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Diagnosing pathogenic illnesses with DNA analysis?
I am wondering if there are techniques for diagnosing pathogenic illnesses with DNA analysis.
For example, imagine a person has a staph infection on their skin. A scraping could be taken and then analysed. In this cases there will be two sources of DNA: the person and the staphylococcus bacteria. My understanding is that statistics can be done to separate the two and thereby positively identify the DNA sequences unique to the staphylococcus, and thus exactly diagnose the pathogen, even telling what family or strain it is.
Now, imagine a harder situation. The patient has a viral infection like a cold. In this case we may still be able to do the same procedure using nasal mucus, but there may be other passive viruses in the mucus. Is it possible?
Now, imagine an even harder situation. The patient has a internal viral infection causing a fever. There blood has thousands of retroviruses in it. Is there any way to isolate the virus causing the fever and get its DNA?

This is all routine, to the point of being trivial.  Genome-based diagnosis is very common and is the preferred approach for many, if not most, infectious diseases. Here is a list of over 150 FDA-approved genome-based assays for pathogens.
Some quick examples include influenza:

Rapid Molecular Assays
Rapid molecular assays are a new kind of molecular influenza diagnostic test for upper respiratory tract specimens with high sensitivity and specificity.1 One platform uses isothermal nucleic acid amplification and has high sensitivity and yields results in 15 minutes or less. Another platform uses RT-PCR and has high sensitivity and produces results in approximately 20 minutes.
Other Molecular Assays
Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and other molecular assays can identify the presence of influenza viral RNA in respiratory specimens with very high sensitivity and specificity.

--Influenza Signs and Symptoms and the Role of Laboratory Diagnostics
RSV ...

A newer test protocol (RT-PCR) is more reliable and is replacing the antigen-detecting test in many hospitals and community laboratories.

--Respiratory Syncytial Virus (RSV) Infection
Meningitis ...

Over the past several years, conventional and real-time PCR assays have been developed for detection of bacterial meningitis pathogens. Reliable assays have been extensively evaluated using invasive clinical isolates and/or clinical specimens from around the world (8, 12, 15, 17, 29, 35, 52, 60). In general, validated assays should have high sensitivity and specificity. They can be used as complementary approaches in bacterial disease diagnosis.

--https://www.cdc.gov/meningitis/lab-manual/chpt10-pcr.html
and many, many more.
An important trend now is using genome detection methods to look for many different potential pathogens in a single sample; these "lab on a chip" approaches (e.g. here are just entering clinics but will probably be routine in a few more years.

That is fine if you know what you are looking for, but what if it is uncertain what the disease is? Can you test a sample against all known diseases, or only a few likely guesses?

@ImprisonedRhesus - The "shotgun" approach you ask about is unwise and exceedingly expensive. Physicians who do not use their intelligence in making presumptive diagnoses and testing for the most likely culprits first do no one (or no institution) any service. Rare diseases do exist, and are a diagnostic challenge, but to use this approach (test for everything) is just sloppy and calamitously expensive.

Okay, so you seem to be saying that we can do DNA diagnosis, but only if we have a good idea of what it might be already and can check for that specific possibility, is that right?

@Imprisoned Rhesus That's a very different question from your original one, which asks about detecting specific agents. I suggest you ask it as a separate question. Short answer, there are research-level tools for identifying unknown agents, but as far as I know none that are clinically approved


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Mackerel evolutionary health affected by loss of predators?
I notice that Atlantic Mackerel (Scombrus scombrus) is endemically affected by parasites. In one study I read that the researchers found that over 70% of the mackerel sampled were infected with parasites.
Is there any evidence that the diseased state of the mackerel population is possibly due to loss of natural predation? The major predators of mackerel are tuna and cod, both heavily fished by humans. At one point cod was fished nearly to extinction and is still considered endangered. Since cod will typically catch the laggards and least fit of their prey fish, like mackerel, I would expect that over time this predation would tend to eliminate sick or unfit fish. Without this natural predator, perhaps it is leading to sickly conditions in mackerel?
Is there any basis for this thinking?

A few comments: 1) For thinking about whether your hypothesis is plausible, it would be handy to know how these parasites transmit (but it is likely there are several parasites and the mode of transmission varies from parasite to parasite). 2) Can you please link to the study you refer to? 3) Do you have any reason for thinking that the rate of parasitized individuals has changed over the period of over fishing? 4) I think (but might be wrong) that warm waters often tends to increase parasitism and climate change might be a potential cause as well.

source: Stack Exchange

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How does a drastic change to the genome persist and spread?
I just read the article on songbirds in the November, 2019 Scientific American. The article explains that songbirds have an extra chromosome, called GRC (germ-line restricted chromosome) that other bird species don't have, and there's a hypothesis that this may have been partially or wholly responsible for the diversity of this group of species.
The following line caught my attention:

Once the GRC originated in the last common ancestor of songbirds, members of that ancestral species that carried the GRC could produce fertile offsping only with mates that also had the GRC.

But when the mutation that created the GRC occurred, who did that bird mate with in the first place?
My belief is that most genetic changes are relatively minor, so they don't immediately result in incompatible mating. Speciation occurs as genetic changes accumulate over time. But the above quote implies that an entirely new chromosome is too drastic to allow interbreeding at all.
Wouldn't there need to be a whole bunch of birds who all had this extra chromosome at the same time to allow it to spread through the population? That seems unlikely to occur.
Am I just reading the line too literally? Could early birds with the extra chromosome mate with other birds, until the new chromosome accumulated too many changes?

It isn't necessarily true that individuals with different numbers of chromosomes are infertile. Even though common wisdom has it that horse (64 chromosomes)/donkey (62 chromosomes) hybrids are invariably infertile mules, that's not true; a significant number of fertile horse/donkey offspring have been documented.  Here is an example where the chromosomes were checked and confirmed to be 63 in the fertile mule parent.
Even more dramatically, the common shrew (a single species) has many different chromosome numbers as natural variability (at least 50 different chromosomal variants were identified in one paper) and this doesn't affect their interfertility.
So there are three general answers to the question here, though I don't know which is the most likely.

The extra chromosome arose and the original variant was very fortunate to have offspring; similar to the rare horse/donkey fertile hybrids.
The extra chromosome arose but had little effect on interfertility; similar to the common shrew. (The quote from the article in the question argues against this, but I don't know if it's a presumption made by the researchers, a presumption made by the writer, or a demonstrated fact.)
The extra chromosome arose in a single litter, so that several siblings shared it, and then interbred. Although incest avoidance is generally quite strong, animals that colonize islands or distance geographic areas (invasive species, often) commonly do interbreed this way.

When I was thinking about it myself, incest was one of the possibilities that came to mind.

The article seems to directly contradict your #2.

Not clear to me from your quote whether that's a presumption made by the researchers, a presumption made by the writer, or a demonstrated fact. In any case, I'll leave #2 in as a general possibility but will note that the article argues against it

Indeed, the article was written by a SciAm editor, not one of the researchers. So she may have been simplifying.

It seems like one of the rare cases in which the duplication of the specific chromosome  is not lethal, but actually advantageous. This means it can happen from time to time to see this extra chromosome by errors in cell-division.
Now although its unlikely, it eventually happened, that two birds with the same duplicated chromosome meet and mate: They replicate their "new species".
Note that the name of this "germ-line restricted chromosome" might be the cause of confusion! Any additional chromosome would be "germ-line restrictive": Unless all chromosomes are matched, cell-division is prevented by control mechanisms.
And some direct answers:

But when the mutation that created the GRC occurred, who did that bird
  mate with in the first place?

It needs to find a bird with the same additional chromosome!

My belief is that most genetic changes are relatively minor, so they
  don't immediately result in incompatible mating. Speciation occurs as
  genetic changes accumulate over time.

True, it takes considerable mutations for 2 chromosomes being unable to be paired, but here we speak of an additional chromosome: It intrinsically cannot be paired.

But the above quote implies that an entirely new chromosome is too
  drastic to allow interbreeding at all.

Exactly!

Wouldn't there need to be a whole bunch of birds who all had this
  extra chromosome at the same time to allow it to spread through the
  population? That seems unlikely to occur.

It takes 2 birds and coincidence!

Am I just reading the line too literally? Could early birds with the
  extra chromosome mate with other birds, until the new chromosome
  accumulated too many changes?

I don't think so!

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Can you please help me identifying these parasite (eggs?) on rose?
My aunt today saw the following objects on roses in her garden

and asked what it is but nobody could tell her yet, but it seems to be some kind of parasite or some caterpillar eggs.
As you can see, they differ in size since they appear in larger groups, but each egg (I call it so since I have no better name) has a diameter of about 1 cm. On the outside, there are red spikes.
Loaction is Germany.
Would be great if someone could tell me what this is and whether it should be removed from the roses.
Thanks in advance

Please insert the pictures into your post rather than links.

Looks like galls; growths of the plant in reaction to an irritant. Generally not necessary to remove them.

These are not eggs, they are rose leaf galls caused by the spiny rose gall wasp (Diplolepis bicolor) larva that encases itself inside the gall and then matures and chews a hole in the gall to escape in spring, laying its eggs on a newly emerged leaf bud. The larvae generate the gall in the fresh leaves, perpetuating the cycle.
Remove the galls in late summer or winter if you want to get rid of the larvae. Personally, I like them, so I would leave them. New larvae will generate new galls, but they will usually only be a few each year.

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Decreasing signals in assay measurements
I'm working with a calcium assay to study the effects of different virulence factors. The assay works, but from day to day the signals of cell lysis go down. Unfortunately, I haven't found an explanation for why this is happening.
The particular assay I use measures cell lysis. The virulence factors I use cause pore formation and lead to a calcium influx (from the buffer). Esterase proteins activate the fluorophore and need calcium. Increase in cell lysis leads to an increase in signal.
As I already mentioned my signals are dropping (from day to day). But I don't know why.
Have you got an idea of what could lead to such effects?
Here are some factors that might be involved.

