text:
Where do garbage flies come from?
I want to know the origin of those very small insects/flies which we see over kitchen garbage or when some surface is wet for some time. Where do they come from? Who actually reproduce them?

I suppose that they reproduce themselves. How a new garbage bin becomes infested with them is a good question - probably because they already live nearby, eithe rin other garbage bins or everywhere, but in less noticeable concentrations.

But I have seen them even when there are no nearby piles.

As I said - they are everywhere... not sure what is the question then.

Not spontaneous generation: https://biology.stackexchange.com/a/97165/16866

“All things bright and beautiful all creatures great and small…”

Q-> Origin of Insects/flies and Who reproduces them?
A-> Eggs laid by adult female flies.
Q-> Where do they come from?
A-> Nearby sewage, society waste-disposal areas, drainage systems.
The very common flies such as - Musca domestica and fruit flies often feed on rotten kitchen food, overripe fruits/vegetables, human excreta, animal dung. They prefer food that is either in liquidy or soluble in their saliva. Water is also required by them as they're also living creatures after all. Other food sources can be milk, sugar syrup, meat broth, etc.
Since dustbins are a food source for such insects, these are the perfect places for breeding as well (their babies also need nutrition). Female flies from near by sewage or locality waste disposal area often lay eggs on the home-based garbage and organic material. Eggs of flies are hatched within few hours and one can see a sudden increase in the number of flies around their bins.
In the daytime, when they are neither hungry nor breeding and prefer resting, that time they are seen in non-waste areas such as walls, floors, ceilings, clothes, etc. These resting places are nearby of their feeding places only.
For more info- Check https://www.who.int/water_sanitation_health/resources/vector302to323.pdf

Another major source for these flies is produce that is brought into a house, which may have fly eggs laid on it already.
While you aren't likely to eat maggot-filled fruit, it's quite easy for waste (e.g., peelings, cores, rinds) to end up sitting for long enough for the eggs to hatch in a trash can or down an imperfectly cleaned garbage disposal.


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Do E. coli change color (from white/grey to yellow) when they grow older?
In my experiment, I had white colonies initially and they turned yellow. So I thought it´s natural that mature E. coli colonies are yellow and young are white. But it could be that I had two types of E. coli and the yellow one just dominated the white.
I research the affect of vitamin C on susceptibility of E. coli to H2O2.
First I treat bacteria with vitamin C, incubate for an hour and H2O2.

That is what I have on all of the plates. It really seems like there are 2 species present.

Can you please add more information about the experiment that you are doing?

It would be really helpful if you could attach pictures of experiment results.

source: Stack Exchange

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How do we know genes that are considered endogenous retroviruses are actually endogenous retroviruses and not just ordinary genes?
What makes these genes different as to be classed as an endogenous retrovirus? I've read the entirity of Wikipedia on retroviruses and didn't find the answer. I think it could be that these genes are identical to some viruses making the conclusion appear sound. But I'm not sure. If this is the case is there any other ways to conclude a gene is an endogenous retrovirus?

That’s a good question. However on this list you need to tell us what research you have done already to try to find the answer. You should also tell us what possibilities you have come up with yourself after thinking about the problem. You can check out the form here in the Help on asking good questions.

The APMIS article link I provided in my answer to your earlier question (https://biology.stackexchange.com/questions/101276/what-book-teaches-you-about-endogenous-retroviruses) answers your question, either directly or in its references (e.g. refs 2 and 3). In particular "HERVs have been historically classified within several different groups, formerly designated as families, based mainly on sequence similarity and other structural features"

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Is there a specific English term for this vessel for microbial sampling?
In Russian, such a container (see pictures) for microbial sampling is called бакпечатка (bakpechatka), as I learned just now. I've no idea about the etimology of the Russian term. Probably "bak" stands for "bacterial" and "pechat" is for "print" (to press).
This deep container is used for taking bacterial samples by pressing a part it against the patient's skin or mucous membrane and then putting the material that stuck to it into an agar medium. Probably the "pressed part" used for sampling is the white cup, and agar is inside the container. At least that's what I gathered from scarce descriptions online.
Are there similar containers for bacterial sampling in the West and what is their name?
Thus far, I'm calling them "bakpechatka culture cups" in the document I'm translating, in the hope that the English-language reader will google and look at the pictures online.

Apparently it is called Count FlexiPlate, although this might be a brand name of a product produced by HiTouch (just as Aspirine can be only the acetylsalicylic acid  produced by Bayer), see here. Note also that it is a modified version of Petri dish, so the latter name may apply as well.


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Can Ni-NTA-Atto Conjugates bind to single His-tag
Can I label a protein with a single His-tag with Ni-NTA-Atto conjugates?
Papers generally use this technique to label 6His-tag.

Please don't substantially change your question after it has been answered. The changes you made completely invalidated my answer. If you have a new question, ask it.

According to the unreferenced introduction to Wikipedia's article on poly-histidine tags, the number of His residues can vary from two to ten, with six being the most common. Since histidine is a naturally-occurring amino acid in many (most?) proteins, adding just a single one at either end likely won't do much of anything. In my work with His-Tags (20-something years ago), I seem to remember that 3-4XHis was about the minimum that produced any kind of differential binding in the purification system we were using (Ni2+-agarose, elution with imidazole). However, for our purposes (scaling up protein purification), the quality of the end product wasn't great, and there was a lot of our target protein in the flow-through, so we ended up going with either five or six His residues, I forget which one.
As always, your mileage may vary, so I strongly suggest testing out a range for your application, if for some reason using the full 6X-His isn't an option.

Thank you for your answer.
I am doing single molecule and I want to count how many 6His Tags I have in my molecular construct.
Do you think I will have one or multiple binding of Ni-NTA-Atto conjugates by 6His Tag ?

If you have a standard, and are able to reproducibly load exactly the same amount of protein in each lane, you should be able to. I haven't used this particular system before, so it'll be interesting to see how it turns out.


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Is there a difference between human neuron cells compared to those of other animals?
Thanks for looking.
Firstly, I am nowhere near biologist, just a student, so my apologies if this isn't a "good" question.
Background:
So I was searching about intelligence, brains and computers, and noted 2 videos, one where a person tries growing human neurons to be connected to a computer, and a mouse brain connected to a supposed robot car.
It made me curious, if there's any major difference between neurons between species.
Question
Is there a difference between a human's brain cells compared to other species?
For the sake of the question, it will be limited to a mouse or a dolphin's, but if you can bring more info from another kingdom, it would be really welcomed.
I'll be really grateful if you coupled it with some illustrations!
Note:
This question is NOT about brain-size, but rather, a single unit of whatever that makes a brain, brain.

Not really.
There really is little difference in neurons in mammal and indeed not much change across vertebrates. You have to go back all the way to jellyfish before you find major differences in neurons.
https://pubmed.ncbi.nlm.nih.gov/30826503/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159607/

As you mentioned yourself, there are differences in brain size, form and structure. This difference also affects the size and shape of cells, i.e. you won't find meter-long neurons in mice, but rather in bigger animals. However, the types of cells are overall the same among the mentioned species. It was found that the ratio of glia cells to neurons greatly varies between species and follows a function of overall body mass, i.e. blue whales have an increase glia cell ratio.
https://www.pnas.org/content/103/37/13606

The basic structure of a neuron is conserved across animal species. This is what is taught at universities and can be found in most textbooks. This does not mean that there are no differences, it just means that we do not have any clear/good evidence of any major differences.
There have been some recent studies suggesting that there may be subtle differences between a typical human neuron and that of another mammal e.g. longer dendrites, differences in the electrical properties of the neuron, differences in cell-signalling within the neuron, more compartmentalisation within the dendrites etc. Here is an example of one such study:
https://www.cell.com/cell/fulltext/S0092-8674(18)31106-1


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Is the Orca a Whale?
I've read that "all dolphins are whales". I've also read that "the killer whale (orca) is a type of dolphin" and that "orcas are not whales, they're dolphins."
But if the orca is a dolphin and all dolphins are whales, aren't orcas whales?

Where are you quoting from? Please provide your sources. Also, we ask that all posters provide evidence of trying to answer their own question. Please update with additional info to avoid having your post closed. Thanks!

When common names are misleading, it can help to look at the taxonomy. Cetaceans include both MYSTICETES (baleen whales) and ODONTOCETES (toothed whales). Odontocetes include the family Delphinidae (dolphins), which includes the orca species (Orcinus orca).
I think your confusion might stem from the common use of the word "whale" to sometimes refer to mysticetes in particular (baleen whales) and sometimes refer to cetaceans as a whole (including both mysticetes and odontocetes). And to be extra confusing, the common name of Orcinus orca is "killer whale", but it is a "whale" (in the sense of a cetacean) in the dolphin family.
Does that help?
Here is another article from the International Fund for Animal Welfare that dives into this question quite nicely.

