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Skeletisation in space
A space pod containing an astronaut drifts out to space and cannot be rescued. The space pod contains no insects, and the only bacteria present are those originally brought in by the astronaut. There is plenty of oxygen (assume 20%) and the interior is heated in the long term to 20 degrees C by a radioisotope heater.
The astronaut eventually dies through lack of food or water. His body is found many years later. What will the rescuers find? A body or a skeleton?

What's the humidity of the air? In dry air you'd get a mummy, like in the desert or in some church crypts.

First I assume many years equals 10 years or more, although the presence of oxygen may drastically speed this up or it may interfere it is hard to say. Nobody was tried to figure out how something will rot in sealed but consciously oxygenated container since is basically does not exist without a custom built chamber.
Your main factor is humidity that is whether the pod has humidity control, if it keeps a human comfortable humidity you will have a skeletal mummy since skin and hair will survive but much of the body will desiccate. If you just treat it like a sealed container the body fluids breaking down will ramp up the humidity and you will just a have a pile of bones and rather disgusting soup. A sealed container is one way to rot down an animal carcass to get bones, it is called maceration and something that has been well studied. I have done it many times and a few years is more than enough to reduce a carcass down to a skeleton.  Note depending on how long you wait even the bone may be damaged or destroyed although the restricted biota may prevent the final stages of this leaving you with extremely fragile skeleton remains.
I must emphasis the smell will be disgusting, as in even seasoned investigators will be tossing their cookies if they smell it. Almost nothing can describe the disgust of the smell of a human body rotting in a sealed container. Our brains have evolved to find human rotting flesh as disgusting as possible.
for additional comparison  a a paper comparing decomposition of several pig carcasses sealed in concrete.
Source link addresses
https://pubmed.ncbi.nlm.nih.gov/2738563/
https://onlinelibrary.wiley.com/doi/10.1002/9781118953358.ch33
https://journals.lww.com/amjforensicmedicine/Abstract/2013/03000/Burial_of_Piglet_Carcasses_in_Cement__A_Study_of.13.aspx

What breaks the body down in a sealed container? Is this purely microbiological?

yes you are covered in microbes as is your gut and many are more than happy to breaks you down if given access to your juicy bits. You also have a lot of microbes trapped in your clothing (this can actually be worse for astronauts). cell for cell you have about as many microbes as normal human cells.  Mythbusters does a rather telling experiment using a pig carcass sealed in concrete and a sealed car which might interest you. .

Mythbusters [https://mythbusters.fandom.com/wiki/Stinky_Car_(Episode)] certainly demonstrated that fresh pig corpses placed in a car sealed with pressure-sensitive tape for two months decomposed - I could find nothing about bodies encased in concrete. However, Mythbusters found the carcases were covered in maggots, so it seems flies still managed to penetrate the car and lay eggs. They would find that harder to do in space. I really want to know whether bodies will decompose in the absence of insects through the action of microbes naturally contained on or within the astronaught's body.

listed as Buried in Concrete MiniMyth

Presumably this process must end some time when all the chemical energy has been used up and all organic compounds basically have been converted to carbondioxide. Any idea how long this might take? Years, decades, millennia?

@StephanMatthiesen hard to say with the continuous influx of oxygen, likely never there are a lot of materials that will not break down without mechanical breakup. That is how fossilization starts after all. I have held mammoth bones that came out of Wyoming topsoil that have not fossilized.

@john That's true, but I was rather thinking of the disgusting smelly soup which can't be there forever and will at some point not have any chemical energy left to sustain microbial life. In an open environment like your mammoth bones it will disperse in the soil and enter the general carbon cycle again, but in a sealed container the mass must remain there but become really dead at some point, no?

@StephanMatthiesen The smell is some of the byproducts of decomposition, the chemicals resulting from the decomposition of amino acids mostly. it does not last forever but that is very different then when all chemical energy has been expended. expect it to last for decades or more in highly concentrated quantities many hundreds of years for detectable levels. the issue is these byproducts do not break down quickly in a sealed container.

@John Thanks, so it slows down a lot before the final oxidation products are reached. Although I guess at that stage it depends very much on the actual space pod (how large it is, if the systems keep circulating and/or filtering air etc.) so it's hard to say.


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Time taken for species to become endemic
Is it known how long species take to become endemic? I know from examples such as Canada which have no endemics following the end of glaciation that the process must take at least 10 thousand years, but this merely demonstrates endemism must take a longer time. Has any technique been developed that provides some measure of the time needed for species to become endemic?
I am especially interested in the rate of endemism on a small and extremely isolated island such as St Helena.

From wikipedia: Endemism is the ecological state of a species being unique to a defined geographic location, such as an island, nation, country or other defined zone, or habitat type There is no time component to it. If a species is found only in Canada, then it is endemic to Canada. If it is found only in your garden, then it is endemic to your garden.

@Remi.b That can probably be an answer and is the best OP is likely to get.

From wiki: "There are two subcategories of endemism: paleoendemism and neoendemism. Paleoendemism refers to species that were formerly widespread but are now restricted to a smaller area. Neoendemism refers to species that have recently arisen, such as through divergence and reproductive isolation or through hybridization and polyploidy in plants." So the time of the former is the one of the extinction of all populations of a species but one, while for the latter is the speciation time. Which one are you referring to?

From wikipedia > endemism:

Endemism is the ecological state of a species being unique to a defined geographic location, such as an island, nation, country or other defined zone, or habitat type.

There is therefore no time component to it. If a species is found only in Canada, then it is endemic to Canada. If it is found only in your garden, then it is endemic to your garden. No matter the duration in which the species has been found in this specific location.
That being said, in conservation biology, it is common to oppose endemic species with invasive species. An invasive species
Wikipedia > invasive species

An invasive species is a species that is not native to a specific location (an introduced species), and that has a tendency to spread to a degree believed to cause damage to the environment, human economy or human health

As the linked wikipedia page explains the concept of invasive species (or if you prefer the concept of non-endemism) is open to a lot of critics and is in no way well defined. There is no time limit under which we would stop considering an invasive species as invasive. It is rather the ecological impact of this species that will people to call it invasive or endemic based on purely subjective notions.

Endemism is dependant on time and location. A long time period is required and this is what my question addresses. The role of location in endemism is self-evident.

You seem to disagree with the Wikipedia definition, then. Can you please give a trusted source that would back up your claim?

Are you sure you are not confounding the concept of endemism with another one such as the concept of being indigenous for example?

The Wikipedia statement that "endism is the ecological state of a species being unique to a defined geographic location, such as an island, nation, country or other defined zone, or habitat type" is a wordier version of my statement, which I believe to be self-evident, that Endemism is dependant on location. I also said it is dependant on time - this does not happen overnight. The question I am asking, which is not addressed by Wikipedia, is whether it is known how long a time endemism takes? I hope that makes my question easier to understand.

@user8654 I don't understand your comments but anyway. You might want to have a look at the edit in my answer. Your stance on the importance of time might come from invasive vs endemic discussions.

Could you add some non-wikipedia sources? I know this is your field, so I'm sure you have them. Wikipedia isn't reliable by it's own standards. We have access to an expert (you). I'd love to see references that represent where you learned these things. For a really basic concept, that might be an authoritative textbook.

@DeNovo Is it my field though? :) I'm a population geneticists / computational geneticist but am not an ecologist and definitely not a conservation biologist. To be fair, I have published a paper on the evolution of invasiveness in domesticated sunflowers but I have not be brought to consider the semantic difficulties behind the concept of invasive vs native species. I don't know of a reference that talk about this semantic difficlties, sorry.

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Why do lychee seeds come in different shapes?
I've been eating lychee fruits recently and noticed that every once in a while (in about 1 of 10 fruits or so) the seed in the fruit is shriveled, while in other fruits from the same batch the seeds have regular ellipsoid shape:

Top: regular seed, bottom: shriveled seed
The fruits with the shriveled seeds don't look or feel or taste any different from those with the regular seeds.
It seems like a binary trait, i.e. seeds are not more or less shriveled, they are either shriveled or not.
Why are the seeds so different? Do they come from different cultivars, or it's some kind of Mendelian development, or maybe some kind of a plant disease?

The shrivelled seeds are aborted seeds, known as 'chicken tongues'. Some cultivars of lychees mainly produce fruits containing chicken tongues. These cultivars are usually considered more desirable, because they have more flesh.
Source: https://www.crfg.org/pubs/ff/lychee.html

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how origin of koi carp is different from goldfish
where did koi-carp originate? how are they different from goldfish? Wikipedia say that goldfish originated by genetic mutation but what about koi-carps?

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Excess proteins in cells
Damaged proteins are broken down in cells by ubiquitin-proteasome pathway. Do cells experience excess of proteins? If yes,  how excess proteins are taken care of?


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Mutations in organisms
I was researching mutations and came across an interesting question:
Do mutations occur in the DNA or mRNA of an organism? Is this more opinion that science?
Thanks in advance!

What do you mean by opinion?

DNA. mRNA is transcribed from DNA.

specifically I assume that the mRNA base changes are a result of the exons, correct?

A more complete answer would be great (I could write it myself but I just wanted to give you some ideas if you wanted to expand your answer). It could be stated for example that not all mutations will ever be transcribed and that of course if there is a mutation in a coding region that is being expressed, then you'll find the mutation in the mRNA also.

Simple questions are best answered with simple answers. You can have your opinions, but in my opinion, I am often annoyed by long winded answers.

@KarlKjer Fair enough. +1

From Wikipedia:

A mutation is the permanent alteration of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA or other genetic elements.

