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What is the name of this sea creature?
I found this creature on the beach in San Diego. It is 8cm long and the end to the right is the mouth. The underside is exactly the same as what is visible. What is the name of this species.

This animal is a sea cucumber. It is probably a "sweet potato" sea cucumber (Molpadia arenicola). Here is a useful link describing this animal with pictures quite similar to yours:
https://mexican-fish.com/sweet-potato-sea-cucumber/

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

@tyersome I have a question about the accepted behaviour in this site. If an answer is correct but very short like this one are we supposed to edit the answer with photos and references or should we write a new answer?

@trinitrotoluene — I'm not sure there is a clear standard, but anything that results in a better answer is good. Constructive editing is always acceptable (and your suggestions will be reviewed). I would personally give the original answerer a day or so to respond and then post a better supported answer if they don't. You could also ask about the etiquette for this in the [chat] or post a question on [meta]. I had a quick look in the latter and didn't find anything related, but I could easily have missed something ...

@tyersome thank you for the insight. This was the most relevant answer i could find on meta. It seems it is best to discuss such changes with op in comments before editing.

@trinitrotoluene For an answer as short as this one, don't feel bad about adding a proper separate answer that includes citations and an explanation. For a longer answer that's just missing a citation you could comment or edit first, but it's also not a problem to write a new answer. We expect most answers here to be cited (some very basic biology that you would find in a "bio 101-like" freshman textbook probably doesn't need a citation, but I usually add a note to answers of mine like that to check a basic textbook, or at least link to wikipedia).

Thank you for editing, but please add a discussion of the features that lead you to this conclusion and upload at least one supporting image. If you do this, the banner can be removed from your answer and you will receive at least one upvote (mine). Thanks!


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Help identifying plant
I saw this plant during the summer in Yorkshire, in the north of England. It was found near in a lowland area not too far from a river, but not in a boggy / marshy place. I’ve also seen them ok roadside verges as well.
I think it’s possibly related to a Lily, but I’m not sure at all about that.
Does anyone know what species this might be?

This plant is a bellflower. Either a Campanula Takesimana or a Campanula Alliariifolia

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In a skeletal muscle contraction, what happens after ACh binds to the nicotinic iontropic receptors on sarcolemma?
Does the bound ACh becomes unbound and then gets hydrolysed by acetylcholinerase?

Acetyl choline, which is released at the neuromuscular junction is continuously broken down by the enzyme acetylcholineesterase into acetate and choline. Choline is once again taken up by the neuron through choline carriers to regenerate acetylcholine. This process continues as long as an the neuron is stimulated.
Source:
Wikepedia

That's correct, acetylcholineesterase is a hydrolase (An enzyme which hydrolyzes choline esters (Such as Acetylcholine).

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


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


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Is grip force a reflex?
When we reach for an object, for example, a cup, is the force used to hold it a reflex? Which sensorial information is used to select the force to hold it?
Why I am interested in this question

With the development of robots with dexterity, it is necessary to develop a minimal amount of sensors so they can choose the strength to hold an object. Objects that look heavy and slippery need more force, while objects that are delicate need a lower force. Do we unconsciously use visual information to decide the force to hold an object? Can this be called a reflex?

When we reach for an object and it feels painful to hold it (it is too hot or too sharp) we immediately release it, is that a reflex?

In my search I found mostly results about the grip reflex of newborns. Is it Completely lost in adults?

(a personal reason) recently, I noticed that my grip force calculation is kind of “uncalibrated”. I am dropping cups, tools, my cellphone, more frequently than before. However this is not a problem of grip Force or shaking, I can hold myself on a bar with one hand and I have zero hand shaking on my hands. So, when I consciously choose to hold it, I have force, but when I am not thinking of which force to apply, I drop things. Note: this question is not for self diagnosis, this is just the initial observation that sparked my interest in the question.

Seems more like a feedback loop than a reflex.  That is, the grip force is adjusted depending on the weight & texture of the object.  That is, when you hold an empty paper cup, a full on, a ceramic mug, or a mug used as a container for nuts & bolts, you automatically use feedback to control how much force to apply.  And you can do this with your eyes closed, so visual information isn't the primary source.

holding an object is usually a task that requires visual and mechanical processing (i.e. what the object looks like (i.e. what material does it seem to be made of, what is your former experience with that material, how heavy does it feel) and muscle memory.
according to the physiological definition of a reflex:

Reflex, in biology, an action consisting of comparatively simple segments of behaviour that usually occur as direct and immediate responses to particular stimuli uniquely correlated with them.

according to this same source, innate reflexes such as walking, blinking and swallowing require skeletal muscles but are still considered reflexes despite the fact that for some of these tasks (such as walking and standing) we do not know from birth (meaning reflexes can be taught and unlearned/lost).
There are other reflexes such as intestinal smooth muscle contractions etc... that we are usually completely unaware of and are controlled by the central nervous system (CNS) unconsciously.
The response to pain is also a reflex; the thermal/mechanical neural sensors in your arm (for example) send the information to your spine which directly sends a signal to your muscles to contract in order to avoid/release the object.
the palmar grasp reflex is one of many reflexes babies have that they do not need to be taught. Adults usually unteach these reflexes as some of them are not as frequently necessary in later stages of life. Newborn apes for one use the palmar grasp reflex to hold on to their mothers (it is possible that is where that reflex came from from an evolutionary standpoint).
consider that all reflexes are caused by cues that your nervous system senses and responds to. Some of these reflexes can be controlled and others not and may vary depending on your environment. A famous example of this is the pavlov's dog experiment which proved that you could also be conditioned to respond to a certain stimulus. In your case, seeing or feeling the cup is supposed to provide a stimulus to your brain reminding you that you are holding an object that requires a specific mechanical maneuver which you have learnt over time.


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Is this a termite wing or flying ant wing
I saw this on the bottom corner of my pantry in the Washington DC area. I can't tell whether is termite wing or something else. The wing is 3/4" long.

I agree it is a great photo but as a person who has had both problems, can you give more details, inside outside any debris ? And where in the world are you! In the Pacific Northwest I can say yes it is!!! Oops not much info so my answer oops comment could be?

If you don't find an answere here find an entomology forum or "what's this bug" because the ID is very specialized entomology.

FYI the Comstock-Needham system might be useful here.

This appears to be the wing of a crane fly (Tipulidae).  Using this figure you can begin narrowing down the possibilities for wing venation. Searching diptera wing venation, I think, brings up this excellent diagram (see bottom left for Tipulidae) which quite closely matches your photo if rotated in a graphics program (GIMP):

 Wing photo from OP paired with wing outline image copied and rotated from Batsdiet.com
You could likely drill this down further by searching Tipulidae venation or the like on Google Scholar, which pulls up many papers with detailed information on various regions and taxa of crane flies.

You might further cite evidence that crane flies have wings this size. For example, quickly Wikipedia suggests they can range from 1-6.5(11) cm, which safely includes the size of the OP's specimen. You might also note that crane flies are present in DC.


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Myelination of 1st Order Neurons in Spinal Cord Ascending Tracts
When a 1st order sensory neuron enters the Dorsal Column Ascending Pathway (i.e. Spinal Cord), does it get its myelination from Oligodendrocytes (as inside CNS) or it retains Schwann Cell myelination?

Is anyone at least up for a discussion?

Welcome. I think this is a great question. What have you found so far?

I haven't come across any text addressing this issue. But I think when the 1st order neuron enters the spinal cord it should retain Schwann Cell myelination (Considering Embryological Origin). But it contradicts with the statement that inside CNS oligodendrocytes myelinate Neurons. :(


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Tree Identification - California Bay Area
I've seen these trees in the Bay Area in Mountain View and Fremont, and have been searching for different pine tree varieties that have wider canopies. Does anyone here know what trees these are, they are very beautiful.

Here is the link to the exact location where I saw them recently:
https://goo.gl/maps/NSfAXZSgzypWXKqj9

Welcome to Biology.SE! Identifications questions should include clear closeup photos of the organism (photos from multiple angles if possible) — for trees please include pictures of the bark, leaves/needles, and any reproductive structures. Habitat information and an estimate of the size of the organism are also helpful. Please [edit] your post to include this essential information. ——— You may also benefit from taking the [tour] and then going through the help pages starting with [Ask] questions effectively on this site. Thanks!

For California trees, my go-to is A Californian's Guide to the Trees Among Us by Matt Ritter (Heyday, 2011).  California trees can be challenging due to the extremely varied habitat and many introductions over the years.
Your trees appear to be younger specimens of Pinus pinea or the Italian Stone Pine, based on the description on page 14 in Ritter. No other conifer in the book matches better.  Going to Wikipedia the description also seems to fit, in particular they mention "...in youth it is a bushy globe..."  There is also good information at Kew where I found this image, which looks to be very similar to what you observed.
Of course, if you can visit the location again you can check for needles in pairs, and orange-brown scaly bark.

Yay, this is perfect! Thank you for the book link - checking out!


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Can 'human' become a genus due to space colonization?
I have read that during the Second World War, some mosquitoes got trapped in the London underground railway system. The mosquitoes never got out and eventually they became a new species by themselves.
I had a similar thought. In the next few centuries, if humans could, in theory, colonize other planets like Mars, Proxima Centauri and beyond, then the environments there are not the same as Earth. So, in the long term, humans who would be born and who would grow up on Mars, for example may become more and more suited to Martian conditions than Earths.
Now, when early humans explored and ventured into new geographical areas, they did change characteristics, but we are still one species Sapiens. But living extraterrestrial, is a whole new thing. The gravity alters, the entire atmospheric composition does. So that is going to have some significant changes on humans.
So, my question is: is it possible that in millions or even billions of years, if humans expand to space, there may arise separate species of humans? And would this new emergence of human species actually result in humans moving one step up the taxonomical ladder: becoming a genus?
EDIT: To avoid confusion and create speculations at the answers, I should specify that I am talking about a very particular case: if Sapiens are living in different planets, then is there a chance that Sapiens will become a new genus, and that Homo can be taken one step higher in the taxonomical order? There would still be Sapiens on Earth, but considering the environmental changes that could happen here too, humans then can be drastically different from humans now. So the question is: can 'Sapiens' become a genus?
Thanks to @tyersome and @jamesqf for pointing this out.