All dolphins are whales but all whales are not dolphins.
Orca, the killer whale is the largest member of oceanic dolphin family.
https://en.m.wikipedia.org/wiki/Killer_whale


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What are proliferating, but "normal" (non-cancer, non stem) cells of the human (mouse)?
What are proliferating, but "normal" (not cancer, not stem, not differentiating) cells of the human (mouse) ?
Typically after differentiation process finished the cells stop proliferation.
But as far as I understand some cell types still proliferate.
But I cannot find much information about what types exactly and what is known about that.
I have heard about fibroblasts, but details are welcome.
Some pair (but slightly different question) is here:
https://www.biostars.org/p/9476880/

Gut epithelial cells have the highest proliferation rate in the human body (and probably mice too). They are essentially proliferating constantly, with complete turnover of the gut epithelium every 3-5 days.
One caveat, regarding the biostars question, is that these cells are also maturing (i.e.  differentiating) into at least 5 different cell types that I can think of off the top of my head. However, I think the proliferation should only be occurring among the epithelial stem cells at the base of crypts, which differentiate as they mature and migrate towards the villi, so it might be possible to use single-cell sorting techniques to separate them for experimental purposes.
Another cool thing about the gut is that the entire structure of the epithelium (crypts, villi, cell differentiation, etc.) can be grown in vitro with various different primary cell culture systems.
References:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7211432/
https://www.frontiersin.org/articles/10.3389/fbioe.2019.00144/full

Interesting, so the epithelial cells produce senescenting cells on a weekly basis. All those cells are evacuated?


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Will a Kozak sequence within a coding sequence interfere with eukaryotic expression?
I want to make a DNA vaccine for fish by using plasmid pcDNA3.1(+) with a bacterial antigen. Unfortunately, there is a Kozak sequence in the middle of my target gene.
I am concerned that this Kozak sequence will interfere with translation inside fish cells.
Can I still use this gene of interest to make a DNA vaccine?
Is there any way to deal with this unwanted Kozak sequence?

You could always try codon editing to interrupt the Kozak sequence, yet still have the same protein sequence.

Thank you so much @MattDMo, such a good idea to try :))

Welcome to Biology.SE. Please take the [tour] and carefully read through the [help] to learn more about the site — in particular focus on how to [ask] questions effectively on this site. Please also ensure your future posts are formatted correctly — writing clearly is an essential part of scientific communication. ——— I have edited your post extensively — I hope that this has preserved the essence of your question. Please check and [edit] to correct any errors I may have introduced.


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Is circular DNA the same as plasmids?
Chloroplasts have circular DNA, but would it be right to say that they have plasmids? Are plasmids and circular DNA even the same thing?
Thank you in advance.

A plasmid is a length of circular or linear double stranded DNA that exists independent of chromosomal DNA with a cell (i.e. extra-chromosomal DNA) and often confers a selective advantage to an organism such as antibiotic resistance.  Plasmids have been identified in archaea, prokaryotes, and eukaryotes and allow horizontal gene transfer within a population, in processes such as conjugation, which proliferates the selective advantage contained within, if any exists.
Bacteria contain genomic DNA in chromosomes while a plasmid in the same bacteria contains non-genomic DNA such as genes that provide AR, virulence, pathogenicity, etc.. Bacteria may survive without plasmids depending on environment but without the chromosomal DNA survival is not possible.
Circular plasmids are often utilized in genetic engineering to transfect a target species with a desired gene for various reasons such as to enhance the performance of the organism, to understand the function of the gene, etc..
Not all plasmids are circular but all plasmids contain extra-chromosomal DNA.  Chloroplast DNA is contained within a chromosome and is not a plasmid.  Symbiotic theory of eukaryotic origin asserts that chloroplasts were once independent bacteria and this will perhaps allow you to develop an intuition as to why chloroplasts DNA is chromosomal rather than a plasmid.  The chloroplast could not survive without the DNA contained within the chloroplast chromosome so it is not categorized as a plasmid.

Your answer would be much better if you started with an actual definition of the term “plasmid”, based either on its original introduction or textbook or journal usage. Only then is listing of attributes really meaningful. (And the singular is bacterium.)

Hi thanks David, this is my first answer to give so I appreciate the feedback.  I can see you're reputation points and found your suggestion to be insightful to help me be more clear.  I've given a revision to my answer and would welcome further  suggestions.

I'd like to hear about "membranes" in that context: chloroplasts if in  membranes should thus make a difference.


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Why is neutralizing important when carrying out the Benedict test?
When testing for non-reducing sugars, acid is added, then the solution is boiled, then it is neutralized, benedict solution is added and then it is boiled again. Why is neutralizing the solution important?

Benedict's reagent is used mainly to test the presence of reducing sugars.
However, it can also be used to test non-reducing sugars indirectly. For that to happen, non-reducing sugars are first converted to reducing sugars by breaking glycosidic bonds in the presence of acid (ex: HCl).
Now, the next step is to check for the presence of reducing sugars using Benedict's reagent. Before adding our reagent, neutralization is done because the benedict's reagent requires an alkaline environment to work properly.
After neutralization only, the benedict's test proceeds further.
Note -> Since, Benedict's reagent is an alkaline solution, so the test solution is only neutralized and not made alkaline in nature.
For more info -- https://www.enotes.com/homework-help/what-steps-testing-non-reducing-sugar-704998


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Help identifying snake? (Southern California)
I just got home after a brief, surprise thunderstorm ... to find a pretty good size snake lounging in the breezeway at the garage side door.  (Presumably, it was seeking shelter from the rain?)

Could anyone please identify this type of snake?
Is it poisonous?
And in any case, is it likely to bite if it felt disturbed or provoked?

Thank you very much in advance!
Diameter: ~~4cm (~~1.5")
Length: ~~1m (~2-3'+) [though hard to say, since it's only been seen curled up]
Location: Southern California, mountainous desert region (~3K' altitude)

EDIT (~11pm PT):  It's still there. :O

Welcome to Biology.SE. Please upload your pictures rather than just providing links (posts should be self contained and not require anyone to follow links). In addition, please  give an estimate of the size of the snake. For more information on how to use this site please take the [tour] and then see the [help] starting with [ask] questions effectively on this site. Thanks!

Hi, @tyersome --
I appreciate the welcome, and the tips.  (I'd tried to upload the photos, but wasn't familiar with the resulting syntax.)
I've updated the question accordingly, and hope this helps.
Any insights appreciated.  Thank you!

Almost certainly the Western Rattlesnake (Crotalus viridis, which is probably the most common rattlesnake in California. It has the characteristic fat body and stripes of a Rattlesnake.
Western rattlesnakes are very common in much of the western part of the USA from southern Canada south into Mexico and across the Great Plains.
See second link for photos with similar colouration to yours.
Like all rattlesnakes, it is venomous and will bite and envenomate when threatened. Get a professional to deal with it.

Thank you VERY much.  The snake eventually left on its own, though we've since been in contact with Animal Control, in case it returns.
They say rattlesnakes are considered "emergency" service calls -- so your identification was VERY important info in that regard.


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Is there an published method for removing the effect of isolation by distance from genetic distances?
Isolation by distance is the phenomena that (even partial) reproductive isolation due to geographical distance between reproductive populations will result in greater genetic distance between those populations. This phenomena is not the only thing that can affect genetic distances, including other forms of reproductive isolation.
Given that the example plot of genetic distance on wikipedia appears to be a linear-ish relationship, perhaps the effect that geographical distance has on genetic distances could be subtracted via a linear regression model. I'm not sure how common linear relationships are for this type of data, but you can find examples of non-linear relationships such as found in "Genetic and phenotypic divergence in an island bird:
isolation by distance, by colonization or by adaptation?". Other studies, such as "Direct and indirect measures of dispersal in the fairy shrimp Branchipodopsis wolfi indicate a small scale isolation-by-distance pattern", show pretty marginal linearity.
Is there a conventional procedure in the literature for removing the isolation by distance effect on the genetic distances?

I think that a first question might be why you would want to do such a thing. I am sure that you can come up with a statistical approach that "removes" isolation by distance effects, but isolation by (geographic) distance would be pretty convoluted with genetic distance in the first place, is my intuition.

You can kind of do this with Mantel tests and related methods. As always there are issues.
If we look at this publication, we for example find a similar motivation:

Another possibility for using the Mantel test is to compare the relationship between two matrices, but taking into account the effect of a third one (usually the geographical distances), as originally proposed by Smouse et al. (1986). When analyzing spatially distributed data, the main issue is to find out if the two matrices are “causally” related (i.e., in the sense that they indicate an ecological or evolutionary process), or if the observed relationship appears only because both variables are spatially structured by intrinsic effects (i.e., distance-structured dispersal causing more similarity between neighboring populations).

In this case, you would be correcting in some way for the effects of isolation-by-distance, probably using some measure of geographic distance as the third matrix in question. However, Mantel tests can't really be interpreted in terms of variance partitioning, which is what you seem to want.
There are more spatial regression methods available that may be able to do this, though they seem to be less popular (probably because Mantel is simple and relatively assumption-free). They treat the isolation by distance effect as a spatial autocorrelation, which makes a certain degree of sense. If you are interested in a variance-partitioning type analysis, these are probably a better bet than Mantel.
But there are issues because it is not clear how to interpret isolation by distance in the absence of the genetic distances; simple distance is probably not good enough, and there are multiple plausible formulations of the distancing mechanism that are not restricted to naive measures of distance. All this is to say, you can do this, but beware of the assumptions that you're making going in.


text:
Understanding the paper "Why war is a man's game"
I have read this article
https://royalsocietypublishing.org/doi/10.1098/rspb.2018.0975
but I don't understand the mathematics which tries to explain why war is male-exclusive. In which branch of mathematics the mathematical theory outlined here can be seen? Is it Game theory? Which mechanisms this mathematical model predicts?
Is this really a new theory?

One has to follow the references, since the method is not explained: judging by the figures it is non-linear equations analysis, such as appears in common population, competition or epidemiologic models. These are obviously motivated by some game-theoretical analysis and basic population biology/genetics considerations.

I am sorry but questions here have to be comprehensible in themselves. Unless you can include the mathematics that you do not understand then it doesn’t fit the SE model.