The virulence factors lose their activity? (I don't feel like that this causes the problem because new stocks also show a decrease in activity, and also the signal from the positive control decreases. I would say it decreases in a similar ratio. The positive control is triton.
The dye loses its activity? The bottle is normally stored in a freezer. I just take it out for the assay. Before I use it, I place the bottle on a shaker for about 30 minutes. I just open the bottle for a few seconds and then put it then back in the freezer.
The plate reader is broken or the reading protocol has changed? I already checked the protocol and every thing is the same as in the beginning. Coworkers get the same results with the same plate reader as before. So I guess, this should not be a problem.
The buffer gets destroyed from the procedure? I store it in the freezer and take it out and put in a waterbath. After I used it I place it back in the freezer. I carry out this procedure every time, can this lead to negative effects? The medium contains calcium, can something happen with it (Calcium plays an important role in this assay)? A colleague already told me that he stores his buffer in the fridge not in the freezer, and he didn't got such effects. But perhaps it's not the only thing he does different..
The cell number changes? The negative control does not change over the experiments, and the signal from it is still higher than the values from the blank. But i will check that.
Could my cells cause problems? They look still good under the microscope.

Welcome to Biology.SE! Thank you for taking the [tour], but please also go through the [help] and [meta] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, please make sure your question is clear and as concise as possible (this includes spell and grammar checking). In addition, please don't include signatures etc. — your post has your ID attached and by posting you've already asked for help! Thanks!

I've edited your post to correct language problems, but I suggest you add much more detail about exactly what fluorophore you are using (and in what solvent) and the constituents of the various other buffers you are using. Please check to make sure I've not changed your meaning. ——— I'll post a preliminary possible answer as well, but you probably need to get someone in your lab to teach you how to trouble shoot. IMO learning how to trouble shoot experiments is the most important lab skill!

Freeze-thaw cycles are often suspected of causing degradation in organic molecules 1,2. My first guess would be that your fluorophore is breaking down due to those repeated cycles. Alternatively, you might be getting precipitation of a calcium compound from the buffer you are freezing that your colleague is not.
Standard laboratory practice is to make aliquots of frozen solutions. Before thawing the solution for the first time, set up pre-labeled smaller containers (e.g. Eppendorf tubes) and then aliquot the amount you expect to use for each experiment. That way potentially sensitive compounds are only thawed twice.
References:
1: Kozikowski, B. A., Burt, T. M., Tirey, D. A., Williams, L. E., Kuzmak, B. R., Stanton, D. T., ... & Nelson, S. L. (2003). The effect of freeze/thaw cycles on the stability of compounds in DMSO. Journal of biomolecular screening, 8(2), 210-215.
2: US Food and Drug Administration. (2008). Guidance for Industry. Drug Stability Guidelines.

Hey MattDMo, thanks for your answer! Today I made a special test, to eleminate some of the possible factors which could lead to such mysterious effects.  I seeded out some cells and instead of treating them with my virulance factors i treated them with triton X. By the way I also seeded out higher and lower cell numbers than normaly used in the assay. More Cells led to more fluorescence, but the effect was small. I found something! When I observed the cells afterwards with the microscope, I saw that they haven't been lysed. How can that happen? They incubated over an hour in triton X?

I guess that the triton was fine because also the virulance factors showed a signal loss. At the moment I feel like that the cells have changed, dispite the fact that they look like they should. Perhaps I should mention here, that this culture was startet about 3 weeks ago, the Inocolum was stored in liquid nitrogen. No abnormalities.

*The cellline was startet 3 weeks ago. I guess the cells have been splitted now for about the sixth time.


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Why are diseases generally specific to a particular species
"Zoonosis" is the process of transmitting a disease from an infected animal to a human. This suggests that animal-to-human transmission is not common. HIV is believed to have first spread to humans zoonotically, but has since mutated to a human-only strain.
This all raises the question: Why do diseases mostly just target a particular species? Aren't most metabolic processes very similar across species, especially within the same order and class? Dogs and cats can't catch the common cold, but they have similar diseases of their own.
There are obviously enough similarities that mice can be used in preliminary tests of human drugs, but the results are very tentative until human trials are done.

The pathogens which are responsible for certain diseases have adapted to their hosts. Viruses need to attach to structures on their cells they invade to replicate. These structures usually consist of proteins and are unique for the respective species (e.g. the ACE2 receptor in the case of Covid-19). During an infection, there will be billions of viruses released and some carry mutations, which are just mishaps in the replication process. In most cases, these errors are leading to a virus that is not viable or cannot infect, i.e. the mutated virus can't replicate and the mutation gets lost, but sometimes it can infect the host better and thus will have a higher chance to propagate.
If this happens with a zoonotic pathogen after it has spread to a human, a new disease has emerged.


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How do eradicated diseases make a comeback?
It's in the news this week that a case of polio was encountered in Gaza, the first case there in 25 years. The conflict between Israel and Hamas is blamed for reduced vaccination, so children are more susceptible to the disease.
But even if people are susceptible, how does the disease resurface? According to WHO, type 1 poliovirus remains in two countries, Pakistan and Afghanistan, but the child was infected with type 2, which was eradicated in 1999.
BBC wrote

According to the UN, Gaza, now in its 11th month of war, has not registered a polio case for 25 years, although type 2 poliovirus was detected in samples collected from the territory’s wastewater in June.

Where could the virus in the wastewater have come from?

One answer to the general question is "not so perma" frost. Smallpox appears to be a candidate to make a re-appearance.

Type 2 polio was still included in vaccines up until 2016. Recipients of the polio vaccine become immune, but in rare cases it's possible for vaccinated people to transmit disease to unvaccinated people, and for the virus to spread from there. Wild type 2 polio is eradicated; but some vaccine-derived cases still circulate. See also:
https://medicalsciences.stackexchange.com/questions/30853/why-is-the-rate-of-circulating-vaccine-derived-poliovirus-disease-booming
There's a tough decision as far as when to stop distributing a particular strain via vaccine; on one hand, you keep open the potential of vaccine-derived spread. On the other hand, the protection against vaccine-derived spread is vaccination of everyone, since if everyone is vaccinated there cannot be spread.
Not every type of vaccine holds these risks, but the oral polio vaccine involves a live, attenuated virus, so that's one that causes a risk.

So the baby, who wasn't vaccinated, caught it from someone who was? They have the virus, but the vaccine prevented them from getting the disease?

@Barmar Not necessarily someone who was directly vaccinated, but someone who got it from someone who was (or someone who got it from someone who got it from someone who was).

But your point is that the virus is still around, because it's in the vaccines, but no one is symptomatic, because they've all been vaccinated? And they can then infect someone who isn't vaccinated?

@Barmar Other unvaccinated people can be symptomatic and spread it as well to other people who aren't vaccinated. That's why we keep vaccinating people. Polio also isn't always a severe disease even in people who are unvaccinated, so unvaccinated people who spread it to others may have brief/mild/no symptoms. The initial spread from someone vaccinated is an extremely rare event, but also many many people have been vaccinated against polio.

"Other unvaccinated people can be symptomatic". But the whole point of my question is that there have been no cases in 25 years -- there are no symptomatic people. Isn't that what we mean when we say a disease is eradicated?

@Barmar The only claim of eradication is of wild-origin type 2 based on a very long time passing with no observed cases of wild-origin type 2. We know there are vaccine-derived cases around. There is no funding to test every single person for polio, cases persist even if you're not aware of them.

Please see the link in my answer to the Medical Sciences Q&A and read the links in timeskull's answer like https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8393165/

OK, I hadn't considered the possibility that there were cases we didn't know about, since it's such a severe disease. Although it seems unlikely that none of the cases in 25 years would be diagnosed. Not to mention that a 10-month-old baby would have been exposed to one of them, they don't have very active social lives, especially in a war zone.

@Barmar The typical infection by poliovirus is not a severe disease, poliomyelitis is. Ordinarily polio replicates in the gut and causes at most a minor illness. Not something you'd even consider unusual. Occasionally, it gets into the blood and if so then it can possibly affect the CNS, where it causes chronic illness. The vast majority of people that are infected with poliovirus do not get poliomyelitis.

My question was about the disease, although I conflated it with the virus. I assume that when we say "So and so has polio" they're referring to the poliomyelitis disease. Is this analogous to the distinction between HIV (the virus) and AIDS (the disease it causes, which is now mitigated by various medicines)?

@Barmar A bit, but not really. I wouldn't bother with any analogies, just read about poliovirus, it's pretty straightforward and I've already described it: the virus ordinarily causes an infection in the gut, and spreads fecal-oral. Sometimes, it spreads to the blood. Sometimes when it spreads to the blood, it also makes it to the CNS and causes poliomyelitis. The people who that happens to definitely know about it. The people who have just the simple gut infection almost certainly do not know about it. It's all the same virus, so it can spread around without being known.

‘Some vaccine derived cases still circulate’ I’m far from an expert on this, but my understanding is that as of right now, these actually account for almost all reported cases of paralytic poliomyelitis. I believe the official numbers from the WHO for 2023 were 12 reported cases from WPV compared to 524 from cVDPV.

@AustinHemmelgarn Yes, the linked post to Medical Sciences discusses this. For Type 2, it's all of the cases.

@Barmar: Over 99% of polio infections are either completely asymptomatic or indistinguishable from those caused by other gastrointestinal virusses, even for the wild-type virus (and even-more-so with cVDPV).

When they say this is the first case in 25 years, do you think they're being imprecise and referring to poliomyelitis, not polio in general? When millions of children were dying from polio, was that actually poliomyelitis?

I always assumed they were the same thing, just as "flu" is short for "influenza".

@Barmar Usually "polio" as a disease is short for poliomyelitis. We don't really have a short name for the normal, non-poliomyelitis version of the infection because, well, it's so minor.

BTW, I did hear on the news today something like "only 1 in 1,000 cases are symptomatic, so it's probably widespread in Gaza."


