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Cellulose structure
In cellulose structure, some beta glucose are inverted. I’ve read that therefore the hydroxyl groups stick on both sides, but aren’t there hydroxyl groups on both sides anyways whether it was inverted or not and whether it was alpha and not beta? So why is this considered so special about cellulose?

Although cellulose is an important bio-molecule, this question concerns polysaccharide structure, and I believe it would garner more attention on chemistry.SE.

@Dirigible — Structural Biology is on topic here.  The question, however is unintelligible to me as it stands. What does the poster mean by “the structure is inverted” and “stick out on both sides”? Unless and until he presents molecular structures — which would probably answer his problem — it is a waste of everyone’s time considering his question.

Indeed, there would be hydroxyl groups in both sides independently of the orientation in space of each glucose monomer. The alternating inversion of each glucose residue reduces the steric effects between each monomer, simultaneously allowing the formation of more hydrogen bonds between each glucose. So it is a matter of molecular stability, and this is not special to cellulose, as it can be seen in other polysaccharides (e.g. chitin).


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Can hand sanitizer kill a fertilized human egg cell?
If you took a human egg cell that was fertilized in vitro and sprayed some hand sanitizer on it would it die?

Hello and Welcome at Biology SE! Please take our tour to see how to ask good questions on this site.

Yes, most likely.  Alcohol-based hand sanitizers are at least 60% alcohol (ethanol or isopropanol).  Alcohol concentrations as low as 15% are efficient at killing cultured mammalian cells.
See: Toxicity of Ethanol in Low Concentrations: Experimental Evaluation in Cell Culture

All cells were killed by a 15-s exposure to 30-40% ethanol while a concentration as low as 15-20% gave a total response after 5-10-min exposures.

source: Stack Exchange

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

sort: votes


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Does the human eye’s field of view shrink when focusing on far away objects?
It seems like the lenses of the eye is like a fisheye lens that flattens out to a normal lens when looking at far away objects. Does that also mean that the field of view gets narrowed down as well? Or is that not how light works?

It's not quite as simple as a plain camera lens.  For instance, the different types of photoreceptors aren't evenly distributed on the retina: https://www.ncbi.nlm.nih.gov/books/NBK10848/  Then the brain does a lot of image processing, so while the optical field of view might stay the same, the field of attention will change.

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


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How does the shoulder joint stay in place?
I read that a human shoulder is a ball and socket joint, but when looking at a picture of a shoulder the socket part seemed way too small to hold the ball in place like a ball and socket joint. Usually the socket covers a little over half the ball and the shoulder socket covers almost none. How does the shoulder stay connected? Are the illustrations wrong?

Because it's

held together by muscles, tendons, and ligaments.

(image from Wikipedia.)
It's somewhat complicated how all these parts contribute to holding the joint in place because it depends on the position of the joint. E.g.

Shoulder muscle forces are usually powerful stabilizers of the glenohumeral joint, especially in mid-range positions when the passive stabilizers are lax. However, muscle forces can contribute to instability as well. Certain muscle forces decrease glenohumeral joint stability in end-range positions. We found this to be the case with both active and passive pectoralis major forces.

That study has some data based on computational models and actual tests on cadavers.


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Large Alpine Hymenopteran Seen in the White Mountains
I was hiking in the White Mountains in New Hampshire, USA, and at the peak of Mount Eisenhower saw a number of large bee-like insects. They appeared to be nesting in a rock cairn, and were strikingly large---length was about 1.5" (~40mm). Weather was clear, sunny, about 65 degrees Fahrenheit. Time of year was early July. Environment was alpine tundra, a few hundred feet above the treeline. Besides the habitat and large size, they seemed like fairly typical bees (I'm saying bees because they were almost certainly hymenopterans, but didn't have the typical "narrow waist" of wasps). The abdomen was the longest part of the body. Behavior-wise, they flew in and out of the cairn, and often rested on the ground (or on backpacks, water bottles, etc). Does anyone know what species this may have been?
(I'm sorry I don't have any photos; even if species is impossible to determine without them I'd be happy for any information on possible family or genus)

Did you notice anything about their flying? Did they seem to hover and linger? Did the sound of their "buzzing" sound "off" to you (i.e., unlike a normal bee buzz)? If yes to these, then you most likely saw a bee mimic fly called a hoverfly. [I'm not sure if hoverflies vs bees are more likely to be above tree line in NH]....If you answer "no" to my above questions, any further information you can provide (coloration, detailed behavior, number of individuals, etc.) would be helpful.

@theforestecologist I don't remember the sound, but they didn't hover at all. There seemed to be about one or two dozen individuals out and about at a time, but they didn't swarm or gather in groups. Abdomen was dark, if I remember correctly. Again, most striking feature was the size: 1.5 inches long and maybe 2/3 inch wide.

@Sol you might want to visit bugguide.net and look at the Hymenopteran families Siricidae (horntails) or Cimbicidae (Cimbicid sawflies); what you've said so far suggests to me that one or the other of those might be the answer to your question.

@ArthurJFrost thank you! Looks like they were probably some sort of cimbicid sawfly

Looks like some sort of cimbicid sawfly. Thanks @ArthurJFrost !


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How do obligate carnivores not have nutrient deficiencies?
I know that if a human eats just meat without plants, they develop issues like scurvy. If my understanding of it is correct that there are nutrients not found in meat, then how do obligate carnivores not suffer from certain nutrient deficiencies?

To add to Bryans answer there are a few other issues.
mainly pickiness and brains.
Human can handle an all animal diet surprisingly well, look at the modern Mongolian nomad diet, which is exclusively animal based. One problem we see in modern humans in industrialized nations is they often avoid eating organ meats, eating only muscle tissue "meat" can easily lead to a nutrient deficiencies. Ask yourself when is the last time you sat down to a liver or kidney dinner. many vitamins are almost exclusively found in organ meats and not muscle tissue. So many times when people from first world countries end up on an all meat diet they end up with deficiencies because they are not eating the vitamin rich portions of the animal.
The other problem is humans have very big brains, and brains can't burn fat. They can only burn carbohydrates or protein. you may already see the problem, animal tissue is rather poor in carbohydrates. But, you say, they have lots of protein,  which is true, but humans along with many animals do not metabolize proteins well, doing so on a large scale leads to ketone and other toxic byproducts. Human brains demand so many calories that they burn thorough what little carbohydrates animal tissue have, very quickly forcing ketosis. So humans must burn far more protein than most other animals on a all animal diet even when lipids are available because carbohydrates are lacking.
Carnivores also have adaptations to better deal with ketones, they still produce a lot of ketones but have better methods for managing them, mostly better ways to excrete them. Most apes only eat small amounts of meat and rarely lack carbohydrates in their diet, have not needed this adaptation. This is true for most of human history and the exceptions are very noticeable. The Mongolians I mentioned earlier also eat a lot of milk and cheese which contain a decent amount of carbohydrates.

Humans are pretty unusual in their inability to synthesize vitamin C (in humans, scurvy is caused not just by a lack of dietary vitamin C but the important factor that we can't simply make our own).
Wikipedia lists just a few mammals as examples of those unable to synthesize vitamin C: simians, tarsiers, capybara, and guinea pig. None are obligate carnivores.
Humans, like the others on this list, have a gene for the L-gulonolactone oxidase necessary in the synthesis pathway for vitamin C, but it's non functional. It seems that either losing function of this gene provided some evolutionary benefit (without a cost if diet was a sufficient source at the time), or it simply didn't provide any benefit and so there was insufficient selective pressure for it to remain functional.


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Can 2 eggs come from ONLY 1 ovary?
I only have 1 ovary due to previous pregnancy and was told that, that pregnancy was a twin pregnancy. I know I can have identical twins but I wanna know the odds of fraternal twins.

It would seem to be obviously yes, since it's possible to have fraternal triplets: https://en.wikipedia.org/wiki/Multiple_birth#Triplets  I would guess that the odds for you having fraternal twins are about the same as a woman with two ovaries having triplets: about 1 in 1000.

The answer to this is yes, you can have fraternal twins. I don't know the likelihood of this happening, and I don't think there is any literature on it in the scientific community.
There is a phenomenon called superovulation, which is where more than one ova (egg) is released during a cycle. The classic model of one egg being released per cycle is still being investigated, and it is possible that it will be found to be true.
I had assumed (me not being an expert on fertility) that such a phenomenon was uncommon, but it seems that it is more the norm than not.
The most recent and most complete study I could find on this is an article on the development of follicles (pre-egg phase) in normal women from Canada. In the article they found that despite the current model of single waves of development and ova release, in most women there are at least two waves of follicular development per intraovulatory interval (IOI)1.

Nonrandom  changes  in  the  number  of  follicles >5mm and the diameter of follicles >6 mm (Non-Identity Method) were observed in all 50 women during the IOI, indicating a wave pattern of follicle development. Thirty-four of the 50 women (68%) exhibited two waves of follicle development; the  remaining  16  women  (32%)  exhibited  three  waves  of follicle development...  ...None  of  the  women  evaluated  exhibited  only  a single wave of follicle development during the IOI.

They didn't go so far as to say that each wave resulted in ovulation, despite several editorials claiming this was may be case in very reputable scientific journals (e.g. this British Medical Journal one).  In fact they say that only the final wave in each IOI is ovulatory (anovulation being without ovulation):

The final wave of the cycle was ovulatory and the preceding waves were anovulatory in all 50 women.

Of note is that for women who have undergone unilateral (one-sided) oophorectomy, the remaining ovary seems to compensate to some extent, producing regular menstrual cycles. I haven't been able to find out if there is an egg released from the one side each cycle or not, but I think most women don't necessarily alternate sides between cycles.

