} N}$$
In consequence, in a 2 island model the expected $F_{ST}$ is almost twice as low $\left(\frac{9}{16} = 0.5625\right)$ than in the infinite island model.
The above equation is an approximation that assumes...

low mutation rate (would not apply to microsatellite data)
relatively low migration rate (there is a $m^2$ term that is dropped)
symmetric migration rate (backward and forward migration rates are equal)
equal population size per island
equilibrium!

Further Reading
I recommend reading this paper (Slatkin 1991), it is IMO one of the best on the study of $F_{ST}$. I would also recommend Nei 1973, Slatkin 1985 and Whitlock and McCauley 1998.
The specific software to use depends on the kind of data you have. In any case, if you average $F_{ST}$ over a number of loci, make sure to use Weir and Cockerham 1984 method.
Bioinformatics
The first step for you is to calculate your $F_{ST}$. Assuming you have a number of SNPs, you will want to use Weir-Cockerham estimate of $F_{ST}$. There are a number of solutions to compute such estimates. One solution to calculate this is vcftools. The following (Bash) will do the job
./vcftools --vcf MyFile.vcf --weir-fst-pop individual_list_1.txt
--weir-fst-pop individual_list_2.txt --fst-window-size 800 --fst-window-step 100

, where MyFile.vcf are your data in vcf format (you might eventually want to use PGDspider to reformat your data). individual_list_1.txt and individual_list_2.txt are files containing the list of individual names (seperated by \n) belonging to the first and second population, respectively. The options --fst-window-size and --fst-window-step allows you to compute the estimate over a sliding window. I chose arbitrary numbers above. EggLib is another good alternative.


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Do distinctions between dry, tickly and chesty coughs have any medical basis?
Background
At least in Britain you normally come across distinct kinds of cough medicine "chesty", "dry" and "tickly".

Questions

Are "chesty", "dry" and "tickly" coughs always due to microoganisms?
For the types of cough that are infectious, are differences due to different species of micro-organism or the same micro-organism at different stages of its development?
Do the alternative treatments (e.g. levomenthol, squill, liquorice for chesty vs. glycerol for dry/tickly) merely deal with symptoms or do they actually help fight the infection?

Related
A related question is: What is the cause of dry cough?

Cough need not be essentially because of microorganisms. It is basically because of airway irritation.

@WYSIWYG Thank you for pointing out that glaring hole, adjusted

I'm not sure what a tickly cough feels like, so I'll leave the answer to someone else. A dry cough produces no mucus, so the lungs are irritated but there's no extra mucus in the upper branches of the lungs. A chesty or wet cough implies both irritation(you're coughing) and extra mucus production. All three are immune responses. As far as treatment goes, blanket anti-cough medicines don't help fight the infection, but deal with symptoms. Expectorants make coughs wetter which help them clear, others just reduce the cough reflex, etc.

If I may add to what Resonating has said, when it comes to infections, dry cough is usually associated with a viral infection, whereas wet cough is usually caused by bacteria. The two are treated very differently - dry cough is remedied with cough-supressing drugs (antivirals are rarely needed), whereas bacterial infections are medicated with antibiotics (antivirals are NOT antibiotics) and drugs that help clear the mucus from the respiratory pathway. Treating wet cough with dry cough medications is not only ineffective, it can also be dangerous. One more thing - not all bacterial infections necessitate antibiotics which should be used sparingly because the world is running out of antibiotics.


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Are humans the only primates being engaged in group sex?
There are quite many examples of humans being involved in group sex. I won't say it is a common thing and won't say whether it is "natural" or "cultural" (but "cultural" only means induced to majority by minority).
What I'm asking is if there are any other primates being involved in group sex (or how is it called in biology?). Under "group sex" I mean a sexual intercourse where several males or females can see other males and females being involved in sex too, right as they themselves are.

I haven't looked this up specifically, but bonobo's are sort of literally crazed sex monkeys - I'd be surprised if they don't do this.

@Nicolai Their sex has 13 seconds duration. I'm not sure another male or female has time even to come there.


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Does the X/Y sperm ratio in male ejaculates depend on circumstances of sex and who they are mating with?
Male mice are known to have different X/Y sperm ratios in their testis. Possibly, this phenomemon is not limited to the mice. However, can the males utilise that to their advantage?
For example, produce ejaculates with higher Y sperm concentration when mating with a female they have not mated before. Or when mating with a female who they perceive as more masculine (regardless of how they do that, be that pheromones, appearance or other signs).

The Trivers-Willard hypothesis says that females should change the ratio of female-to-male offspring based on her condition (https://pubmed.ncbi.nlm.nih.gov/27170721/). Maybe something similar is happening here, where males ejaculate more X-chromosome carrying sperm when in better health and less when in poorer health. I have never heard of the TWH being applied to males though, so that is honestly just my best guess.


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Is there any evidence for sperm parameters being connected to fitness of the offspring produced by that sperm?
In most (if not all) sexually procreating species the amount of offsprings a male can produce is limited not by the amount of sperm he can produce, but by the amount of eggs his sperm can fertilize (with rare individual exceptions).
Because of that the optimal strategy would be to fertilize eggs with the best sperm.
Therefore it is reasonable to assume that there would be adaptations making sperm with deficient genes less likely to fertilize an egg.
But is there any evidence of this happening? E.g. would fertilizing eggs with less motile sperm (potentially with IVF) produce a less genetically fit offspring or result in a miscarriage?

The only way that natural selection can act on genes is when they're expressed, there's no mechanism for reading and assessing the "quality" of a gene in a sperm. Obviously the genes that effect the quality of the sperm will be selected for/against.

Well, it could be that genes which would make a "lower quality" offspring also would make a "lower quality" sperm. How is an interesting question, but genes should be seen as a part of the whole system (genome) rather than indepedent individual entities.


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Does lack of adaptations for sperm competition necessarily shows the species are monogamous/serially monogamous/polygynous?
On the one hand adaptations for sperm competition, such as large testes, mate guarding, etc. are used to support that female in species are promiscuous.
On the other hand we know multiple eusocial species where most inidividuals don't reproduce letting their kin (e.g. the bee queen) reproduce. Which means that in some cases it is more beneficial to let your kin reproduce than to do it yourself.
For that matter, would not there be intermediate states, where multiple indivuduals reproduce, females are promiscuous, but since reproducing as much as possible yourself is not necessarily good, sperm competition adaptations would not get developed? Are there any candidates for such species?


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Books on machine learning applications in Biology
I have recently engaged with a collaboration, which requires me to construct, then train an unsupervised artificial neural network (ANN).
However, I have only a very coarse understanding of what machine-learning classifiers try to do, and how they work. For example, Chen et al.'s random forest (RF) classifier (ensemble of decision trees) for protein-protein interaction prediction. Additionally, I have very little idea about which types of machine-learning are useful to different classes of Biological problems.

