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circular pattern of mold on quince
Could someone explain why mold on my quinces grows in well separated circles around a center? To make clear, what I mean I post the picture

Somewhat related to fairy rings?

Looks like you may have Monilinia fructigena, brown rot, or at something similar (possibly also called brown rot, but from a different species). This pattern isn't special to quince, but to this fungus.
The formation of these rings is called "zonation", and the concentric rings are from areas of growth that are primarily spore-forming versus not.
Hall (1933) gives an extensive description of the different factors necessary for observing this growth pattern, but ultimately the key factor is light. Patterns of light-and-dark conditions while the fungus spreads causes alternating phases of growth, with one phase comprised of more sporulation.
Another source: https://www.cabi.org/isc/datasheet/34747

Byrde, R. J. W., & Willetts, H. J. (2013). The brown rot fungi of fruit: their biology and control. Elsevier.
Hall, M. P. (1933). An analysis of the factors controlling the growth form of certain fungi, with especial reference to Sclerotinia (Monilia) fructigena. Annals of Botany, 47(187), 543-578.

Thank you for your answer, I have no access to the publications, which are not online. Is it possible that the factor light means just day and night?

@trula Yes, day and night.

thank you again


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"Bacteria don't have membrane-bound organelles." Are sulfur bacteria or Cyanobacteria exceptions?
Can bacteria have membrane-bound organelles?
I read this many textbooks:

Bacteria cells are simple cells that do not contain a nucleus or other membrane-bound organelles. However, they do contain other cellular structures that aid with their life processes.

Or here:

Prokaryotic cells (Figure below) are usually smaller and simpler than eukaryotic cells. They do not have a nucleus or other membrane-bound organelles. In prokaryotic cells, the DNA, or genetic material, forms a single large circle that coils up on itself

Are sulfur bacteria or Cyanobacteria exceptions?
Sulfur bacteria because they have big vacuoles. (Vacuoles do have membrane, don't they? Or maybe something is different about prokaryotic vacuoles that I don't know?)

A vacuole is a membrane-bound organelle which is present in plant and fungal cells and some protist, animal and bacterial cells. (1)

And
Cyanobacteria because they have gas vesicles. (These vesicles are membranous, aren't they?)

(1): Schulz-Vogt HN (2006). "Vacuoles". Inclusions in Prokaryotes. Microbiology Monographs. 1. pp. 295–298.

source: Stack Exchange

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

sort: votes


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Are there any fluorescent proteins capable of transforming 500-600 nm light to 400-500 or 600-700 nm?
In order to improve photosynthesis, which doesn't use 500-600 nm light, I wonder if that light can be transformed into useful light?
The idea is to transfect photosynthesis organisms with the gene for that protein to improve growth.

Fluorescence always absorbs photons of higher energy and emits photons of lower energy so transforming light to 400-500 nm won't be possible.

@Cell Only in most cases: https://en.wikipedia.org/wiki/Fluorescence#:~:text=In%20most%20cases,%20emitted%20light%20has%20a%20longer%20wavelength

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


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When and Why does G0 phase occur?
I've asked this question, specifically because i've seen this question.

As we see in this diagram , G0 phase occurs after M phase and at a specific point within G1 phase.

Is there a meaning to saying "end" in this case?
What is the checkpoint for causing a cell to enter G0 instead of continuing with the cell cycle, in case of heart cells and neurons? (what exactly is "checked"?).

Regarding when, I would answer at the end of Mitosis (check also this link:  https://biology.stackexchange.com/questions/70323/what-determines-the-reversibility-of-cell-of-g0-phase-in-cell-cycle?rq=1 ).
I wouldn't know what to answer to your second question, but maybe the link I posted above will help.


