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How did interspecies reciprocity involving cleaner wrasses originate?
The small bluestreak cleaner wrasse (Labroides dimidiatus) will approach a much larger fish (for example a grouper such as Cephalopholis miniata), enter its mouth, and spends several minutes cleaning its teeth. How did this behavior evolve? Wouldn’t the first cleaner wrasse that was bold enough to approach a larger fish have been immediately eaten? Since, in this encounter, the behavior of both fish isn’t learned, it must be encoded in their genomes. How could the appropriate coding gradually evolve?

Cleaner wrasse don't only clean within the mouth; although some species may specialize towards mouth-cleaning, it's likely that this behavior began with cleaning elsewhere on the fish's body.
Some studies (e.g. Bshary, 2003) suggest a large effect of cleaners on fish populations/diversity, so it seems that there are strong selective pressures for evolving behavior permissive to cleaning fish.
The cleaners themselves seem to have evolved cleaning traits on many occasions (see Baliga & Law, 2016). Although there are some obligate cleaner species, it's more common for cleaners to clean as juveniles, and the most common transition between cleaner behaviors is from non-cleaners to juvenile cleaners.
Therefore, it seems like the first cleaners were very small fish outside the typical prey target size of the cleaned fish. If there is strong selection towards individuals who tolerate these small, non-prey cleaners, it's reasonable to expect that this behavior could expand towards larger cleaners, and eventually to the more extreme versions of the behavior like allowing cleaners in the mouth.

Baliga, V. B., & Law, C. J. (2016). Cleaners among wrasses: phylogenetics and evolutionary patterns of cleaning behavior within Labridae. Molecular phylogenetics and evolution, 94, 424-435.
Bshary, R. (2003). The cleaner wrasse, Labroides dimidiatus, is a key organism for reef fish diversity at Ras Mohammed National Park, Egypt. Journal of Animal Ecology, 72(1), 169-176.

How are specific behaviors learned during one's life encoded in the genome of germ cells so they can be passed on to offspring?

Specific behaviors learned during one's life are not encoded in genomes, and there is no implication that that's the case here. Behaviors, and tendencies toward behaviors, can be genetically encoded and selected for. This is a very different question than originally asked, and should be asked separately (though I think it has already been asked and answered on this site)

@igorbrznovskaya For an example of the sort of thing that can be learned during the lifetime, think about a human's preference for a treat, let's say ice cream. The behavior of seeking out ice cream is indeed a learned behavior, but the evolved part that is transmitted in the genome is the preference for fats and sugars. Similarly, there is some underlying evolved behavior here (perhaps the physical sensation of being 'cleaned' is pleasurable? like scratching an itch), but there may be learned components ('fish that look like this scratch itches').

The behavior is beneficial for both species. To use your explanation, perhaps the first L. dimidiatus that was bold enough to approach C. miniata was immediately eaten, but some proportion of C. miniata did not eat the L. dimidiatus, and the alleles responsible for the cooperative behavior increased in frequency for both species, while the alleles responsible for the non-cooperative behavior decreased in frequency.
See symbiosis


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What insect is this case from?
I found this insect case in my garden in the south of Melbourne (Australia), on concrete under some dried leaves of a tree that I'd cut down.

It is 8 cm long, which is pretty big for an insect! The photo is of the underside. I don't recognise it. What species is it?

This appears to be the exuvia (i.e., molted) pupa of some sort of moth.
One Australian species with a similar-looking and sized pupa is the bardee or rain moth (Trictena atripalpis; or Abantiades atripalpis):

 Credit: Dianne Clark ; Source: Coffs Harbour Butterfly House
See another similar looking (and coincidentally 8cm long) specimen here:

source: Stack Exchange

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

sort: votes


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How much heme is in cooked pork and beef; why is cooked pork ("the other white meat") not red?
The new video See how Impossible Pork will make you forget about pig meat includes a very short discussion of

the addition of heme to the product to make it taste like beef
the deep red color of a heme solution
that pork is not nearly as red as beef, (after cooking it's essentially off-white)

Does pork (pig/swine muscle tissue) have substantially less heme content than beef (steer/bovine muscle tissue)? If heme is contributing to the flavor of cooked meats (rather than raw) such as pork and beef, why do they no longer have a red color after cooking?

Note that the muscle composition of farm pigs and wild swines will be very different.

Yes.
Pork has substantially less heme than beef (Cross et al. 2013).

As to why the red colour is lost, it is due to the Maillard reaction, by which the iron in the myglobin is oxidized from Fe(II) to Fe(III).  This results in a colour change in the meat (Tamanna & Mahmood 2015).

Sources:

Cross AJ, Harnly JM, Ferrucci LM, Risch A, Mayne ST, Sinha R. 2013. Developing a heme iron database for meats according to meat type, cooking method and doneness level. Food Nutr Sci 3(7): 905–913.

Tamanna N, Mahmood N. 2015. Food Processing and Maillard Reaction Products: Effect on Human Health and Nutrition. International journal of food science 2015: 526762. doi:10.1155/2015/526762

Thank you for the concise yet complete and well-sourced answer!

Sorry for being so concise; in a bit of a hurry.  :)  The papers referenced are really pretty good reads if you want more info.

I'll definitely check them out tomorrow; this turns out to be pretty interesting!

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


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centiMorgan distribution among human chromosomes
Using the rough estimate of 7,000 centiMorgans in a human... Is there an estimate that breaks down this total by chromosome (including the sex chromosomes)?  E.g., in the human karyotype, do chromosome pair 1a and 1b have n1 cM, 2a and 2b have n2 cM, etc. so that n1 + n2 +...+ n22 + sex chromosomes = 7,000?
If you understand what I'm getting at and can re-phrase my question to clarify it, please do so.

The short answer is "yes". Here is an early example: https://science.sciencemag.org/content/265/5181/2049.abstract
I am sure that with some searching around you can find the most recent version. I was able to find somewhat more recent maps here. The data has to be in the UCSC genome browser somewhere. Most likely you should find your 7000 cM estimate source and figure out which map that estimate comes from if you like that source.
These data structures are called "genetic maps" or "linkage maps". Each chromosome has positions that are defined by cM, and you could use that for your purpose I believe by just taking the largest cM value marker for each chromosome.
(Note that the two copies of a chromosome do not have independent genetic maps- after all, the map is defined by recombination between the two homologs. e.g. for chromosome 1 there is usually just one map, and therefore one maximum cM value- the map is an average across the human chromosomes sampled.)
Edit
The question seems to be related to a genealogical heuristic for identifying relatedness in cM values. I'm still not 100% sure how they measure this exactly.
The source shares expected values for relatedness here: https://secureservercdn.net/184.168.47.225/35b.ded.myftpupload.com/wp-content/uploads/2018/12/Relationship_Chart_FINAL_August_2017.jpg

The short answer suits my purposes well, as I am trying to get a rudimentary grasp on the mathematical and biological factors that apply to genetic genealogy.  I understand that parent/child relationships are a special situation, and with all other familial relationships "damned statistics," recombination, etc. are strong factors.  For some reason, self-reported sibling relationships in a 25,000+ person study by Blaine T. Bettinger are averaging significantly lower (about 2600 cM shared ) than the expected 3500 cM for a 50% DNA match.  Can you direct me to a source with a layman's answer?

@JosephFilip it would help to see the actual source to evaluate this. I am not sure what it means to share cM between sibs as it's a measure of physical linkage on chromosomes rather than genetic relatedness.

Edit: it appears to be related to this: https://thegeneticgenealogist.com/2018/12/17/examining-outliers-shared-cm-amounts/. I'm not a genealogist per se, I guess this measure kind of makes sense in that context, though it's unfamiliar to me. The layman's answer might be that blog post.

@JosephFilip Note: sibs aren't 50% matches, but rather a bit less than. Parent-child are 50% because of Mendelian inheritance (one chr copy from each parent), but sibs are comparing the outcomes of two such random draws (one for each sib). In other words the values you note 2600 cM are expected for sibs (see the chart linked in answer/blog post). see here for more details: http://hoylab.cornell.edu/relatedness.html

To a hammer, everything looks like a nail. To a 1970s math major, everything looks like an equation.  I did my own analysis of the grandparent/grandhild inheritance probabilities, but I can't figure out how to post it.  I used the assumption, known to be wrong, that chromosomes behave as identical immutable coins being tossed.  My calculations for averages and "normal ranges" match with "summary info" on genealogy and DNA test websites. They give a figure but don't say how it was derived.  The hoylab site says that sibs SHOULD BE 50% matches.  btw I do know that cMs are a rate not a distance.

ah- you know what, you're right, I faked myself out. siblings do share 50%, for some reason I just went crazy for a second there because the genealogy site said it was true. but if you do the simulation (which i did as sanity check) or check any reasonable source it is absolutely 50%, e.g. https://en.wikipedia.org/wiki/Sibling. i have no idea what's going on with the genealogist. possibly it is lower due to non-informative haplotypes (i assume you need good haplotypes to infer cM)?

Thank you for your patience!  The genealogy and DNA-test sites use very loose or incorrect terminology.  E.g. Ancestry returns a group of matches for, say, "6th-8th cousins", but there are a couple of dozen other familial relationships with the same degree of separation.  Gedmatch goes by "generations removed" so you get a list of people 2.1,2.3,4.2,...5.7 gens removed, whatever that means.  And they treat cMs as a distance.  If 1 cM=1% observed rate of occurrence, and there are 7000 cM, does that imply an avg of about total 70 "recombination" events in a specific sperm or egg cell?