So -if they exist- I would very much appreciate information on books that discuss applications of machine-learning classifiers in Biology/Bioinformatics. Preferable criteria are:

Intuitively introduces key concepts.
Illustrates a variety of Biological/Bioinformatics problems and their solutions by appropriate types of machine-learning (e.g. when is it appropriate to use ANNs versus RF classifiers?)
Relatively short (I'm planning to read from cover to cover).

Related

Stack Biology: Machine-learning for light microscopy problems to solve (I would consider this question a sub-class of the present question; personally, I am more interested in the sequence analysis / genetics domain of Bioinformatics problems)
Stack Biology: Historical connection between neuroscience and machine intelligence
Blogs about deep learning implementations in Biology
GitXiv: Collaborative on-going (and also published) computer science projects pertaining to machine-learning (search using relevant Biology-related queries to filter)

Tarca et al. 2007 could be a good reading.

At NIPS 2016 most ANN implementations I saw were related to biology were trained on imaging data, thus the kind of comprehensive book you are looking for probably doesn't exist yet.
However, if you utilize the search feature on Amazon.com you'll find:
Neural Networks for Applied Sciences and Engineering: From Fundamentals to Complex Pattern Recognition
Artificial Neural Networks (Methods in Molecular Biology)
and this, which seems to best meet your need:
Neural Networks and Genome Informatics, Volume 1 (Methods in Computational Biology and Biochemistry)

I own a book entitled Bioinformatics, The Machine Learning Approach, by Baldi and Brunak. I haven’t done more than glance at it, but it might be of interest. It’s more geared to bioinformatics than general computational biology.


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Species ID: Buckyball-like fungus
Previous research

A friend of mine shared a link of some beautiful fungi: https://i.sstatic.net/B81Pu.jpg. I was intrigued by the curious critter below -- it seems to have honed the power of buckyball geometry, presumably much before we Humans ever did (search: Buckminsterfullerene to learn about a feat of chemical engineering).
Google reverse-image search almost got me the answer I needed, but no species name.
I've asked friends on Facebook with no answers yet.

Question
What is the name of this species of fungus?

Related Questions on Stack Biology

Here's a related Species Identification question of a fungus: Puffball mushroom species ID? (by @rg255)

EDIT: I'm an idiot... the Imgur had species names, thus answering my question, post-mortem. Thanks @skymningen for pointing that out.

If you like the general idea of how wondrous mathematics in nature can be, read "What Shape is a Snowflake?" by Ian Stewart. It's a nice read, I loved it as a youth and I blame some of my fascination for biology to this book.

I understand the face palm, but it might be more useful to future readers if you change the title again.

@AtlLED, I'm not quite sure what you mean? As in to add the species name?

The question would appear as "answered", and @Ilan did technically answer it before I read the comments. I would suggest you voting to close my answer down, let the community decide.. I was about to delete it but then I read the deletion message

Sorry, I mean the top heading title not the question title.  The "Edit: I'm an idiot..." part is kind of jarring.  I don't think it needs to be deleted.  Maybe a more subtle note after the link?  Anyway, I guess this is more of a style point so feel free to ignore.

@skymningen, I am intrigued: why did you use the word "blame"?

@hello_there_andy I am not a native english speaker. Connotations of words might be different in my native language. It was supposed to be a cheeky comment.

I see @skymningen

Looks very similar to Clathrus ruber fungus.
Be careful, it is poisonous.

Actually... the link the OP gave has named pictures and it was also named as Clathus ruber there. So I guess you got it right.

@skymningen I didn't use the link in question. Hm, nice to know.

@skymningen thanks for pointing that out... I genuinely didn't notice those... *facepalm*... *re-edits the question*

@hello_there_andy Happens. Without that question I would have never known this interesting fungus!

Who knew fungi could be so... fun. Sorry that pun had to be done. @skymningen


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Is my RNA-seq experimental design correct to use it for SNP calling?
I am a newbie here and would highly appreciate your advice about one particular experimental design.
We have data from RNAseq experiment which was originally designed to assess differential expression. The details of experiment are as follows:
2 modalities of the phenotype
Each phenotype is represented by 4 samples. 1 sample = 60 individuals pooled together at the stage of RNA isolation.
Molecule – polyadenylated mRNA
Sequencing chemistry – Illumina paired-end, read length - 2*100 bp
My question is whether it is correct to use this RNAseq data to call for SNPs? I made previous search and found that most of people calling SNP from RNAseq use 40-1000 samples (= individuals). But they initially designed RNAseq experiment for further GWAS. I see that this analysis cannot be applied to my data (at least because in my case individual flies were pooled without barcoding – 60 flies per a sample). However, can I still call for SNPs and upload the list to database as a list of potential targets for GWAS with, for example, estimation of functional impact upon protein structure? Will they be “true” SNPs, or our experimental design makes even this step invalid?
I found this paper https://www.ncbi.nlm.nih.gov/pubmed/27458203 where people used 2 phenotypes each represented by 2 samples what is almost like our experiment, but still have doubts.


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Is it likely that humans will evolve to be less affected by dangerous food additives or tobacco smoking chemicals?
I recently had a discussion with a few colleagues about food additives and there were two major "arguments" about how some of these affect the human body in the long term:

some food additives will become less dangerous to humans, they evolve. The same rationale for smoking. The only similar thing I know to support this would be the ability humans gained to drink non-human milk.

the first argument is very unlikely to hold because in the vast majority of cases these substances do not affect reproduction and thus people getting sick and/or dying in their 50s+ is not affecting the evolution (food additives and smoking allow one to have children that can reproduce).

Neither of those involved has any in-depth knowledge of how evolution works in these cases and I am wondering if any of these arguments make sense from a biological point of view.

This is a really hypothetical question, since it assumes that particular food additives, or the practice of smoking tobacco, will be around for long enough to actually have an evolutionary effect.  But most additives have only been around a couple of generations.  Even widespread smoking was only around for a century or two. and is in decline most places.

Evolutionary effects only show up when they have a strong impact on the number of descendants that are produced.
Any disadvantageous effects due to things like food additives and tobacco appear to be quite small with respect to the ability of people to produce children and grandchildren. Moreover, since humans are social animals whose reproductive success is strongly determined by their social relations, there may be all sorts of other effects that interact as well, such as tobacco use being socially desirable or undesirable in particular (sub)cultures.
Thus, there is virtually no chance of evolutionary effects showing up before cultural or technological changes render the issue moot by changing the nature of the environment against which evolution would occur.