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Fatty acids into glucose
I have a question regarding the synthesis of glucose from fatty acids. In my book as well as in other posts on stackexchange, it states that fatty acids CANNOT be turned into glucose for the following reason:
Fatty acids are converted into acetyl-CoA, which cannot be reverted into pyruvate because humans do not have the enzyme, but some plants do. Therefore, fatty acids cannot be turned into glucose.
Glycerol however can be converted into glucose by gluconeogenesis.
However, fatty acids can be turned into acetone by ketogenesis and acetones CAN be converted into pyruvate and therefore also into glucose. So doesn't that mean that fatty acids can be turned into glucose?
Fatty acid -> acetyl-CoA -> acetone -> pyruvate -> glucose.
Ketogenesis happens during a carbohydrate deficiency (or diabetes mellitus). The brain is able to use ketones for energy, but preferably uses glucose, so I'd assume some ketones are converted to glucose as well?

This question has already been asked and answered on this site. Please search previous questions. If you have a hypothesis about a reaction sequence, write out the reactions in full. That way you will discover the fallacy of your argument yourself. Arrows between compounds don’t cut it.

As stated in the original comment, I have looked at other posts on Stackexchange and I have also presented the answers that I found. Yet I haven't seen anyone say anything about the conversion of fatty acids into glucose via acetone.
@user1136: It isn't really about net synthesis of glucose, the question is: are fatty acids able to be converted into glucose? If acetone can be converted into glucose and fatty acids into acetone, then isn't the conclusion that fatty acids can be converted into glucose via ketogenesis? I am not talking about fatty acids into to acetyl-CoA to glucose

Fatty acid chains are used to form acetyl-CoA molecules. Two acetyl-CoA molecules condense to form 1 molecule of acetoacetic acid. Part of acetoacetic molecules are converted into acetone & beta-hydroxybutyrate.
If fatty acids can be converted into glucose, then isn't the book and the posts wrong? They state that fatty acids can't be converted into glucose because acetyl-CoA into pyruvate isn't possible, but the conversion via acetone should be possible?

I don't know the exact chemistry behind it, but when I look up reactions of the conversion I find the following: acetone -> acetol -> methylgloxal -> pyruvate -> glucose, so maybe this explains how acetone is converted into pyruvate?

I don't believe that there is significant conversion of ketone bodies to glucose in starvation. There is no evidence that the methylglyoxal pathway is used in normal animals, and indeed methylglyoxal is highly toxic. Experiments in 1984 feeding rats with high concentrations of acetone (which is only produced from ketone bodies by non-enzymic reactions) fail to convince.


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Can elephants trumpet when they have water in their trunks?
I am writing a fun story about elephants and want to know if elephants can trumpet or at least, make noises when they have water in their trunks, like when they are drinking water. Thanks for your help!

I think no. Because the elephant uses its trunk to make noise and if the trunk is filled with water then there is no chance the voice would come out.


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What is the difference between a myofibril and a myoblast? (In skeletal muscle)
I read that a muscle fibre (myofiber) is formed when myoblasts fuse.
https://teaching.ncl.ac.uk/bms/wiki/index.php/Skeletal_muscle#:~:text=The%20multinucleate%20feature%20is%20established%20in%20myogenesis%20where,cells%20%28each%20muscle%20cell%20is%20one%20muscle%20fibre%29.
On google I saw that a muscle fibre is formed from many myofibrils.
https://biologydictionary.net/myofibril/#:~:text=Myofibrils%20are%20long%20filaments%20that%20run%20parallel%20to,are%20made%20up%20of%20repeating%20subunits%20called%20sarcomeres.
Does that mean that myoblasts and myofibrils are the same thing?

Myoblasts are the embryonic precursors of myocytes (also called muscle cells). Myoblasts differentiate into muscle cells through a process called myogenesis.
A myofibril (also known as a muscle fibril) is a basic rod-like unit of a muscle cell. Muscles are composed of tubular cells called myocytes, known as muscle fibres in striated muscle, and these cells in turn contain many chains of myofibrils.
So, to answer your question, No. These two are different and one is the precursor of the other.


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Why does dryness irritate mucosal surfaces, and what exactly is this "irritation"?
The mucosal surfaces of the body function to moisten the epithelial linings and keep them from becoming dry. Why is this important? As an example, the respiratory tract moistens and warms the air that we inhale before it gets to the lungs, to protect it from damage and "irritation". How would cold, dry air cause those things?