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Photosynthesis in Higher Plants
Q:Photosynthesis in C4 plants is relatively less limited by atmospheric CO2 levels because: 1) Four carbon acids are the primary initial CO2 fixation products 2) the primary fixation of CO2 is mediated via PEP carboxylase 3) Effective pumping of CO2 into bundle sheath cells 4) RuBisCO in C4 plants has higher affinity for CO2.    Now the correct option is 2 but can you explain the reason for not choosing 4th option?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

If that is the case, why would C4 plants make PEPcarboxylase the primary acceptor instead of RuBisCO? Since it is not so, C4 plants were forced to take this alternative and make RuBisCO confined only to the bundle sheath cells. The problem in C3 was photorespiration, since oxygen used to competitively inhibit the uptake of carbon dioxide by RuBisCO. Hence it turns out that RuBisCO has more affinity for oxygen. If RuBisCO had more affinity for CO2, C4 plants would not have required to take the alternative pathway that they follow.
For the fact that why C4 remains unaffected by atmospheric CO2 levels is that because PEP carboxylase concentrates CO2 levels inside bundle sheath cells. So no matter what is the atmospheric CO2 level, the level inside bundle sheath cells remain always high and perfect for RuBisCO to act upon.


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Evolution of the unique mating system of the scorpion Androctonus australis
Sperm transfer in the scorpion Androctonus australis involves a sclerotized spermatophore, which is formed in the paraxial organs of the male reproductive system. The right paraxial organ produces the right half of the spermatophore (hemispermatophore), and the left paraxial organ the left hemispermatophore. The hemispermatophores are mirror images of each other, and are always produced one pair at a time.
During mating activities, a sexually mature male locates a receptive female, grasps her pedipalps, and proceeds to drag her along in his search for a suitable substrate onto which the spermatophore will be glued. This search may last for several hours. When the male finds a suitable substrate, the hemispermatophores slide out of their respective paraxial organs, move past the genital atrium (where the hemispermatophores are glued together), and the spermatophore is attached to the substrate.
The spermatophore contains the sperm mass in a concealed vesicle so that sperm aren't dessicated. The male then pulls the female over the spermatophore, guiding her so that her genital opening reaches a position directly above the spermatophore. A brief struggle ensues and the female's rocking motion helps to engage the spermatophore with her genital operculi. Continued rocking by the female triggers spermatophore opening, and the sperm mass is transferred into her genital pore. The transfer requires a pressurized vesicle that forces the sperm into her genital pore.
The spermatophore originated in aquatic organisms, but it has undergone extensive modification for use in terrestrial organisms like scorpions. Which evolutionary developments caused the transition from an aquatic deployment of the spermatophore to a terrestrial deployment involving the various interdependent behavioral and physiological elements described above? Since the behavioral elements are invariant, they must be encoded in the genome just as the physiological elements are. A rigorous answer to this question necessitates the elucidation of a series of intermediate steps, each of which was driven by natural selection, and each of which involved a set of mutations whose overall probability was not prohibitively low. If one or more of the steps was driven by genetic drift, then we must take into account the fact that, although the time for fixation of a neutral mutation is shorter in small populations (such as occurs during a population bottleneck), there is less opportunity for mutations to appear in small populations.

Hi and welcome to Bio.se! I learned something today, thanks! Be careful about asking "why" evolution occurred. Maybe tweak the question to ask for more literature on this. Currently, it sounds like you are asking generally about (i)"is the behaviour genetic", and (ii) "has the genetic evolution been mirrored by the behaviour"? The second point is incredibly subjective.

Is this homework?

Dear James, thanks for your comments. You are right -- more literature on this would be appreciated.

What specific part of the process is problematic we see most of this behavior represented in other species as well. As it stands this is not asking for an answer it is asking for a dissertation.

Dear John, the transition from aquatic deployment to terrestrial deployment necessitated extensive physiological changes acting in concert with behavior changes. I am interested in the details of the process.

Why would it need both a behavioral and physiological change at the same time. plenty of aquatic animals use spermatophores. you seem to be confused about what a transition to a terrestrial environment looks like, from what we know from the fossil record of other animals it is a gradual process that happens is shallow swamps were better osmotic balance, limbs are already valuable and humidity hovers around 100%, it is not a single sudden event. there was likely even an amphibious stage like some crabs.

@John  I can’t think of any functional intermediates between aquatic spermatophores, which are attached to the female’s body as she floats in the water (see Cephalopods), and terrestrial spermatophores, which are glued to the ground, as in scorpions. As soon as the evolutionary transition is made to a spermatophore that is glued to the ground, then there must be the associated searching and dragging behavior to find a suitable spot on the ground to glue it to, as well as all the other behavioral steps listed in my original post.

@john  Moreover, there must be the secretion of glue, which is absent in aquatic spermatophores. Vague scenarios won’t do -- you have to deal with these unique points.

not all scorpions use glue, and plenty of aquatic organisms use glue for spermatophores and egg cases, why look at cephalopods when you have much more closely related crustaceans. You seem to think evolution has to go right from marine crustaceans right to this one modern species, all the steps don't have to evolve at once, heck the variation in reproductive apparatus is so diverse  in scorpions has been proposed as a way to classify them. I think the issue is your not very familiar with scorpions or their relatives.

I will research this and get back to you.


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What are the disadvantages of myelin
The myelination of axons has plenty of advantages. It increases signal speed in axons, and thereby reduces reaction times. This is, of course, very good for the survival of the animal in question.
Most invertebrates do not have such a myelin coating. I know, that evolution does not just evolve features, because they are useful, but it seems to me, that invertebrates are entirely outclassed by vertebrates, because of how important reaction times are to an animals survival. So if such a trait is not impossible to evolve, it would most likely have evolved multiple times in different animals. If it was as advantagious as I imagine, invertebrates without myelin would have been outcompeted by now.
So there must be a significant disadvantage to having myelin coating.
Can you explain to me, what that is exactly?
Is it just the associated energy cost?

When you say "outclassed", I hope you realize the most numerous and diverse members of the animal kingdom are insects. And please think about your assumption that reaction time only depends on myelination... I think we could agree that flies or mosquitos have faster reaction times than your average mammal due to the architecture of their muscles and cuticular exoskeleton. The efficacy with which they respond with movement is very much quicker than the tugging of a bone by a partially contracting muscle pulling a tendon.

Apologies for the late reply, I kind of forgot about my question. I know, that insects are the most numerous. But at their size, intelligence is not as important as it is for bigger creatures, because of the limited number of neurons.

I kind of forgot, that insects have increadible reaction times :) Thank you for pointing that out :)

Many invertebrates possess myelin. It is a misconception that invertebrates lack myelin.
The world speed record for a traveling bioelectric signal is held by the myelinated axons in the abdomen of the Penaeus shrimp!
Please take a look at this website or this review to find a highly recommended comprehensive website about invertebrate myelin from about a decade ago. Here you will find a list of references and additional readings if you are so inclined.
As an additional note: invertebrates also possess and very often make use of ensheathing glial cells, such as is the case with sensory neurons in lepidopterans (moths and butterflies) as depicted below. I've labeled the sheathing cells in pink and red. Please understand that it is currently still unclear whether these cells secrete myelin, though they are thought in some way to insulate the neuron. What you are looking at is a hair-shaped sensillum that is innervated by one or several sensory neurons; these are the basic functional units for sensing movement, proprioception, smell and taste and they exist across all invertebrates, often lining the cuticle and across the entire body, e.g. on legs, on the antennae, in genital tracts, etc. They are best studied in hexapod insects.

Thank you very much for the detailed answer (and apologies for the late reply...) I am a complete novice, when it comes to biology, so I have to admit, that I don't fully understand your answer, but I will read through the linked sources more thoroughly, and then post follow up questions, if necessary. Thank you very much for your time :)

Quick follow up question: In what way are intelligence of an animal and signal speed (and myelination) related. If you were to create a mouse with much less myelin in the brain, would it be less intelligent, or would only things like reaction speed decrease? Likewise, could we increase the intelligence of some invertebrates like octopuses by increasing the myelination in their brain?

I think intelligence and myelination are not directly linked. Intelligence is a very complex (multifaceted) word that is typically poorly defined. In evolutionary biology, it typically means the ability to respond to entirely novel problems with a pre-existing machinery; it has little to do with the speed of transmission or speed of thinking. Sloths have myelin too! Maybe you are asking what the effects of hypo- and hyper-myelination would be. Take a look here, it may be of help.

thank you very much :) My idea was, that the brain of the octopus is specialized to achieve high reaction speeds etc despite the lack of myelin. Could it have more neurons, to achieve higher intelligence, because the size of the neurons could be reduced? Also, what are your thoughts on this paper: https://www.sciencedirect.com/science/article/abs/pii/0191886994900493


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Do any non-human species have juveniles that cannot communicate with adults?
Human babies take 1+ years to begin learning how to speak (though sign language can be learned a bit earlier1).
I know that cries, yells, and other non-linguistic sound are a simple form of communication, but they don't actually get across a specific point (e.g., what is causing a cry).
I understand that no other species use language, per se, and that linguistic development is complex and therefore requires time.
However, I'm wondering if other species have similar periods in which the adults "don't understand" the babies/juveniles.

In other words, do any other animals have a period of communication development early on in life before which the juvenile's cannot communicate with adults?

Boughman & Moss (2003) mentions the development of call types in some birds based on exposure to parents or certain social groups, but it doesn't quite address how these individuals communicate prior to the development of these calls (if at all). The paper also discusses individualization of sounds and recognizing variations to identify individuals, but again, this doesn't quite capture my question about a period of ontogenetic communication incompatibility.

