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How do we know if a trait is genetic rather than via rearing environment?
In articles like this one, I often read that several "genes variants are associated to a given trait". It is often added: "genetic factors explain (say) 20% of the trait variance."
The way I understand this is the following: researchers regress the trait upon the genome, find correlations between some variants and the trait and give some measure of the fit (or explained variance) like the $R^2$. Is my understanding correct?
If my understanding is correct, I am uncomfortable with the interpretation that the trait is partly genetic. Indeed, it could be due to rearing (that is, from the parents, yet not from the genes). I am aware of the practical difficulty (or impossibility) of finding a trait that we know for sure is from rearing and not genetic, but one can use models (described below) to study my concern. The basic model feature a random trait and the advanced one a trait transmitted by rearing.
The basic model runs as follows: define an arbitrary trait as the indicator of a random subgroup of the (global human) population. Would a study really fail to detect a genetic causality in this model? How common is it to find some gene variants associated to this arbitrary trait, and explaining (say) 20% of the trait variance? More formally, what is the distribution of the variance (apparently) explained, in function of the size of the arbitrary subgroup? I am sure there is a paper (or even a literature) about this: I'd like a reference to get the main insights.
Now, let's turn to the more advanced model, for which I am also seeking for references (I am sure it exists as well but have no clue how to look for it).
The model simulates genomes of the whole population among successive generations. Some trait appear at a given generation (call it t=0, although it is not the eldest generation modeled) among random individuals. The trait is not uniformly distributed at t=0, but has more chances to be found in individuals "close to the spatial location where it appear" (you can think of the trait as "listening to techno", and the location as Detroit). Suppose the trait is not genetic, in the sense that no gene variant influences the trait occurrence in one individual. Instead, the trait is transmitted through rearing environment: e.g. an individual has the trait with probability P if one of their parents has it, and with probability p<P otherwise (we could refine the assumption and say it could also be transmitted by acquaintances, or that it has more chances to be transmitted if both parents have it, but I think such refinements are not needed, and we could perhaps even simplify further and take p=0, P=1). Then, after T generations of breeding (realistically modeled), some biologists try to assess whether the trait is genetic. They will surely find some genetic correlations as (i) the trait has originally appeared in a specific location where people were relatively close genetically, (ii) the trait is transmitted by the parents, like genes, and (iii) there are many many genes, so that the probability is high that those who got the trait at t=0 share some gene variants. Now, let me recall that the trait is not genetic: for example, we could take the babies from their biological parents at t=T and have them raised by randomly drawn couples, it would be the adoptive children of techno listeners who would share the trait, and the (apparent) genetic link would be lost.
Hence my question: how do biologists know whether a trait is genetic or transmitted by rearing, despite the two seeming hard to distinguish in the advanced model? When I read a study claiming that a given trait is genetic, do they employ subtle statistical method to really prove so, or do they mean by that "genetic or reared", in the sense that the trait could fall in the case of the advanced model above? Does "explain 20% of the variance" mean that it is (probably) partly genetic?

Is https://biology.stackexchange.com/a/42280/27148 helpful at all?

Left-handedness is probably a good example: having a left-handed parent, especially mother, increases one's chances to be left-handed, but it is not necessarily genetic.

Thank you @Bryan, it helps because I learned that the "20% of variance explained" notion I referred to in the question is called "heritability" (and interestingly, not "geneticity"). However, the core of my question remains unanswered and I am all the more surprised because in your link, they seem to overlook the issue I mention, because they don't draw a distinction between non-biological environmental heredity and genetic, or at least do not provide a method to distinguish them.

I really don't understand this question.  How can a trait be genetic OR hereditary?  Genetic IS hereditary.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

How could I make it clearer? I thought the title said it all: "How do we know if a trait is genetic rather than hereditary?" I don't understand what isn't clear :-/
@jamesqf hereditary (transmitted by the parents) encompasses genetic (transmitted by the genome) but not the other way around. Or am I not using the correct definitions?

Does this answer your question? Why is a heritability coefficient not an index of how "genetic" something is?

@bixiou: I may be wrong, but my understanding is that genetic == hereditary.  You seem to be asking about genetic versus environmental, which could include prenatal influences such as chemical exposure (fetal alcohol syndrome comes to mind, or being taught something by parents &c. Acquisition of language would be an example of the latter: humans have the genetic ability to learn language, but what particular language(s) they learn is environmental.  A child of Chinese parents adopted as an infant by an English-speaking family will grow up to speak English, not Chinese.

I've tried to rewrite the question to avoid the redefinition of "hereditary", which I think even with your explanation in the first paragraph will mostly confuse or frustrate readers. Hopefully I've kept the meaning you intended. If in a population rather than a single family lineage we might call this "culture". "Environment" would be broader and would include all of these factors.

Thank you all, in particular @BryanKrause. I learned the word "rearing" thanks to you :-) Indeed, I had a wrong definition in mind for heredity. Your edits were fine, I just changed "influenced by rearing" into "transmitted by rearing".

It's purely and simply that there is no single answer - as in the linked paper, there's no "gay gene", there is a group of identified genes that contribute, but not all the variance in the population seen can be attributed to those genes. i.e. you can have some or none of those genes and still be gay, or indeed all the genes and not be gay.
This could mean that there are other genes still to be identified as playing a role, or it could mean that environment, epigenetic factors (e.g. methylation, some of these seem to be hereditary too!), expression levels etc. play roles in this trait, but as it is multi-factorial, we don't know the answer(s) yet. It may well be that we will never know, or that there are more than 1 answers to the trait.

I am sorry but this does not answer the question nor does it add information with respect to it.

@bixiou - yes it does - if you want me to spell it out explicitly - your "models" make some assumptions that are simply incorrect. There are heritable traits of which we know no genetic component - e.g RogerVadim's handedness in comment above, and this is partly because we don't fully know what all of our gene products do and how they are regulated. Have a look at the functional interactions of p53 at stringdb - keep clicking the "more" button. We've known and heavily studied this protein for ~50 years and are still finding interactions...

@bixiou ...there are about 25,000 genes in the genome, each would need to be studied to the same level and we would need to be able to work out the undoubtably multi-factorial models to explain some of these traits. We don't have the technology yet, though we are just starting to scratch the surface. We are also finding new ways in which we regulate genes and gene products - M6A (6-methyladenosine) in RNA is a good example of this, known for 30+ years, only now being identified as to what it does.

That's interesting that we are not able to study all genes at the same level, it shows that my understanding (as I have defined it at the beginning of the post) is wrong. I'd like to know how they do though, because knowing that I am wrong does tell me the correct answer.

@bixiou why they aren't studied has many answers, partly funding, partly man-power, partly reagents, partly we haven't looked for that interaction (yet). p53 is heavily studied because it is a cancer gene, one of the more common changes, it also happens to be a cell cycle regulator, so it is easy to get money and thence man-power to study it. A lot (almost all) of the interactions at a protein level are determined empirically and 1 by 1, so you can see that it takes a long time and a lot of work to get it done.

General remark
One does not necessarily need to use a subtle statistical method, but one does need good understanding of the experimental design and statistical analysis in order to draw reliable conclusions from the data (or know when not to draw such conclusions). It is for a good reason that statistics is a field of its own (just like biology) and there exist a dedicated stack exchange community (by far more active than biology). Pubmed is also full of articles explaining why this or that approach needs to be carefully - just try to search for spirious correlations and see how many articles come up.
Correlations and non-correlations
Closer to the point: the model in the OP assumes that certain trait can be a consequence of the location (or other non-genetic factor, not necessarily hereditary) and the genotype. The co-occurence of certain genotypes and locations confounds the problem. Moreover, it is possible that this co-occurence actually leads to real correlations between these two factors.
One thing to look for is the appropriate sampling procedures, especially the sample size. As an extreme example, let us consider preference for wearing warm clothes in winter - is it a function of location (Moscow vs. Miami) or a trait coupled with Y-chromosome? We could do the analysis of variance, proposed in the OP and easily prove that there is no correlation with the presence of Y-chromosome... unless most of the individuals sampled in Moscow were men and most of those sampled in Miami were women, in which case we may erroneously attribute the preference to warm clothing to possessing Y-chromosome.
It is clear what has gone wrong in the example above:

the experimental design was not balanced
statistical analysis was not corrected for this lack of balance

One can thus expect improvements along these two axes: by designing experiments that allow disentangling undesired correlations and by employing the approrpiate methods of analysis. Let me however add a few more remarks:

not all correlations can be disentangled - sometimes creating appropriate design is difficult or even impossible. This is especiallyw hen we are talking about complex genetic traits.
there may be genuine correlation between the traits - e.g., the trait of interest and settling at a certain location may be both functions of genotype.
In regard to the correlations that may arise after several generations, as the OP suggests, it is worth keeping in mind that such correlations require evolutionary timescales - they are a real issue when comparing Native Americans and Chinese, but less of a problem when comparing populations in New Yorkers and Detroit.

Suggested Reading
I suggest starting with the Wikipedia article on the Experiment design or an equivalent chapter in a biostatistics textbook. Statistics community Cross Validated is rather welcoming to biostatistics questions. Finally, there are many good statistics and biostatistics textbooks - the obstacle is usually not the availability of materials, but the level of math and abstraction.

The reason why I am asking on a biology forum is because 1. geneticists have for sure thought about that (and master the relevant statistics), 2. I am interested in what geneticists do, what statistical methods they use, whether and how they are able to distinguish heredity from genetics. I am sorry but your answer does not really help answering the questions I raised.