How do you think it would cause those things?

I genuinely have no idea, I sat down a few times and looked it up as much as I could, nothing really describes how dryness and coldness irritates a cellular lining.


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Colorful Large Wasp (?) on Milkweed Arizona USA
Observed this very colorful insect on Asclepias subulata (Desert Milkweed) in Phoenix Arizona. About 8 am, temperature about 90F, sunny, late-September.  When flying it seemed to have a narrow waist like a wasp.  About 5 cm long, appears rusty-red in flight (not surprisingly given its size).  As the pictures show, it was enjoying a bit of nectar from the flowers. Would love to know its name so I can greet it properly next time!

Possibly a tarantula hawk (because of its red wings and metallic blue body), and because they inhabit the Southwest US. It being on the flower in the picture makes sense as “...adult tarantula hawks are nectavores and feed on flowers”. They have very painful stings, but as with most insects, if nobody bothers them, they won’t bother you.
The females hunt down and paralyze tarantulas and lay their eggs in them, hence the name. Freaky, isn’t it?

Reference

Very good.  I also found this info https://www.desertmuseum.org/kids/oz/long-fact-sheets/Pepsis%20Wasp.php


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Can a bacterium infect another bacterium?
I researched about it by searching on Google and reading some bacteriological articles, but I did not get any answer. I also asked some of my teachers, and they were also a bit confused. Some said that it is possible and others said not. So the question remains:
Can a bacterium infect another bacterium? If so, how?

Not exactly what you asked but the YouTube channel Journey to the Microcosmos may be interesting along those lines, a recent video "Our Paramecia Are Infected" discusses some of this and has very pretty microscope video
https://www.youtube.com/watch?v=foKz81ElCjM

Bdellovibrio bacteriovorus (BV) “infects” other bacteria:

Similar to a virus, BV attacks bacteria such as Escherichia coli (E. coli) by attaching to and entering its prey, growing and replicating within the cell, and then suddenly bursting out, releasing its progeny into the surrounding environment. — How bacteria hunt other bacteria

Note that a lot of the answer to this question hinges on what you mean by "infect". Bdellovibrios (as Laurel has already established that this does happen) do something that does look a lot like infecting eukaryotic cells- but it is still spoken of as "hunting". Why? I am not sure.
There are lots of different ways that bacteria can have negative interactions with each other- though they often resemble "hunting" or "warfare" more than "infection".
Getting a bit more into the "how" of the question, a common mechanism for inter-bacterial negative interaction is the Type VI secretion system. This apparatus is often spoken of as a "weapon" that bacteria can use to kill each other, by adhering to the other cell and shooting toxins in through its membrane. They can use this to great ecological effect.
The type VI secretion system is also used in some contexts for infecting non-bacterial hosts, so by that logic you could argue that it resembles infection.
Update: for a short discussion of inter-bacterial killing (including Bdellovibrio + secretion systems) in the context of biotechnological applications, see here.


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Probability of all alleles represented in a sample
I'm trying to wrap my head around some formulas presented in the 1992 paper from Chakraborty Sample Size Requirements for Addressing the Population Genetic Issues of Forensic Use of DNA Typing, but I have not been able to.
Specifically, the right hand side of formula (16) and it's relation with formula (13).
$1-\sum\limits_{i=1}^{k}(1-p_{i})^{2n}$ (13)
$[1-(1-p)^{2n}]^{r}\geqslant1-\alpha$ (16)
Formula 13 indicates the probability, for a locus with $k$ segregating alleles whose frequencies are contained in the vector $p$, that all alleles are represented in a given sample of size $n$, and the right hand side of formula 16 indicates the probability of $r$ alleles to be represented in a given sample of size $n$.
First of all, why, based on 13, the expression inside the summation indicates the probability of an allele of frequency p, to remain unobserved in a sample of size n?
I tried to understand this from the Hardy-Weinberg equation but did not have any success.
Second, Why to take the expression in (16) to the r'th power?
Which biological concepts am I missing?