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Why DNA needs histones to be packaged and ordered?
I know that histones are proteins that package and order the DNA into structural units called nucleosomes, my question is Why DNA needs histones to be packaged and ordered ? Why DNA cannot do that by itself ?

Not all organisms have histones. Prokaryotes generally don't.

Structural packing of a lot of DNA into a small space is a useful function.

The packing and ordering also facilitates mitosis/meiosis.

Packaging also controls gene expression under certain conditions.

@Galen You could probably attempt at an answer from all of your comments.

Sort of like having one of these:

instead of this:

Surely you could simply wrap DNA up in a coil, but to do it in a neat fashion that allows you to package and repackage sections as needed, it's a lot better to have some dedicated machinery.
It is also difficult to organize DNA without a supporting structure because the negative charge of the DNA polymer repels other parts of the molecule, whereas histones are rich in positive charges.
As Galen mentioned in comments, histones both pack DNA into a smaller space (human DNA from one cell would be about the height of an adult if it was all in a straight line) and contribute to gene regulation. Modifications of histones control whether the DNA around that histone can be accessed by transcription machinery and therefore whether those genes will be expressed.

The wrapping of DNA around each histone is ~1.6 rotations.

Yes, indeed I didn't mean to be literal.

Great visual analogy! :)

You might like to add the point that DNA is itself negatively charged, so it cannot pack by itself due to repulsion. Histones have positive charge (lysine and arginine rich proteins) so that they can easily hold DNA around them.

Why DNA needs histones to be packaged and ordered?

Histones counteract retroelements, and this defense against parasitic (viral) DNA is presently considered to be their original physiological role.
see: Madhani, Cell, 2013: "The Frustrated Gene: Origins of Eukaryotic Gene Expression"

Why DNA needs histones to be packaged and ordered ? Why DNA cannot do that by itself ?

Histones are not needed to package and order DNA; Another way to order DNA would be through supercoiling – which can also be done by bacteria (lacking classical histones or histone-like proteins).
see: Griswold, Nature Education, 2008, "Genome Packaging in Prokaryotes"

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Does anybody know what kind of tree is this?
I saw this tree yesterday and I liked it. It is around 1.5 m. I did some search on internet and thought it might be Holly, but I'm not an expert on trees. So I wanted to ask you, does anyone know what kind of tree is this?
Location:The Netherlands

Looks like a holly, similar to English holly ( at least that is that it is called in the US ) .There are different cultivars . It has been pruned to a tree shape .

Thank you for the answer.


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Since nature highly favors the pyranose forme of Ribose, what explains the fact we find it in the form of furanose in DNA and RNA?
I read in my notes that relative abundance of ribopyranose represents about 80% of all ribose in solution (including the alpha and beta anomeres).
I'm curious as to why evolution favored the use of the least abundant conformation for DNA and RNA.
Do we have enzymes that convert pyranose to furanose in order to achieve this? or are we just using the furanose?
Thank you,
Pierre-Eric

Because the ribose in RNA is a component of a nucleotide and is not a molecule unto itself. It has the 5' phosphates and 1' nitrogenous bases attached, and those functional groups will alter the conformation of the ribose in the nucleotide.

But then, my question should be read like this:
Is the cell using ribofuranose or ribopyranose  in the synthesis of nucleosides?
and if it is the latter, how.... or when is it converted?
or even... does the cell synthesize nucleosides at all? Or do we simply use the one we get from digestion of food?
If we do get it all from digestion, then wherever the nucleosides are formed in the foodchain, wether it is in bacterias or protozoas...
How does it go from pyranose to furanose (if the pyranose are used), and why are the furanose used and not the pyranose if it is the other way around?

Look at your textbook for the De Novo Purine Nucleotide synthesis. You do not start with ribose you start with 5-Phosphoribosyl-1-pyrophosphate and its precursor is ribose 5-phosphate. The 1,3-diaxial interactions of a C5 phosphate group likely pushes the molecule into favoring the furanose form as the negativity of the phosphate and the lone pairs on the ring oxygen are likely not very happy that next to each other to assume the pyranose conformation.

Can you provide a link to the reference that says that pyranose structure is more abundant? That may be true but I am not too sure about it.


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How protein denaturation affects digestion?
Which one of these is a) easier to digest, b) more nutritious (in whatever sense):
1. scrambled egg,
2. raw egg.
Bascially is "denatured protein are worse than not denatured" a myth, or not?

This article specifically looks at the question you're asking.  Just jump down to the conclusion if it's too technical.
To summarize, cooking the egg (or heat pre-treatment as they call it in the paper) leads to a significant increase in protein uptake.
I'd call that myth busted via radiolabeling.

For some proteins denaturation can make them insoluble. This is not so in the case of egg albumin though.


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How long a dog can remember its owner's smell?
Can dog remember multiple smells? and how long it can remember a smell?

There are a lot of misconceptions about dogs memories. They have short attention spans but they do form long term memories. If my partner has been out for the day and they return home several minutes before I return home for a walk with our beagle, he will excitedly alert to their scent. He does not do that otherwise, so he is picking up on the particular chemical signature that they produce.


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Why do animal cells "mistake" rubidium ions for potassium ions?
So, I was browsing the Wikipedia article for rubidium, and came across this interesting tidbit:

Rubidium is not a known nutrient for any living organisms. However, rubidium ions have the same charge as potassium ions and are actively taken up and treated by animal cells in similar ways.

This immediately struck me as interesting, and a completely wrong explanation, as all singly-ionized ions have the same net charge.
Now, from my basic understanding of chemistry, elements of the same group have the same valence electron structure, which accounts for much of the element's chemical effects. And if you look at the periodic table, sure enough, rubidium falls below potassium, in the Group 1 alkali metals.

But, from my old memories of basic biology, even saying "these elements are vertically adjacent on the periodic table" is an incomplete explanation, because, for example, the body has no problem "telling apart" sodium from potassium, or plenty of other vertically adjacent elements.
A survey of other potentially relevant features reveals the calculated radius of rubidium (265 pm) is relatively close to the radius of potassium (243 pm), and the first ionization energy of rubidium (403.0 kJ/mol) is also pretty close to that of potassium (418.8 kJ/mol). So they do seem fairly similar, but question still remains, how "similar" does an element need to be to become a biological proxy?
This leads to me to the following questions:

Why does rubidium act as a biological proxy for potassium? Also:

Why is cesium also a decent, but less good, biological proxy for potassium?
Why is potassium not a biological proxy for sodium?

If rubidium acts as a biological proxy, why is it still not a "nutrient" and not considered to play a biological "role"?
Which other sets of elements can act as biological proxies for each other? (I presume expanding this question to molecules yields too many answers to be useful.)
Is this rubidium-potassium proxy effect specific to animals or to all life?

Some good references I've found, skimming the literature (I started by looking at some references in this article):

Relman AS. The physiological behavior of rubidium and cesium in relation to that of potassium. Yale J Biol Med. 1956;29(3):248–62.

Relman notes that this phenomenon was first noted by Sydney Ringer in experiments begun 1882, published in the Journal of Physiology in the year 1884 (or so).

Fieve RR, Meltzer H, Dunner DL, Levitt M, Mendlewicz J, Thomas A. Rubidium: biochemical, behavioral, and metabolic studies in humans. Am J Psychiatry. 1973;130(1):55–61.

But I'd rather someone present an intuitive explanation for this before or after I attempt to dive in.

Not what you'd call a useful proxy, but arsenic is poisonous because it's similar enough to phosphorus to act as a substitute in the ADP/ATP cycle, but then fails to provide energy to cells the way ATP does.

To be fair, the Wikipedia article does not actually say that rubidium ions are taken up in the same way as potassium BECAUSE they have the same charge. It just says that they have the same charge AND are taken up in the same way, which is true. A similar statement appears at the end of the article.

@barbecue Yes, I realized this later on. Still, I think that sentence in Wikipedia could have been phrased more clearly.

@JonathanJeffrey someone seems to have updated the article to make it clearer, was that you?

@barbecue No, it wasn't me! But I'm glad that someone got around to it (probably after reading this question).

As a side note, we use this property in nuclear medicine. Rb-82 is radioactive and can be used in heart studies - myocardial PET scans - as it enters the myocardial cells in a similar way to potassium. Pertechnetate - TcO^-4 is similar to iodine, and there are a lot of other examples.

The Na⁺/K⁺ pump discriminates sodium ions by their smaller size – that’s why in no way can (a larger) Rb⁺ pass for Na⁺ in this important application. But obviously Rb⁺ can pass for K⁺ there, and does it.

There are multiple biological mechanisms that can be brought to bear for distinguishing between atoms. In addition to binding properties (e.g., ionic charge, electronegativity, bond strength), there is also the size of the atoms and even their vibrational properties.
For one of these mechanisms to actually be used, however, it needs to be evolutionarily selected for in some way. The binding properties are by far the simplest to select for, since they are fairly local and permissive in nature, while the others require much more carefully tuned mechanisms.
Thus, we should expect to see most biological selectivity to be developed in terms of binding properties, as seems to be the case. For same-group covalent-binding such as one encounters with oxygen vs. sulfur, there are major differences in the properties of the bonds, giving ample opportunity for biological selectivity.
For Group 1 alkali metals like sodium, potassium, and rubidium, however, ionic bonding is much more uniform. Thus, we should expect mechanisms that apply to one to apply to all unless strongly selected for distinguishing.  In the case of potassium versus sodium, which are both very important in biochemistry, a recently discovered mechanism in sodium-potassium pumps uses binding properties to grab both, then atomic size (via steric hindrance) to distinguish sodium versus potassium as described nicely in the answers to this question.
Presumably, there simply has not been sufficient evolutionary pressure to establish mechanisms for distinguishing rubidium from potassium in the same way.  While sodium and potassium have approximately equal abundance, rubidium is approximately two orders of magnitude less abundant than either. Cesium, in turn, is nearly two orders of magnitude less than rubidium, and rapidly decaying francium mostly doesn't exist.
Thus, unless there is a particularly problematic effect of occasional incorporation of rubidium or cesium, then, we should expect these elements to be essentially indistinguishable from potassium biologically, but not from sodium, since sodium/potassium distinguishing mechanisms will reject them all along with potassium into the "not the right size to be sodium" bin.