1. Fitzpatrick, E.M., Thibert, J., Grandpierre, V. and Johnston, J.C., 2014. How HANDy are baby signs? A systematic review of the impact of gestural communication on typically developing, hearing infants under the age of 36 months. First Language 34(6):486-509. pdf
2. Boughman, J.W. and Moss, C.F., 2003. Social sounds: vocal learning and development of mammal and bird calls. In Acoustic communication (pp. 138-224). Springer, New York, NY. pdf

Plenty of species don't meet their parents. I don't suppose those meet your criteria?

@JohnDvorak they do not. I'm interested in the ontogeny and ethology of communication, not its absolute absence

Problem is, human baby crying still counts as communication. It's a far cry from Shakespeare, but I doubt that even chickens or baby eagles fare any better than just one utterance (no idea how to support that claim with studies though...). And it's not purely a matter of age either - get plopped into a random country in Africa or Asia, and you'll soon learn just how much you can say just by pointing at the right thing and saying "this".

@John Dvorak:  And similarly, there are multitudes of people with whom I share a common language, but seemingly can't communicate beyond what could (with some effort) be done by pointing & grunting.

Following up on the comment by @JohnDvorak — there is pretty good evidence that human babies communicate in ways that are much more sophisticated than just screaming until they get what they want. See for example: this review and this article. Based on this (and personal observations that some individuals seem to do a very good job of understanding what babies want) I think the premise that humans have non-communicative juveniles isn't well supported!

@theforestecologist We are starting a Bioacoustics Stack Exchange for people interested in the studies of non-human animal sounds and the impacts of sounds on animals. Please join us! https://area51.stackexchange.com/proposals/126698/bioacoustics?referrer=YjZmYjUxYzJkNDI1YmY5NDk3NzdhMzViMmZlNzI4ZDdiYTAyMWQxNTM5ZWFiNzRhODNkMmFiMzIxZjI3MmY1N_gFvrICTvBsmYNJ2ptRM6lIZEAV-VGkXtIwNyVDja680

@ASimonis thanks for the heads up-- yes I'm aware (and excited!), and I'm pseudo-interacting with it (limited by time constraints). As per this comment (and the other dozen you've made site-wide the last few days advertising Bioacousitcs SE): Such serial advertising (or really any post advertising other SE sites) has been deemed inappropriate and spammy (meta post). Please desist from writing such comments. They will be flagged as spam and deleted. Chat is where to be active

Thanks for the heads up @theforestecology. I'm sorry if the comments were inappropriate - just trying to figure out how to help our community grow and thrive. I was not aware of the Chat space, but now I am and will check it out.  Much appreciated! :-)

@ASimonis no worries. Just trying to prevent you from getting spam flagged. Carry on! (well, without posting ads for Bioacoustics :p). See you in chat sometime :)


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From which end of mRNA does transcription start?
The book "Understanding bioinformatics", says that "RNA polymerase transcribes the anticoding strand in the direction from 3' to 5', so that the mRNA strand is produced from the 5' to the 3' end".
But from Khan Academy's article, I got "RNA polymerase builds an RNA strand in the 5' to 3' direction, adding each new nucleotide to the 3' end of the strand". Also "the codons of an mRNA are read in order (from the 5' end to the 3' end)". Which one is correct?

@Thymine's answer is correct. I just thought I'd post a more graphic answer for clarity.
                  <==(RNA Pol)3'------------------------- 5'
5' ------------------------------------------------------ 3'
3' ------------------------------------------------------ 5'

The RNA Polymerase is synthesizing on the 3' to 5' strand, but nucleic acids are always added in reverse direction to the template strand (this goes for DNA replication as well as RNA synthesis).
The confusion arrises, of course, because there are several different ways of looking at it.  If you're looking at the polymerase's template strand, you would (like the book) that the RNA Pol is synthesizing 3' to 5'.
On the other hand, if you're looking at the strand being synthesized, you'd say (like Kahn Achademy) that it's being synthesized 5' to 3'.  This is why Kahn says

[...] adding each new nucleotide to the 3' end of the strand.

There is an incomplete mRNA fragment with the RNA Pol sitting on the 3' end.  That's where it adds each new nucleotide.

They're both correct. The confusion stems from the book talking about the anticoding strand as well as the newly-formed coding RNA strand, whereas Khan Academy talks only about the coding strand.
From the book:

The anticoding strand is transcribed from 3' to 5'.
  Therefore the coding strand is produced from 5' to 3', meaning the very first nucleotide added by the RNA polymerase is the 5' end, and you add to it in the 3' direction.

From Khan Academy:

The RNA polymerase produces a strand of RNA from 5' to 3'.


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Do plants refix some of the carbon dioxide in the Calvin cycle that they produce through cellular respiration?
Plants do cellular respiration and release CO2 into the air, but does the plant also use some of this CO2 to do the Calvin cycle? Or does all the CO2 required for the Calvin cycle come in through the stomata?

Gases like CO2 move quite freely in biological systems, approximating the laws of diffusion (note: there are of course some exceptions, especially underwater, as well as with proteins that assist in bulk transport of CO2 like hemoglobin).
If you were to measure the net amount of CO2 coming into the stomata, it would indeed approximate the net CO2 use by the plant. From this, you could make a claim like "the CO2 a plant needs comes in through the stomata": this is true for the net, and that's usually what's most important to a biologist.
However, if you want to get picky about what really happens at a molecular level, the flux of CO2 coming through the stomata is not the same as the net: no one is keeping track of the individual gas molecules, they just float around back and forth. The only reason there is a net flow at all is due to a concentration gradient: because the plant uses some CO2, there is less inside than outside. When molecules move around randomly, that means that a few more end up coming inside than are leaving. When we talk about net diffusion we are talking about the averages of many many molecules over time.
Included in that random motion are not just the CO2 molecules present inside and outside the plant, but also those that the plant is producing through cellular respiration. By chance, certainly, some of these molecules could end up back in the Calvin cycle. Some could even exit through the stomata and come back in (my intuition is that this is quite improbable for an individual molecule but I haven't done the math...the important concept is that it's all one "pool").
If you really wanted to know, you could set up a Monte Carlo simulation (or use differential equations) and calculate probabilities of all sorts of event sequences for individual molecules. You could also tilt the scales a bit if you, say, put the equivalent of a 'plastic bag' over a leaf, either physically or in a model: if there's a limited amount of CO2 in the "outside" space it would be much more likely for individual molecules to be "reused".
From a biologists' perspective, though, and especially for ubiquitous, freely moving molecules like CO2, it's usually only important to think about net flow.

Great answer — thanks for fixing the egregious mistake I introduced into the title!

@tyersome Haha no problem. Shh don't tell anyone but I edited my answer before the time edits register to fix the place I referred to CO2 as an "ion" - maybe a bit too much neuroscience for me. Happens to us all sometimes :)


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Why majority of synthesized mRNAs are halted at Nuclear Pore Complex?
I was reading about mRNA export process. I came to know that only 36% of synthesized mRNA transport events at Nuclear Pore Complexes(NPC) of the nuclear membrane get successful in crossing to the cytoplasm. I have heard that transcription machinery is a highly accurate one and so why would NPCs want to regulate mRNA transport like this?

Is NPC acting as a quality checker? Are there any errors mRNAs facing in between the transcription and meeting NPCs? (Please share related literature, if you find some.)
Any other hypothesis someone would want to share?

I think this is so specific that you might want to consider contacting the authors directly, they've probably been thinking about this since their paper in 2013 found the same fraction of mRNAs unable to cross the NPC

One thought, upon re-reading. It says 36% of events are successful. This doesn't mean that 64% of mRNPs never cross, it just means that out of every 100 attempts to cross, 36% are sucessful. Perhaps most of the 64% that failed simply try again later and succeed?

@Thymine my bad. Should I delete the question?


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How does natural selection explain sexual display?
As I understand it, animals sometimes grow more vibrant colors, bigger feathers, elaborate dances, build shiny nests, all to impress the other sex. However, these are all superfluous to survival -- any nutrition or energy spent developing these attributes or conducting these rituals are no longer usable for hunting or child rearing, for example. Given the same animal who does one of these wasteful practices versus the same animal who doesn't, in theory the latter should have the advantage in its chances of passing its genes down.
Why is it then, that sexual preference grows towards these wasteful growths and habits, rather than ignoring these sexual displays for sheer survival efficiency?

Does this answer your question? Why does sexual selection evolve beautiful features?

@kmm No, because the answer doesn't explain why those sexual traits are interpreted as beneficial

Short answer
Survival does not get your genes into the gene pool, reproduction does.
thus reproduction based selective pressures can be stronger than survival based ones. there are plenty of organisms that die during or right after mating because of this.
Consider an example In species A finding a mate is fairly rare, it may only happen a few times in an organisms life. if individual X is guaranteed to mate and reproduce when they find a mate but will die after mating, and individual Y will not die after mating but only has a low chance to mate then the genes from X will spread much faster than the genes for Y, because mating is already a rare event, but X genes spread every time while Y genes will also only spread once or often not at all, and will also take much longer.
Or to put it another way, a chicken is just an eggs way of making another egg, the survival of the chicken is only useful as much as it facilitates reproduction.
Any mutation  that happens to make you better at attracting a mate will spread, how it does so is basically irrelevant as long as it works, loud noises, bright colors, eye spots anything that draws the females attention works. studies on several bird species have shown even the colored bands used to identify birds for study effect their mating chance is they are right colors. Animals often already have a variety of biases for their attention hijacking them is an easy way to improve your chances of mating.  Of course once a way evolves that reliably improves mating chances preference for that becomes favorable as well which can lead to a run away selection feedback loops AKA Fisherian runaway
https://link.springer.com/article/10.1007/BF00172135

I don't understand, how does this explain the development of sexual display traits and the attraction to them?