@bixiou you asked a very general question - one cannot describe all possible statistical methods used in genetics in a short answer. Try to ask a more specific question, and also give an idea on how much background you have in genetics and statistics. Alternatively, you may consult books, such as https://www.springer.com/gp/book/9780387953892

I have a good background in statistics but close to none in genetics. Thank you for the reference! Don't you know a reference that studies more specifically the problem I am talking about? I guess there must be some papers about the models I described.
As for a more specific question, it would be the following: when an article claims that a trait is (partly) genetic (because some share of the variance is explained by genetics), should we interpret this literally? Or could it be that the trait is hereditary but not genetic? And if it is truly genetic, how do we know it's not just hereditary?

PS: your book may contain the answers to my questions, but I don't have time to read an entire book, so I'd like to know what chapter to read. That's the reason why I am on this forum: I don't know what keywords to search with on Google Scholar, and similarly I don't know where to look at in the book.

@bixiou three people tried to answer your question, but it seems that none of us understands what you are really asking. You know better what your question really is, so try reformulating it, and adding some references, so that we can have a better idea of what you mean.

I think I got the source of the confusion. I checked the wikipedia page of 'heredity' and in turns out it does not mean what I thought. I don't know what word to use then: what I mean by 'heredity' is "transmitted by the parents" (including adoptive parents), but that can be socially rather than genetically transmitted, genetic for me is just a subset of hereditary.

@bixiou - that's environmental, language is a fine example. The reason for our confusion is that often biologists have a very strong understanding of genetics and heredity and use those terms to mean specific things... hence my answer talking about factors that we don't know about yet.

@bixiou Re: "when an article claims that a trait is (partly) genetic (because some share of the variance is explained by genetics), should we interpret this literally?" Sometimes yes, sometimes no. As Roger points out, It depends on how well the experiment and statistical analysis were designed and executed. If you don't feel you can evaluate this yourself, you might want to stick to review articles and textbooks, where someone has already done at least some evaluation and vetting.

Thanks @Armand. Suppose it is well done. How is it done?

Some papers that should help and provide further info in their refs:
An oldy but goody:
"Genetic dissection of complex traits: guidelines for interpreting and reporting linkage results" (1995) Eric Lander & Leonid Kruglyak
Here's a discussion of techniques involved, with an emphasis on linkage analysis but discussing association studies as well:
"Genetic linkage analysis in the age of whole-genome sequencing" (2015) Jurg Ott, Jing Wang, and Suzanne M. Leal
A more recent example:
Höglund, J., Rafati, N., Rask-Andersen, M. et al. Improved power and precision with whole genome sequencing data in genome-wide association studies of inflammatory biomarkers. Sci Rep 9, 16844 (2019).

Thank you @Armand! These references should answer the question. I'll probably accept this answer once I have read them.


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Does surface to volume ratio matter for cold-blooded species with regards to temperature?
While surface grows quadratically with scale, volume growth is cubic. Temperature exchange (gain and loss) of animals is mostly dependant on surface area  (the more area, the faster) whereas heat generation is largely dependant on mass / volume. For warm blooded animals, this implies that specimen in colder climates are usually larger than members of the same species in warmer climates, in order to lose less heat relative to their heat generation.
I'd expect cold blooded animals to approach the environmental temperature faster if they were smaller, having a more suitable surface-to-volume ratio. This obviously is of advantage when warming up, but should be as much of a disadvantage when cooling down. So how does surface-to-volume ratio matter for cold blooded species?

I don't think you understand "zero sum game".

mgkrebbs: What do you mean by that? The point is that while warm blooded species have something to gain by being of larger size, I wonder whether the same is the case for a cold blooded one. Granted, if this was to be a game, who are the players you may ask - and I could only give a rather unprecise answer; so indeed, I'll rephrase.

large size usually offers a gain in savings on food and water needs.  1 elephant eats less than 1 elephant weights worth of mice.

Surface-to-volume ration would predict scaling as multiples of 1/3, which is not what is observed across many domains of life. See this, e.g.: https://biology.stackexchange.com/a/97655/59521

I am a little confused about what you mean in terms of advantage/disadvantage with regard to warming up/cooling down. It seems like it would depend a lot on the environment and the organism in question? Perhaps an illustrative example might help.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

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Would green light look different if blue and red cones were deactivated
When looking at a graph plotting "blue", "green" and "red" cones reponses to different wavelengths, you can see that any wavelength trigerring a response from green cones is also able to trigger a significant response from blue and red cones.
Excluding colorblindness, that must mean the green we're used to is the result from not only green cones activation, but also red and blue cones activation.
My question is: given the current knowledge of cones, the optical nerve and image processing in the brain (or anything else relevent of course), if my blue and red cones suddendly stopped reacting to light, would a 520nm wavelength light look "purer and greener" than it would in a normal situation, or would the brain interpret this as a different "unknown" color? Or perhaps might it not be able to interpet it at all until it forms new connections in order to understand it?
(While this is most likely a hard question to answer, perhaps knowledge about how the brain processes images is advanced enough to form a "likely" hypothesis, which is why I asked.)

The genetic condition you are describing is called green cone monochromacy (GCM). This condition is exceedingly rare because it requires the dual inheritance of tritanopia (absence of blue retinal photoreceptors) and protanopia (absence of red retinal photoreceptors).1 Consequently, I can find very little information on the experience of people with GCM. In general, however, people with any type of monochromacy are considered completely colorblind. This is because color is perceived not by the excitation of specific cones but rather by the relative excitation of different cones and rods.  So, a person with only one functional cone type can perceive the intensity of light but not the color.
If you're interested in the science of how the eyes and brain work together to process color, I suggest reading up on opponent process theory.

References

Simunovic, M. Colour vision deficiency. Eye 24, 747–755 (2010).

I understand that, perhaps I phrased it wrong, what I meant is a more hypothetical (and possibly off-topic I am aware) where someone was trichromatic before switching to this situation, so that their brain would be wired for trichromatic vision and they would have memories of trichromatic vision to compare what they were now seeing to. While this is purely hypothetical (until very good prothetic retinas are invented I guess), I hoped current knowledge of the brain would have a crumb of hypothesis regarding the outcome. I will be checking that link, thanks.

(cont.) My line of reasoning was that "green" cones would send signals using the preexisting circuitry that was built up from living as a trichromat, but the total received signal would be unique in that the brain would be receiving nothing from "blue" and "red" cones, something that never happened in a normal situation since green cone activation implied red and blue also activated. Even if it's not the cones themselves that encode color, the circuitry behind, in the brain, would still be there (at least for some time).

@Uretki It was not that long ago when black-and-white monitors were in fact light-and-dark-green. ;)

Found a likely answer from the "See also" section of the link provided in acvill's answer.
Turns out it seems that you can somewhat approach this situation by exploiting cone cell fatigue to lessen blue and red cone cells's response to green light.
While this isn't exactly the situation described in the question (since I assume red and blue cone cells remain sensitive, just less), it seems to be pointing towards the "purer and greener" answer.
Link: https://en.wikipedia.org/wiki/Impossible_color#Chimerical_colors
Quote:

A chimerical color is an imaginary color that can be seen temporarily by looking steadily at a strong color until some of the cone cells become fatigued, temporarily changing their color sensitivities, and then looking at a markedly different color. The direct trichromatic description of vision cannot explain these colors, which can involve saturation signals outside the physical gamut imposed by the trichromatic model.
[...]
Likewise, staring at a bright magenta template may result in an impossibly highly saturated green afterimage.

So, I assume the result of deactivating red and blue cone cells and looking at a green light would be to see an exceptionally impossibly saturated green color.

one can trick the brain to see only green for a short time,spend some time in a room brightly lit by grow lights(red and blue light with all the green removed)when you leave the room everything will look green until the brain adjusts back to normal lighting.

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Saving a Maize Landrace from Inbreeding Depression
I have 10 seeds of a rare corn landrace. I probably won't be able to acquire more and the cultigen's long term fate is unknown. So, I want to do my best to preserve it for future generations.
Corn is largely out-breeding and used to growing in very large populations, so it's very susceptible to inbreeding depression. The seed I got came from a small but reasonably heterozygous, healthy population with a modest/good amount of diversity.
If I want to preserve the corn without crossing it to anything else, what should I do?
My thoughts are that I have to ensure that it does not breed true for maladaptive recessive alleles. So, I plan to increase seed stock until I have enough genetic material to grow out thousands of individuals and cull any sick plants over several generations, while trying to keep the population contributing to the next generation large. In other words, purging the poor genetics.
I also thought it might be a good idea to breed a few lines from the initial stock to ensure even more diversity.
Is my plan viable? What are my chances of success? Are there any better protocols?
Thanks.

I don't suppose you have the space for rudimentary cloning tech handy? Just a thought, but keeping some of the original plants handy in slow-growth mode might help with later crosses.

@ARogueAnt. As a matter of fact, I do. That is a very good idea. Thanks.

After planting the 10 seeds, manually cross-pollinate the plants with each other to ensure that (1) there's no self pollination, (2) every seed contributes equally to the gene pool, and (3) no foreign pollen contaminates your gene pool.
Cross plant 1 with plant 2, plant 2 with plant 3, plant 3 with plant 4, plant 4 with plant 5, ... and plant 10 with plant 1. Then you can pick an equal number of seeds from each cob to build a population from which you can start eliminating weak or off-type plants.
(A second round of controlled cross-pollination to ensure that seeds from the same cob don't cross pollinate may not be a bad idea: cross plant 1x2 with plant 3x4, 2x3 with 4x5, 3x4 with 5x6, ... and 9x10 with 1x2)
Controlled crossing ensures that no "good genes" from the initial set of seeds are lost by accident.