Baerwald et al., A new model for ovarian follicular development
during the human menstrual cycle. 2003. Fertility and Sterility 80(1).


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Is centrosome one of the structures that red blood cells lose during maturation process?
Centrosomes are microtubule organising centres- their function is to facilitate cell division.
RBCs don't undergo division. They are produced via hematopoeisis in the bone marrow. It doesn't even have a nucleus, hence there is no use for centrosomes in mature RBCs and they probably don't have it.
I couldn't find any paper indicating this point. Is that true?

I was aware that mature red blood cells (RBCs) lose their nucleus, ER and Golgi apparatus. However, I wasn't sure about the centrosome! Centrosomes, being MTOCs (microtubule organising centers), have known functions beyond those in cell division. Some are cell type specific! So be wary of thinking that all cells that do not undergo mitosis lack centrosomes. I find it flawed to reason along the lines of
mature RBCs are anucleated cells =  no nucleus = no nuclear membrane = no mitosis = no mitotic spindle = no centrosomes

After a little research, I've found the following unreferenced statement in this opinion piece by Rieder, Faruki & Khodjakov from 2001 in Trends in Cell Biology:

In some cells such as megakaryocytes, myocytes and red blood cells of
higher animals, the centrosome degenerates. As a rule, however, such
cells are terminally differentiated and no longer capable of entering
the mitotic cycle.

If somebody finds a concrete example (or better yet, image!), that would be more convincing than an opinion piece.


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Does this evolutionary model of mutations have a flaw?
In a youtube video by an evolutionary biologist titled Creation Myths: Genetic Entropy at 14:50 he explains that the ratio between beneficial + neutral mutations and deleterious mutations decreases over time since the probability of a beneficial mutation increases over time because the more deleterious mutations the more opportunities for a deleterious substitution to back mutate creating a beneficial mutation until there is an equilibrium.
My issue with this is that this model only includes substitutions and according to one study 16% - 25% of mutations in the human genome are indels. And the probability of a indel reversing is incredibly low as far as I understand. What I would like to know is how does indels and other mutations beyond substitutions affect this model of mutations? Surely it shouldn't be ignored.

On the contrary, stepwise mutation (adding/subtracting one unit from a repeat array) is one of the canonical mutational patterns for indels, and it is eminently repeatable/reversible. And 25% is probably too low!

@MaximilianPress I agree with answer

Hugely complex question. It has been considered and reconsidered many times. There is the neutral theory, which states that the vast overwhelming majority of mutations have no effect on the phenotype. The nearly neutral theory and the classical theory. Neutral theory is a big subject.
On indels, these can be "neutral" and reversing depends how much selection pressure they are under. Microsatellites do "reverse".
Essentially, this is a massive question and its better to consider a single species as an example for a single type of mutation
See the comment by @MaximillianPress. That is a good answer, the step-wise mutation model is not a bad model for (microsatellite indels) and states indels can "grow" and "shrink" one repeat unit at a time. I know what the OP is saying alot of indels occur in protein genes and must have a specific function.

Indels under selection pressure are common in the surface antigens of many pathogens including HIV. The distribution for codon indels in env was modelled by Fletcher and Yang 2009 here. This is a strongly skewed distribution and maintenance of very long indel lengths of up to 100 could only be maintained by selection pressure, however the preponderance of small copy number indels is massively dominant.
The stepwise model (SMM) is not a skewed distribution it assumes that there is equal probability for increasing the indel size as it is reducing it. This was used for microsatellites which are assumed to be neutral (not under selection pressure).
In protein modeling under the old DUET model (now deprecated) by Pires and Tom Blundell 2014 showed maximum structural disruption for indels.

Can you elaborate on how indels are able to be reversed? Or do you just mean reversed as in taken out of the gene pool due to selection?

done as requested


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What book teaches you about endogenous retroviruses
I'm interest in ERVs as evidence for evolution and want to learn more about them.

The Sverdlov book is from 2005, and much work has been done in the 15 years after that. Here's a more recent review article with many useful references:
Escalera-Zamudio M, Greenwood AD. On the classification and evolution of endogenous retrovirus: humanendogenous retroviruses may not be ‘human’ after all. APMIS 2016; 124: 44–51. PMID: 26818261 DOI: 10.1111/apm.12489

can you please add appropriate links (PubMed, DOI, etc.)?

Try this one:
Retroviruses and Primate Genome Evolution - Eugene D. Sverdlov
Hope you find this answer helpful.


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What portion of the human genome is dedicated to the developement of the fetus?
I was thinking about how we don't know the function of a large portion of DNA and I thought maybe it's because it's only used during the development of the fetus

"Only used during the development of the fetus" fetus dev is pretty important, no? Depends a lot on what you mean by "dedicated to". Not much of the genome is "dedicated to" an artificial human concept. But this random paper estimates that in fish (a developmental model similar to humans), 5-10% of genes are not only used in but critical to development. This is a subset, and in humans there's more neural development, and genes != genome, but that's a start. (It's recommended to do a little googling before you ask a question.)

I'm guessing this question is coming from misunderstanding "junk DNA" etc and not realizing that there is no confusion about any DNA that codes for proteins that could lead to "missing" some because it's only used in development.


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Octopus out of water
I was watching a YouTube video where a guy saw an octopus out of water. It was far from a puddle, and looked like it was struggling. He decided to help it get to the next puddle, so he picked it up and said he hoped it did not bite him or ink.
It got me to wonder, what happens when an octopus produces ink out of the water? I tried looking up a video or a Wikipedia entry about it, and did not find anything. Does the ink squirt out in a jet? Does it dribble out into a puddle? Looking it up, I know the ink is expelled from their siphons, but I have not found anything about octopuses expelling ink when out of water.

Does this help https://en.wikipedia.org/wiki/Cephalopod_ink?

It is definitely interesting information, but it does not address what happens when (or if) an octopus tries expelling ink when out of water.


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If we evolve from microbes then why so many microbes are still here?
Researchers say that we evolve from microbes then why there are still so many microbes ?

https://blogs.iu.edu/sciu/2017/09/26/why-are-there-still-apes/

To answer the intention of the question: evolution works by branching. To use this language of 'microbes', imagine a world with only microbe A. Say there are 100,000 individuals of the species microbe A.
Now let one of the microbe As reproduce and produce a mutation leading to the first microbe B. This evolutionary step would not transform every microbe A into a microbe B. The change would only be in the offspring of one of the 100,000 microbe A. This would create a new branch as the new microbe Bs reproduced, but would not affect the 99,999 other microbe As.
There is no reason for microbe A to die out just because a small portion of them had children that eventually became microbe B (unless they were in direct competition for limited resources, or one was a predator for the other, etc.). The other microbe As can just go on living as before, and either stay the same or branch into even more species-- say microbes C, D, E and F.
Let this run for hundreds of millions of years and you get more and more complicated life eventually resulting in what we see around us, including many species that have evolved into other species.
Note that this is very simplified for the sake of clear explanation. A mutation does not necessarily result in a new species.

As noted in the previous explanation, but said in other way:
Our evolutionary lineage may have a common ancestor (aka, a "parent species", say, another microbe [a microbe that no longer lives today, probably]) with some of today's microbes many years ago.
In this scenario, if we look at the "childs of that parent species", we may find a variety of genotypes, which will express different phenotypes.
If we look at the different childs generated in the previous step, and iterate that process, eventually you could get some organisms more similar to the common ancestor between us and microbes (aka, the microbes), and some individuals with a great amount of divergence from the common ancestor (aka, us).
This divergence process has to do with genetic mutations generated at reproduction of each individual.


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Why do the mRNA vaccines for COVID need special lipids?
I've read that the Pfizer mRNA vaccine is delivered to the cell by encapsulating the fragile mRNA into a lipid nanoparticle. However, the lipid has to be PEGylated in order to avoid immunogenecity. Why is that? How does PEGylation reduce immunogenicity in general?

Lipid nano particles are bound by serum proteins, the opsonins which are part of the innate system and are subsequently eliminated from the body by uptake through macrophages.
Binding PEG to the surface of these particles increases their hydrophilicity (and obviously creates a hydrate hull around the particles) and functions as well as a steric barrier. Both measures prevent the opsonins from binding the particles and thus marking them for removal, which extends their half-life (see the references for more details).
References:

PEGylated liposomes: immunological responses
Rationale and Application of PEGylated Lipid-Based System for
Advanced Target Delivery of siRNA


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difference between biotic and living?
how  can we differentiate between biotic and living things,is  there any difference? and same for abiotic and non-living?
I think it is that biotic is like biomass and living should carry out life processes.

Have you tried googling dictionary definition of biotic/abiotic?

biotic: relating to or resulting from living things, especially in their ecological relations (Oxford)

While there may be a field-specific connotation that I'm not aware of, I've never heard "biotic" as a category of "things" before. I am most familiar with it's use in the context of ecology, e.g. a parasite might be a biotic factor in the survival of a population of animals in a particular ecosystem.
To get to the heart of your question, I don't think there is a difference, but rather a relation: biotic factors refer to currently or formerly living things (and abiotic refers to things that are or were not alive).

But don't you think that a dead animalis non-living but still biotic facor.

Fair point, I edited my answer to make it hopefully clearer. The main point is that "biotic" and "living" are not two categories to compare; but that "biotic" refers to factors relating to or originating from "living things".


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Pedigree probability question
The following pedigree shows the inheritance pattern of a trait. From the following, select the possible mode of inheritance and the probability that the daughter in generation III will show the trait.
a) X-linked recessive, probability is 1/2
b) X-linked recessive, probability is 1/4
c) Autosomal recessive, probability is 1/2
d) Autosomal recessive, probability is 1/3

This question is from an examination. The answer key says c) is the answer. I get how c) could be the answer, but I also think a) is a possibility. Please tell me if a) is possible or not.

