text:
What keeps a virus from spreading from one species to the other, when it can infect both?
I have read that there have been cases where animals (some tigers, also a dog) have been infected by Covid-19 through a human host. At the same time, I read that currently it is deemed unlikely that the virus can spread back from those animals to humans (in the same source). Regarding the infection of other animals like tigers there is also this question which has some sources.
That makes no sense for me, I would think outside of the body, a virus is the same independent of the source and so any species that can catch it should be able to spread it to any other species that can also catch it. Are there any reasons why this would not be the case, in general?

One reference for the human-to-tiger transmission: https://www.nytimes.com/2020/04/06/nyregion/coronavirus-new-york-update.html (scroll down towards the bottom)

Your question would be improved if you could cite the things you've read.

@UuDdLrLrSs That seems to be a news ticker that updates constantly. The tiger thing doesn't seem to be there anymore.

I'm pretty forgiving when it comes to questions, probably more so than a few would like, but there are a lot of uncited assertions in this that make it really difficult to answer.

@BryanKrause Added a link to the german news page where I read it. It is about the tigers, but also contains a bit about dogs and house cats which can be infected, but that at the same time the virus couldn't spread back to humans.

@AlexReynolds Sure I am interested in this particular disease, but I don't expect a definitive answer here. But the general case can probably be answered - are there viruses which jump from one host species to the other, but can't jump back? If so, why?

@kutschkem its still there - search for "tiger" in the text of the page


text:
By what physiological mechanism do we not feel microbes (bacteria, etc.) living on our skin?
 Background
I know our bodies have a handful of ways to threshold our awareness of sensory stimuli:

Neural density

Sensory acuity
I assume really tiny stimuli could fit between receptors

e.g., Oaklander (2001) found nociceptor densities of 2-4000/mm2

Impacts summative abilities to surpass postsynaptic impulse thresholds

Varying thresholds of individual receptors.

Dubin & Patapoutian (2010), for example, show variations in classes of neurons based on their temperature (°C) and mechanical force (milli-newtons) thresholds (see thresholds listed in Tables 1 and 2).

Reticular formation involvement in regulating what we are consciously aware of

My question:
Which of the above physiological mechanism(s) are primarily responsible for our lack of sensation (or lack of conscious awareness) regarding microbes on our skin?

Update: My question is explicitly about physiology. Regardless of the impacts, benefits, evolution ,etc. of not feeling them, they're there. But even though we're covered in microbes, we don't sense them -- how not? I want to know by what physiological mechanism(s) we don't feel microbes on our skin.

I don't think any metazoan has evolved mechanisms to 'sense' microbes in the way you are describing. Microbes are everywhere, in fact, more microbe cells than human cells in adults. So, it is not that 'we don't feel them', quite but the opposite: we don't know how it feels to be 'sterile' of microbes. From the time we are born until we die, we are constantly hosting microbes, just as we don't 'feel' the atmosphere pressure, or gravity: these all are environmental constants to us. For such environmental constants, why would we be conscious of its presence/absence if it has no adaptive value?

I'd argue that we do have awareness of such organisms, only via smell: https://www.medicalnewstoday.com/articles/173478#what-is-body-odor, https://www.healthline.com/health/sudden-change-in-body-odor, https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-018-0588-z

@TumbiSapichu  sure. I allude to some of your comment  in my post -- perhaps some part of our brain (e.g., the RF) prevents us from "feeling" them. Even if we don't know what it feels like to be sterile, you're suggesting that we feel something but we don't know how to interpret it (or that we haven't had reason to evolve a way to be conscious of it). That would be suggestive of CNS level of regulation (vs the PNS options I also propose in my question). I understand that no metazoans (including us) feel microbes, but my question is why (in a physiological sense) that is the case.

Nociceptors probably aren't the most relevant sensory receptors for the question; they aren't really responsible for any feeling of "touch"; you'd expect them to be activated only if a microbe released something chemical like damaged tissue does.

@Bryan I know they're not. It was just an example paper (the 1st I found) demonstrating density of a type of sensory receptor. I mention it solely for an example of receptor density. I assumed that the density of other sensory receptors are in the same ballpark (though, perhaps this was an incorrect assumption for me to make?). Regardless, I guess it's not really relevant to understanding the main question: which of these reasons would be most responsible for us not feeling microbes?

Ask yourself, what benefit would it have?
Keep in mind you will always bee covered in them, this is the state you evolved in. Thus sensing them would serve no purpose, and sensory organs are expensive in terms of resources so why would we evolve a useless sense?

But I'm not asking about the benefit. I realize there is nothing to gain feeling them. But that doesn't make them not there. And so even though we are covered in bacteria, we don't sense it. My question is about physiology. I want to know by what physiological mechanisms we don't feel microbes on our skin.

@theforestecologist because we lack a mechanism to detect them, I don't understand what more you could want, it is like asking why humans can feel beta particle emission.

but is that true? Are we lacking detection or awareness? You say this very definitively (and it may be true), but I haven't been able to find literature discussing the mechanism. Is this entirely an issue of PNS not sensing or of CNS not making us aware? If the PNS, is it because thresholds aren't met (for mechanoreceptors for example), or some other reason? I get that you want to simplify the answer because the question doesn't seem important to you. However, I have a biology student who asked me quite earnestly for an answer, and I'd like to provide one if such knowledge is known.

your not going to find a paper about a lack of a mechanism, scientists don't usually write papers about non-existent hypothetical structures. There is literally an infinite number of things we can't sense. For explaining it to a biology student the answer is to think of what senses we do have and what purpose they serve, they need to flip their thought process and think of what we can sense and how each mechanism works. we can't sense it because there is no mechanism to sense it because we can only sense things we have mechanisms to generate sensory signals for.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


text:
Why don't carrier proteins require energy to change shape?
I know that carrier proteins can be used for both passive and active transport, but I am referring to the facilitated diffusion aspect. Even though facilitated diffusion via carrier protein goes along the concentration gradient, the protein still must change its shape, from what I understand. Why does this process still not require ATP, and why does it require ATP to go against the concentration gradient in the same manner?

The carrier proteins that participate in passive transport do not require energy in the form of ATP molecules, which is the primary form of metabolic energy of the cell, but this does not mean that the transport process is energetically 'neutral'. Many proteins bind their ligands via hydrogen bonds, partial or full ionic bonds, van der Waals interactions, etc. These interactions build up a type of energy known as 'binding energy', which can be enough to induce a conformational change in the transporter. In addition, consider that a chemical gradient in itself is a form of energy, which effectively drives the movement of many solutes across the membrane. In fact, the gradient of a molecule can be used to transport another type of molecule, without using ATP. For instance, consider the Lactose permease. Its mechanism is, I quote:

Hydronium ions from the outside of the cell bind to a carboxyl group
  on the enzyme that allows it to undergo a conformational change. This
  form of lactose permease can bind lactose from outside the cell. The
  enzyme then everts and lactose is transported inward.

Below a diagram of this protein, with its ligands in the center:

That being said, some proteins that are involved in passive transport do not require conformational changes like these I described, because they are simply 'open' (like a tunnel), and the solutes can freely diffuse across the channel. This is the case, for instance, of aquaporines. The advantage of the carriers that need to change conformation is that the binding to their transported molecule implies a recognition mechanism, which gives high specificity, whereas the proteins that are simply 'open' are less selective and thus transport many different solutes. See, for instance, the central pore of an aquaporine:

Regarding your last question, the hydrolysis of ATP can release enough energy that (similarly to the binding energy described above) can induce a conformation change in the transporter protein (active transport). This is often used when going 'against' the gradient because, as I mentioned, the gradient in itself contains energy that if not used passively (as in passive transport) then it is not favorable to transport something against the gradient. Thus, an external source of energy is needed (ATP!).

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
What are the implications of tigers being susceptible to SARS-CoV-2?
It was recently reported that a handful of tigers and lions tested positive at the Bronx Zoo for SARS-CoV-2 (see here and here). Does this imply that the SARS-CoV-2 strain in humans mutated into a form that can infect these other species? I thought these sorts of mutations required a long time and prolonged contact between the species (which I wouldn't have thought would be present with such large cats).
Alternatively, is it possible that a single strain of the virus is capable of infecting multiple species?

A partial answer, to the question of how the virus might spread to animals I found several references

The HongKong dogs, the New York tiger, the Netherlands mink farm and the French cat have been sequenced and can be seen on nextstrain. Note the low amount of mutations in each case, which is intriguing because we expect for example that different ACE2 genes will induce some adaptation at in the viral spike. Those animals had an infection and detectable RNA in the nose for several days. For the dogs the viral load was low and in one case the sequence was identical to the owner. The minks and tiger had noticeable symptoms. A Wuhan cat partial sequence has been uploaded too, as well as a full-length French cat sequence.

A lab paper said "SARS-CoV-2 replicates poorly in dogs, pigs, chickens, and ducks, but efficiently in ferrets and cats", in particular dogs can't transmit the disease efficiently. According to them subadult cats are susceptible while adult cats are not, and the disease is upper respiratory tract.
There is a new preprint on a 4 month cat who developed severe disease, dyspnea, and had to be euthanized.

A paper found antibodies in several Hubei cats from animal shettlers and vet clinics, some of the positive cats are "stray cats", others are sick cats, and a few were cats owned by covid positive people, in those the antibodies were found to be neutralizing the virus much better than in others.

Another one found that ferrets are efficiently infected in lab and transmit the disease to each other, even if it is mainly upper respiratory tract (no severe pneumonia).

Rabbits are susceptible though less than ferrets, and asymptomatic.