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Can blood transfusion help to fight cancer cell?
First of all, I'm not a biology student or have sufficient knowledge of biology so I apologize if this question appears silly. Let's say patient A has cancer cells and a healthy person B has the same blood type as patient A, by using a blood regulator device to regulate the blood between A and B, will the white cell in patient B recognize the normal cell in patient A as foreign cell and attack it? Is there a chance the white cells of person B recognize the cancer cell in patient A as a foreign cell and attack it?
So far what I understand as below from internet
At early stage white blood will detect cancer cell but as the cell evolve, the white blood cell will no longer recognize the cancer cell as foreigner cell which enter the escaping phase, in this phase the cancer cell start to growth without obstruction. However, I am not able to find article like the membrance wall constitution for different people so logically if it is similar, the white cell will not recognize normal cell in both people as a foreigner cell, correct me if i'm wrong but a cancer cell that enter the escaping phase may not treated as normal cell in person B due to difference membrance wall constitution? If this is true, then can this method use to save patient with cancer especially for family members that willing to use a blood regulator device to constantly regulate the blood between both hence regulate the white blood cell of person B into A to fight cancer cell? If this work, this can also use to save patient with Covid at critical stage where an immune person can regulate the blood between both people as if lending the person immunity system to fight covid infected person?

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

White blood cells have antibodies that target specific proteins on the surface of different cells- this is why blood transfusions need to occur with the same blood type in each patient. (If this were to happen, your body would produce antibodies to attack the foreign blood cells.) To address your first question, as long as the blood types are the same, the cells inside of patient B's blood will not attack any of patient A's blood. Even if patient B had a different blood type as A, if his blood was introduced into A's bloodstream, a healthy amount of B lymphocytes (these are cells that stem from bone marrow and differentiate to create new antibodies) would need to be introduced along with it. Otherwise, the cells would not have the capability to create antibodies that are compatible with A's blood. However, doing this wouldn't really be a good idea, as this would cause an indiscriminate attack- all of A's blood cells would be attacked. And to answer your second question- after cancer cells get past a certain stage in their development, they lose important proteins that the body uses to identify them. In other words, they sneak past its immune system and begin to spread. The escape phase is a direct result of this- the tumor begins to metastasize throughout the body and the body fails to stop it. To be frank, there is very little to do here- the issues with the blood transfusion method are detailed above. And to address your final statement about Covid- from what I understand, this is mostly correct. If you may remember, people with antibodies often donate their plasma to be used in other patients. However, the key part of this is that the blood cells are not the useful part of this transfusion. The antibodies are. It isn't a matter of blood transfusion- it's a matter of antibody transfer. For the most part, however, your logic is correct. I could help you a little more if you linked the websites that you researched. Thanks.

Would you edit this answer so it's not a wall of text that breaks people's eyeballs, also, adding references to support your claims. Please take our [tour] and refer to the [help] for guidance as to our ways. Welcome to Biology.

https://news.cancerresearchuk.org/2019/02/28/science-surgery-why-doesnt-the-immune-system-attack-cancer-cells/ this is the article I refer to but that is from the perspective of immune system A couldn't recognize the cancer cell. If the same cancer cell that enter escape phase in A put into healthy person B,C,D and so on, there a 100% chance it escape the immune system of all these healthy people?


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What causes Erythroblastosis fetalis?
So this is what I understood about the disease by researching about it
When a Rh-ve mother has a Rh+ve baby in her womb,

The placenta prevents mixing of fetal and maternal blood preventing antigen detection by her immune system.
There are no pre-made antibodies that can attack the fetal RBCs to kill them
At the time of birth, the placenta breaks thereby exposing the fetal RBCs to her immune system
The WBCs get sensitised and begin antibody formation which takes atleast 6 months
The first baby is born safely
In the event a second Rh+ve baby is conceived, the antibodies aleady present in the blood
cross the placenta and destroy the fetal RBCs killing it.(secondary immune response)
To prevent this an injection of Rh antibodies is given to the mother after first birth which
destroys all fetal RBCs before they sensitise the immune system preventing secondary immune
response.

My Question is
Why does this happen only with the Rh antigen?
I know many people whose mothers have B+ve/A+ve blood but their children are born normally even when they have A+ve/B+ve blood(opposite of the mother). There even are people whose mothers have O+ve blood while they have B+ve/A+ve blood groups.
The body has pre-made a and b antibodies which should kill the fetus unlike in case of Rh where 1st birth is safe. Also much lesser time is needed to produce these antibodies which is why there cannot be any blood transfusion between incompatible ABO system blood types while one transfusion is possible between incompatible Rh blood types
My take on this will be that antibodies against ABO blood groups can never cross placenta but most antibodies do so this seems less like a solution
A lot of research failed me a solution.
I found a somewhat similar question here but it does not address my query completely
Erythroblastosis Foetalis

You may find this helpful: https://www.exxcellence.org/list-of-pearls/management-of-pregnancy-with-abo-incompatibility/


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What are the factors affecting reaction time and/or reflex velocity?
So there was this video of a cat killing a snake: Cat reaction time
and another of a bobcat killing a rattlesnake Bobcat kills rattlesnake
And then this from wikipedia on sand cats:

In the Ténéré, a desert region in south central Sahara, sand cats were observed preying foremost on small rodents, and the young of cape hare (Lepus capensis), but also hunting greater hoopoe lark (Alaemon alaudipes), desert monitor (Varanus griseus), sandfish (Scincus scincus) and venomous Cerastes vipers.
This paper claims that vipers and rattlesnakes have fastest strike rateMongoose are known predators of cobra.

These mammals are able to hunt them because of their faster reaction time and/or relex velocity.
So how is it that these animals have faster reaction times given that the length of signal transmission is actually lesser in those reptiles?
From wikipedia:

 Myelin  is considered a defining characteristic of the jawed vertebrates (gnathostomes), though axons are ensheathed by a type of cell, called glial cells, in invertebrates.
A reflex arc is a neural pathway that controls a reflex. In vertebrates, most sensory neurons do not pass directly into the brain, but synapse in the spinal cord. This allows for faster reflex actions to occur by activating spinal motor neurons.

So those factors are eliminated. For the mentioned case, it might be that those reptiles don't have as good of a perception as their predators but again they have a higher ratio of electrical:chemical synapses. (In case of a fly it is probably the smaller body and electrical synapses)
So what are the general factors affecting the speed of a reflex/reaction time? If a specific system is of help, the visual reflex system of the feline will do just fine.
Why was the snake unable to escape being hit by the paw?(The snake has an extremely fast strike velocity and the most likely factors are eliminated. At such close ranges, stimulus perception should not differ much either)

PS Those links are mostly posted to show source and research but most of that is GK so don't read unless you wish to

Given the finishing sentence, are you asking for the structures and delays within a reflex arc including musculature? Any specific species and sensory system you are interested in? As you rightfully indicate in your post, species and size matter.

Yes I am asking for those kinds of factors other than the mentioned.  Also feline relexes are fast so that will do. As for sensory system, not so specific but in the above fight it was probably visual vs (visual+thermal)

Having said that - does this answer your Q? One of the As is pretty good

That is pretty good. Can  you also tell why a rattlesnake is unable to retract its head despite its high strike velocity to avoid the paws?

That might have to do with agonist being quicker than the antagonistic muscle's, like a croc's beak that crushes bones but cannot counteract two hands holding it shut.

I recommend specifying the Q to focus it on the snake's evasive maneuvers when your original post is answered by the linked post, otherwise your current Q might face closure, being a suspected dupe.

Strike velocity isn't a reflex arc, it's just the motor side; no sensation involved necessarily. Doesn't seem to make sense to compare it to stimulus-response.


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How can animals defecate or urinate in fear if the nervous system seems to opposes it?
How do animals defecate and/or urinate in fear even though their 'flight or fight' response seems to oppose it? I have seen many cats and dogs urinate and defecate when they experience extreme fear. It also happens with most other animals in shock or fear including humans.
The 'why' is probably to deter predators which has been made excessively clear by my research but this is what is puzzles me despite my attempts.
From a book(made by doctors and teachers for medical exams ): Another website for medical exams
It is clear that sympathetic nervous system inhibits both these functions.
My teachers said that adrenaline is complementary to the sympathetic nervous system and has the same effects on the body.
But the real life observations seem to contradict.
Also this question:
Fear induced defecation does not clear my question regrading the aforementioned contradiction.

Not sure where you're getting these materials exactly, but I don't think anyone has called norepinephrine "sympathetin" for 75 years.

@Bryan Krause Probably because this is in context of sympathetic nervous system. In the chemical coordination chapter of the same book, it says "epinephrine/adrenaline and norepinephrine/noradrenaline" when talking about adrenal hormones

Even so, the only places I see the word used are (often sketchy) test prep websites. There are only 12 results on Google Scholar and many of those are duplicates/not actual papers. It's not as if the word is suddenly used when you start talking about the sympathetic nervous system, it seems like it's just used by some pathetic test prep materials that probably all copied each other.