@user338907 That's fascinating about lithium... do you have any information about mechanism? To me, that would suggest that the sodium selectivity is not just "small enough" but "just the right size", which would cause lithium to not work right either. It sounds like we're getting to the edge of known science here, however.

Excellent answer. I have to say, the pore selectivity in (for example) voltage-gated channels permeable to sodium or potassium but not both is something that I find to be one of the most remarkable feats in evolution.

Nice answer. Upon looking at things more, it appears the verdict is out on whether rubidium is an essential nutritional element (i.e. a mineral) or not for humans and other animals. How that ongoing research bears with the question of how animals evolved rubidium-potassium compatibility is an interesting question.

Although I accepted this answer, I think there are still lots of interesting insights and questions in this area, so I welcome others to write their own answers. (I myself am currently being quite fascinated by this paper that describes how some bacteria require lathanides, but can't tell them apart!)

I've just asked Help understanding how "steric effects" are distinct from "electronic effects"?


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How many calories do gut bacteria burn?
It has become well-accepted that microbiota of the gut (a.k.a. gut bacteria) consume calories that are ingested and can have significant effects on energy metabolism in humans. For example, if you take the feces from mice that have had a gastric bypass and transplant those into the colon/GI tract of obese mice, then the obese mice lose weight (See here for article about this study).
Are there any known estimates on how many calories the typical gut microbiota in an adult human consumes? That is, about how many calories your gut microbiota use per day?
For more information there is a freely available source on Pubmed, "The Human Microbiome, Diet and Health Workshop Summary."

Depends on the diet, right?

@WYSIWYG I don't necessarily think so (but definitely not sure). If someone is eating a diet high in fiber I'm sure that the microbes have increased access to that compared to amino acids, carbohydrates and fatty acids that can be transported across the intestine into the body. The GI bacteria must be in some sort of steady-state because they aren't overtaking anyone's body, thus you could assume the energy utilization by the entire gut microbiome is somewhat constant (I think) - I'm wondering how many "calories" that would be overall that we're eating, but they're actually using.

A recent study by Bahr et al. found that "healthy" gut microbes increased non-aerobic resting metabolism by 16%, compared to gut microbes being treated by risperidone. Risperidone is an antipsychotic drug that causes weight gain and Bahr et al. were trying to determine why. In addition to to the article, their university issued a non-technical press release on the article.
This article doesn't exactly answer your question but does provide a good staring place.


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Can bacteria metabolize fatty acids for fuel?
I'm not a microbiologist, but rather a physiologist  curious about microbial metabolism. Much like humans bacteria can utilize glucose, but when it comes to long chain, medium chain, or short chain fatty acids, what are the pathways that microbes use to break these compounds down for fuel?
It seems plausible that bacteria can take up short chain fatty acids, but with longer chain species are there impediments to uptake? Are the oxidative enzymes similar between bacteria and humans?

Beta-oxidation happens in mitochondria. So there is a good reason to assume that bacteria can metabolize fatty acids.

I don't see the connection between bacteria and mitochondria. Bacteria don't have mitochondria. If you are referring to the endosymbiosis theory, mitochondria are likely descendants of archaea, not bacteria.

I found this review about bacterial lipid metabolism. There it says:

Exogenous long chain fatty acids are utilized by E. coli in two ways. Firstly, they can
  be incorporated into the membrane phospholipids by the acyltransferase system (PlsB
  and PlsC; Section 4). Secondly, they can be used as the sole carbon source for growth,
  and are in fact an important source of energy for E. coli in their normal habitat, the
  intestine [16]. The CoA thioester of the fatty acid is the substrate for both of these
  pathways. Fatty acids greater than 10 carbons in length require the fadL gene product
  to be taken up from the growth medium in sufficient quantities to support growth.

So yes, bacteria can grow on fatty acids alone and they can utilize long fatty acids as an energy source. However the uptake of the long fatty acids requires the protein produced by the fadL gene.

+1 that's a great review included in your answer. I was mostly interested in whether or not bacteria could use triglyceride as fuel because I was unsure if they expressed a lipase to break down the triglyceride to individual fatty acids (like pancreatic lipase produced by humans for lipid digestion). I wanted to start by trying to understanding if there were limitations to fatty acid metabolism. However, in that review it states that some bacteria do express an outwardly directed, membrane-bound lipase for that purpose. Very cool!

Glad I could help :-)

I wanted to start by trying to understanding if there were limitations
  to fatty acid metabolism.

There are aerobic bacteria that can reduce fatty acids. However, there are no bacteria that reduce fatty acids without any oxygen equivalent to, say, fermantation (sugar->alcohol).
You can try this in the lab or even at home. Put tomato purée or sugar in a bottle. Put a layer of oil above it. Keep one bottle open and the other one closed (air-tight). You'll see that the bottle that is open will get molded while the closed bottle will not. This is because there are no bacteria that can penetrate the layer of oil because there are no enzymes strong enough to work anaerobically.
Also, good tip to preserve your food at home.
Source: I'm a biotech engineer.
Carlson, Karin; Linder, Claes et al.


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DIfference between diversification and differentiation
In Adaptive dynamic :
what is the difference between Ecological Differentiation and Ecological Divergence ?

I would say that ecological divergence emphasizes on the process of speciation by niche differentiation while ecological differentiation emphasizes on the process of niche differentiation due to overlapping niche of non-necessarily closely related species. But it's no more than a guess! What do you think?

As already said in a comment: I would guess that ecological divergence emphasizes on the process of speciation by niche differentiation while ecological differentiation emphasizes on the process of niche differentiation due to overlapping niche of non-necessarily closely related species.
But looking to some articles, it seems that they use both term without making any difference. As found on this article for example.
Therefore, I would rather advice to no consider too much difference in meaning between ecological divergence and differentiation. But take time to define accurately the words you're using, especially if you talk about cases that fall on the border of two concepts!


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Is there a maximum pain threshold?

Is there a maximum threshold of pain a Human can experience, beyond which point there is no noticeable difference?

I ask this question in part to better understand the definition of pain and its different facets, e.g. Is there a quantitative measure of pain? Are there various types of pain, or are they all part of the same fundamental experience?
It would also be interesting to know since I could perhaps be allowed to claim:

"well at least I know I cannot feel more pain than X"

Thank you for your opinions.

it only goes to 10. http://en.wikipedia.org/wiki/Pain_scale  ha ha just a little levity

"But this one goes to 11!"

Haha! Interesting how many scales there are, cheers

When the pain receptors are fully loaded then it's not possible to excite these receptor greater. However the perception of pain has a large psychological component and is not well understood. Your brain could modulate your perception of pain naturally or due to illness.


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Why don't we have more cone cells (bigger fovea)?
Background
Apart from being able to sense color, cone cells are able to perceive finer detail and more rapid changes in images, because their response times to stimuli are faster than those of rods.
The fovea centralis is where cone cells are most concentrated and is responsible for sharp central vision (foveal vision), which is necessary in humans for reading, driving, and any activity where visual detail is of primary importance.
Question
It is hard to imagine what it would be like to be missing the fovea centralis, and even harder to imagine what it would be like to have one the size of the entire retina! In any case it seems that having a bigger fovea centralis would be beneficial for survival, so why do we have so much peripheral vision?

Fovea has very high resolution , color vision but low light sensitivity. So, if we consider the fact that most mammals are nocturnal doesn't this make sense ?

See this

We use central vision for a lot more things today than in the past. Peripheral vision is most important in navigation, so those who lose their central field retain the ability to navigate around objects. It is important that this is fast and sensitive in the dark as well as light. It isn't important for it to be in colour; this would mean it would be less sensitive in the dark and colour isn't important in navigation and also it would take longer. Navigation is of vital importance as it can be the difference between survival or death in the flight or fight response. Similarly it is important in the fight part, being able to see a foe.
Let's our foveas were bigger, well we would lose the above. What would we gain? The ability to see more at full resolution and colour. It's impossible for us to concentrate on more than we can see in our central field already. in fact we dart our gaze around to focus on many things because we can't focus on multiple things at once. By this I mean thinking about what we see not processing it. Of course we would also require a much larger brain to be able to process it all, processing the central field takes a lot of brain matter.
So in conclusion, it's not helpful.


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Ka/Ks (dN/dS) analysis module for Python?
From this wiki article:

In genetics, the Ka/Ks ratio (or ω, dN/dS), is the ratio of the number
  of Nonsynonymous substitutions per non-synonymous site (Ka) to the
  number of synonymous substitutions per synonymous site (Ks), which can
  be used as an indicator of selective pressure acting on a
  protein-coding gene.

Question:
Are there any modules/packages available in Python for doing Ka/Ks analysis? I wish to carry out whole gene Ka/Ks analysis and then maybe "codon level" Ka/Ks analysis (i.e. within gene via sliding window).

Do you know about BioPython?
Here, on another website, someone already asked this question and a pretty nice answer was provided by Brad Chapman. He gives already written functions to perform this kind of analysis (I personally haven't tried the codes).
In Perl there is Bio::Align::DNAStatistics. You might adapt it to Python.
This might be useful as well.
I think there are plenty of possibilities that are offered to you. You can go through some others by doing google search with the keywords synonymous, non-synonymous and BioPython.

Cheers, i'll give this a go soon!

I've looked into BioPython, they have an output parser for PAML but that software is not recommended when you only have pairs of protein sequences. I ended up programming my own version which implements the approximate Nei-Gojobori algorithm.


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Infant tissues, organs, body parts or reflexes in an adult organism
What is the phenomenon, when a normal useful tissue, organ, body part or an inborn reflex or instinct existed in the infant organism and normally should disappear or at least completely lose its function in the adult organism but it won't? Atavism and vestigiality don't seem the right terms. Is there a specific word that refers to the phenomenon?