Judging from the plots it seems like non-linear dynamics. Steven Strogatz's book on the subject is a good introduction.

you are probably better off changing the title to reflect the need for help with the math. you need very specific help. you should also edit your question to include the math itself, this will help as not everyone will be able to access the full article.

@John the article is open access, so everyone (with an internet connection) should be able to access it. Understanding the math is another issue entirely...

evolutionary game theory is probably the closest rubric.


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What's this bug that is pretending to be an ant?
I found a bug with a yellow banding in the South of France. At first I thought it was an ant, and then it appeared to be a related to a cricket.
What type of bug is it?

If you look at the wings, they look partially formed and hard -- this is indicative of this being a nymph of some type of hemipteran. (The developing wings are sometimes called "wing pads").
One group that comes to mind is the family Miridae since some species have ant-mimic nymphs.
One possibility (well, one jumping off point) is Miris striatus *

 Credit: Tristan Bantock (2008) ; Source: BritishBugs
GBIF confirms this insect is in France.
*I'm not convinced this is your species given the darker limbs and more prominent and abundant yellow in your specimen. Genus seems likely though. Miridae is a very large family of true bugs, so there are lots of potential options I'm not even familiar with...

Update: I just returned to this. I'm actually more certain this is the OP's species. I think the more prominent abdominal yellow is simply a camera angle causing the two most anterior striations to "blend" to appear as a larger spot. The prominent yellowing in this image [archive link] appears much more like the OP's specimen.


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Do all stem cells have a full number of chromosomes?
Do all or only some stem cells have a full number of chromosomes?

Are you attempting to distinguish between totipotent and pluripotent stem cells here?

Not really, but is that one of the differences between totipotent and pluripotent stem cells? (one has a full number of chromosomes and the other has half the full number of chromosomes)

I guess I'm just confused by your question. What causes you to think stem cells wouldn't have a full set of chromosomes, since by definition they're the cells that can differentiate into many different types of cells, which means they generally need all that genetic information.  People have created artificial haploid stem cells, but I don't know if that's what you're trying to get at. And how would you count something like a muscle cell, that has many nuclei?

Yes, you're right. I also thought that it would make sense for them to have a full set of chromosomes, but I just read it somewhere (that stem cells don't have a full set of chromosomes) and so I thought maybe only some had half the full set and some didn't so I decided to ask to make sure. Well, thanks for the help. I guess they were (somehow) referring to the artificial haploid stem cells. It seems like I don't know enough about this topic so I'll just read about it more.


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What's the difference between mRNA and inactive virus vaccine?
If the techniques used in both vaccines are similar and if both use the spike protein approach, then how is the mRNA vaccine more effective than the other ones and more importantly how come it is also effective towards the new variations of the virus such as the Delta variant whereas the others are not? The same protein should be built with the same mRNA, right? I am a little confused here.

The techniques used in mRNA vaccines and inactivated virus vaccines are not similar. Here's some info on inactivated virus vaccines at ScienceDirect: https://www.sciencedirect.com/topics/medicine-and-dentistry/inactivated-virus-vaccine and here is info on the Covid mRNA vaccines at the CDC: https://www.cdc.gov/coronavirus/2019-ncov/vaccines/different-vaccines/mrna.html

Re: "more importantly how come ..." is a different question and your premise is not quite correct. Here's a paper from a decade ago about SARS that discusses why the spike protein makes a good vaccine target in these viruses: Du, L., He, Y., Zhou, Y. et al. The spike protein of SARS-CoV — a target for vaccine and therapeutic development. Nat Rev Microbiol 7, 226–236 (2009). https://doi.org/10.1038/nrmicro2090

I will definitely look more into those. Thank you!

In molecular biology, a ribonucleic acid vaccine or messenger RNA vaccine is a type of vaccine that uses a copy of a natural molecule called messenger RNA to produce an immune response. The vaccine transfects molecules of synthetic RNA into immunity cells.
An inactivated vaccine is a vaccine consisting of virus particles, bacteria, or other pathogens that have been grown in culture and then lose disease-producing capacity. In contrast, live vaccines use pathogens that are still alive. Pathogens for inactivated vaccines are grown under controlled conditions and are killed as a means to reduce infectivity and thus prevent infection from the vaccine. The virus is killed using a method such as heat or formaldehyde.
mRNA vaccines are a new type of vaccine to protect against infectious diseases. COVID-19 mRNA vaccines are given in the upper arm muscle.  the cell displays the protein piece on its surface. Our immune systems recognize that the protein doesn’t belong there and begin building an immune response and making antibodies, like what happens in natural infection against COVID-19.
They do not affect or interact with our DNA in any way.
mRNA never enters the nucleus of the cell, which is where our DNA (genetic material) is kept.
For more info - mRNA and Inactivated (Killed Vaccine)

The mRNA vaccine doesn't transfect (much) into the immune cells directly, most is apparently into the muscle and vascular and lymphatic cells at the site of injection, then some transported around the body, ending up in the liver largely. Your later description is closer. You also have the links for mRNA and inactivated swapped.

Your description of inactivated vaccines is partially confused with a description of live attenuated vaccines. Both of the vaccine type descriptions are missing key elements such as how they generate an immune response, and advantages and disadvantages of each.


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What's the most recent common ancestor of reptiles and humans?
In the Phylogeny of humans and reptiles, what is/are some of the most recent common ancestors?

related: https://biology.stackexchange.com/questions/82206/why-arent-mammals-and-reptiles-considered-amphibians?r=SearchResults&s=14|11.8981, https://biology.stackexchange.com/questions/47957/why-are-turtles-classified-as-reptiles-and-not-amphibians/47968?r=SearchResults&s=15|11.3526#47968

I think that you are looking for the amniote common ancestor.
Amniotes are the group of organisms that have an amnion, a specific membrane around the egg, among other features. This includes reptiles, mammals, etc. but excludes amphibians and fish as indicated in your tree.
Wikipedia says:

The first amniotes, referred to as "basal amniotes", resembled small lizards and evolved from the amphibian reptiliomorphs about 312 million years ago,[7] in the Carboniferous geologic period. Amniotes spread around Earth's land and became the dominant land vertebrates.[7] They soon diverged into synapsids and sauropsids, which persist today. The oldest known fossil synapsid is Protoclepsydrops from about 312 million years ago,[7] while the oldest known sauropsid is probably Paleothyris, in the order Captorhinida, from the Middle Pennsylvanian epoch (c. 306–312 million years ago).

That citation 7 points to this paper, which used paleontological data to assign time estimates to various diversification events inferred from molecular phylogenies; this allowed them to approximately estimate the time of emergence of amniotes from the amphibian clade.

Could you please add in the [7] citation?

@MattDMo thanks, done.


text:
Why is ammonia converted to urea rather than secreted in the urine?
Since ammonia is highly soluble in water, my senses keep telling me something like, "Just a little bit of water is enough to flush it, given that a lot of it would dissolve per liter of solvent". But who knew, it's exactly the opposite.
I keep seeing articles saying that since ammonia is very soluble in water and it takes lots of water to eliminate this waste in vertebrates. Uric acid, on the other hand, is very easy to eliminate, since it is not easily dissolved in water.
Why does the water solubility of ammonia would make it much harder to eliminate in birds, reptiles or the human body, compared to urea/uric acid?
Humans also eliminate ammonia, but, apparentely, its high solubility in water, and toxicity, would make it so that is actually more favourable to just convert it to urea inside the liver. On the other hand, its quite easy for bony fish to eliminate ammonia as a nitrogenous waste, since there's plenty of water around to help them flush it.
Once again, i don't get it, if ammonia is highly soluble in water, why does it take an ocean for some vertebrates to eliminate?
Some links: https://en.wikipedia.org/wiki/Metabolic_waste
https://courses.lumenlearning.com/boundless-biology/chapter/nitrogenous-wastes/

Welcome to SE Biology. I would advise you to prepare and edit future questions beforehand to produce a more compact and structured question. This will help you examine your logic and assumptions, and will produce something that is more readable and hence likely elicit an answer. In this case you provide no basis for the assumption in your title that ammonia is more difficult (please avoid non-scientific terms like “tougher”) to eliminate than urea. Where did you read that? Why don’t fish have problems? If you didn’t read it anywhere isn’t it just possible that the problem lies elsewhere?

I am trying to help you. Some people charge for this sort of educational advice. I am giving it to you for free. Your link says nothing about ammonia being difficult to eliminate — the erroneous assumption of your question. It does contain the statement "Nitrogenous wastes in the body tend to form toxic ammonia, which must be excreted." If you had read that, then the only question I can imagine you could have is one about why transferring ammonia to the bladder would not be enough to prevent its toxic effects on the body. But that is not what you asked.

I have edited my answer. It would appear that one has to consider the actual mechanism of secretion of ammonia as well as whether there would be any problem with an otherwise toxic concentration of ammonia in the bladder. The problem would seem to be talking about "flushing" and "filtering" without thinking about the mechanism, and not considering the role of ammonia in acid/base balance. It would be good if you removed the red herrings of uric acid and volume of water from your question and title as it might encourage a physiologist to interest himself in your question.

What exactly are you suggesting? Because the question i have in my mind is exactly the one that is written.

I am suggesting that you accept 1. that the toxicity of ammonia means that land animals have to convert it to a non-toxic compound for excretion, 2. That animals that can afford to carry and loose water convert it to urea which is soluble in water, whereas birds which cannot convert it to the insoluble compound uric acid, which is excreted with their faeces. The valid questions then become 1. Would secreting ammonia to the urine in the bladder solve the problem of toxicity? If so 2 Why does this not happen? A title might be "Why is ammonia converted to urea rather than secreted in the urine?"