Welcome to Biology.SE! Thank you for taking the [tour], but please also go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, questions must be clear — how are you defining "human"? I would say the genus Homo is equivalent to "human" in which case your question is trivial. In addition, as written your question is speculative and thus will generate opinions rather than factually based answers — this makes the question off-topic as currently written. Thanks!

Human, or in Latin, "Homo", already IS a genus.  It's just that the other species in the genus -  Homo habilis, Homo erectus, Homo neanderthalensis, &c - have died out.

@tyersome thanks for the note, I edited it.

Define "species". IIRC there's been research that has shown that there's a bigger genetic difference between white and black people than there is between dogs and wolves, and there's a gigantic amount of physical variation between different breeds of dogs, who are all considered one species.

@nick012000 I don't know about the difference compared to wolves/dogs, but there is significantly more diversity within each human "race" than there is between "races", which is to say that any two black people or any two white people are generally more different than the average of all white people are from the average of all black people (and the same is true of all "races"). All that is to say that there is not much genetic difference between black people and white people

@KevinWells My point is that the definition of "species" is basically arbitrary and there's no concrete way to tell whether or not two distinct populations are different species or not.

@nick012000 does not a common definition of species require that mating between Earthling and Martian could not produce fertile offspring?

@MatijaNalis Dogs, wolves, and coyotes are all considered different species and they can produce fertile offspring.

@nick012000 Dogs and wolves are not considered different subspecies, dogs are just a domesticated sub-species. You are right about coyotes though, they are considered a separate species, but can interbreed with wolves. It's possible that they should therefore be considered sub-species, but it really just shows how complicated species distinction is

The concept you are referring to is speciation and it has been well studied in a wide variety of different natural organisms. I suppose here we are talking about the biological species concept.
The overall answer is yes it is possible, but critically depends on a few different factors. The reality of speciation in the wild is very complex, but these are some things to consider:
Genetic isolation
If two groups, such as your Martian colony and humans on earth isolate from one another, then for speciation to occur, there needs to be a significant level of genetic differentiation between them. This means substantial differences in the kinds of genetic variants found at positions along the genome.
Genetic differences are eroded by post-isolation gene flow – in your example, that might mean a spaceship flying back to Earth with Martian colonists, who then have offspring with people on Earth.
Although there is plenty of evidence that speciation with gene flow can occur, the general rule of thumb is that increased gene flow means a longer divergence time is required to fully speciate.
In nature, this is often caused by some kind of geographic barrier to gene flow, such as mountains or rivers forming, but it can also be caused by morphological differences, such as variation in sexual appendages. Of course, in our example, this barrier to gene-flow would be the large and difficult to traverse distance between the Earth and Mars.
Divergence time
You alluded to some kind of separation time, and you are right to be talking on the scale of millions of years. Speciation can occur extremely quickly; in Lake Tanganyika cichlids, it has occurred probably within the last 15,000 years. Humans have created whole new species of crops, such as maize, within the past 10,000 years. There is even evidence of some fish speciating in 3000 generations.
However speciation is often a much longer process. For example humans and chimps were thought to speciate in 4.5 millions years.
Of course, there is an interaction with several other factors. All other things being equal, less post-isolation gene flows results in a shorter time to speciation and vice versa. Stronger selective pressure between the different environments leads to a more rapid accumulation of genetic differences.
As Konrad Rudolph correctly points out, divergence time is strongly related to generation time, with all other things being equal, a shorter generation time, results in faster speciation.
Selection pressures & differing environments
I think the last main factor governing speciation is how different the Martian colonists environment was from that on Earth.
Different environments can lead to natural selection occurring in opposing directions in the two populations, leading to ecological speciation. Speciation can proceed without differing environments, where neutral drift in allele frequencies can eventually cause speciation, but this will be a long process.
Speciation will occur much more rapidly if there is a start difference in environment and selection pressures between the two groups.
So in conclusion, given enough time, genetic isolation and differential selection pressures (or some combination of the above), it is plausible that a new species of human could form. However, given the time-scales required, it seems a bit unlikely to me.
EDIT
I think it is worth pointing out what @Jaquez said in the comments. If current terrestrial humans split from an extraterrestrial source to form another species, it would be named as another species within the Homo, such as Homo extraterrestrialis, for example. The addition of a new species does not move the group Homo up to become an e.g. Tribe or Family.

Your answer currently implies that speciation time is the same for all species. This is very crucially not true, it depends on effective population size and generation length. The former is small in humans and the latter is very long, both of which imply that splitting into separate species will take much longer for humans than it takes for cichlids or maize, independent of selective pressure.

Which part of the answer do you think implies that? It wasn’t my intention.

Yeah, I didn’t think it was intentional. But the paragraph under “Divergence time” reads as if the numbers from cichlids and maize could be used as a proxy for humans (or rather, they could if it weren’t for “natural” vs artificial environments — which anyway only applies for the maize example, not for cichlids). That said, the 3000 generations you cite sound about right as a (very rough) ballpark estimate.

Right, I understand. In hindsight that was quite a tangential point and potentially confusing, thanks for noticing it.

Excellent answer, +1.  However, I feel it would benefit from clarifying that speciation would not, as the OP asked, move either Homo or sapiens up the taxonomical ladder.  It would result in a new species within Homo, for example Homo extraterrestrialis.

I do not believe it will happen.  There are multiple roadblocks:
First, speciation time is measured in generations, not years.  The human generation time is long, the 3000 generations mentioned in another answer for a fish translates to nearly 100,000 years.  Are human populations not going to interbreed over a time span that long?
Second, the speed of speciation is a function of the evolutionary pressure.  We radically alter our environment and change the whole driving force--genes which make one more or less able to survive the rigors of the environment have almost no effect anymore.  To the extent that human evolution will occur it will be mostly towards things that favor reproductive success--things which attract mates, a desire for children, contraceptive unreliability.  These things aren't going to be substantially different on Mars than on Earth.
Finally, we are already to the point that we can make designer babies to some degree, although we can't yet do it with the sort of reliability needed to ethically do it on humans.  I find it inconceivable that we can remain a technological species (as would be required to have a population on Mars) without reaching the point that we can freely rewrite the genetic code at least during reproduction.  If there is a speciation event it will come from the lab, not evolution.  It's possible that some day there will be a modification developed that is a substantial upgrade but which is not compatible with existing humans--those with the modification can only breed with others that have it.

Indeed. For such a speciation to occur, we had to first terraform Mars to a degree where a non-technological human population can survive, and then we would need a total societal collapse on both planets, so that space travel would become impossible for a long long time. But even then, in those 100000 years humans would either rediscover technology and space travel, or die out.

"is it possible that in millions or even billions of years" - so definitely.  Chimps and Humans diverged 5-7 million years ago.  As for @vsz, that's not true.  You would just need to have limited interaction.  If you are imagining societies with regular flights between the planets then maybe not.  But even on Earth we get 'ring species' that can interbreed at the boundaries while populations at the ends cannot.

@JasonGoemaat A requirement for speciation is that you have populations that do not interbreed.  That means a lack of mobility.  I'm questioning how you could have a population on Mars that for a vast period of time doesn't interbreed with the population of Earth.  If they fall too far for spaceflight they also fall too far for survival in the Martian environment.  And that doesn't even address my other points.

As others have noted, the key concept is speciation. Imagine some H. sapiens living on Mars. How are they going to breathe? Presumably we have a nuclear reactor generating power, which in turn is used to make oxygen. What is it breaks down? Those who can tolerate low oxygen levels might do better.
Here on Earth we invest a lot of energy in building bones and things to resist gravity. On Mars there may be less need to do this, and more need to be efficient with oxygen and tolerate higher levels of CO2. So some mutations that would be sub-optimal on Earth might be beneficial to the colonists.
Couple this with isolation, as others have mentioned, and the two populations may drift apart, leading to the eventual emergence of H martiansis (or whatever.).

A driving force producing natural selection is not required for speciation.  Separate two identical populations and give them identical environments and they will eventually diverge due to random changes in the genome.  One of the main factors causing this is in the proteins in the coating surrounding the egg.  They are like a lock that sperm have the key to.  The selective pressures preventing change are simply that a male cannot reproduce if it cannot find a female with compatible proteins. Small changes aren't a problem, but the drift over time would lead to speciation with no other changes


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What do spider digestive fluids look like?
What is the general appearance of the fluids that spiders use to digest their prey before they ingest it into the body?

In most species of spiders, this liquid is thick and brownish (Brown)
This digestive juice helps spiders to feed of prey even larger than spiders.


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The fraction of the genome that is evolutionarily conserved through purifying selection is less than 10%?
I would appreciate help in understanding the meaning, logic, and, in particular, how to interpret the phrase:

The fraction of the genome that is evolutionarily conserved through purifying selection is less than 10%

I could ask numerous question regarding the biology (including what happens to the rest of the genome, and positive selection) and formal logic of this statement, but maybe I could impose, and just leave it to whomever kindly replies.
This remark comes from the abstract of Grauer & al. "On the immortality of television sets: "function" in the human genome according to the evolution-free gospel of ENCODE"
And the Abstract itself:
A recent slew of ENCyclopedia Of DNA Elements (ENCODE) Consortium publications, specifically the article signed by all Consortium members, put forward the idea that more than 80% of the human genome is functional. This claim flies in the face of current estimates according to which the fraction of the genome that is evolutionarily conserved through purifying selection is less than 10%. Thus, according to the ENCODE Consortium, a biological function can be maintained indefinitely without selection, which implies that at least 80 - 10 = 70% of the genome is perfectly invulnerable to deleterious mutations, either because no mutation can ever occur in these "functional" regions or because no mutation in these regions can ever be deleterious. This absurd conclusion was reached through various means, chiefly by employing the seldom used "causal role" definition of biological function and then applying it inconsistently to different biochemical properties, by committing a logical fallacy known as "affirming the consequent," by failing to appreciate the crucial difference between "junk DNA" and "garbage DNA," by using analytical methods that yield biased errors and inflate estimates of functionality, by favoring statistical sensitivity over specificity, and by emphasizing statistical significance rather than the magnitude of the effect. Here, we detail the many logical and methodological transgressions involved in assigning functionality to almost every nucleotide in the human genome. The ENCODE results were predicted by one of its authors to necessitate the rewriting of textbooks. We agree, many textbooks dealing with marketing, mass-media hype, and public relations may well have to be rewritten.
Thanks

Fine. I’ve deleted.