Mice are not succeptible but human-ACE2 transgenic mice are and develop a mild pneumonia. Note that SARS-CoV and OC43 produced instead a deadly encephalitis.
However, through 6 ($10^{5.8}$PFU) passages into mice lungs the researchers could adapt SARS-CoV-2 through acquisition of a single mutation in the RBD allowing the virus to produce a moderate pneumonia into both young and aged mice.
The same researchers after 30 more passages obtained a super-deadly mouse adapted strain effective even at $10^2$PFU with 3 mutations in the RBD and 9 others mainly in nsp3-4-6 and N. Of note, two of the RBD mutations are in the South African variant N501Y.V2.
Something similar had been done with SARS-CoV.

The Baric lab has compared the RBD from SARS-CoV-2 and previous sarbecoviruses,
the human and mouse ACE2 protein, and through computer simulations they could find two amino acids to change in order to switch the virus from humans to mice. With 10 more passages they obtained a deadly strain in aged mice.

There are several mink farms in Netherlands where the animals got infected, this is possibly the most promising species for inter-species transmission. Edit : as predicted (first reported case) of animal to human transmission is believed to have occurred in such a mink farm. A detailed story including severe pneumonia is described in a paper.

In lab, SARS-CoV-2 is provoking a severe disease in minks as well as in Roborovski dwarf hamsters.

The Pangolin outbreak(s) : not SARS-CoV-2 but the newly discovered Pangolin-CoV in the same lineage, it killed 16 of 21 Malayan pangolins in March 2019. The virus was identified only in February 2020. The Pangolin-CoV whose RBD is very similar to SARS-CoV-2 was in this outbreak.

Cats can transmit the virus to each other. In the nose the peak was $10^{4.5}$ PFU / ml which is a medium viral load.

Similar for hamsters and macaques, the latter are used for vaccine development.
Racoon dogs show high shedding and can transmit the virus through present only minor clinical signs.
This kind of result is not surprising, most human viruses can transmit to some species and not to others, often producing a different and milder disease, which is a problem for vaccines and antibodies development.

This paper https://onlinelibrary.wiley.com/doi/pdf/10.1002/jmv.26621 has a lot of references on zoonotic potential of SARS-CoV-2

Your question may be based on a misconception. Mutations occur all the time. In almost all cases, it leads to decrease in reproductive viability. For a virus with one or more established host species, it has already evolved to be quite efficient at reproducing within those species. For it to jump to a new host species and spread in that other species, it must not only be able to infect the new host species, but must also have the opportunity to cross over. If it cannot normally infect the new host species, then it has to acquire some mutations. But mutations occur all the time, whereas the opportunities are not always there. So this is a matter of relative likelihoods. The more contact between wild animals and humans, the greater the likelihood of such inter-species infection happening, because of low prior contact between humans and wild animals.
Since we now have probably 10 million or more humans infected, we have provided a great number of opportunities for the virus to jump to other species, many orders of magnitude more than the original opportunities for the virus to jump to humans. This is why such large-scale events can have knock-on effects of much bigger scale than the events themselves.
While zoo visitors may not go close to large cats, they may sneeze or cough and thereby transmit the coronavirus in mucus droplets that can last very long even if alcohol-based disinfectants are applied. The zoo keepers themselves may be infected and have close contact with the animals. It is difficult to trace the source of infection when we have so many cases. Although the Bronx Zoo was supposed to be closed from 16 Mar onwards, it is not impossible that some animals were already infected prior to that, so any hypothesis is going to be guesswork.
Furthermore, viruses that already regularly infect more species tend to be able to infect more new species than other viruses. So once the coronavirus managed to jump to humans, it is reasonable to expect it to be able to infect other new species more easily than the strain in the original host species. So the fact that tigers are susceptible to the strain that infects humans does not imply anything about whether that strain has acquired some new mutations or not.

A single strain of virus (such as rabies) can infect multiple species of hosts.
The big question is whether domestic cats also get infected?
If they do, two main problems.
There would be a reservoir of virus circulating in cats allowing reinfection of humans. And worse, the virus may acquire mutations in the cat population that make it more virulent in humans.
Personally, I recommend keeping a good distance from all big cats to be safe.

Lol agreed.  Only one thing is worse than being bitten by a tiger, and that is being bitten by a tiger with coronavirus.

Interestingly I got quite a lot of downvotes and negative criticism for this (inc. request for citations). Never make a joke on an intercultural site unless it’s OK for people to miss it.


text:
Are there any studies on the solar latitude limits of different plant species, beyond which they wouldn't thrive even with suitable weather?
Not sure whether this belongs here or in the Gardening & Landscaping StackExchange, but here goes...
According to maps provided in the paper Present and future Köppen-Geiger climate classification maps at 1-km resolution which assumes no reduction in greenhouse gas emissions, by the end of the century climates (for example) suitable for Theobroma cacao (with rigorous irrigation) and Cocos nucifera may extend at least to Porto Santo Island (33.08(3)°), the latter possibly to the Azores (38°) given that they are more tolerant of anemic winter heat than frost, for Carnegiea gigantea Northeast Kazakhstan (43.208(3)°), for Olea europaea North-Central Iceland (66.525°), for Malus domesticus Knivskjellodden (71.18(5)°), for Trachycarpus takil Knivskjellodden (71.18(5)°) or potentially even Southwestern Svalbard (77.5(3)°), and for trees in general the Eureka area on Ellesmere Island (79.48(3)°).
However, even though poleward areas may become suitable for species previously restricted to areas closer to the equator in terms of their thermal and precipitation profile, they may not in terms of their solar profile. I mean, while a Windmill palm would be able to accept the mid-10s °C summers and slightly-above-freezing winters of future Finnmark, would it accept the month of darkness and low solar angle except in mid-summer? Would olives tolerate the midnight sun? Would coconuts withstand the sub-30° zenith angles of the mid-latitude winter? This question could also apply to the extreme low latitude limits of species; for example, could hemiboreal Hol/Nearctic winter-deciduous trees live in the modern Southern Altiplano where average monthly temperatures are vaguely similar but the latitude is inside the tropics?
So... Have there been any studies on the potential latitudinal limits for different plant species? They don't have to be for the species I've mentioned, those were just examples.


text:
How far can free radicals from UV radiation diffuse through the skin?
UV radiation damages DNA through two separate mechanisms. Direct damage occurs when a photon is absorbed by DNA. Indirect damage occurs when a photon is absorbed by a chromophore, and the excited chromophore then reacts with DNA, or reacts with other molecules, forming free radicals and causing harm via an oxydative stress mechanism.  How far can these free radicals travel?  The Wikipedia article on indirect DNA damage states

Unlike direct DNA damage, which occurs in areas directly exposed to UV-B light, free radicals can travel through the body and affect other areas—possibly even inner organs. The traveling nature of the indirect DNA damage can be seen in the fact that the malignant melanoma can occur in places that are not directly illuminated by the sun.

This seems extremely dubious to me, but I know very little about the topic and can't find any more reputable sources discussing the question. Can indirect damage occur in adjacent non-illuminated cells?  Can it occur millimeters away from the illuminated area? Centimeters?  Can UV light harm inner organs?

The part about melanoma vs basal cell carcinoma is nonsensical.  All types of skin cancer can occur in any area of the skin since things other than UV radiation can damage DNA.

The life of the radicals decides how far they move.
This paper https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4310837/#!po=6.92308 has a table of half lives of radicals, the longest lasting ones (the radical of nitrous oxide and nitrogen dioxide) have half lives of seconds.
Diffusion theough the skin would be slow
Technically the problem is "reactive oxygen species" (ROS) and "reactive nitrogen species" (RNS) that are the damaging chemicals that includes free radicals. The reactive species that are not radicals have a longer half-life or are even fairly stable and so could diffuse further before making mischief.
The wikipedia article has problems - that is mentioned on the talk page.


text:
Why does inbreeding cause genetic defects, but cell division in one's own body does not?
I was watching a DNA transcription video when I realized that cells basically create copies of DNA all the time in our body. There may be a few mutations/errors, but it works out fine. However, when the haploid DNA in sperm combines with the one in the egg, there's so much extra work to be done to avoid errors. It's like if I write some software in one project and try to combine it the code I've written in another project, it's easier for me to do it because my coding style is similar and I know the code. But if I have to merge somebody else's code into my code, there would be a heck of a lot of merge conflicts and errors. Sure, I may learn better programming from the other person's efficient code, but the amount of bugs, testing etc. will be much more cumbersome.
Some research says:

Malformations or harmful traits can stay within a population due to a
  high homozygosity rate, and this will cause a population to become
  fixed for certain traits, like having too many bones in an area, like
  the vertebral column of wolves on Isle Royale or having cranial
  abnormalities, such as in Northern elephant seals, where their cranial
  bone length in the lower mandibular tooth row has changed. Having a
  high homozygosity rate is problematic for a population because it will
  unmask recessive deleterious alleles generated by mutations, reduce
  heterozygote advantage, and it is detrimental to the survival of
  small, endangered animal populations. When deleterious recessive
  alleles are unmasked due to the increased homozygosity generated by
  inbreeding, this can cause inbreeding depression.

But bed bugs for instance, have managed with inbreeding without any problem (goddamned creatures!).
The question I'm asking is from the perspective of how the DNA combination and copying happens. Since the regions chosen during meiosis is random, shouldn't a similar DNA from sperm and egg resulted in a more stable genetic code since they are similar? I'm not looking for simplistic answers like "because Nature wanted diversity" or "because recessive alleles are unmasked".
I'm looking for a more fundamental explanation about the property of DNA, or the process of copying/merging these complex structures. Why does merging two similar things cause more problems than merging two dissimilar things?

You are citing texts with terms "recessive alleles", "homozygosity" and "heterozygote advantage" but you not using them in your own questions makes me think you don't fully grasp them. Are you fully fammiliar with Mendels laws?

Homozygocity etc. are like telling grandma that the "internet" is a bunch of connected computers. My question is a more fundamental "why" about the genome.