Further to my reply. I feel that I have answered 2 in relation to the competition with the blood buffering role of ammonia produced in the tubule, although a clearer title of the sort I suggest might elicit a more detailed answer. I assume you do want to understand the system, rather than pretend it doesn't make sense and argue about what people may or may not have written (but not explained).

I'm starting to doubt my ability to comunicate in this language because both 1 and 2 were never really in question for me. I knew that more evolved vertebrates, as they started to populate more dry habitats, had to come up with a solution for the toxicity of ammonia, and that would be the urea and uric acid cycles. What i don't know is if the solubility of ammonia worked as an evolutionary pressure to this shift - in response to dry habitat colonization - or was it simply a matter of toxicity.

@DiegoMenezesPamplona Toxicity. What the sources you are reading (and David's answer) are trying to convey is that a lot of water is needed for ammonia excretion despite the high solubility, not because of it.

In other words, does the fact that ammonia is highly soluble make it more costly for the internal organs to flush it, or was it simply a matter of higher toxicity, when concentrated in the plasma, pushing evolution for a less toxic waste for the same concentration budget?

@BryanKrause But it’s more than that apparently. As far as I can see it’s “would be needed if there were a way of removing blood ammonia by secretion” although I suspect most general authors are not aware of the problem that tubule’s own ammonia generation system poses. The poster has changed his title but not his question which is still obsessed with the irrelevant concern with solubility. Surely there are some molecular physiologists on the list. I remember being involved in teaching acid-base balance to medical students — I was on firm ground with bicarbonate buffering, but not the kidney.

@BryanKrause So you're saying that high solubility doesn't have anything to do with the fact the ammonia needs a lot of water to dilute and flush?  So, for the same degree of water availability, ammonia would be more concentrated in the plasma than urea, for example?

@DiegoMenezesPamplona Yes I am saying the high solubility has nothing to do with needing a lot of water to flush it. No, this does not mean ammonia would be more concentrated in the plasma. It means if you didn't have enough water to dilute the ammonia enough to remain below toxic levels, you would die of ammonia poisoning.

@David Not sure I'm exactly following your point about secretion, but I think if a textbook is mentioning it they probably intend a contrast with uric acid as a nitrogenous wastes strategy rather than saying anything particular about ammonia.

OK. I don't have a queston anymore. I think it's best if @David posts a new one. If you prefer you can write it on the comments and i can edit mine.

What I propose to do is to do a little reading and then edit both question and answer. I live in a part of the world where the sun rarely shines, so that when it does one has to go out and take advantage of it, because it won't last. This week the sun is shining, so it may be next week before I do this. However the point is not to do things in a hurry but do them properly. That way we may increase our understanding of the topic.

The comment of the poster to my request for clarification cites “The formation of ammonia itself requires… large quantities of water to dilute it out of a biological system” I conclude that he assumes that the problem with animals eliminating ammonia as such is one of solubility in water. This is not the case. The solubility of ammonia is such that saturated solutions exceed a concentration of 10 mol/L.
The problem is that ammonia is extremely toxic at low concentrations, so that decreasing its concentration to non-toxic levels would require a large volume of water. The writer of the cited text is, in my reading of it, presenting this as a hypothetical solution, and then rejecting it because the demands of supplying this volume of water would be prohibitive to the organism.
This is not my field, so the best information I have about the toxicity of ammonia comes from an anonymous web page on the University College London web site. It states:

Ammonia is highly toxic. Normally blood ammonium concentration is < 50 µmol /L, and an increase to only 100 µmol /L can lead to disturbance of consciousness. A blood ammonium concentration of 200 µmol /L is associated with coma and convulsions.

The page goes on to state (in red):

200 µmol /L is far too low a concentration of ammonium to affect plasma pH or the normal transport of sodium and potassium ions across nerve cell membranes.

I know almost no physiology, but my inference of the significance of this is that it would be difficult for the kidney to respond to this concentration of ammonia by filtering it out. Hence it needs to be converted to a non-toxic (or much less toxic) compound — urea, in the case of vertebrates.
Further reading suggests that the problem is that there is indeed a renal system involving the proximal tubule for secreting ammonia into the urine by a mechanism coupled to the cation transport and responsive to pH. In fact this system exists to control blood pH by generating ammonia to neutralize blood acid. This would explain the second part of the quotation above — the organism’s mechanism to control blood acid is inconsistent with a secretion mechanism for blood ammonia.
It would be good if a molecular physiologist could comment on or edit this section.

But why do you think it has nothing to do with soulubilty? I have a Portuguese school textbook that, as this website,  states crystal clear that as solubility in water increases, so does the need for water in the process of elimination. It would be great if i could find a peer reviwed article abou this and not just a school textbook. I think your explanation is good enough, but why are you so sure?

You can see this idea literally everywhere, but it's never thoroughly explained. Check this out http://www.bio.miami.edu/dana/dox/nitrogenouswaste.html. Here the relation between solubility and elimination is stated separately from the toxicity, which makes me think that something is missing.

My answer hardly gives the impression that I am “so sure” when I apologise for using an anonymous web page as a source of information and ask for help (answers can be edited) on physiological aspects of the question. As I have a chemical background I knew that ammonia was soluble in water, which is why I felt that solubility was not the problem. As for the Miami U page, that does not impress me. Lists of advantages (like debating arguments) generally contain weak or dubious members to make up the numbers. I imagine a single factor prompted the evolution of ammonia modification. I may be wrong.

You said, quote, "I conclude that he assumes that the problem with animals eliminating ammonia as such is one of solubility in water. This is not the case.". I felt here you were sure about this. The miami page was just to illustrate that this is a common idea which shows up now and then when reading about nitrogenous wastes.

Please don’t take offence. Your written English doesn’t suggest that you are a non-native speaker, but I just wonder whether you are confusing “dilution” with “dissolution” / “dissolving”. Ammonia is so soluble in water that you can dissolve 0.88 g per ml.  None of the texts mention solubility. The Miami U page talks about “more water to dilute”. You can only dilute a solution where the solute is already dissolved. This will decrease its concentration. Why would you do that?

The miami page mentions solubility on the uric acid section. I'm not native and definitely not fluent, so feel free to correct anything.

@DiegoMenezesPamplona It does, but it doesn't mention solubility in the others because it's not a limiting factor for those.

For reference, I am linking this answer of yours: https://biology.stackexchange.com/questions/82379/why-is-urea-not-converted-to-ammonia-in-the-body/82400#82400


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How are random mutations in cells of an organism controlled?
Even in the most stable conditions cells undergo mutations. So in humans(an example) with millions of cells, mutations must be a common affair. But how is that we are still basically the same throughout the life, and no random mutations cause sudden disorders in us. Even if mutations are rare, they cannot be nil and how are they controlled.

A rule of thumb is one mutation per cell division. Most cellular organisms have various error proof and repair mechanisms, to reduce the number of mutations. When these accumulate, they do cause sudden disruptions, such as cancer.

I think you haven't researched on the topic. Try googling "Mutation Repair" or "DNA Repair". You'll find various articles related to the same.

There are many reasons why humans rarely experience the deleterious effects of mutations. Many mutations arise from errors in normal biological processes such as DNA replication or recombination. DNA repair mechanisms and apoptosis (programmed cell death) are some ways of 'dealing with' mutated or damaged DNA. Another reason that we rarely see deleterious effects of mutations is because of the way amino acids are encoded.
There are approx. 20 amino acids encoded by the genome, yet each amino acid can be encoded by approx. 4 different codons. For example threonine is encoded by ACU, ACC, ACA, ACG. This means a point mutation is unlikely to make any difference to the final protein product as there is a high chance that the mutation will still code for the same amino acid. This is what is called a silent mutation, and there are other types mutations that do not have deleterious effects.
https://www.nature.com/scitable/topicpage/genetic-mutation-441/

There are no amino acids in the genome — it is DNA.

Sorry about that, clearly what I mean is there are 20 amino acids encoded by the genome.  I will edit that.


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The average of Ct values in real-time PCR
The Ct value is the number of cycles when the "PCR amplification curve with the horizontal axis as the number of cycles" and the "predetermined threshold" intersect, and is not necessarily an integer value.
Real-time PCR was performed on n series of samples under the same conditions, and the Ct values, ${Ct_1},{Ct_2},\cdots {Ct_n}$, were obtained for each. Then, in many instructions, the average of these Ct values is determined as follows;
$$\bar{Ct}:=\frac{{Ct_1}+{Ct_2}+\cdots +{Ct_n}}{n}\tag{1}$$

My question:
What is the meaning of such an average? How do I justify taking such an average?