So basically you want someone to explain the ENCODE position that DNA can be functional without it being subject to purifying selection, carefully defining functional conservation and purifying selection and the level (base or greater) that they apply. With examples. I think this is a good question and hope you will get a good answer. Methinks Grauer et al. protest a little too much. One doesn’t imagine they have made a great effort to understand the other point of view. But I may be doing them an injustice.

@David On the most basic level, I'm stuck trying to understand their verbiage. Conserved = kept, through purifying selection = discarded. So I don't understand how they line up. Then, less than 10%, so what about the other 90+% and positive selection; or is that irrelevant to their assertion?

I will try to tackle the terminology first

Conserved: That remains identical (or at least very similar) across species.

Purifying selection: Is one of the possible forces that lead to conservation of important sequences of DNA, by removing deleterious alleles.

So, the phrase simply means that the proportion of the genome that is very similar in sequence with the genome of other species (i.e. evolutionarily conserved) is less than 10%.
This is the answer to you question. Then, I just want to add that I share David's view on the abstract.


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Where can we see professional discussions about vaccine development of the covid-19?
Is there any place where people keep talking about the vaccine development professionally? I need the
latest news.

Private companies, not quite open science.

oh...how about relatively professional？Guys with strong biology background, but not work in vaccine companies.

Please see Biology Meta for a question and answer giving various sources of information about coronavirus. However the links provided are to information not chat.

The New York Times maintains a decent vaccine progress tracker: https://www.nytimes.com/interactive/2020/science/coronavirus-vaccine-tracker.html
I also follow Derek Lowe's In The Pipeline blog: https://blogs.sciencemag.org/pipeline/
(It is not purely coronavirus-focused, but it has a lot of good information, and cites sources that you can go to for even more detail)


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Why do dragonflies lose all of their coloration once they die?
At 06:43 in The Secrets of Nature video Sky Hunters, The World of the Dragonfly - The Secrets of Nature the narrator says:

Scientists have been collecting dragonflies since the eighteenth century, but there’s always been a difficulty. Dragonflies quickly become deathly pale, they lose all their color. That’s why collectors have usually preferred to concentrate on butterflies...

and an image of rows and rows of uncolored dragonflies pinned to a display are show.
Question: Why do dragonflies lose all of their coloration once they die?
 click screen shots for full size

I have also seen spiders losing colors when they die.

This is probably because the color in dragon fly wing is due to chitin crystal and which is protected by some secretion over the entire wing something like cuticle upon leaves and when dragon fly dies that secreted substance upon wing washes away when not maintained resulting in shredding off of the color from wing. Sorry I can't comment (<50 reputation) so I did answer even tho im not clear with it.
Try reading this you might find something useful maybe Insect Wing
Also this journal said that while studying the wing of dragonflies they killed and kept them in lab it didnt mention that wing lost color Mechanism of the wing colouration in the dragonfly Zenithoptera lanei (Odonata: Libellulidae) and its role in intraspecific communication
So it might be possible that the video shows dragonflies after some long time maybe a week after death and body is intact because of chitin layer but wings bleached away in sun or degraded in environment.
Also wings have supply of veins so something related with continuous production might be cause of that thing too.

Dragonfly wings are usually transparent, or at most have brownish patterns.  (At least in the North American species I see flying around - the species in the link is apparently an exception.)  It's the body that is often brilliantly colored.

Oh thanks for the information :)

@jamesqf here are some bright red wings! Identify these two big, beautiful dragonflies in Taiwan?

@uhoh: Well, I did say usually :-)

@jamesqf yep! But I was so excited to see such deeply pigmented wings I had to tell somebody :-)


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How close is the U.S. to herd immunity, assuming long-term immunity?
Assuming:

infection always results in death or immunity (unproven, but no evidence of repeat infections yet)
official COVID-19-related death counts are accurate (142k at the time of this question)

How close is the U.S. to achieving herd immunity to COVID-19?
The CDC has published estimates of infection rate, mortality rate, etc. However, I haven't yet seen anyone actually do the math of how close the U.S. is to herd immunity.

You need to infect 60-80% of the population. So: Far, far (any many deaths) away.

I’m voting to close this question because it is not about biology in the terms of SE Biology but a request for statistical information about the medical state of the population in a particular country which will be out of date next week.

You are very welcome to SE Biology, but please read the [tour] where you will find what sort of questions are suitable here. There is a list of sources of information about coronavirus in answer to one of our Meta questions, or your question may be more acceptable on SE Medical Sciences.

@David I understand your criticism, but you are applying it very inconsistently, as many other answers are tied to particular "current" timeframes and events. https://biology.stackexchange.com/questions/94024 https://biology.stackexchange.com/questions/90793

I am not applying it inconsistently, thank you. I voted to close each of those questions and downvoted them. I was responsible for the Meta post (later adopted as a Community post) aimed at deflecting such posts in a more appropriate direction. The fact that sufficient others did not support me makes no difference to whether or not my view is correct. My reading of the Tour and Help for this site gives me no reason to believe it is not.

The CDC estimates R0 to be 2.5, meaning that (2.5-1)/2.5=60% of the population must be immune to achieve herd immunity.
(That is, under 60% immune and the # of cases will increase; over 60% immune and the # of cases will decrease.)
The estimated IMF (infection mortality rate) is 0.65%.
So 60%*0.065%=0.39% of a population will die to reach herd immunity.
To date, 142k people in the U.S. have died from COVID-19, out of a population of 328M. So 142k/328M=0.043% of the population has died.
Thus, based on reported deaths, the U.S. has 11% of the required infections/immunity to produce herd immunity.

Note that this assumes that high- and low-risk individuals are exposed at the same rate. If more of these infections happen among low-risk individuals, the effective IMF is lower, yielding fewer deaths to produce herd immunity. And the inverse is also true.

I am curious why you are using the SE Q&A format to post your calculations on SE Biology.  Would I be allowed to tell Stack Overflow about the current stock market price of computer chip companies or the percentage of European networks that depend on Huwai?

Paul, perhaps you should generalize your question, e.g. to be about how one can find out how close a country is to reaching herd immunity.  Then your answer can be modified a bit to explain how to calculate and use current U.S. numbers (showing how they were found) as an example.

@mgkrebbs I feared that would be too broad. FWIW, StackOverflow would be an odd choice for your computing cost question, as SO is  focused on software, but people can and do ask such questions on ServerFault.


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types of cells in a pharyngeal specimen
I would like to ask what type of cells should someone expect in a pharyngeal smear, in a person, who is infected with a viral infection. Thank you a lot!

I’m voting to close this question because it seems to be a medical question rather than one primarily about biology. This means it is not on-topic for this site. While this might be a better fit for [MedicalSciences.SE], please don't repost (instead request migration). Please consult the [tour], [ask], and other [help] pages for more information.  Thanks!

The tissue in the pharynx include:
Stratified squamous epithelium & mucus-producing glands.
However other cells that could be found would be other types of bacterial, is this what you're referencing?
Commonly scientists start with a gram stain to determine the classify the bacteria.
Gram+ bacteria have cell walls composed of thick layers of peptidoglycan. Gram+ cells stain purple when. Gram- bacteria have cell walls with a thin layer of peptidoglycan. Gram- bacteria stain pink.
The microbiome of a human consists of 100,000 billion bacteria. Therefore there are many types. E.g. Prevotella has been shown to be the most common type of bacteria in the human pharynx.
In a pharyngeal smear you would expect to find Stratified squamous epithelium, mucus-producing glands, bacteria and if a virus is present. Viral particles. This can be determined by RNA or DNA analysis.
E.g. COVID-19 is an RNA virus. If PCR analysis was completed on a sample obtained from a pharyngeal smear then we could confirm the presence of the aforementioned mammalian cells, bacteria and viral genetic material.

should someone expect lymphocytes?

@Marilu, lymphocytes continuously circulate between the lymph and blood until they encounter a foreign antigen. It would be possible, but it's usually not the aim of a pharyngeal smear. A blood test would provide better results to identify how 'hard' the immune system to working.

thank you so much!

Happy to help Marilu.


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

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

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

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

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

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

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

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

However, Lyttle goes on to describe

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

Jaenike (2001) says

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

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

As for your final question,

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

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

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

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

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


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is there a limit to how much humans can taste?
kind of a weird question, sorry, but i was wondering--is there a threshold at which our taste buds become overwhelmed? if i, say, put some supersweet compound in my mouth, would there be a point at which adding more compound would not increase the level of sweetness i perceive? i'm sure that if i experienced too much sourness or spiciness, my tongue would probably go numb, but what about sweetness and bitterness? and what is that amount? does it vary from person to person, or are people's opinions on different sorts of food just preferences, and the threshold at which they become unable to process more of a specific taste the same for everyone?
thank you. i hope this makes sense.

Have you done any research by yourself?

no, i felt like i couldn't word my question such that a search engine would understand.