"Remnant" is the closest term I can think of; "residual" is also used. You can find both used to describe the foramen ovale for example, which typically closes at birth (and has served its purpose at that point), but remains patent in a substantial proportion of adults, sometimes causing symptoms.
However, these terms are of course not specific for the circumstance you describe; I don't know of any that is.


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Live cell imaging using confocal microscope - Question about the microscope settings and laser wavelength
I am doing some calcium imaging to measure calcium levels in HeLa cells. To do this I have expressed cameleon calcium indicator (YC3.60) in the cells and I am using confocal microscope Fluoview for the live imaging. I am having trouble to fully understand some settings about the microscope. As indicated on the picture settings below, I am using 440nm wavelength. However since the argon laser does not emit 440nm but 458nm I do not understand what does this 440nm stands for?
Also after performing the live cell imaging, I analyze the data ratiometically. Is is possible to tell from my confocal settings what would be the ratio of Channel2/Channel1 in nm? I suppose it is 530nm and 480 nm but I am not sure if this is correct.
I have read different papers using confocal microscope but it is not very clear to me since this is my first time using it.
I would appreciate it a lot if someone can help me with this.

Your best bet will be to ask the person who runs the facility - they will have an idea on the set up at your facility and what will work best for your needs.

I thought about that but for the moment I don't know yet someone I can ask there.


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Does your body type affect the rate at which you age
Out of the 3 body types: ectomorph, endomorph and mesomorph, does one age quicker/slower than the others or does it not matter so much?
There are many factors that affect the rate of ageing, but I'm just wondering if body type plays a role.
I've read that humans age slower due to a slower metabolism, so does that mean that ectomorphs have, on average, live longer or is there something about endomorphs that means they live longer?

Welcome Pencilcase. We are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on. Enjoy the Stackexchange network.

The term endo/meso/ectomorph just describe shape, vaguely. These are not strict nor scientific definitions. Your question would be better posed by asking whether BMI, body muscle percentage, fat percentage, height or weight affect aging. I would also advise you to define what you mean by 'aging', which itself is poorly understandable. Do you mean life expectancy? Do you mean actual well-being (what kind?), or the incidence of specific aging diseases?

Hello, thanks for answering!
I'm not a biologist but I think by ectomorph I mean people with a high metabolism and a lower percentage body fat and by endomorph I mean someone who puts on weight easier and has a slower metabolism (so generally a higher fat percentage.)
I heard that the reason why humans age slower is due to a slower metabolism and I want to know if that means ectomorphs live longer than endomorphs or if there's something else at play.
And by ageing, I mean how quickly it takes for damage to accumulate (eg: does one experience more inflammation or take longer to repair)

@Pencilcase I have never heard words like 'ectomorph', 'endomorph' and 'mesomorph' used in a scientific sense. Even whether such things as 'body types' exist is doubtful.


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What are the roles of ATP and ADP in muscle contraction?
I've always known that the hydrolysis of ATP generates ADP, P, and energy, so I'd assume that if energy is necessary in a given process, ATP hydrolysis should occur (or another exothermic process).
What I don't understand is how this works in muscle contraction. I assume that part of my misunderstanding might be due to the lack of knowledge of how the contraction works at a molecular level, as well as how this phenomenon relates to the contraction at the macroscopic level (my arm contracting), hence I'm writing this question.
From a number of sources, including the image below (which is taken from an book in Italian, so I don't include the text; with reference to the figure, stadio means stage, by the way) and the one in this related question, I understand that the mechanical energy is released (i.e. the muscle exerts power on the external world) both when P is released when ADP is released, but definitely not when ATP is hydolised.
Now I do understand that the cycle in the image has to repeat a tremendous number of times while I simply raise my hand to say hello, for instance, but my knowledge of physics tells me that, whatever the amount of energy required to raise my hand is, the two power srokes summed up on all the elmentary cycles have to provide that energy (plus some more to overcome losses, like joint friction or whatever).

But where is the energy that the two power strokes are exerting coming from? It looks like the energy is coming from the release of ADP and P, which makes me think that this is itself an esothermic process, otherwise how could it result in power strokes?
And also, why is ATP needed, then?
From the image I see that the ATP hydrolysis happens between stage 5 and stage 1; does this mean that stage 1 is a high energy state?

In the meanwhile that I write, I start to think that probably the core of the matter is that I mistakenly thought that ATP is what provides the energy for the mechanical action, whereas probably it provides the energy (between stage 5 and 1) that is stored in the myosin (stage 1), such that when the mechanical energy is required (between stage 1 and 2), the myson is able to release it (from stage 2 to stage 4). Does this make any sense?

As a first approximation, I think your explanation makes sense. You can imagine the system having a spring, and the hydrolysis of ATP providing the energy to load the spring  (store the energy in the myosin). Afterwards, this energy is released as mechanical work in the power stroke(s).
However, this analogy will not lead you far because things get complicated, especially if you want to study this process from a physical perspective. In biological textbooks (such as the one you provided), you will find the whole cycle being portrayed as going in one direction only (clockwise red arrows in your image). But because this is happening in the molecular world, most of the reactions/processes are actually reversible. In fact in molecular motors (such as your example with myosin), thermal motion frequently leads to backward steps, especially when the muscle is under high load. This can nowadays be directly measured with various single-molecule techniques:

The simplified biophysical models for molecular motor are ratchets, using thermal motion. They are in a way analagous to Maxwell's demon. But the same way as Maxwell's demon is not feasible because it violates the second law of thermodynamics, a molecular (Feynman–Smoluchowski) ratchet cannot generate macroscopic work by solely extracting the thermal motion. And that is where the energy of ATP comes into play: the energy is used to keep the system out of equlibrium and break the symmetry of motion in space and time (steps forward become more frequent than steps backward).
My answer is really far from being self-sufficient or self-explanatory, but I hope it provides at least some starting keywords for your further research of the topic.


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Producing a genetically modified animal with cell walls
I'm curious if there has been any genetic experiments transferring cell wall producing genes into the genome of a animal model organism such as the fruit fly (Drosophila melanogaster) or a larger animal such as a mouse (Mus musculus).
If there hasn't what do you think would happen, if anything at all?
Thanks!

I don't know of any animals with cell walls unlise your considering something like chitin as a cell wall, which it isn't. Please provide examples if you have any. Thanks!

The short answer is it's very complicated. Plants devote a significant portion of their genomes to cell wall construction and integrating that into an animal, I imagine, would be like integrating a helicopter into a battle tank.

Unless some experiments have been made testing this (which I doubt) this question can only generate speculation.  Voting to close as primarily opinion-based.

Mammalian cells have a semi permeable membrane not a true cell wall like a plant cell. I could imagine that if the semi permeable membrane were replaced with a plant like cell wall then osmosis and other biochemical processes necessary to the organisms growth and survival could not occur correctly.


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Do ants within a colony ever fight or come to conflict?
I'm investigating how hierarchical groups of a larger organization with a common goal tend to come to conflict with one another over time.  As you decompose a large group (for example a corporation), peer groups may compete in an effort to accomplish short-term goals in an effort to further the corporation as a whole.  For example, two groups of software developers might fight for time on the corporations computer system to finish their immediate deadlines.  Though this typically can be resolved through mediation and compromise, there is a human element where one group might inflate the real need to use such a resource.
I was then wondering if the same situation could ever arise in an ant colony.  Are ants truly purely social and never come to conflict within a colony?  Or can they end up fighting internally if food or space is ever scarce?

There has been several major transitions (John Maynard Smith and Eors Szathmary) and systematically there is opportunity for conflict to arise…. and it does! There is conflict along genes within a chromosome (example the Psr gene of Nasonia vitripennis, see R. Trivers and A. Burt Genes in conflict), along chromosome within an individual and along individual within a colony.
Ants has been much studies (see E.O. Wilson, L. Keller, M. Chapuisat) and it has been found that there are tons of different reproduction system in those species. There are conflict between queens, between workers and between queen and workers to reproduce. In some species, a colony have several queens, in others, there are several queens fighting early in life for the right of being the unique queen. In some species, workers can fight to take over the queen and take her function. In some species, workers reproduce sometimes even if there is a queen. There is conflict over who will survive depending on how much related one is to the other one. For example, there is conflict over sex-ratio, the queen is as much related to her sons than to her daughters but the workers are more related to their sisters than to their brothers (because of haplo-diploidy, see Robert Trivers).
There are various factors limiting the conflicts: high relatedness (Hamilton, Trivers), Cost of a fight, absence of information, power asymmetries. Ants evolved various strategy. There is a "police" who kill worker's spawn. We might as well consider lineage selection that select for cooperative colonies (note that L. Lehmann and L. Keller argue that group selection and kin selection are the same concept!)
I basically repeated some stuff I read (or learned in class) but I am personally not sure that all that makes sense! I don't know if really the frequency of conflicts is not simply related to the mutation-selection balance. Criticisms are welcome!
UPDATE:
In reaction to your comment:
Conflicts always have to do with reproduction or survival in evolutionary biology. One might make three categories of conflict:
1)Those involving the right of reproducing
2)those involving the probability of dying (I prefer not to be a forager because forager have a very high mortality)
3) Those that concern the survival of kin individuals. The "purpose" (if I might use this agency way of speaking) of any one to to increase its inclusive fitness (Hamilton, but don't read Hamilton, there is lots of easy source of information on kin selection). Therefore, one will rather help its brother to survive rather than his cousin as it is more closely related to its brother. Similarly, beccause of the haplo-diploidy nature of sex determination system in hymenoptera, workers are more closely related to other workers than to the males while the queen is as much closely related to her daughters and sons. Therefore, we would expect a conflict over the sex ratio, queen trying to have a sex-ratio of 1:1 while the workers are trying to have a sex-ratio of 75:25 (if there is only one father).
Hope this helps!
If you want more specific information about sex-ratio in ants, kin selection, group selection please ask it in another post. Note that there is already some discussions one these subjects on Biology.SE.