Cell division involves mitosis primarily. In sexual reproduction there is meiosis. Genetic recombination occurs primarily when there is sexual reproduction. In short, your cells are simply multiplying, they do not have sex, and thus there is no novel genetic material (which there is with sexual reproduction). In sexual reproduction, there is a 'purging' effect: if there is a bad allele in some parental DNA, it could be masked by a good copy of the other parent. Your question stems from a misunderstanding of sexual reproduction and a mixup of inbreeding, very different to somatic cell divison.

I suspect your problem is grasping what is a deleterious recessive allele. Wikipedia and textbooks explain it much better but I will try to illustrate with respect to your question.

I have to merge somebody else's code into my code, there would be a heck of a lot of merge conflicts and errors.

Problem with this analogy is that when merging code both variants are written by people. People tend to write code that works on its own. This is not the case for DNA since mutations are usually random and more often than not result in gibberish. Better analogy would be maybe combining information from two coppies of the same data to overcome bit rot.

Since the regions chosen during meiosis is random, shouldn't a similar DNA from sperm and egg resulted in a more stable genetic code since they are similar?

Lets consider two made up genes A and B.

A is a dominant functional version of A gene involved in development of hand. In very abstract (code-like) way it could be read as: "If at the end of hand initiate 5 fingers"
a is a mutated nonfunctional version of A gene. In very abstract way it could be read as: "If at the end of hand initbzngers". It produces nonfunctional protein. In biological terms "a" is called deleterious recessive allele.
B is a dominant functional version of B gene involved in development of brain. In very abstract way it could be read as: "If in neuron keep junctions together"
b is a mutated nonfunctional version of B gene involved in development of brain. In very abstract way it could be read as: "If in geuron keep junctions together". It never produces the needed protein.

Now lets consider cross between two dissimilar individuals:
father AaBB X mother AABb
Following Mendel's laws they produce progeny:

AABB - has at least one functional copy A and B gene and thus develops fine.
aABB - has at least one functional copy A and B gene and thus develops fine.
AABb - has at least one functional copy A and B gene and thus develops fine.
aABb - has at least one functional copy A and B gene and thus develops fine.

now let's consider cross between two similar individuals:
father AaBB X mother AaBB
Following Mendel's laws they produce progeny:

AABB - has at least one functional copy A and B gene and thus develops fine.
AaBB - has at least one functional copy A and B gene and thus develops fine.
aABB - has at least one functional copy A and B gene and thus develops fine.
aaBB - fails to properly develop fingers.

cells basically create copies of DNA all the time in our body. ... Why does inbreeding cause genetic defects, but cell division in one's own body does not?

During normal cell division AaBB cells should produce only AaBB copies which have at least one functional copy A and B gene and thus are fine.
Big picture
In a real population imagine every individual has tens of thousands of genes and each of them can be made nonfunctional by random mutation. The nonfunctional copy often does not have effect since the individual has another functional copy. When two non-related individuals procreate, chances are mutations they carry are in different genes and their progeny are fine as illustrated above. When related individuals procreate chances are thay both have the same deterious mutation(s) and not all their progeny will be fine.

But bed bugs for instance, have managed with inbreeding without any problem (goddamned creatures!).

Species for which inbreeding is normal have much less recessive deleterious mutations prevalence in populations for simple reason. If new deleterious mutation appears the inbreeding leads in two generations to aa homozygots that die or fail to procreate and the "bad" mutations are selected out fairly fast. Inbreeding is normal state for some species. Today inbreeding-resistant species are descendants of individuals who have survived many generations of inbreeding.

You say

cells basically create copies of DNA all the time in our body. There may be a few mutations/errors, but it works out fine.

and

Why does merging two similar things cause more problems

Well, it doesn't, at least not in the way you seem to understand it. Cell division in the adult human leads to problems too. Every time a cell of yours divides, there is a chance that something goes wrong and the new cell receives an imperfect copy of the DNA. This is what is called a "somatic mutation" (the opposing term would be "germline mutation"). This is the reason people get cancer - when you are unlucky enough that a cell of yours gets all its anti-cancer mechanisms get mutated away, it can become the "granddaddy" of a tumor in your body. It (and its descendents) start multiplying exponentially. And of course, there is even more mutations in this large number of new divisions, which makes for subclonal tumors, complete with a perfidic kind of natural selection when exposed to some of the newer targeted therapies we have. So this kind of mutation happens frequently, and it does lead to quite large problems for individuals and for humanity as a whole.
The problems with inbreeding also exist, they are just a different kind of problem with a different cause and effect. Here, what you are afraid of is not a mutation. Rather, as explained in more depth in the other answers, if the father has one good and one malfunctioning copy of a gene, and the mother has one good and one malfunctioning copy of the same gene, you get very high chances of having a baby with two malfunctioning copies of that gene, without any transcription errors coming into play at all. And it is very rare for this to happen if you randomly select a mother and a father from the population, but if the two of them share a significant proportion of their genes (because they are related), it happens fairly frequently - enough for basically all human societies to have noticed it even in ancient times and to have created taboos around inbreeding.
A third thing can also happen, which is a de novo mutation in the very early stages of cell division of the zygote. It is not necessarily a result of merging the genomes of the mother and the father, but rather a cell division problem after this merging has happened. It is not necessarily more rare, per division event, than the somatic mutations (the first kind of problem). But it will affect all the cells emerging from that mutated cell, which will be a significant proportion of the baby's body. This is an event that is not very noticeable, since many of the problems at that stage will not result in a life birth - in fact the pregnancy/conception can end so early that the mother never realizes she conceived. It is also not as prominent in social norms, since it is not correlated to something obvious like inbreeding, so there are no traditional prohibitions for events that lead to it (actually, there are modern prohibitions, like warnings in situations which can cause mutations in a fetus or a zygote).
All three of these exist, and all of these lead to problems. So your wondering why one is a problem and the other isn't is based on a misunderstanding.

Why does inbreeding cause genetic defects, but cell division in one's own body does not?

Inbreeding does not cause genetic defects, it just makes already existing ones more likely to be problematic.

Why does merging two similar things cause more problems than merging two dissimilar things?

You have two copies of each gene, one from each parent.  For many possible defects all that matters is that you have at least one working copy, which can compensate for the other not working.  If you take two parents that each have a bad copy because they inherited from a common ancestor, there is a high likelihood that their children will receive two bad copies, and thus the previously hidden defect will be expressed.

I'm looking for a more fundamental explanation about the property of DNA, or the process of copying/merging these complex structures.

The fundamental part is just that you have two complete copies of your genome, one from each parent.  If you didn't, inbreeding would be much less of a problem.


text:
What was the evolutionary benefit of enclosing hemoglobin in cells?
The ancestral solution to oxygen transport is with hemoglobin (or, similar proteins) dissolved in blood (or, "hemolymph", but, basically, dissolved in water. ) What was the advantage of enclosing the oxygen-transport proteins in cells?

Hello, looks like this is your first question. Please notice that although I got your point and I think your question is good, you should do your own researches before posting here: this will not only improve the general quality of this SE, but will also make other expert users eager to answer, while short questions without references usually get no answer.Welcome to Biology SE by the way :)

Does this answer your question? Why isn’t Haemoglobin a plasma protein, rather than being encompassed by the erythrocyte?

@David what do you think yourself?

My angle is that, if you know, with certainty, the answer, then I'd like to hear it. If you just scan for something that "might" answer the question, you are no better than a search engine. If you know for a fact that a url you shared does answer it, then, good. In your opinion, does that url answer the question? Tumbisapichu suggested concentration as main factor. Sounds plausible. I've thought myself that oxidative stress might be it, ROS is in proportion to oxygen pressure, and I'd assume it is highest inside the oxygen transport cells, that also lack mitochondria (the main source for ROS)

The “does this answer your question” is the new and misleading auto-generated text when you flag a question as a duplicate. The point is not whether it answers your question, but that duplicate or similar questions are closed. I have no particular interest in the topic I just remember it coming up previously.

Well you flagged it as duplicate, so, you claim that it does answer the question. That the comment is auto-generated does not change that. Does it answer the question, in your opinion? What was the evolutionary advantage of enclosing hemoglobin in cells?

If you enclose the globin in a cell you can achieve a high concentration of the globin, which makes for a faster, readily usable pool available, and it is not subject to degradation (via proteases, or other mechanisms) as if it was just dissolved. In addition, all other functions of the globins (pH regulation, CO2 metabolism, etc) will be more tightly controlled if the globin is on the same site (i.e., inside a cell), instead of being mixed in a milieu. All of that has probably more to do with the evolution of the entire circulatory system, as a whole, and only sequentially as the 'enclosure' of globins in specialized cells. You can find some more details here.

If a higher concentration is the main benefit, is the primarily factor viscosity, that enclosed cells can have higher concentration without decreasing viscosity of the blood?

That's also a good point, but more than viscosity I'd say that a factor would me osmolarity. Dissolved proteins in a circulatory system make for higher osmotic pressure, which would need to be compensated.

Good point. My own analysis is that the cells then prevent endosmosis by tension in the cytoskeleton matrix. (I'd guess a way to compensate for the osmolarity is necessary, otherwise the cell would be in the same situation as a hyperosmotic blood. )

What is the scale of concentration increase, roughly? 10-fold? (albumin is 1/10th globin in red blood cells, guessed from that if osmolarity is main factor)

This might be informative: https://en.wikipedia.org/wiki/Mean_corpuscular_hemoglobin_concentration

have seen that, easily attainable. and albumin concentration is roughly 1/10th of MCHC

the hemocyanin concentration (or whatever pre-blood cell animals tend to use) is what it harder to find. if osmolarity was the main factor, I was guessing albumin could be a good estimate, that it is 1/10th of the MCHC. since roughly 50% of blood volume is red blood cells, concentration increase as advantage driving evolution of blood cells would be half of that, 5x. just guessing. do you know the scale of concentration increase?