The key word here is genome. A mutation is defined as something occurring in the genome, and the genome of living beings is made of DNA. Hence, mutations arise in the DNA.
A special case concerns viruses (which, for the record, are often not considered living beings): they can have a RNA genome, so they can have mutations in the RNA.
BUT!
This does not mean that mRNA transcription is an error-free process! As an example, this link gives you a nice overview on the error rate in transcription and translation,which apparently are quite high. It's just that, by definition, mutations arise in the genome.


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Why food is still tasty?
I'm not a biologist, but it seems that plants with disgusting taste have evolutionary advantage to tasty plants. Same about animals.
There are some species that can not be eaten by man (sharks have poisonous meat). Being eaten by a human — is one of major threats for a shrimp. Does it mean that shrimps are going to become less and less tasty (for a human taste)?

Why do you think sharks are poison ?

mercury accumulates in top level predators

@blacksmith37 "Unprocessed shark meat may have a strong odor of ammonia, due to the high urea content that develops as the fish decomposes". You can eat it, but it's unhealthy. In most countries only shark fins are used as food — other parts are concidered waste.

Things are not fundamentally tasty or disgusting. A dung fly loves that taste of dungs while I personally prefer the taste of an apple and my dog prefers the taste of duck fat. A classic example is the gene family TAS2R and the evolution of bitter taste in rodents and primates.
Predator (incl. herbivores) evolves as to like the taste of what he should be eating (Carlsson et al., 2009). Preys (incl. plants) can eventually play out with their taste though, trying to either taste bad to avoid specific predators or taste good to attract specific predators that may disseminate their seeds. I have failed to find evidence that plants can deceive animals at being more tasty than nourishing but you might still want to have a look at Dethier (1980), Sorensen (1983) and Goff and Klee (2006).
One could therefore expect an evolutionary race (red queen) between preys and predators upon how they taste. It would likely be a rather complex race as most species have several predators and several species they prey upon. However, such race on taste would work only if plants can deceive animals which I failed to find evidence for. Arms race for toxic compounds relating to evolution of taste in animals are very much known though (Edger et al., 2015).

So is it a Red queen taste version?

Yes. But see edit where I made sure to be a bit more safe in not claiming more than it is known. I also added a few references.

Well, my dog likes long-dead deer bones, and eats horse droppings and hoof parings, among other things I don't think I'd find at all tasty.  OTOH, my horse likes to snack on bitterbrush (https://en.wikipedia.org/wiki/Purshia_tridentata ), and eats a lot more hay than I'd care too.  Tastes differ :-)

Right now mankind is a major predator for a lot of species (shrimps for example) — does it mean that in future generations shrimps will evolve to be less attractive for people?

@StanislavGoldenshluger More than half of the world production in shrimps are farmed (according to WWF), so it is not really a good example.


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What are the sizes of individual cells of the cyanobacterium Nostoc spheroides?
In this article Nostoc spheroids are described as edible blue-green algae, but they are mostly named cyanobacteria, which are prokaryotes.
In the above and other articles about Nostoc spheroids only sizes of the colonies are mentioned and i couldn't find the individual cell sizes.
Can the sizes of individual cells of Nostoc spheroids, and other cyanobacteria like Nostoc commune and Nostoc muscorum be found somewhere on the internet ?

We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

@tyersome  If you read my question well, i did some research. I thought this is a very straight forward question. It's not my fault if it can't be answered !

You may have done some research, but IMO posting a link to Wikipedia page notifying us that there is no such page isn't convincing. 2) Lack of interest in searching out trivia for you isn't a sign that the question can't be answered. ——— If you really care about this information I encourage you to either write a convincing argument for why this is interesting or spend the time to find out the answer yourself.

If you have a question about a bacterial species. Bergey's manual is your friend: it is the definitive manual for bacterial morphology. Most universities have it as a pdf —I am unable to speculate on whether it is also available on say sci-hub (a paper pirating site). Check out figure 810.78 on page 576. Their shape can vary a large bit, but it is in the 1-3 µm range, so the usual size for diderm bacteria (2 µm is the length of an E. coli).

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book on human sexuality evolution
i am interested in Lynn Margulis' book Mystery Dance: On the Evolution of Human Sexuality.
i don't find it in libraries and it's too old and i am too poor for paying 20 euros for a 1991 book.
Does anybody know a more modern book about human sexuality evolution?

Perhaps The Evolution of Desire by David M. Buss. I haven't read it myself (yet), but I've had it recommended.

Wild connection by Jennifer Verdolin is good, it shows the source of many of humanities sexual behaviors, but it really depends on what you are looking for is there a specific area you are trying to learn about?
The Third chimpanzee might interest you, it compares human behavior to the other chimpanzee species, sex is only a small part but it is there.
I a can warn you against a book I used to like,sperm wars by Baker, A lot of the research is his own and there have been a lot of issues with people being unable to replicate many of them, so a lot of it untrustworthy, which is a shame because I really liked his writing style.


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What percentage of a complete Denisovan genomes lives on in the union of the sets of overlapping pieces in extant humans
In studies like this one mapping out distributions around the world or the analysis described in this article (suggesting a contribution from a non-Denisovan but Denisovan-like unidentified hominin to Melanesian populations, various single digit percentages are given of an average as high as 6%.
One complication in talking about this is what we mean by percent. Just through shared DNA we'd have over 99%, if we knew which DNA was shared. There are surely other complications, like how do you count repetitions toward the percentage, etc. But I mean to ask what percentage of  DNA that is DNA descended from introgressions adds up to, if you put together the different and overlapping pieces various people have.
I realize it may also be hard to pin down exactly what one would mean by a Denisovan genome -- as I said one of the linked articles suggests there may at least one Denisovan-like hominin species represented in the introgressions.
Note: Someone already asked this about Neanderthals.


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How do cells relocate transmembrane proteins from one side of the cell to the other? Is it possible?
Is there a process by which cells can relocate proteins residing on the cell membrane in areas of low demand to that of a high demand location somewhere else in on the cell? What's that process called?
Through protein catabolism, cells can break down the proteins into their individual amino acids and then reuse these resources to build new proteins in needed locations. This process seems inefficient if the cell simply needs to move a transmembrane protein (for example integrin or cadherin) from one side of the cell to the other.
I hope the question is clear. I haven't taken a biology course since early high school (8 years ago) so if there's something i need to clarify let me know!

Transmembrane proteins can move laterally through the plasma membrane (see fluid mosaic model) and this movement can be actively directed along the cytoskeleton. The following paper is the most salient example that I found of transmembrane proteins moving from one side of the cell to the other:
Moss WC, Irvine DJ, Davis MM, Krummel MF. 2002. Quantifying signaling-induced reorientation of T cell receptors during immunological synapse formation. PNAS 99(23):15024-15029.

Productive T cell recognition of antigen-presenting cells (APCs) is normally accompanied by the formation of a cell–cell contact called the “immunological synapse.” ... T cell receptors are recruited in bulk within the first minute after the onset of activation...

The following figure, adapted from the paper, shows the time-lapsed movement of GFP (ie fluorescently) labelled CD3, which is part of the transmembrane T-cell receptor complex, during synapse formation with an APC:

Time is in minutes, and zeroed at first contact between the two cells. I've put a red dot on the T-cell and a blue one on the APC in the DIC images (left panes); hopefully that proves more informative than annoying. The right panes show GFP fluorescence and thus CD3 localization. As time progresses, CD3 is re-localized from one part of the membrane to another (the synapse). There is supposedly a video of this is in the supplementary information of the article, though I was unable to open it.
The rate and directionality of the movement implies that an active process is occurring, rather than simple diffusion. However, they did not find the actual mechanism for movement and I haven't found any follow-up papers in a brief search (though many subsequent papers implicate the cytoskeleton in this movement). Just to show that movement of transmembrane proteins can, in fact, be actively directed by the cytoskeleton, I refer you to this paper:
Grabham PW, Foley M, Umeojiako A, Goldberg DJ. 2000. Nerve growth factor stimulates coupling of beta1 integrin to distinct transport mechanisms in the filopodia of growth cones. J Cell Sci 113:3003-3012.
They show that membrane-spanning integrins are moved along actin filaments of the cytoskeleton by myosin motor proteins. Expectedly, the abstract does a good job of summarizing the paper:

The cycling of membrane receptors for substrate-bound proteins via their interaction with the actin cytoskeleton at the leading edge of growth cones and other motile cells is important for neurite outgrowth and cell migration. Receptor delivered to the leading edge binds to its ligand, which induces coupling of the receptor to a rearward flowing network of actin filaments. This coupling is thought to facilitate advance... [T]ransport was dependent on an intact actin cytoskeleton and myosin ATPase...

Here's a few more papers I found, but did not use, in case anyone is interested: one, two, three.

@BryanKrause Thanks! And likewise, obviously; I thought they’d work hand in hand.

As this is my first question I've asked on this site, I am VERY impressed with the quality of the answers, thanks! My lab has seen hints of this happening when using epithelial cells with fluorescent labeled E-cadherin protein. When stimulated on one side with external E-cadherin protein, it seems the E-cadherin inside the cell decreases in areas far away from the stimuli and correspondingly increases in the area of the stimuli.

@SethH You're welcome, and that sounds like an interesting experiment.