No, it cannot be X-linked recessive, because in this case, the right-most son would have a trait.


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Why is it easier to spin in one direction than in the other?
When I use a rotating floor disk to spin fast (while standing), I notice that I can keep balance much easier and rotate much faster in clockwise direction rather than in counterclockwise direction. I can even spin while standing on one leg clockwise, but not counterclockwise.
How this asymmetry can be explained? Does it happen for all humans? If yes, is clockwise spinning direction is always simpler or sometimes it is vice versa (like left-handedness)?

Welcome to Bio.SE! This seems like personal experience that isn't a universal phenomenon. Have you looked into its generality at all? We ask that posters try to research their own question and explicitly indicate what research they've already done, what they learned, and what is still unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Good old-fashioned learned behaviour, just like crawling, but I have no proof.

You are right handed, no? Handedness extends to many, many other factors, including vision. Visual connections to parts of the brain are stronger form the dominant eye. This is probably the reason, but I'm happy to be wrong if you're left handed.

@bob1 - Don't just take a guess... Physiology is complex.

@anongoodnurse, I am indeed right handed.

@Anonymous - If you are right-eye dominant (which is likely), your visual "skills" (such as spacial orientation, etc.) are better for the right side of your upper body. It makes sense that you would commence practicing a skill demanding good spacial orientation in the direction in which you are most confident. And that doesn't even take into account footedness)

I’m voting to close this question because it is unsuitable for the following reasons: 1) idiosyncratic and therefore not of general interest; 2) a personal medical question; and 3) multiple questions (i.e. unfocused) — there is also no evidence that any prior research was attempted.

It is just idiosyncrasy of practice and learned behavior, and it almost certainly has little-or-nothing to do with some genetically-determined asymmetry within one's vestibular system. Humans of the same handedness prefer to spin one way, or the other, and footedness and handedness are often not shared on the same side. It's like preference for holding the phone with one hand, or turning in one direction during a startle reflex, or using a tool such as a hammer with a preferred hand. All these are reversible with training and the less dominant side is eminently trainable, even beyond the comfort level of the dominant side. To my knowledge there are no studies that would indicate otherwise (hence the "lack of sources" mentioned in the comments). I think the reason that we have sidedness, or handedness for instance, is because of small initial preferences being reinforced, conditioning, and habit. These of course can present as differences in relative nerve or muscle or tendon sizes - however, I stress that these are very individual-specific and subject to change throughout life, i.e. idiosyncratic and plastic.
Here is a review from 2019 from Marcori et al. which goes into some of the underlying neurological phenomena, which tries to detail exactly how dynamically handedness can change. It is only a primer and does not delve into the sidedness that you specifically ask about (spinning) nor the vast majority of sidednesses that you may allude to.
Everyone has some deep, personal experience with their vestibular experiences, be it during exercise, sport or movement, so I feel a comparison of a few anecdotes can do this topic justice, for the sake of understanding the variety of experiences humans have.
If I may: I have a natural preference for keeping balance in counterclockwise spinning, unlike you. Though like you, I am right handed, right footed, and with board sports I ride goofy stance, which is less common than regular stance. With practice you can very obviously and overtly build comfort for the 'lesser preference'. Time spent playing team sports has resulted in a high degree of ambidexterity (confidence, or comfort) in both arms and legs, but with skateboarding, a newer hobby (which incidentally require a considerable degree of 'detaching yourself from the ground', as well as lateral motion, both being new and unfamiliar sensations), I find myself far from able to comfortably ride fakie or in switch stances (with weak foot toward direction of motion, for goofy riders). They are very alien feelings, just as kicking or throwing a ball used to be with my less dominant limbs. There are right-handed musicians that play left-handed instruments (e.g. guitars) and vice versa. The same goes for archers, martial arts, the list is surely endless. There are myriad examples that disprove your suggestion, so I hope that you now better understand that there is no universality, and that the extent of your suggestion was limited in the first place.
However, to elaborate on the biology of things... Certainly at the neural (circuitry) level, and perhaps even within the vestibular system, there are - and must be - differences that cause you to have a preference. Preferences are ultimately physiological, and the fact that you turn this way or that to cover your face from incoming objects is not completely random or indeterministic. But there is no universality that you suggest for a certain direction among humans, especially for spinning or correcting for experienced centrifugal force. Even handedness, which to us may seem fixed, is not fixed; in many parts of the world, left-handed writing was frowned upon and children were forced to write with their right hands, and became right-hand dominant. Certainly some folks from the older generations have experienced this first hand and can attest to how plastic handedness can be.

Re the plasticity of handedness, that's not entirely true, at least in my experience.  You can certainly train yourself to do things with your off hand, but unless you are naturally fairly ambidexterous (or in my case, ambi-clumsy :-)). you'll never do them as well.

So many...incorrect statements, and all without sources! And some bolded no less!!!

"[T]he "lack of sources" mentioned in the comments" is not because this is unstudied, because it has been studied enough to easily find multiple sources with a quick google search. Otherwise I could not say that "Visual connections to parts of the brain are stronger form (sic) the dominant eye." Which is the tip of the iceberg in eye sidedness. Heck, it's even been studied in flounders (which, given, is kinda unique.) And the edit? If I could downvote again, I would. So many incorrect statements...

Sorry to disappoint. As a more informed person on the matter, you should feel encouraged to write a better answer to help OP out. If this has not already resolved the relatively simple question posed, I made a deeper search and found a few that truly do not seem an ideal fit, but perhaps to others. I add them here for posterity: somewhat of a tangential review of recent findings, vestibular processing in rats and handedness-depedence to vestibular function.


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Is the Amazon forest O2 and CO2 neutral?
In these days, we receive a lot of concerning news about the Amazon burning. Recently, I came across widespread claims about the production of O2   and the absorption of CO2 by the Amazon forest, something known as "carbon dioxide in, oxygen out". However, I also found claims that the Amazon ecosystem uses up all the oxygen it produces, and that it is a stable carbon sink, i.e. it acts like a carbon storage system, not as a sponge for carbon.
What are the real facts about oxygen and carbon dioxyde dynamics in the Amazon forest? I'd intuitively say that the second hypothesis is stronger, but I'd like to have a confirmation backed by some papers.

tl;dr We don't really know. A reasonable guess is that it's a weak sink, gradually turning into a source via increased drought frequency, but it's extremely hard to measure; carbon flux is highly variable both spatially and temporally (so it matters both when and where you measure), and it's difficult to make sure that you're accurately measuring all the different components of carbon flux.
Dolman and Janssen 2018 say:

Ground observations suggest that, through tree growth, the Amazon forest acts as a net carbon sink to the atmosphere (Brienen et al 2015), which is confirmed by atmospheric studies (Gatti et al 2015). However, the sink strength appears to have been declining since the 1990s and recent drought events in 2005, 2010 and 2015 might have temporarily reversed the Amazon carbon sink into a source (Feldpausch et al 2016, Gatti et al 2015)

They go on to discuss the great difficulties in constructing an accurate model of Amazonian carbon dynamics (for the purpose of predicting future source/sink relationships).
Rice et al. 2004
summary based on measuring living trees and coarse woody debris [CWD], it looks like a particular patch of forest was a small net source, but this may be a transient effect.

Amazon forests could be globally significant sinks or sources for atmospheric carbon dioxide, but carbon balance of these forests remains poorly quantified.

In other words, "it's still unclear [as of 2004], so we did another study."

We surveyed 19.75 ha along four 1‐km transects of well‐drained old‐growth upland forest in the Tapajós National Forest near Santarém, Pará, Brazil (2°51′ S, 54°58′ W) in order to assess carbon pool sizes, fluxes, and climatic controls on carbon balance.

So they took a very small sample of a particular forest type.

The gain in live wood biomass was exceeded by respiration losses from CWD [coarse woody debris], resulting in an overall estimated net loss from total aboveground biomass ...

So this particular patch of forest was a carbon source at this particular time ...

... a period of high mortality [probably] preceded the initiation of this study ... transfer of carbon between live and dead biomass pools appears to have led to substantial increases in the pool of CWD, causing the observed net carbon release.

... but that may be due mostly to a recent die-off - maybe not true over a longer time scale ...

... the hypothesized sequestration flux from CO2 fertilization ... would be comparatively small and masked for considerable periods by climate‐driven shifts in forest structure and associated carbon balance in tropical forests.

... it will probably bounce around a lot (i.e., it's not wise to extrapolate this result either in space or time).
Miller et al. 2004

We used two independent approaches, biometry and micrometeorology, to determine the net ecosystem production (NEP) of an old growth forest in Pará, Brazil. ... Biometric inventories indicated that the forest was either a source or, at most, a modest sink of carbon from 1984 to 2000 ... biometric and micrometeorological measurements in tandem provide strong evidence that the forest was not a strong, persistent carbon sink during the study interval.

and a more recent reference ...
Antonucci et al. 2018

The objective this paper was to quantify the hourly variability of CO2 fluxes in the year of the El Niño, in 2015, in a tropical rain forest in the Western Amazon ... The average daily behavior of CO2 fluxes showed higher concentrations of absorption during the day than emissions overnight, behaving as a carbon sink, corroborating the importance of the forest in assimilation of the atmospheric carbon.

references

Miller et al, "Biometric and micrometeorological measurements of tropical forest carbon balance". Ecological Applications 2004, https://doi.org/10.1890/02-6005
Rice et al., "Carbon balance and vegetation dynamics in an old-growth Amazonian forest". Ecological Applications 2004, https://doi.org/10.1890/02-6006
Antonucci et al, "CO2 fluxes in a wet tropical forest area in Western Amazon in year of El Niño". Ciência e Natura, v. 40, 2018. https://periodicos.ufsm.br/cienciaenatura/article/view/30718
Dolman and Janssen, "The enigma of the Amazonian carbon balance", Environmental Research Letters 2018. https://iopscience.iop.org/article/10.1088/1748-9326/aac78e/meta


text:
Is transition more common than transversion during the evolution of duplicated genes?
Transitions are base mutations of purine to purine (A <-> G) or pyrimidine to pyrimidine (C <-> T). Transversions are purine to pyrimidine or vice versa (A <-> C, A <-> T, G <-> C, G <-> T). And it is well-known that transitions are more common than transversions in the populations.
So what is the condition in the evolution of duplicated genes? Suppose a gene A is duplicated with two copies A1 and A2 in the same genome (not two alleles in different sets of chromosomes, or the same gene in two different cells/organisms). At first A1 and A2 had the same sequence, but then they went through an evolution process and each got some mutations. Now let's check the sequence of A1 and A2 again, are the differences between A1 and A2 mainly transitions instead of transversions?
Although I think it would not be surprising to find that transitions are more common in this condition, I've searched some papers focusing on the evolution of duplicated genes to look for some support. However, they mainly discuss what happened to their functions instead of sequences.