Probably not, if for no other reason than tobacco companies and other drug producers have been intentionally breeding their plants to produce stronger and stronger doses of the chemical so that their customers can get a stronger high. It's just another form of biochemical arms race.
As an example, there was once a species of caterpillar that fed on a drug-producing plant, either tobacco, cannabis, or coca, as part of its natural lifecycle, incorporating the toxins into its body. The modern, selectively-bred versions of this plant are so toxic that this caterpillar, which was once specialized to feed on this toxic plant, can't handle it anymore and can only feed on wild, non-cultivated plants. Sadly I have been unable to locate a reference with the exact species.


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Is it possible that nearly human mammals existed before the last mass extinction dinosaurs?
From time to time I am hearing people discussing about the possibility that men and dinosaurs meeting some time ago.
The oldest mammal remains seem to be about 35 million years old, quite some time after dinosaurs have perished.
Also, it is very implausible for a primitive man to manage to survive near the dinosaurs (I think they would be very hard to handle even using current technology).
Question: is it even remotely possible for advanced mammals (nearly humans) to have coexisted with dinosaurs?

Just a quick comment, the article that you linked exists on the ICR page, Institute for Creationist Research, which is more of a religious organisation than a scientific one. If anything, they're doing pseudoscience, so please, do take their claims with a (big) grain of salt.

Is it possible that nearly human mammals existed before the last mass extinction dinosaurs?

Short answer
No!
Longer answer
The ancestor of all mammals lived about ~180 millions years ago (see here), so much before the Cretaceous–Paleogene extinction event (~65 millions years ago). The ancestor of all primates lived ~65 millions years ago (see here), so pretty much at the same time as the C-P extinction.
But please, don't picture the ancestor of all primates as something that is too human like. It looked more like a lemur, a tarsier or a loris, than like a human!
The first great ape lived about 14 millions years ago (see here) and the most recent ancestor of chimpanzee, bonobos and humans lived about 6 millions years ago (see here). The discovery of how to control fire happened about 1.5 millions years ago (with a pretty wide confidence interval, see the wikipedia article). The first generally considered Homo sapiens lived about 200,000 years ago (see the wikipedia article). The wheel was first invented about 5'000 years ago (see the wikipedia article).
Related: Who are humans' closest relatives, after primates?

So, the answer is clearly to my question is No and such coexisting is pure fantasy. Thanks for the relevant references. Onezoom dynamic tree is particularly nice and useful for newbies.

Indeed it is no! I added this simple straight forward answer as a short answer. Yes OneZoom.org is pretty neat. You can find other good resources to represent the tree of life in the post The best free and most up to date phylogenetic tree on the internet?.


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What animal / insect carcass is this? (Victoria, Australia)

During a hike on a mountain in Victoria, Australia, I came across this unusual shedding in one of the small rainwater pools. The pool looks small, but was developed long enough to have several insect species thriving in it such as water fleas and others of which I'm unsure.
This was the only shedding found and no other large insects or animals were found in this pool.


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Do plant orders have easily recognizable characteristics like the families do?
I know that many plant families have recognizable characteristics, and a recommended way to learn botany is to become familiar with these families before moving into genera. I'm curious why I haven't seen this advice applied at the order level before. Are orders too high-level to have a concise list of recognizable characteristics most of the time? Are there too few orders for them to be useful, but few enough families to make learning them within reach? Are there any resources that list the characteristics of the orders similar to what Elpel's "Botany in a Day" does for families?

I wish I had previously known about 'Botany in a Day' - sounds very helpful! A short (and unsatisfying) answer would be that yes, there tend to be shared features between members of a given order, but I am not sure whether they are universally helpful, reliable or recognisable (e.g. Asterales are supposed to share a common stamen morphology...).

Orders are, like you say, too high-level for this - the Caryophyllales for example, the order that contains the familiar pinks and carnations grown in gardens also contains cacti, tropical pitcher plants, beetroot, Lithops, plumbago and amaranth - all of which at first glance seem to be completely unrelated.


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Enzyme Concentration vs Reaction rate curve
I aware that the Michaelis-Menten plot (Substrate concentration vs Reaction rate) is a hyperbola. Would the shape of enzyme concentration vs reaction rate also be a hyperbola? I would assume substrate concentration and enzyme concentration would be similar variables. I am wondering what the curve is when there is a limited amount of substrate, as unlimited substrate would lead to a linear curve. Thanks in advance :)

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works.  Have a think about the conditions for generating a M-M plot and what you are measuring.

A plot of (initial) reaction rate vs enzyme concentration should be linear at all substrate concentrations, regardless of enzyme mechanism.
Doubling the enzyme concentration should exactly double the (initial) rate, and halving the enzyme conc should exactly halve the (initial) rate.
This must be the case at both high and low 'fixed' substrate concentrations.  By 'fixed', I mean the concentration of substrate at which the experiment is done.
If, in determining a Km for an enzyme, the lowest substrate concentration used is 10µM and the highest is (say) 1mM, then a plot of vI (initially rate) versus eo (enzyme concentration) should be linear at both 10µM and at 1mM.
To spell it out, doubling the enzyme concentration at a substrate concentration of 10µM should double the rate, and halving the enzyme concentration should half the rate, and the same applies at 1mM.
In kinetic parlance, "the vi versus eo should be linear", and is a prerequisite for a meaningful (steady-state) kinetic analysis
There are exceptions, such as some preparations of phosphofructokinase, where doubling the enzyme concentration does not double the initial rate (perhaps because of enzyme oligemerization) and this makes kinetic analysis very difficult.
Let's think about the consequences of this not being true.  How does one determine a meaningful Vmax?  If you determine the kinetic parameters at one enzyme concentration and I at another, we will come up with different values for Vmax if the vi versus eo is not linear.
Furthermore, what happens if, during the course of determining the kinetic parameters, I need to double the enzyme concentration in order to produce a detectable rate (typically, this happens at low [S])?  The assumption is that I can divide this rate by 2 in order that all rates are quoted at the same enzyme concentration.
I said above the this applies for all enzyme mechanisms. This includes Michaelis-Menten.  Pick any Km, Vmax, and [S]o, assign an arbitrary value of 1 to eo, and calculate the rate.  Now double this arbitrary value: the calculated initial rate doubles.
Finally, the above applies to steady-state enzyme kinetics where eo << [S]o
A comprehensive analysis of the case where the enzyme concentration is high is given by M. F. Chaplin in The effect of enzyme concentration on the Michaelis-Menten equation published in the January 1981 issue of Trends in Biochemical Sciences, but which does not seems to be indexed in PubMed or the like, and a link to a scanned copy may be found here (which amazingly still works).