The breakdown and reassembly of proteins is a ubiquitous process within cells, and yes this is expensive but transport is expensive, too, and recycling has the added benefit of dealing with proteins that become misfolded or otherwise damaged as well as allowing for transcription and translation to regulate overall protein levels. The Toyoma & Hetzer 2013 review (see references below) cites estimates of the median protein half-life in a non-dividing mammalian cell to be about 43 hours, though they discuss some exceptions that do last much longer.
However, it is possible to relocate transmembrane proteins via vesicles.
Essentially the same way proteins are put in the plasma membrane in the first place, but in reverse. Endocytosis is often taught as a way that cells (often macrophages are used as an example) take in materials from the outside world, but it is just as applicable to internalizing chunks of membrane. Nature has an entire 'web focus' on entocytosis reviews.
One situation where this happens is in synaptic plasticity; receptors can be internalized or trafficked to the membrane to decrease or increase the potency of that synapse, respectively (see Carroll et al., 2001), but similar processes occur all over (and some proteins constantly cycle back and forth; see Trowbridge et al. 1993 for a more general review, though a bit dated).
However, to your specific question, I don't know specifically of examples where transmembrane proteins are literally cycled from one side of the cytosol to the other. There may be examples I am not aware of, but my understanding is that it is more typical to think of a "store" of certain proteins in endosomes, from which they can be trafficked to the membrane and reinserted via exocytosis. Probabilistically, some will be transported from one place to another, but not so much in a stepwise fashion.

Toyama, B. H., & Hetzer, M. W. (2013). Protein homeostasis: live long, won't prosper. Nature Reviews Molecular Cell Biology, 14(1), 55.
Carroll, R. C., Beattie, E. C., von Zastrow, M., & Malenka, R. C. (2001). Role of AMPA receptor endocytosis in synaptic plasticity. Nature Reviews Neuroscience, 2(5), 315.
Trowbridge, I. S., Collawn, J. F., & Hopkins, C. R. (1993). Signal-dependent membrane protein trafficking in the endocytic pathway. Annual review of cell biology, 9(1), 129-161.


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Veritasium video about mosquitoes
In the recent veritasium video about mosquitoes , the host says that the researchers used identical female twins and fraternal female twins to understand the effect of genes on attractiveness to mosquitoes.
Is there a scientific reason to use only female test subjects for the experiment?
The video:
https://youtu.be/38gVZgE39K8

My guess is that there is no reason for choosing female per se. Rather, I'm guessing that they simply wanted to avoid complications regarding sex differences, so they simply created the experiment with participants being of the same sex. So I suspect the experiment could just as well have been created with only males.

Female and male mosquitoes are quite different, studying both would be like studying different species in many ways and females are the ones that bite, so likely that is why.


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Where is cleavage site located?
I feel a bit confused about cleaving!
Is cleavage site always located on the substrate or on the enzyme?

Hi. Your question seems incomplete. Please provide some context to your question. Also I really think this question can be googled and found easily their. Thanks.

The cleavage site is always located on the substrate. It is specific sequence of bases (if we speak about DNA or RNA) or amino acids (proteins) that is recognized by the particular enzyme and cut.

Yes, and the site on the enzyme's side is called the "active site" or "catalytic site".


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Inexperienced divers damage coral, but parrot fish eating coral doesn't do damage?
I've been learning about life on coral reefs. Recently I've become aware of the damage to coral reefs caused by tourism and inexperienced divers:
1) Corals have a thin membrane which keeps them healthy. Touching them could break this membrane, causing infection which can lead to death.
2) Stepping on, leaning on, and sitting on coral could smash their polyps.
I am not against being responsible as a diver, respecting nature, arriving and leaving without a trace. I'm just curious what the difference is between human and animal contact. Parrot fish eat coral, taking bites out of it, leaving exposed areas and this damages the coral. I've seen footage of sharks having feeding frenzies on reefs, where they smash into the reef during the commotion and while trying to catch their prey. Fish rub up against coral and peck at them to get algae, and crustaceans walk on the coral with legs that seems like it would break the thin protective membrane on the coral.
Obviously, as humans we technically do not belong in their world, so I'm sure there are reasons for damage with that alone; but why does marine life causing damage not cause actual damage? Or does it, and it just repairs differently or faster somehow?

If I am not mistaken, most parrot fish species eat algea that live on corals, not corals themselves.

I'm voting to close this question as off-topic because, however well-meaning it is, it is not a question about biology in the terms of SE Biology. It is merely an exhortation for social responsibility in relation to the environment.

@Remi.b some species of parrotfish do eat the coral and the algae that live within coral.

Yes, some. That's why I said "most" and not "all"

@David I disagree, the core of the question is what is the ecological role of parrotfish and how does it not pose a threat to the ecosystem.

Why do you assume that this doesn't cause actual damage or pose a threat to the ecosystem? Perhaps it does; ecosystems may change (and get destroyed) by natural causes as well.

You are absolutely correct in regards that marine life does cause damage to corals. In particular, parrotfish have been found to play an important role in regulating the biodiversity of coral reefs through their feeding behavior. Certain species of parrotfish feed on certain species of coral, typically faster growing species that branch out into easier access bits of corals that the fish can consume. This has the effect of allowing slower growing species that may also be harder corals to consume (in terms of hardness, shape accessibility, or other factors) to grow and compete in the coral reef and prevent the reef from being overgrown with the faster species. A similar process is seen on the land with grazing herbivores which help propagate biodiversity by consuming certain plant species thereby giving increased chances for other species to grow. These ecosystems and the relationships between corals and species like parrotfish have had an extremely long time to come to shape through evolutionary pressures on both sides of the organisms, consumer and producer.
The problem with divers who cause damage to corals is that it is an introduction of artificial stress and arbitrary damage to the coral reef in a short time without much time to adapt, placing additional stress on the environment which is already stressed. Unlike the parrotfish, divers may not discriminate on what corals they damage. Additionally, areas where inexperienced divers damage coral generally will see more inexperience divers often at the same diving site, so from the standpoint of protecting the coral reef, minimizing the damage caused by divers becomes an important priority to the stewards of those areas and the diving shops which bring divers to those areas.

The core answer is great and ultimately applicable to all environmental stress caused by man: the problem is not the interaction itself, but is its intensity coupled with its suddenness. The environment can adapt to a variety of stresses, but it needs its time.

OTOH, it is indeed true that a coral reef can be overgrazed by animals. An example that readily comes to mind is the infestation of the Great Barrier Reef by the crown-of-thorns, Acanthaster planci:

Normally, these starfish help the ecosystem by feeding off fast-growing coral species, thus promoting diversity. However, every so often, there is a boom in the population of these animals, and overgrazing thus occurs.

Do things like this ever happen naturally, or do they occur directly/inadvertently because of man? Like the lionfish invasion of Altlantic waters that was due to captive fish getting into the ocean; or jellyfish blooms due to several manmade causes.

I can't point to a specific example offhand, but it would be quite strange to assume that population blooms are always caused by man.

I think an essential part of this is the fact that there really is nothing particularly special about humans. We are as much a part of the environment as any other animal and produce our own evolutionary pressures (See proliferation of household/farm animal populations vs. almost a total annihilation of large predators).
The problem usually is that we (i.e. humans as a race, but mostly the developed world) don't like the results. We both like the idea of the great cats (albeit from a distance or behind glass/bars) and are afraid that the evolutionary pressures we generate are too large.
From what I understand it is very unlikely that we are able to destroy nature/life on earth, but it is very likely we are able to cause enough devastation that it won't be able to sustain the human race at the very least short term (couple hundred thousand years). This is bad for us and as such we should be mindful about not causing too much evolutionary pressure too fast to keep the planet in the state where it is capable to support us and possible also look really nice.


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What spider is this? Found in Hawaii
I found this spider at the edge of a park in Hawaii. ~1cm in length. The area I found it was very dry and had thick tall grasses just a few feet away.

Looks to be an araneid (orb weaver spider).

You have a Spotted Orbweaver (genus Neoscona). Likely either a Western Spotted Orbweaver (N. oaxacensis) or Red-femured Spotted Orbweaver (N. domiciliorum)


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What direction is a sequence in databases written?
In many databases, the DNA sequences for proteins are given as a string of a,t,g,c without specifying whether the starting is from 5' or from 3'.
Also it is not specified if it is the coding or non coding strand.
Is it because all the sequences are written from 5' to 3' of coding strand only?

Is there a specific database you have in mind that is ambiguous?

@James I was writing a code that calculates the #g-#c at each position for an E coli genome. It's supposed to show a specific variation when walked in 5' to 3' direction. I was wondering whether the genome (essentially the string of characters that I have) is from 5' to 3' or not. Sorry if it was too apparent. I'm new to this.

Directionality
It is indeed the convention to represent nucleic acid sequences in the 5ʹ to 3ʹ direction.
This is implied in the IUPAC/IUB document on Abbreviations and Symbols for Nucleic Acids, Polynucleotides and their Constituents, although not stated explicitly — presumably because this was written in 1974, before the large nucleic acid databases were established.
Strand
In general you can assume nothing about which strand a particular feature is located on. You need to refer to the context or documentation for the particular database that you are using.
I prefer the term ‘sense strand’ to ‘coding strand’ as explained in another post. However this only has meaning in a restricted set of circumstances relating to mRNA, particularly considering cDNA copies of eukaryotic mRNAs. Only if the context indicates that this is the case can you assume the strand presented as a ‘sense strand’.
The problem arises from the fact that for all (or almost all) genomes, different genes are located on different strands of the DNA — the chromosome has no unique ‘sense strand’ or ‘coding strand’. Thus, for DNA sequences in a database such as Genbank, the following are possible:

The DNA sequence presented does not encode protein or structural RNA.
The DNA sequence presented contains genes on both strands.

An example of the latter is given in the Sample GenBank Record which should be consulted to understand the feature annotation in DNA sequence entries in GenBank. This 5028 bp yeast chromosome entry encodes two genes. The first, AXL2, is annotated:

 gene            687..3158
                 /gene="AXL2"

The second, REV7, is annotated:

 gene            complement(3300..4037)
                 /gene="REV7"

This indicates that, when presented in the 5ʹ to 3ʹ direction, the gene REV7 lies on the complement of the strand presented.