It's overly simplistic to think of the sympathetic (SNS) and parasympathetic (PNS) as purely inversely activated; it's possible to activate both at once or suppress both at once. It's also overly simplistic to think of them as unitary responses; it's possible to activate parts of the SNS and not others, or parts of the PNS and not others.
Freezing, urination, and defecation in stressful situations are associated with corticotropin releasing factor (CRF, also known as CRH) in rodents. CRF is part of the response to stress and influences both parts of the autonomic nervous system. The effects of CRF are different in different parts of the digestive system (Taché & Bonaz, 2007; bold emphasis added by me):

In contrast to the inhibitory effects of CRF and urocortin 1 injected into the CSF on gastric and small-intestinal motor function, these peptides stimulate colonic transit and defecation and induce diarrhea through increased sacral parasympathetic outflow to the large intestine in female and male rats, mice, and gerbils

In humans, parasympathetic activation is also associated with some peoples' responses to trauma and PTSD, specifically the feeling of immobility or inability to act (Corrigan et al 2011).

Corrigan, F. M., Fisher, J. J., & Nutt, D. J. (2011). Autonomic dysregulation and the window of tolerance model of the effects of complex emotional trauma. Journal of psychopharmacology, 25(1), 17-25.
Taché, Y., & Bonaz, B. (2007). Corticotropin-releasing factor receptors and stress-related alterations of gut motor function. The Journal of clinical investigation, 117(1), 33-40.


text:
Can citrate in semen be utilized as a source of energy by the sperm?
Prostatic secretions of semen include citrate as one of the component.
The role of citrate in motility has been suggested by some researches.
(Kavanagh JP. Isocitric and citric acid in human prostatic and seminal fluid: Implications for prostatic metabolism and secretion. Prostate. 1994;24:139–42).
Is there a possibility, that it can be utilized as an energy source, and enter the citric acid cycle of mitochondria of spermatozoa?

Many microbes can use citrate as a carbon source for catabolism or anabolism. Citrate however is not a dominant (if at all) energy source for human cells  because transport of citrate across the cell membrane is not as efficient as those of monosaccharides such as glucose and fructose. Semen has high levels of fructose compared to other fluids in the body, and glucose and fructose are the primary sources of energy for sperm 1. It is possible that citrate is important for sperm motility and viability through other mechanisms. If I can speculate, citrate could be a chelating agent in semen, but I do not have a source to back this up.


text:
How do viruses/bacteria survive in extremely cold conditions?
So, recently, i watched a video, it was about a anthrax outbreak in Siberia.
The cause, supposedly were reindeer carcasses, infected by anthrax. Due to the thawing ice they resurfaced, and that lead to a outbreak.
So, i was wondering, how do viruses/bacteria manage to survive in extremely cold weather conditions?
I already did check Google and Youtube (in multiple languages), had a look into the book "Purves Biology" for answers, yet i did not find something specific enough to answer my question.

Anthrax is caused by the bacterium Bacillus anthracis, which is a spore-former. https://en.wikipedia.org/wiki/Endospore

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Does not answer the question properly. I was wondering how bacteria or viruses generally manage to survive in such cold conditions. You only told me about how Bacillus anthracis survives in the cold. But what about other bacteria, do they survive differently than this virus? Or are "endospores" the general approach to survive these conditions? And what about viruses, do they do the same?

Thank you for adding more detail — however, unless you confine you question to anthrax your question is too broad. Bacteria  have been evolving for billions of years and there can be no universal answer that covers all of them — for example many of them won't survive freezing. Likewise viruses have probably been around for just as long (or possibly even longer) and whether they should be thought of as "alive" is debatable.


text:
Is there any possibility at all, that anything, bacteria, viruses, etc, can survive the plastic recycling process used for food and drink plastics?
The Question
-    Is there any possibility at all, that anything, bacteria, viruses, etc, can survive the plastic recycling process used for food and drink plastics ?

Since I notice that some bacteria ? viruses ? survive on undersea volcanic vents, or other extremely hot places on earth.

I am not wanting to put that industry on any disrepute. I wonder if bioplastics ( made from plants ) could be used for food and drink plastics or even for computers.

I did some research into this topic, and definitely could not answer it.

I assume that even if anything could survive the plastic recycling process, it would not be anything that could transfer and reside in the human body .

I have put the second part of my question, into another question  An experiment to confirm if anything can survive the plastic recycling process, and, if it could transfer itself into the food/drink, or human body?

Could you show us the results of your prior investigations as per the [help], which you may remember being reminded the previous occasion that you asked this question. Also focus it a bit, the part about bioplastic computers seems to be a different topic.

I was thinking of removing that part about bioplastics and computers, however, it helps to show alternative plastics when looking at this subject from a greater distance

I have now added a second part to the question, asking what would be an experiment to confirm if this is possible - If anyone can indicate if or not that should be posted as a separate question ?

Please take the [tour] and read [ask] from the [help]. You need to limit yourself to one question per question - this post has at least three. Also, "I did some research into this topic, and definitely could not answer it" is not acceptable as a prior research attempt. Tell us what you looked for, what you did learn, and where exactly you are stuck and need help.

Prions can survive higher temperatures than those required to melt plastics. They cannot be sterilized or cooked away (the temperatures and times required aren't really cooking anymore).
https://dwr.virginia.gov/wildlife/diseases/cwd/what-are-prions/
https://deq.nd.gov/publications/AQ/documents/Chronic_Wasting_Disease_Burn.pdf

That's a good answer, I have no qualifications in this area so I didn't know about that one. I wonder if there are any types of spores ( en.wikipedia.org/wiki/Spore ) that can survive these temperatures

Please add references to support your claims.

@MattDMo Isn't this common knowledge? Fine I'll get you references.


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how to extract garlic fructan?
can anyone tell me a not complicated way to extract fructans from garlic (i have access to highschool lab). I need this to be able to make an experiment on garlic extract and just fructan from garlic prebiotic activity

It seems that the basic method is just a water extraction - soak some powder from your garlic in water for a period of time. Ideally you would determine experimentally the optimal time and temperature for this using a quantitative method (e.g. HPLC or a biochemical assay of some sort), but you probably don't have access to those.
Here's an example of the method from this paper1

Water extraction procedure
Conventional solvent extraction was carried out in a water bath (model WB/0B7-45, Memmert Company, Schwabach, Germany). Ten gram of Serish root powder was suspended with distilled water under treated condition shown in Table 1. The suspension was then filtered through muslin cloth to remove the insoluble residues. The extracted slurry was centrifuged at 4,500 × g for 10 min to collect the supernatant. The resulting solution was diluted with water to obtain a 1 % solution and kept at 4 °C until the day of experiment.

Edited to add:
Note that this won't just get the fructans out, it will get any soluble components including sugars, water soluble proteins, polysaccharides etc - hence the need to quantitate the fructan component to be scientifically accurate. Ideally for proper fructan isolation you would also need to extract the fructan, which I think you could do with a FPLC via ion exchange chromatography. But this is also very unlikely to be part of your high-school's equipment.
1 Pourfarzad et al, J Food Sci Technol. 2015 May; 52(5): 2657–2667.


text:
vitamin D in mushrooms
How could I test vitamin D levels in mushrooms? (I am a high school student, our lab is pretty modern, but my resources are limited)
I found an article about it (https://www.hindawi.com/journals/jfq/2020/8869279/) but I cannot understand it. Also, it is on a few different types of vitamin D. I want to test the active(usable?) vitamin D amount in different grown mushrooms.

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

In addition, we have no idea what "pretty modern" means — if you want useful answers you need to put in more effort on your part. Do you have access to an HPLC/FPLC machine or any kind of set up for doing column chromatography? In not, then the paper you linked is of no help to you. Have you researched what forms of vitamin D are "active"? If not, that would seem to be your first step — I suggest editing that information into your question along with what you can find on your own about methods for detecting those compounds.


text:
Why do plants flap their leaves?
Simple question really, I have a plant, that I'm not sure of the species. Every few days I watch its leaves droop (which scares me because I worry the plant has died), but then a few days later I find it's perked right back up. Then a few days later it does the same thing again. I don't think it's dying, in nature documentaries with time lapse I've seen plants do similar things while growing and I was curious what it's called, and why they do it?
It kind of looks like the plants are flapping their leaves, one day they're hanging down drooping, the next they're up in the air.
Photos
There's more to come, but here's a photo of what it looks like right now

Update
I've got a timelapse here I took frames once every hour, for about a week.
https://youtu.be/VE_D3E_Mioc
Two days ago the big leaves were dropping down the sides of the pot

Are you observing your plant at the same time every day? Does it receive enough water daily? How stable is it's environment (temperature, humidity, sunlight, etc.)? A plants leaves can droop and wilt when they don't have enough water, and they will perk up again when they are watered, possibly explaining the movement you described. They can also respond to environmental stimuli. These responses are known as tropisms. For example, plants that grow towards a light source exhibit phototropism.

I observe it regularly in the morning and the evening, I water it every week. But if I water when it starts wilting, then it just keeps wilting, it seems to wilt and perk up on a regular interval of every week or so.

The environment is pretty stable around 70 degrees, same with the humidity, I think. It sits in the window in my dorm room. It gets sunlight for a few hours every day, less than I think I'd like to give it, but it's the best I can do given my limitations of the dorm. Does that help @MikeyC

watch sped up footage of plants growing.

I know, that's what I'm asking about, so you've seen it then? What's it called? @John

this may be helpful https://pubmed.ncbi.nlm.nih.gov/33888615/

Welcome to Biology.SE. Can you add pictures of your plant over time (from the same position) showing the "flapping" and more detail about the pattern/timing? For example, is there any correlation with bright vs. dark days or outside temperature (might be relevant if it is right next to a poorly insulated window)? In general, these sound like "Nastic movements", but the time scale seems slower than I would expect.

@tyersome I can try to start doing that, but I haven't been taking any pictures up to this point, I will add pictures once I get them taken

@tyersome I added a photo of what my plant looks like right now

hi @iggy12345 you can take a look here https://en.wikipedia.org/wiki/Heliotropism and here https://en.wikipedia.org/wiki/Phototropism i know too little about this to make an answer.