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Is stroma lamella and intergranal thylakoid the same?
My textbook says that "Thylakoids are arranged in stacks like the piles of coins called grana or the intergranal thylakoids. In addition, there are flat membranous tubules called the stroma lamellae connecting the thylakoids of different grana"
"Grana are connected by stroma thylakoids, also called intergranal thylakoids or lamellae"
"Wrapped around the grana are multiple parallel right-handed helical stromal thylakoids, also known as frets or lamellar thylakoids."
Source: wikipedia

Source: By Yuv345 - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=93345037
This image has stroma lamellar sheets. Is that synonymous to stroma thylakoids?
My confusion is regarding the synonymous terms used.


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Is a FoldScope microscope suitable for plant cytogenetics?
I have recently been getting more interested in amateur botany, and have some background in genetics and genomics (PhD+). I have used standard light and confocal microscopes but don't have much expertise in microscopy.
I often find myself wondering what the ploidy is of some plant that I'm looking at, as I know that this is a major life history feature and genetic variant in wild plants.
I was curious whether a cheap little scope like a foldscope would be an adequate microscopy instrument for looking at the cytogenetics of a (probably rather crudely prepared) plant sample, assuming that I can come up with a suitable home protocol. (I don't currently have access to lab space.)
I have found this question, but it doesn't really explain much about the required parameters for cytogenetic microscopy.
So:
1) What microscopy parameters need to be satisfied to do cytogenetics?
2) Does a foldscope meet them?
3) If not a foldscope, what other cheapo scope would work?

Foldscope has resolution of two microns, not enough for this purpose. Sorry no extra refs.

@PolypipeWrangler Can you comment on why? E.g. I found this: "...the size of an average condensed mitotic chromosome, which is about 6 by 0.7 microns..." That is in the same range, which might mean it's either easy, hard, or impossible, but I don't know because I don't have the background. To reiterate, what are the parameters necessary for the task?


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What are the relative frequencies of dominance and codominance in genes underlying phenotypic characters?
Many questions already exist regarding dominance/recessive relationships, see e.g. here. I am asking this question because I have often wished to have it to refer to, and also genuinely curious whether someone has a clear answer grounded in evidence.
A common misconception that one encounters in genetics (especially as received from a high-school level class) is that all genes affecting a phenotype follow the classic Mendelian relationship of a dominant / recessive inheritance pattern yielded by diploid organisms. See for example this recent question.
It follows that many consider this relationship to be foundational to genetics rather than largely the result of ascertainment bias. In contrast, most quantitative genetics models perform well assuming linearity / additivity, i.e. "co-dominance". It is not clear whether this is an outcome of the real state of affairs, or simply that the additive model is "good enough" for summarizing the complex reality of underlying epistasis, dominance, etc (I believe "good enough", but that's somewhat philosophical).
My question is this: what proportion of variants with quantifiably large phenotypic effects fit a dominance model of inheritance?
The question is muddied somewhat by incomplete (but not co-) dominance, or the possibility of multiallelic loci with many alleles with a complex dominance hierarchy, as in this example. But I'd be satisfied with a rough quantitative estimate.
My vague sense is that most variants are better explained by an additive model, if only because their effects are rather small. In other words, I think that our fixation on dominance is a result of ascertainment bias inherited from Mendel. We then teach it to early students because it's simple and illustrates some important features of genetics. Am I wrong?

This seems like it would be exceptionally difficult to quantify. By far the most common cases of apparent dominance are going to be those involving enyzmes where a recessive allele is somehow non-functional, yet the product isn't limiting or negative feedback is present such that haplosufficiency is observed. Even then, though under some circumstances you may see some evidence of haploinsufficiency, or there may be some other allele that shares a phenotype with the "true" dominant allele, yet shows haploinsufficiency when paired with a true nonfunctional allele. How do you count that?

@BryanKrause I agree with the sentiment- it's hard! This is the kind of thing that variance partitioning claims to handle, but doesn't actually. Perhaps a more viable question would be something like how frequently variable characters segregate in a true Mendelian fashion following dominance, vs. complex, vs. additive or whatever. In which case, almost none would be dominant I'd bet! But it's highly contingent on the population and whatever other variation exists.

It is not clear whether this is an outcome of the real state of
affairs, or simply that the additive model is "good enough" for
summarizing the complex reality of underlying epistasis, dominance,
etc (I believe "good enough", but that's somewhat philosophical).

I think it is likely that it is both. Additivity is real biologically and isn't just convenient, but it is also true that if we had complete information about every genotype-phenotype relationship, we would improve our models a bit beyond the purely additive model (for many phenotypes).

My question is this: what proportion of variants with quantifiably
large phenotypic effects fit a dominance model of inheritance?
Proportion of variants in the genome would be hard to define. Most nucleotides are probably useless and don't significantly affect any phenotype, drastically reducing the proportion of dominant and additive alleles. The proportion of variants that effect a given trait is easier. This is different than "importance" of dominance/additivity: you can have a lot of dominant alleles with little affect, so the phenotype is overall additive but has more dominant alleles governing it, or vice versa.

We can try to get an idea of both the raw number and the variance explained. For a raw number, and picking educational attainment as an example, Okbay et al. 2022 looked at 2,574,253 people and found that their "dominance GWAS identifies no genome-wide-significant SNPs. Moreover, with high confidence, we can rule out the existence of any common SNPs whose dominance effects explain more than a negligible fraction of the variance in EA." The "combined variance explained by dominance deviations in common SNPs is negligible." Since they found thousands of additive alleles, the proportion of dominant alleles for this phenotype is zero. For other phenotypes, I'm sure someone has found non-zero dominance alleles.
It seems like the core of what you want is how much variance is explained by additive vs. dominance/epistasis effects. I don't like this too much for the reason you stated in your comment, but it's interesting nonetheless. There have been a number of estimates on this.
A study on 70 complex traits on 254,679 individuals "found strong evidence for additive variance," but negligible dominance variance" and "epistatic variance... not significantly different from zero." "Genetic variance for complex traits is predominantly additive." "Epistatic variance is likely to be extremely small in human complex traits." This replicated a similar earlier result that looked at 79 phenotypes. This was replicated again here with 50 phenotypes. Each time, dominance is negligible.
Hill et al. "evaluate the evidence from empirical studies of genetic variance components and find that additive variance typically accounts for over half, and often close to 100%, of the total genetic variance."
Twin studies also support the additive model being predominant, with no effect of dominance for most phenotypes, but some effect for some phenotypes.
You wondered if it was the "the real state of affairs" or just "good enough." Here are some reasons why there might be real biological bias for additivity--though this isn't mutually exclusive with it being "just good enough."