@ArjunDevdas If this answered your question, you can mark it as accepted by clicking the checkmark.

The convention is to provide the sense strand from 5’ to 3’.


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How is the gradient in density gradient centrifugation made?
From the literature I read, I came to understand the following. Please correct me if wrong.

In CsCl gradient centrifugation, the gradient is achieved by centrifuging the CsCl solution at high rpm, which causes the heavy Cs ions to distribute unevenly throughout the solution, due to sheer centrifugal force.
In Sucrose gradient, solutions of decreasing concentrations of sucrose are layered one over the other slowly.

Why can't we achieve the sucrose gradient by simply centrifuging it like in the CsCl gradient?

Sucrose gradient separations are an example of a rate-zonal centrifugation technique (fair technical document on centirfugation separations). The idea is you layer lighter sucrose solutions on top of one another, for example, 35% at the bottom of the tube (the most dense zone) and 15% at the top band (the least dense zone). There might be 5 or 6 layers. You then layer the sample, which may contain cell lysate, at the very top.
This method is done on a centrifuge, and the idea is that in order to penetrate down to a more dense layer, the component of the lysate must exceed the density of the preceeding sucrose layer. Quite literally the dense components are pushing down through the sucrose layers. The method is suitable for organelles and proteins. The layering must be done deliberately and carefully, however, because the sucrose layers and sample will easily mix if they're disturbed. The same concept applies to ficol density gradient separations: If there's no density of solution below the sample for it to pass through, there's no separation.
On the other hand, the CsCl method is an example of an isopycnic centrifugation suitable for the separation of nucleic acids, see the above mentioned reference. This is because the DNA migrates to where the denisty of the DNA equals the density of the gradient, referred to as the neutral buoyancy or isopycnic point.

Thanks for the answer. But, if you have a solution of sucrose of a particular concentration and you centrifuge it at high rpm, would it be enough to form the density gradient like the CsCl, or is it necessary to layer solutions of varied concentrations and then centrifuge? Why exactly do we need solutions of different concentration unlike CsCl method where we use just one solution of CsCl of a specific concentration?

It's necessary to layer the sample on top of the sucrose solution. In the CsCl method the sample is in suspension and works on a different principle. If you suspend your sample in the sucrose solution, you won't accomplish anything. For example, if you want really dense things like organelles, you could put a single dense layer of sucrose under the sample and spin that, but you'd only obtain one fraction: The constituents with the highest density.

The principle behind the sucrose gradient is denser things push down from layer to layer until they're no longer dense enough to get through and end up as a band somewhere along the gradient, or pellet completely to the bottom.

So, if you mix them together and then spin, everything will just pellet to the bottom and you get no separation.


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By definition, will some children always be stunted?
I had a question about stunting i.e. height-for-age. The WHO defines at as any child whose height-for-age is 2 standard deviations below the median height-for-age.
Given this definition, wouldn't there always be stunted children? I must have misunderstood the definition because this seems like one of those challenges that needs to be "fixed" but my current understanding means its sort of unfixable.
Any insight is appreciated.

I'm voting to close this question as off-topic because it seems like its asking more about statistical/mathematical distributions vs biology.

You are correct, that under that definition; unless there were no variation (which would be impossible), there would always be individuals that fall below 2 standard deviations. However, "stunted" under this definition would not be a problem if variation was extremely low. So yes, it would be unfixable by definition, but if variation fell, then the "problem" would be fixed, because it would no longer be a problem.

I disagree with the last sentence. No matter what the actual distribution, there will always been extreme observations.

Karl Kjer: Many thanks for your answer! I think it encapsulates the trouble I am having with this but I think you may be pointing to an answer. Perhaps what WHO need to do is to add to the definition suggesting an SD cutoff after which this stops being relevant. That is, if the spread is much lower and most of the world's population are more tightly centered around a mean, then stunting stops being relevant as a public health challenge.


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The 4-chambered heart
Birds and humans have a four chambered heart. All animals having 4-chambered hearts are warm-blooded.
Why are crocodiles an exception? Why are they cold-blooded even though they have a 4-chambered heart?

https://news.ucsc.edu/2014/12/crocodile-genomes.html

So, the slow evolving genome is the reason...

The short answer is crocodiles may be secondarily cold blooded, but the long answer is warm blooded and cold blooded is not a binary condition but a spectrum.
It has to do with how much heat you generate with your own tissue as all organisms generate some heat and gain some from the environment when they can. on one end you have extreme ectotherms (some insects) at the other extreme endotherms (such as arctic mammals) and a huge range between them covering nearly every level of metabolic activty. The ancestors of crocodiles (Crocodylomorpha) were terriestial and highly active and was thus likely near the warm blooded end of the spectrum and thus with a four chambered heart. They actually look like what you would get if you tried to turn a crocodile into a wolf.  But it is believed that as the line that led to modern crocodiles adapted more for an aquatic environment they switched back to a more ancestral metabolism. Although  I should mention crocodiles and esspecally alligators are capable of producing considerable metabolic heat and activity even for prolonged period, more than other "reptiles", comparable to slowest metabolism mammals. they kep many anatomical adaptation to a higher metabolism as they also aid in diving and still benefit their higher metabolisms.

https://www.livescience.com/51162-dinosaurs-warm-blooded-growth-rates.html interestingly enough there's some evidence that dinosaurs may have been in the middle of the spectrum

If by in the middle you mean the same as mammals. Also growth rings have been shown to be really poor indicators as they can be caused by all kinds of things.


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How do tumor cells 'gravitate' towards each other?
In a popular article it is mentioned that in centrifugal experiments with cancer cells that

When subjected to microgravity-conditions, the cancer cells were unable to sense each other and therefore had a very hard time coming together.

which is because

[...] the process through which cancer grows and spreads would seem to indicate that there is a means through which the cells are able to sense each other and gravitate together to form a tumor.

I would now be interested in the role of such fundamental forces in cell-signaling.
How does gravity interact with cell-signaling and lead to the 'gravitation' of tumor cells towards one another?
To my knowledge, cell signaling is a bunch of processes that involve the propagation of electrical signals by chemical means, so I am rather surprised that gravity would play any role in this.

That article looks like incoherent gibberish, to be honest. Very little in it makes any kind of sense. The statement that "the only way cancer cells could sense each other is through mechanical forces" is nonsense. You can't get microgravity with a centrifuge - all you can do is put the cells in higher "gravity" and then reduce the "gravity" back to 1. And so on. Undoubtedly the actual scientist knows these things, but the person who wrote the article clearly didn't understand what they were being told. Trying to figure out the reality is probably a waste of time, until Chou publishes.

@iayork: Yes, I was very confued upon reading it as well. The fact that the article on Universetoday is essentially a copypaste of the UTS article, and also misspells Chou's name is not very indicative of quality science journalism. However I was just curious if in the biology world there is some indication that this might be a real effect and what its provenance should be.

It actually looks like the original article was in fact written by Chou, and is still just as confusing. Statements like "By disabled, I mean they either die or float off because they can no longer hold on" sound a bit like https://xkcd.com/1217/ to me, and comes with no citation, nor does any of Chou's previously published work have any relevance to this. It kind of sounds like they shook up some cells growing in a dish and they fell off the dish.

Microgravity can affect the mechanical forces of the cell and alter gene expression; there are some reports on this. However, the statements made in the popsci article are ridiculous.

@WYSIWYG: I'm happy to upvote any credible source that goes beyond "Gravity affects pathways somehow". I'm interested in the microphysics, you could say.

@AtmosphericPrisonEscape I don't have time to write a full answer, at the moment. But have a look at this article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5007526/

@WYSIWYG Interesting article. So it seems that they essentially point to macroscopic shear stresses, blood pressure drops etc. to be responsible to deform cells and then cause all sorts of trouble. Wouldn't this cell degradation then also show up in a petri-dish under full $\vec g$, but with enough space for cells to expand, instead of squished together? It seems the cells rely on the effects of accumulated weight to keep their shape, so I'm surprised that a cells in a small petri dish show those effects...

It is reported that 99 genes are significantly upregulated in presence of normal gravity, whereas in absence of gravitational force no gene expression is seen in case of T cell activation. Research article attached concluded  that gravity is important for regulating various essential T-cell activation signalling pathways, which play key role in cell proliferation and apoptosis.
Transcription factors like NF-kB, CREB, ELK, AP-1, and STAT are responsible for tumor cell development. And NF-kB and CREB showed gravity-mediated gene expression. As, the PKA
signaling pathway regulates expression of these transcription factor, so it means that gravitational force moderates PKA signalling. And PKA signalling also mediates tumorigenesis. So, by regulating various cell signalling pathways, gravity controls the tumor cells.
Gravity also modulates the activity of Epidermal growth factor, which are implicated in tumor progression. (Via: https://www.ncbi.nlm.nih.gov/pubmed/7757250)

Thank you for this, but your answer doesn't answer my question. You say 'So, by regulating various cell signalling pathways, gravity controls the tumor cells.' and I asked 'How are cell signaling pathways regulated by gravity?'

The article (summary?) you've linked gives a hint at the end: "The physical mechanisms by which the T cells respond to gravity remain an intriguing enigma [...]". However the article is from 2005, so maybe there is some more recent insight? Or are we simply not there yet...

As gravity controls the expression of various Transcription factors, which are responsible for proliferation and death of cells by regulating signalling pathways. So this effects progression of tumor cells.

@TwinkleSheen You're repeating the same thing. "Controlling transcription factors" is not a mechanism for gravity to have an influence, it's just a synonym for "regulating cell signalling".


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How can census population size be smaller than the effective population size in some species? is that possible?
The only way I can think this could happen is through a recent population bottleneck. Can it be possible though ?

Why are you asking? Have you encountered a case where the census population is considered smaller than the effective pop size?