The amplification curves are ideally considered to consist of the following when the initial template quantities are ${N}_{1}(0), {N}_{2}(0), \cdots N_{n}(0)$, respectively;
$${N}_{i}(k)={N}_{i}(0){a}^{k}\tag{2}$$
It is my understanding that the Ct value is for calculating ${N}_{i}(0)$ backwards.
Let the threshold value be X, then, for all $i=1,2,\cdots n$,
$$X={N}_{i}(0){a}^{{Ct}_{i}} \tag{3}$$
therefore, for all $i=1,2,\cdots n$,
$$X{a}^{-{Ct}_{i}}={N}_{i}(0) \tag{4}$$
therefore,
$$\bar{{N}(0)}
:=\frac{{N}_{1}(0)+ {N}_{2}(0)+ \cdots + N_{n}(0)}{n}
=X\frac{{a}^{-{Ct}_{1}}+ \cdots + {a}^{-{Ct}_{n}}}{n} \tag{5}$$
therefore, a better Ct average , $Ct_{avg}$ shall satisfy
$$X=\bar{{N}(0)}{a}^{Ct_{avg}} \tag{6}$$
therfore ,
$$X{a}^{-{Ct}_{avg}}=X\frac{{a}^{-{Ct}_{1}}+ \cdots + {a}^{-{Ct}_{n}}}{n} \tag{7}$$
$${a}^{-{Ct}_{avg}}=\frac{{a}^{-{Ct}_{1}}+ \cdots + {a}^{-{Ct}_{n}}}{n} \tag{8}$$
Based on the above discussion, wouldn't it be more natural to use the following?
$$Ct_{avg}=-{log}_{a}(\frac{{a}^{-{Ct}_{1}}+ \cdots + {a}^{-{Ct}_{n}}}{n}) \tag{9}$$

I believe 'a' may vary depending on template, primers and reaction conditions.

I only just noticed that biology.SE supports LaTeX. Finally.

I’m voting to close this question because this isn't a biology question. It might be appropriate for a statistics site, but there is nothing about a biological process or mechanism.

I'm only used to seeing technical replicates averaged in the way you describe at the beginning (arithmetic mean), and I think it makes sense in that case (I could be wrong), because you're measuring technical variation in the measurements, not variation in the amount of starting material in your sample. If you're talking about averaging Ct values across multiple samples from a statistical population, then you are correct that an arithmetic mean is rarely the appropriate measure of center. But I'm not convinced this approach is either.


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What is the methodogy used to determine the exact genetic flow from one area to another and the times in which it flowed?
For example, I take the instance of Central Asian migration into India.
Say geneticists studied a) ancient bones in CA b) ancient bones in India c) living people in Central Asia d) living people in India.
Case 1: -
Say they found a particular haplogroup (A) which is present only in Central Asians, and another one B, which is present in Indians (both living people, aka options c and d). Then they also found another haplogroup C, which is present in both individuals.
Question 1: - How do they then determine that it was the Central Asians who migrated and not Indians? Is it due to coupling this evidence with other sorts of evidence like general climate/vegetation? Or is it due to the fact that progressively, unique genes found in Central Asians decline in quantity when moving north to south, and the unique Indian genes aren't found outside India at all (Indus Valley genes)? And if I am not wrong, Indus Valley civilization people were descended from Africans who migrated via Yemen/Oman and the historical Elamites were their cousins, so even the so-called unique Indian gene can be found outside India...how do they then describe the direction of the gene flow?
Case 2:- Say the ancient bones of Central Asia (dated to 3000 BC) showed some genes which were common between ancient bones found in India (dated to 1500 BC).
Question 2: - Does this lead to the conclusion that the migration was from CA to India, latest by 1600-1500 BC? Is there any other technique to find the timing of the gene flow?
Question 3: - Modern ancestry tests have several obscure ancient groups like Neolithic Iranian farmers, Oriental Hunter-Gatherers, BMAC etc. Are all of these from bones taken in specific areas like Zagros Mountains (for iranic hg), Central Asia and Bactria (Afghanistan)? And these bones were dated to the specific time periods when these proposed civilizations were also historically dated?
Overall, I want to understand the nuance of the genetic tests which offhandedly say, that xyz group migrated to pqr location at abc era without giving the details.

I would love to answer this question since it's what I study - but I will encourage you to try and trim it down to a single question, since we expect posts to only contain one question.

In any case, this article should give you an idea of the complexity of the subject: "Ancient genomes reveal complex patterns of population movement, interaction, and replacement in sub-Saharan Africa" Science Advances  12 Jun 2020: Vol. 6, no. 24,  eaaz0183 DOI: 10.1126/sciadv.aaz0183

thanks guys! both user438383 and Armand


text:
bird that might be a young one that didn't fledge happily
Can anyone identify this bird - located in Massachusetts

Welcome to Biology.SE. For identification questions please include an estimate of the size, what part of Massachusetts, and include any behavioral, habitat (e.g. types of plants), or other details that you noticed. In addition, if possible clearer pictures from multiple angles would be very helpful. Please [edit] your post to include as much of that information as possible. Also, what do you mean by "didn't fledge happily"? ——— Please also take the [tour] and go through the [help] starting with [ask] questions effectively on this site. Thanks.

It is difficult to be sure without clearer pictures, but my best guess would be a female (and/or immature) Brown-headed cowbird.
This is based on the heavy conical beak, my guess at the size, the overall grey-brown coloration, dark eye, dark beak, dark legs, and the faint suggestion of a line behind the eye. In addition, this is a common species in many parts of Massachusetts.
If you have seen these cowbirds (the males are quite distinctive) in your area that would support this idea.

Public domain image from USGS.

Cowbirds do not raise their own young, they lay their eggs in other birds nests . The cowbird young are generally larger then and push out the original young. It could be the adoptive parents have abandoned this one as it seems big enough to be on its own .

Yes, does that have something to do with my answer?

Looks like a young Cowbird to me, for the same reasons that tyersome gave.  Young Cowbirds, like young Starlings, are pretty bland and unmarked.  The short neck and big round head also point in that direction.

Another similarity that could be added to your reasoning is the culmen/dorsal ridge of the upper mandible (The upper prong of the mandible is embedded into the forehead) that looks quite similar when enlarging the OP's picture.


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Why did the dinosaurs not have gigantic brains and become really smart?
All my life, I've heard that all these gigantic dinosaurs that used to live on Earth had peanut-sized brains. I just accepted this as a fact, and I guess it may be a fact.
But now I wonder: why?! If their bodies were so incredibly huge and everything was so big back then, why did the brains not also follow that rule? How is it possible that such big animals (or elephants/whales today) apparently have such small brains?
Why doesn't the size of the body roughly dictate the dimensions of the brain inside? Or do they mean this in a more metaphorical way, such that "small brain" really means "low-capacity brain" rather than it actually being physically small? I would assume that if a brain is big, it automatically features more "raw power" rather than being full of empty, unused space.

And this was downvoted why exactly?

Why not check on the sizes of brains vs. bodies for various big animals today and for various dinosaurs?

Welcome to the site. Your question seems to be unresearched from your side. I recommend you to read this (https://biology.stackexchange.com/help/how-to-ask) before putting your question on the site.

whales and elephants have very large brains.

It is quite possible that the dinosaurs were very intelligent - we have no way to know it. It is also possible that a few millions years from now, some creature will wonder, how humans, being so intelligent, managed to run down themselves to extinction.

@Z. B.: I would imagine that it was downvoted because there's really no answer to "why" questions about evolution, and even more so about "why didn't" questions.  The most you can say is that there was no evolutionary pressure to develop great intelligence.  When it comes to intelligence, size isn't everything.  Elephants & whales DO have large brains: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4053853/  And some of those dinosaur descendants, the birds, can be quite intelligent despite having small brains.


text:
How much of male parental matter is still there in an infant organism after birth?
Are the atoms from the father's sperm still there in his baby's cells? Do they get lost during pregnancy? If they are still there, are they in a particular cell? Are they dispersed among many cells? Is it a regular mechanism or a matter of chance?

What do you mean by the term - "The atoms from father's sperm"? Is it chemical atoms or something else?

In most animals, humans included, the normal pattern of fertilization ends up with precisely one sperm contributing precisely two things to the egg: a haploid nucleus and a centriole. That's it. No more physical matter from the father ever enters the baby.
A typical human nucleus is about a 6 micron sphere of material, and a centriole is much smaller, so we're talking about mass in the picogram range. A healthy newborn child is a little over 3 kilograms, so the fraction of paternal atoms in a newborn child is definitely less than $10^{-12}$.
The actual location of those atoms would be fairly arbitrarily dispersed with each cell division, with the biggest chunks being the chromosomes and centriole, which could end up in at most 24 different cells. Don't forget, however, that not all cells in the fetus make it to the baby (some die, some are shed or otherwise disposed of), so some of that paternal matter might well be further lost. Other paternal atoms will be in materials less carefully managed by the cell (e.g., non-chromosomal materials of the haploid nucleus), and so will disperse more evenly and also be diluted by the regular processes of recycling and dilution.
Bottom line: there will likely be a few atoms from the father in the child, but only a vanishingly small fraction.  That doesn't really matter, though, because the information contributed from the father is still in every cell.

The father contributes information just once, doesn't he?

Yes, via that one sperm. The mother also contribute genetic information just once, via the egg (which has a little more genetic information than the sperm, due to the addition of mitochondria). The mother also has, of course, a major impact on development by providing the gestational environment, but the information content of that is difficult to define.

Doesn't the mother contribute genetic information as many times as there cells in the embryo and then in the foetus?

@yewgeniy No: just the once, via the egg, just like the father does just the once via the sperm. After that, the genetic information of both gets replicated. The atoms come from the mother (or, more properly, mostly from her food, delivered to the growing fetus by her body), but they no more deliver genetic information than your dinner gives to you.

"... the genetic information... gets replicated..." by whom?