Yes, there is a threshold of taste.
According to this article

The taste system encodes information about the quantity as well as the identity of stimuli. In general, the higher the stimulus concentration, the greater the perceived intensity of taste. Threshold concentrations for most ingested tastants are quite high, however. For example, the threshold concentration for citric acid is about 2 mM; for salt (NaCl), 10 mM; and for sucrose, 20 mM. Since the body requires substantial concentrations of salts and carbohydrates, taste cells may respond only to relatively high concentrations of these essential substances to promote an adequate intake. Clearly, it is advantageous for the taste system to detect potentially dangerous substances (e.g., bitter-tasting plant compounds) at much lower concentrations. Thus, the threshold concentration for quinine is 0.008 mM, and for strychnine 0.0001 mM. As in olfaction, gustatory sensitivity declines with age. Adults tend to add more salt and spices to food than children. The decreased sensitivity to salt can be problematic for older people with electrolyte and/or fluid balance problems.

Interestingly,

In fact, all of these tastes can be detected over the full surface the tongue. However, different regions of the tongue do have different thresholds. Because the tip of the tongue is most responsive to sweet-tasting compounds, and because these compounds produce pleasurable sensations, information from this region activates feeding behaviors such as mouth movements, salivary secretion, insulin release, and swallowing. In contrast, responses to bitter compounds are indeed greatest on the back of the tongue. Activation of this region by bitter-tasting substances elicits protrusion of the tongue and other protective reactions that prevent ingestion

And in most of the individuals, this threshold is same for both right and lefts parts of the tongue.
Reference
Now as stated by the first article, taste threshold depends on the age of the individual.
More interestingly, it also depends on the individual's state of mind, i.e. whether depressed or anxious.

Circumstances in which serotonin (5-HT) and noradrenaline (NA) are altered, such as in anxiety or depression, are associated with taste disturbances, indicating the importance of these transmitters in the determination of taste thresholds in health and disease.

Measurement of taste function in healthy humans before and after a 5-HT reuptake inhibitor, NA reuptake inhibitor, or placebo showed that enhancing 5-HT significantly reduced the sucrose taste threshold by 27% and the quinine taste threshold by 53%. In contrast, enhancing NA significantly reduced bitter taste threshold by 39% and sour threshold by 22%.
Reference

Hence threshold value varies from substance to substance as well as from individual to individual.
Here is a good article giving threshold values of different chemicals in various food items.
Hope all your questions are solved :)

thank you so much!!!!

@mye Welcome to Biology SE. You should always give an upvote atleast or accept the answer, if you are satisfied with the answer; so that it will encourage other users to answer your questions


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Absence of cytoplasmic Intermediate Filaments in Arthropods
Cytoplasmic intermediate filaments such as vimentins support the architecture of the cell and have been known to aid signaling processes. However, as in this article, it is stated that out of all eumetazoans in Kingdom Animalia, only arthropods do not contain such structures. How is this possible? Are there any replacements to the conventional intermediate filaments present in cells? Do arthropods have special cellular behaviors or signaling networks to correspond with this absence?

It is stated that out of all eumetazoans in Kingdom Animalia, only arthropods do not contain such structures.

I found this paper(1), eliciting an exception (within an exception)- Isotomurus maculatus:

Here, we report the first evidence for the expression of a cytoplasmic IF protein in an arthropod - the basal hexapod Isotomurus maculatus. This new protein, we named it isomin, is a component of the intestinal terminal web and shares with IFs typical biochemical properties, molecular features and reassembly capability.

I would suggest you to read the paper, for more information.

How is this possible? Are there any replacements to the conventional intermediate filaments present in cells?

Both electron microscopy and molecular cloning studies have been unable to detect any cytoplasmic IF protein in these organisms, although they do express a nuclear IF system made of authentic lamins. Other cytoskeletal components have been proposed to have assumed, in arthropods, the mechanical functions that are usually played by cytoplasmic IFs in other organisms. For example, wing epithelial cells are stabilized in insects by a cytoskeletal array consisting of parallel bundles of 15-protofilament microtubules and actin filaments.

Do arthropods have special cellular behaviors or signaling networks to correspond with this absence?

I am not sure if this is what you might be looking for, but the Delta/Notch signalling, which may be involved in posterior elongation in arthropods, does not require IF's.(2)

The Notch cascade consists of Notch and Notch ligands, as well as
intracellular proteins transmitting the notch signal to the cell's
nucleus. The Notch/Lin-12/Glp-1 receptor family was found to be
involved in the specification of cell fates during development in
Drosophila and C. elegans.

1- https://bmcbiol.biomedcentral.com/articles/10.1186/1741-7007-9-17
2-https://en.wikipedia.org/wiki/Notch_signaling_pathway#Mechanism_of_action


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Why do some karyotype graphs contain 46 pairs of chromosomes?
The human genome consists of 23 pairs of chromosomes. Two copies of each pair connect to each other at the centromere. Normal karyotype graphs should look like this:

But some karyotype graphs contain 46 pairs of chromosomes, such as this one:
Why is this the case?

They both contain 23 pairs of homologous chromosomes (and... yes as Luis suggested the first one is male and the second one female).
In Figure 1 each chromosome is composed by 1 chromatid, while in Figure 2 each chromosome is composed by 2 chromatids. This is probably because the two pictures were taken at different stages of Mitosis.
In Figure 1 the picture was taken probably in anaphase, while in Figure 2 was probably taken in or before metaphase.
You might want to search the internet to check the difference between chromatids and chromosomes and to read something about the cell cycle and mitosis.


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How do we know that selective agonists are indeed selective?
Suppose we know that compound X is a selective agonist of receptor Y, meaning that it binds only this receptor Y and no other. But how do we know this that it doesn't bind some another receptor? I suppose that screening for the binding strength of a given ligand to all known receptors would be very tedious and not feasible.

Unfortunately, it's really hard in the general sense. Even for FDA-approved drugs with well-characterized mechanisms of action, the binding profiles are incomplete.
For GPCRs, it's you can run your compound(s) against a full panel of many GPCRs. For example, the PDSP (Roth Lab) can test for binding against multiple GPRCs using radioligand binding assays. See: https://pubmed.ncbi.nlm.nih.gov/23235874/, Figure 2 in particular. Most receptor binding assays are competitive, meaning they detect the displacement of known ligands. This is inherently limited because your compound could bind to a different site -- even a novel site.
You'll notice that in Figure 2, the GABA A receptor was conspicuously missing. One of the reasons is that binding is subunit-specific, which is another complication -- many receptors are oligomers, and it's often hard to prepare them for the assays.
For many well-known enzymes, there are specific activity assays available. These measure the level of a reaction product (often by fluoresence). This of course doesn't rule out binding without activity, and these assays are not available for all enzymes.
Another class of assays measure changes in potential across a membrane. For example, the FLIPR assay for GABA A receptors (https://pubmed.ncbi.nlm.nih.gov/31127604/). These tend to be very time-intensive and expensive, they're limited in the number of receptors, and of course they can't detect binding without activity.
As a last resort, you can use pull-down assays. One of the popular methods is immunoprecipitation (IP). You make an antibody that's selective for your compound and use to cross-link to any protein your compound might be binding to. Then these proteins get pulled out with your compound. These are generally very time-intensive and expensive, and they can need a lot of tweaking. And, of course, they won't detect all proteins your compound might bind to.
It's currently impossible to show that a compound is completely selective. To show that it's "likely" to be very selective, you can expect to invest a year or more for one compound.
But! To take a first stab, you can check out commercial assays offered by Eurofin (ex https://www.eurofinsdiscoveryservices.com/cms/cms-content/services/in-vitro-assays/gpcrs/binding/). They have a GPCR panel and a number of activity assays. Unfortunately their services are quite expensive.

Probably also worth noting that selectivity is always relative. Even research compounds that are used specifically for their high selectivity have some off-target binding, one just hopes that it is negligible at the concentrations used.


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TMB vs ECL for ELISA: which detection method is more sensitive?
I failed to find a comparison, does anyone know which ELISA detection method is more sensitive of these two: ECL, TMB?
Many thanks!

In general, ECL is more sensitive than TMB for ELISA detection. The minimum detection limit of TMB is 60pg/mL and 20pg/mL for ultra TMB [1], whereas the detection limit of ECL can be as low as about 1.7pg/mL  [2].
Resources:

https://info.gbiosciences.com/blog/elisa-substrates-a-selection-guide

https://www.thermofisher.cn/cn/zh/home/life-science/antibodies/immunoassays/elisa-kits/elisa-enzyme-substrates.html


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Activated carrier molecules and their relationship to enzymes
I am reading Molecular Biology of the Cell, and one thing I don't quite get is the difference between an enzyme and an activated carrier molecule. I understand that enzymes lower the activation energy for a reaction, and in that sense speed up the rate at which a reaction occurs. I also understand that activated carrier molecules act as a source of energy that can drive unfavorable reactions (like anabolic reactions) forward. But I still don't quite grasp the exact difference. I was wondering if someone could shed some light on this.

I will focus on the meaning of ‘activated carrier molecule’ as descriptions of enzymes abound. In order to do that I need to introduce two other ideas first. I apologize to the purists for tailoring this to the level of the question.
1. Gibbs Free Energy in Biochemical Considerations
There are different ways of considering energy, and in chemistry one may be used to considering bond energy in relation to a particular molecule. However in biochemistry (which is what this question is concerned with) the focus is on the energetics of overall processes. For example “Are the reactions involved in the synthesis of glucose from pyruvate energetically favourable?" or “How can the synthesis of glucose from pyruvate occur if the overall reaction is not energetically favourable?” Likewise for individual reactions, such as the formation of peptide bonds between amino acids.
For considerations of this sort the thermodynamical concept (Gibbs) Free Energy (G) is most useful. This is because the change in free energy (ΔG) during a reaction (or other change of state) indicates whether a reaction can occur spontaneously. To quote from a useful section in Berg et al.

A reaction can occur spontaneously only if ΔG is negative.