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Coefficient of relatedness for a locus on the Z chromosome
So i know that the ZW determination system is the equivalent for XY in birds. Moreover, I know that the coefficient of relatedness between siblings for the X chromosome is 0.5 so im guessing that the coefficient of relatedness between siblings for the Z chromosome is the same ??

but isnt it different between brother and sister and between sisters and between brothers. Isnt the Z chromosome considered as haploidiploid ?


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How is (Insect) population control through male sterilization effective
This is no doubt a simple question.
I was reading about Sterile Insect Technique where sterile males out-compete non-sterile ones to mate with females and thus reduce the population.
My question is - why don't the females just re-mate after they don't reproduce?
I'm assuming that the number of sterile males will be much less than the existing male population.
Is it because my assumption is incorrect and there are more sterile males?  Or my assumption is correct and given the life-cycle of the organism, the females have only once chance to mate?  Or something else?

Sterile insects are typically produced by radiation. A sufficient dose is used to cause substantial DNA damage in the gametes of the males. However, this doesn't mean the sperm are completely non-functional.
In fact, it is important that the sperm are functional and simply contain dominant-lethal mutations at a sufficient probability (Robinson, 2005 describes this in detail as well as the dosing strategies to optimize the desired outcome).
The males still mate and fertilize the eggs of the female; it is only later that the eggs will eventually fail to develop, but there is no way for the females to be aware of this (nor much that can be done even if they were - once the eggs are fertilized they cannot be fertilized again).
It is also important to release a sufficient population of sterile males to impact the population. Depending on the species, it may or may not be necessary to completely overwhelm the existing population, but a typical goal seems to be 10-100x the native population. By raising males in laboratory conditions, it may be possible to produce a larger population than would typically survive to mating age in the wild.

References:
Cockburn, A. F., Howells, A. J., & Whitten, M. J. (1984). Recombinant DNA technology and genetic control of pest insects. Biotechnology and genetic engineering reviews, 2(1), 68-99.
Klassen, W., & Curtis, C. F. (2005). History of the sterile insect technique. In Sterile insect technique (pp. 3-36). Springer Netherlands.
Robinson, A. S. (2005). Genetic basis of the sterile insect technique. In Sterile Insect Technique (pp. 95-114). Springer, Dordrecht.

Finally some quality content. What a relief. +1

@AliceD Haha I've been trying where the questions warrant it. Unfortunately it seems most of my answers have gone unnoticed lately, based on the very low total view counts in the 30-40 range even after several days. Just not much of a voting population around lately.

Excellent answer @BryanKrause.  As to your dilemma, perhaps this is due to the rise of pseudo-science.

Yes, voting is a hitting rock bottom. I'm trying to spend more time here again. I've been investing my spare time over at Psych mostly.

Good answer, but "In the cases I am aware of, this technique is used with species that only produce one batch of offspring" - the main case I'm familiar with is mosquitoes, where this isn't true.

@arboviral Thanks - I'll remove the statement. Although from some brief research it looks like mosquitoes still only mate once? Can you confirm that?

@BryanKrause As far as I know females have one receptive period, and normally mating is inhibited once sperm are transferred (hence mate once), but you sometimes get incomplete sperm transfer and therefore multiple mating (https://www.cambridge.org/core/journals/bulletin-of-entomological-research/article/multiple-mating-in-female-mosquitoesevidence-from-a-field-population-of-anopheles-freeborni-diptera-culicidae/1CA5BD9936FA474774B638280CC5DD03). Males can mate with several females.

@Bryan it's fine as a first approximation though - the vast majority will only mate once. So it makes virtually no difference to your original statement now I think about it - sorry :)

No worries. I'll leave it removed. I think if anything it distracts from the main point of my answer, which is that these sterilization strategies are predicated on making sterile embryos rather than males completely incapable of mating.


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What's this housefly-like bug?

When it flies around it looks like a slightly lazy housefly.
About a centimeter long.
Has a pointy beak (slightly blurred here by the shadow).
Loves flying at people. Tickly when it sits on you. Hard to brush off - clings on hard. Very resilient - you can swat it a couple of times and nothing will happen.
Makes a crunch when properly squashed. Sighted in central Israel (Beit Shemesh).
What is it?

it is a louse fly https://en.wikipedia.org/wiki/Hippoboscidae they bite and the wound can take several months to heal completely.

Good to know. Thanks @trondhansen !

BTW Your reference points to another reference that says this particular type is a Pigeon fly and a further reference says that they will not normally bite humans unless they can't find their regular host (pigeons) around - and there are lots of those here! Also says that if desperate enough to bite humans, their bites are just "itchy".

i know too little about them to make an answer,one of the types we have here is the deer louse fly and they bite many types of mamals including humans,i live in norway but the deer louse fly is common in most areas where one can find deer-roe deer-moose.


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Can flow-FISH be used on metaphase cells?
I know flow-FISH can be used on interphase cells but was wondering if it only works on interphase cells or can work on cells regardless of stage in the cell cycle.

Don't know if this will help but Maurizio Carbonari in cytometry A in 2016 published on methods which allow for cell cycle analysis.
The abstract

Formamide has long been one of the most widely used reagents in the study of nucleic acids. However, the use of formamide for treating cells to be analyzed by flow cytometry is a recent development and is restricted to measuring telomere lengths by flow‐FISH. In this field, we have published several papers in order to observe the effects of formamide treatment on cells at room temperature. We therefore discovered that, with suitable modifications, a short and simple incubation in this ionizing solvent facilitates cell cycle analysis by flow cytometry, equivalent or superior to that obtained with treatments in alcohol, acetone or detergent in hypotonic solution. Even using a bulky and problematic stain (low quantum efficiency and G‐C base preference), such as 7‐aminoactinomycin D (7‐AAD) which, on the other hand, has the advantage of being excited at 488 nm and does not bind to the RNA, it is possible to obtain excellent coefficients of variation and (G2–M) mode/(G0–G1) mode ratios. These parameters, especially if stained cells are washed before acquisition, arrive at optimal values. It is noteworthy that the ability to wash the cells stained for DNA content analysis without affecting the stoichiometry of the staining has not been described elsewhere in the literature. With formamide treatment the doublets are practically absent, sample recovery is efficient, as well as the preservation of physical parameters, and the stained cells can be stored for at least 10 days at room temperature before acquisition.

As for Flow-FISH, it is a method used to measure telemore lengths.
Vyacheslav I Borisov et al. in Current Protocols in Cytometry. 2014
Published on applying flow-fish to look at M phases.


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Does octopus eye presents the equivalent of fovea in primates?
I'm working on a simple computational model of Primate eye:  as we know, it presents a central part, the fovea, that is very rich of receptors in comparison with eye periphery. I'm wondering if other species eye, like octopus, present a similar structure: a central fovea.
Thanks


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Negative spikes in neurons
I'm new to neuroscience research and came across a term called negative spikes (sometimes also used in conjunction with terms biphasic spikes or positive-negative spikes), but could not find what it meant from scientific papers. Can a spike occur in a negative direction (hyperpolarization from the resting potential first, followed by depolarization) or does this term mean something else entirely?

Please add context as to where you found the terms. What papers etc.

this question reminded me of: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804433/

Intracellular recordings of action potentials always show the same format with which you are familiar. There is polarisation which the stimulus reduces, a threshold is reached, there is a positive spike, then repolarisation, hyperpolarisation, a refractory period an a return to the baseline polarisation.
The term "negative spike" applies to extracellular recordings. These measure the potential between a point close to but outside the cell and a reference point. The inflow of cations into the cell causes a drop in extracellular potential, which appears as a negative spike in the recording.


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Coronary circulation
It is said that the coronary artery that gives the posterior descending artery(PDA) determines if the heart is right dominant(most cases) or left dominant. Is there any reason to this? Why PDA?

Where/ By whom is that said? Could you please provide a reference?

source, please...

This is purely an anatomical definition: right dominant is defined as coronary circulation where the PDA (posterior descending artery) is a branch of the RCA (right coronary artery) and left dominant is defined as coronary circulation where the PDA is a branch of the LCX (left circumflex artery). The Wikipedia article on coronary circulation is a reasonable reference for this question.
There's nothing else special about the statement "dominant" and it doesn't have any other importance for cardiac function, except that someone who is left dominant would have more serious issues if there is a blockage in their left main or LCX.
Typical human coronary artery anatomy consists of two ostia off the aorta, right and left. The "left main" branches fairly early on into the LAD (left anterior descending) artery, which follows the septum between left and right ventricles down the anterior side, and the LCX, which follows the 'top' of the left ventricle counter-clockwise (if looking down at the top of heart and rotating the heart so the atria are on top; in an actual human heart the atria actually point towards the midline a bit more than other species). The RCA travels in roughly mirror fashion, following the 'top' of the right ventricle in clockwise fashion. The RCA and LCX nearly meet on the other side of the heart, at the posterior septum.
In a majority of people, the RCA continues and follows the septum down to the apex (kind of like the LAD but on the opposite side). In a non-negligible minority, the supply of the posterior descending artery is either shared by RCA and LCX or is completely supplied by the LCX.

Thank you for the answer. Could you elaborate on 'someone who is left dominant would have more serious issues if there is a blockage in their left main or LCX' Please?   For wouldn't someone right dominant have equally serious problem with a blockage in left main artery?

@ADP Of course a complete left main blockage is pretty much fatal already, but I meant it just as to a matter of degree: the more of the heart is supplied by that vessel the more severe a blockage is. The same goes on the other side: someone who is right-dominant would have more severe impacts from a RCA blockage than someone who is left-dominant.