Imagine if a gene for having a long neck was dominant in giraffes--it
would be impossible to eliminate the recessive allele from the
population (aside from genetic drift), as there is no phenotypic
difference between heterozygous and homozygous long-neck individuals.
Now imagine if there was simultaneously a different, additive pathway
to having a long neck. Selection would favor increasing neck length
via the additive pathway, as there would be decreased risk of one's
offspring having a short neck. In this case, selection inherently
favors additivity.
Mutations happen randomly. By definition, in
order for a new dominant interaction to occur, two mutations must
happen. If the mutations require each other to be useful, they'd have
to occur simultaneously to be selected for. On the other hand, a new
additive mutation being selected for only requires that a single new
mutation is beneficial.
Most
allele frequencies are biased towards one extreme or another.
Therefore, the remaining genetic variation between individuals is
likely to be of small effect and polygenic.
[Multilocus epistasis
itself mostly contributes to additive variance.][6]
The existance of polygenicity alone can be sufficient for a lack of dominance effects.

I like your list of arguments about "the real state of affairs", and it seems to be a good set of arguments that dominance is very uncommon, which is great because that's the point of the question. However, it is not a good set of arguments that additivity has a real biological basis- e.g. your point 4 is explicitly a "additivity is good enough" point. Overall, thanks for the comprehensive answer!

Right. I also agree that it is "good enough." However I do think at least points 1 and 2 are relevant to the biological basis of additivity.

Mm... I think that points 1+2 make arguments for the relative frequency of additivity under a toy model of selection. But they're not really biological arguments (as I usually think of them). They're saying effectively, "if additivity existed, then selection would like it." (A corollary of these is that additive variation would become fixed!) They're not saying "under the hood, there are biochemical, cytological, developmental, and ecological reasons why a certain genotype::phenotype map exists". The latter is more interesting to me, which shows my biases.

You may be interested in this paper: https://academic.oup.com/genetics/article/121/4/869/5997956

I don't have a citation for this, but I imagine a common biochemical reason as follows: imagine you have a typical protein-coding gene or promoter. You alter a random base pair. Odds are, the promoter or the protein is still going to function, just slightly better or worse as most amino acid sequence changes wouldn't have devastatingly large effects outside of specific critical regions (BRCA2 is a good example of this). You mostly modify the binding affinities by modifying a random base pair, which wouldn't result in dominance. If most mutations killed the gene, dominance would be more common


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Can you "fight" a coma or serious illness?
In an article about the latest earthquake to strike Mexico, I read that a rescuer said to someone in a gurney, "Fight for your life, please!"
I've seen similar things in TV shows and movies where a character is in a coma or seriously injured or ill.
But how much—if anything—can mentally "fighting" a coma, injury, or illness do?


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Transpiration Process
During periods of rain/showers, does the transpiration process in plants slow down as a result of an equilibrium of water in the interior and on exterior of a plants foliage?


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Failed attempts at changing ecosystem in order to preserve it?
Have there been any notable tries in the recent past (think 20th century or later) to purposefully change any ecosystem in order to save it or some particularly species in it, but which have instead produced the opposite effect? I am sure there must have been, but can't bring any to my mind at the moment.
Like, for example, if you have an island that has some large felines, which frequently attack sheep that are becoming scarce, so the felines are starving and becoming scarce, too. So you introduce feral goats, which were supposed to provide meat for felines, however, goats were (a) too nimble for felines to hunt well due to, eg. geography of the island (too many rocks that goats can prance about, but cats not so well), and (b) ate all the grass that sheep still had. So the net effect was that sheep died out, cats died out and there remained a few goats.
I am aware of a number of cases, where these things could have happened due to humans not aware or not caring about the problem (eg. introducing rabbits in Australia), but I am wondering specifically about misplaced efforts to save/stabilize an ecosystem.

Perhaps not quite what you had in mind, but it seems like the introduction of the mongoose into Hawaii is close. In the late 19th century sugar planters introduced mongooses into Hawaii in an attempt to control rat populations. It turns out that rats are mostly nocturnal, and mongooses are mostly diurnal, so the two species rarely interacted. The mongoose population boomed and had a huge negative impact on native bird and turtle populations, since the mongooses would eat the bird and turtle eggs.


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Is it considered feasible to genetically improve plants for better Carbon dioxide breakdown?
I have found several somewhat related questions and answers here and elsewhere, but I couldn't find, if any  scientist groups are researching genetical improvement possibilities of existing plants' photosynthesis processes to produce plants, which would be net oxygen producers and/or significantly increase their CO2 removal abilities.
For the most part, it seems people are preoccupied with getting energy out of plants, but if we allowed that potential energy to be used for photosynthesis, wouldn't such plants be useful even if we can't harvest energy from them?

Plants already do this on their own in the presence of high CO2.

I'm not sure from your question if you're clear on the relationship between carbon fixation and 'energy', so just to be clear: carbon fixation in photosynthesis is the process of capturing CO2 and using it to store light energy in the form of carbohydrates. More CO2 capture = more harvestable 'energy'. Improving the efficiency of photosynthesis therefore captures more CO2 and generates more harvestable energy in the form of carbohydrates (edible or not).
There are three carbon fixation pathways in plants: C3, C4 and Crassulacean acid metabolism (CAM). The relative efficiency of the different pathways depends on the environment; for example, C4 plants are able to more efficiently fix carbon in drought, high temperatures, and limitations of nitrogen or CO2.
Because of this, scientists are indeed interested in engineering crop plants to use alternative carbon fixation pathways. One such project is the C4 Rice Project: http://c4rice.irri.org/.

Thank you, this explains a lot. I was wondering if maybe there were plants who were not cultivated, but which were particularly effective at tying up CO2, but this shows the other implications.

@Gnudiff no problem - glad it's useful!

Many if not most plants undergo less photosynthesis than they possibly could. This is because water availability is often their major limiting factor. Plants have to keep the tissue they respire through moist just like we do, so they are constantly losing water to the environment as long as they are taking in CO2. Because of this, many plants slow or limit their gas exchange and photosynthesis. Changing the efficiency of their photosynthesis will not have any effect on the plants ability to sequester carbon. Simple high efficiency irrigation might however.

I don't think OP is specifically asking about "Changing the efficiency of their photosynthesis"; I think his question applies equally to, say, genetically modifying a plant to be able to retain moisture better so that it will happily photosynthesize more (if that is indeed its limiting factor).

its the same problem either way, biological gas exchange just forces you to lose moisture because it has to work through diffusion. plants have already done everything they can to limit it, including creating microclimates.

Thank you I upvoted this for indicating the issue being broader.