@personjerry What part don't you understand.

You've explained why a male would develop such features if the female finds it attractive, but why would the female evolve to find these features attractive in the first place?

@personjerry they don't have to anything that grabs the females attention works, there are plenty of existing attention managing processes tp exploit survival has already shaped brains to notice things that stand out with bright colors, to notice eyes, and react to loud noises. to use a human example we evolved to notice red colored fruit and plenty of males and advertisers exploit this with red coloration. there was a study on crows that showed putting any brightly colored tag on a bird made it more likely to mate.

So it's not so much that we evolved a taste for sexual display specifically, rather sexual display traits hijacked existing systems to become relevant? Do you have any citation for that? And if you edit this part into your answer Ill accept it

The point is that it's not only wasteful, but counter-productive to survival.
If you're a red bug in the lush green of the amazon you are painting a target on yourself. This has the effect of increasing your selective pressure. If you survive with a target on your back, and wasting energy on pigments, then you must be very good all of the other things necessary for survival.
So, with natural selection, the higher selective pressure on an organism with a target on its back will be a more selective filter, only allowing the most performant little red bugs to survive and mate with each other, "quickly" giving them an edge over their less colorful brethren, and resulting in a biodiversity that flaunts its ability to survive today with extravagant colors and nests.
The mating dances might be a different story, I'll let someone else tackle that.

Don't many of these displays also function as health indicators, as unhealthy individuals are likely to have less vibrant colors/feathers?

How could natural selection come up with the logic to figure out that surviving with a target on your back suggests a more fit individual?

Natural selection doesn't come up with anything. You have 100 bugs, 10 of them are bright red and die at a faster rate than the other 90. So of these 10 bugs at a disadvantage, 9 die before reproducing. The last one, with the highest fitness, is the only one to reproduce, so its offspring inherit its fitness. For the other 90 non-bright red bugs, that process is less selective, because they have an easier time surviving with their natural camouflage. So fitness enhancing changes take longer to set in the population.


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A question about L-Citrulline
I know that L-Citrulline enters in the second step of urea cycle in the liver mitochondria and I wonder if a person takes an overdose of L-Citrulline wouldn't that cause mild hyperammonemia or at least cause an increase in the glutamine amino acid?


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what happens to rna length if we have a termination site in additional to the original one
if we have an RNA transcription and we add an additonal temination site in  the middle , will i have two RNA molecules or just a short one ?

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Assuming that by termination signal you mean transcription termination signal (and not a stop codon), you would have one shorter RNA molecule. You can have two shorter RNA molecules if there is another transcription start site after the termination signal, but there is no reason to assume this will be the case.
In some cases the RNA polymerase will skip a base and frameshift while transcribing a new RNA strand. This is known as transcriptional slippage, and it is taken advantage of by some viruses in order to make their genomes more compact by having several different mRNAs overlap each other.
In this rare case, having a termination signal does not necessarily mean transcription will terminate, it might be able to skip through parts of the termination signal and continue to the next termination site.


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What happens to the molecules of the pathogens after phagocytosis?
For example, what happens when a bacterium gets digested by a macrophage? I suppose that the macrophage produces the presented antigen from leftovers from the digested bacterial particles. What happens to the rest of the bacterium? Can the molecules from bacteria be used as a source of nutrients for the body? Or will they accumulate/get transported as waste products?

The ingestion of a bacterium by a macrophage involves phagosome lysosome fusion, which you can read about in Abbas Basic Immunology, Ch 2. As you suspected, in addition to bacterial killing and antigen processing, the phagolysosome breaks down bacterial macromolecules, as any lysosome does, using a variety of lysosomal hydrolases. There are export pathways for the end products, including lipids, carbohydrates, and amino acids, as discussed in this review, which does allow for re-use by anabolic pathways. As discussed in the linked review, the process of digestion and catabolite export is regulated, as should be expected. In culture models, nutrient availability appears to be important.


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What does it mean to share similarities among living organisms "both horizontally and vertically"?
I came across the following lines in a textbook (NCERT biology for class 11).

Systematic and monumental description of life forms, brought in, out of necessity, detailed systems of identification, nomenclature and classification. The biggest spin off of such studies was the recognition of the sharing of similarities among living organisms both horizontally and vertically

What does "both horizontally and vertically" mean?

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I find it unclear. Maybe "among organisms alive during the same time period ('horizontally') and between organisms and their evolutionary ancestors and descendants ('vertically')" ???

Ben Bolker's comment is correct; the next sentence in the passage helps to clarify (bold added):

The biggest spin off
  of such studies was the recognition of the sharing of similarities among
  living organisms both horizontally and vertically. That all present day
  living organisms are related to each other and also to all organisms
  that ever lived on this earth, was a revelation which humbled man and
  led to cultural movements for conservation of biodiversity.

The relationship between species in the present day are the horizontal relationships; one can define species horizontally by looking at and grouping organisms existing today (or at any other time "slice"). You can compare species horizontally by, say, looking at the skull of a human and the skull of a chimpanzee.
The relationship between species today and species that have existed in the past are the vertical relationships. For example, you could look at the skull of a modern horse and compare it to the skull of Mesohippus.
I've included a couple sources below that use this distinction, though I'm not sure where it originates.
I'd say the "horizontal" terminology comes up more frequently and may be more familiar, for example in reference to horizontal gene transfer one is talking about genetic material moving between species living at the same time. "Vertical gene transfer" can also be defined as the transmission of genetic information from parent to offspring, but more typically you would just call it inheritance.

Alvarez-Venegas, R., Sadder, M., Tikhonov, A., & Avramova, Z. (2006). Origin of the bacterial SET domain genes: vertical or horizontal?. Molecular biology and evolution, 24(2), 482-497.
Stamos, D. N. (2002). Species, languages, and the horizontal/vertical distinction. Biology and Philosophy, 17(2), 171-198.

although in the OPs case horizontal relatedness is not being assumed to be due to horizontal gene transfer, but just due to inheriting genes from a common ancestor.

@John Yes indeed, I'm just giving another example for where the "horizontal' term is used to refer to organisms existing at the same time.

Horizontally refers to organisms alive at the same time, All living organisms share similar genes.
Vertically means into the past and presumably future. How both fossils and genetics show relationships between ancestors and descendants.

Basically the sentence is saying When you study biology and how organisms relate to one another, you see massive amounts of organized similarities in organisms both backwards through time and in extant animals inherited from common ancestors. these similarities form a predictable pattern best explained as a complex web of relatedness stretching backwards in time.
When you realize these and a lot of taxonomic terms originated from paleontology and thus ultimately geology, in which organism relationships were discussed before genetics were even discovered, it makes more sense. phylogenetic trees would have been overlaid on geologic sections. Horizontal groups were organisms in the same horizontal layer of rock thus presumably alive at the same time, vertical meant vertical depth in the rock which was of course different time periods, the deeper you go the further back in time you went. It is a poor choice of wording for a textbook, the less jargon the better, but completely normal in the scientific literature.
here is an example of one of those early combined geologic, taxonomic "trees"

http://museum2.utep.edu/mammalogy/systematics1.htm


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Why are Excavata called "Excavata"?
The explanation given in my textbook is:

Some members of this diverse group also have an “excavated” feeding
  groove on one side of the cell body. (Campbell Biology)

This still isn't clear, though. What does it mean that this groove is "excavated"? Is it hidden inside the organism and then dug out?? Several websites just say the same thing.

This is just a reference to the feeding groove - a morphological feature that groups these organisms. The presence of the term in quotes as "excavated" is an indication that the word is not meant to be taken literally. Quotation marks used like this are referred to as scare quotes - they are meant to alert the reader that the phrase in quotes is not to be interpreted by its standard meaning.
Instead, you could read the sentence as meaning:

Some members of this diverse group also have a feeding groove on one side of the cell body, as if part of the cell was excavated.

One should not take the etymology of species names too literally - they are really just names. This is also true of common names of organisms.


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How do enhancers induce transcription?
DNA response elements are DNA sequences that are could be found upstream, downstream of genes that regulate gene expression at the transcriptional level.
One type -Enhancers- bind specific transcription factors called activators, this binding leads to the bending of DNA, bringing the otherwise distal enhancer near the promoter region of the gene, leading to induced transcription.

My question is:

How and by what mechanism do enhancers induce and increase transcription rates? i.e how does the interaction between the activators and the transcription complex, increase transcription rates?

The activators are proteins that bind to specific DNA sequences in the enhancer region. These activators also bind to the RNA polymerase and other associated members of the transcription complex, which makes it more likely for an RNA polymerase to hang around the promoter sequence of the region it enhances.
This in turn increases the chance of the gene being transcribed.
It's basically a little magnet that sucks in the RNA polymerase and then nudges it towards the promoter.

If the RNA polymerase is already near the promoter, why would it need an activator to bind to it?

This way if the RNA polymerase is near the promoter it binds to it, but if it's near the enhancer and the activators it also binds to the promoter. It extends the reach of the promoter, like how a magnet can help you grab things from further away, even though you can still grab them by yourself if they're within arm's reach.