So is it safe to say that any conflicts that would arise are centered around the confusion of a queen or general reproductive differences?  I'm a little confused by the answer but you did give a lot of references and subjects to explore so this is good stuff and a much better start than I already had with naive google searches.  :)

@ngramsky See my updated answer


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Which organs need to have fluid compartments in order to develop properly?
I am a student, slightly struggling with the new concept of fluid compartments. I know that there are two main types of fluid compartment, extra and intracellular fluid. I also read that most organs need to have these fluid compartments (established by cell-cell adhesions within tissues) in order to function and develop properly.
My question is what type of organs require these fluid compartments? Would it be the kidneys and the intestines for example?
thanks

Organs consist of different tissues and cells. To function properly each cell needs intracellular fluid. All cellular processes (energy metabolism, signal transduction) occur in aqueous environment, otherwise the required chemical reactions could not take place. Extracellular fluids provide nutrients to the cells and also information from other cells or organs. It can be divided in three categories:

Interstitial compartment: between tissue cells; provides nutrients and helps the cells to communicate within a tissue or organ.
Intravascular compartment: content of blood vessels; transports nutrients, information and immune cells within the body e.g. from one organ to another.
Transcellular compartment: all spaces in the body where only a small amount of fluid is present, normally between organs.

So all organs need these fluid compartments to function properly. The only organ where this is different is the skeleton. But the bone building cells (Osteoblasts) also need extra and intracellular fluid to build a scaffold of collagen. Only after that, they can fill up the interstitial space with hydroxylapatite.
The kidneys clean up the blood and excrete the waste via the urine which occurs in aqueous environment. The intestinal tract absorbs nutrients which are solved in water. Hence, saliva and gastric juice are produced when you ate something.
So every organ needs fluid compartment to do its job. So does the whole organism to make sure all organs are working together (via blood circulation and nervous system).


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Why do we have two eyes?
Humans, animals and birds all have two eyes. Why? In addition to why two instead of one, why aren't there more than two?

Two eyes are important for 3D vision.

First, it's not true that all animals have two eyes. For example many spiders have four, six or eight eyes whilst worms have none, but all are animals.
In simple terms, the reason typical mammals have two eyes is probably similar to the reason that cars usually have four wheels, the reason houses keep out the rain and why coffee cups have handles. It's because that's what works.
Each time an organism develops, there is a high chance that the genetic information that built it will include something new. When that happens, most often the phenotype (essentially, the organism's appearance, such as how many eyes it has) does not change. The organism looks the same as its parent(s) did. If something significant does change, it is most likely to be bad news for the new organism. The chances are the organism will not survive and the particular genetic information that built it will not used again. Hence, organisms don't tend to be that different to their parent(s). Dogs don't give birth to cats.
But just rarely, this new combination produces something different and useful - useful enough that the organism is particularly successful and a good fit for its environment. In that case, simply because it can, the organism has more offspring and more of those offspring themselves survive to have offspring of their own. The genetic information that built the organism is thus used to create more, similar organisms.
So, the first eyes were produced by accident. When eyes turned out to be useful, subsequent generations from the first organism with eyes were more likely to have eyes themselves. As it turns out, analysis of genomes shows that eyes have evolved like this multiple times.
We can only assume that since mammals typically have two eyes, either the random genetic accident that would produce different numbers of eyes in mammals has never happened, or if it did happen, the result was not a good fit to the environment.
Why not no eyes? Human beings are occasionally born without eyes and the cause may be genetically inherited. One might reasonably imagine that for much of human history such a child would be unlikely to survive into adulthood and thus pass on this mutation.
Why not one eye? One reason in the case of primates is that two eyes are useful for estimating distance, which is difficult with one eye. A two-eyed animal has an advantage against predators, making it more likely the next generation is going to have two eyes.
Why not more than two eyes? Perhaps a larger number of eyes requires a larger head making childbirth impossible, or perhaps it requires too much energy to sustain. Who knows? What we observe today - humans typically have two eyes - means that, if that mutation for more than two eyes did happen at some stage, then more than two eyes wasn't optimal for the environment in which the resulting organism found itself, so it didn't get passed on to the next generation.

Please answer questions here with facts, preferably supported by citations. Hand-waving and conjecture are generally not welcome here.


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What is the general term for tree-dwelling animals?
Many different types of animals live primarily in trees, from birds to monkeys and beyond.
Is there a general term that I can use to refer to all of them?
The closest I've been able to come is "arboreal", and I'm not sure that that particular term is appropriate for the broad range of animals encompassed by the casual usage of "tree-dwelling."

What do you mean by "the casual usage"? Dictionary.com seems to make the meanings rather explicit and clear. An animal that lives in or amongst trees is arboreal.

Arboreal is indeed the correct term to use.


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What are 'acid stable' amino acids?
I tend to see terms amino acid, acid stable amino acid, and free amino acids used often in the field of nutrition, but they are sometimes used interchangeably which confuses me.
I know that:

amino acid is a general term to describe organic compounds that encompass both essential and non-essential amino acids.
free amino acids is a general term for amino acids that are not broken down from a protein source; instead it exists in its original form 'freely'.
acid stable amino acid ... no idea

Is that right (correct me if I'm wrong)? What is the larger relationship amongst all three terms? Would consuming a free amino acid be better than one from a protein, or from an acid stable amino acid? Why would one choose to consume a particular class of amino acids over another?

a reference to the source of acid stable amino acid may help place it into context. If its is 'acid-stable amino acid' it may refer to its stability in acidic environments like the stomach?

The amino acids asparagine and glutamine have hydrolysable amide groups on their R groups, as shown here:

Note the leftmost amide group on both amino acids. When exposed to acid, these groups would hydrolyse, releasing ammonia.
This was of interest when people used to determine amino acid compositions by acid hydrolysing purified proteins (example paper which does this) and then running them through HPLC or mass spectroscopes. This method, however, fails to distinguish asparagine/aspartate and glutamine/glutamate due to their acid-unstable nature.
So to answer your question, an acid-stable amino acid is any amino acid that does not degrade under acid treatment.
Additional amino acids that degrade under such treatment can be found here, and includes serine, threonine, tyrosine, tryptophan and cysteine in addition to the two above amino acids. These amino acids degrade by alternative pathways distinct from the one by which the above amino acids degrade.
Finally, assuming you are talking about amino acids in dietary supplements, the reason acid-stable amino acids are reported is because acid hydrolysis is usually the method used to hydrolyse the proteins into amino acids, and therefore the manufacturer would not be able to produce acid-unstable amino acids by this method, leading to that label on your supplements.


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importance of cDNA sequencing of a specific gene in different plants
i want to know what if i made a sequence of cDNA of a specific gene in different plants - what is the important from the sequence and can if found difference between plants , and can i use this sequence to determine cis regulating element

No, cDNAs are copies of spliced mRNAs, and typically contain a 5'-UTR (untranslated region), an open reading frame, or ORF, and a 3'-UTR.
The cis-regulatory information might be revealed by sequencing the genomic DNA upstream of the gene(s).  That is where one usually finds the promoter (although there are some rare exceptions, particularly for genes transcribed by RNA polymerase III).

ok , thanks alot however, how can i obtain the sequence of promoter of a specific gene with a simple method ( only primer and PCR)

The importance of sequencing
Sequence comparison is important because biologists tend to use prior knowledge to make inferences about the function of unknown entities.
Determing flanking sequences
You can use Genome Walking to isolate flanking regions of known sequences. It's a simple repetitive method. The amount of repeats will depend on how far you want to go upstream or downstream of your gene of interest.

One point is cDNA sequence encoding a specific protei, you will find differences in the coding sequence bewtween plants of different species and, within the same species, difference when you compare the genotypes
for promoter analysis you must use the genomic DNA, at leasst 1 kb upstream the ATG, or more (may be there are introns)


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Does music enhance neural activity/cognitive or cerebral function, or is it just mania?
I always find myself drew upon curiosity whilst studying, to whether certain types of music are or are not, effecting me in a sense of cognitive ability.
Take a fantastic piece such as, Mozart's, Symphony No. 40 in G minor, K. 550, for example. Whenever i'm listening to it, at the same time as studying, I feel more fluid... and somewhat enthusiastic. Is there a reason for this?
So to conclude, does music of specific  genre's (i.e. Classical) or, music in general, have any impact on cognitive performance? In particular, cognitive performance, in regards to Mathematics.

This sounds like it would be better received at cogsci.SE.


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Why does my grass luminesce when I step on it?
I live in Austin Texas. My grass is in pretty bad shape but I have noticed small luminous spots on some areas after I step on them.
I'm guessing this will be seasonal so, for the record, this is during November and December that I've noticed it.  It's been quite wet and about 40F to 60F at night. I've seen it a dozen times over the last several weeks. I've attempted to collect samples and when I bring it inside to study it, there is nothing there but grass and maybe some young root systems.  I've googled and haven't seen anything like this discussed.  Does anybody have an explanation?
I can see about 5 spots after trampling a few square feet of my grass.  Using a DSLR and a time exposure, this is the best photo I've been able to get of one:

On one attempt, I pinched the glowy part, held it in my hand, confirmed it was glowing, brought it inside, and this is what I had:

Can anyone explain this?  Is this significant?  Or perhaps the right question is where should I go for a question like this?

Neat! How long does the glowing last? And can you not see the luminescence when under artificial lighting?

I'd guess that you have some kind of glow worms/fire flies - when you walk across the grass you are disturbing them causing light to be emitted. It's going to need a much better photograph to capture the luminescence event (I appreciate that is very difficult!) to be answerable.

It lasts for about 30 to 90 seconds.  It's conceivable that I'm squishing something, like glow worms. Are glow worms tiny like a quarter of an inch?  And would this be the right season, weather, and location for there to be several of them per square foot? And would their ..uhm.. juices glow when they get squished?  Oh, and this is so faint that anything more than moonlight and you wouldn't see it.