So in the reaction sequence just mentioned, the overall synthesis of glucose from pyruvate (gluconeogenesis) has a positive ΔG and is energetically unfavourable, whereas that of the reverse process (glycolysis) is energetically favourable. And likewise peptide bond formation, not surprisingly, has a positive ΔG and is not energetically favourable.
2. How are Energetically Unfavourable Reactions Accomplished in Living Cells?
The question posed in the heading arises from the fact that gluconeogenesis and peptide bond formation occur in living cells, even though taken alone the core reactions that represent the processes are energetically unfavourable. The answer is given in the title of [section 14.1.1. of Berg et al.]

A Thermodynamically Unfavourable Reaction can be driven by a Favourable Reaction

As already stated, it is the ΔG of the overall process that is important, so if a reaction with a positive ΔG is ‘coupled‘ to one of negative ΔG of greater magnitude, the overall reaction can proceed. For example:
A → B           ΔG =  20 kJ/mol (unfavourable)
C → D           ΔG = –30 kJ/mol (favourable)
A + C → B + D   ΔG = –10 kJ/mol (favourable)

If reaction C → D proceeds alone, the free energy is liberated as biochemically useless heat. If it is coupled to reaction  A → B it drives the latter with the balance being lost as heat.
3. The Role of Activated Carrier Molecules in Energy Coupling
Clearly, any coupled reaction can cause water to run uphill, as it were. But in order to continue one needs to regenerate the starting molecules for the favourable reaction. It is more efficient to specialize this regeneration process by using a limited range of specialist reactions with a negative free energy change. One description of the substrates (reacting molecules) of such specialized favourable reactions is “activated carrier molecules”. Alberts et al. define them as:

Small diffusible molecules in cells that store easily-exchangeable energy in the form of one or more energy-rich covalent bonds. Examples are ATP and NADPH.

Berg et al. also use the term, but describe it in terms of the following examples:

ATP as an activated carrier of phosphoryl groups, because phosphoryl transfer from ATP is an exergonic process (i.e. has a negative ΔG)
Nicotinamide adenine dinucleotide (NAD+) is a major electron carrier in the oxidation of fuel molecules. (Although in this case it is the half reaction involving the oxidation of the reduced form, NADH — or NADPH as mentioned by Alberts et al. — that has a negative ΔG).
Coenzyme A… is a carrier of acyl groups (but it is the transfer of the acyl group of acyl-CoA molecules — e.g. acetyl CoA — with the generation of CoA that has a negative ΔG).

Examples of the participation of such molecules in metabolism can be found in the volume referenced, however I would emphasize that it is the specific reactions of these molecules involving the groups (or electrons) that they carry that is important.
And what about Enzymes?
As the poster stated “enzymes lower the activation energy for a reaction”. They are (generally) large proteins catalysts that have no effect on the ΔG, and they are unchanged at the end of the reaction.
Of course they are important for biochemical reactions, they participate in them, and provide binding sites to bring the substrates and activated carriers in juxtaposition so that they can react. But they couldn’t be more different from the small activated carriers.

@user1136 — Whether a reaction proceeds or not depends on the delta G. Only If you start putting numbers in do you have to deal with delta G0. I deliberately didn’t do that to avoid obscuring the basic idea. If the poster reads the links he can, if he wishes, take things further.

@user1136 — I see what your point is. Because as a result of the reaction proceeding the concentration of substrate and product changes, then the deltaG changes. Thus the action of the enzyme, catalysis, has changed the delta G. I think that is more than pedantry, it's casuistry. I wouldn't try it on a class of undergraduate students though.


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

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

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


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Peak-calling in CLIP: What is the effect of RNA-concentration?
I hope it's ok to repost my question from 8 months ago from StackExchange:Bioinformatics, that is still in beta.
https://bioinformatics.stackexchange.com/questions/10730/peak-calling-in-clip-what-is-the-effect-of-rna-concentration

Question:
I would like to ask how RNA-concentrations influence the diverse CLIP peak-callers in their evaluation of peaks. The peak-callers I would like to understand are: Piranha, CIMS, Paralyzer and the one used in eCLIP (CLIPper). (After weeks of literature research I still can't find an answer!)

More details:
If the concentration of an RNA is too low it can't be cross-linked to the tested protein and no cross-link-peaks will be found, independent on the peak-caller and independent on whether there would be physicochemical interaction hot-spots (peaks). (obviously)
But what is the consequence of increasing the RNA-concentration from a "sufficient", to a high or extremely high level?
Which of the peak-callers will find more peaks on an RNA, the higher it's concentration and which peak-callers could be considered to be robust? (Robust in a sense that the score of the peaks is independent of the RNA concentration. Also the number of called peaks of a particular RNA-protein interaction depends mainly on the number of "real interaction-hotspots" and would not necessarily increase with concentration. )
Also let's assume the interaction frequency/density is quite uniform (no physical hot-spots): Then which peak-callers would almost necessarily start calling (more) peaks, the higher the concentration of the RNA was in the experiment?

Some considerations:
I know that there are many RNAs that don't interact with any proteins (in the databases) and that there are some RNAs that interact basically everywhere throughout their sequence to almost all tested proteins. (Potentially this is observed due to concentration dependencies!)
CIMS & Paralyzer, to my understanding, take the fitted crosslink-induced mutation rate at the specific sites to evaluate peaks. This ratio (mutated/total), in theory seems robust to me.
Piranha, as I understand, tries to fit the raw data to a sum of many individual binomial-functions, basically assuming the bulk of reads as background noise, only evaluating local peaks in read-counts relative to the background. This seems robust to effects of very high concentrations.
I would be thankful for any comments or references!


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My dog and I are wondering: is this a biting midge, or another bug?
A week or two ago, my dog started scratching, and it only increased. Not long after, I started getting bit by something that itches something awful. I thought it was fleas so got some medication and moved my dog out of my room. He stopped scratching immediately. After deep cleaning, I let him back in my room the next day. He shortly thereafter scratched again, but not intensely or frequently. My bites have continued.
I set out a flea trap (water, dish soap, flashlight on the water) and it caught the bug you see in the pic (it has only caught four of them).
Is that a biting midge, or something else?
Also, I'm in New York City.

https://i.stack.imgur.com/GC0iL.jpg -- close-up pic, color and pattern
https://i.stack.imgur.com/CVgnl.jpg -- several from a distance to show size
https://i.stack.imgur.com/rQqp4.jpg -- same one as in the first pic

The size is maybe as big as the hole a small nail makes in the wall, a very small ant, or a freckle.

Please mention which country/region this photo was taken in.

Right. I'm in NYC, so it doesn't make a ton of sense, but I know there is a small presence. I have several houseplants and am on the second floor. I rarely have my window open, but shortly before this started, there was an entire day I kept my window open. It does have a screen, but midges would easily fit. Walking my dog could also be a way to pick them up, i guess

I added a section picture for scale.

Welcome to Biology.SE! Identifications questions should include: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible) — photos must be uploaded (not links) — this is both to ensure the post remains relevant (links can and do break) and for the convenience of other users; 2) an estimate of the size of the organism; and 3) the species-identification tag. Please [edit] your post to include this essential information. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

@tyersome The photos were uploaded to the image hosting service that stack exchange uses.

@Brindle Cruncher, did you actually see the insect biting you or your dog? If not, the itching could be something totally unrelated. (As mentioned, you found these insects in a trap, not on your dog/yourself.)

@adhish I did not, so good point. My dog has stopped scratching like crazy, and my bites have gone away, so totally plausible. I did feel bites happening, but maybe that was in my head. Still curious about the insect identification though.

@tyresome thank you! When I uploaded the photos, they were automatically turned into stack exchange service links. I'll add the other two points.

It seems to be a Yellow-banded polybia wasp (Polybia occidentalis), a species of Potter wasp.

my doubts with this conclusion is that the abdomen of the insect in your photo is quite large compared to other observations of the species. Also, Polybia occidentalis is a species that exists in South and Central America, not up north in New York, Perhaps it is able to exist there due to the warm summer weather though I am not entirely sure.
It might be another species of potter wasp. Potter wasps are able to sting but rarely do so to large organisms and their stings don't hurt much. They usually prey on caterpillars and beetle larvae and use those to feed their own. They create these nests that look like a ceramic pot. each of these "pots" contains one larva of the wasp (along with all the food the wasp has collected for their larva when it hatches).
here's a photo of the pots (wasps seem to be willing to create these pots on pretty much any solid surface including under leaves):

Wasps are not parasites, they are hunters of other insects, if my identification of this species is correct, then you and your dog are likely not going to suffer any direct harm from this species let alone parasitic behaviour.

I don't think so. Its bites are painful, but most importantly my bugs are tiny (see the second picture I added).

I'm a bit confused, are you talking about the insect with yellow horizontal stripes? because that is the only one I have noticed.

Potter wasps are extremely tiny as well (as seen from the image i put which has multiple wasps easily fitting on the last joint). If you are talking about the same stripey insect, then perhaps I can post more images to make my identification more clear and possibly more convincing? I merely chose that photo because it has different angles of the morphology of potter wasps.

check out the three different pics.

Thank you for the clarification, unfortunately I cannot identify the species in the third picture. Perhaps taking it out of the water might help take a clearer picture of the more detailed characteristics of the insect?

It's the same insect. Just wanted to provide it for context on size.


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What author citation and abbreviation does (would) a monarch or a crown prince get after publishing a new taxon name?
Even though taxonomic rules appear to be silent about this (I've checked ICN Art. 46 and ICZN Art. 51), author citations, as well as abbreviations, are usually based on a surname. However, monarchs and crown princes don't have surnames per se, at least in the Western culture. Even though they have dynasty names, they may only get referred to by their personal name and dynasty name used as (instead of) a surname after the monarchy was overthrown, and for our purpose let's assume otherwise.
Has there ever been a case when such a person, while practicing biology (either as a hobby or professionally) published a name for a new taxon and there was a need to make up an author citation/abbreviation? If yes, how was it (they) made? If no, what would be an author citation/abbreviation for someone like, e. g., British Prince William?