If we consider that the biochemical impact of transitions vs transversions is constant across the two scenarios, then the only discrepancy can be due to the level of purifying selection, or the level of positive diversifying selection, or both, between the two duplicates.
By far the most common fate to one duplicate copy is for purifying selection to be relaxed, leading to accruing deleterious mutations and eventually loss. This means that fixation of non-synonymous mutations are more common, and as transversions are more likely to be non-synonymous, this implies that the rate of fixation for transversions would increase.
Similarly, one might expect functional change leading to positive diversifying selection, which implies a greater rate of fixation of non-synonymous mutations and, following the same logic as above, a greater rate of transversions.
Whether or not this contributing increase to the rate of fixation of transversions mean that transversions actually outnumber transitions, or instead merely decreases the ratio of transition:transversion, will be dependent on the particular gene and selective scenario.
As a final note, while the first cause I identified (biochemical)  actually changes the rate of mutation, the selection-specific factors are changes to rate of fixation, which is a population-level process. So while the relative rates of transition and transversion may stay the same, the fixation rates of these two categories of mutation between the two duplicate copies are the important difference.


text:
Mechanism of Octoxynol-10 as a preservative in vaccines
I noticed that the Fluarix Quad flu shot this season contains Octoxynol-10 rather than Thimerosal as a preservative. I am not expert in this area, so I did a Google search of "Octoxynol-10", and noticed that it has lysing properties and so speculated that this must be how it would kill any bacteria present and thus act as a preservative. Nonoxynol-9 is an active ingredient in anti-spermicides, I speculate for the same reason.
My question is: What does the Octoxynol-10 do when injected into my muscle tissue? I speculate that there may be some lysing of my cells. Perhaps only the cells with very thin membranes lyse? bacteria, sperm, nerve?

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Can a hairpin (stem loop) within a transcript stall a eukaryotic ribosome?
Is their evidence of RNA secondary structure causing a stall in translation within a eukaryotic cell?

Hi @LeeAnn, and welcome to biology.SE. Someone has voted to close your question because you haven't shown an attempt at the answer. What prompted the question and how have you tried to solve it before coming here?

Can a hairpin (stem loop) within a transcript stall a eukaryotic ribosome?

It seems that could happen.
C9orf72 translation is one of the examples. In this gene, GGGGCC repeats exist in 5' UTR of the mRNA (upstream of the first ATG). The repeats expand in subsets of neurodegenerative disorder such as ALS. The repeats can form a stem loop structure and stem loops of expanded repeats are more stable.
mRNAs having expanded repeats seems producing poly-GlyAla, poly-GlyPro, and poly-GlyArg peptides which codons are GGG-GCC, GGG-CCG, and GGC-CGG from different frames from GGGCC repeat.
This means the translation starts somewhere in or upstream of the repeat without ATG. To explain this, there is speculation that ribosomes stall because of the tight structure of the stem loop by expanded GGGGCC repeats, mistakenly take tRNAs and start translation. It is called "Repeat-associated non-ATG translation".
You might want to refer to:
Repeat-associated non-AUG translation and its impact in neurodegenerative disease.
https://sites.tufts.edu/als/the-answer/c9orf72/
RAN translation and frameshifting as translational challenges at simple repeats of human neurodegenerative disorders

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Why is competence useful for a starving cell?
I know that some bacteria become competent when there is not much food available in their environment.
I don't really understand why this is useful for the cell. I've seen some other organisms form a biofilm or get together to become a slime when starved and I understand the utility of this mechanisms (reducing energy consumption and being able to move around easily to look for nutrients).
The only plausible explanation that I see is that being competent might be useful to take advantage of the DNA of dead cells. Am I right?

The wikipedia article you link gives four current hypotheses: genetic diversity, "DNA as food," repair of DNA damage and Horizontal gene transfer. Are you looking for additional hypotheses, or a clarification of what's in the article?

@AJK I would like some clarification. For instance I don't understand the "DNA as food" hypothesis. In my understanding if all the cells became competent then there would be no available DNA in the medium they're growing in and they would die, making one of the above forms (biofilm - slime) preferable.


text:
Electrodes for electroporation of bacterial cells
Wikipedia says

"The process {electroporation} requires direct contact between the electrodes and the suspension."

However I've read the process is an effect of the field strength alone, and ideally no current passes at all, due to its heating and other unwanted effects. Why can there not then be a resistive layer between the electrodes and sample to stop any current flowing?

Hmmm, I'm not sure that this is the right site to answer this question - you might be better migrating to electrical engineering or  physics for a complete answer. I suspect that if it worked without direct current, then it would be done that way - perhaps you have a new idea and you can test it and potentially get a patent.


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What are the key mechanisms of control and transport of ATP from mitochondria to synapse in active firing neurons?
I am working with a group in the field of neuronal activity (in computational neuroscience), in specific the firing rates at different ensemble/population hierarchies.
It is well established that neuronal activity, particularly in the synaptic areas, is energy-intensive, and ATP consuming. There is vast scientific research literature on the molecular mechanisms of how ATP in the membrane area of synapses is being processed. However, in contrast, there is a challenge to understand the molecular mechanisms of how the synaptic cellular membrane regions communicate at the neuron's molecular level with the mitochondria to ensure tight energy control. There are two central questions which I want to understand:

How and by which mechanisms, at the molecular level, the synaptic areas of the membrane ensure an efficient system control of ATP delivery adapting to the neuronal activity requirements.
The mechanism of transport of ATP from mitochondria to the synaptic regions of the cell membrane.

I would appreciate comprehensive information on both aspects. The answer should optimally:

describe the key molecular mechanisms at a high-level,
including clearly key and major steps of the control and transport process, and
referring to scientific reference papers for further detailed insights.

Research results must not be focused on human neurons, and can be on model organisms or cells.
Thank you in advance.

I've posted an answer, but please do recognize that StackExchange is a site for specific questions and answers. We're not a lit review service and it's not appropriate to request answers that themselves would make up an entire book or even paper.

Synapses are full of mitochondria - Palay, S. L. (1956). Synapses in the central nervous system. The Journal of biophysical and biochemical cytology, 2(4), 193.
So, it's not so much that ATP needs to be delivered to synapses; ATP is manufactured there. Trafficking of mitochondria to synapses is regulated by neuronal activity, see for example:
Sheng, Z. H., & Cai, Q. (2012). Mitochondrial transport in neurons: impact on synaptic homeostasis and neurodegeneration. Nature Reviews Neuroscience, 13(2), 77-93.
This review talks about kinesin and dynein motors that are involved in this transport along microtubules. Like many other aspects of neural transmission, mitochondrial transport is regulated at least in part through calcium concentrations. Like other elements of the synaptic machinery, mitochondria are anchored to synaptic protein complexes which keeps them in place. The more places to dock, the greater eventual concentration of everything in the synapse. Additionally, both calcium and ADP concentration slow down mitochondrial transport and can lead to a process where mitochondria stop moving around and settle where they are needed. Calcium concentration is increased when synapses are active, and ADP is high when ATP is being used, so both of those signals cause mitochondria to "stop" when they pass by an area that needs more ATP production, and keep on moving through otherwise.
Other relevant reviews:
Misgeld, T., & Schwarz, T. L. (2017). Mitostasis in neurons: maintaining mitochondria in an extended cellular architecture. Neuron, 96(3), 651-666.
Devine, M. J., & Kittler, J. T. (2018). Mitochondria at the neuronal presynapse in health and disease. Nature Reviews Neuroscience, 19(2), 63-80.
Rossi, M. J., & Pekkurnaz, G. (2019). Powerhouse of the mind: mitochondrial plasticity at the synapse. Current opinion in neurobiology, 57, 149-155..

Thank you. I knew about Palay et al. 1956 but did not trust because it was old and not mechanistic. The other references, particularly Rossi et al., really exciting and new to me. Your description helps to deep dive.


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Please help strang micro warm like thing found in dogs kennel in Conyers Georgia
I found this strange tiny warm under my five months old puppy's cage can someone please help find out what it is their was about thirty of them her cage is cleaned regularly and is dry and cozy I've checked her poop nothing in it but she is constantly scratching and losing hair rapidly no flea's on her

Welcome to the site - we would need to know where in the world you are, and preferably get some better pictures and a sense of how big these "worms" are. Could the scratching be caused by shedding (spring/summer coming in the Northern hemisphere...)? Do you groom the puppy and get these off her, or were they only found on her bedding?

If you're concerned about the health of your puppy, please take them to a veterinarian.