Hmm, no I don't know.

here it looks like it is 9 g/L, 1/4th of that of erythrocytes. https://www.sciencedirect.com/science/article/abs/pii/0014489472901117. with 50% red blood cells in blood, that means concentration is only doubled.

my intuition was that blood cells protect against oxidative stress, primarily, by moving oxygen into the cell. they also die pretty quickly... that as endothermy evolved etc, and metabolic rates and oxygen consumption increased, it was necessary.

Also, hiding the Iron from invading bacteria is good. Free iron is a limiting factor for bacterial growth.


text:
What is the probablity that SARS-CoV-2 will mutate?
In many epidemic/pandemic situations, a lot of time the pathogen in question will mutate. For reference, this is the definition of mutation taken from Wiki:-

A mutation is an alteration in the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA. Mutations result from errors during DNA replication, mitosis, and meiosis or other types of damage to DNA (such as pyrimidine dimers that may be caused by exposure to radiation or carcinogens), which then may undergo error-prone repair (especially microhomology-mediated end joining) or cause an error during other forms of repair or else may cause an error during replication

So my question is,
1》What is the probablity of SARS-CoV-2 mutating?
2》 How can we predict, in advance the mutation of the virus? (Maybe by studying the environmental factors of a specific place)
3》Lastly (something that makes the biologist cringe) is there any way to prevent mutation? Any way at all to somehow limit the mutations which can be used widely?

BTW I am not a biologist, only a person among the millions out there, trying to find a way to help prevent the spread of the disease. My aim is to somehow use ML with Covid data to predict mutations (if possible...)

Please use the correct terminology: Covid is the disease caused by the virus, which is correctly named SARS-CoV-2. The disease itself cannot mutate.

@Chris Agreed. I thought the terminology was used so widely that I forgot that they weren't inter-replacable...

HIV is a virus. AIDS is the disease caused by HIV. No one says AIDS mutates. Not to be a jerk about it, but the terminology you choose is important.

https://biology.stackexchange.com/a/92213/5075

Although @Chris has sorted out the misconceptions you have as a non-biologist, I would point you to authoritative sources of information about the virus and epidemic that are listed on Meta, in case you did not see the banner. We would all like to do our bit in the current circumstances, but you should realize that there are thousands of elite experienced professional scientists of all types working in this area. You might wish to find out what they are doing.

I don't see how you want to prevent mutations - and these don't have to be a bad thing as the mutation of SARS (the original one from 2003) shows, here the mutation (or better the deletion of a part of the viral genome) led to an antenuated pathogenic virus. Since this mutation happened in the early phase of the spreading, it became the major virus. See reference 1.
Mutations are a statistical process which happens all the time, especially for RNA viruse due to errors in the polymerases (see reference 2). So the answer to your first question would be: 100%. It is mutating, which can also be seen in the sequences which have been published so far. The differences are only minimal with a sequence homology between 99.91 and 100% (see reference 3), but this can already lead to changes in the amino acid sequence. You can see this in the screenshot from phylogenetic tree of all sequenced SARS-CoV-2 viruses on [Nextstrain] (see the site for the actual development):

To your question 2: You cannot really predict where mutations happen and which will come through in the long time, as this is a statistical process and the sheer number of viruses around in each infected patient. But there are positions which are more prone to mutations, while mutations at other parts of the sequence will lead to much less fit virus. There is not so much data available yet (remember that this virus is only around since the end of last year), but reference 3 has some data on it (figure 3):

Question 3: I don't see how this should happen, as this involves the polymerases which are involved in replication.
References:

Attenuation of replication by a 29 nucleotide deletion in
SARS-coronavirus acquired during the early stages of human-to-human
transmission
Why are RNA virus mutation rates so damn high?
The establishment of reference sequence for SARS‐CoV‐2 and variation
analysis
On the origin and continuing evolution of SARS-CoV-2

@reuns Good idea, I missed that site. Thanks for the notification.


text:
Help me understand voltage patch clamping
Before I type my question it is important to know that I already tried looking this up on my own and could not find an answer because the answers are all in complicated physics terms and this topic is only half a page in a chapter on Action potential in my 1st year physiology textbook.
My textbook says:

This apparatus is used in the following way: The investigator decides
which voltage to establish inside the nerve fiber. The electronic
portion of the apparatus is then adjusted to the desired voltage,
automatically injecting either positive or negative electricity
through the current electrode at whatever rate is required to hold the
voltage, as measured by the voltage electrode, at the level set by the
operator. When the membrane potential is suddenly increased by this
voltage clamp from −90 millivolts to zero, the voltage-gated sodium
and potassium channels open and sodium and potassium ions begin to
pour through the channels.

1: Does that mean that the change in membrane potential that I did resulted in changes in the conformational states of ion channels which in turn changed the membrane potential that I need to control ?

To counterbalance the effect of these ion movements on the desired
setting of the intracellular voltage, electrical current is injected
automatically through the current electrode of the voltage clamp to
maintain the intracellular voltage at the required steady zero level.

2:Is this all still the step of setting the membrane potential to a certain specific value ?

To achieve this level, the current injected must be equal to but of
opposite polarity to the net current flow through the membrane
channels.

3: I'm not sure I understand this.

Finally, the investigator adjusts the concentrations of the ions to
other than normal levels both inside and outside the nerve fiber and
repeats the study.   When sodium is the only permeant ion in the
solutions inside and outside the squid axon, the voltage clamp
measures current flow only through the sodium channels. When potassium
is the only permeant ion, current flow only through the potassium
channels is measured.

4: do they make sure that the flow is only from sodium channels by setting the membrane potential to the equilibrium potential of other ions or a potential between the equilibrium potential of the other ions (so greater than it) and the equilibrium potential of Na (and also less than it )?

I'll try to answer the sub questions 1-by-1

Does that mean that the change in membrane potential that I did resulted in changes in the conformational states of ion channels which in turn changed the membrane potential that I need to control ?

It's the other way around; your book is right - "When the membrane potential is suddenly increased by this voltage clamp from −90 millivolts to zero, the voltage-gated sodium and potassium channels open and sodium and potassium ions begin to pour through the channels". So the voltage step (depolarization) induced by the apparatus triggers voltage-operated channels to undergo conformational changes, this in turn results in additional current flowing through them. On the other hand, hyperpolarization of the potential from say -40 to -90 causes the neuron to close these channels, blocking current to flow. In other words; the patch clamp apparatus controls the membrane potential, the state of the ion channels has little to do with that, as the apparatus will automatically adjust the current injection.

Is this all still the step of setting the membrane potential to a certain specific value?

Yes.

"To achieve this level, the current injected must be equal to but of opposite polarity to the net current flow through the membrane channels."
I'm not sure I understand this.

To set a certain stable potential across the membrane, the flow of current needs to be stable, otherwise it will fluctuate; Ohm's law tells us U = IxR. The resistance R is set by the channels. Let's consider that R is stable for the moment. In that case, you will set the membrane potential U by tightly controlling the current I. If I fluctuates, i.e., when the apparatus doesn't balance the flow of current through the membrane channels exactly and oppositely, a net current will start flowing and u will change. You don't want that to happen.

do they make sure that the flow is only from sodium channels by setting the membrane potential to the equilibrium potential of other ions or a potential between the equilibrium potential of the other ions (so greater than it) and the equilibrium potential of Na (and also less than it )?

This part has nothing to do with equilibrium potentials. They substitute negative ions simply by ions that are not membrane permeable, and the only positive ion available in the test tube is Na+. In that case, only Na+ can flow and you are sure that it is Na+ that is flowing. At least, this is what I make up of this text.


text:
Lifetime of clothes moths
Cross-posting, as I'm not at all sure which StackExchange this belongs in. Very happy to move / delete where I've chosen poorly, and a better SE can be recommended.

Question:
Can anyone advise on how long clothes moths eggs can last unhatched, and how long the larvae would then be able to survive without any natural fibre food.

I'm currently trying to deal with a clothes moth infestation, and your site has been invaluable.
Are you able to advise how long the larvae can survive without any available food?
We've removed the carpet and soft-furnishings from a room, and thoroughly hoovered, but there are nooks and crannys (especially around the skirting boards), which I suspect still have eggs in. I've thoroughly removed any fibres left from the carpet, so my plan is to leave the room for 10 days to ensure any remaining live eggs have hatched into larvae (which then have nothing to eat, and then ... X? ... days to ensure that those larvae have all died.
Are you able to advise what X should be?
We're under the impression that the larvae can ONLY eat natural fibres, so they can't eat, e.g. artificial foam underlay or cardboard boxes & books. Even if those are the only things around them, they can't consume those and will thus starve.

If you are dealing with a real clothes moth, your natural plant fibers should be safe, they can digest only keratin, which translates to hair and feathers.


text:
What is the disadvantage of circular DNA?
I have searched online and there is little information about the disadvantage of a circular DNA. Since I know that with chromosome arrangement like human, we have telomere that held the DNA strands together, which loosens as the organism ages and the cell divides. With circular DNA there is no need for telomere and the number of times for the cell to divide is greatly increased. Then comes my question, does circular DNA has major disadvantages? And if a multicellular organism has circular DNA arrangement, does it have a longer lifetime?

This question is similar to a previous one — What is the advantage of circular DNA in bacteria? — so I suggest that you refer to that.

@David, that question asks about advantages, not disadvantages, and the answers there address that question, not this one.

@mgkrebbs — Oh, come on. It’s all a single question about the relative occurrence of the two types of chromosome. Whether it has been answered properly is not the point. The question is poorly expressed and there is no reason to regard its wording as sacrosanct.