I know nothing about taxonomic nomenclature, but my gut feeling on this matter seems to be correct — the Christian or given name is used. The “List of organisms named after famous people” on Wikipedia includes:

Callicebus bernhardi — Prince Bernhard of Lippe-Biesterfeld
Megaselia mithridatesi — Mithridates VI of Pontus
Mitra kamehameha — King Kamehameha I
Ornithoptera alexandrae — Alexandra of Denmark
Paroxyna cleopatra — Cleopatra VII Philopator
Pinus montezumae — Moctezuma II
Victoria Lindl. — Queen Victoria

However this is not always unqualified — perhaps because he is not the monarch?:

Hyloscirtus princecharlesi — Charles, Prince of Wales

and there are exceptions:

Lepidoteuthis grimaldii — Albert I, Prince of Monaco (born Albert Grimaldi)


text:
Book recommendation: protocols and recipes handbook for molecular biology / biochemistry
I'm a 5th-year PhD student in chemical biology. I've mostly been doing computational work, so my bench skills are rusty. To help me, I'd like a handbook of common techniques -- transformations, ELISA, protein purification, DNA extraction, SDS-PAGE, column chromatography, etc. I'd especially like a collection of recipes for buffers, etc.
I can find some protocols, but it's hard to find ones covering the more basic methods, and I'd like something cohesive. And there's something satisfying about an actual book.
I found these (and browsed through them in an HHMI library once):

https://www.amazon.com/Kathy-Barker/dp/0879697083/
https://www.amazon.com/Lab-Ref-Handbook-Reagents-Reference/dp/1936113791/

But they're pretty out of date! Most of the techniques are still valid, but I know many have been superseded. There are still a lot of radioligand assays (which are now uncommon in most labs).
So, can anyone recommend a book that could help someone relearn basic techniques?

My experience is that techniques are almost most often taught by hands-on, one-on-one training -- you find someone who knows the technique and ask them to show you, but COVID-19 distancing protocols make that nearly impossible. (The good news is that I often have the lab to myself and an underused supply of chemical stocks and reagents.)

Not a book recommendation but you should check out : https://www.protocols.io/ As someone with a computational background, I'm not the happiest about the about the way they write the protocols but they are definitely legit.

The extremely old-school answer here would be Maniatis' Molecular Cloning. They put out a new edition every decade or so, there is one from 2012 that is updated.
To get an idea of the book's impact in molecular biology, see this review from their website:

“In every kitchen there is at least one indispensable cookbook...Molecular Cloning: A Laboratory Manual fills the same niche in the laboratory (with) information to help both the inexperienced and the advanced user. (It) has once again established its primacy as the molecular laboratory manual and is likely to be found on lab benches...around the world.” ——Trends in Neurosciences

Likely there are more streamlined books out there at this point (this book runs at 3 volumes), but it's hard to see how to dispense with Maniatis.
It includes recipes for buffers etc. (see end of listing below). It is a little lighter on protein techniques, though, so I don't think you will find e.g. ELISA in there, though you will definitely find SDS-PAGE.
Here is a current chapter/protocol heading (you can scroll through the monospaced text). I had to delete a bunch of subheadings to make it fit under 30K characters:
Volume 1
Chapter 1: Isolation and Quantification of DNA1
Protocol 1: Preparation of Plasmid DNA by Alkaline Lysis with SDS: Minipreps
Protocol 2: Preparation of Plasmid DNA by Alkaline Lysis with SDS: Maxipreps
Protocol 3: Isolating DNA from Gram-Negative Bacteria (e.g., E. coli)
Protocol 4: Precipitation of DNA with Ethanol
Protocol 5: Precipitation of DNA with Isopropanol
Protocol 6: Concentrating and Desalting Nucleic Acids with Microconcentrators
Protocol 7: Concentrating Nucleic Acids by Extraction with Butanol
Protocol 8: Preparation of Single-Stranded Bacteriophage M13 DNA by Precipitation with Polyethylene Glycol
Protocol 9: Plating Bacteriophage M13
Protocol 10: Growing Bacteriophage M13 in Liquid Culture
Protocol 11: Preparation of Double-Stranded (Replicative Form) Bacteriophage M13 DNA
Protocol 12: Isolation of High-Molecular-Weight DNA Using Organic Solvents to Purify DNA
Protocol 13: Isolation of High-Molecular-Weight DNA from Mammalian Cells Using Proteinase K and Phenol
Protocol 14: A Single-Step Method for the Simultaneous Preparation of DNA, RNA, and Protein from Cells and Tissues
Protocol 15: Preparation of Genomic DNA from Mouse Tails and Other Small Samples
Protocol 16: Rapid Isolation of Yeast DNA
Protocol 17: Using Ethidium Bromide to Estimate the Amount of DNA in Bands after Electrophoresis through Minigels
Protocol 18: Estimating the Concentration of DNA by Fluorometry Using Hoechst 33258
Protocol 19: Quantifying DNA in Solution with PicoGreen
Chapter 2: Analysis of DNA81
Protocol 1: Agarose Gel Electrophoresis
Protocol 2: Detection of DNA in Agarose Gels by Staining
Protocol 3: Polyacrylamide Gel Electrophoresis
Protocol 4: Detection of DNA in Polyacrylamide Gels by Staining
Protocol 5: Detection of DNA in Polyacrylamide Gels by Autoradiography
Protocol 6: Alkaline Agarose Gel Electrophoresis
Protocol 7: Imaging: Autoradiography and Phosphorimaging
Protocol 8: Recovery of DNA from Agarose Gels Using Glass Beads
Protocol 9: Recovery of DNA from Low-Melting-Temperature Agarose Gels: Organic Extraction
Protocol 10: Isolation of DNA Fragments from Polyacrylamide Gels by the Crush and Soak Method
Protocol 11: Southern Blotting
Protocol 12: Southern Blotting: Simultaneous Transfer of DNA from an Agarose Gel to Two Membranes
Protocol 13: Southern Hybridization of Radiolabeled Probes to Nucleic Acids Immobilized on Membranes
Chapter 3: Cloning and Transformation with Plasmid Vectors157
Protocol 1: The Hanahan Method for Preparation and Transformation of Competent E. coli: High-Efficiency Transformation
Protocol 2: The Inoue Method for Preparation and Transformation of Competent E. coli: Ultracompetent Cells
Protocol 3: Easy Transformation of E. coli: Nanoparticle-Mediated Transformation
Protocol 4: Transformation of E. coli by Electroporation
Protocol 5: Cloning in Plasmid Vectors: Directional Cloning
Protocol 6: Cloning in Plasmid Vectors: Blunt-End Cloning
Protocol 7: Dephosphorylation of Plasmid DNA
Protocol 8: Attaching Phosphorylated Adaptors/Linkers to Blunt-Ended DNAs
Protocol 9: Cloning PCR Products: Addition of Restriction Sites to the Termini of Amplified DNA
Protocol 10: Cloning PCR Products: Blunt-End Cloning
Protocol 11: Cloning PCR Products: Making T Vectors
Protocol 12: Cloning PCR Products: TA Cloning
Protocol 13: Cloning PCR Products: TOPO TA Cloning
Protocol 14: Screening Bacterial Colonies Using X-Gal and IPTG: -Complementation

Chapter 4: Gateway Recombinational Cloning261
Protocol 1: Propagating Gateway Vectors
Protocol 2: Generating an ORF Entry Clone and Destination Clone
Protocol 3: Using Multisite LR Cloning to Generate a Destination Clone
Panel: Gateway Recombinational Cloning261
Panel: Basic Principles and Applications of Gateway Cloning262
Panel: Disadvantages of Gateway Cloning and Alternative Cloning Systems264
Panel: Generating Gateway-Compatible Vectors280
Chapter 5: Working with Bacterial Artificial Chromosomes and Other High-Capacity Vectors281
Protocol 1: Small-Scale Isolation of BAC DNA and Verification by PCR
Protocol 2: Large-Scale Preparation and Linearization of BAC DNA
Protocol 3: Examination of BAC DNA Quality and Quantity by Pulsed-Field Gel Electrophoresis
Protocol 4: Two-Step BAC Engineering: Preparation of Shuttle Vector DNA
Protocol 5: Preparation of the A Homology Arm (A-Box) and B Homology Arm (B-Box)
Protocol 6: Cloning of the A and B Homology Arms into the Shuttle Vector
Protocol 7: Preparation and Verification of the Recombinant Shuttle Vector
Protocol 8: Electroporation of Competent BAC Host Cells with the Recombinant Shuttle Vector
Protocol 9: Verification of Cointegrates and Selection of Resolved BAC Clones
Protocol 10: One-Step BAC Modification: Preparation of Plasmids
Protocol 11: Preparation of the A Homology Arm (A-Box)
Protocol 12: Cloning of the A Homology Arm into Reporter-Shuttle Vector
Protocol 13: Transformation of the BAC Host with the RecA Vector
Protocol 14: Transfer of the Reporter Vector into BAC/RecA Cells and Selection of Cointegrates
Protocol 15: Growth of S. cerevisiae and Preparation of DNA
Protocol 16: Small-Scale Preparations of Yeast DNA