Terms to investigate: Water pressures + wilting + water regulation

@theforestecologist I think that's what's happening, but I added a timelapse, just in case, if you add that as an answer, I'll accept it

Strongly agree with all of what @bob1 wrote. In addition, that pot looks like the type of container that is terrible for plants because it has no drainage and also doesn't breathe — this usually results in excess moisture accumulating at the bottom after watering leading to root rot. If you really like the container, I encourage you to put your Coleus into a separate pot (preferably an unglazed ceramic) with a drainage hole. You can then display your plant as you like, but pull out the inner pot to drain off the excess water.

Having looked at the time-lapse:
I suspect you might get a better answer out of gardening on this one, but I think it is entirely water related and that you are underwatering or watering poorly. It could also be that there is some problem with the pot - it may not be draining properly and the water is pooling in the bottom, which can cause root rotting.
What happens when you let a pot dry out is that when you add water, it takes some time for the soil/potting mix in the pot to hydrate. In fact, the potting mix can even become hydrophobic, so even though you see water flowing through the pot, it isn't actually soaking in.
Water won't be taken up immediately, it takes some time to soak into the potting mix, and then be taken up by the roots and transported to the leaves.
If the pot has holes in the bottom, try soaking the pot in water from the bottom once a week (I suggest about 1h - stand it in a tray), rather than adding water to the top, and/or more regular watering.
The plant you have is a Coleus, which are good pot plants. They do, however need regular watering, about every 2-3 days and good drainage to do their best. There is a good guide to growing them at TheSpruce.com.
I would say, the pale colour of the leaves is an indicator that it is suffering in some manner. There are a few possible causes - it possibly needs a bit more sun, but the few hours in your window should be enough. Having said that, the pale colour could also be from nutrient deficiency, particularly nitrogen, or caused by being too dry. The dry edges/tips on the leaves also indicate that it has been too dry at some point in the past few months.


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What happens to quality of breast milk when twins of two different sexes are born?
It says here in Scientific American

Mother's milk may be the first food, but it is not created equal. In
humans and other mammals, researchers have found that milk composition
changes depending on the infant's gender and on whether conditions are
good or bad. Understanding those differences can give scientists
insights into human evolution.
Researchers at Michigan State University and other institutions found
that among 72 mothers in rural Kenya, women with sons generally gave
richer milk (2.8 percent fat compared with 0.6 percent for daughters).

Now I'm curious as to what happens when fraternal twins of different genders are born?

Welcome to Biology.SE. Please take the [tour] and consult the [help] starting with [ask] for details about what is expected on this site and then [edit] accordingly. I've made some minor edits, but I encourage you to think about whether the last paragraph adds anything to your question — my recommendation would be to delete since it not based on scientific evidence. It would also help if you could indicate where you've looked for answers to this specific question.

@trondhansen is Scientific American not a reliable source? Also it's Kenyan women, I don't know which ethnicity is being reffered in Wikipedia. Does Ethnicity influence nutritional content? Economic status can also influence it.

@MrGreenGold i removed my comment because the article in the scientific american does not have a reliable source and Marissa is a freelance science journalist not a scientist.it is unlikely that the mother produces milk with only 0.6% fat if the baby is a girl and the same mother produces milk with 2.8% fat if the baby is a boy,it is an increase of 5x the fat content(normal fat content in mothersmilk is 4.2%).


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Where in the cell does this enhancer RNA knockdown take place?
In Pnueli et al., 2015, they knock down an enhancer RNA using RNAi, testing whether it is a mere byproduct or whether it has a key role in the enhancer's function. They find their system works: the siRNA knocks down the enhancer RNA that it's targeted to, enabling further study. Hooray!
... but I've read that RNAi and the RISC work outside the nucleus, and intra-nuclear effects are further downstream and indirect (example: Gosline et al. assume that effects on introns are indirect). I assume the paper's not wrong, so what's going on?

Conventional wisdom is wrong or incomplete: RNAi can work inside the nucleus too.
Pneuli et al.'s enhancer RNA gets exported to the cytoplasm and then re-imported to act on its target gene.
Something else?

Pnueli, L., Rudnizky, S., Yosefzon, Y., & Melamed, P. (2015). RNA transcribed from a distal enhancer is required for activating the chromatin at the promoter of the gonadotropin α-subunit gene. Proceedings of the National Academy of Sciences, 112(14), 4369-4374.
Gosline, S. J., Gurtan, A. M., JnBaptiste, C. K., Bosson, A., Milani, P., Dalin, S., ... & Fraenkel, E. (2016). Elucidating microRNA regulatory networks using transcriptional, post-transcriptional, and histone modification measurements. Cell reports, 14(2), 310-319.

Are you sure an antisense RNA against this enhancer RNA uses the cell’s microRNA RISC system? I don’t know, but a priori would expect not.

I have no idea. What else would it use?

Hybridization? When antisense RNA was first introduced the microRNA Dicer system was unknown, and the strategy was based on the idea of inactivating mRNAs by hybridization. The reason I would not expect such antisense RNAs to use the Dicer system is that they do not have the imperfect stem-loop structure of the natural substrate. I may be wrong as this is not a technique I have used, but you should check it out before assuming your assumption is correct and there is a problem with the paper

Would hybridization lower concentration of the target RNA as measured by e.g. qPCR? Or would it affect activity without altering concentration?

FWIW, the system they describe using is shRNA, which I thought worked via RNAi. That's what wikipedia says anyway. If it's more complicated than that, well, that's basically my question.

RNAi can happen in the nucleus as well. This is better documented in C.elegans but there are some references supporting nuclear RNAi in mammalian cells too:

https://doi.org/10.1073/pnas.1707440114
https://doi.org/10.1016/j.celrep.2013.12.013
https://doi.org/10.1093/nar/gkv1305


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Are all fibrous roots considered as adventitious roots?
I have just started studying about morphology of angiosperms.
I'm learning about roots right now and I came across the following.
In monocots, adventitious roots are a characteristic feature whereas in dicots true roots are a characteristic feature.
When I was younger, I had learnt that fibrous roots are a characteristic feature of monocots.
So I studied further to find that, in monocots, the fibrous roots develop from the base of the stem after the radicle goes absent. And since the roots here do not develop from the radicle but the base of the stem, they are called adventitious roots.
So with this information, I have the doubts:

Are all fibrous roots adventitious?
If all fibrous roots are adventitious, then are all adventitious roots always fibrous?
Are all monocots fibrous rooted?

Are all fibrous roots adventitious?
-Yes. Take note that adventitious roots do NOT originate from a radicle (first root of a germinating seed). Adventitious roots grow primarily from the nodes of the stems and leaf of some documented plant species. In case of germinating monocot seeds, they do have radicle but the embryonic root dies as the monocot plant grows. The dying embryonic root will soon be replaced by new growing roots from the nodes of mature stems of the monocot plant. These thin and numerous roots are now the fibrous roots which are classified as adventitious roots since they now originate from a stem, not from a radicle.

If all fibrous roots are adventitious, then are all adventitious roots always fibrous?
-No. Example are the plant cuttings of dicot plants. Stem cuttings of a dicot plant will still produce roots that resemble the taproot system yet they NO longer originate from a radicle. Hence, they are now adventitious roots since their new origin is the stem. Therefore, dicot plant cuttings develop adventitious roots that are not fibrous.

Are all monocots fibrous rooted?
Yes.

I'm not sure that I get #3 in the question because of the odd phrasing. Anyhow, welcome to the site. Please take our [tour] and refer to the [help] for guidance. Enjoy Biology.

Adventitious roots are plant roots that form from any non-root tissue and are produced both during normal development and in response to stress conditions, such as flooding, nutrient deprivation, and wounding.[1]

Are all fibrous roots adventitious?

As per the definition, yes, the fibrous roots system consists of adventitious roots that arise from the base of the stem.

If all fibrous roots are adventitious, then are all adventitious roots always fibrous?

No.

Are all monocots fibrous rooted?

Yes, a fibrous root system is universal in monocotyledonous plants and ferns.

References:

Bianka Steffens, Amanda Rasmussen, The Physiology of Adventitious Roots, Plant Physiology, Volume 170, Issue 2, February 2016, Pages 603–617, https://doi.org/10.1104/pp.15.01360


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Why do we have to scrape the inside of the cheek twice to get the sample of epithelial cells?
I was studying the theory of a practical exercise of preparing temporary slide of animal tissue from my laboratory manual.
In the section about epithelial tissue, the first few steps of the procedure contains the following.

• Rinse your mouth well with water.
• Gently scrape the inside of your cheek with the broad end of a clean
toothpick. Discard this material.
• Scrape again, and spread these cells gently on a clean slide. Add a drop
of 0.9% NaCl solution or physiological saline and a drop of methylene
blue with the help of a dropper.

Why is it mentioned to scrape and discard the first time and scrape again?
I've tried searching about it on the web but couldn't find any mention of scraping twice to obtain the sample, nor it is mentioned in my book. There doesn't seem to be any apparent reason to scrape twice to me.

What do you think? What have you found in your research? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure. Please see our homework policy for more information.