I don't think there is any biology here, just concepts of probability

@BryanKrause Probability in this case is been used as a tool for a specific application, like in every other problem involving probability. The main issue here (for me) is to understand the underlying biological concepts to give sense to, for example, why is it that the power in (13) is 2n. Is not a problem related to solve for n in (16) or something of that nature, I'm more interested in understanding the concepts that dictate the reason(s) why the expressions adopt that form to estimate the probability of interest.

@BryanKrause, I absolutely agree that these are probability questions not pop gen questions per se. If I wanted to answer anyway, is it your opinion that (1) answering here would be harmless or (2) we should tell OP to go away, post it somewhere, leave a link here, and close it?

@BenBolker Grey area. I think if you want to answer the probability question here I'd appreciate if you narrate it with the biology, and I think that will overall be well received.

I'm going to strictly answer the questions, rather than step through the proof, because it involves a lot of formatting that I'm not familiar with.  Other folks are welcome to edit this!
Equation 13
This equation assumes a diploid genotype, given by the $2n$ power with $n$ individuals.  For anything with greater ploidy than mono-, it's mathematically simpler to determine the probability that an allele is not present.  As an example, see this calculation of a triploid Hardy-Weinburg equilibrium equation.  Using this simplification,
$P(single$ $allele$ $not$ $present)$ $= (1$ $- P(allele$ $present))$ ^ $(ploidy)$ ^ $(n)$
$= (1$ $- P(allele$ $present))$ ^ $(ploidy$ * $n)$
With $k$ segregating alleles, each allele has its own non-presence probability.  The probability of total non-presence is $1 - (sum$ $of$ $P(each$ $non$-$presence))$
Equation 16
In this equation, the author describes the probability that all alleles are present at a given frequency.  These allele presences are independent of each other and therefore multiplicative.  Since $P(allele$ $present)$ is vectorized, this product can be simplified to $^r$

Tip - to format equations, you should use the $ symbol rather than the grave accent.

Aha, thanks!  That's a lot better :)


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Cell culture media L-Glut dilution?
Cross-posted on r/labrats.
I haven't done cell or tissue culture in about 4 years.
Protocol:
Volume: 200ml media (academia so using sparingly, not the whole 500ml bottle!)
1% L-Glut (250uM)
My L-Glut comes in a 100ml bottle of 200mM.
What should I make up a stock dilution of 250uM in? Distilled H2O? PBS?
Should I then add 2ml (1%) to my media? Or should I add 250uM of L-Glut directly to the media?


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What motivates children to start walking?
Crawling is a way we first learn to translocate but  , in all our lives, there comes a point where naturally try standing up and try to walk.. but why? What really pushes us over the edge to start walking?
When we first start walking, usually we fail many times but still we have this natural motivation learn walking despite the failure. Is this some sort 'intuitive' intelligence which babies have? To be more specific I can't imagine a baby to consider the pros and cons of walking vs crawling and then logically argue to himself/herself that learning how to walk would be something worthwhile to spend his mental resources on.

Reference video

In my experience (I have 2 kids), they are motivated by being able to move faster and reach more things. In the case of the second, he was also motivated by the fact that his older brother could walk, and he wanted to keep up (or sometimes get away!). They follow the example of the other humans around them - Mommy and Daddy do that, so I want to also - and see the benefits of being able to do it. Kids are smart, and they're able to reason and make choices based on advantages and disadvantages.

To get away from their parents?  (Been there, done that, had it reciprocated in turn.)

Why do newborn fawns struggle to stand up yet keep trying?  Why do young kangaroos come out of their mother's pouch and try to stand and hop?  Could it be instinct?  I can't imagine them considering the pros and cons of trying these things.

I did consider it to be instinct but what is 'instinct'? Is it a result of some predetermined genetic fate? I mean.. if that is the case that's scary because in a way our life actions are predetermined by our genetics

Some acounts of feral children describe them walking on all four mimicking thair animal caretakers movement style. If walking upight was purely inborn instinct one would expect even feral chidren walking upright.