Cells replicate themselves.


text:
Which molecular changes make certain SARS‑CoV‑2 strains more contagious?
Articles  often state that certain SAR-COV-2 strains are more transmissible, e.g:

Most studies indicate Delta is 50-60% more transmissible than the
Alpha variant

How dangerous are covid-19 Delta and Delta Plus variants?
I believe that these studies are all based in statistics of people infected — that higher transmissibility has something to do with changes in the virus attachment and entry into human cells — but without much further detail. Is it known which changes lead to a virus strain becoming more contagious, and whether one can predict that when certain molecular changes appear in a virus strain it will be more contagious, or is our knowledge based solely on observation?
Is it known which molecular changes make certain SARS‑CoV‑2 strains more contagious?

Aside from changes in virus attachment and entry, other changes affecting transmissibility would include those affecting number of viruses given off by the infected and in what form (e.g. aerosolized), survival of the virus outside an infected individual, mutations affecting course of disease once virus enters a cell, and so forth. Some of those mutations can be studied in the lab in animal models or in tissue culture. Mutations affecting structure such as in the S protein can be modeled and can be tested to see if convalescent serum or monoclonal antibodies will still bind to them.

There are many approaches as described above -- it's worth looking into them if you're interested.

Pablo, two things. 1. Infectologist is not an English word. 2. Questions of the sort “Do experts know?” are unnecessarily contorted. This site is for questions about biology, not biologists. Your title would be better if you deleted the first three words. Likewise in your last sentence.

@RoniSaiba The  important thing is not whether virologists know, but whether it is known on the basis of peer-reviewed published science that is supported by other findings. The paper could be published by a Nobel Laureate or an Undergraduate student. Emphasis on status has no place in science. I therefore feel obliged to edit the post in the way I hoped the poster would. He will not learn if you do it for him, especially if you do it wrong.

@David sure. Feel free to edit as you see fit. "Infectologist" was too much of an eyesore so I suggested an edit.

We can only see this in retrospective. So here are some mutations that have enhanced the transmissability of the virus:

ORF1b:P314L in combination with S:D614G (Pango lineage B.1 and all subsequent lineages)
S:N501Y Most prominent mutation of Alpha, Beta, and Gamma. It often licences S:E484K which on its own does not seem to boost transmission.
S:P681R The key mutation in the Delta variant, enhancing the Furin cleavage site

In order to be efficient the mutations need to be embedded in a fitting virus, the same mutation may enhance transmission for a certain variant, but being inefficient in another variant with different co-mutations.

To improve this answer, you could 1) provide links to references for your points. 2) discuss why retrospective analysis is not the only method we can use to see these sorts of things, and 3) what sort of changes are seen in similar viruses that also lead to enhanced transmission (cough polybasic cleavage site cough).


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

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

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


text:
Is MPseq more cost effective than FISH when looking for chromosomal abberations?
There are some papers out there that propose to use MPseq in addition to or instead of FISH when looking for chromosomal aberations in the context of cancer
e.g. this one on infiltrating lobular breast cancer refractory to standard therapy or this one even claims that MPseq outperforms FISH...
I do understand that pricing may vary widely given the individual contracts a hospital may have with a certain vendor. But can anyone answer this roughly.
I've never done FISH myself so  I don't know how time intensive it would be. Considering prep and interpreation of the results. I could imagine that it keeps a lab tech busy for some time.
For MPseq, I imagine that several samples can be run a the same time and I would imagine that the output is less prone to operator bias.
I know it is not a simple yes no question and more of a discussion but your thoughts on this would be much appreciated.

There are many high-throughput products that perform roughly this function of finding karyotypic variants. Bionano sells an optical mapping product that claims to do this, I have not directly inspected their viability; their tech is slightly complex.
Hi-C-seq is rather simpler and there are several competing firms that offer products that perform karyotyping:

Arima,
Dovetail Genomics,
Phase Genomics (of which I am a former employee and equity holder).

I am sure that there are other methods including mate pairs and even plain whole-genome shotgun sequencing that could do ok at this task.
The Hi-C companies sell relatively inexpensive kits for library preparation, and some will also sell analysis services at fairly high throughput.
All of those methods should outperform mate-pair sequencing (which I think you call MP-seq) significantly, due to the relatively high rate of chimera formation (on the order of 0.1-1%) and generally the lower signal of mate-pairs, which are restricted by the insert sizes chosen. All of them should find the large karyotypic events found by FISH, ideally with more precision and sensitivity.
Traditional karyotyping services (such as FISH) run ~\$11000 per diagnosis, whereas the high-throughput methods I note (not the ones in that paper) probably are closer to ~\$500-1000/sample for preparation + ~\$500-1000 for sequencing plus maybe ~\$2000 / sample for analysis costs with a vendor (at a guess, for many samples). The companies in question may also do your sample preparation at a significant increase in cost (an extra $2000, perhaps). This would be a total of ~\$4000 / sample, as a high estimate.
Mate-pair costs would be cheaper at the sample level but more expensive at sequencing and analysis, not sure about the exact numbers. I don't think there are providers offering the package as a service, as it may not be economically viable, but I could be wrong about that.
I don't have refs for these prices, the providers themselves are the source of truth for that. Any of the companies above would happily prepare a quote for you.
If my very rough math above is correct, any of the sequencing methods should be cheaper, except possibly for Bionano (which is still probably more precise).
I'll note again my conflict of interest with Phase, though I don't work there anymore and I don't speak for them.


text:
Does Tryptic Soy Agar (TSA) contain L-cysteine? (Question about Legionella)
I ask because Legionella sp. requires the presence of cysteine. If TSA does contain L-cysteine, is it sufficient to grow Legionella?

Legionella also requires other nutrients. Our general recipe includes ACES, Bacto Agar, Charcoal, Yeast extract, L-cysteine, ferric pyrophosphate, potassium hydroxide to make BCYE agar which is used to grow legionella.


text:
Which others human species/subspecies are known to have coexisted in the past with anatomically modern humans?
According to this article,
interbreeding between archaic and modern humans

There is evidence for interbreeding between archaic and modern humans
during the Middle Paleolithic and early Upper Paleolithic. The
interbreeding happened in several independent events that included
Neanderthals and Denisovans, as well as several unidentified hominins.

According to this other article discoveries change picture of human history-evolution,

Now, new research reveals that a third human ancestor was hunting and
gathering in the same landscape. Two studies published Thursday in the
journal Science describe a previously unknown hominin called the
Nesher Ramla homo

And this other article enigmatic human relative outlived neanderthals also mentions,

The provocative find joins a number of recent discoveries that
continue to point to a stunning diversity of hominins in ancient Asia,
including the announcement just yesterday of a new species, Homo
luzonensis, in the Philippines.

So far 4 species Neanderthals, Denisovans,  Nesher Ramla homo and Homo luzonensis are mentioned.
Which others human species/subspecies are known to have coexisted in the past with anatomically modern humans?

This is a difficult question to answer exactly - I think it might be useful to split it up based on the degree of evidence.
Since you asked about Anatomically Modern Human (AMH), it's worth considering their distribution and timing. The oldest and most basal individual which is still considered AMH is Jebel Irhoud, Morocco, which is dated to ~315kya. In Europe, we have the Apidima samples from Greece which date to ~200kya and in Asia we have Misliya1 which is the oldest West Asian sample from slightly earlier 180kya.
Of course, these are the only specimens that have been positively identified as AMH. Therefore, it seems highly likely that there would have been earlier migrations out of Africa that didn't leave fossil remains.
Certain

Neanderthals and Denisovans. There is very solid genetic evidence that humans have lived alongside two archaic species; Neanderthals and Denisovans. There are fairly large, unambiguously archaic chunks of Neanderthal and Denisovan DNA in many present-day non-Africans.

It's likely that there was a single mixture event with between modern humans and Neanderthals.
On the other hand, there was likely several admixture events between Denisovans and modern humans, particularly modern humans in Southeast Asia.
Possible

Nesher Ramla Homo, dated to 140–120kya from a cave in Israel. There is evidence that AMH lived in Western Asia as early as 200kya, so it is possible they may have lived aside one another. However, it's also possible that the AMH lineage present in Misliya may have gone extinct before the Nesher Ramla was present.
Homo naledi lived in South Africa 335–236kya. This appears to be well within the likely dates of AMH occupation of Africa, given the Florisbad skull is AMH and dates to 259kya. It's been proposed that the signals of superarchaic admixture in present-day Africans could be Homo naledi.
Homo heidelbergensis, dates to roughly between 200-600kya and is found at least across parts of Southern Africa and Southern Europe. Given AMH almost certainly existed in Africa at this point, it seems plausible that they may have lived alongside heidelbergensis.

Possible but unlikely.

Homo floresiensis lived on the island of Flores, Indonesia, approximately from 50/60kya - 100kya. Data suggests that modern humans did not inhabit this part of the world further ago than 50kya.
Homo luzonensis lived in Luzon, Philippines and has also been dates to 50kya. Note that humans have existed in this region for almost 1 million years, but these would not be considered anatomically modern humans, who would only have arisen within approximately the last 350ky.
Middle Pleistocene East Asians hominins. There is growing evidence of a clade of modern, but with archaic features, hominins who lived in East Asia (particularly China) ~150kya. It's proposed that these may have been the result of a mixture between an early out of Africa migration and some archaic lineage such as Denisovan. It's highly unlikely there was a major AMH lineage present in East Asia at this point, but they may have interacted with early dispersals out of Africa.

It's also worth considering that we only have snapshots for these samples. It's possible, for example, that the Nesher Ramla Homo lived between 500-100kya, but that we only have samples from 200kya. The same goes for the dates of AMH presence in certain locations; even though we only have samples for AMH in e.g. North Africa at 315kya, it seems plausible the true date is somewhat older.
This probably isn't an exhaustive so happy for others to edit in things where necessary.