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How is it possible that animals that produce venom do not end up being poisoned?
My question is kind of naïve. Some living organisms are known to be capable of producing highly lethal venom to defend themselves (snakes is probably the first example to come to mind, but it is also true for many kinds of toads, marine organisms, various insects and so on). So, they must store it some where within their bodies. One could expect these substances to gradually diffuse into tissues surrounding the venom reservoir that would result in killing cells, poisoning or necrosis of the tissues. It is not difficult to arrive at a conclusion what would be the final outcome of this process for the whole organism. We know it does not happen. Why? What prevents venom from spreading?

Have you searched this site? I’m almost sure this question has been asked before. And what research have you done elsewhere?

the venom injected by a snake will break down in the digestion of the prey,venom is different from poison,venom is injected and poison is eaten.

If an animal produces a venom, most likely immunity to that venom co-evolved along with it. If it didn't, obviously the species would no longer exist.

Quite various strategies: Specialized cells, glands and organs, protective molecules (e.g. inhibitors), physical barriers (e.g. tough, fibrous capsules), pH and activation required (change in pH or the presence of a certain enzyme needed for activation), target specificity (receptors' specificity), and most fascinating: autoimmunity.


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Is there a database for fossilized coral reefs that have been reported?
Given that coral lives only up to 5,000 years, and I assume marine biologists have maps of where all known living reefs are around the world for research and monitoring, where can I find information on locations of known dead coral, and especially fossilized coral as I once encountered on an island in the western Caribbean?
Is there a scientific database, oceanography software/framework, or perhaps publications such as by NCBI, which provide records of instances of fossilized coral which have been located and which perhaps document their age, conditions that led to their demise, etc.?

NOAA has a helpful short article called "What's in a Name? - Coral Reef" by John K. Reed which has a section on "Coral Growth and Reef Age" which was useful for finding references to more recently developed fossils: https://oceanexplorer.noaa.gov/explorations/02sab/background/corals/corals.html

Yes, have a read from:
The Paleobiology Database (PBDB): A comprehensive online resource that compiles data on fossil occurrences from various scientific publications and databases.
The Ocean Biogeographic Information System (OBIS): A global database that provides access to marine species occurrence data, including fossil corals.
Fossil forums and reddit fossil ID have direct access to pro geologists.
The Fossilworks Database:  It aims to provide a comprehensive record of fossil species including corals from all ages.

Thank you. On OBIS how can you filter for fossil corals specifically?

Perhaps this:  https://obis.org/taxon/1292 https://obis.org/dataset/89e23fc8-3f61-4480-9de3-358fe6eefe0b


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Cellulase Sample Digestion Protocol?
Is there an effective way to use cellulase(s) and/or lignase(s) to remove unwanted plant debris from a sample?
I'm working with a series of fresh water grab samples for environmental assessment. The objective is to separate out the benthic invertebrates as a proxy for biodiversity and habitat health. We use 500 micron mesh to remove the bulk of the sediments but this leaves several liters of fine plant material in a variety of stages of decomposition. While searching through yet another petridish of rotting sphagnum I wondered if there might not be a better way to do this?
Is there an effective protocol for decomposing the plant matter using some mixture of cellulases and lignases? Or am I barking up the wrong tree?

Welcome to Biology.SE! No experience with this but I would guess that cellulase treatment would be far too slow and I wouldn't have thought there was much lignin in sphagnum. Are these samples of living organisms or have they been fixed in some way? If live, could you use a variation of the technique I've seen where leaf litter is heated in funnels? Maybe you could try using noxious chemicals or heat to drive the invertebrates from the sphagnum slurry?

Thanks tyresome. The samples aren't entirely sphagnum and have a healthy amount of grasses, leaves, etc. Pretty much a stew of anything that fell into or grew in the river. The critters have been preserved in ethanol and are hopefully dead.

You could try experimenting with enzymes on some samples you've already analyzed — if you find something that works publish it and post your answer here!  The only alternative I can think of is if you could find a stain that was selective for invertebrates (I was thinking about chitin, but then realized your samples must be riddled with fungi). Good luck!


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Help id mushroom found in West Midlands, Egland
I found this mushroom yesterday. It looks like an oyster but it grows in some poorly kept lawn. I am sure there was no tree there in the past. This spot was landscaped a couple of years ago after building some blocks of flats. I turned it over, hoping to find some piece of wood, but there was nothing. It has a mild mushroomy smell. Do you have any ideas what it may be?

They look like pleurotus, i'd ask a mycology specialized forum like reddit or facebook mycology.

https://www.flickr.com/photos/shentsonebirder/8284582392 unsure


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Function of amatoxins
There are a couple of papers and "lots" of anectodal evidence which imply that mushroom hunting does not have any adverse effects on the fungi, neither short nor long term. One of the counter arguments for that is that some fungi developed deadly toxins and what reason do they have other than stoping animals from eating them?
So, I had this discussion recently and I raised this point. I was told that many compounds that fungi produce do nothing for the fungus and they are producing them just because they are not costly enough to be cut by evolution. I don't find this argument particularly compelling, so I was wondering whether we know anything about the function of such compounds, say amatoxins.
Do they have any function other than killing us? Are they used by the fungus for anything during its life cycle? Do they kill insects or larvae? Do we know anything about them?

I think this is a great question with minimal research in this area. There are superagonists that bind to human receptors better than our endogenous ligands. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4813425/


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How do *Polistes sulcifer* (cuckoo paper wasp) eggs hatch so quickly?
The Polistes sulcifer wasp is a brood parasitic species, which parasitizes colonies of the paper wasp Polistes dominulus. During an extremely brief time window in the spring, just before the P. dominulus workers have emerged, the P. sulcifer female will invade a P. dominulus nest. Once inside, it will kill or evict the host queen, ensure its cuticle hydrocarbon profile will not lead to its being attacked, and then lay its own eggs. It will rely on the host workers to tend to these.
(Note: I don't know whether it just alters its own hydrocarbon profile, or whether it also alters that of the nest. It's tangential to this question.)
The P. sulcifer wasp needs to time its attacks precisely. If it invades too late, the workers will have emerged and the colony will have a lot more wasps to defend it. If it invades too soon, there will not be enough host workers emerging to tend to its brood, especially if the host queen has not laid many eggs. P. sulcifer itself does not have a worker caste, and so is entirely reliant on host workers.
Research published in 2004 (paywalled, unfortunately) showed that the parasite wasp eggs took an average of 5 days to hatch after being laid, with the minimum observed being 3 days. This was in marked contrast to the host eggs, with average time 8.6 days in an unparasitized host colony, and 9.1 in one which was parasitized. Likewise, the parasite larval stage was much shorter, lasting an average of 9.8 days as opposed to 16.6 for host larvae in a parasitized nest (14.8 in an unparasitized colony) and the pupal stage also slightly shorter.
The parasite larvae were able to attract more attention from the workers than the host larvae - including being fed more often - which would appear to offer an explanation for the faster larval development and shorter larval/pupal stages. But this does not explain the shorter egg stage. Rapid development is clearly advantageous in terms of maximising the number of offspring produced, so a shorter egg stage is advantageous to the parasite, but the mechanisms behind this short incubation period are not known.
In the famous example of an avian brood parasite, the cuckoo, the parasite eggs also hatch more rapidly than the host eggs. This is, at least in part, because the female cuckoo holds the egg in her oviduct for an additional 24 hours prior to laying, at a higher temperature than an egg being incubated in the host nest. This gives the cuckoo egg the equivalent of a 30 hour head start on the host eggs.
In the aforementioned 2004 research paper, it was speculated that the wasp might use a similar mechanism, but this was not known, and no research into this had been carried out. A later 2006 paper also stated that no information was known about this, and I have been unable to find any further research on the topic.
Has there been any subsequent research into how P. sulcifer has been able to ensure its eggs hatch abnormally soon after being laid?
Sources - paywalled:
Cervo, R., Macinai, V., Dechigi, F., & Turillazzi, S. (2004). Fast growth of immature brood in a social parasite wasp: a convergent evolution between avian and insect cuckoos. The American Naturalist, 164(6), 814-820.
Ortolani, I., Turillazzi, S., & Cervo, R. (2008). Spring usurpation restlessness: a wasp social parasite adapts its seasonal activity to the host cycle. Ethology, 114(8), 782-788.
Sources - non-paywalled:
Cervo, R. (2006, January). Polistes wasps and their social parasites: an overview. In Annales Zoologici Fennici (pp. 531-549). Finnish Zoological and Botanical Publishing Board.
Cervo, R., Dani, F. R., Cotoneschi, C., Scala, C., Lotti, I., Strassmann, J. E., ... & Turillazzi, S. (2008). Why are larvae of the social parasite wasp Polistes sulcifer not removed from the host nest?. Behavioral Ecology and Sociobiology, 62(8), 1319-1331.
Other sources:
Davies, Nick B. (2015). Cuckoo: Cheating by Nature. Bloomsbury. ISBN 978-1-4088-5658-1.