Thanks, can you please provide refrences that propose this mechanism.

There's a pretty good review here https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6795546/?report=classic

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How many generations are required for a specific neutral mutation to reach fixation?
In population genetics, the term “time to fixation” is defined as the time it takes for a specific mutation to appear in a population, plus the time required for this mutation to spread throughout this population. My question is, how many generations are required for a specific neutral mutation to reach fixation? I need a general formula for number of generations as a function of mutation rate and population size, valid for all kinds of biological entities. Note that a neutral mutation is not fixed by selection, it is fixed by genetic drift.

The only definition of fixation (in genetics) I've seen involves one allele completely replacing all other variants of that gene. 2) I doubt that there can be a "universal" law for all biological entities. Some examples: many organisms are not sexual, ploidy varies particularly within plants, and dispersal rates within a population are going to be different. All these factors seem likely to affect how long fixation takes.

How many generations are required for a specific neutral mutation to reach fixation?

Kimura and Ohta (1968) showed that the expected time for a neutral allele to reach fixation is
$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0),$$
where $p_0$ is the initial frequency and $N$ is the population size. The model assumes a Wright-Fisher population (panmixia, constant population size, exclusively sexually reproducing hermaphroditic individuals, ...) and negligible mutation rate at the locus of interest.

how do i calculate po in terms of known quantities, such as mutation rate?

You can compute the expected allele frequency at mutation - drift balance (e.g. see here or any decent intro textbook to population genetics). In short, let $\theta = 4N\mu$, where $\mu$ is the mutation rate, the expected heterozygosity is
$$H = \frac{\theta}{\theta + 1}$$
From that you can compute the allele frequencies $p$ and $q=1-p$ by solving $H = 2pq$.
If needed, you can get the entire distribution of allele frequency given $N$ and $\mu$ (and even $s$ and $h$ if needed) in Wright (1937).

I think your answer would be more generally useful if you provided some examples of actual numbers.

Maybe worth noting what assumptions are behind this model? I could easily be wrong, but I would expect that how fast individuals, propagules, and gametes disperse through a population must have some effect. Also, is this true for species that aren't obligately sexual (e.g. many plants can reproduce vegetatively) ...

@tyersome The model assumes a Wright-Fisher population. Information added to the post. Thank you

thanks for the formula. Since neutral mutations are often phenotypically silent, it can be difficult to detect their presence in wild populations, which means it can be difficult to assign an accurate value to po. So, I would be very grateful if you rewrite the formula in terms of the mutation rate, which is known for a broad range of organisms. I apologize that my math skills are too low for the job, otherwise I would do it myself. Actually, I found a paper (Lanfear et al, 2014:36) that gives the rate of neutral evolution as a function of mutation rate, but I can’t see how it reduces to your

Lanfear, R. et al, (2014) Trends in Ecology & Evolution 29:33-42  http://dx.doi.org/10.1016/j.tree.2013.09.009

I found a paper (Lanfear et al, 2014) that gives the rate of neutral evolution as a function of mutation rate, but I can’t see how it reduces to your formula. I would be grateful if you show me how it reduces. Once that is accomplished, the number of generations to fixation is easily obtained as the reciprocal of the rate of neutral evolution. Thank you for your valuable time.

@igorbrznovskaya If you are looking for the time to fixation, then you cannot ignore the allele frequency. If you are looking for the rate of fixation, then of course, it is a different story. In a Wright-Fisher population, the rate of fixation at a neutral locus is simply equal to the mutation rate (see this post)

@Remi.b  In Kimura's equation, how do i calculate po in terms of known quantities, such as mutation rate?

@igorbrznovskaya Please see edited post that attempt to answer this follow-up question

@Remi.b  Thank you very much for the new formula


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qPCR to detect viral load
In an experiment qPCR was used to determine viral load. Alongside this conventional PCR was also performed and ran on an agarose gel. However I do not understand why both methods would have been used, any insight would be greatly appreciated?

Can you please add some more information about the experiment? Or add a link to the reference where you found the description of the experiment. Otherwise this question will be hard to answer, since there may be many reasons to do a conventional PCR.

It was an experiment we did in the lab. We performed qPCR on samples from 2 patients to test them for HIV. I understand why qPCR was used however I do not understand why we were also asked to perform Conventional PCR alongside this.

How did the two experiment differ or what did you do with the samples (besides letting the samples from the conventional PCR run on a gel)? Which qPCR machine did you use?

qPCR primers are typically designed to amplify a single, small (<200 bp) amplicon.  Most modern qPCR machines allow the user to perform a melt curve analysis at the end of the experiment to determine if there is more than one amplicon species.  If you are using an older device without this capability, conventional PCR and gel electrophoresis could be used to determine primer specificity.  As for why the experimenter didn't just load the qPCR product into a gel, perhaps they forgot.


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Total number of animals in Australia
In the last weeks there have been a lot of news reports about the number of animals that died in the current wild fires. However, I was wondering, what that is as a percentage of overall animal population in Australia. So:
What's the total number of animals living in Australia?

I wasn't sure about the tags, you're of course free to change it to more fitting ones

Hi, and welcome to the site!  It would be best if you could include actual quotes from the news articles you are looking at.  Thanks!

Note that the definition of "animals" behind the "# dead in fires" numbers going around is not the same as a biologist's definition of "animal"


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Which type of test tube should not be used for blood collection?
The following question is presented in my biology textbook:

You are required to draw blood from patient and keep it in a test tube for analysis of blood corpuscles and plasma. You are provided with the following four types of test tubes. Which one of them will you not use for the purpose?

Test tube containing calcium bicarbonate
Chilled test tube
Test tube containing heparin
Test tube containing sodium oxalate

In thinking through the question, I reasoned that since we are collecting blood from a patient for biochemical assay or hematocrit, we would want it to be in an anticoagulated stage. Sodium oxalate and heparin are both anticoagulants and therefore should serve my purpose well. I don't think a chilled test tube would have any effect directly, except the fact that low temperatures delay clotting. So, I had chosen the test tube containing calcium bicarbonate to be unsuitable, as $\ce{Ca++}$ is one of the factors required for clotting and hence would accelerate the clotting procedure.
The textbook disagrees with me, and gives (3) as the answer.
Is this an error in the textbook key, or a flaw in my reasoning? Which should be the correct answer, and why?

Your reasoning is sound and correct. The answer key is wrong.
An unclotted blood sample needs something to prevent clotting. Extracellular calcium is required for both the coagulation cascade and platelet activation. It even has its own name in this context, Factor IV. This why EDTA, a calcium chelator, is used in some blood collection tubes to delay clotting.
So, as you say, the most correct answer would be (1): Test tube containing calcium bicarbonate. That is the opposite of the kind of tube you should use for this type of sample.
The answer given by the key, (3): Test tube containing heparin, is incorrect. Heparin tubes are a good choice for plasma and whole blood analysis, as you indicated. Heparin is a good anticoagulant, both in vitro and in vivo.
See this nicely laid out list from UCI medical school for an example of specimen requirements for specific tubes.


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Is feeding wild pigeons really "weakening the entire species"?
While reading about what foods are healthy for pigeons, I came across the following paragraph: (Source)

Human interaction and improper feeding of domestic and wild pigeons is believed to be one of the reasons for the birds' decline. While many urban areas claim that pigeon populations are out of control, the truth is that around 59 species are currently threatened by extinction, which is over 20 percent of the pigeon population. Since the 1600s, 10 species of pigeon have become extinct. While habitat loss and over-hunting are partly to blame, bird specialists believe that domestication and improper feeding has weakened the entire species.

There are no sources cited. What does "weakening the entire species" even mean? What evidence is there to support the claim that improper feeding is weakening entire species of pigeons? How would overfeeding by humans lead to extinction? And how would domestication be contributing?

This might be a good question for Skeptics.SE

I did wonder whether an ecology question was on topic for this site. But how would I migrate the question?

The quote is silly. All the declines noted are for species other than Columba livia, the domestic and common wild pigeon. Indeed other species have been lost to habitat loss and hunting, but not to feeding.  Feeding and human activity have helped C. livia explode in population, which is not a sign that (entire) species has been weakened.

It might also be noted that those extinct pigeon species might well include the dodo: https://en.wikipedia.org/wiki/Dodo

Yes, [tag:ecology] questions are on topic here.

Yes, my comment about Skeptics was about the form of the question, not the topic

Oh, and the passenger pigeon.  Extinction of those had nothing to do with feeding, everything to do with human hunting and the introduction of new predatory species.


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Differentiating Antaresia (Children's Complex) Pythons using something other than color pattern
I have a standard wild-type Children's python (Antaresia childreni) that I'm planning on breeding in the next few years and was just sold a male "Children's python" that I think might actually be a spotted python (Antaresia maculosa). Unfortunately, he's of some kind of reduced pattern morph (granite, I think) that has completely blown out his natural patterning, so my main method of identification is useless.
I know that along with the Stimson's python (Antaresia stimsoni) all of these snakes have been identified as "Children's pythons" at some point in the not-too-distant past, but someone saw fit to distinguish between them and I can't seem to find any basis for doing so that isn't based on range and pattern, both of which are meaningless for a captive-bred snake of a morph that makes its natural pattern indiscernible.
Is there some reliable way to tell the difference between these snakes other than coloration and range? Perhaps some difference in number or placement of certain scales or details about the eyes?
I've included a picture in case anyone can comment and tell me what this little guy actually is on the basis of the modified pattern - but I'd still like a better way if anyone can provide a real answer.