@David, they are obviously related, but the concern of the questioner is different in the two cases, and the direction of the answers should specifically address the particular concern, as the two sets of answers do.  I would also suggest that the concern expressed in your comment below, "the interesting question is why eukaryotes have linear chromosomes", deserves its own separate SE.Biology question.

@mgkrebbs — I do not flag a lot of duplicates, but the policy seems to support my attitude. The question was poor and the poster accepted an answer that was not very informative (imho), so it doesn’t matter too much whether it is closed or sinks into oblivion on its own.

Does this answer your question? Is there an advantage to linear chromosomes?

Per se, there is no disadvantage of one type of DNA over the other. They evolved for different reasons, and the fact that both are still present indicates that they fulfill their role(s) satisfactorily. There is no competition between the two types of DNA. Even multicellular organisms (eukaryotes) have circular DNA within their mitochondria, and both genomes cooperate for a proper functioning cell (and there's even gene transfer from the mitochondria to the nuclear DNA, and there is also translocation of mitochondria). Most multicellular organisms have chromosomes instead of circular DNA, although there are some multicellular bacteria with circular DNA, so these would not 'suffer' from the shortening of the chromosome ends, but take into account that aging is due to many factors (oxidation, protein degradation, membrane degradation, etc), so it is not the sole responsability of telomeres to extend the lifespan of an organism.

I see. Thanks for the excellent answer.

The interesting question is why eukaryotes have linear chromosomes.


text:
Why is the ratio between action potential and threshold value called the 'safety factor'?
"AllorNothing Principle. Once an action potential has been elicited at any point on the membrane of a normal fiber, the depolarization process travels over the entire membrane if conditions are right, but it does not travel at all if conditions are not right. This principle is called the all-or-nothing principle, and it applies to all normal excit- able tissues.
Occasionally, the action potential reaches a point on the membrane at which it does not generate sufficient voltage to stimulate the next area of the mem- brane. When this situation occurs, the spread of depolar- ization stops. Therefore, for continued propagation of an impulse to occur, the ratio of action potential to threshold for excitation must at all times be greater than 1. This “greater than 1” requirement is called the safety factor for propagation."
This might be a more basic, straightforward question but for some reason, there's not much info on it on the web.
I'm guessing its called the 'safety factor' because it means that not any stimulus can cause an action potential and that the cells remain at equilibrium/their un disturbed state for most of the time, but this is only a guess.
Source of Info: Guyton & Hall Medical Physiology textbook

Can you please quote from your book? I think you may be missing some context.

Action potentials propagate by depolarization of one section of the membrane causing depolarization of an adjacent section.
It is necessary that this depolarization be greater than threshold. If the amplitude of the action potential were to drop below threshold, it would fail to propagate. Additionally, it would be quite slow and inefficient.
Therefore, the action potential amplitude is far greater than the threshold. This helps speed and builds in a "safety factor" to ensure the action potential propagates - that's what your book is saying.

Got it, thank you so much but may I ask one last question ? What determines  the maximum potential (the peak) reached in action potential ? I read in some student's notes that the the membrane potential never goes above 0 for small nerve fibres. To specify, he wrote : "Overshooting (meaning that the Inside potential becomes larger than zero)  happens in large nerve fibers but not in smaller fibers and many central nervous system neurons. " Does that mean that the larger the nerve fibre the higher the peak ? I'm also uncertain whether he means nerves of the CNS overshoot or not

@LiaAhmed That should probably be a separate question

Could you please explain why they use the number one? What  is the ratio exactly?


text:
Is the human iris concave or convex?
Most drawing and 3D modeling tutorials show the iris to be concave. But all the diagrams I Googled show the iris is at best flat, otherwise even a little convex (discounting the optical distortion in photographs). So is it concave or convex?
Edit: Just to be clear, the question only concerns the concavity of the iris. The reason I mention drawing and 3D modeling here is that because it's such a common practice to make the iris explicitly concave in a somewhat exaggerated way, which is at odds with countless profile diagrams of the eye that I could google.
For example, this video (at about 5:52) even says that "it is convex according to anatomical diagrams, but I like to draw it as if it is concave". Or in this video (at about 7:46), the modeler pushed the concavity of the iris quite far, it's like a deep indent.

I'm not sure I understand the question. When I searched for diagrams of the iris, I usually saw cuts of the eye in the medial plane. The few ones which showed a frontal view of the eye showed the iris as a regular circle. You presumably draw eyes from a frontal viewpoint, which also tends to show a circular iris. So where is the discrepancy? Can you post an image from a tutorial with a concave iris and a diagram with a convex iris?

I didn't really say anything about at which angle I'd draw the iris, because it's not very relevant. I said "most drawing and 3d modeling tutorial show the iris to be concave", meaning that regardless of the view angle or the viewpoint, you'll always have to take into account that it is concave. Thus, when you draw, even in front view, remember to to shade as if it is concave; when you model an eyeball, don't forget to make it concave.

An iris is three-dimensional. A drawing is two-dimensional, so it represents a cut through the three-dimensional object. For many three-dimensional objects, some cuts are concave and others are convex within the plane of the cut. So it makes the question clearer to explain in which plane you are looking for convexity or concavity.

@rumtscho By "concave" and "convex" I simply mean the general tendency, nothing too deep into the weeds of whether some cuts of it could be concave and others are convex. All I care about is whether the iris tends to poke forward toward the cornea ("convex") or recede backward away from it ("concave"), and all that seems to have been easily understood by the answerer below. We could argue all day about how 3D objects manifest in space, but I think the general idea of the question is clear enough.

Thank you! I came up with several different definitions of "convex" and "concave" that would be consistent with your question, and didn't know which is the right one. Funnily enough, it turns out none was the one you had in mind - the explanation of poke forward to the cornea/recede backward is exactly what I was missing.

Iris curvature seems to be dependent on the state and health of the eyes.
See Prevention of blinking alters iris configuration in pigment dispersion syndrome and in normal eyes :

Initial iris configuration was concave in all eyes with pigment dispersion syndrome, whereas in control eyes it was concave in four eyes, planar in four eyes, and convex in two eyes.

Other resources :
Accommodation-induced changes in iris curvature
Ultrasound biomicroscopic analysis of iris profile changes with accommodation in pigmentary glaucoma and relationship to age
Quantification of Iris Concavity

Nice answer! +1

It seems they can be all three of them. Convex, concave or flat.
Was wondering the same thing and ran some searches on google to come across this:

I find it more convincing to have it concave in my artistic preference.
Ref.>
https://www.aao.org/disease-review/gonioscopic-grading-systems

Welcome to Biology.SE. Please take the [tour] and consult the [help] pages for advice on [answer] and [ask] effectively on this site. In particular, please do not post text as images. Copy and paste the text into your question. Images are not searchable, and can not be interpreted by screen readers for those with visual impairments. Use the [edit] link to modify your question. See this for more information. In addition, this seems to duplicate an already existing and better answer — your time could be better used on unanswered questions.


text:
Im struggling to see how these are presynaptic terminals/knobs and not post synaptic

How are these presynaptic terminals ? The action potential is generated at the axon hillock and moves down the axon (in this case to the right) , then at the end of the axon should be axon terminals and presynaptic knobs. Shouldn't the dendrites shown here have post synaptic knobs with receptors for the neurotransmitters ?

The fibers in green are axons and axon terminals from other neurons, not the one colored orange.
Yes, there would be post-synaptic structures associated with these but those are not drawn in this cartoon.

The green ones you see are the synaptic knobs or presynaptic terminals of other neurons of which some lie on the surface of dendrite of the given neuron(Axodendritic) and some on the soma of the neuron(Axosomatic). Also please note that the synaptic knobs(green) on soma is not peircing it rather imagine it in 3d, where the synaptic knobs are coming from top, outside your book to the neuron making a synapse.


text:
What do we know about "continence" in animals?
What do we know about continence in animals? In particular, what do we know about the development of continence in animals?
By "continence", I'm referring specifically to whether or not a wild animal, free from human influences, appears to exhibit discrimination in when and where it relieves itself, and to what extent. For example, rats are allegedly incontinent, at least by this definition. (The article would seem to imply they are physically unable to control themselves, but other sources state that rodents can learn continence, which would imply that they normally just don't bother, which is what I want to know about.) Conversely, cats can be quite fastidious, and kittens are reportedly "unable" to void themselves without their mother's assistance. In fiction, we have an example of a species which is said to uncontrollably void when they eat.
Based on what we know from studying real animals, is it plausible that an animal would be unable to control its voiding out of a habit of not trying to do so (I'm ignoring physical problems, here), or is the cited source, if you'll excuse the highly apropos expression, full of sh--? If it is plausible, what types of animals, generally speaking, would exhibit this, and to what extent? Also, how does this change from birth to maturity?
Ultimately, what I am looking for is a set of guidelines that would allow me to predict an animal's voiding habits and the extent to which the animal is able to control the same given the animal's age/maturity and other general information (e.g. dietary tendencies). I am not worried about outliers, unless the answer is that it is not possible to make a prediction with any reasonably accuracy, in which case I would still like to know what range of variation I might expect.

Edit: I'm increasingly suspect of the cited source on rats. If that's bunk, I would still like to know; are there any examples of animals (perhaps excluding humans, because that can turn into quite the argument) who, at any life stage, do not exhibit continence and/or exhibit feline-like "hyper-continence" (i.e. inability, or at least instinctive disinclination, to void on their own) absent physiological abnormalities? (Alternatively, am I also wrong about cats?)

Please don't disrespect what folks on another SE forum have offered to you in the way of criticism, whether you "buy" it or not.

@elemtilas, to be fair, you're saying that the question, even as I have posed it here, cannot be answered because no one knows? No one has done any studies in this area? Because I really do find that hard to believe. (Conversely, I'd readily believe that the WB question has failed to attract anyone with the requisite knowledge, which is what I'm hoping to rectify by asking here instead.) FWIW, I attempted to reword that statement.