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What to do if someone breaks a bone?
What is the best first aid someone an do in events of fractures? I am sports physician - just wondering if there is a specific certification for something like this.
thanks

Depends on the bone.  Any good first aid guide should cover this, and in more detail than could reasonably fit in an answer.

Try health.se for this question

When a person meets with an accident or a traumatic injury and the spot of injury goes numb or turns bluish, there are high chances that the victim might suffer a fracture. In case if you suspect that the person might have a fractured bone, then here are some of the things that you can do to help the person feel better at the earliest.
Once you are done accessing the other injured areas, the first thing that you have to do to treat the broken bone is to make sure it doesn’t move. Get anything that is strong and tie it to the place of fracture. This will stop the bone from moving any further. The next thing is to apply ice to the injured part and see if you can provide the person with some medication that can temporarily reduce pain. However, remember to rush the person to the hospital at the earliest.As for the course , I think this one is pretty popular. You can also check St John's Ambulance as they are pretty much the standard in NZ and AU.

So a bruise is an indication of possible fracture??


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Are molecular machines encoded in the DNA?
I don't know much, if anything, about molecular biology. I watched the "inner life of the cell" on Youtube which triggered my curiosity about how these molecular machines came to be. My simple understanding is that if these molecular machines are encoded in the DNA, then they are "evolve-able" by mechanisms such as natural selection. Is that case? And if so, can we identify which part in the DNA sequence have the encoding for these molecular machine such as the Kinesin? Do molecular motor machines get synthesized by the RNA as well?

I added an answer to your 'can we identify which part' subquestion to my answer.

Yes.
The "molecular machines" you are referring to are particular proteins.
The specific one you are referring to, kinesin, is involved in movement along microtubules, part of the structure of the skeleton of a cell, but other proteins act as their own kind of machine to do their own tasks: sometimes catalyzing a biochemical reaction, or responding to a type of stimulus, or forming a shape or structure, or combinations of all of the above.
Protein-coding sections of DNA are well-studied, and there are substantial databases of known proteins. If you go to wikipedia you will see a whole list of different kinesins, if you click on one, for example, KIF1A, on the right hand side it shows you it is found on chromosome 2 in a human, starting at 240,713,764 base pairs and ending at 240,820,308 base pairs. Information for the mouse is also located there.
Proteins in DNA-based life are all synthesized by first producing an RNA transcript from the DNA, which is effectively an RNA copy of a short stretch of DNA, which is then translated into protein. Other RNA molecules are involved in this process, too, as the rRNA part of the ribosome (sort of a 'protein factory') as well as tRNA which carries the amino acid components of proteins as they are being built. Transcription and translation are central to understanding biology at the molecular and cellular level.
Not only can all proteins, from kinesin to collagen, evolve, they all have evolved through natural selection and other evolutionary mechanisms, and they continue to evolve today in all living organisms. Without evolution, no biology would exist. RNA-based biology (today, mostly some of the viruses) is also subject to evolutionary mechanisms, so that isn't something unique to DNA, but rather to heredity and biology in general.

Some molecular machines are also be build entirely of RNA, in otheres like ribosomes, the functional portions is made of RNA and the proteins are there to stabilize the RNA.

Yes, it's fair to say molecular machines are encoded in the DNA.  As you say, kinesin is a molecular machine - a motor protein that moves molecules along microtubules, which are also proteins.  Protein enzymes are one of the most common molecular machines in cells - they build and break down molecules, among other things.  Membrane channels are proteins, too, and they could be called molecular machines - I'm picturing a drawbridge that lets tall ships pass when it's open and not when it's closed, though channels are more like holes in the cell membrane than like drawbridges.
The sequence of bases [A, G, C and T] in the DNA tells the cell what protein to make. And, yes, mutations occur in the DNA sequences, which results in mutant proteins - or, variant proteins, because there are often several versions of a protein that work fine.
Wikipedia's article - https://en.wikipedia.org/wiki/Kinesin - tells about the family of kinesis proteins, which are coded for by a corresponding family of genes in DNA.
Yes - RNA is important in synthesizing molecular machines. It carries copies of the DNA codes for different proteins in our genes.  It has 3 of the same bases ['letters'] as DNA - A, G, and C, but instead of T it has U, which goes in the RNA sequence wherever T would be in DNA.  The RNA copies of the genes go to the ribosome, an amazing molecular factory that takes the information in the RNA copies of the genes and uses it to make proteins, which have amino acids instead of the 4 bases of DNA and RNA.


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How plausible would it be for animals to normalize the birth of monozygotic twins in their reproductive cycles?
I'm currently trying to develop the world of a sci-fi story I'm working on, and a concept I've thought of adopting with the environment and characters is a common breeding system where identical twins (or sometimes not, asymmetric twins from the same egg have also been under consideration) are a commonplace byproduct of the world's evolution.
I'd like to know the plausibility of this. My idea is for two twins to be born with natural, pheromonal connections between each another. The sexual organs of the twins would be the same, thus preventing immediate inbreeding. I'd also envisioned [most] twins consistently having lifelong reliance on one another. i.e. I also want to know how reasonable it would be to expect them to coordinate efforts in the acquisition of food and evade potential predators. As for mating, I thought if they shared the exact same DNA there would be less ingrained concern over which gets to spread its genes. Would this be accurate?
Thanks in advance for anyone that tries to answer me. I'm doing what I can to keep things in the realm of reality, so it'd be much appreciated to know whether or not the universe I'm creating has a strong enough footing in the real world.

Welcome to Biology.SE. Your question appears to be a good fit for worldbuilding.SE but is rather off-topic here on Biology.SE.

Parthenogenesis, apomixis and fragmentation exist in many animal species.

Okay, I apologise. Thank you for pointing me to a more suitable venue.

As a whole, your question is opinion-based, speculative and not really suitable for Bio-SE.  However, several of the building blocks that you describe have a reasonable biological foundation, which might be useful to know.
For instance:

There seems to be a genetic component To monozygotic twinning (see e.g. ghr.nlm.nih.gov). This means that the trait could, very hypothetically, be selected for, and a population with a higher level of monozygotic (identical) twins could develop (ignoring other possible detrimental effects). Different frequencies of MZ twins is also know from castle breeds and other species.
The level of shared genes is the driving force between kin selection. This is part of the explanation  for the reproductive system in social bees (and other eusocial insects), where (usually) a single queen reproduces and her workers (all sisters), which are 75% related to eachother due to the haplodiplod genetic makeup, all work towards the common "goal" of producing new sister queens (which will then be 75% related to all the workers).
This gives some (again, very hypothetical) basis for your idea that "...they shared the exact same DNA there would be less ingrained concern over which gets to spread its genes".
Monozygotic twins often describe an especially strong sibling bond, which lends support (again, very hypoythetically) to your idea of "...expect them to coordinate efforts in the acquisition of food and evade potential predators.". There is also some research to back this up (e.g. Fortuna et al. 2011. Twin relationships: A comparison across monozygotic twins, dizygotic twins, and nontwin siblings in early childhood), but there are also studies that indicates that monozygotic twins show similar sibling behaviors as other types of sibling pairs (see e.g. Mark et al. 2017. Using Twins to Better Understand Sibling Relationships). This is not a field I know well and there is most certainly many more relevant sources to look at.

The introduction to Mark et al (2017) contains many references on MZ twins that should be relevant to your "thought experiment", e.g.:

...Fraley and Tancredy’s (2012) later work, which suggests that twin children rely more heavily on their co-twin for safety and security than do non-twin siblings.


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Why does white light viewed through optical chopper appear purple/blue?
I looked at a light like the one shown here through a fidget spinner (I believe I was observing near where the "blades" meet the inner portion) and noticed that it appeared purple/blue, particularly when viewed for a prolonged period (I looked at the reflection of sunlight from snow and observed this as well.).  I believe this is either an optical effect (the spectrum is convolved with the Fourier transform of the "chopping function or pulse" ) or has something to do with the eye/my perception.
So what's going on here?

I didn't expect this to be as easy to see as you described, but I found it right away. I'm almost certain it's an effect of the time-response of the eye. Would this question fit better on [biology.se]? We'd be happy to migrate it for you.

I totally wasn't expecting to immediately duplicate this with a fidget spinner and the fluorescent light in my office.  What a neat effect!
My technique: I hold the spinner quite close to my eye, so that it occupies nearly all of my field of view, and look through the spinning part at my ceiling light.  If the spinner is very fast or very slow, I don't see any change in the hue of the light.  However there's an intermediate rate where the back part of the fluorescent lamp takes on a patchy blue tint with colored edges. The tinted region is irregular and unpredictable in the same way as a pressure phosphene, if you're familiar with that better-documented effect, and has kind of the same "feel" to it.
Trying to photograph the effect just gives the rolling shutter problem, so that's no use.  (No color change in the photo, either.)
At the rotational speed where the color change effect is the most pronounced, I estimate the frequency at which the spinner blocks nearly all of the light to be 10-20 Hz.  (How? I let the thing hit a fingernail and listened to it tap; it sounds like thirty-second notes, four to a click, at a good presto tempo.)  I've read elsewhere that the human eye can process images at 10-15 Hz. So some sort of biological stroboscopic effect, where the eye has just enough time to begin to respond to the reduced light before the light returns, seems plausible to me.


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How is mankind important to nature?
Like mosquito eggs are important for fish, what’s our role in balancing the life on earth or its ecosystem.
Please suggest if this question doesn't fit in this community.
I am a mechanical engineer with interest in knowing biology and biochemistry.

Hi and welcome to BIO.SE. Although humans clearly play a major ecological role in the world, the wording/focus of your question (specifically within the context of your use of the word "role") causes your question (and therefore any answers) to be opinion-driven. You can try to to read up on top-down control of ecosystems, given that we are clearly top predators.