It is very interesting you saying "plants have already done everything"... it would imply that there is no actual way to improve the process. However, plants don't have the same goals as us, when it comes to process usability.

the lose of water is their major limiting factor meaning their is massive evolutionary pressure to do something about it. as long as gas exchange relies on diffusion, water lose will occur across the same membrane.


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Sports of western sword fern: descriptions or resources?
I found a western sword fern (Polystichum munitum) growing in a home garden that appears to be showing a sport. Notably, the sportive fronds come off the same rootstock as more normal-appearing fronds (see image).
Prominent features include duplicated frond apices and pinnae, and a "lacy" appearance with marked serrations (see images). There is also possibly some chlorosis and/or necrosis, suggesting that the sportive leaves are unhappy in some way.
Fern sports are a well-known phenomena, and have been described in the Polystichum genus previously.
Questions:

Is this truly a sport? If not, how could I tell?
Are spores from this fern likely to be viable?
Is anything known about the mechanism, other than mutation? I know that fern karyotypes and genome sizes can be pretty unwieldy, I suppose ploidy change is a good hypothesis.


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What kind of spider is this?
This large white spider has made her home on our garage. We live in the upper peninsula of Michigan. I believe it's an orb spider but couldn't find any with the large black almost hourglass shape on the back

A creepy one... Is that a good answer?


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What does the total membrane current vs time plot of an action potential look like?
What does the total membrane current vs time plot of an action potential look like? I see that there are voltage vs time plots, but I can't seem to find the current plots.
Thanks

Check out panel b for total current, panel c for K+ and panel d Na+ currents separated...

This is from this website: imageWebsite

Could you please also provide a link to your source in case someone wants to read more about how these currents are measured?


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Why are the Watson Crick base pairs normally found in RNA helices cis with respect to the glycosidic bonds?
I know that Watson Crick base pairs found in RNA helices are cis with respect to their glycosidic bonds, but I am having great difficulty seeing why this is true. Since RNA secondary structure is defined by a single RNA strand that loops back on itself forming helices, it seems to me that nucleotides in an RNA helix should have their 5' phosphate groups oriented in opposite directions, which should make their glycosidic bonds trans. Is there no relationship between the direction of the glycosidic bond and the orientation of the phosphate group? What am I missing here?

I am afraid that without a diagram to illustrate what “you know” very few members of this list will be able to follow it, never mind answer it. Certainly I can’t. Only real specialists can talk about structure envisaging it intheir mind. At the very least reference a paper or web page illustrating your point.

@David Page 501 of this paper provides a useful illustration, and I think enough information to answer the question.  We see the antiparallel helices both interacting at W-C surfaces will be cis when antiparallel.  Cis is defined as both sugar backbones on the same side in the plane of the bases (creating a minor groove), NOT phosphates both on the same side in the plane of the backbones.  I'll leave this as a comment because (a) I could be wrong and (b) it's a hard one to talk about in a way that makes sense.


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How many types of tRNA are there in a human cell?
If the genetic codon on mRNA is a triplet then this means the four bases (A, T, G and C) can have 64 possible combinations. But since three of these codons are non-sense (non-coding) so we are left with 61 codons.
So this means there should be 61 types of tRNA bearing anticodons complementary to these 61 codons? Since I've read that there are no tRNA having anticodons complementary to these stops codons.
Also why does a quick google search tells you there are 20 types of tRNA? Is this completely wrong?

Welcome to SE Biology. Please do us the courtesy of finishing the [Tour] and then read the Help on asking good questions. You will see that you are expected to "thoroughly searched for an answer before asking your question". It is clear from your question that you have never consulted even an introductory text on biochemistry or molecular biology on the topic of translation. You need to do so as your suppositions, conclusions and the results of your Google search are incorrect. The topic has a greater complexity than you imagine, and is too broad for an answer here.


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Are cockroaches attracted to the dust particles is that a primary reason that I have cockroaches in my kitchen? Would like to know more about yhat
Same as title, are cockroaches attracted to the dust particles is that a primary reason that I have cockroaches in my kitchen?

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.


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Can someone please solve this question I think it is 3 but answer scheme says that is wrong

My reasoning for the option 3 is that the ratio of amino acids to carbons is more than 2 is to 1 and the ratio of amino acids to nitrogens is greater than 1 is to 1 and that is the only correct choice with these criteria

The question asks you to choose 2 options. Please [edit] and show us the second you have chosen and explain your reasoning for choosing that one.

Yes I am aware but I do not see another possible option using nitrogen and carbon ratio method

Welcome to SE Biology. Please finish reading the [Tour] to find out how this site works. There are two general problems with your question in this respect. First your title should not be a “please help me” request but an indication of the biological subject matter that your problem relates to. This helps readers decide whether to read a question, and allows indexing. Second, we discourage posting text as graphics, as this discriminates against the visually impaired. It may seem a chore, but questions should be typed out.

I'll answer this on https://bioinformatics.stackexchange.com this is probably the wrong site, hence despite my attempts to upvote you - its been downvoted


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What's the aestivation in Onion (Allium cepa)? Is it valvate or imbricate?
In my textbook it's written Liliaceae has valvate aestivation but in a question asked in a popular entrance exam (NEET UG), onion is mentioned to have imbricate aestivation...I am confused.

Both members of Liliaceae (sensu stricto) and Allium can have imbricate aestivation.
I unfortunately couldn't find good images with shareable permissions. But if you look here you can see a photo showing buds where an inner tepal is overlapped on both sides by other inner tepals.
This image is a bit more ambiguous, since some of the key areas are cropped out, but it could be showing valvate aestivation.
If you google "Lilium bud cross section" you'll find several images, most of which nicely show imbricate aestivation. I also found a reference that Lilium philippinense has imbricate aestivation.
However, it's commonly recognized now that Allium is not a part of family Liliaceae or even order Liliales, but a separate order, Asparagales. So, it's not entirely surprising that these groups might have different aestivations.


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How did humans know the process of domesticating animals?
If people in ancient times had no scientific knowledge  about natural selection and Darwinism, how were they knowledgeable about animal domestication and artificial selection?
What tools and techniques did they use to intercept animal reproduction and obstetrics? Did they use any artificial insemination tools?

Humans do not need to understand it to do it, nor is any technology needed. Just keeping the wolves we liked and driving off/eating the ones we did not for hundreds of generations got us dogs. there is no forthough necessary just favoritism.

It's common sense for 3-4 generation families living in tribes and cities to see heredity around them and learn from spoken tradition. tempers and physical traits are inherited. Conceptually they would also understand from mixing food ingredients, from mixing inks, that when you add two things together, you get a combination of the two. It's easy for them to consider using the largest animal of every generation to make the largest stock. Prehistoric people would not use freezers and condoms:) they would not complicate the act of putting two animals in the same room.