I finally got frustrated enough to dig up A Revision of the Liasis childreni species-group (Serpentes: Boidae) L.A. Smith, 1985 - the original paper that split up this species complex, and when even Smith made primary determinations off of pattern and color alone, I took matters into my own hands and dug into the his raw data.
I have compiled the mean scale counts for each species into a table, and truncated any rows that showed no useful degrees of deviation for any species, resulting in the following:
             A. Childreni  A. Maculosa  A. Stimsoni  A. Stimsoni Orientalis  A. Perthensis
Ventrals     272.8        263.5         279.5        263.8                   232
Subcaudals   47.3         42.1          46.2         42.8                    38.7
Midbody      41.3         38.3          43.4         40.3                    32.7
Loreals      7.9          4.7           12.2         7.9                     7.3
Postoculars  3.6          3.1           4.2          3.8                     3.4
Pits         4.5          4             5.6          4.8                     3.1

I am including this table in its entirety to assist future identification efforts within the complex, as the original paper did a poor job of presenting this data.
The most useful difference for my purposes - distinguishing between A. maculosa and A. childreni - appears to be loreal scale count. The loreal scales sit between the eye and nostril of the snake, and do not include scales which belong to the orbital and nasal structures (The region marked "l" in the diagram below).

Following up on this, I examined a number of close-up photos of known examples of both species, and very quickly identified a distinctive difference in not just the count but also the pattern of loreal scales. Once you're looking in the right place, the difference is obvious.
A. Childreni showing its distinctive granularly-clustered loreal scales:

A. Maculosa showing its smaller number of tightly structured loreal scales:


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Why is centriacinar emphysema more common in the upper lobes compared to the lower lobes?
I suspect it's because the upper lobes get less ventilated (the volume of their alveoli change less during respiration, and they receive less new air with each breath) compared to the lower lobes, and this causes air to stagnate there more in comparison. Since centriacinar emphysema is usually smoking related, I assume it's because smoke remains in the upper lobes more. I feel like this doesn't really make sense, could be because it's incorrect or it just needs a change of wording.
Also, an extra question if it's okay, why is panacinar emphysema more predominant in the lower lobes? Is it because the lower lobes get better perfusion?


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Can bacteria pick up lethal plasmids?
I am sorry if this question is too general, and does not have any concrete answer.
I was explaining to my non-biology-background friend about plasmids and how they are picked up by bacteria from the remains of other dead bacteria during stressful conditions. This is when this question arose:
Why would bacteria pick up plasmids released from the dead bacteria, as this means that these plasmids either did not help it survive in those conditions, or could have in fact been the cause of their death? This also lead to the question of whether plasmids can be lethal? (I believe there could be, for example plasmids which are translated into proteins which are endonucleases which would probably kill the bacteria, yet I am not sure).
Moreover, if this sort of plasmids exists, then why could we not engineer them specifically and use them as medicine as an “antibiotic”?

You might be interested in this answer, and the other answers to the question.

The ability of bacteria to take up intact environmental DNA is called natural competence.
One problem with trying to take advantage of this in a therapy is that it is not very efficient. Importantly, natural competence is regulated and tends to be activated when bacteria are already stressed. This is also likely part of the answer as to why a bacterium would take up DNA from the outside: if they are already in bad shape, they don't have much to lose. Bacteria growing in non-stressful conditions are less competent, and possibly negligibly so.

Ween et al 2002 compared competence in two bacterial strains, one with a "normal" regulation of competence. At most bacterial concentrations, the "normal" strain showed less than 1% transformation, and this is still in sort of an ideal laboratory condition, where the culture medium is flooded with plasmids. There wouldn't be a feasible way to even approach delivering that much plasmid DNA into a human.
Ween, O., Teigen, S., Gaustad, P., Kilian, M., & Håvarstein, L. S. (2002). Competence without a competence pheromone in a natural isolate of Streptococcus infantis. Journal of bacteriology, 184(13), 3426-3432.

The other big problem is you are working directly against selection pressures. In the case of a plasmid that improves survival (say, one containing a gene that confers antibiotic resistance in the presence of that antibiotic), then the population will more quickly increase the expression of that plasmid, as bacteria with it grow and reproduce while other bacteria die. However, if you have a lethal plasmid, all the bacteria you are able to transform simply die. They don't spread the plasmid by reproducing, and as they die the non-transformed bacteria will continue to reproduce.

This also lead to the question of whether plasmids can be lethal?

Yes, genes in plasmids could be beneficial, neutral or even lethal, although lethal plasmids may have trouble surviving for long since they depend on a live cell for replication.

Moreover, if this sort of plasmids exists, then why could we not engineer them specifically and use them as medicine as an “antibiotic”?

Efficacy aside, they're relatively large, highly immunogenic molecules. Not great properties in an antibiotic.


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what is this insect? just curious
Thank you for replying my question..and sorry for my broken english (https://i.stack.imgur.com/5GXs5.jpg)

@PriyanshuDas Answers should be posted as answers, not comments. Additionally, from How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. - we should encourage questions to be improved rather than answering ones that do not fit the guidelines.

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What is the oval shaped bone in the heads of some fishes?

I had a dish of fish and found 2 oval shaped nearly 1cm long bones in its head.What help does it do to the fish? what is its name?
I have clicked the picture myself .

perhaps you can put an arrow on one of these pics so we know where it's from https://www.google.com/search?biw=1241&bih=646&tbm=isch&sxsrf=ACYBGNQoji81vb-xuKWibW4RhulDGDMTmw%3A1578738792915&sa=1&ei=aKQZXqy-N7KMlwSem5mQCw&q=Channa++skull&oq=Channa++skull&gs_l=img.3...8758.8758..8869...0.0..0.149.463.1j3......0....1..gws-wiz-img.......35i39.mfErXoy7XxM&ved=0ahUKEwisksenrPvmAhUyxoUKHZ5NBrIQ4dUDCAc&uact=5

Seems like otoliths. Put a more detailed image for better identification.

Thanks priyanka das

Haha, it's Priyanshu. I'm not cent percent sure if its otolith or not. Just in case you don't know what otoliths are, let me tell you we too have them. They are calcium carbonate granules present in our inner ear. They strike against the sensory hair cells present in there whenever our head moves, thus giving us a sense of movement and balance.

I am a professional fish biologist and those are otoliths; I have aged thousands of them. They are primarily used in maintaining equilibrium, hearing, and balance. The details of the shape of the otolith can vary between species but generally look very similar. They are located in the skull of the fish, usually at the back.
Here is an image of other otoliths:
Photo source: Examples of common fish otoliths found at archaeological sites in Florida. Images from the Florida Fish and Wildlife Conservation Commission http://www.flickr.com/photos/myfwc/sets/72157625872804969/
Otoliths are calcium based structures located within otolithic organs (the sacule, lagena, and utricle) and make up the inner ear of boney (teleost) fishes. They come in pairs and there are three of them: Sagittal (within the saccule), lapillali otoliths (within the utricle) and asterisci (within the lagena). They are made of calcium carbonate and are generally composed in two different crystalline formations, aragonite and vaterite; crystalline form and amount depend on the otolith and stress induce metabolic processes. Otoliths are formed as the fish grows. In periods of fast growth (warmer months) the otolith forms faster and in periods of slow growth (colder months) the otolith forms more slowly. Given the cyclical pattern of warm and cold months in the year, the otolith form annuli (growth rings); annuli can be used to age fish just like rings on a tree. Additionally, they are metabolically inert and cannot be reabsorbed as calcium reserves like other boney structures in the fish; thus, they are a permanent record of the fish's age. This permanent record can also be used to evaluate the life history (i.e., movement patterns) using trace element analysis.
Specifically, how do they work/help the fish? Within the sacule, lagena, and utricle the otoliths are suspended in endolymphatic fluid within their respective organs. The organs have hair-like sensors in them that detect vibration or movement of the otoliths within, triggering an associated nervous stimuli. The nervous stimuli are then interpreted as movement and orientation.
Here are some sources:
https://dfo-mpo.gc.ca/science/aah-saa/otoliths/info/introduction-eng.html
https://en.m.wikipedia.org/wiki/Otolith#Description
https://www.sciencedirect.com/topics/earth-and-planetary-sciences/otolith
https://www.daf.qld.gov.au/business-priorities/fisheries/monitoring-compliance/monitoring-reporting/commercial-fisheries/species-specific/estimated-fish-age
This book is also an excellent resource for a much more in-depth look:
https://fisheries.org/bookstore/all-titles/professional-and-trade/55078c/

Answers should be complete. It's great that you added the citations, but your post needs to indicate why it's correct without reading external links that may die or change. Either summarize these sources in your own words or find photo evidence, etc. Include this info directly in your answer so users can know why you're right without *needing" to click on your links. Citations are for support, not to send users elsewhere for answers. Also, indicating you're an expert is irrelevant -- convenient for having proper knowledge to cite, but not necessary here or adequate to use as "support"

I have edited the original post to provide example photos, additional detail, and more external information if the readers wish to explore further.

Excellent. Thanks for the added effort. +1


text:
What are the methods of prophylaxis against exposure to radioactive isotopes?
Potassium iodide is used as prophylaxis to prevent illness when one is likely to be exposed to Iodine-131 and other radioactive isotopes of iodine. Are there any other prophylactic treatments for exposure to other radioactive isotopes, such as Cesium-137, Tritium, Strontium-90, etc? If so, how do they work?

What research have you done to find this out yourself?