The classical division of humans and animals has always been self-centered and artificial. Humans are animals, competing with other organisms under exactly the same rules. Evolution involves trade-offs, strategies, and adaptation. Humans have been set on a path to use their brains to compete, rather than claws. But the concepts are the same. It happens that this is a very effective strategy, such that humans now dominate virtually every ecosystem on Earth, to the point that some are now calling the age we live in as the "Anthropocene". Humans are the apex predator. We now have no natural enemies, however as vectors of disease, mosquitos control our populations more than any other animal.

very useful @KarlKjer
Can we say, human is producer of enough carbon dioxide-- useful for photosynthesis? Though I know, we have been brutal to nature in all the ways.

The carbon dioxide we produce has a benefit to Northern climates, but  is balanced by the detrimental effects of warming in the tropics. Given that plants are also evolved to live in the climates where they exist, and are often tightly linked to their pollinators, the potential decoupling of this relationship with increasing temperatures is not beneficial to plants. Some crops in some places will produce more (as the planet and most life on it suffers)


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Do chromosomes change with time?
An offspring is 23 chromosomes of mother and 23 of father, if one of the mate learns say music after the birth of their first child— will their second offspring have better music skills than former? about my knowledge of biology, so far I read about DNA, Genome, chromosomes and genetic engineering, I am an engineer by profession.

You might want to read about epigenetics

@Remi.b — But the Wikipedia article you cite is a mish-mash of misleading nonsense.

Short Answer: Probably, at least a little, much research still needs to be done.  For a great paper on this see here.
Your question can be answered in two parts:

Can Epigenetics be inherited - The answer to the simple question in your title, do chromosomes change with time, is yes.  There are copying errors, and carcinogenic mutations that can permanently change cells' genomes.  Less permanent is epigenetics, which are temporary chemical modifications to the DNA which changes how it is expressed. The epigenetics of the cell may change for various reasons from the cell undergoing mitosis to a wildly changing diet.  However, when sperm and egg cells are formed these epigentic modifications are typically wiped from the genome in order to remove any possible damaging marks.  However, there is a growing body of literature which states that some marks escape the purge and change the characteristics of the progeny.  Studies include scare-treating mice, 1836 famine, fatty rats, human psychological changes.  While the exact genes causing the change is unknown, there is clearly a strong correlation
Can Music Skill be Captured in Epigenetics - Music skill is to difficult to measure biologically, but likely has some links in speech skills, which would be captured in the brain, and muscle skills.  While there is some evidence for there being an muscle epi-memory, brain epigenetic inheritance is more tenuous (although see this exciting paper on RNA causing memory changes through epigenetics).  I would say the general scientific consensus is that there is some relation between epigentics, and memory, and music skill - there is a great deal of work still to be done.

Until recently, the answer to your question would have been a definitive "no", because is smacks of the rejected Larmarckian ideas of the inheritance of acquired characteristics. And the example you provided, about musical skills, that would be "no" as well from a genetic perspective, although the hearing of music around the house may have cultural impacts on the second child. However the new field of epigenetics has revealed that DNA methylation, over the course of ones life can influence offspring of future generations. There was a community in Sweden that took very detailed health records over generations. The effects of a famine in 1836 showed up in the grandchildren of the survivors. It is further explained here: https://io9.gizmodo.com/how-an-1836-famine-altered-the-genes-of-children-born-d-1200001177

Still smacks of Lamarckism, and there is absolutely no evidence or intellectual framework for acquired music skills being associated with methylation of genes, this changing the musicality of an individual, or being responsible for musicality in offspring.

No, it was a good question. The Swedish study was rejected for years, with the simply statement that what had been observed could not be. The question was not about music, but about change in inheritance over time. Music was just an example.

The question has obviously been asked by an outsider. I think a good answer should start with an introduction to epigenetics.

Can you provide an instance of a mammalian gene that:
(a)  is normally unmethylated at some site but has been shown to be demonstrate changed expression following methylation at this site (even just turned off or on),
and
(b) this specific methylation has been demonstrated to be induced by some environmental stimulus,
and
(c) methylation at this site following the said stimulas has been shown to be passed on to the offspring,
and
(d) the offspring have been shown to exhibit the changed gene expression resulting from the methylation?


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Why was IVF in Rhino not believed to be possible?
This line from here:

We achieved together something which was not believed to be possible.

suggests IVF in Rhino was not believed to be possible.
Why was IVF in Rhino not believed to be possible?

I’m voting to close this question because the function of this site is to answer questions about biology, not about the perceived difficulty of a particular obscure process, according to authors of a paper.

@David - Once again, I disagree with your somewhat narrow definition of Biology. Ecology is a specialty field in biology, just as is Molecular Biology or Medicine. Questions about ecology on topic. This isn't a question about reproductive medicine, but one of Ecology (though the OP misunderstood that.) To answer ecology questions, and in so doing to teach, who knows what might come of it? Close for lack of research if you will, but not because "it's not about Biology".

This is actually an English language question, not a rhino reproduction question. The line before the one you quoted is

The technique could be used to save the northern white rhino from total extinction.

The northern white rhino is on the verge of extinction, and it looks like a sure thing in the natural world. As with climate change tipping points, for animals the tipping point for extinction is followed by a rapid decline in population numbers because there are too few remaining individuals on earth to reverse the process; extinction is considered irreversible.
The article states that there are only two female white rhinos left on earth, a pretty sure sign that they will become extinct soon.  However, suddenly the zoologists have hope to prevent extinction (through IVF). It's not that IVF was impossible. It's that the white rhino may not disappear off the face of the earth after all.
They did what they thought was impossible. They may have saved a species from extinction.


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What is the standard method for measuring soil and substrate acidity
Soils and other plant substrates differ a lot in their moisture content. In dry matter a pH is not measurable without adding water, but this has the problem of the resulting value not being independent of the amount of water added. In controlled conditions pKa measurements would be used instead as they are independent of the amount of water, but would this would require information about chemical composition that is generally unobtainable.
What is the standard way of reporting acidity of soils? I would think that there is probably some kind of measurement based on mass or volume. Or, perhaps the log scale renders the amount of water negligible for most purposes?

Soil should first be processed by drying the soil to ensure a standard "dry" sample is analyzed. 55$^o$C in drying ovens for 24 hours works for most non-water-zone soils, but more time at 50 - 55 $^o$C (as long as it's consistent between samples) can be used to dry out wetter samples. One can then put the soil through sieves to remove rocks and other debris (2mm sieve is common).
To actually measure soil pH, one combines 1 part soil with 1 part water and then measure with an electrode (McLean 1982)$^1$.
By always using 1 part soil to 1 part water, you maintain a consistent relative amount of water per sample and therefore can account for different sample sizes.
The final value is reported as pH.
You can find the McLean (1982) resource here for $15 or likely for free from a nearby university library. The paper has been cited over 2800 times.
[1] McLean, E.O. 1982. Soil pH and lime requirement. In A.L. Page et al. (ed.) Methods of soil analysis, part 2. Agronomy Monogr. 9, 2nd ed. ASA and SSSA pp 199–223.
EDIT:
As @Roland pointed out in the comments, other standards do exist.
For example, the International Organization for Standardization (ISO) maintains reports describing  standard protocols for different methods (which therefore are sometimes used):

ISO 10390:2005 specifies an instrumental method for the routine determination of pH using a glass electrode in a 1:5 (volume fraction) suspension of soil in water (pH in H2O), in 1 mol/l potassium chloride solution (pH in KCl) or in 0,01 mol/l calcium chloride solution (pH in CaCl2).
ISO 10390:2005 is applicable to all types of air-dried soil samples, for example pretreated in accordance with ISO 11464.

The USDA describes several standard protocols used by their laboratory at the National Soil Survey Center to measure soil pH (Hydrogen-Ion Activity) in their Soil Survey Laboratory Methods Manual (version 5, 2014). See specifically, pages 265-281 for various soil suspension and soil extract methods.

Note: They cite repeatedly the McLean (1982) paper as a  source for determining pH using an electrode.

They also provide further notes in this technical note.

The EPA (US Environmental Protection Agency) similarly has a protocol that they use. Their electrometric approach using a digital pH meter involves the insertion of a glass electrode into a soil suspension made by mixing the soil 1:1 with a reagent solution (see referenced notes below).

EPA protocol for soil pH (Method 9045D): Revision 4 (2004) available here

References "Chapter One" of technical note SW846 (I link to Update V revision 2, July 2014), which relates back to 2-2 of EPA-600/4-79-019

Again, the overall takeaways are:

Reporting soil acidity as pH is standard
There are multiple standard methods to measure the pH; Just be sure to properly cite your approach!

At least among soil scientists, it's pretty common to use 0.01 M CaCl solution instead of pure water. The top answer there briefly explains why. See also: http://www.iso.org/iso/catalogue_detail.htm?csnumber=40879


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Does the SMUG1 enzyme break single-stranded DNA?
The SMUG1 gene codes for the enzyme single-strand selective monofunctional uracil DNA glycosylase.  This enzyme can remove uracil from single-strand (unpaired) DNA.  (Uracil can occur in DNA due to deamination of cytosine.)
What happens when this enzyme removes uracil?  It seems what would be best is that a cytosine would replace the uracil in the DNA strand to restore the original DNA sequence, but I haven't found mention of this.  The alternatives would seem to be that the enzyme simply splits the strand into two strands by removing the uracil (which are then unconnected since this is single-strand DNA), or it joins the two adjacent bases together, deleting the uracil but keeping the strand intact.

I think you needed to click just one more link: https://en.wikipedia.org/wiki/Base_excision_repair
It just cuts out the base so there's an empty spot on the ribose. I was looking for a picture and the top hit was actually this site (at A):
What is the mechanism of monofunctional glycosylases?