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Long-term viability of induced parthenogenesis
Short version:
Some parasitic bacteria, such as Wolbachia, cause hosts from sexually-reproducing insect species to reproduce asexually instead, with an all-female line. Sometimes, all members of the species end up reproducing in this way - see e.g. Encarsia formosa wasps. How many generations can this remain viable before the effects of

reduced genetic diversity/inbreeding
possible reduced parasite resistance
etc.

take their toll?
If that's too vague a question, what is the longest time/no. of generations that induced-parthenogenetic species have been known to survive?
NOTE: This only applies to induced parthenogenesis resulting from e.g. parasitic bacteria infections. Not to naturally-occurring parthenogenesis.
Full version:
Certain parasitic bacteria, such as Wolbachia can induce thelytokous parthenogenesis in their haplodiploid insect hosts. The infection is passed on down the generations, from mother to daughters. Eventually, this can lead to speciation.
(In non-technical language... the effect of this is that infected female insects lay unfertilised eggs, which hatch exclusively into females, which later on lay unfertilised eggs which hatch into more female insects...
Members of a species which previously reproduced sexually now reproduce asexually, and the asexually-reproducing members of the species may eventually diverge so much from the others genetically that they become a separate species.)
All Hymenoptera (ants, wasps etc.) are haplodiploid.
One would expect that this would reduce genetic diversity in the infected population. A species which previously reproduced sexually, and now reproduces entirely asexually, might be expected long-term to lose biological fitness as a result of inbreeding depression. See also: "Muller's ratchet"
However, a 2001 paper investigated the effects of Wolbachia-induced parthenogenesis on Trichogramma wasp species, comparing such wasps to those that reproduced sexually and to those that were naturally parthenogenetic. Fewer of the infected wasp embryos survived to adulthood, but this was due to direct effects of the infestation on embryonic growth. Inbreeding depression was not a factor.
A 2000 paper also noted that Wolbachia can be horizontally transmitted through the sharing of a common food source, and stated:

horizontal transfer of parthenogenesis-inducing Wolbachia among offspring of infected females offers the potential for recombination between different Wolbachia variants and thus for circumventing Muller's ratchet.

Though I think that would only apply to the bacteria, not its host.
A notable example of Wolbachia-induced parthenogenesis is the chalcidoid wasp species Encarsia formosa. I don't know how long this has existed as a distinct species. Antibiotic treatment to kill the Wolbachia can restore their ability to give birth to males.
Is there a theoretical limit on the number of generations an induced-partheogenetic species should be able to survive? And what is the longest amount of time that any such species has been observed to survive?
Sources:
Tagami, Y., Miura, K., & Stouthamer, R. (2001). How does infection with parthenogenesis-inducing Wolbachia reduce the fitness of Trichogramma?. Journal of Invertebrate Pathology, 78(4), 267-271. (Paywalled, unfortunately.)
Huigens, M. E., Luck, R. F., Klaassen, R. H. G., Maas, M. F. P. M., Timmermans, M. J. T. N., & Stouthamer, R. (2000). Infectious parthenogenesis. Nature, 405(6783), 178-179.
Stouthamer, R., & Luck, R. F. (1993). Influence of microbe‐associated parthenogenesis on the fecundity of Trichogramma deion and T. pretiosum. Entomologia Experimentalis et Applicata, 67(2), 183-192. (Paywalled.)

What a good question!I think that Wolbachia infections could be sustainable on the long term.Lots of species are currently infected by Wolbachia (looks like at least 25% of all insects species could host Wolbachia) and some scientists call it a symbiosis rather than an infection.In other words, I think Wolbachia doesn't lower the evolutionary success of its hosts.

@Zafalija Bear in mind that Wolbachia infection affects different hosts in different ways. In some areas, there are species with 100% of the population infected, but no apparent symptoms. (Not even Wolbachia's famous biasing of sex ratios.) For example, in the Carpathian Basin, three of my favourite butterfly species - the Large Blue (Phengaris arion), Alcon Blue (Phengaris alcon) and Mountain Alcon Blue (Phengaris rebeli) are all 100% infected. And in the UK, 19 populations of another butterfly, Euphydryas aurinia, also have 100% Wolbachia prevalence, without any apparent effect!

Sources for the above: https://www.researchgate.net/publication/276509070_Controversial_patterns_of_Wolbachia_infestation_in_the_social_parasitic_Maculinea_butterflies_Lepidoptera_Lycaenidae and https://en.wikipedia.org/wiki/Euphydryas_aurinia

@Zafalija OK. I just wanted to get across that my question is explicitly about host species that it induces parthenogenesis in. It doesn't do that in any of the butterfly species with 100% infection that I mentioned.

And Wolbachia can be lost of course, e.g https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6493766/
Loss of cytoplasmic incompatibility in Wolbachia-infected Aedes aegypti under field conditions

I knew about entire populations infected by Wolbachia.I was trying to say that Wolbachia infection doesn't have any negative impact on the survival of the species due to lack of genetic variability; lots of species have been infected for centuries without becoming extinct, so I guess their altered sex ratio is not an important factor for survival, at least until some male survives: having a unisex population is obviously a serious evolutionary threat.

Since wolbachia infections can be "entirely cleared" as stated by @PolypipeWrangler, you won't have entire species with no males at all.Maybe you could find some populations totally infected by wolbachia, but since wolbachia infections are 'reversible' some male could appear here and there, restoring a little genetic variability in our pool.Please notice that parthenogenesis could be beneficial in some cases: it seems that lots of invasive species are parthenogenetic (https://scholar.google.com/scholar?hl=it&as_sdt=0%2C5&q=parthenogenetic+invasive+species&btnG=&oq=parthenogenetic+i)

@Zafalija You mention "species infected for centuries". Did any of these become parthenogenetic as a result of the infection? If so, could you tell me the names of these species? Thanks!

@PolypipeWrangler Thanks. But that scenario relied on the high temperatures in the locality, and not all species with Wolbachia will live in regions that get that hot.

Check this: https://www.karger.com/Article/Abstract/104228                                     Wolbachia was discovered in 1924.It is likely that it has been around for centuries, if not millennia, before its discovery.Also, @PolypipeWrangler's comment pointed out that wolbachia can be lost.We surely do know that it can be lost due to high temperatures, but you can't exclude that wolbachia could be lost due to other environmental factors.Please notice that wolbachia could actually improve the fitness of certain species!

@Zafalija I've looked at the abstract (I can't read the full article due to the paywall). It mentions Culex pipiens (but misspells it "pipientis"). Wolbachia induces cytoplasmic incompatibility in that species, but that's not the same thing as parthenogenesis.

That abstract was meant to be a reference to the fact that wolbachia has been discovered in 1924, not to parthenogenesis induced by wolbachia.If it's true that wolbachia has been around for centuries, if not millennia, there could be lots of species infected by wolbachia on the long term, with its effects being parthenogenesis or cytoplasmic incompatibility (which could lead to rapid speciation events), but I don't think there's enough literature about this.These are only my speculations, but keep in mind that centuries and millennia are nothing in evolutionary time, hence I think

that lots of species have been hosting wolbachia for long periods of time (maybe losting it after some environmental change), and the fact that we currently know about species infected by these bacteria means that it isn't awful in evolutionary terms.This theory is probably true if wolbachia is really old, while it's totally erroneous if wolbachia is recent.


text:
educational sources for learning biochemistry
I just finished high school and am going into a biology undergraduate degree, I'm getting into biochemistry too and would like to learn more about it through online platforms or even non-fiction books to use my time effectively this summer. So far I've been using online flash cards to learn more about the jargon and would like to hear some suggestions of platforms or books to read that teach concepts strongly tied to biochemistry beyond what a basic high school curriculum would teach.

It might be prudent to find out which text books are used at your university.

There are several reference books for biochemistry, some more readable than others. I personally recommend two of them: (1) Lehninger et al. Principles of Biochemistry and (2) Voet, D., Voet, J., et al. Fundamentals of Biochemistry: Life at the molecular level. Both books contain the most important and basic features of each subject. The chapters are generally well written. I have to say that, from my own experience, I consider that Voet's book is more enjoyable, given that some of the sections of Lehninger's can be a bit tricky. Whichever book you choose, make sure you get relatively new editions. Good luck!
As a side note, even though biochemistry is one the first proper biology classes one takes in undergrad, there are some background requirements. Taking organic and inorganic chemistry courses before is important and some understanding of thermodynamics will certainly come in handy.

How are either of these books “online” platforms? What value are personal preferences without reference to the background required, your own background, the other courses the poster may be following, any teaching experience you may have and comparison with other books available. And these are introductory text books, not reference books. It is for these reasons that I regard text recommendations off-topic on a site devoted to answering problems in biology.

''books to read that teach concepts strongly tied to biochemistry beyond what a basic high school curriculum would teach.'' I assumed he was also interested in reading non-fiction books. I do agree that adding the background needed is important (as I edited the question), but I do not think the rest is needed. As a side note, what I meant by reference books is that they are very commonly used in undergraduate courses. In your view, what is a reference book then?

I'd add Stryer et al. Biochemistry as another Option. I never read Lehninger, but compared to the Voet the Stryer is a bit of an easier and more accessible introduction in my opinion. Though it's a long time that I've read those two. You can search it for free on NCBI Bookshelf, though you can't browse the book freely there.


text:
Biological term for close species rivalry
Is there any phenomenon/force in biology when two very close species fiercely fight each other (as a sign of a strong tendency to deepen the difference between species)? If there is, what's the name of the phenomenon or any similar phenomenon? (Question from a layman in biology, thanks for an answer.)

What do you mean by tendency to deepen the difference between species? Are you talking about evolutionary process that yield the two species to differ due to competition?

Oh you are talking about speciation? Not talking about relationships between the two lineages of interest, I answered your question below but I am not sure this is exactly what you were looking for.

Citing wikipedia

Character displacement refers to the phenomenon where differences among similar species whose distributions overlap geographically are accentuated in regions where the species co-occur, but are minimized or lost where the species’ distributions do not overlap. This pattern results from evolutionary change driven by competition among species for a limited resource (e.g. food). The rationale for character displacement stems from the competitive exclusion principle, also called Gause's Law, which contends that to coexist in a stable environment two competing species must differ in their respective ecological niche; without differentiation, one species will eliminate or exclude the other through competition.