Chapter 6: Extraction, Purification, and Analysis of RNA from Eukaryotic Cells345
Protocol 1: Purification of Total RNA from Mammalian Cells and Tissues
Protocol 2: Isolation of Total RNA from Zebrafish Embryos and Adults
Protocol 3: Total RNA Isolation from Drosophila melanogaster
Protocol 4: Total RNA Extraction from Caenorhabditis elegans
Protocol 5: Total RNA Extraction from Saccharomyces cerevisiae Using Hot Acid Phenol
Protocol 6: Quantifying and Storing RNA
Protocol 7: Precipitation of RNA with Ethanol
Protocol 8: Removing DNA Contamination from RNA Samples by Treatment with RNase-Free DNase I
Protocol 9: Isolation of Poly(A) Messenger RNA Using Magnetic Oligo(dT) Beads
Protocol 10: Separation of RNA according to Size: Electrophoresis of RNA through Agarose Gels Containing Formaldehyde
Protocol 11: Separation of RNA according to Size: Electrophoresis of RNA through Denaturing Urea Polyacrylamide Gels
Protocol 12: Transfer and Fixation of Denatured RNA in Agarose Gels to Membranes
Protocol 13: Transfer and Fixation of Denatured RNA in Polyacrylamide Gels to Membranes by Electrophoretic Transfer
Protocol 14: Northern Hybridization
Protocol 15: Dot and Slot Hybridization of Purified RNA
Protocol 16: Mapping RNA with Nuclease S1
Protocol 17: Ribonuclease Protection: Mapping RNA with Ribonuclease and Radiolabeled RNA Probes
Protocol 18: Analysis of RNA by Primer Extension

Chapter 7: Polymerase Chain Reaction455
Protocol 1: The Basic Polymerase Chain Reaction
Protocol 2: Hot Start PCR
Protocol 3: Touchdown PCR
Protocol 4: PCR Amplification of GC-Rich Templates
Protocol 5: Long and Accurate PCR (LA PCR)
Protocol 6: Inverse PCR
Protocol 7: Nested PCR
Protocol 8: Amplification of cDNA Generated by Reverse Transcription of mRNA: Two-Step RT-PCR
Protocol 9: Rapid Amplification of Sequences from the 5 Ends of mRNAs: 5-RACE
Protocol 10: Rapid Amplification of Sequences from the 3 Ends of mRNAs: 3-RACE
Protocol 11: Screening Colonies by PCR

Chapter 8: Bioinformatics541
Protocol 1: Visualizing Genomic Annotations with the UCSC Genome Browser
Protocol 2: Sequence Alignment and Homology Search with BLAST and ClustalW
Protocol 3: Designing PCR Primers Using Primer3Plus
Protocol 4: Expression Profiling by Microarray and RNA-seq
Protocol 5: Mapping Billions of Short Reads to a Reference Genome
Protocol 6: Identifying Regions Enriched in a ChIP-seq Data Set (Peak Finding)
Protocol 7: Discovering cis-Regulatory Motifs

Volume 2
Chapter 9: Quantification of DNA and RNA by Real-Time Polymerase Chain Reaction631
Protocol 1: Optimizing Primer and Probe Concentrations for Use in Real-Time PCR
Protocol 2: Constructing a Standard Curve
Protocol 3: Quantification of DNA by Real-Time PCR
Protocol 4: Quantification of RNA by Real-Time RT-PCR
Protocol 5: Analysis and Normalization of Real-Time PCR Experimental Data

Chapter 10: Nucleic Acid Platform Technologies683
Protocol 1: Printing Microarrays
Protocol 2: Round A/Round B Amplification of DNA
Protocol 3: T7 Linear Amplification of DNA (TLAD) for Nucleosomal and Other DNA < 500 bp
Protocol 4: Amplification of RNA
Protocol 5: Direct Cyanine-dUTP Labeling of RNA
Protocol 6: Indirect Aminoallyl-dUTP Labeling of RNA
Protocol 7: Cyanine-dCTP Labeling of DNA Using Klenow
Protocol 8: Indirect Labeling of DNA
Protocol 9: Blocking Polylysines on Homemade Microarrays
Protocol 10: Hybridization to Homemade Microarrays

Chapter 11: DNA Sequencing735
Protocol 1: Preparing Plasmid Subclones for Capillary Sequencing
Protocol 2: Preparing PCR Products for Capillary Sequencing
Protocol 3: Cycle-Sequencing Reactions
Protocol 4: Whole Genome: Manual Library Preparation
Protocol 5: Whole Genome: Automated, Nonindexed Library Preparation
Protocol 6: Whole Genome: Automated, Indexed Library Preparation
Protocol 7: Preparation of a 3-kb Mate-Pair Library for Illumina Sequencing
Protocol 8: Preparation of an 8-kb Mate-Pair Library for Illumina Sequencing
Protocol 9: RNA-Seq: RNA Conversion to cDNA and Amplification
Protocol 10: Solution-Phase Exome Capture
Protocol 11: Automated Size Selection
Protocol 12: Library Quantification Using SYBR Green-qPCR
Protocol 13: Library Quantification Using PicoGreen Fluorometry
Protocol 14: Library Quantification: Fluorometric Quantitation of Double-Stranded or Single-Stranded DNA Samples Using the Qubit System
Protocol 15: Preparation of Small-Fragment Libraries for 454 Sequencing
Protocol 16: sstDNA Library Capture and emPCR
Protocol 17: Roche/454 Sequencer: Executing a Sequencing Run
Protocol 18: Validation
Protocol 19: Quality Assessment of Sequence Data
Protocol 20: Data Analysis

Chapter 12: Analysis of DNA Methylation in Mammalian Cells893
Protocol 1: DNA Bisulfite Sequencing for Single-Nucleotide-Resolution DNA Methylation Detection
Protocol 2: Methylation-Specific PCR for Gene-Specific DNA Methylation Detection
Protocol 3: Methyl-Cytosine-Based Immunoprecipitation for DNA Methylation Analysis
Protocol 4: High-Throughput Deep Sequencing for Mapping Mammalian DNA Methylation
Protocol 5: Roche 454 Clonal Sequencing of Bisulfite-Converted DNA Libraries
Protocol 6: Illumina Sequencing of Bisulfite-Converted DNA Libraries

Chapter 13: Preparation of Labeled DNA, RNA, and Oligonucleotide Probes943
Protocol 1: Random Priming: Labeling of Purified DNA Fragments by Extension of Random Oligonucleotides
Protocol 2: Random Priming: Labeling of DNA by Extension of Random Oligonucleotides in the Presence of Melted Agarose
Protocol 3: Labeling of DNA Probes by Nick Translation
Protocol 4: Labeling of DNA Probes by Polymerase Chain Reaction
Protocol 5: Synthesis of Single-Stranded RNA Probes by In Vitro Transcription
Protocol 6: Synthesis of cDNA Probes from mRNA Using Random Oligonucleotide Primers
Protocol 7: Radiolabeling of Subtracted cDNA Probes by Random Oligonucleotide Extension
Protocol 8: Labeling 3 Termini of Double-Stranded DNA Using the Klenow Fragment of E. coli DNA Polymerase I
Protocol 9: Dephosphorylation of DNA Fragments with Alkaline Phosphatase
Protocol 10: Phosphorylation of DNA Molecules with Protruding 5-Hydroxyl Termini
Protocol 11: Phosphorylation of DNA Molecules with Dephosphorylated Blunt Ends or Recessed 5 Termini
Protocol 12: Phosphorylating the 5 Termini of Oligonucleotides Using T4 Polynucleotide Kinase
Protocol 13: Labeling the 3 Termini of Oligonucleotides Using Terminal Deoxynucleotidyl Transferase
Protocol 14: Labeling of Synthetic Oligonucleotides Using the Klenow Fragment of E. coli DNA Polymerase I
Protocol 15: Purification of Labeled Oligonucleotides by Precipitation with Ethanol
Protocol 16: Purification of Labeled Oligonucleotides by Size-Exclusion Chromatography
Protocol 17: Purification of Labeled Oligonucleotides by Chromatography on a Sep-Pak C18 Column
Protocol 18: Hybridization of Oligonucleotide Probes in Aqueous Solutions: Washing in Buffers Containing Quaternary Ammonium Salts

Chapter 14: Methods for In Vitro Mutagenesis1059
Protocol 1: Random Mutagenesis Using Error-Prone DNA Polymerases
Protocol 2: Creating Insertions or Deletions Using Overlap Extension PCR Mutagenesis
Protocol 3: In Vitro Mutagenesis Using Double-Stranded DNA Templates: Selection of Mutants with DpnI
Protocol 4: Altered -Lactamase Selection Approach for Site-Directed Mutagenesis
Protocol 5: Oligonucleotide-Directed Mutagenesis by Elimination of a Unique Restriction Site (USE Mutagenesis)
Protocol 6: Saturation Mutagenesis by Codon Cassette Insertion
Protocol 7: Random Scanning Mutagenesis
Protocol 8: Multisite-Directed Mutagenesis
Protocol 9: Megaprimer PCR-Based Mutagenesis

Chapter 15: Introducing Genes into Cultured Mammalian Cells1131
Protocol 1: DNA Transfection Mediated by Cationic Lipid Reagents
Protocol 2: Calcium-Phosphate-Mediated Transfection of Eukaryotic Cells with Plasmid DNAs
Protocol 3: Calcium-Phosphate-Mediated Transfection of Cells with High-Molecular-Weight Genomic DNA
Protocol 4: Transfection Mediated by DEAE-Dextran: High-Efficiency Method
Protocol 5: DNA Transfection by Electroporation
Protocol 6: Analysis of Cell Viability by the alamarBlue Assay
Protocol 7: Analysis of Cell Viability by the Lactate Dehydrogenase Assay
Protocol 8: Analysis of Cell Viability by the MTT Assay