Prehistoric people had a similar intelligence as today, they just didn't have books. They knew absolutely millions of things about nature and conception. If you go to a yanomami village you realize that there is a lot of method and the magic explains only things that are not logical, linear, additive, related, visible, heredity is fairly straightforwards, it's very additive and visible.

That might be more a history or archeology question than a science question.
Early domestication
While there was no concept of long term evolution, many people could witness that offspring of individuals (whether plants or animals, incl. humans) looked like their parents. From there, it is not much of a stretch to understand that by breeding individuals with desired traits, you would get offspring with desired traits. This is artificial selection at play.
Artificial insemination
Early animal domestication did not use much artificial insemination. According to Britannica.com, the first successful artificial insemination in animal was in 1780s only.
Intended vs unintended selection pressures
Note however that I do not want to claim that most of the domestication traits evolve by the human intention to make them more frequent in the population. It might be just that individuals poorly adapted to domestication would flee or get harmed or something and would therefore have lower survival. For example, aggressive individuals could get hurt by their farmer.
Note btw, that wether the selection pressure by the farmers were intended or not, we still typically use the term artificial selection.

It would be good to leave a comment when down voting so that I can improve upon the answer.

I think this is a very interesting question but not necessarily directly related to genetics. This is more a question related to fields such as cognitive archaeology/anthropology and technological lithic analysis of how tools were made.
I'm not too familiar with Homo sapiens myself as it's unrelated to my field, but a close friend of mine is an evolutionary anthropologist who specializes in Homo neanderthalensis but knows a whole lot more about this than I do. I asked him for some suggested reading about this and here are his suggested introductions to the subject.
General interest but very comprehensive and in depth: Stringer, C. & Andrews, P. (2011). The complete world of human evolution. London New York: Thames & Hudson, Inc.
College textbook: Boyd, R. & Silk, J. (2009). How humans evolved. New York: W.W. Norton
The 2nd source actually delves into the topic of evolution of human intelligence, behaviour, culture, genetics and mating. If you want to learn more about the technological evolution, development, production and sophistication of stone tool making I suggest reading about things such as the Levallois technique. I hope this provided an answer to at least some of your questions! :)

That sort of makes sense, but I was interested in the techniques and practices of agriculture, animal domestication, and possibly plant domestication. How humans were able to control the mating of species to get them to do what they wanted to do, and even though the knowledge of how animal reproduction wasn't there, they still had instinctually messed with nature--whether it was for good or for bad you decide.


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Why is blood collected at crime scenes?
I have read that mature red blood cells (MRBs)do not have DNA.  So I am curious why crime scene technicians collect blood. Is it to collect and amplify segments of white blood cells?

Blood was collected and analyzed long before DNA techniques.  E.g. blood typing could rule out suspects with a different blood typing, or the blood on a suspect's clothing could be from an animal...

I appreciate the comments.  Just to be clear, I wasn't being lazy when I made the question.  Of course I could use a search engine.  I've been exposed to this StackExchange for maybe two weeks, and I find the questions and the depth of knowledge that contributors bring with their answers to be amazing.  I plan to make a Toastmaster's speech on aspects of DNA later this month.  No one in the speech club knows anything about cell biology.  I'm sure they will be surprise to learn that MRBC's do not have DNA.  The input given to me was just what I hoped for!

three words; white blood cells.

There's still white blood cells with DNA.
Some forensic blood tests are:
Conventional serological analysis:

Analysis of the proteins, enzymes, and antigens present in the blood, for general doctor tests: (black/white/drunk/stoned/heroin addict/polio vaccinated/hiv pos...)

Restriction Fragment Length Polymorphism (RFLP) DNA :

Direct analysis of certain DNA sequences present in the white blood cells. This method also usually requires a "large" sample size to obtain significant results.

Polymerase Chain Reaction (PCR) DNA :

Analysis of certain DNA sequences that have been copied multiple times to a detectable level.


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Is there a term for a sequence of genomes for a family?
Suppose that I am following how a "familial" genome changes throughout generations. That is, I have the genome of a grandmother, father, and daughter, and my objective is to see how the genome of each generation changes. Is there a better word for "familial genome," which defines the sequence of genomes through genetically related individuals?

When you write "sequence" in the titles do you mean "sequence" in terms of DNA sequencing, or are you using in a more general way to mean successive arrangement of grandparent/parent/child?

@BryanKrause Great question. I meant the latter. Thanks for clarifying :)

Update
Based on conversation in the comments below, it seems that the the OP is interested in how reference genomes can be used to represent the background genome on which variants can be used to represent the specific genomes of individual people.
Original answer
May be misunderstanding, but I am not sure that the concept that you are talking about actually exists. Recombination in each generation will break up contiguous chromosomal sequences into shorter regions that are passed down each generation. Furthermore, such a familial genome has an artificial bound, as ultimately all humans are related in a single pedigree due to the likely single origin of humankind.
Some related concepts are:

pedigrees
trios (parents and child genomes sequenced, usually to track where a child's genetic disease comes from)
quads (parents and two child genomes sequenced, usually where one child is affected by some genetic disease- no convenient link but similar to trios)

The closest thing to what you are talking about is probably the haplotypes shared by all family members. Haplotypes are the regions of sequence that can be shared by families that are not broken by recombination. You could speak of the set of common haplotypes between some set of people (in a family or just in a population).
However, haplotypes will necessarily get chewed up by recombination over time, so they're more of a heuristic for talking about the set of shared genotypes in a group of people (who are after all still related in some big pedigree), not something that's specific to lineal descent of families such as you suggest.

Thank you for your answer. This makes more sense. Suppose that I have genome sequences of different people in NYC (who are likely not family members). Would it be fair to treat their collection of genomes as a single genome that varies through time? I know this is odd, but just curious!

@RonSnow I don't know how you would make it "vary through time", but one standard practice for representing human genomes is to have a "reference" genome with some set of sequences for each chromosome, and then to represent individual peoples' genomes only by how they vary from that reference. This simplifies genome analysis somewhat, though it has its own set of issues. It seems like it might be similar to what you mean?

I think that is the closest thing to what I mean - you're correct. Thank you for your help! :)

@RonSnow updated answer to reflect this, no problem.

Perfect, thank you so much!


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What is a simple small scale procedure for plastination of a cucumber?
Question
In words a high school student will understand, what procedure can a student apply to plastinate a cucumber?
A cursory article on plastination can be found here.

Motivation
When someone shares a procedure on how to plastinate a human body parts, then students can be guided through that same procedure in order to a sun-flower, or rose, or carrot, or potato.
Perhaps students could enjoy making re-usable carved potato stamps to use outside of biology, in their art class.
For now, the only thing that I have seen plastinated seems to be human flesh and organs, but the original research in 1977 mentioned a cucumber.
I tried aluminum sulfate on a specimen of Gaillardia pulchella, but the results were terrible. The inflorescence was dry and crumbly, not like a proper plastinated human heart or liver.