In ecology, the competitive exclusion principle, sometimes referred to as Gause's law of competitive exclusion or just Gause's law,[2] is a proposition that states that two species competing for the same resource cannot coexist at constant population values, if other ecological factors remain constant. When one species has even the slightest advantage or edge over another then the one with the advantage will dominate in the long term. One of the two competitors will always overcome the other, leading to either the extinction of this competitor or an evolutionary or behavioral shift toward a different ecological niche. The principle has been paraphrased into the maxim "complete competitors cannot coexist"

Character displacement is very close to what i'm looking for. When small differences suddenly start to play a big role and result in split. Cheers

Can you try to explain what is the difference? Maybe you are specifically including a (allopatric/sympatric) speciation event into the story...

I'll accept your answer, i'm new member, it says to wait for 5 mins. The crucial point you made right - when small differences are accentuated. I was looking for this thing

Sure take your time. I just wanted to invite you to explain why the answer does not answer if it does not. Make sure to wait to see if others agree with my answer or if they downvote or comment on it.

For my non-biological purpose it fits well. I was looking at the term that denotes the situation when differences between two very close species get accentuated in their proximity.


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Pepper plant leaf curl and "sweating"
The "sweating" and leaf curl have been going on for about a week. I've done some extensive googling and have found mixed diagnoses. For context, the ambient temperature is 74°, I'm using 6,500 K lamps and there are some flies around, but they are small and seemingly harmless. The plants are about 67 days old. Pls help.


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Do vitamins protect you from common cold?
Do vitamins (taken as pills) boost your immune system, and make you less likely to contract diseases such as common cold or flu?

Welcome to Bio. Consider posting this on Health.SE

Sorry. I wasn't aware of "health.SE".  Maybe it's better to close this question then.

I'm voting to close this question as off-topic because it may be better of at Health. SE

@Christiaan the OP has already reposted it there...

@Nemo please don't post questions on two different sites. If it doesn't belong on the first site you post it at, it will be migrated to the better fitting one.

There are two answers to your question, "emphatically yes" and "sort of."  Vitamins play a critical role in immune function, and a deficiency of certain vitamins can lead to a higher risk of developing an infection.  Specifically, vitamin A, B2, B6, C, D, and E deficiency are linked to depressed immune function.  However that is deficiency, not supplementation above what most people need.
There's a popular idea that megadosing with vitamins, usually vitamin C, lowers the risk or length of common upper respiratory infections (eg the common cold).  The evidence on that is much less convincing.  A metanalysis of studies finds weak or no evidence that it is effective, but may be associated with a small effect.  More study is recommended by the researchers, but they don't go as far as recommending large doses of vitamin C.  (It is also worth noting that large doses of fat soluble vitamins, A, D, E, and K, can be quite toxic and should be avoided).
The magnitude of the first effect is quite large: people with a vitamin deficiency certainly have a depressed immune system.  However it is not clear that larger doses are helpful.


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Insertion of synthetic DNA sequence
If I have some synthetic DNA sequence (<=20 bp long), is there a way for me to reliably insert this sequence next to some n-bp motif?  I'd like for this to be possible in humans.  If so, are there any restrictions on the size of n?
I have explored the use of CRISPR/Cas9 for this end, but it is limited in the sense that the gRNA target sequence must be adjacent to a PAM sequence.  Attempts have been made to solve this problem (http://www.nature.com/nature/journal/v523/n7561/full/nature14592.html#affil-auth), but they fall short of full generality for n.  Are there any better approaches?

How big is the n (size of one/both flanks)? Also have a look at this post.

Just use something not restricted by PAM site, such as Zinc Finger nucleases or TALENs. But NOTHING about DNA insertion is reliable. The most likely repair route would be nonhomologous end joining, but you're looking for homology directed repair based on your 19 base template. Also 20 bases is way too short for good homology. You might be able to improve insertion rates by using a single-stranded template though.

gRNA is just for the targeting of the cut in order to engage site directed homologous recombination. You need to insert your synthetic sequence in between homology arms to get it to incorporate.


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Is water vapour a product of fossil fuel oxidation?
In textbooks, while water vapour and carbon dioxide are said to be the greenhouses gases which are most abundant in the atmosphere, when a table is given showing the top greenhouse gases emitted by humans, water vapour is omitted (carbon dioxide and methane are the top two).
However, when methane is oxidised to release energy from fossil fuels, the products are carbon dioxide and water (i.e. water vapour), therefore, aren't humans responsible for the concentration of water vapour present in the atmosphere?
Why is water vapour generally omitted from the tables?

Most likely because our atmosphere contains already huge amounts of it. This is different for CO2.

Your title confuses me. Is your question if water vapour is produced by fossil fuel combustion (answer: yes) or if water vapour is a greenhouse gas (no, not really, see answer EdM)?

@RHA the terminology here is tricky. The ACS page I linked suggests that water vapor accounts for over half of the total greenhouse effect, so it should be called a greenhouse gas. It's not, however, a greenhouse gas that's being affected by human activity in a way that increases the greenhouse effect, unlike carbon dioxide.

I'm voting to close this question as off-topic because it is not about biology. It appears to be about climatology or some such subject.

Althugh water vapor contributes to greenhouse warming of the atmosphere, changes in atmospheric water vapor tend to follow rather than drive changes in temperature. Also, in the form of clouds, atmospheric water can have a cooling effect on earth temperature.
Clouds illustrate why water vapor, unlike carbon dioxide and methane, is not thought of as a driver of recent changes in earth temperature but rather is more of a follower. Unlike those other two gases, if you keep trying to put water vapor gas into the atmosphere it will convert to liquid water at some point, leaving only a constant level of water in the form of gas. That's what happens when a cloud forms; what you see and what can shield you from the sun is a collection of water droplets or ice crystals. Large amounts of water vapor are also regularly put into the atmosphere by evaporation of water from the earth's surface, dwarfing the contribution from human respiration. Eventually the atmosphere gets locally saturated with water vapor and it falls back to earth as rain or snow in the hydrologic cycle.
In principle methane and carbon dioxide could similarly condense out of the gas phase, but not at temperatures that occur in our atmosphere. You need to go far out into cold reaches of the Solar System to find naturally occurring methane lakes or solid carbon dioxide. There is no equivalent of rain to remove excess of those gases from our atmosphere. Carbon dioxide can dissolve in water to leave the atmosphere, but at the cost of acidifying the water. Ocean acidification is another serious result of adding carbon dioxide to the atmosphere.
The amount of vapor you can add before conversion to liquid water increases with the temperature. So as land temperature increases the rate of evaporation of water into the atmosphere can increase, and as atmospheric temperatures increases the amount of water vapor that the atmosphere can hold also increases. So in principle water vapor might thus serve to amplify the greenhouse warming from other gases, although its transition to liquid or ice in the atmosphere might tend to counteract that. This is a major issue being investigated in attempts to understand the interplay of factors that determine earth temperature.
A focus on carbon dioxide has an important practical aspect. If you control the excess release of carbon dioxide due to fuel combustion, you necessarily also control the associated excess release of water vapor.
In summary, human activity ends up having much less direct influence on changes in atmospheric water vapor than it does on changes in carbon dioxide or methane. That's why the latter two gases rightfully receive more attention as controllable greenhouse gases.
The American Chemical Society also discusses this issue.

The answer from the ACS foes not make sense. They contradict themselves in order to support the main party line that CO2 is the problem. Water vapor is a far more potent greenhouse gas than CO2.The ACS concedes it makes up 60% of the entire earth's greenhouse effect. According to the chemical reaction of combustion of greenhouse gases twice as much water vapor is created as CO2. Thus, if there was a substantial greenhouse effect at all it must be due to water vapor. The data does not support it at all so it is left out of all EPA, IPCC and other political discussions of climate science.
The two main contention of the ACS are invalid. First, CO2 rise also follows temperature, as they report is the case for water vapor. This is separate from anthropogenic sources of the gases, though! The reason is that CO2 solubility in the ocean decreases with temperature rise, thus the ocean releases CO2 into atmosphere from warming. The other claim is pure speculation that the water vapor saturates the air and forms clouds. They do not present any evidence of increased clouds due to combustion, which would actually cool the surface temperature by blocking sunlight, the main source heating the earth.

Water vapor has a positive and a negative green house effect. Clouds cancel out the sun. Additionally: The concentration of water in the athmosphere should be more or less constant, while the concentration of CO2 is rising...

Natural feedback mechanisms control the amount of water vapor in the atmosphere.  Added water vapor vapor becomes rain in short order, increasing sea level by a miniscule amount.  OTOH, CO2 is a driver because there are no feedback mechanisms that regulate its concentration, at least on any timescale relevant to humans.


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Germ cells vs. gametes
Naively, I thought that germ cells are diploid (in diploid species like human/mouse at least). Then, germ cells undergo meiosis and become haploid. I thought this was the critical change that defined these derived cells being named gametes (spermatozoon/ovum) rather than germ cells. However, I read that while XX mammalian germ cells undergo meiosis during embryonic development, XY germ cells don't go through meiosis until well after birth (puberty). This would mean that female gametes arise over a decade before male ones in humans. Is there an accepted definition of when germ cells differentiate into gametes and the terminology?

Your observation is right.

In females( having  XX mammalian germ cells), Oogenesis starts with
the process of developing primary oocytes, which occurs via the
transformation of oogonia into primary oocytes, a process called
oocytogenesis. Oocytogenesis is complete either before or shortly after
birth.(1)

The "germ cells" are called oogonia. Ovum is not a direct product
of meiosis I, the oocyte forms a primary oocyte in meiosis I, which
undergoes meiosis II after fertilization to give an ovum.