The (limited) answers there are somewhat light on details (especially with respect to how things change during maturation) and examples. To wit, so far the examples cited in the question (baby cat, adult rat) are the only "hard" facts I have. Surely someone must know more? Most of what I've gotten is instead "this is a bad question, we can't answer". BTW, feel free to suggest edits. I've tried very hard to be clear about what I'm asking.

You likely can't have it both ways: you want a general answer but you also want it to be specific enough to cover multiple life stages? It does seem like you've gotten good worldbuilding-style answers over there. Have you also tried simple searches such as: https://scholar.google.com/scholar?hl=en&q=rat+continence to better inform your question?

(elemtilas) Eh, fair enough. Done. (Bryan) Well, what I'm looking for may not be a short answer. My guess would be something like "rats are the only species that are actually incontinent, and den-residing animals need a parent's help until they're old enough to move around"... but I don't know if that's accurate? (I suspect "only rats" isn't; I'm using that as an example of where I could use help!) Also, most of my attempts to do research (including your suggestion) keep running into incontinence due to physiological problems, which is not what I'm after.

@Matthew The search I linked is full of discussion of continence (rather than incontinence) in rats; it seems a bit unusual, then, to consider them incontinent. I think probably the reference you used to refer to rats as incontinent is not meaning what you think it is, I think they're just referring to pest rodents not utilizing human toilet facilities.

@BryanKrause, the page explicitly claims that "[rats and mice] have no control over their bladders". If your claim, however, is that that's bunk, well, I'm increasingly inclined to believe you. So, are there any (non-human) examples of animals which are incontinent (absent physiological abnormalities) at any life stage?


text:
Is there any case in which excitability increases with lowering the RMP?
My professor says , at a more negative RMP, less sodium ion channels are inactivated, so if you take 2 of the exact same neuron with the same threshold potentials, and try to excite them starting from different membrane potentials, the one you try to excite from a more negative membrane potential excites faster and fires an action potential faster because more sodium ion channels are activated .
I might have missed something from what he said, and I hope I did because this makes no sense to me.
Shouldn't excitability increase with an increasing positive resting membrane potential ? The closer I am to the threshold potential the weaker the stimulus that I need to fire an action potential, isn't that right ?
The only article I found on this is https://www.sciencedirect.com/topics/neuroscience/excitability and its specific to cardiac muscle so perhaps the excitability in cardiac muscle  is an exception ?

A typical voltage-gated sodium channel has 3 gating states: open, closed, and inactivated. The third category is the important one here.
Open channels are open: they let ions through.
Closed channels are closed: they don't let ions through, however, they are available to open and their probability of opening increases as the membrane voltage rises from negative towards positive.
Inactivated channels don't pass ions, but it also cannot be opened by depolarized voltage. Instead, it needs a negative membrane voltage to pass back to the Closed state.
When a sodium channel opens, it only stays that way briefly before going to an inactivated state. Recovery from inactivated back to "closed but openable" requires the
If you depolarize a cell gradually, this will open sodium channels, but it will also increase the number of channels stuck in this "inactivated" state. That means there are fewer channels available to flip from closed to open.
When a cell is hyperpolarized, there are fewer channels stuck in the inactivated state, and so the threshold potential can actually become more negative: it takes a smaller voltage step to open enough channels to trigger an action potential, because there are more channels available to open. You can describe this situation as being "more excitable" despite the hyperpolarized potential.
Some cells, including cardiac cells and other types of pacemaker neurons, will actually depolarize spontaneously from this hyperpolarized potential and reach threshold all on their own without external input.

Oh, I understand but, when does 'a more positive RMP makes the neuron easier to excite' argument apply ?

@LiaAhmed When it is transient. It takes awhile for the population of voltage gated channels to equilibrate; brief depolarization gets you closer to threshold without substantial inactivation. Note that different neurons have different populations of voltage gated sodium channels so they may show different properties.


text:
Is it impossible for some female songbirds to sing?
I have read that in northern hemispheres, most female songbirds can't sing (for example, the Blackbird). Things are different in tropical regions. Birdsong is for males in some species; it is utilized to defend territories and/or attract other females.
While it seems impossible that female songbirds can't perform complex songs, can it be possible for captive birds?
I have read some reports that females are able to sing after being injected with testosterone. But the interesting question is whether females can be trained to sing without testosterone injections or other interventions?
There is an article showing that for one songbird species it is possible to produce female birdsong without testosterone injection (while older research claimed, females sang only when treated with this hormone): https://www.newscientist.com/article/2151727-female-birds-that-used-to-be-silent-are-now-singing-like-males/
There are dissertations about birdsong and sexual hormones: https://research.vu.nl/ws/portalfiles/portal/42186406/complete+dissertation.pdf
And here it is reported that female songbirds sang after getting testosterone: https://journals.sagepub.com/doi/abs/10.3181/00379727-41-10631?journalCode=ebma

It's usually helpful for people trying to answer the question if you include some links to the places where you have found these ideas. Thanks.

Here is an example link: https://www.newscientist.com/article/2151727-female-birds-that-used-to-be-silent-are-now-singing-like-males/

Great, could you edit your question and link it in the relevant part?


text:
I just had my genome sequenced. Can someone tell me what these different file formats are?
I just had my whole genome sequenced and now I want to play a bit with bio-informatics. However, the documentation is quite scarce on the file standards used.
These are the files I have been given (the "raw" data):

Can someone explain me with some detail what is each file format, and for what are they used?
Transcribed list of file-formats from the picture:

Indel (TBI)
Indel (VCF)
SNP (VCF)
SNP (TBI)
CNV (TBI)
CNV (VCF)
BAM (BAI)
BAM
FASTQ R2
FASTQ R1

I'm voting to close this question as off-topic because isn't a biology question as defined for this site. Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site for details. It might fit within [Bioinformatics.SE], but please check their help pages before posting there. Thanks!

"I just sequenced my whole genome": Out of curiosity, how did you do that?

@tyersome sorry, please forgive me. I actually looked for a bioinformatics stack but google brought me here :X

@bli I am living with this condition for almost 20 years, and it had no progress, so I though: It probably isn't "cancer/leukemia/MPN" (i.e. a malign for of PV). So it was important to get the raw data to compare my genes with the most recent literature discoveries (standard sequencing tests do not cover most genes that justify this). Now I have the raw data and I already used apps on sequencing.com to browse and search these genes (DanteLabs also has a Gene Browser, but I like to compare). So, what I have found today: (next comment)

@bli the test used saliva, and there's a debate if saliva is fully germline or not, but either way, given that my JAK2 is neg, and I live with this "PV" for at least 20 years (I have 30) I doubt I have any somatic mutatiion, so it must be congenit... If it were true PV I would maybe be dead by now. So without further ado, I found that: (i) I have a very high chance to develop Hereditary Hemochromatosis (HFE, ELAC2), (ii) then I search for all the genes I could for PV, and I found Familial Erythrocytosis mutations, several SNP mutations in two big genes (EPAS1, EGLN1), and (iii) ...

@bli ...and (iii) I was suspecting that I also have very high ocygen affinity (gonna test my p50 soon) so I looked for the (apparently ONLY?) documented gene that can cause erythrocytosis with high affinity, these gene is a2-globin gene, and I have a very very clear mutation like this: chr16 173,183 G>A. The paper I learned this from: doi: 10.1111/j.1365-2796.2008.02014.x (Blood p50 evaluation enhances diagnostic definition of
isolated erythrocytosis)

@bli regards the Hereditary Hemochromatosis, I probably still not have it as my iron levels are normal... But again, I have this form of PV, so they might cancel each other... lol

@bli probably I am going to organize this data and publish it online freely available to the world (DNA, diagnostics, etc).

"Polycythemia vera (PV) is a chronic myeloproliferative neoplasm. Virtually all PV patients are iron deficient at presentation and/or during the course of their disease." || So lol, what were the odds? I have no iron deficiency, so maybe my Hematochroma is already here and PV cancels it out, because my iron levels always measured normal in the past (as well as my EPO levels btw - not secondary PV)

Related: What is the difference between FASTA, FASTQ, and SAM file formats?.

@PedroD Out of curiosity too, concretely, how do you "sequence your genome" from saliva? Do you do it yourself, using a machine available at your research lab? Or do you send your saliva to a lab (what kind of lab?), what kind of price is it to have your full genome sent as computer files?

"I just sequenced my whole genome" : this is so cool, sounds like Sci-Fi :)

No lol, I did it in DanteLabs (they arefrom Italy), and besides the classic reports, they also give you all the raw data in the formats above.

The machine they used was Illumina nextseq 6000, I paid ~250€, it takes about 2 months

@PedroD Then perhaps the title should read "I had my genome sequenced..."

@CarstenS Better now?

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

Your genome has a sequence that is unique to you, gifted to you by your parents and by small changes from random chance.
Your genome is pretty close to what is called the reference genome, which gets updated — infrequently1 — as sequencing platforms, pipelines, and algorithms change.
The reference genome is the "standard bearer". All other individual genomes are compared against it. This lets everyone compare apples to apples when trying to say something about the genome, in the aggregate or "big picture" view.
The files associated with the VCF format specify places in your genome that differ from the reference genome — and how they differ. These differences include:

Indels — insertions or deletions of DNA, as compared with the reference.
SNPs — single bases that differ from the reference.
CNVs — repeated stretches of DNA that differ from repeats in the reference.