@MattDMo I've added info. accordingly.


text:
Why does the Scatchard plot have a negative gradient?
I am very confused as to why the scatchard plot has a negative gradient. If the x axis shows increasing B, specific binding to a receptor, and on the y axis the specific binding (B)/concentration of ligand ([A]), then why is the gradient negatively sloped. Textbooks will assume that the concentration of ligand remains constant, so it seems intuitive that as you go along the x axis and increase the specific binding to the receptor, the gradient would be positively sloped, as values on the y-axis would also be taking greater values for the specific binding (as it is just B/[A]).
The only way that I can make this work would be that as B increases, then [A] will also have to increase so that overall B/[A] will decrease (and thus provide the negative gradient as seen on the plot) However this is also unintuitive as:
i)We assume that [A] is constant anyway and this is what most textbooks do
ii)Even if [A] can change, we would expect it to get smaller, as [A] represents the concentration of ligand, so as the number of bound receptors (B) rises, then we would think there would be fewer free ligands as they are binding to the receptor.
Any help understanding where I have gone wrong in this reasoning would be greatly appreciated, as I have clearly fundamentally misunderstood either the biology that this is seeking to model, or the mathematical model used to generate the graph.

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

I have now edited my question to include additional details.

I think you probably misunderstand which quantities exactly are represented on the Scatchard plot. Let's start from the beginning. Binding between a receptor, $\mathrm R$, and a ligand, $\mathrm L$, can be described as an equilibrium reaction
$$\ce{R + L <=> RL},$$
with the corresponding equilibrium constant
$$K_{\mathrm{eq}} = \frac{[\ce{RL}]}{\ce{[R][L]}}.$$
For the simplicity, we have assumed that only one ligand binds to the receptor. Usually, we use the inverse equilibrium constant, called disociation constant
$$K_{\mathrm d} = \frac{1}{K_{\mathrm{eq}}} = \frac{\ce{[R][L]}}{\ce{[RL]}}.$$
Both the ligand and the receptor can be either free or bound, but their total concentration remains constant. So we write
$$\ce{[L]_{total} = \underbrace{[L]_{free}}_{[L]} + \underbrace{[L]_{bound}}_{[RL]}},$$
$$\ce{[R]_{total} = \underbrace{[R]_{free}}_{[R]} + \underbrace{[R]_{bound}}_{[RL]}}.$$
Let's first look at the fraction of occupied receptors, namely $\ce{[R]_{bound}/[R]_{total}}$
$$\ce{\frac{[R]_{bound}}{[R]_{total}} = \frac{[RL]}{[R]_{free} + [RL]}} = \frac{\frac{\ce{[L][R]}}{K_{\mathrm d}}}{\ce{[R]_{free}} +\frac{\ce{[L][R]}}{K_{\mathrm d}}} =  \frac{\ce{[L]_{free}}}{K_{\mathrm d} + \ce{[L]_{free}}}.$$
This curve is probably familiar to you, and it is usually called saturation curve. It relates the concentration of free ligand with the fraction of occupied receptors.

We are now interested in the ratio between bound and free ligand,
$\ce{[L]_{bound}/[L]_{free}}$. Let's derive this quantity
$$\ce{ [L]_{bound}} = \ce{[RL]} = \frac{\ce{[R][L]}}{K_{\mathrm d}} =
\frac{\ce{[R]_{free}[L]_{free}}}{K_{\mathrm d}},
$$
$$
\ce{ \frac{[L]_{bound}}{[L]_{free}} }  = \frac{\ce{[R]_{free}}}{K_{\mathrm d}}=  \frac{\ce{[R]_{total}}-\ce{[R]_{bound}}}{K_{\mathrm d}} = \frac{\ce{[R]_{total}}}{K_{\mathrm d}} - \frac{\ce{[L]_{bound}}}{K_{\mathrm d}}.
$$
We have obtained the Scatchard equation, relating the concentration of bound ligand with the ratio of bound and free ligand
$$ \boxed{\ce{\color{red}{\frac{[L]_{bound}}{[L]_{free}} }} = \frac{\ce{[R]_{total}}}{K_{\mathrm d}} - \frac{\color{blue}{\ce{[L]_{bound}}}}{K_{\mathrm d}}}.$$

Thank you that makes much more sense


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Melting Points of Animal Fats and Body Temperature
Melting points of animal fats used in cooking vary quite significantly. In some cases being above the body temperature of the animal, and in other cases being well below (cf the examples below).

Lard: melts 30-48°C depending on where in the pig it's taken from. Back fat mostly melts below the pig's body temperature (39–40°C), whilst leaf fat mostly melts above it.
Goose fat: melts 25-37°C, so quite cool, and whilst I wasn't able to find a number for adult goose body temperature, I found the numbers 39–42°C for goslings online, meaning all the goose fat would be expected to be liquid.
Beef tallow: melts around 45–50°C, so well above a cow's body temperature of 38-39°C, meaning all the fat would be expected to be solid.

Obviously the fats here are in the form they're used for cooking, after they've been rendered out of whatever structure they're stored in in the living animal (presumably within cells and not in bulk), but does the fact that some of these fats will be solid, and others liquid, at their animal's usual body temperatures have any effect on how the body stores, moves, and uses the fats?

From your question, I would expect that really well-marbled beef cattle would have some difficulty with some movements (though I admit to having little knowledge of where every cut of beef comes from on the body.) Do you believe that animals walk around with solid fat? I have difficulty imagining that, but I could be wrong. Solid fat would seem so... restrictive.

@anongoodnurse I'm assuming that the fats are not stored in bulk but within cells, which could allow for the necessary flexibility. Having solid fats stored in bulk definitely does seem like it would cause problems

you basically want a book on lipids in the body, lipids are used for all kinds of things in the body and in many states.


text:
How does genetic feedback shape the evolution of whole ecosystems?
While looking into the organization of ecosystems and how evolution shapes it, I've been reading "Ecology" (1975) by Eugene Odum. In chapter 6, p. 167, Odum speaks about the mutualistic relationship between bullhorn acacia and acacia ant, and writes:

As one species evolves to take a selective advantage of the
association, the other species comes under selective pressure to
strengthen the interdependence. We can see how a genetic feedback
process of this sort could shape the evolution of a whole ecosystem.

I don't understand the first sentence. So, the acacia increases its fitness through the association with the ant, and the ant would come "under selective pressure to strengthen the interdependence" with the acacia? What is Odum trying to say here?

Welcome to Biology.SE. 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, your title question is much too broad and doesn't reflect the body. It would also strengthen your question if you referenced more current material (or at least sources available online) that you had used to try to work this out yourself.

Thank you for your welcome. I read what you recommended and I edited my question, making the title and the question more specific, with the detailed question about Odum's own answer being better integrated with the question. I also explained why I read this old source.

Can you add the page number for your quote of Odum?

Sure, it's page 167. I see you also suggested an edit of my question. Thanks, however the phrasing is too specific and doesn't match my real interest. That being said I would welcome someone simply explaining the Odum quote. Odum does reply to the question I'm asking, so explaining his reply is a way of replying to my question. (Reposted for more concision and clarity.)

I have approved the edit (with minor adjustments). I think that the edit at the least clarifies an answerable question. It is not obvious what else beyond this was of interest (except perhaps that you are looking for more general principles of the phenomenon). I encourage you to a) further edit or b) ask a new question building on the specifics in this one if you are not satisfied with the edit.

@MaximilianPress I don't see how my original question was unanswerable. It is in fact the question Odum is answering in this quote. Had you written an answer to explain why you think it was unanswerable, that might have been helpful. On the other hand I can see how asking both a general question and a specific one about a quote may have seen undesirable. As it stands the question is a bit strange but it's at least restricted to the quote; let's see if someone will be able to explain it.

Not that it was unanswerable. Simply that the answerable part of it has been clarified and made much more obvious by the edit. (I upvoted the question, contingent on the edit!)

I don't claim that this is a fully fleshed out answer, but it's too long for a comment.
I suggest taking a look at some of the classic models for the evolution of cooperation. One example would be Axelrod and Hamilton (1981) in Science, who formulate a series of theoretical conditions under which cooperation 1) arises, 2) is a robust strategy, and 3) stabilizes. The paper was then treated at book length by Axelrod.
Briefly, they argue that cooperative strategies are more successful when the frequency of cooperating partners is higher (and obviously, when the benefit of cooperation is higher).
In a very simple example, cooperation in the Prisoner's Dilemma becomes a better strategy as the game is iterated, and you learn whether your partner is trustworthy or not.
Extended to the evolution of associations like ant-acacia, if one species (say acacia) "takes selective advantage of the association", then necessarily the frequency of acacia individuals willing and able to cooperate will increase. This could be either because there are more acacias or because more of a stable population of acacias will cooperate with ants.
Therefore, the benefits of cooperation will increase for ants, because the frequency of cooperating acacias is higher. This would then be the "selective pressure" for cooperation that Odum writes about.
Increased fitness of cooperators relative to non-cooperators is "selective pressure" to cooperate, meaning more cooperation in the long term under assumptions of a stable environment.
The paper itself is light on equations, using instead mostly simulations. Others have gone so far as to build more modern simulation packages implementing a variety of strategies, in case that is helpful.

I read the article you suggested (Axelrod 1981). They do show how, within their game-theoretic model, constant defection is evolutionarily stable relative to any kind of cooperation, and therefore cooperation can only prosper in an environment with some cooperators -- which I guess is what you are alluding to. Still I'm not convinced that you are explaining the quote satisfactorily. I think Odum is making (in 1975) a general statement about how mutualistic relationships arise from coevolution and end up shaping whole ecosystems. But I don't understand his sentence. It may be a phrasing issue.