Yes, I now see SMUG1 just removes the base, leaving the sugar and phosphate. It seems then that the information that U had been present (and thus cytosine is appropriate) is lost.  The fate of the baseless sugar-phosphate is unclear to me from the Wikipedia articles; most of the discussion seems to suggest that breaking of the phosphate backbone is usual (which would leave two unconnected DNA molecules).


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Reconstruction of wildlife distribution based on poorly-sampled data
cross-posted to Signal Processing, Cross Validated, and World Building Stack Exchange
Hi, I thought I'd also put this here in case there are any field biologists with ideas on the matter.
Problem: After reading a series of fantasy novels, I noticed that the biosphere in that world made no sense. To clarify, this is a world where despite magical occurrences, the world itself is almost entirely non-magical. 'Alternate history magical realism,' perhaps. i.e., unlike, for example, Harry Potter, in which almost all plant and animal species mentioned are fictitious and magical, this series uses real flora and fauna. This allows me to extract information about the fictional world's environment based on the distribution of these animals, by assuming that similar animals will live in similar climates on Earth and in the fictional world.
Ignoring the likelihood that the original author did not put enough thought into worldbuilding to make this a necessarily reasonable endeavor, my idea for how to proceed was as follows:
As maps exist of the fictional world, and the path of the characters can be plotted, I hoped to mark every mention of a specific plant or animal in the text, along with the location of the characters when it occurred, and from this reconstruct a plausible distribution for each species. I've created a theoretical example (in photoshop), for illustration:

where the red dotted line represents the paths of various characters, the orange, green, and blue splotches represent the true distribution of the species; the stars, triangles, and circles represent the locations at which a species is mentioned; and the brown, green, and blue lines represent the reconstructed contours of the distribution.
Is there a method to do such a reconstruction? It sounds a bit like a Monte Carlo analysis, but I figured I should check... (It also sounds rather like the magical programs detective shows use to plot serial killers' locations)
Note: It should be clear from the problem statement that just because a species is not mentioned at a specific location does not mean that it does not exist there. i.e., a sample at a specific location returning only 'A' - 'Bill and Jeff saw a lemur.' - does not exclude the possibility of 'B' and 'C' also at that location, but not sampled. Just because the text may specifically say that Bill and Jeff saw a lemur, and doesn't mention any other flora or fauna doesn't mean we should assume that they are in a universe devoid of anything but the occasional lemur.
Final Thoughts: Ideally, the analysis method would further:

take into account the coverage of the paths, and not assume that (in
the example above) nothing exists in Mexico or northern Canada, just
because there are no samples taken there. Remember that samples can
only be taken along paths.
take into account edges, in this case coastlines. If A, B, and C are
land animals, it does not make sense that a reconstruction of their
distribution would include water, even if their range surrounds a
lake or something.

Sorry for the long-winded explanation. Any thoughts?

I'm voting to close this because it is not a biological question.

This is not a biological question though these kinds of measurements are performed by ecologists. It is mostly about placing sensors and tracking movements. Even if the question was on-topic it is not clear what you want to ask.

I think the question is valid and voted to keep open, even if the background is purely hypothetical and without any direct connection to real-life biology. The problem of inferring species distributions from species occurrences is a common problem in ecology, and this question is dealing with exactly that.

@terdon - so this should be deleted then?

I don't get why this question is closed. Yes, the background is hypothetical, but the actual problem is embedded within ecology and population biology. And to say that this is "only" dealing with methodology does not make sense, as long as we allow questions on sequencing, PCR, BLAST etc, since these methods/lab techniques aren't "biological questions", only methods to observe biological features or to estimate biol. parameters. Which is the case here as well, but this deals with another level of biol. organization. The Q could be reframed though, to put less emphasis on the fantasy parts

The problem of how to infer species distributions from scattered species occurrences is common in ecology, and there exists a number of methods to construct distribution maps. As a start, you should have a look at Species Distribution Models (SDMs) using regressions models or Maxent, and the paper by Elith et al (2009) is a good starting point and a standard reference. SDMs using maxent is now a common approach, which integrates species occurrences as point data along with environmental layers (e.g. temperature, moisture and topography) to predict species distribution maps, and this can also include absence data or "pseudo-absence" data (randomly sampled data from a region of interest). The maxent software is described and can be downloaded here: http://www.cs.princeton.edu/~schapire/maxent/
A common criticism against distributions produced by Maxent is however that they ignore e.g. species interactions, and they only considers the species occurences and the environmental variables that has been included in the model.
In your "Note", you touch upon the issue of detectability, which is an important issue that has received much attention recently. The problem is largest when you only have presence data, and to have real presence/absence data is preferable. Even if you don't have real absenses (the species has been searched for but not found), an estimate of sampling effort in different areas is still very useful, since this means that you can at least evaluate whether absenses is due to "real" absense or lack of sampling. In your case, the movement paths of characters could be used as a measure of spatial "sampling effort". The main issue with detectability in studies of distribution of species trends is if there is trends or bias in detectability, which means that apparent changes over time or patterns in distribution might be due to differences in detectability and not real differences between areas or over time. This could for instance be the case if observers are more likely to spot a species in one type of habitat (open savannah) then in another type of habitat (closed forest). Useful starting points for issues of detectability are Dorazio (2014) (technical though) and Kery et al (2010).


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What is this butterfly?
The following guys (about an inch long) were seen in the Willamette Valley of Oregon in summer.  When one would fly by a resting one, they'd get into a high-speed little "dogfight".  What genus might they be (or species, if you know).  Are they in the "skipper" group of butterflies?

That last picture reminds me of an Underwing Moth. But the clubbed antenna don't match.

Yes, it's a skipper. But I don't know the species.

Yes, it is a skipper (family Hesperiidae) and very similar to European species in Ochlodes, and my guess is that it belongs to one of the North American species in this genus. For instance, it is very similar to Ochlodes sylvanoides (also called Woodland Skipper), which is common in the western parts of the US. However, I'm not familiar with North American butterflies, and there might be closely related similar species that I'm ignoring.
Images of Ochlodes sylvanoides from http://butterfliesofamerica.com/t/Ochlodes_sylvanoides_a.htm:

More pictures can also be seen at Bugguide.net

This led me to open my copy of Robert Michael Pyle's The Butterflies of Cascadia (Seattle Audubon Society, 2002); the species of the question IS Ochlodes sylvanoides, which Pyle illustrates on Plate 4 (page 81), and discusses in full (with further pictures) on pages 99-101; the range map provided on page 99 is a solid mass of blue (which means the species is found throughout the region Pyle covers).

A late addition to my comment above: Pyle also illustrates Ochlodes sylvanoides on Plate 3 (page 77), and covers two additional species of the genus; the range maps given for both of the latter have no blue in Oregon's Willamette Valley.


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How would you use readthrough as part of a genetic circuit design?
Traditionally, in synthetic biology, researchers tried to avoid some transcription phenomena (like roadblocking of tandem promoters or readthrough of weak terminators) since they are not in line with the discipline's strive to design modular, digital genetic circuits. However, some researchers have started using these "problems" as part of the intended design (see Bordoy et al., for example).
How do you think transcriptional readthrough could be used as part of a genetic circuit design? When would you want to have a readthrough? What kind of logic or function would this emulate?

Readthrough has already been used to implement transcriptional NOR gates, wherein tandem input promoters express a repressor that represses an output promoter. (First time I recall here: 21150903, used widely here: 27034378, roadblocking modeled here: 32141239.) An advantage of this design is that the repressor need only be encoded in DNA once, which can significantly reduce the DNA footprint of the design and the likelihood of recombination if the repressor's DNA sequence is long (e.g., protein-based repressors). OR gates have similarly been implemented as two tandem promoters expressing a common output gene. (An alternative NOR design—which is common with repressors with short DNA sequences (e.g., sgRNAs)—is to duplicate the repressor and express it separately from both input promoters. This approach circumvents the roadblocking and input asymmetry that can occur with tandem promoters.)
Readthrough has also been used with antisense promoters to tune gene expression (see 26769567). In these designs, an input promoter must read through a downstream antisense promoter, and the strength of the antisense promoter can be used to tune the response of the input promoter.
Another application that comes to mind is encoding the relative ratio of expression of multiple genes by separating them with weak terminators (e.g., to achieve X-fold expression of the first gene relative to the second). This begins to evoke an operon, as jakebeal notes. The closest example I can think of comes from this paper: 23727987, although they actually used readthrough to address the inverse problem of characterizing terminator strength.

I think this is an interesting proposal to try to turn a problem into a benefit.
What you are considering is conceptually similar to the organization of an operon, in which multiple genes are controlled by a single promoter, with multiple ribosome binding site (RBS) entry points for translation, and read-through can certainly occur in these cases too. Structurally, this would be the same behavior, except that the entry points are promoters instead of RBSs.
At a logical level, in effect the second promoter ends up implementing one of two functions:

If it is positively regulated, then it would be an OR, activated either by its own transcription factor or read-through from the 5' sequence.
If it is negatively regulated, then it would a NOT IMPLY, activated by the 5' sequence, but dominated by its own repression, since steric repression mechanisms will tend to block the read-through as well.

There are lots of potential concerns regarding signal strength of the read-through, but if one wanted to make use of this mechanism there is no reason to think they would not be susceptible to engineering.

Exactly. So how stochastic is the readthrough? Is there anything analogous to electrical engineering? How/when it is used in electrical engineering? Is there a logical equivalent for transcriptional readthrough?

I think the closest analog would be wired logic gates, though that's not asymmetric like read-through is. I wouldn't worry too much about the stochasticity, though: the promoter is stochastic too, so one would just want to appropriately match their levels.