I know this is a late reply, but I observed the same phenomenon this morning. I live on 12 acres with horses. It is my ritual to jog with my horse in the morning early before I get started with my day. It was before sunrise and very dark (the moon wasn't out). I had a red-filter flash light so I could see what I was doing, but once I started my jog I turned it off. I saw a speck on the ground that I thought at first had to be the neighbor's security light shining through some trees. After I looked closer I was certain it was it's own light source, so maybe a firefly then? A firefly usually has

first of all, this is not an answer to the question. This is also not a question on its own.Usually, I vote to remove these kind of answers but in your case, I will make an exception since its a well written anecdote and others get to know that this is not an uncommon occurrence.

If it were fireflies or glow-worms, you would have seen them pretty quickly with your searching and collection of grass. I would guess that this is some kind of bioluminescence caused by bacteria or Dinoflagellate.  I have seen this effect when walking on wet sand at the ocean. It is quite fascinating and fun to watch. According to wikipedia, bioluminescent bacteria and Dinoflagellate can exist in fresh water. The moisture in your yard might be enough to support their growth.
https://en.wikipedia.org/wiki/Bioluminescent_bacteria
https://en.wikipedia.org/wiki/Dinoflagellate :

The luminescence occurs as a brief (0.1 sec) blue flash (max 476 nm) when stimulated, usually by mechanical disturbance. Therefore, when mechanically stimulated—by boat, swimming, or waves, for example—a blue sparkling light can be seen emanating from the sea surface.[66]


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Calculation of solute, pressure and water potential
What would be the water potential (Ψw), solute potential (Ψs) and pressure potential (Ψp) at equilibrium when a cell with Ψs= – 0.7 MPa and Ψp= 0.7 MPa is placed in a solution with Ψs= – 0.5 MPa?  (Source)
a. Ψw= – 0.2 MPa, Ψs= – 0.5 MPa, Ψp= – 0.5 MPa
b. Ψw= – 0.5 MPa, Ψs= – 0.7 MPa, Ψp= 0.2 MPa
c. Ψw= – 0.5 MPa, Ψs= – 0.5 MPa, Ψp= 0 MPa
d. Ψw= – 0.3 MPa, Ψs= – 0.3 MPa, Ψp= 0 MPa
Water potential in the cell (before being placed in the solution) will be zero. But after it is placed, due to exosmosis water should move out thereby decreasing its water potential. But by how much does the water potential decrease (when the cell is in equilibrium) and what effect that might have on the cell's solute and pressure potential is what I am unable to calculate.


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Firstly, Spider ID? Also possible relation to ~100+ serious bite reactions in past 1-2yrs
Might have been occuring since day 1 in new residence about 2 years ago. Bites are painful to touch, when fresh, very odd sort of void filled with black stuff under skin which regularly shows fang type trackmarks.(golf ball size swelling, pussing, twin &/or parallel punctures wounds, black(necrotic?) Substance under hardened skin cap as healing, long term healing) Spider found in nightstand drawer, maybe stranded in bottom of SS can cooler.
I have many pics of the live spider in a jar. Thankyou...;)>!

Please add information such as size of spider and your geographical location. Clearer pictures of the spider would also help.

Thank you for reply... I am located at Northern border of 54121 zip code, I'll transfer it to a better container than old mason jar and try for better pics... was having issues uploading here,

Will confirm and post better pics asap, ... but body appears to be ~15mm and leg spread in standard stance ~35mm. I'm not sure, but it may have shrunk a little after spending the last few days in an empty jar.  I will say that thing is very aware and has great sight through that distorted glass, it tracks and follows me around the room from 10-15 feet away even after 2 days of ignorance to it...

https://drive.google.com/folderview?id=1By0VjOmEnhSb-zVieAbHfEjwVg2jpnYf

The link above has a dozen of the best pics

Holy fk 100 bites sounds like a spider drive thru.

It is a wolf spider. It grows from about 1cm to 5cm long. Wolf spiders are usually gray with brown to dark gray markings. It does not spin webs, instead it actively hunts it's prey. Wolf spiders are agile, robust and have excellent eyesight$^1$. That is why you have noticed that it is quite aware of your movements.
Hogna radiata:

Alopecosa Kochi:

The bite of this spider leaves prominent marks$^2$.

In severe cases, the surrounding area may develop redness, swelling, and even ulcers that spread beyond just the bite location. Allergic reactions may cause even more severe symptoms in some people$^2$.

Since the wolf spider is not poisonous its bite can be treated by cleaning the area with soap and water and then placing a bandage over it$^2$.
Note:
I am unable to identify the exact genus of the spider. I believe it could be Hogna or Alopecia. Someone more knowledgeable could inform me.
References:
1.Wikepedia
2.Healthline

That is what I was leaning towards too, it's not identical to any pictures I can find but it's closed of course a lot of the other ones are close to each other being different spiders too.   I don't understand why I'm getting consistently bitten over such a long period of time, all seasons.  Some bites are much worse than others, but fang marks and spread are pretty consistant. But doesn't seem like nesting type, more territorial, I would guess.  I bomb the place three times w/ double doses: doesn't seem to have much effect, not permanent one for sure. I've added bite pics to drive link

@CustomCreations I am not experienced enough to know the answers to these questions. Hopefully someone else will give a solution to your issue.


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Why are Chromosome Territories important?
Chromosomes occupy discrete regions of the nucleus, referred to as 'Chromosome Territories'. This spatial organization is emerging as a crucial aspect of gene regulation and genome stability in health and disease.

But how is this the case when:

Most eukaryotes seem to have Chromosome Territories, but yeast S.
cerevisiae is an exception to this.

So if some eukaryotes do, and some do not, what information do Chromosome Territories provide? Some literature uses the phrase 'non-random chromosome territory arrangements'. Thus, I am confused.
Chromosome territories are randomly arranged in some eukaryotes.
How are chromosome territories crucial for gene regulation and genome stability in health and disease in some  eukaryotes, but random in other eukaryotes?

First, this idea was discredited or ignored during several decades, some studies suggest that CT is random in some eukaryotes that isn't necessary the truth. It is not easy at all to determine is CT are random or not
Second, not all eukaryotic organism are the same. Plants and Fungi have cell walls, animals do not. Fungi can have a dikaryotic cell or even undergo somatic hybridisation.
Third, "chromosomes are more unfolded in lower eukaryotes such as yeast."Chromosome Territories: The Arrangement of Chromosomes in the Nucleus
This article does not mention that S. cerevisiae is an exception, on the contrary "and may even hold for single-cell eukaryotes, such as budding and fission yeast".
Thank you for the question, I learnt a lot while searching for an answer


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What causes a selective shift of colour perception after removing wavelength filtered glasses?
Background
To improve sleep by reducing blue-light melatonin disruption, I wear night-glasses that filter short wavelengths (e.g. something like these). With these glasses on, both the top and bottom bars of this test image will appear visually identical:

(Source: Personally derived from this public domain image and released to public domain)
But the colour spectrum you "see" while filtering the blue light will not appear to be either of these bars; instead some partially de-saturated hybrid of the two. I think this is probably due to a pervasive blue wavelength of the LCD back-light regardless of defined colour contrast.
However, there is something else odd going on. If I wear these glasses for several hours and then remove them for some reason - all the blue colours I should see will be muted, partially de-saturated or even interpreted as a shade of green for at least several minutes afterwards (I haven't stop-watched the effect). Freaky.
Question
Why is this selective shift of colour perception occurring for a while after removing wavelength filtered glasses?

I presume that, like sunglasses, when you first put on the glasses you notice a difference.  If you leave the glasses on for a while, is that difference still noticeable?  If you take them off for a brief moment then put them back on, does it look weird again for a bit?

@Amory I'd need a spare day or two to throw my sleep schedule completely out of whack to get a wider range of information. What I already know from prior use is that depending on the underlying spectral mix, blue light sources will appear green, amber or an extremely dim brown while the wearing the glasses. To be expected; but the persistent interpretation of vivid blues as a greenish-cyan or a rather muted washed-out blue for approximately several minutes after removing physical filtration is the unusual thing. I have some ideas what might cause this, but I'd be speculating.

The short answer is you don't see light you see a reconstruction of your environment made by a learning organ, your brain adapts to changes in stimuli. Color in particular is tricky because there is no objective way for your brain to determine somethings color, it can only see the wavelength that reaches the eye which are affected by everything along the way including the color of your eye's tissues.  Your brain adjusts to the filter, until it sees the colors it expects to see again. It does this by becoming less responsive to some signals, in the case of the glasses the colors in between certain ranges. when the glasses are removed the brain is still largely ignoring those signals and has to learn to accept them again in exactly the same way it learned to ignore them.
You can do something similar with glasses that flip the visual field, (turn everything upside down). The work was done by This is a good article. Follow the link for more information. George M. Stratton, and after wearing the glasses eventually you start seeing things right side up again, then when you remove the glasses everything is upside down again, the brain has to again relearn to see right side up.

Wearing colored glasses forces the eyes to work harder to see the normal colors the way they are supposed to be seen.  In other words, when you wear, say, green glasses, the sort that overwhelmingly turn everything green, the eyes are trying harder to detect all the colors that are not green, and to desensitize themselves to green.
So when you take the glasses off, your eyes have become used to disregarding green in favor of everything else.  Anything green will look a bit washed out, until your eyes adjust.  The effect is less pronounced or non-existent with grey or grey-green glasses.
This has been my experience.  The exact mechanisms by which it happens?  Can't say, don't know.

Welcome. Can you add resources to your answer?

John's answer is correct, in that the color adaption mostly happens in the brain and not the eyes. The eyes mainly adjust to light intensity (e.g. 'nightvision')


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Phantom Limb | Is that even possible?
I am fascinated by the fact that an amputee can control their robotic arm by thinking of the actions they would normally execute when the limb was present.
The mind sends signals to the nerve endings of the amputated limb, which gets picked up by the robotic sensor to perform actuation. Can we send similar signal if we assume we have additional limb (Say a third hand)?
E.g. A phantom hand attached to certain part of our body or is it bit of a stretch. Can we train our mind to control a Phantom hand we never had?