@David I read the Wikipedia articles on Iodine-131 and Potassium Iodide. I also searched "Tritium Poisoning Treatment" on Google and got this result: https://io9.gizmodo.com/drinking-a-beer-can-save-you-from-radiation-poisoning-1648955835 , so apparently one method of prophylaxis against tritium poisoning is diuretics and increase fluid intake, but I'm wondering if there are others. The Wikipedia article on Cesium 137 claims that exposure can be treated with Prussian Blue. This: https://www.dhss.delaware.gov/dph/files/strontiumfaq.pdf claims that there are no direct treatments for Strontium-90

So I am wondering whether there are any measures one can take (Besides donning protective equipment) before being exposed to Strontium-90 and Cesium-137, rather than after.


text:
Is withdrawal Euphoria possible?
It is known that when the human organism is supplied with certain hormones and/or drugs that serve a certain function for a sufficiently long amount of time, he reduces, and may eventually entirely stop, production of those hormones. It is one of the reasons stopping drug abuse by going cold turkey is so hard, because the happiness hormones produced normally in the brain before, are now produced at a reduced quantity now and their neural receptors are atrophied too, so that their effect is even further decreased.
My question then is this: Could we reverse this? Create drugs with catecholamines or some other such hormone so we bombard a patient negative emotions so incredibly potent for an amount of time that after we stop injecting him with the drug, he's chronically euphoric? Maybe a way to kickstart the life of a suicidal person with depression, have them live at least a year or two in that blissful state of withdrawal symptoms to have them want to keep living, knowing it is at the very least possible to feel that way

Welcome!  It's an interesting question and I look forward to seeing the answers.  The obvious issue is that you have to keep a patient on medication for quite a while before the withdrawal will have an affect, and during that time, the patient will be far worse.  Therefore, far from preventing suicidal depression, you are rather pushing the patient that much closer to suicide for weeks or even months of time. Furthermore, I'm guessing the result would be relatively transient as compared with the treatment time.


text:
Is brewer's yeast a good source of protein for humans?
I read that brewer's yeast protein is not a "real protein" and is not usable by non-ruminants. Is that true?
If yes, how can I know what kind of protein is good for humans (especially athletes)

brewers yeast is generally used as a  niacin (vitamin B3) supplement not protein. it prevents pellagra.

Please state the source. What is a “real protein”? Why would ruminants be any different from other animals? And this site is the wrong place for dietary advice.

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 it would be helpful if you were to include where you read about this and what you have done to check whether that information was true. Also note that almost all foods contain protein, but it isn't accurate to say that any of them are protein. Thanks!


text:
Can microbes become "overweight"?
Just out of some weird thoughts, can a microbe (any single-celled organisms, accepting answers for both prokaryotes and eukaryotes) ingest too much food (e.g. via absorbing too much involuntarily because the surrounding has too much of it,or via phagocytosis) and retain part of it somehow?
Being "overweight" can be characterized by larger than average cell size/mass, presence of numerous intracellular food reserves (like glycogen?). I am guessing these (increasing cell mass and food reserves) would likely happen to some extent. But do these changes affect reproductive fitness (readiness to cell division) of the microbe? (In humans, we can safely say that being overweight is detrimental to reproductive fitness.)
For instance, What would happen when microbes are over-supplied with energy-rich and carbon-rich molecules but not the other nutrients (e.g.NPK)? And once it is switched back to a "stoichiometrically/nutritionally normal" diet, would it likely have a higher/lower reproductive fitness (compared to microbes normally-fed the whole time)?

what have found yourself? That will help focus your question and guide answers

Well, it is hard to find any relevant experimental information (if that's what you meant) because studies of stoichiometric imbalance in microbes are mostly done in the sense of "lacking" rather than "surplus". This question is rather "unusual" as such so it warrants a more "exploratory attitude". I welcome theoretical answers that explore possibilities and not having concrete evidence as well.


text:
What might earlier versions of caddisfly shelter-building behavior have looked like?
The caddisfly has an amazing ability to build armor for itself by using a self-produced underwater glue to hold together pebbles: https://www.youtube.com/watch?v=Z3BHrzDHoYo.
How could this behavior and the ability to produce the glue have evolved? The survival advantage of the current level of the caddisfly's ability is clear, but how were the incremental stages advantageous? How could it have developed its armor-building ability without a strong enough glue? And how could it have developed a stronger glue without the armor-building ability that would make it useful?
My guess would be that before it was building a full shell like it does now, it started just by holding a pebble or two to itself. Then perhaps the bodily fluid that is now used as glue gradually increased in stickiness and helped the organism keep hold of the rocks or keep them together. It seems, however, like any modest amount of increase in stickiness that could occur due to mutations wouldn't have been enough to keep the rocks together.

Your intuition seems fairly correct. Mouro et al 2016 show some findings relevant to your question...

Caddisflies have been around for a very long time. Much of the fossil record of their existence is of preserved shelter cases rather than the insects themselves.
Early cases seem to be made up of more variety of materials, whereas selective cases made of very specific materials are observed more recently in the fossil record and today. This suggests that they first just collected random pebbles and organic materials, and later evolved more refined construction techniques.

As far as evolution of their silk, I think it's important to recognize that these insects are closely related to Lepidoptera, the moths and butterflies. Many Lepidoptera species, like caddisflies, spin silk cocoons as part of their development cycle, so it can be inferred that the silk and many of its properties precedes any construction behavior using other materials.

Mouro, L. D., Zatoń, M., Fernandes, A. C., & Waichel, B. L. (2016). Larval cases of caddisfly (Insecta: Trichoptera) affinity in Early Permian marine environments of Gondwana. Scientific reports, 6, 19215.

Beyond what is shown in the fossil record and in genomic analysis, the evolutionary advantage of a phenotypic feature can only be guessed at and its plausibility gauged.
That said, here's a guess that seems plausible: the sticky silk might have first served as a way to tether the caddisfly larvae to stationary rocks in a river current.  The tether would have naturally and coincidentally picked up small rock grains, sticks, and the like.  If the tether broke, the grains would stay attached to the remaining silk strand and, if "reeled in" by the larva, might have served as makeshift armor as the larva tumbled downstream in the current.  This would open up a new adaptive opportunity, channeling adaptations in the direction of improving the shell-constructing behaviors and physiological tweaks that support shell construction.


text:
How to derive Hill equation (one specific part)
There is just one specific step in the derivation of the Hill equation for haemoglobin which I can't understand.
Step from: $Y = \frac{(p\ce{O2})^n}{K_d + (p\ce{O2})^n}$
To: $Y = \frac{(p\ce{O2})^n}{(K_d)^n + (p\ce{O2})^n}$
I don't understand where $(K_d)^n$ comes from. (I can go from this second equation to the Y/(1-Y) equation afterwards).

How I derived my equation is the following.
$\ce{Hb.(O2)_n <=> Hb + nO2}$
Hence the dissociation constant $K_d$ should be:
$K_d = \frac{[\ce{Hb}][\ce{O2}]^n}{[\ce{Hb.(O2)_n}]}$
And Y, which is the fractional $\ce{O2}$ saturation would be:
$Y = \frac{[\ce{Hb.(O2)_n}]}{[\ce{Hb.(O2)_n}] + [\ce{Hb}]}$
If you multiply the top and bottom by $K_d$, the following is obtained:
$Y = \frac{(p\ce{O2})^n}{K_d + (p\ce{O2})^n}$
This is where I became stuck. What am I doing wrong?
Thank you very much for your answer.

In your second step $(K_d)^n$ should be $(K_A)^n$.
Where:

$K_d$ is the apparent dissociation constant and
$K_{A}$ is the ligand concentration that results in half occupation

See for example the relevant wikipedia article.

@user1136 Apparent because the association/dissociation reaction is not a single step kinetics.


text:
What's unique for vitamin B-12 group?
I've been trying to figure out what makes the vitamin B group really big with 8 vitamins.
Chemically they have different structures.
Solubility: not only vitamins from this group are water soluble vitamins (also vitamin C).
Function: not only this group of vitamins are cofactors for metabolic processes.
So what's the reason for this grouping, or why we can't include other vitamins in this group?
Also, what does the letter B stands for?

Related: https://chemistry.stackexchange.com/questions/63956/why-is-the-vitamin-b-complex-a-complex

The common scientific belief around 1900 was that the only dietary components needed to support life were protein, fats, carbohydrates, and salts.[1]  In 1912 Hopkins reported on experiments showing that "accessory factors" seemed to be needed.[1]  In 1916, some of the factors began to be characterized in the paper "The Relation of the Unidentified Dietary Factors, the Fat-Soluble A, and Water-Soluble B, of the Diet to the Growth Promoting Properties of Milk."[2]  The title itself designates two factors as A and B.  Lack of factor A seemed to be associated with various problems particularly with the eyes, and factor B with a condition similar to beriberi.  Before long, another factor was found that was associated with scurvy. In 1920, the literature had a confusion of terminology in use, and Drummond, using a variant of Funk's word, proposed:

that the substances be spoken of as Vitamin A, B, C, etc. This simplified scheme should be quite sufficient until such time as the factors are isolated, and their true nature identified.[3]

It was only later that the factors became well characterized. Vitamin B came to be known to be a complex mixture, and its components took decades to be characterized.(Wikipedia)  As components of Vitamin B came to be known, subscripts were assigned.  Some of the subscripts were assigned to compounds that later turned out to not to be fundamental and essential, and so are no longer used. Vitamin B12 took a particularly long time to characterize.(Wikipedia)
The vitamins are now well understood, and each has a specific name unrelated to the vitamin naming scheme, yet the vitamin terminology continues to be used because it is well known and useful to people at many different levels of technical knowledge. The significance of the name of the B group of vitamins is that "B" follows "A" and precedes "C" in the alphabet, and the history of discovery is still embedded in the names we use.
[1]  Hopkins FG. Feeding experiments illustrating the importance of accessory factors in normal dietaries. J Physiol. 1912 Jul 15;44(5-6):425-60. doi: 10.1113/jphysiol.1912.sp001524. PMID: 16993143; PMCID: PMC1512834.
[2] EV McCollum, N Simmonds, W Pitz. The Relation of the Unidentified Dietary Factors, the Fat-Soluble A, and Water-Soluble B, of the Diet to the Growth Promoting Properties of Milk - Journal of Biological Chemistry, 1916
[3] Drummond JC. The Nomenclature of the so-called Accessory Food Factors (Vitamins). Biochem J. 1920 Oct;14(5):660. doi: 10.1042/bj0140660. PMID: 16742922; PMCID: PMC1258930.