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How does exercise cause weight loss if the corresponding chemical reactions have the same mass on the LHS and the RHS?
How does weight loss take place in the body during physical activity, given that the corresponding chemical reactions would have the same mass on the left hand side and the right hand side?

What chemical reactions would these be? We cannot answer question if you don’t specify the problem.

Please give example of chemical reactions you're referring to, It will help us answer your question.

Better yet, look yourself at the reactions and think about what might happen to the products...

I don't know what chemical reactions take place. I just remember studying years ago that the metabolic activity in the body is basically chemical reactions. And chemical reactions don't involve a change of mass between LHS and RHS is another thing I remember studying. So how does weight loss take place then (apart from sweat and bodily waste being expelled from the body)?

This is a layman question -- I have no knowledge of biology or chemistry beyond high school level which was years ago

Excretion. You've really answered your question in your own comment, except that you don't seem to have realized that there is no "apart from sweat and bodily waste being expelled from the body".
Simplistically, say the body has some stored fat, which has the general formula CH3(CH2)nCOOH.  When you exercise, the fat is burned for energy, converting it to CO2 and H20.  The CO2 is exhaled, the H20 leaves either as perspiration or urine. https://en.wikipedia.org/wiki/Lipid_metabolism#Lipid_catabolism

Thanks, this is exactly the answer I was looking for.


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Remarkable attempts of studying biological systems axiomatically
I am reading Anti-Tech Revolution by Theodore Kaczynski, in the second chapter the author talks about how technology will cause problems in society and before he begins the discussion, he introduces proposition. Here is the first:

Proposition 1. In any environment that is sufficiently rich, self propagating systems will arise, and natural selection will lead to the
evolution of self-propagating systems having increasingly complex, subtle,
and sophisticated means of surviving and propagating themselves.

This I felt was an additional assumption one would make after accepting the Darwinian proposition of natural selection... so I wondered.. does there exist any fleshed out sub field of biology which have axiom systems from which experimental predictions can be worked out from?
Definition of an axiomatic system:

An axiomatic system is any set of axioms from which some or all axioms can be used in conjunction to logically derive theorems.

The proposition is wrong. In the context of explaining the origin of life, it has been shown that in some environments self-replicating molecules can arise... but we are not certain that such conditions ever existed on Earth.

Hmm how does that make it wrong though..? It doesn't state the conditions, just leaves it to be defined somewhere elese 'sufficiently rich'

Well, if we want to be mathematically rigorous, it is not "wrong", but "meaningless" without definition of what is sufficiently rich. However, I think what is implied is that such conditions are common and rather general to system composition and its other properties, while in practice there may be only one combination of chemicals and external parameters that produces self-replicators.

@RogerVadim the point is that assuming the environment is such that allows self-propagating systems to arise, then these systems which will arise will be subject to natural selection and will change over time to make themselves better at propagating. Now, yes, this assumes the sufficient complexity and also seems to ignore the need for lossy replication to drive evolutionary change, but essentially it says that if there are self-propagating systems, then they will evolve. That's correct (if you assume lossy replication).

@terdon I interpreted the proposition more generally, as it seems to appear in the context not even related to biology. But I haven't actually read this book, so I won't argue.

I feel like it's worth noting that Ted Kaczynski is better known as "The Unibomber". He carried out a bombing campaign across the US resulting in the murder of three people. He's currently imprisoned and serving 8 life sentences.
This doesn't necessarily disqualify his neo-luddite ideas, but they ought to be approached with a heavy dose of skepticism. The point of his book is not to forward ideas about mathematical biology, but to predict tech-caused apocalypse (with his solution being the incitement of societal collapse and rebirth).

I agree with the general sentiment but it's the unabomber, not the unibomber. @Brickman

I think a stronger argument against taking Kaczynski's work prima facie is that it was (as far as we know) not peer reviewed prior to publication. That means it should be read in conjunction with scientific reviews of it that are out there. In that vein you may want to look at Kevin Kelly's "What Technology Wants" https://www.econtalk.org/kelly-on-technology-and-what-technology-wants/

In a way, all biological research is based on certain axioms, just as all scientific study is bound certain foundational principles. The proposition you shared sounds like something straight out of General Systems Theory (GST), an inherently interdisciplinary field based on the premise that complex systems share common organizing principles, and that these principles can be discovered and modeled mathematically. GST also attempts to follow certain axioms. Such as:

Every system is bounded by space and time, influenced by its
environment, defined by its structure, and expressed through its
functioning. A system may be more than the sum of its parts if it
expresses synergy or emergent behavior... (more GST here)

And many of these these principles (or axioms, if you prefer) are universal across biology. For example, the concept of the relationship between structure and function is fundamental in some way to every biological discipline I can think of.
Systems biology is another concept related to GST that can be applied a few different ways. The most common is probably by those who simply favor a top-down research approach of complex biological systems, motivated by the knowledge that there are certain biological phenomena that cannot be fully understood or predicted through reductionist study of a system's component parts alone. Of course, top-down and bottom-up approaches are complementary, and can seldom replace one another.
There are also those who take a more GST-based approach to biology. For example, I once worked with a mathematician who took some well characterized mathematical models describing road traffic patterns and applied them to molecular genetics, ultimately generating an improved model of how RNA polymerases travel along a DNA strand during transcription. But one could also draw parallels or generalities (as your proposition does) from looking at different types of evolving systems, like biological populations, communities, nations, religions, corporations, economies, and so on.

It's hard for me to know the degree to which the Kaczynski quote is wrapped up in what you are interested in, so I will answer your question very narrowly without considering that quote:

does there exist any fleshed out sub field of biology which have axiom systems from which experimental predictions can be worked out from?

Yes, fields exist in which such axiomatic systems exist (as I understand them). Probably the best example is mathematical population genetics, which was mostly worked out before we had molecular methods, but which has been enormously useful in the interpretation and formulation of hypotheses regarding such data as it has accumulated. For a somewhat less mathematically involved introduction, see also here.
It uses Mendelian inheritance (or even simpler systems) as a set of basic assumptions, and tries to figure out what should happen in evolution across generations based on that.
I make no claims about other fields of biology, though probably there can be good arguments that such fields exist.

I am not completely sure, but I think mathematical biology, bioinformatics and/or computational biology are what you are looking for. However, the assumptions in these fields are not always fundamental "truths" like with mathematical axioms or Einsteins postulates. The issue with axiomatizing biology is that the systems that are studied, unlike algebras or fundamental forces, are complex, composite and non-homogeneous. That makes reductionistic approaches generally quite unproductive.
However, that does not mean all hope is lost. Usually, in the cases of, for instance, cancer modelling and swarming behaviour, the assumptions are simplifications that allows us to create mathematical models that can make predictions regarding those systems.
The field I think most closely resembles what you may be looking for is evolutionary game theory. This is an application of game theory where players have been replaced by populations and strategies have been replaced by genetic traits. This approach has contributed to the understanding of sexual selection, co-evolution and more.

On the question "does there exist any fleshed out sub field of biology which have axiom systems from which experimental predictions can be worked out from?", we do have axioms for FOL elementary theory groups (Shoenfield, pg. 22) in which predictions (FOL proofs?) in a certain sub-areas of biology (e.g. genetic code) can be had, as alluded to in "In this section we review some work describing the genetic code in groupoid and group theory terms".


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Little owl as decoy for skylark
I read that hunters used (now is forbidden) little owls tethered to attract skylarks.
They say this is due to their magnetic look of the eyes.
I didn't find any scientific documentation of this. Any one knows a scientific explanation of this, if any? Why, if true, should the skylark be attracted by the owl?

Found the reference. Skylarks react to the presence of the owl to mob it.
Van Nieuwenhuyse, Dries; Genot, Jean-Claude; Johnson, David H. (2008). The Little Owl: Conservation, Ecology and Behavior of Athene noctua. Cambridge University Press. p. 6. ISBN 978-0-521-71420-4.


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Are autoantibodies against intracellular proteins "functional"?
Autoantibodies against intracellular proteins have been detected in some autoimmune diseases (For example, TRIM21 in Sjögren's syndrome and NALP5 in Autoimmune Polyendocrine Syndrome Type 1).
My question is are these autoantibodies functional (e.g. play certain roles in the diseases) or are they just the byproducts of pathological processes?
Regarding the first case scenario, it is highly unlikely that these autoantibodies can penetrate the cell membrane to interact with the intracellular autoantigens.
The second case scenario sounds more probable to me. For example, some processes may cause cell death and lysis, thus release intracellular proteins. Local inflammation can co-occur and may trigger the formation of autoantibodies.

This review sketches out some of the scenarios from the point of view of cancer therapy.  Some of them are unlikely, though I wouldn't say impossible, to happen naturally, but others are likely to be relevant.

@MikeSerfas Thank you. The third possibility "Antibodies can also be generated that bind cell surface major histocompatibility complex class I (MHC-I)-presented peptides that are derived from intracellular proteins." is brilliant. I should have thought of it.

Thus your question "are these autoantibodies functional" is to be answered to the positive: yes, cells presenting these antigens are led to apoptosis by T cytotocic cells? Just to make sure.


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Why and how do Stomatal Guard cells turn flaccid at night time and cloudy days, and turgid during the days?
If I'm correct, the guard cells turn turgid during the day and flaccid at nights. What is the reason behind the same and how is it done? (im a noob highschool student, so basic explanations are welcome)

What is the result of each type of guard cell status (turgid or flaccid) on the stomatal opening? What are the functions of the stomatal opening?