@MartinP. I guess I have a very different reading of that paper. I see the paper as making a series of arguments about why cooperation evolves even in the presence of incentives for defection (title: "The Evolution of Cooperation"). To me, all that Odum seems to be saying is that cooperation is a comparatively better bet when there are lots of cooperators, relative to when there are few cooperators. In other words, it only makes sense to have a credit card when the stores you shop at mostly accept credit cards.

I was not making a summary of the paper, but of the part that seemed to justify your reference to it in your answer. My impression is that the paper's model has very specific assumptions and is not much help for ants and acacias. One such assumption is that all individuals can cooperate with each other. Acacias can't cooperate with each other.

In your bank and credit card example, how are the credit cards holders pressured "to strengthen the interdependence", as Odum writes? I'm thinking more of an employee-company analogy. The employee is happy with their job, so they go the extra mile to make sure the company is happy with them and keeps them. That is "strengthening the interdependence". See my own answer.

@MartinP. Imagine that I sell tacos out of a truck in 1970. 0% of my customers want to use a credit card to buy tacos, I have no reason to accept cards. However in 2022, probably 80-90% of my customers will want to use a card. Likewise, over those years those customers went through a change where more and more businesses accepted cards (and now some don't accept cash). Both agents adapted to each others' behavior to strengthen the interdependent behavior (where behavior == "credit card transactions"), driven by increasing frequency of cooperating behavior.

My guess is that Odum is trying, and possibly failing, to provide a general reasoning about how stable mutualistic relationships might naturally evolve and shape ecosystems. Consider ants and acacias.
At first, a particular mutually beneficial exchange happens by happy coincidence between some ants and some acacias: the ants find shelter in the acacia's thorns, and their natural reaction to intruders serves as a defence for the acacia. The acacias figure out through evolution that if they can thus count on the ants then they can stop the costly production of the bitter alkaloids that acacias usually have for their defense, which gives them an edge relative to other acacias that bear that cost. To make sure the ants do keep coming and the happy coincidence becomes a way of life, they also evolve to produce (less costly) Beltian bodies on which ants can feed.
The ants are glad to have have found a provider of free food and shelter (free, because it was a happy coincidence at first and by hypothesis the ant hasn't yet evolved to specially adapt to it). However, now that they have found such a worthwhile partner, they don't want to lose it and therefore evolve to "strengthen the interdependence" (as Odum writes). Perhaps they become even better defenders of the acacia by making their pheromones even more repellent to the acacias' ennemies. And that is how what was a happy coincidence becomes a stable mutualistic relationship.
I'm not sure this second part makes sense as it is (we'd probably need a more precise explanation of why the ant needs to do anything more), but it may be the logic Odum was suggesting in 1975.
It may be that, contrary to what Odum suggests (and to what I assumed as well), there is in fact no generally accepted evolutionary mechanism that explains mutualism, only particular stories for particular cases. Someone in fact writes, in an article that I should probably read, "Simple, general principles governing the evolution of mutualism have proved elusive" (The evolution of mutualism, 2012).


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How is brain calorie intake affected after hemispherectomy?
So, I hear brain consumes 20% of the body's energy, and also according to studies people with only one hemisphere can function mentally fine with little to no problems.
My question is, how does that affect calorie intake of the whole body or the brain? Is the calorie intake halved for the brain, cause it only has one hemisphere?
Source how it's done:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4729844/

Welcome Hormoz. Do you have any reference to support that the entire central nervous system is halved? This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask.

I mean that's what it is for, either partially or fully. That's like asking "do you have any source that addition is actually done in math?". A simple google search would suggest that such a thing exists. There are MRI scan pictures to suggest this too.
Of course I don't have all the details so I might not be right on everything, but that doesn't change the nature of the question which is about calorie intake after it.
I can include some source though regardless. Edited.

What I'm saying is, there needs to be a differentiation between "brain" and "cerebral hemisphere", there's a category mismatch in the question. Please re-read my previous comment.

So, as far as I know, there several ways to go about this, some which might not remove as much brain matter, some which can remove nearly half of it. Some parts might remain though.
As you say, the wording might not be completely accurate, but due to variety in how this is done, I am not quite sure how else I should word it? I can replace the word brain with hemisphere so edited.
I am asking for cases where nearly or completely half of a brain is removed.

How much energy is used by a missing hemisphere? None. Brain energy use is determined roughly by number of neurons. One would need to know the % of total neurons removed by that resection to give an estimate. If you provide that information, we'll approximate the reduction of energy by the reduced brain mass. Thanks

So the reason I am asking is not because I want to know how much energy on hemisphere consumes normally. It's mainly because when you remove one hemisphere, the other hemisphere takes over most of the work done by other. In other words, one hemisphere is doing the work of both. I wanted to know if that would mean the energy consumption of that hemisphere would rise due to that.

Ah, interesting. I don't think the remaining neurons do twice the work most of the work is "silent"), but they may increase dendrite formation. I don't think the answer is known, but it doesn't remain the same.


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Movement of solutes across a semipermeable membrane in a U-shaped tube

The solutions in the two arms of this U-tube are separated by a membrane that is permeable to water and glucose but not sucrose. Side A is half-filled with a solution of 2 M sucrose and 1 M glucose. Side b is half-filled with 1 M sucrose and 2 M glucose. Initially, the liquid levels on both sides are equal.
When it reaches equilibrium, the sugar concentrations on both sides of the U-tube will be 1.5 M sucrose and 1.5 M glucose.
Can somebody explain the answer (D) to me? My understanding is that the membrane is permeable to glucose, therefore glucose will reach equilibrium, with 1.5M on each side. Since the membrane is not permeable to sucrose, the concentration of sucrose will not change. Water will move from B to A. Does the movement of water causes the sucrose solution on both sides to be equal? But wouldn't that alter the glucose concentrations too? I'm sorry I just know what my bio teacher told me but I don't quite get the reasoning. Thanks.

Please do not post questions as graphics. They do not index and discriminate against people with visual impairments.

OK I'll modify it

The membrane allows movement of particles which will cause a balancing of the concentrations.
There is one hint in the text: "Initially, the liquid levels on both sides are equal" which gives away how this will happen.
Water and glucose can freely move through the membrane and this is what will happen. Water will move through the membrane, the level in side A will rise until both concentrations of sucrose are equivalent. Glucose will also cross the membrane from B to A until the concentration is equal on both sides.
You are right, the movement of water will lower the concentration of glucose in side A but since the glucose can move across the membrane as well, this will not affect the equilibrium.


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Intersexual competition regarding energy investiture of offspring
A while ago I remembered reading about a species that had evolved so that the male sperm cells promoted the energy investiture of the female in this offspring upon fertilisation. Since this was a r-selected species this hurt the females by reducing the likelihood that they would be able to give birth as many times due to the increased strain and so evolved some method that reduces the energy investiture in offspring.
Unfortunately I haven't been able to find references to this and was wondering if anyone here would be able to inform me which species I had likely heard about (or give examples of a similar behaviour), preferably with some references (I'm an academic, so probably able to access paywalled journal articles from the main journals).

Hi and welcome to the site. What is a "high" K species? (in what manner is it high?) Are you sure it wasn't seminal fluid? Try searching "effect of seminal fluid on female" (without quotes) and see if that helps. if it doesn't, edit to show what you found (showing research effort is expected on this site; "Nothing" is not accepted.) Try rephrasing the question to m.ake it clearer. Thanks

by high K I actually meant r-selected (don't work in biology so use the term very rarely and always get it mixed up). I have tried searching intersexual competition and only seemed to get results about macroscopic competition between animals rather then competition at a biochemical level. I did manage to come across t-Haplotype sperm in mice (see https://www.inverse.com/science/selfish-sperm-have-a-deadly-advantage). Most of my searches came up with results that were on a completely different track to what I was looking for, but I'll have to add "seminal fluid" to my searches and see

I think you'll find a lot more information on that different search.


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What is this colorful bug from Germany?
a friend found this little fella just outside of Berlin and managed to snap a blurry picture.

This boy or girl is probably the size of a finger nail and features fly like skin wings with no hard cover. There are thin curved antennas at the head.
On the internet I found the same color scheme in "Festive Tiger Beetle (Cicindela scutellaris)", but the shape doesn't seem to match.
Can you identify this creature?
(surely not spider, right?)
Thanks

Welcome to the site. Could you please provide some sense of scale - approximately how big do you think the insect is? With the poor photo, it is hard to tell if it is winged, or any features besides the distinctive colouration. Any further details you could provide would be useful in ID.

Festive tiger beetle seems to be only north America, though I am no expert.

It could be a ruby-tailed wasp.

That sounds indeed quite possible

Perhaps it's some form of jewel beetle. Their wings are traditionally used in jewel and clothesmaking and some of them are detrimental invasive species.
It will be nearly impossible to say which species based on that photo, which is too blurry.
https://www.lsuagcenter.com/profiles/lbenedict/articles/page1590086881287
https://en.wikipedia.org/wiki/Buprestidae


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model organism for maize
Since I am trying to find the functions of some transcription factors of the maize,  I would like to try a search on the model organism transcription factor databases.  Which model organism would anybody suggest?
Edit:
Sorry for the incomplete information provided.  Since a transcription factor database could provide the experimentally verified information about the model organism, some transcription factors of the maize have one defined function, e.g. matters about flowering and I would like to know the transcription binding in the model organism in order to clarify the function of these transcription factors.  As a result, I could connect these functions dot to dot instead of carrying out the actual experiments.
The model organism provided in the ans. helps me limit the further searches and helps me use the right algorithm to relate the transcription binding of different plants, e.g.  I could relate the transcription factor of flowering in maize to the similar motif in model plant (organism).

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or 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!