The specifics of each of these classes of variants can be associated with various diseases or other attributes that make you unique and interesting. More on that later.
Each of these VCF files in your dataset has an associated TBI file. This is an index file, which helps you to quickly retrieve elements of interest from these datasets using a command-line tool called tabix.
If you are looking for differences within a specific genomic interval — say, all the differences on chromosome 4, from bases 123456 to 567890 — then you can pass that interval to tabix along with your VCF file of interest, and it will return all the indels, SNPs, or CNVs within that range, if there are any within that interval. This subset is VCF-formatted, so by knowing the format, you can get more detail about those differences.
The BAM-formatted file collects all the individual sequencing reads in a form that is mapped or aligned to the reference genome, along with some summary information to tell you how those reads differ from the reference genome.
As with the VCF files, this BAM file has a BAI index file to go along with it. Like tabix, you can use the samtools command-line tool to extract the set of reads over your genomic region of interest, if you want to examine them further.
Both tabix and samtools are available from the same author. If you have questions about these tools, the Bioinformatics Stack Exchange site is a great place to ask questions3. Lots of bioinformaticists  there have a great deal of experience with those toolkits and can help answer more specific questions.
The two FASTQ files are the raw sequence data coming off the sequencer, along with quality data. The sequence reads in these two files are paired for higher quality and longer reads, which makes the sequencing platform faster, cheaper, and better.
I walked a bit backwards, here, on purpose.
The raw FASTQ files are starting material for making the BAM file. The BAM file is then, in turn, used with variant calling software (example) to generate the variation (VCF) datasets.
Why walk backwards through these datasets?
Most people don't care about the raw FASTQ data, except perhaps to do manual alignment or check data quality. What is often more interesting or useful to most is how one's genome differs from the reference, which is captured in the variation data.
Those differences, in aggregate, are how companies like 23andme sell a product2 that tells you that you are more related to so-and-so population than so-and-so population, or whether you are more or less likely to have some disease or other odd, interesting phenotypic trait.
1. Even when new versions of this reference genome are released every few years or so, if you know what original reference genome was used to generate your BAM and VCF files, you can redo analyses based on that knowledge. There is likely some metadata associated with your sequencing results that you can look up to find this out, or you can ask the sequencing center from where you obtained these results.
2. For a bit more context, in this answer to another SE question, I talk a bit about SNPs and how they are used for testing association with so-called Mendelian disorders, diseases caused by single base changes, which may be of interest to you given what motivated you to get your genome sequenced, in the first place: https://biology.stackexchange.com/a/88839/5075
3. You can ask questions about them here, too, but you'll make certain people grumpy. Better to go to the other SE site for that.

OMG this is the most complete explanation I've read. Thank you! You should create a blog post with this, I could not find any that introduced all formats this way, actually the info is scattered around in an unorganized way. Thanks!

+1, but it seems to be missing an essential piece of information. If the reference genome is regularly updated, how does one know which version of the reference genome the data is relative to?

@JBentley you can't tell from the file formats (which this question is about). Sometimes the bam files can have indications, but the only way sure way is asking the person who generated the files.

@JBentley Reference genomes are not updated too frequently. But they do change every few years, and the selection of reference determines the outcome of BAM and VCF files, which are analysis products of the raw FASTQ reads. For humans, a couple common reference genome keywords are hg38 and, perhaps less so, hg19. Perhaps some metadata file not shown here in the question makes use of one of those labels, but as mentioned by @Nicolai, asking the sequencing center where the data come from should get an answer, as well.

Please have an upvote! I'm a bioinformatician too, and this is an excellent answer. Also, just the fact that someone is able to ask this question suddenly brought into focus how far sequencing has moved on since I started.


text:
Identify this gray spider with distinctive white mark
I was out back in the garden tonight and found an extremely long strand of web running about 10 ft. At the end was a kind of spider I’ve never seen before. It’s about a .75-1 inch, fat body, with a distinctive white mark on its back. It was very docile while I took the pic. I’m in Austin, TX and this was night time. Any clues?

An Orb Weaver - I dont know what sort. Giant lichen?


text:
Do plant cells recycle carbon dioxide from their respiration during photosynthesis?
It seems one of my colleague's biology textbook claims that plant cells, with presence of light, feed back 100% of carbon dioxide molecules from their respiration into photosynthesis. Can you say that carbon dioxide molecules, gas or dissolved, get transferred from the mitochondria to the chloroplast?

Please provide a source for your colleague's text book and quote verbatim what it says. That way we can help clarify questions that may arise from misunderstanding what the author intends.

Will do that tomorrow, but it's in Korean so it has to undergo translation. Thank you anyway.

@tyersome It does I think! Gaseous carbon dioxide must be no exception from random diffusion.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884119/
This paper found mitochondria move to be next to chloroplasts when exposed to light. So carbon dioxide is  more likely to be recycled in lighted conditions.

Wow, it's a whole new perspective!


text:
Difference between infectivity and cell fusion abillity of Virus. (COVID 19)
I'm a computational chemist who have interest in COVID-19.
As a physical chemist, I'm lack of basic knowledge for biology.
What is the difference between 'infectivity' and 'membrane fusion activity'?
I thought that, for corona virus, infection is equal to membrane(cell) fusion, but it seems wrong idea.
Thank you for reading!

From what I read there are the concepts: there is the receptor binding, then either the S protein does active membrane fusion and genome releasing near the cell surface, or the receptor+virus is engulfed as endosome and the fusion+releasing is achieved later, closer to the ER & Golgi (where the ribosomes and the target membranes are located). You may think to the cell as a labyrinth of membranes and the virus needs to reach the correct one to do the translation and anchor its transmembrane proteins to achieve the replication and assembly. So infectivity = releasing many virions.


text:
simple explanation of a crispr screen vs pooled crispr screen?
I'm familiar with how CRISPR works to make either knockdown or amplification effects for a single gene because you can make precision cuts.
What exactly does a pooled crispr screen do & how does it work?

In the context of pooled CRISPR screen, you first design a library of gRNAs against a certain set of targets (instead of just one target).
The library can have the size you want, most commonly it is either targeting the kinome, or the whole genome (genome-wide).
In this context, you would add the full library on your cell of interest in which you want to make the perturbations.
Depending on how the screen is set-up you try to select the perturbations which either allow you to pass a selection process (toxicity, fluorescent readout, etc). Usually an elegant way is to have either a label also code barcode which helps you to identify the gRNA which generated the surviving/selected phenotype. With the barcode/gRNA you can track back which gene was likely perturbed in the screening process.
Hope that helps and that answers you question, please don't hesitate to further refine it if this is not clear to you.

Hi, i am not a specialist in CRIPSR but should I understand from your answer that the cripsr method is robotic with a computer interface?

@totalMongot: no screen should be interpreted as a biological screen for example in the context of CRISPR, genetic screen: https://en.wikipedia.org/wiki/Genetic_screen

So if I understand well, this works this way: 1/ I analyze my cells to have the genetic screen 2/ I choose from the genetic screen which gene (gene X) I want to alter 3/ the genetic screen tells me for example that gene X is ATCA 4/ I send with crispr vector an enzyme to alter ATCA?


text:
Are specific primers or detectors, or both, used in COVID-19 tests?
I am trying to learn about the rRT-PCR testing procedure used to test for COVID-19, but I am slightly confused on one point. Are highly specific primers used with a non-specific detector, or are highly specific detectors used, or are both specific primers and detectors used? Some of the sources say that multiplex PCR is used, which indicates a specific detector, but as I am still a beginner on the subject, I am not sure. I would also really appreciate it if somebody could also point to a source that details the some of the testing procedures.
Thank you

It is often helpful to do a little background research using google before asking a question, or to link to specific sources that you need help with; e.g. It would help to know which sources you're looking at. Technical information on one testing procedure is available here (methods section): https://jamanetwork.com/journals/jama/fullarticle/2761044. The community has collected COVID-19 information here which may be helpful: https://biology.meta.stackexchange.com/questions/4035/information-about-coronaviruses-how-to-ask-and-external-resources?cb=1

When you run a PCR reaction, you are making copies of a DNA sequence of interest (cDNA in case of retrotranscription, since retrovirus have RNA as the genetic material). The sequence of interest is presumed to be in a sample, that you take from the patient, or some organism (I say 'presumed' because the PCR is precisely to confirm this). These copies are made by a group of 'generalist' enzymes, called polymerases, and by generalists I mean that they do not discriminate on which DNA sequence they are copying. But, they cannot copy DNA de novo (from scratch). The copying process needs to be 'primed' by a short sequence of nucleotides that is complementary to the DNA of interest. These are called primers, and they effectively serve as probes to target the copying of the specific sequence you need to amplify. And this is where scientists put a lot of care on: primer design. Bad primers will not be very specific, or will not be very efficient during the amplification process. As for the 'machine' that actually detects the copies, there are many variants. The most typically used in research and diagnostic laboratories, involves staining the amplified DNA with some molecule that binds nucleic acids (which there are many), and visualize it via DNA electrophoresis. What you visualize is a population of DNA copies (via the staining you make), so you need to know beforehand what to expect. For instance, do you expect a small fragment (a couple hundred basepairs) or a big one (a few thousands?). You have a 'ladder' (also called marker) that gives you a reference to compare, like in this image:

People know what to expect because they already know the DNA (or RNA) sequence they are amplifying (otherwise they could not have designed the target primers). They know the sequence because they've done some form of nucleic acid sequencing (labs, health institutes, and so, do this all the time and deposit the sequences in some platform, for instance GeneBank).
A 'positive' amplification will give you a band in the expected size range, and no other bands (because your primers are targeted for a particular DNA sequence). But as you mentioned, there exists also a multiplex PCR reaction. In it, you design multiple primers to target different sequences (using the same DNA sample -e.g. from a patient or organism-), but the verification process is basically the same. Here people are extra careful to avoid cross-interactions among the primers added to the reaction.
PCR is a family of techniques, not a single one. There are variations in the actual process, and also in the 'detection' (for instance, qPCR uses real time detection of copy numbers). But the general principle is the same: primers are specific, while the 'detection device' is not really.