(Umm, I forgot to add the 'how' part to my question...) Coming to that; i guess
flaccid = close; - doesn't allow transpiration
turgid = open; - does allow transpiration

There is a good free recent review by Brodribb et al., 2020 which explains much of this biology.
The most fundamental mechanism, dating back to the evolution of stomata before they were even used to regulate photosynthesis, seems to be potassium regulation.  As a rule, water follows dissolved material (osmosis): if you enclose a bag of water and salt underwater in a membrane permeable to water but not salt, the particles of salt will push out on the bag with the same amount of pressure as if they were particles of gas floating in the bag and there were no water present inside or out.  Cells usually hoard potassium ions - they will also passively allow some negative ion, such as chloride or malate, to flow in to counteract the charge on the potassium.  Without those negative ions, a positive charge would quickly build up inside that would stop the potassium from moving in.  Thermal energy inside the cell gives every particle a random energy of motion (which leads to pressure at a boundary) that is equal on average, whether it is potassium, chloride, glucose, or a protein.  So when you double the amount of potassium in a cell, also doubling the corresponding negative ions, that is most of the particles in the cell - so the amount of water will also nearly double and the cell will get double the size.  In guard cells the amount of potassium can more than double to open stomata.
There is another mechanism to get to the same end: increasing the amount of glucose in the cell.  Normally, cells store energy as starch, which has a tremendous number of glucose molecules physically linked together.  These don't count as much more than a single particle for purposes of osmotic pressure, so starch isn't going to make the cell turgid.  But if you "mobilize energy reserves from starch" - split it up into glucose - those glucose molecules will all be moving around separately, each bashing against the membrane (and supporting cell wall) with its own random thermal energy.  Once again the guard cell will expand.
But everything I've described is relative.  A pile of dry salt or sugar won't exert any pressure at all, and a guard cell in a desiccated plant will not be able to expand.  Passively, a drying plant's guard cells will tend to close from lack of pressure.  However, the review explains that it would be dangerous for the plant to leave that to chance - it can't let air bubbles get into its water distribution network - which is one reason for all the active regulation described above.
Active regulation means "thinking" in some sense at the cellular level, so it is much more complicated than the physics of opening and closing.  People can tell a beautiful story that is pretty much wrong by trying to present the process without it.  You can see some of this complex regulation covered in the related question here about crassulacean acid metabolism plants, which open stomata only at night to conserve water.  Our review covers it under "Molecular evidence..." and it is quite complex; I would probably damage it in the retelling.  Key steps are abscisic acid production, H+-ATPase, and KAT/AKT-type Shaker channels.  But this is pretty much the on/off switch for a plant, so there could be quite a bit untold there, or unknown altogether.

thank you for the detailed explanation :)


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What are the prospects in synthetic biology, especially in the introduction of biological computers?
One of the interesting areas of synthetic biology is the so-called biological computers. A biological computer refers to an engineered biological system that can perform computer-like operations. I have read a large number of articles on this topic, and in almost all of them the logic gates are made of DNA or RNA inside bacteria. What are the prospects? For example, are there developments that imply the construction of logic elements and microcircuits directly inside the cell: DNA encodes the necessary proteins that are synthesized and assembled into logic gates and other components in the cell?

I wonder why people put a minus without any explanation?

1 downvote is from me - people aren't obliged to explain why they downvoted. I downvoted because, whilst certainly interesting, your post doesn't ask a question with an objective, fact-based answer. 'What are the prospects' is quite open-ended and will encourage opinion-based answers. If you have a specific quesiton about synthetic biology, I'd encourage you to focus on that. Thanks.

@user438383 a specific question: are there developments that imply the construction of logic elements and microcircuits directly inside the cell: DNA encodes the necessary proteins that are synthesized and assembled into logic gates and other components in the cell?

@ArmanArmenpress If you can formulate more specific and less opinion-based questions, I would encourage you to ask them as separate questions, rather than asking them in comments.

What are the prospects? For example, are there developments that imply the construction of logic elements and microcircuits directly inside the cell: DNA encodes the necessary proteins that are synthesized and assembled into logic gates and other components in the cell?

Yes, there is an entire literature on this called "genetic circuit design", which Brophy and Voigt 2014 introduce nicely. Xiang et al. 2018 provides a discussion of developing biological computers. Karkaria et al. 2020 provides an excellent overview of what this field has accomplished, what the current challenges are (such as metabolic load and non-orthogonality of parts), and how they might be tackled by having community (distributed) circuits.
For a school assignment I performed a rudimentary citation analysis of the genetic design literature (Seilis 2020). While it isn't publication-quality work, and certainly isn't peer-reviewed, you might find some interesting papers are cited there.
In terms of logic gates, you'll find that both unary gates and all sixteen possible binary gates, and many others, have molecular implementations. And in terms of prospects, they could be used for monitoring and control, production of medicine and goods, and literally run molecular experiments, among others. I recall Xie et al. 2013 constructed a circuit that when put in non-cancerous cells did nothing, but when put into HeLa cells would trigger apoptosis.

Might be worth mentioning that computation is possible without every logic gate type. In fact, the minimal set of logic gates requires only a single type-- either NAND or NOR. These are called "universal logic gates", since they can be combined with themselves to produce any other logic gate. In practice this is often very convenient in that it allows for device construction with only one process, rather than many different processes (one per gate type).

The functional completeness of certain sets of boolean functions is worth mentioning because it motivates the intuitive idea that we could program a system to do whatever we want within the physical limitations of the system.

One of the physical limitations that prevents us from just using compositions of NAND or NOR everywhere is the non-orthogonality of parts. Unlike in a silica circuit where identical parts would have isolated behaviour, solution chemistry leads to things dispersing  across the cell. To have two independently-acting NAND/NOR gates one would have to implement them using different interactions to prevent undesired behaviour. This is one of the challenges discussed in Karkaria et al 2020 among others.


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Using PCR to add the overhangs to gBlocks for NEB HiFi
Does adding the overhangs to gBlocks for NEB Hifi using PCR pose a big problem? The IDT website suggests that one should design the gBlocks with the overhangs. However, if I did not do this, will it be a problem?
Edit: I intent to use Q5 High-Fidelity Polymerase and the gBlocks range from 500-2200 bp in size. It's not necessary for the exact sequence to be present.

Welcome to Biology.SE. Please [edit] your question to provide more details such as: the error rate of the polymerase you intend to use, the size of the gBlock, and how critical it is to you that the exact sequence be present for your application. You may also benefit from taking the [tour] and consulting the [help] starting with [ask]. This will familiarize you with how this site works and what the expectations are for questions. Thanks.

You could add the overhangs with PCR, then gel purify or PCR purify. I don't think it will pose a big problem as I've done it before and all of the colonies I screened were correct.

Welcome to Biology.SE. We're looking for long answers that provide some explanation and context. Don't just give a one-line answer; explain why your answer is right, ideally with citations. In particular, you are ignoring a potentially significant problem with this approach — the error rate of the DNA polymerase being used. I've posted a comment to the OP asking them to give us more detail, but please also edit your answer to be more complete. Please see the [tour] and [help] starting with [answer] questions effectively for details about site expectations. Thanks!

Error rate here of Q5 polymerase is 5.3 x 10^-7 [1].  One would have to be remarkably unlucky for error to propagate into your final clone.  [1]  Paulo Cseri Ricardo, Elaine Françoso & Maria Cristina Arias (2020) Fidelity of DNA polymerases in the detection of intraindividual variation of mitochondrial DNA, Mitochondrial DNA Part B, 5:1, 108-112, DOI: 10.1080/23802359.2019.1697188


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Can anyone identify this Australian tree?

This tree is found in the Wrights Hill area on the New South Wales/Australian Capital Territory border.
Bark at breast height is curled and dense, becoming less dense at height.

Eucalyptus, but which one?

Welcome to Biology.SE. For tree identification we need close-up pictures of leaves and flowers — this is especially true for a large group like the eucalypts! Thank you for taking the [tour], you may also find it helpful to go through the [help] starting with [ask] questions effectively on this site. Thanks.

The changes in the bark makes it look like Eucalyptus melliodora (Yellow box).

Locations recorded are in this link. http://plantnet.rbgsyd.nsw.gov.au/cgi-bin/NSWfl.pl?page=nswfl&lvl=sp&name=Eucalyptus~melliodora
Some photos of this tree can be seen at:
http://www.nccma.vic.gov.au/sites/default/files/publications/nccma-41853_-_box-gum_grassy_woodland_identification_10-11_web_0.pdf


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What is the effect of an acidic solution on hydrolytic enzymes?
I'm working on a school research project and my research question is "What is the effect of increasing concentrations of Acid X on hydrolytic enzymes, measured through the loss of mass of leaf litter after 30 minutes?"
Note that the acid to be used will be chosen later and the time of the reaction can be altered. I plan to use at least one of these hydrolytic enzymes: endoglucanase, cellobiohydrolase, and β-Glucosidase.
I have spent days on end searching for information on hydrolytic enzymes and acids (their relationship). I have been unable to find anything. Do hydrolytic enzymes follow the normal trend of denaturation under a change in pH?

There is a good amount of information about this online, I was able to find information in one google search, for example https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4875970/

Welcome to Biology.SE. Not all enzymes behave the same way so, in addition to being under-researched, this is also too broad. Thank you for taking the tour, but please also consult the [help] staring with [ask] effectively on this site, what is on-topic, and what is not. You should also search for and read the "homework" policy for this site. Thanks.