Babies raised by dogs still crawl when they are teenagers. Children copy adults.

You might be interested in Alison Gopnik's book "The Gardener and the Carpenter", where she gives thoughts on how children develop and learn. Children are very disinhibited in their behavior, and this is generally considered to be a consequence of their prefrontal cortex being immature, but she proposes that this is not a bug but a feature. That there is a tradeoff in any algorithm between "exploiting" the possibility space (incrementally improving your solution until it's as good as it can be) and "exploring" the possibility space (casting a wide net to find totally different solutions that might be even better). If you just "exploit" you are liable to stay stuck in local maxima; if you just "explore" you're never going to find a good solution because your search is too random and the possibility space is too large to examine every possibility. Good optimizing algorithms have alternations between the phases, with "explore" phases to look at many different areas of the possibility spaces, and "exploit" phases to optimize the most promising candidates. Gopnik's argument is that children are the "explore" phase of human development, and that is why they are disinhibited: they are motivated to try many different things for the sake of it, with no specific objective in mind or much thought to the consequences. (and in this view, an important job of parents is to make sure the consequences won't be fatal).
This might answer some of your question of babies thinking about "pros and cons". It might be more realistic to see them as thinking only in terms of "pros". Not, "if I do this this will be the consequences, if I do that those will be the consequences, what should I do given the consequences I want", but "what happens if I try this? And that? And that? And that? And that?"
Another factor that wasn't mentioned in the comments is imitation; children like to imitate others around them and odds are they see adults walking all the time.
In terms of walking though I'd expect instinct to play the major role. Not that walking would be hardwired per se, but there are probably movements and reflexes that babies are hardwired to try, and once they get to a physical maturity where walking is possible the odds are that they will try those movements, and find the results interesting at least, profitable at best.

To understand why we must first understand how.
Standing. Standing is crucial to being able to walk, that is, developing the strength to stand on one's feet[1]. Usually, this starts with supported standing by a parent or an object. This builds coordination, flexibility, and further curiosity for the tiny human to keep moving around in the way that they can, most efficiently (which is walking as opposed to crawling).
Now we can attempt to hypothesize why.
As others have said, efficiency is huge. It takes less energy to walk than to crawl 10 feet, once the ability is there. Many might say that it is similar to making the decision to walking 10 miles or learning how to bike so that you can bike 10 miles. Clearly, biking is a more efficient mode of transportation. Getting from one place to another is a very integral part of human development and ability. Efficiency, paired with the curiosity that seems very integral in a baby's psychology, leads to the baby wanting to travel from place to place and see and touch and eat everything it can.
Is it evolutionarily beneficial for babies to move around a lot, efficiently? I think the answer is yes. In order to prove this, let's assume the answer is no. If no, then humans as a whole would just be content not getting around efficiently and have indifference toward them using as much energy as possible during the action. This is clearly inhuman and not self-preserving, and obviously a contradiction. Thus, it must be evolutionarily beneficial for babies to move around a lot. Furthermore, the movement and curiosity may lead to increased exposure to the elements and foreign biological organisms, giving the kids the chance to develop their immune system, like we all know is so crucial at that age. There is probably more examples to help this argument, but this example proves the point and concept. Moving efficiently is evolutionarily beneficial.
A more sociological question would be, would babies try to walk if no one else did? Is it nature or nurture? If we all in society crawled, would the baby too? Mirroring might play a very powerful role here. Testing this would be very interesting, but it would likely violate the Belmont agreement.

Standing. https://www.parentingscience.com/when-do-babies-start-walking.html


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Question in gel chromatography experiment
Here I am trying to do
gel chromatography to separate vitamin B12 and Bovine Serum Albumin (BSA)
in this experiment, I am using sephacryl s-100 HR gel column
my question is can I use Phosphate buffered saline with sephacryl s-100 HR gel column
also since the Bovine Serum Albumin (BSA) is colorless I need some kind of Protine detection reagent to see this protein (I need something other than Coomassie brilliant blue)

Is this a homework question?