Why not maize itself? (And other grasses)
If for some reason you need something that is more explicitly a model organism, I suppose you could look at Arabidopsis. That link actually includes a large number of plants, but Arabidopsis is almost certainly the best described.
But the maize data itself should be quite good (as well as containing orthologs from other Graminaceae.


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Identify species
Would like to know if anyone knows what this is!?
Was attached to human hair off scalp 1/8 inch long

Looks like dust fibre

Welcome Jennifer. There doesn't seem to be anything in the picture or the text to lead us to believe there even is an organism there. Can you clarify?

There was movement and it looked 2 me as two eyes

The first photo object is a few mm (2-4 mm?) length based on those being fingerprints in the background. How big is the second object. If it is smaller, then the tiniest breeze, even the heat rising from your body could make it move, as could slight tremors in your hand.


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Is DNA a Language?
I’ve been thinking about attributes that are unique to humans (not just far more developed in humans than other species) and aside from trivial things like chins, the only ones I can think of are art and language, but I’m not certain of either of these. Some songbirds sing for no apparent reason, which might suggest they have an intrinsic aesthetic sense.
As for language, what separates it from communication, I would argue, is grammar. It seems fairly clear that the other examples of what we would typically call communication in nature are not grammatical. But then I thought about DNA. People often speak metaphorically about DNA as a “programming language”. So, is that more than just a metaphor? That is, does DNA have clear lexical units, whose arrangement determines the relations between them? That is, is DNA, in whole or in part, grammatical?
There is a similar question here, but the answers are too ambiguous in the use of the word “language” for my purposes. For example, English is undeniably a language. We could take all valid English sentences and order them as in a dictionary. This assigns each sentence a natural number. We could then assign the number the meaning of the corresponding English sentence. It would be fair to call this a “code”, but hard to call it a “language” in the strict sense: the digits of the numbers and their organisation would not really have meaning. In comparison, in English, the word “biology” has a specific reference, or placing an adjective before a noun has a specific meaning. I’m not talking about DNA “meaning” what it’s encoding in the sense that it knows what it’s doing, that is of course nonsense. Rather I’m using the word meaning in the sense that lexical units of DNA and ways to organise them would denote specific things, for example, specific ways to fold part of a protein, or bond amino acids. Just like how a computer doesn’t know what it’s code says, but still, in the psuedocode:
while n>1:
    if n even:
        n = n/2
    else:
        n = 3n+1
print “Yes”

every term has a clear meaning, and their arrangement combines these meanings according to clear rules.
This may be an incredibly misguided question. I’m not a biologist.

It would not be fair to call anything to do with DNA a "code" unless you are referring to the Genetic Code. In molecular biology (which predates modern computer programming) it does NOT mean encoded information and cannot be used in this way in scientific language.

Welcome to Bio.SE, Thomas. If you haven't yet, please take the site tour and read the guide on asking a good question. Generally, this forum is dedicated to answering specific questions about biological systems or concepts. Your question strikes me as philosophical, and your edit, while clarifying your point, does not do much to rectify the fact that any and all answers would be speculative and/or opinion-based.


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Where in the biological realm is vitamin B5 chiefly produced?
Can yeast produce pantothenic acid (vitamin B5)?
Do bacteria efficiently produce it?
Or does it only come from plants?
The Wikipedia page for pantothenic acid doesn’t seem to answer the question (other than mentioning that small amounts are found in, i.e. used by, every organism, and hinting at the facts that animals concentrate it and yeasts are, at the very least, inefficient at producing it).

I see that you reverted the title of this question. I suggest that you Google “biological realm” to find the context in which this strange (at least to me) expression is used.

realm /rɛlm/ LITERARY 1. a kingdom. "the defence of the realm"  2. a sphere, domain 3...

The title is an improved version of the initial title. The one you gave changed the meaning of the question. I think it becomes problematic when we change peoples' questions to better fit our answer (it quickly becomes a very lonely world / a monologue). I don't think you had any bad intent but I'm sharing the thought that occured to me when bringing it back to its original meaning with an small edit to the original question better encompassing part of your answer.

— Whenever I am obliged to translate a phrase into German, French or Italian I not only check with a dictionary, but do a Google search to check the phrase is actually used in the language, and with the same sense. That is what I did, and suggested you do, with “biological realm”. If you think my alteration changed your meaning explain. But invented expressions will not do.

Google has ceased to be of any value as a reference a long time ago. It is merely now a tool to dumb down people, increase dependence (consumerism) and serve brainwashing (propaganda). As for most people my personal experience is that most people have a poor mastery of their own language, and that is most true in the case of the English language. This is by design as a systemic effort to limit people's language is needed to limit their conceptualization of reality (reality is made of many nuances and subtilities, the more you restrain the language, the mote you limit people's grasp of reality)

*the more you...

Oh Dear — As people will tell you, I do the bad cop, good cop on this site. With your question I was doing the good cop: not only giving an answer, but explaining how I found the information; commenting to explain how to minimize mistranslation problems between scientific disciplines the way I do for languages. Now you can use whatever search engine you like, or none, or Wikipedia (set to the language of interest) or PubMed or... But the point is if the searched phrase does NOT appear in the context expected, you should SUSPECT it MIGHT not be commonly used in that context.

…and a title is, well, a title. Its function is to communicate to people the flavour of your question. It is not a platform for extending people's grasp of reality. If you use terms that appear strange to biologists, and use outdated terminology to refer to compounds, the chemical nature of which has been known for years, you will certainly communicate something, but not what I suspect you want, and not in a way that will solicit the specialist answer required. To me, at least, such a title signals that you are not a serious biologist and this is probably a naïve question about "vitamins".

I understand you good intent, but I'll happily be considered a non-serious biologists by anyone who mainly only can judge based on my vocabulary (or by anyone at all for that matter).

General Considerations
Pantothenic acid is a precursor for the synthesis of Coenzyme A which is essential for most, if not all, living organisms. As bacteria appeared on earth before plants, and can currently live in environments where there are no plants, it is difficult to envisage their being unable to synthesize pantothenic acid. The situation with yeasts is less obvious, but as independent free-living single-cell organisms, the expectation would be that they had retained this synthetic ability of their evolutionary precursors.
Pantothenic acid synthesis in different organisms
Pantothenic acid is produced by a wide range of bacteria, with the structure of the enzymes of the pathway of its synthesis, e.g. the final enzyme, pantothenate synthetase, available from many different species, as can be seen from a search of the Protein Data Bank.
Indeed far more detail is known about the process than in higher plants, because of the greater ease of conducting molecular genetics on the former.
One way to check for the existence of a pathway in a particular organism is using KEGG, and this approach shows the pathway for the synthesis of pantothenic acid is present in Saccharomyces cerevisiae.
Efficiency
The poster refers repeatedly to the efficiency of production of pantothenic acid but appears to be misusing the word, and it is not clear in this context what he means. In science efficiency expresses the percentage of input energy or material that is converted to an intended output. For example in biochemical thermodynamics, inefficiency might be the loss of chemical energy as heat (in processes where the aim is not to produce heat). In a general sense such efficiency exerts selective pressure on organisms, and this will be greatest in rapidly-growing organisms such as bacteria which are subject to competition for resources. All organisms have regulatory mechanisms to ensure that there is sufficient of the product of a pathway when it is required, but that energy and precursors are not wasted by producing it when it is not required. Such regulatory mechanisms tend to respond more rapidly to changes in bacteria than in eukaryotes (such as plants), with their longer division times, but there is no reason to believe that any organism that synthesizes pantothenic acid does so inefficiently.
It is possible that the poster is interested in which organisms might present the most abundant sources of pantothenic acid for those organisms such as mammals that cannot synthesize it themselves. This may relate to the size of the ‘pool’ of this metabolite in the cell. However that is a completely distinct question from synthesis and efficiency thereof. I doubt whether there is much literature on this as it appears that human deficiency of pantothenic acid is very rare, so that this has not been a particular dietary concern.

For the term "efficiently", let's define it like this: The more efficiently an organism produces pantothenate, the less its growth and replication would correlate, in an environment replete with all other nutrients, with the amount of exogenous pantothenate present in / added to that environment (despite disposing of pantothenate internalization/transport mechanisms/ability).

There might be a better term, and if you find one please tell me and I'll edit the question/text accordingly.

@Hans — I'm sorry but you are not defining anything. You are stating a consequence of this mysterious thing which seems as mysterious as the thing itself. Correlation of growth and replication? Why? And why should pantothenate be in or added to the environment? You seem to have some basic concern or agenda that you are not spelling out. What are you after?

I'm trying to understand which organisms are most pantothenate-"independent" in their growth and replication. As you wrote, it's possible that all life on earth requires it metabolically, if you factor out growth/division metabolic load, there is some logic in assuming that those whose growth/division is most independent of exogenously-sourced pantothenate most efficiently produce it themselves. If you have a better term or a better way to put it, as I wrote, please state it.

@Hans I think the issue is that assuming there is a correlation between growth and any one molecule, you'll only see it if that molecule is a limiting factor. Every organism that has a sufficient amount will see no relationship with growth, whether or not they produce it endogenously or how efficient or whatever.

@Hans — I also wonder if you possibly are thinking that because pantothenic acid is a vitamin for humans, it somehow is a limiting nutrient for all organisms. This would be a misconception. Essential amino acids are not considered vitamins but we require them in our diet, whereas bacteria (and even many lower eukaryotes that have retained the pathways make them quite happily). Of course there may be situations of this sort, where products needed for survival in an extreme environment are chemically difficult to synthesize for some reason, and some organisms have adapted better than others.