Perhaps students would enjoy plastinating straw-hats, if they do not like potatoes. The hat would fray less easily, the hat would be waterproof in the rain, rubbery, and a plastinated straw hat would be more durable than a traditional straw hat.

I’m voting to close this question because I do not think the preservation of dead plants is a topic consistent with the general aims of this site.

I disagree somewhat with David; I think preservation of biological specimens would be a suitable topic for here. Certainly would like to see the 1977 research you refer to - a reference or link would be nice.

This falls between here and our [crafts.se] site. If you have no luck here, then try there (probably leave out the part about human body-parts but fruit n vegetables should be OK).


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Using bovine insulin in bovine cell culture for diabetics
Insulin in the US is very expensive. It uses DNA recombinant techniques on yeast or bacteria, which requires patented techniques to isolate the insulin.
In contrast, bovine cell culture of the bovine pancreas may allow the (relatively) easy production of bovine insulin from the cells, in a manner that does not require patented filtration techniques.
Given the expensive cost of human insulin in the US, could bovine insulin made by individual small-scale labs be a feasible alternative?

Insulin is pretty cheap everywhere else. I don't think there are technical reasons why it's expensive in the US, it's just that country's broken health system.

Besides that, insulin from pigs has been used for decades until it was replaced by human insulin from biotech. As fas as I know, there are less side effects now.

I'd suggest reading up on the history of insulin. Until the 1980s all insulin came from pig and cow pancreases. It took tons of pancreases to generate a few ounces of insulin. That was feasible, because we slaughter a lot of pigs and cows for food. Maintaining mammalian tissue cultures requires skilled labor and a laboratory with excellent quality control standards. You aren't going to do it in a garage, and it will produce minuscule amounts of insulin. Today's insulin is made in giant vats of E. coli. Growing vats of bacteria at industrial scale is pretty much a solved problem.

@CharlesE.Grant I see, so there's no question about using E. coli. This might be unrelated, but is there a reason why projects such as the Open Insulin Project aren't taking off?

@terdon The way I see it, there is no way to decrease US medical prices across the board unless independent, individually producible competition is created. The current price of medicine makes it cheaper (even accounting for human labor, precursors, and perhaps even equipment) to make one's medicines than to buy it from a company. Purificiation is the only step where I see concerns.

@Chris I see. Thank you for the input!

I'm not familiar with Open Insulin. I just read their web page. I suspect they suffer from the problems many inventors face in going from a "proof of concept" project to mass market scaling. Reliable, cost effective, manufacturing with effective quality control is often much harder than simply getting the clever innovation to work on a demonstration scale. You can easily kill people with insulin, and you have to make the process utterly reliable in the hands of ordinary people. Many biohackers are fairly casual about their own safety, but they want to provide this to ordinary end users.

@CharlesE.Grant Yes, its the costs of certification (if it is a drug for distribution then you need FDA registration etc. in the USA) and GMP that make it unlikely for any of these small scale operations to be feasible.

@bob1 I see... Saddening that waivers cannot be signed even

In Estonia there was GMO cow project where human insulin genes were transferred to cow milk secretion area to later extract insulin from milk. I'm not sure if there is any progress in that field.


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Hypothetical scenario where the seed doesn't rot after sprouting the plant
Suppose a seed was sprouted in such a way that after it sprouted, it did not rot and was connected to the plant.
If so, will the connected seed keep releasing enzymes needed for the glyoxylate cycle?

This phenomenon is fairly common in plants, it is called vivipary.

@bob1 Thank you for the input. I am not sure vivipary fits my exact situation, but it seems interesting. If the seed develops while still attached to the mother plant (as seen in vivipary), would it release glyoxylate cycle enzymes back to the mother plant?


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What is a good introductory book on plant genetics for an outsider?
I am interested in plant breeding, but my knowledge about plant genetics itself is unfortunately limited (math major). Would you know of any good introductory '101' books that explain the basic concepts? As elementary as: what exactly is DNA recombination? What is an F1, F2 plant?
Many thanks and kind regards,
David

I am in a PSEO class for plant biology and ecology and I found a book online I believe you would find useful.
Click here
I've used this book to study many times even though it wasn't supplied to me. It does a great job explaining overall concept of plant microbiology. This book will introduce concepts that someone would be new to. I recommend that you give it a read, then after you read it, move to a book specifically on plant breeding.
Hope this helped!
-Sartoaster


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Is it possible to sort droplets inside an oil phase with a FACS
In a nutshell, is it possible to FACS a sample that is in oil rather than in a buffer (water based solution)?
I would greatly appreciate any help with this.
Thank you

Not sure about FACS, but what you describe is similar to droplet digital PCR (ddPCR). The samples are still in an aqueous buffer, but they are emulsified in oil, creating many microscopic droplets that each contain some sample and are isolated from each other. BioRad makes a machine that does this, but whatever you are detecting would have to produce a fluorescent signal.

Thanks ndusek, yes it seems detection of fluorescence is possible inside oil. Its only a question if a FACS could achieve the same.

It's possible that there's some specialized modified machine that can do it, but conventional flow cytometry machines can't do it. This article suggests one possible approach:

Unfortunately, FACS instruments are incompatible with nonaqueous suspensions, so to sort a water-in-oil emulsion, it is necessary to carry out a further emulsification to produce a water-in-oil-in-water double emulsion. The resulting sample, now dispersed in an aqueous phase, is amenable to FACS sorting.

--One in a Million: Flow Cytometric Sorting of Single Cell-Lysate Assays in Monodisperse Picolitre Double Emulsion Droplets for Directed Evolution
There are also microfluidics machines that might be able to do it, but I think you'd have to build your own rather than being able to buy a solution (which would be expensive in any case, I think).


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How to pipe Bwa-mem output without saving SAM file
I'm trying to find circular ARN using the program CIRI2. CIRI2 takes as input SAM file from BWA-mem, but I would like to go straight to CIRI2 output without saving SAM file.
Is there a way to achieve this?

This is an English language list. Do you by any chance mean RNA rather than ARN? And although I may be wrong, I think you are more likely to get an answer on SE Bioinformatics than here.

I never used CIRI2 but I think you can do the same way as I used to pipe with samtools:
bwa mem genome.fa reads.fastq | samtools sort -O BAM -o output.bam -
So it would be something like:
bwa mem genome.fa reads.fastq | CIRI2 <your options>
I think you will need to precise that CIRI2 input is STDIN.
I hope it will help,