Hi @gfdsal. No, where are the nerve endings to this third limb? Non-existent right? (Also it is spelt Phantom)

@Andrew, I can ask the same thing for fhantom limb pain, where your feel pain at the part of the body that is already amputated. The pain lies not on the nerve ending but sent from the brain reference 1, reference 2

Not only can we, it has already been done with primates https://www.nature.com/articles/nn0799_583 behold the first 3 armed monkey.

@John, this is amazing! I reckon with the advent of assistive AI we shall be controlling exogenous limbs just by thinking of actuation!

@john Although the paper added does seem to prove another functioning limb could be added to a body. It is on rats, not primates.

@andrew, my bad wrong link, here is the correct one. http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.208.6192&rep=rep1&type=pdf

@John - please don't answer the question in the comments.


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Gene knockdown vs gene knockout vs knocksideways?
How are the techniques: Knock-sideways, knockout & knock-down different?

Hello and welcome Adil Amchi.
In genetics and molecular biology there are differences between the terms knock-out, knock-down and (the lesser known term) knock-sideways.
Knock-sideways: Inactivates proteins. Could be done using small molecule inhibitors.
Knock-out: Gene removal, no gene expression. Could be done using CRISPR.
Knock-down: Gene expression is reduced. Could be done using interference RNA.
(Another reference for Knock-sideways:

"Importantly, the rapidity of the “knock-sideways” system allowed the researchers to observe a phenotype distinct from siRNA-mediated knockdown of the same protein...")


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What would happen if we place denatured DNA in acidic medium?
DNA can be denatured at high temperatures or in alkaline solutions. But DNA can be annealed at low temperatures. I want to ask, could it be annealed in acidic medium?

Hello and welcome Nandini Yadav,
It is worth mentioning DNA is an acid (Deoxyribonucleic acid) and intracellular pH is most commonly between 7.0 and 7.4.
Alkaline reagent Example

"The sodium hydroxide (NaOH) is a commonly used reagent to denature the DNA by increasing the pH. At an alkaline pH, OH- groups are predominant. They remove the hydrogen- bonds-contributing protons from guanine and thymine, thus breaking the hydrogen bonds between the two oligonucleotides."

Source
You can see in the image below hydrogen bonds between nucleotides Adenine (A), Cytosine (C), Guanine (G) and Thymine (T).

Acid reagent Example

A decrease in the pH was found to deteriorate the thermal stability of DNA

Source
At an acidic pH, the H+ in the surrounding environment of DNA is high and therefore the hydrogen bonds between Adenine (A) and Thymine (T), Cytosine (C) - Guanine (G) will 'break'.
More information here.


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Y chromosome changing sex ratios
Fisher's principle explains why sex ratios in most sexually reproducing species is approximately $1:1$. However, given that in humans and many other animals, males and females differ genetically, it seems that this should cause issues for Fisher's principle.
Say that the Y-chromosome of an animal had a mutation that increased the ratios of males to females produced by the animal. At the extreme, we could imagine a mutation such that the sperm of the animal only carried Y-chromosomes. Although, by the Fisher principle, this would be bad for the overall number of offspring produces by the animal, it seems it would be good for the Y-chromosome itself, since it will now be present in all descendants of the animal (since they are all male), rather than only half the descendants. I would therefore expect that such a mutation would spread, skewing the sex ratios away from $1:1$.
Have scenarios like the one I outlined above actually occurred in species? If not, why not?

not sure why someone voted to close: this seems like a well-thought-out question, and the answers aren't that easy to find ...

@BenBolker & OP — Maybe I'm misunderstanding the question or overlooking some subtlety, but my understanding was that Fisher's principle does a good job of describing the evolutionary forces that generally maintain a 1:1 sex ratio. To me this obviously includes the "selfish"/"driven" behavior of sex chromosomes ...

I think sex ratio distorters can at least temporarily push evolution in the other direction. Carvalho, Antonio Bernardo, Michelle Cristina Sampaio, Flavia Roque Varandas, and Louis Bernard Klaczko. “An Experimental Demonstration of Fisher’s Principle: Evolution of Sexual Proportion by Natural Selection.” Genetics 148, no. 2 (February 1, 1998): 719–31.
Shows Fisher's principle re-asserting itself in the long run ...

Perhaps my question wasn't very well worded, but Fisher's principle as usually stated cannot apply to genes on the sex chromosomes. To understand why, we can imagine a toy example where a Y chromosome prevented the production of sperm with X chromosomes, so that an animal only had male descendants. Although by Fisher's principle this reduces the overall fitness of the animal, for the Y chromosome itself this is adaptive: it now is present in all the animals descendants, rather than half of them, and this factor of 2 more than overcomes the fact that each male has less children on expectation.

I think Fisher's principle would imply that other genes should evolve to counteract the driving from the sex chromosomes, as the papers @BenBolker describe, but I don't know in practice if this is why we see animals with 1:1 gender ratios, or if other mechanisms have evolved to prevent runaway gene drives; any species which were suseptible to such a gene drive would need to become parthenogenic or else go extinct.

This sort of thing absolutely happens; useful search terms are "sex ratio distortion", "segregation distortion" (i.e. modifying the ratios with which different chromosomes segregate), and "meiotic drive" (a specific form of segregation distortion).
Your scenario (Y-chromosome genes forcing all offspring to be male) is much less common than the reverse (X-chromosome genes, or other genomic elements, forcing all offspring to be female), because it's easy for an all-female lineage to maintain itself by parthenogenesis. Lyttle (1991) says:

Strong Y drive is of necessity transitory, since drive
suppression must either evolve very quickly or the population will be pushed
to extinction. This may explain why few Y drive systems have been observed
in nature.

However, Lyttle goes on to describe

W-chromosome drive in butterflies (in butterflies, females are the heterogametic sex — the sex chromosomes are Z and W, ZZ individuals are male and ZW individuals are female). So this is a little bit like your Y-chromosome example, except that the populations end up all-female rather than all-male
male drive in mosquitoes

Jaenike (2001) says

Although several species exhibit Y drive, X drive is far more common.

Table 1 in that paper lists Y-drive examples in houseflies, mosquitoes, medflies, lemmings, and field mice. (I would include an image, but the table extends over 4 pages ...)

As for your final question,

I would therefore expect that such a mutation would spread, skewing the sex ratios away from 1:1 ... Have scenarios like the one I outlined above actually occurred in species? If not, why not?

I haven't dug through all the original literature that Jaenike (2001) cites, to see if there are populations in nature that are male-skewed due to selfish Y chromosomes. The point that Lyttle makes is that, even if you can find evidence of the existence of selfish Y chromosomes hiding in the population, it's very unlikely  that these will persist in natural populations for very long, because of the strong selection against them at the population level (and from the rest of the genome); either the population will go extinct, or moderators will evolve that suppress the driving effect of the Y chromosome.

Jaenike, John. “Sex Chromosome Meiotic Drive.” Annual Review of Ecology and Systematics 32, no. 1 (2001): 25–49. https://doi.org/10.1146/annurev.ecolsys.32.081501.113958.
Lyttle, Terrence W. “Segregation Distorters.” Annual Review of Genetics 25, no. 1 (1991): 511–81. https://doi.org/10.1146/annurev.ge.25.120191.002455.

the one for field mice is so extreme their populations go through boom bust cycles as the gene spread then the population collapses as it starts to run out of females.

I took a quick look for papers that clearly described these dynamics, e.g. would be cool to cut & paste a figure showing population size/gene frequency/population sex ratio over time


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Slinky-like worm/leech identification
In my mulch bed today I came across a tiny red worm, between $\frac{1}{4}$ and $\frac{1}{2}$ an inch long. It moved across the ground by sitting upright on one end, waving the other end back and forth (presumably for some momentum), and then flipping over and standing on the other end. It did this motion flipping end-over-end, kind of like a slinky. Observed in the Chesapeake Bay region.
I haven't been able to find anything on this little creature through searches. An article about leaping nematodes is the only thing remotely in the neighborhood of what I saw but the motion described is different and these sound far too small to be the same creature. Any ideas what this is?

Welcome to Biology.SE! Can you get pictures of your worm — macro images in particular might be helpful for this identification. You might also want to check out iNaturalist — that site is much more focused on identifications and I think you are more likely to a definitive answer there.

Hi @tyersome, thank you for the feedback. Unfortunately I wasn't able to get a picture at the time or locate one again since then but will continue trying. I'll give the app a try I can get a pic. Thanks.

Did they resemble these "jumping worms" ? https://www.youtube.com/watch?v=jrGnUFDXuyQ  this video is not as red or as jumpy as I'm imagining yours to be

@JimN, very different. This was tiny by comparison to those, less than half an inch, and stood upright, never on it's side like a normal worm. Still have had no luck spotting again to get a picture.

@IPoiler how about this one: https://www.youtube.com/watch?v=AFkz-L4wNT0 (starting at the 25 second mark) or this one https://www.youtube.com/watch?v=xVk87DZB6NY (3:30 mark). Neither of these is red, though, but how does the size and shape compare?

@JimN, not quite but slightly more disturbing to watch (0.o). Looked a bit like a miniaturized single red/orange anemone polyp. Great work tracking down a potential hit in a video with less than 70 views though.

@IPoiler to be honest, I've spent a few hours on this :) which I don't mind. I've learned a lot along the way. I can't figure out what would match your description. But there are some parasitic worms/maggots that affect specific plants. I know you described your worms as being in your mulch, but did it seem like they were coming out of a certain plant? the roots? or concentrated around a certain something decaying in compost? Or was it around a particular kind of large tree?

@JimN after doing some reading on locomotion in different types of invertebrates, I'm pretty confident that what I encountered was some type of tiny leech. It didn't have quite the inchworm gait like the one in the video, seeming to instead flip from one sucker to the other like a slinky. It did mostly stand up on one end waving around similar to that one though.