Chapter 16: Introducing Genes into Mammalian Cells: Viral Vectors1209
Protocol 1: Construction of Recombinant Adenovirus Genomes by Direct Cloning
Protocol 2: Release of the Cloned Recombinant Adenovirus Genome for Rescue and Expansion
Protocol 3: Purification of the Recombinant Adenovirus by Cesium Chloride Gradient Centrifugation
Protocol 4: Characterization of the Purified Recombinant Adenovirus for Viral Genome Structure by Restriction Enzyme Digestions
Protocol 5: Measuring the Infectious Titer of Recombinant Adenovirus Using TCID50 End-Point Dilution and qPCR
Protocol 6: Detection Assay for Replication-Competent Adenovirus by Concentration Passage and Real-Time qPCR
Protocol 7: Production of rAAVs by Transient Transfection
Protocol 8: Purification of rAAVs by Cesium Chloride Gradient Sedimentation
Protocol 9: Purification of rAAVs by Iodixanol Gradient Centrifugation
Protocol 10: Purification of rAAV2s by Heparin Column Affinity Chromatography
Protocol 11: Enrichment of Fully Packaged Virions in Column-Purified rAAV Preparations by Iodixanol Gradient Centrifugation Followed by Anion-Exchange Column Chromatography
Protocol 12: Titration of rAAV Genome Copy Number Using Real-Time qPCR
Protocol 13: Sensitive Determination of Infectious Titer of rAAVs Using TCID50 End-Point Dilution and qPCR
Protocol 14: Analysis of rAAV Sample Morphology Using Negative Staining and High-Resolution Electron Microscopy
Protocol 15: Analysis of rAAV Purity Using Silver-Stained SDS-PAGE
Protocol 16: Production of High-Titer Retrovirus and Lentivirus Vectors
Protocol 17: Titration of Lentivirus Vectors
Protocol 18: Monitoring Lentivirus Vector Stocks for Replication-Competent Viruses

Volume 3
Chapter 17: Analysis of Gene Regulation Using Reporter Systems1335
Protocol 1: Assay for -Galactosidase in Extracts of Mammalian Cells
Protocol 2: Single Luciferase Reporter Assay
Protocol 3: Dual Luciferase Reporter Assay
Protocol 4: Using ELISA to Measure GFP Production
Protocol 5: Generation of Cell Lines with Tetracycline-Regulated Gene Expression

Chapter 18: RNA Interference and Small RNA Analysis1415
Protocol 1: Preparation of siRNA Duplexes
Protocol 2: RNAi in Mammalian Cells by siRNA Duplex Transfection
Protocol 3: RNAi in Drosophila S2 Cells by siRNA Duplex Transfection
Protocol 4: Preparation of dsRNAs by In Vitro Transcription
Protocol 5: RNAi in Drosophila S2 Cells by dsRNA Soaking
Protocol 6: RNAi in Drosophila S2 Cells by dsRNA Transfection
Protocol 7: Analysis of Small RNAs by Northern Hybridization
Protocol 8: Analysis of Small RNAs by Quantitative Reverse Transcription PCR
Protocol 9: Construction of Small RNA Libraries for High-Throughput Sequencing
Protocol 10: Preparation of Antisense Oligonucleotides to Inhibit miRNA Function
Protocol 11: Inhibiting miRNA Function by Antisense Oligonucleotides in Cultured Mammalian Cells
Protocol 12: Inhibiting miRNA Function by Antisense Oligonucleotides in Drosophila S2 Cells

Chapter 19: Expressing Cloned Genes for Protein Production, Purification, and Analysis1481
Protocol 1: Expression of Cloned Genes in E. coli Using IPTG-Inducible Promoters
Protocol 2: Expression of Cloned Genes Using the Baculovirus Expression System
Protocol 3: Expression of Cloned Genes in P. pastoris Using the Methanol-Inducible Promoter AOX1
Protocol 4: Preparation of Cell Extract for Purification of Soluble Proteins Expressed in E. coli
Protocol 5: Purification of Polyhistidine-Tagged Proteins by Immobilized Metal Affinity Chromatography
Protocol 6: Purification of Fusion Proteins by Affinity Chromatography on Glutathione Resin
Protocol 7: Solubilization of Expressed Proteins from Inclusion Bodies
Protocol 8: SDS-PAGE of Proteins
Protocol 9: Analysis of Proteins by Immunoblotting
Protocol 10: Methods for Measuring the Concentrations of Proteins

Chapter 20: Cross-Linking Technologies for Analysis of Chromatin Structure and Function1637
Protocol 1: Formaldehyde Cross-Linking
Protocol 2: Preparation of Cross-Linked Chromatin for ChIP
Protocol 3: ChIP
Protocol 4: ChIPQuantitative PCR (ChIP-qPCR)
Protocol 5: ChIP-chip
Protocol 6: ChIP-seq
Protocol 7: Generation of 3C Libraries from Cross-Linked Cells
Protocol 8: Generation of ChIP-loop Libraries
Protocol 9: Generation of Control Ligation Product Libraries
Protocol 10: PCR Detection of 3C Ligation Products Present in 3C, ChIP-loop, and Control Libraries: Library Titration and Interaction Frequency Analysis
Protocol 11: 4C Analysis of 3C, ChIP-loop, and Control Libraries
Protocol 12: 5C Analysis of 3C, ChIP-loop, and Control Libraries

Chapter 21: Mapping of In Vivo RNA-Binding Sites by UV-Cross-Linking Immunoprecipitation (CLIP)1703
Protocol 1: Optimization of Immunoprecipitation Stringency for CLIP
Protocol 2: UV Cross-Linking of Live Cells and Lysate Preparation
Protocol 3: RNase Titration, Immunoprecipitation, and SDS-PAGE
Protocol 4: 3-Linker Ligation and Size Selection by SDS-PAGE
Protocol 5: Isolation of the RNA Tags, 5-Linker Ligation, and Reverse Transcription PCR Amplification
Protocol 6: Sequencing of RNA CLIP Tags
Protocol 7: Gel Purification and Storage of RNA Linkers

Chapter 22: Gateway-Compatible Yeast One-Hybrid and Two-Hybrid Assays1761
Protocol 1: Generating Yeast One-Hybrid DNA-Bait Strains
Protocol 2: Generating Yeast Two-Hybrid Bait Strains
Protocol 3: Identifying Interactors from an Activation Domain Prey Library
Protocol 4: High-Efficiency Yeast Transformation
Protocol 5: Colony Lift Colorimetric Assay for -Galactosidase Activity
Protocol 6: Yeast Colony PCR

Panel: Reagents and Buffers1811
Panel: Tris Buffers1828
Panel: Good Buffers1829
Panel: Phosphate Buffers (Gomori Buffers)1830
Panel: Phenol1834
Panel: Equilibration of Phenol1834
Panel: Phenol:Chloroform:Isoamyl Alcohol (25:24:1)1834
Panel: Deionization of Formamide1834
Panel: Blocking Agents Used for Nucleic Acid Hybridization1836
Panel: Blocking Agents Used for Western Blotting1836
Panel: Commonly Used Techniques1843
Panel: Siliconizing Glassware, Plasticware, and Glass Wool1843
Panel: Preparation of RNase-Free Glassware1844
Panel: Hemocytometry Counting1846
Panel: Viability Staining1847
Panel: Precipitation of Nucleic Acids with Trichloroacetic Acid1849
Panel: Removing Ethidium Bromide from DNA1851
Panel: Disposing of Ethidium Bromide1851
Panel: Decontamination of Concentrated Solutions of Ethidium Bromide (Solutions Containing >0.5 mg/mL)1851
Panel: Decontamination of Dilute Solutions of Ethidium Bromide (e.g., Electrophoresis Buffer Containing 0.5 g/mL Ethidium Bromide)1852
Panel: Commercial Decontamination Kits1852
Panel: Detection Systems1855
Panel: Ethidium Bromide1855
Panel: Methylene Blue1857
Panel: SYBR Dyes1857
Panel: Chemiluminescent Labels1860
Panel: Chemiluminescent Enzyme Assays1861
Panel: Commercial Reagents, Kits, and Luminometers1863
Panel: Horseradish Peroxidase1865
Panel: Digoxygenin1869
Panel: BCIP1873
Panel: AMPPD1876
Panel: Immunoglobulin-Binding Proteins: Proteins A, G, and L1879
Panel: General Safety and Hazardous Material1885

While a little out of date, I do like it. (I found an old copy.)

I know you are asking for books, but for up-to-date basic overview of how some methods work - I would try websites or YouTube instead of textbooks...
One good website is BiteSizeBio. They have their own section for 'how to articles' and educational webinars. Otherwise I would also try YouTube. If you search in YouTube for basic techniques like 'how does the ELISA method work?' or 'principles behind SDS-PAGE' then you will find a lot of instructional movies. There is also the 'the protein man's blog' for purification of proteins, some analysis but also some DNA things.

An additional recommendation would be https://www.jove.com , the journal for visualized experiments. Explains different experiments and methods through videos.

Some protocols are not going out of style anytime soon, such as:
Frederick M. Ausubel, Roger Brent, Robert E. Kingston, David D. Moore, J. G. Seidman, John A. Smith, Kevin Struhl (2002) Short Protocols in Molecular Biology. Wiley, 1512pp. Check the Appendix sections for buffer formulations, etc. My copy is torn into pieces due to heavy use.
If you need the up-to-date form, then I recommend the subscription to Wiley's Current Protocols in Molecular Biology.


text:
What is the word for a group of genes inherited together?
I know the words haplotype and haplogroup, as well as genetic linkage, but...
I recently came across a new phrase describing genes which tend to be inherited as a group, and wrote it down, but now cannot find it...
Also, is there a word or phrase for genes which are expressed together?

"inherited together" (e.g. in linkage) or "expressed together" (e.g. coexpressed)? These are two different situations

@FabioMarroni — He wrote inherited. He is talking about genetic linkage. Why don’t you believe he means what he says? He asks a second question about expression, which is against the rules and also unclear because he doesn’t say whether he’s talking about eukaryotes and prokaryotes. That affects whether the one answer so far to that question is correct or not.

@David, you're right, I didn't understand that the second question was a separate question.

I believe you are referring to operon?

In genetics, an operon is a functioning unit of DNA containing a cluster of genes under the control of a single promoter. The genes are transcribed together into an mRNA strand and either translated together in the cytoplasm, or undergo splicing to create monocistronic mRNAs that are translated separately, i.e. several strands of mRNA that each encode a single gene product.

There is also a term called supergene which is in a way a less strict grouping, suggesting close genetic linkage and possible functional relationship.