The ootid is the immature ovum formed shortly after fertilization, but
before complete maturation into an ovum. Thus, the time spent as an ootid is
measured in minutes.              ....(2)

(In oogenesis, the ootid doesn't really have any significance in itself, since it is very similar to the ovum. It matures into an ovum.)
This diagram sums it up very well:

Oogenesis in Eukaryotic Cells.(A) oogonium where the mitotic division
occurs (B) differentiation and meiosis I begins (C) primary oocyte (D)
meiosis I is completed and meiosis II begins (E) secondary oocyte (F)
first polar body (G) ovulation must occur and the presence of the
sperm penetration (fertilization) induces meiosis II to completion (H)
ovum (I) second polar body               ...(3)

It is commonly believed that, when oocytogenesis is complete, no additional primary oocytes are created, in contrast to the male process of spermatogenesis, where gametocytes are continuously created.

In males, again, as you say, Spermatogenesis is the process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testis. The germ cells here are the spermatogonia. But here, initiation of spermatogenesis occurs at puberty. So, males start producing sperm when they reach puberty, which is usually from 10-16 years old.(4)

(The process is almost similar to oogenesis, I would recommend you to start with the wikipedia page if you want to understand this in detail.)
Take away points:

The first haploid cell formed from a diploid germ cell is not an ovum/spermatogonia.

Ovum is formed after fertilization, whereas sperms are formed at puberty.

Oogenesis starts after birth, whereas spermatogenesis starts at puberty.

1- https://en.wikipedia.org/wiki/Oogenesis
2- https://en.wikipedia.org/wiki/Immature_ovum#Ootid
3-https://upload.wikimedia.org/wikipedia/commons/1/1a/Oogenesis.svg
4- https://en.wikipedia.org/wiki/Spermatogenesis

Thanks, i missed the distinction between meiosis I and II


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Vitrification of Humans for Later Revival
In the video from Tom Scott "I promise this story about microwaves is interesting.
" high success rate in multiple reanimations of a hamster was stated by scientist interviewee J. E. Lovelock who worked on these experiments. In the near end of the video the scientist says that it is not possible on larger organisms partially because you cannot get antifreeze agents to diffuse into the cells quickly enough. Searching on this topic I found out that antifreeze is required because if ice forms it expands and damages the cell walls and more. Although in how Lovelock was describing the experiments, it seemed as if they quickly cooled the hamster to between 0 and 1 degrees celcius, see "Reanimation of rats from body temperatures between 0 and 1° C by microwave diathermy" and "Resuscitation of Hamsters after Supercooling or Partial Crystallization at Body Temperatures Below 0° C.". From the original Nature article

Hamsters, chosen because of their known adaptability to body temperatures between 2.5° and 38° C.,
were cooled by the method recently described by
Andjus and Smith for rats. After transfer to icy
water, the deep body temperature was recorded from a
colonic thermocouple connected to a potentiometer
or a microvoltmeter recording with an accuracy of
±0.3 deg. C. In our experience the hamster ceases
to respire at body temperatures between + 2.5° and + 6° C., and heart beats are no longer visible at +1.8 - 3.5° C.

it is then said that

After cessation of
respiration, the animal was transferred to a 50 per
cent propylene glycol bath maintained at - 4 ° to - 7° C., which reduced body temperature to zero in
7-10 min. Under these conditions, some animals
became supercooled so that body temperature might
reach - 5·5° C. or even below in a further 50-70 min.

Propylene glycol being an ingredient in antifreeze also being non-toxic which is seen in its use as a food additive. Although nowhere in this method is it said that it somehow is administered into the hamster so that it can diffuse into the cells themselves. It is also said that an estimated 15% of total body water crystallized (froze/became ice). These hamsters were then successfully revived. Why does Lovelock then say that it does not work on humans because of antifreeze not diffusing fast enough? From searching around one reason is that it does not work because it is not possible to cool a human body quick enough, although if it became possible to vitrify a body quick enough and heat it up quick enough. Would it then become possible to revive humans and or bigger animals?
My main question is how and why does it matter how big the animal that is being frozen matter? What exactly makes it possible on hamsters and not on for example a dog or a human being? I understand that it takes significantly longer to cool a human being compared to a hamster. But I do not understand how for example the heart cells do not die in the process of cooling a hamster compared to a human. The cooling pattern is the same for both, and the heart in both cases will be deprived of blood therefore oxygen. The amount of expansion caused by potential ice formation will be the same on hamsters and humans because the size of the cells are roughly the same.

Are you familiar with Kleiber's law? Would it be a sufficient answer for you?

I think you may be "assuming facts not in evidence" :)  You are focusing on the size of the animal. However, your quote notes, "Hamsters, chosen because of their known adaptability to body temperatures between 2.5° and 38° C., ", that is hamsters were chosen not for their size, but because they were known to be able to adapt to temperatures as cold as 2.5C.
Determining the mechanisms of how hamsters can adapt to such cold temperatures would certainly be interesting.


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How does free living nitrogen fixing bacteria fix N2 in aerobic condition?
If a Azotobacter is free living nitrogen fixer it will also require ATP through cellular respiration. I am confused here: if Nitrogenase is highly sensitive to oxygen molecule how will Azotobacter be able to fix N2 and carry out cellular respiration at the same time?

https://en.wikipedia.org/wiki/Azotobacter#Nitrogen_fixation

Nitrogen fixation is highly sensitive to the presence of oxygen, so
Azotobacter developed a special defensive mechanism against oxygen,
namely a significant intensification of metabolism that reduces the
concentration of oxygen in the cells.[40]

From that cite "Respiratory Protection nitrogenase complex in Azotobacter vinelandii"(google translated)

The second strategy, dubbed "breath protection ", is based on a
significant increase in the rate of the rate of respiration, resulting
in the concentration of oxygen in the cytoplasm decreases to a level at
which nitrogenase no longer experiences damaging action О2 .

https://en.wikipedia.org/wiki/Azotobacter#Nitrogen_fixation

Also, a special nitrogenase-protective protein protects nitrogenase
and is involved in protecting the cells from oxygen. Mutants not
producing this protein are killed by oxygen during nitrogen fixation
in the absence of a nitrogen source in the medium.[41]


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The primary source for Erich von Holst research for minnow forebrain and shoaling
I am trying to find the primary source of information about the experiments of Eric von Holst, mentioned by Konrad Lorenz in the book “Das sogenannte Böse: Zur Naturgeschichte der Aggression”/“On Aggression”. The essence of the experiment is widely known and retold in many tertiary sources.
Quoting from a secondary source: under the chapter “Die anonyme Schar”/“Anonymity of the flock” from Konrad Lorenz.
"Ein Fisch, der, aus welchen Gründen immer, in bestimmter Richtung
zu schwimmen beginnt, kann ja nicht umhin, in Bälde aus dem
Schwarm heraus ins freie Wasser zu geraten und gleichzeitig damit
unter den Einfluß aller jener Reize, die ihn in den Schwarm
zurückzuziehen trachten.
...
Man kann ganz kribbelig werden, wenn man diesem Treiben
zusieht, und man kann nicht umhin, an der Demokratie zu zweifeln
und Vorteile in der Rechtspolitik zu sehen.
...
Er [Erich von Holst] operierte einem einzelnen
Fischchen dieser Art das Vorderhirn weg, und in diesem stecken,
wenigstens bei diesen Fischen, alle Reaktionen des Schwarmzu-
sammenhaltes.
...
Das operierte Tier war eben durch seinen Defekt eindeutig zum Führer geworden.
"
"A fish which begins, for any reason, to swim in a certain direction cannot avoid leaving the school and thus finding itself in an isolated position. Here it falls under the influence of all those stimuli calculated to draw it back into the school.
...
Watching these indecisive actions one almost begins to lose faith in democracy and to see the advantage of authoritarian politics.
...
Erich von Holst removed from a common minnow the forebrain which, in this species, is the site of all shoaling reactions. The pithed minnow sees, eats and swims like a normal fish, its only aberrant behaviour property being that it does not mind if it leaves the shoal unaccompanied by other fish.
...
By virtue of his deficiency the brainless animal had become the dictator!"
The many-hour search for the words "elritze vorderhirn schwarm erich holst"/"minnow forebrain shoaling erich holst" gives only biographies and obituaries of Eric von Holst and secondary/tertiary / damn knows what sources.
Could it be that with all due respect to Konrad Lorenz it was a false quote or a stretch? Did anyone dig up primary sources?

Not my field, but I found a bibliography of von Holst here. This lists a series of articles between 1934 and 1939, mainly published in Pflügers Archiv, on various aspects of the movement of the goldfish backbone and things affecting it, but (as far as I can see as a non-native German reader) nothing involving surgery or group behaviour. After this time his publications seem to involve mainly insects and birds. If you have any difficulty getting access to the papers, let me know.


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If Melatonin is anti-gonadal, why is it associated with early sexual maturity in congenitally blind girls?
If melatonin is anti-gonadal, that is, it delays sexual maturity, then shouldn’t it delay sexual maturity in congenitally blind girls rather than helping them attain sexual maturity at an early age?

Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, we expect 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 example please provide evidence for your statements that melatonin is: 1) "anti-gonadal" — also under what conditions this is true and what sort of delays occur? 2) "associated with early sexual maturity" — also how early? Thanks!

melatonin released from pineal gland and and its one of the function is that it delays sexual maturity. but there are also a point to remember that pineal gland is activated at that time when light stimulate the retina but in the case of blind person activation of pineal gland is not occurs. that's why hr. like melatonin is not secreted and sexual maturity come before time. it come 2-4 years before the normal age.

Welcome to Biology.SE! We expect all answers to contain references so that readers interested in knowing more may look them up. Please add some references to your answer. Thanks :)

i read this from books so you may find this at : 1. ncert - biology - xii   or 2. allen module-8 chapter 2

Isn’t melatonin secreted during the scotopic phase? That would mean that in blind girls melatonin levels should be higher compared to serotonin (secreted during daytime). Therefore, blind girls should have a delayed sexual maturity rather than early sexual maturity.