According to PeaceHealth:

The vitamin B-complex refers to all of the known essential
  water-soluble vitamins except for vitamin C.
Vitamin B was once thought to be a single nutrient. Researchers later
  discovered these extracts contained several vitamins.
Each member of the B-complex has a unique structure and performs
  unique functions in the human body. Vitamins B1, B2, B3, and biotin
  participate in different aspects of energy production, vitamin B6 is
  essential for amino acid metabolism, and vitamin B12 and folic acid
  facilitate steps required for cell division.

So, vitamins B have different functions, but most of them appear to be involved in the metabolism, especially of carbohydrates (Medical Libre Texts).

B doesn't stand for anything. Originally, the vitamins were name alphabetically which can be traced to Cornelia Kennedy's 1916 Master's Thesis. What separates B-vitamins (and all vitamins) is there function. The function of B-vitamins is in metabolism and certain metabolic cycles, such as the Citric Acid Cycle.
Citations:
http://vc.bridgew.edu/cgi/viewcontent.cgi?article=1029&context=mahpls_fac
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4772032/

Please cite a reference in support of this assertion about B vitamins being classified as such because of an involvement in metabolism. It may be true, but I find it strange as the requirement for a vitamin must have been established before its function was known.


text:
Can the knowledge about torsion angles alone be sufficient for specifying secondary structures of protein?
I have read that Ramachandran plots are used to identify secondary structures of proteins. Also, alpha helices and beta strands cluster around specific regions of the plot which gives us the information about how much of these structures are present in the protein. But, it seems intuitively unreasonable. I can't convince myself "why there can't be other structures with the same torsion angles as alpha helices or beta sheets". Am I missing something?

Perhaps you are missing time with a suitable text book. Try Dickerson and Geis. Long out of print but you might pick up one second-hand if it isn’t in your university library. And this list can hardly respond to your intuition, other than to suggest you do not put too much trust in it.

There is some information on Ramachandran Plots that you may find useful in an answer I posted to another question.

The problem with your question is that you do not quote a source, so it is impossible to know what is meant by Ramachandran plots being used to identify secondary structure of proteins. Why? Because a Ramachandran plot made up of all the amino acids in a protein requires knowledge of the dihedral angles of each amino acid, and so can only be plotted for a protein if its 3D structure is known — in which case the secondary structure is evident as it is defined in terms of repeating dihedral angles. So what do you mean? Some kind of blind recognition quiz? You need to clarify your question.

Its not true that the Ramachandran plot will determine the secondary structure of an amino acid.
Ramachandran plots show the sterically allowed phi/psi angles of an amino acid.  As such nearly all non-glycine amino acids are in alpha/beta spaces.  Random coil segments of structure consist mostly of alpha and beta conformation amino acids in nonsense orders. (alpha/beta/beta/alpha/alpha and etc)
The dihedral angles repeated in a pattern over a several consecutive amino acids create secondary structure (N>4 or 7 for helices - strands need other strands forming sheets).

So, is it possible for two amino acids to have the same sterically allowed phi/psi angles ?

all the amino acids except for glycine have pretty much the same allowed phi/psi angles :) . glycine, having a hydrogen on the alpha carbon rotates much more freely. IN a polypeptide the allowed angles will change depending on the rest of the peptide... this is not as predictable..


text:
Are all carcinogens mutagens?
I assume that all carcinogens must be mutagens, but I've read that this is not the case. However, I can't find any good examples or an explanation of why it is not the case.
How can a non-mutagenic agent be carcinogenic?
How can something lead to uncontrolled division of abnormal cells without changing the genetic material of the organism?
The only explanation I've found is that normal replication of genetic material during normal cell division includes occasional errors, so any physical or chemical agent that simply speeds up cell division will increase the number of errors per time and can therefore be considered a potential carcinogen even though it is not directly mutagenic.
But that example doesn't satisfy me because such a compound would not increase the number of errors created per cell division, but is that the only way something non-mutagenic can be "carcinogenic"?
I've also read in This Question that Alcohol is an example of a non-mutagenic carcinogen because Alcohol does not damage DNA, but I think that's not accurate because I've also read that Ethanol is mutagenic via its first metabolite, acetaldehyde, or are they just using wordplay to say that Alcohol is not mutagenic because only its first metabolite is?

It depends a bit on what you consider carcinogenic. If in the strictest sense possible, it's a long list. For example, the NIEHS list contains estrogen, UV radiation and wood dust. Some of the items on that list will be non-mutagenic.

@Mast But those are all mutagenic

The entire list is long, very long. Did you check them all?

How can a non-mutagenic agent be carcinogenic?
An agent that causes overexpression of oncogenes or inhibition of tumor suppressors, would be carcinogenic but not mutagenic.
HPV, for instance, produces proteins that cause inactivation and degradation of tumor suppressors, p53 and pRb[1].
Regarding alcohol. As you guessed, alcohol is metabolized to form acetaldehyde which is mutagenic as well as carcinogenic. Moreover, alcohol metabolism can lead to production of ROS which can also be mutagenic. Overall, alcohol is considered a potential carcinogen by IARC due to the observed effects. These classifications are not based on molecular mechanisms.
More recently, a study by Riva et al (2020) has found that only three out of the twenty carcinogens they tested had a mutagenic effect.
Thus, to conclude, not all carcinogens are mutagens.

Reference:
 [1] IARC Working Group on the Evaluation of Carcinogenic Risk to Humans. Human Papillomaviruses. Lyon (FR): International Agency for Research on Cancer; 2007. (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 90.) 4, Molecular Mechanisms of HPV-induced Carcinogenesis.

Is there an example of a type of cancer that doesn't have high mutation rates/genome instability or acquired lots of mutations? I expect even viral infections ultimately lead to mutagenesis that make a tumour malignant?

@Cell Any tumorigenic signal has to be sustained for a cancer to become stable. Therefore mutations are necessary. HPV induced tumor is dependent on the virus. Certainly higher growth rate and bypassing of essential cell cycle checkpoints will increase the mutation rate. However, if a cancer cell keeps mutating then it will accumulate deleterious mutations. From the analysis of CTVT (a transmissible tumor), it has been found that five driver mutations are sufficient for increasing the fitness of the cancer cells and cancer cells then undergo selection against deleterious mutations.

@Cell to summarize, I guess there are no cancers (not lab models) without any driver mutations.

Alcohol itself is non-mutagenic because it does not directly alter DNA. (Additionally ethanol enhances carcinogenesis and is itself not a carcinogen - updated) There are similar non-mutagenic carcinogens such as estrogen - which is a carcinogen. Another important thing to realize is that a non-mutagenic carcinogen may not alter DNA, but instead alter receptors. This can lead to changes in expression of the DNA without actually changing the DNA. Research, such as in this article (https://www.ncbi.nlm.nih.gov/m/pubmed/2372870/) show that these compounds may alter membranous receptor sites or base their effects on long-term residence in the cells proper. Also, a somewhat older research article may also help your discovery: https://www.ncbi.nlm.nih.gov/m/pubmed/8476535/?i=3&from=/2372870/related. There are plenty of non-genotoxic carcinogens but also some that do alter DNA via intermediates, so it is important to check which one of these is the case.

Since when has ethanol been classified as a carcinogen? Not in the catalogues of laboratory chemical suppliers who, it least in Europe would have to label it as such with statutory warnings.

Ethanol enhances carcinogenesis induced by other compounds, and it may influence the initial as well as the promotional phase of carcinogenesis.
Reference: https://www.ncbi.nlm.nih.gov/pubmed/7050573

That is not the same as classifying as a carcinogen. In a question about carcinogens you and the poster need to be absolutely precise in your usage of the term.

If Ethanol is not a carcinogen, then it's not a non-mutagenic carcinogen. Also, I read that Estrogen is a weak carcinogen and a weak mutagen, so it's also not an example of a non-mutagenic carcinogen.

@David IARC considers alcohol as a potential carcinogen.

"Some retroviruses contain cancer-causing genes (oncogenes),
and cells infected by such retroviruses are oncogenically
transformed into tumor cells"
Molecular Cell Biology Lodish et al. 8th ed
DNA is integrated into the genome and cancer is not technically caused by "mutation". That is the case in some of the types of cervical cancers(HPV)
I believe that "not all carcinogens are mutagens" and "not all mutagens are carcinogens".
You may also consider the situation in which a chemical/protein effects the DNA in a way that causes a change in epigenetic code of the genome .Consequently that would also result in cancer by changing the gene expression patterns/amounts of products etc.

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