Thanks for your answer. What I have seen is that gel electrophoresis is not used in covid testing. Instead, a dye is added which binds to the dna to be expressed, so you can monitor the fluorescence of the dye to determine the amount of dna present. These dyes can be made specific, like the TaqMan detector. Do you know if these specific dyes are used in addition to the specific primers you mentioned? Thanks

Dyes in general applications are not specific, that's why they are useful, otherwise you'd need to have one dye for each specific sample/sequence. Sometimes a dye is bound to a probe (like a primer), and thus made 'specific', but in reality is the probe which is specific, not the dye. And as I said, PCR and amplicon detection are a family of techniques, you'll find many variations and more sophisticated techniques appear all the time.


text:
I need to identify the genus of this colony just by its morphology, can somebody help me?

it was grown on TSA
it's a mesophilic bacteria.

(it was contaminated by E. coli, so ignore the clearer and smoother colonies).

Do you have any more information? Is this a school project? why only the genus? "mesophilic" --> what exact conditions did you grow it under?

@MaximilianPress yes it was supposed to be a lab work in my uni, but because of the virus I don't have more information about it and still have to write a report and the task is to identify the genus just by its characteristics. I only know that it was grown on TSA, under mesophilic conditions (~30 C) for a week. My guess is this is Bacillus genus since the biofilm is wrinkly, but I want to hear other opinions.

Perhaps you were to do a Gram stain as well; which was cancelled. I had thought Bacillus also.

@PolypipeWrangler yes, I'm sure gram staining was planned too. Thank you for your response!

Maybe present  an analysis based upon each of the possible results of a Gram stain also.


text:
A plant in my aquarium seems to be growing small plants under its leaves, what's going on?
In my aquarium I have this plant. I think it's a kind of swordplant. I've loosely attached it to a large piece of driftwood in the hope that it will grow itself on there, I saw that they had done the same in the petstore.
Now recently other plants have started to grow from under its leaves. I've tried to take a picture of it, these are the biggest ones but there are smaller ones on other leaves:
The plant seems to be doing pretty well, I added some iron and fertiliser to the water. The aquarium is positioned so that it catches a bit of direct sunlight late in the day and tons of indirect sunlight almost all day. It also houses shrimps and two apple snails.
My question: What are these small leaves? Is the plant procreating or does are these some kind of parasitical plants of another species?

From what I see ,it does look like some kind of Echinodorus ( Amazon sword). They do propagate by stems with new plants. They prefer to have roots in substrate.

Yeah I agree it looks like some sort of Amazon Sword, but I also know that grows stems with plants and that's not what I see here, so I'm still wondering what these are.

Java fern has new little plants that start from the leaves but  the photo does not show enough for identification. I have a bunch of java fern and it does not need substrate.

I looked up some more pictures of Java Fern propagating, that is for sure what this is, thanks! Crazy, I never knew this. Will try to get them to grow into mature plants:)


text:
Pedigree - Dealing With Unknown Parent Genotypes
I'm dealing with a pedigree problem, and I'm having some trouble dealing with problems of unknown parental genotypes (where there are multiple possibilities). This is not a homework question; it's an exam practice problem.

The question asks: Suppose brother and sister 6 and 7 are mated. What is the probability that their first pup will be albino?
The answer choices are 1/4, 1/8, 1/16, 1/32, or Not Enough Info.
Here's my attempt at the problem:
Since #2 is black, and some of its offsprings ended up sepia, #2 must carry the sepia gene (since the male mate is cream, and sepia is dominant over cream). So, we know that #2 is $Cc^k$.
Now, the male mate can be either $c^d c^d$, or $c^d c^a$.
This means that in order for the offspring of #6 and #7 to be albino, we need:
1) Male parent needs to carry the albino gene (i.e. male needs to be $c^d c^a$).
2) Male parent needs to pass on the albino gene to both #6 and #7.
3) #6 and #7 both need to pass on the albino gene.
I think the probability that the male is $c^d c^a$ is $\frac{1}{2}$, since the male parent can be either $c^d c^a$ or $c^d c^d$.
If we draw out a punnett square, the probability that the albino gene gets passed onto 1 individual is $\frac{1}{2}$ (since we already know the offsprings are sepia, we only need to consider the genotypes that contain $c^d$).
The probability that #6 and #7 pass on the albino gene is $\frac{1}{4}$.
This led me to think that the final probability is then P(male parent has albino gene) * P(#6 inherits albino gene) * P(#7 inherits albino gene) * P(#6 and #7 pass on the albino gene), which is $\frac{1}{2}$ * $\frac{1}{2}$ * $\frac{1}{2}$ * $\frac{1}{4}$, which gives us $\frac{1}{32}$, but I do not feel confident in my answer. Specifically, I do not know how to account for the fact that the male parent can be either $c^d c^d$ or $c^d c^a$.
Is my thought process correct? If not, where in my logic did I go wrong? Thank you for your help.

Based on the information given in the pedigree, you can actually be certain that #2's mate has a genotype of CdCa because of the following:
Two of 5's siblings are albinos. Since albino is a recessive trait (lowest in hierarchy of dominance), both parents (4 and 4's mate) must have the Ca allele. Let's call 4's mate "8". Since 8 has the Ca allele, at least one of 8's parents must also have the Ca allele. Since you have already (correctly) determined that #2 is CCk, #2's mate must have the Ca allele, and must therefore have a genotype of CdCa.
Thus you can eliminate the extra (1/2) from your calculation, making the answer (1/2) * (1/2) * (1/4), or (1/16).


text:
What factors affect the rate of siderophore production by microbes?
Microbes produce siderophores which are chelators and bind to iron. This is how microbes absorb iron from soil or rock. What causes microbes to increase or decrease the rate of production of siderophores?

Hi Zoe, welcome to Stack Exchange! Despite the biological context of your question, I wonder if this question might fit better on https://chemistry.stackexchange.com/

@Galen, as the question was about microbial mechanisms for siderophore regulation I think that the question is a good fit for Biology. This is likely a gene regulation question.

It might help if you gave a more specific example related to your interest in the question. The answer to your question is going to depend on what type of microbes your are interested in, their specific metabolism, and in what kinds of ecosystems they are found. For example, a gut pathogen might have very different modes of iron acquisition than a chemo-autotroph in a hot spring.

I think that you are interested in how bacteria regulate the expression of genes that produce siderophores. For a technical reference you can see this paper studying Vibrio, or this paper studying Pseudomonas. For a more general review see here.
Note that this is a diverse piece of metabolism and therefore there are likely to be a diversity of mechanisms by which siderophore production occurs, though superficially it appears that there are some general principles you can draw. I recommend looking at those papers and trying to understand the commonalities.


text:
Why are bats so resistant to getting disease from viruses?
I saw in the YouTube video COVID-19 that bats carry so many viruses, yet never or almost never get a disease by any of them. I'm looking for an evolutionary reason as well as a reason based on how their bodies work. However, when you're giving the reason based on how the bodies work, I want you to find some clever way to summarize the reason in a way that I can understand because I hardly know anything about biology.
Could the evolutionary reason be something like this? Bats live in large groups all the time and keep switching around their groupings. Viruses that infect bats evolved by natural selection to do everything they can to spread between bats and survive and not have every last bit of it fought off. Bats in turn evolved by natural selection to not let viruses take over their body more than just a tiny bit. So it was to the evolutionary advantage of both bats and viruses that infect them to form a compromise where the virus gets to invade their bodies to a very small extent but not too much.

Excellent review in the New Yorker, that discusses that very question, among other things.
https://www.newyorker.com/science/elements/from-bats-to-human-lungs-the-evolution-of-a-coronavirus
Here's what Carolyn Kormann writes:
"As the coronavirus family grows, different strains simultaneously co-infect individual bats, turning their little bodies into virus blenders, creating new strains of every sort, some more powerful than others. This process happens without making bats sick—a phenomenon that scientists have linked to bats’ singular ability, among mammals, to fly. The feat takes a severe toll, such that their immune systems have evolved a better way to repair cell damage and to fight off viruses without provoking further inflammation. But when these viruses leap into a new species—whether a pangolin or a civet or a human—the result can be severe, sometimes deadly, sickness."
Hope it helps…

I got the answer to my question in the article you linked. It said bats and viruses have been coevolving for a long time. I also got curious to find out how large flocks of bats can get so I YouTube searched "flock of bats" and got the YouTube video https://www.youtube.com/watch?v=PNPioS_roRE. They go into caves in such large numbers in an inclosed space easy for viruses to spread. Maybe the bats didn't evolve to strongly fight the viruses and instead the viruses evolved to not try to take over the body to such a huge extent in order to not be fought back so hard. It's kind of interesting to

think how they might have coevolved. They probably evolved a compromise where they're all like the common cold to bats. The different types of viruses are probably also in a mixed evolutionary stable strategy. Isn't it amazing that bats constantly live so close together in such large numbers in caves and carry so many viruses and are resistant to getting disease from any of them?

When the video was saying it was something to do with the fact that bats evolved to fly, I couldn't understand what it was saying. After I saw it again in https://www.npr.org/sections/goatsandsoda/2020/02/05/802938289/new-coronavirus-wont-be-the-last-outbreak-to-move-from-animal-to-human which was linked by https://www.npr.org/sections/goatsandsoda/2020/02/09/803543244/bats-carry-many-viruses-so-why-dont-they-get-sick, I quickly figured out what they were saying this time. Bats need to fly. They require a lot of energy to fly so the energy drain of viruses is less compared to the total amount

of energy they burn so they had weaker natural selection to fight off the viruses almost completely. Really they tolerate a larger amount of viral infection in their bodies but not that large an amount. The virus tries really hard not to be fought off completely and the bat evolved  to try really hard not to have the viruses invade to a really huge extent so they evolved a compromise where the viruses can invade to some extent but not too much.