No, it just that I originally not a biologist but a physicist and it is my first time performing this experiment

Within reason, you can basically use any buffer you like with Sephacryl S-100, provided that is suits your purpose in terms of protein/enzyme stability, and phosphate-buffered saline sounds ideal.
There are sometimes a small amount of positively or negatively charged groups associated with a gel-filtration resin, introduced during the manufacturing process, and it is recommended to have some salt present (100mM KCl used to be recommended) in order to counteract anion-exchange and/or cation exchange effects.  In addition, at very high salt concentrations (1M ammonium sulphate or higher), proteins may bind to the resin by a hydrophobic interaction. Furthermore, one or more of your target molecules may be unstable at extremes of pH.  NADH, for example, is unstable in acid.
In other words, you want to set up the experiment where the target molecules are stable, and where separation on the column is by 'molecular sieving' only.
A very common method of measuring protein concentration is to measure the A-280 of each fraction (the absorbance at 280nm). The has the big advantage of being reasonbly sensitive AND is non-destructive (you can fully recover the sample after the measurement).  All you need is access to a spectrophotometer and a quartz cuvette!
In addition, with (pure) BSA the method may be made quantitative as the A(1%, 280),sometimes called the E(1%,280), is known. From memory I think this is about 0.68 for BSA.  That is, a 1mg/ml solution of (pure) BSA will have an absorbance at 280nm of 0.68.  (The 'rule of thumb' for impure protein preparations is that a 1mg/ml solution has an absorbance of 1. But note that many compounds absorb at 280nm, including DNA)
You can, if you wish, calculate the A(1%, 280) from the amino acid sequence of the protein of interest. The refs (Perkins; Gill & von Hippel) are given below.
It should be possible to detect B12 by a similar method, perhaps even at 280nm, but an absorbance spectrum may yield a more sensitive/specific wavelength.
You don't give the pH of the PBS (!important), or the dimensions of the Sephacryl column.
Long, narrow columns work best, but you probably already know that.
Some Refs
Gel Filtration by Reiland (Methods in Enzymology, 1971).  A great article
Protein Purification: Principles and Practice by RK Scopes (Springer Advanced Texts in Chemistry) 3rd Edition
Sober, E. K. & Sober, H. A. (1970). Molar extinction coefficients and E (1%, 280) values for proteins at selected wavelengths of the ultraviolet and visible region. In Handbook of Biochemistry. Selected Data for Molecular Biology, 2nd edn. Sober, H. A., Ed. pp C-71 - C-98. The Chemical Rubber Company, Cleveland, Ohio.
Perkins, S. J. (1986). Protein volumes and hydration effects. The calculation of partial specific volumes, neutron scattering matchpoints and 280-nm absorption coefficients for proteins and glycoproteins from amino acid sequences.  Eur. J. Biochem. 157, 169 - 180. [Pubmed]  [pdf]
Gill, S. C. & von Hippel, P. H. (1989). Calculation of protein extinction coefficients from amino acid sequence data.  Anal. Biochem. 182, 319 - 326.  [published erratum appears in Anal. Biochem. (1990) 189, 283].


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What kind of parasite is this?
I found this strange disease on the leaves of a pear tree. I don't know the tree's species but I found it in South Turkey, 150 km from the Mediterranean. What causes this disease?

Welcome to Biology.SE! If you know this a pear tree then you do know the genus (Pyrus).

Related: https://biology.stackexchange.com/q/10002/16866

This is pear rust (Gymnosporangium sabinae).

It is fairly widespread in the northern hemisphere:

It is a fungal infection and affects pear trees from junipers. Pruning the affected nearby junipers can help control its spread.


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Help identifying a part of a flower
I researched about floral diagrams and this is what I found:-
This is floral diagram of Theobroma cacao. I managed to identify others but this part near the stamens was not found anywhere.
Also the floral diagram includes some circular parts which I have highlighted.
So what exactly are these parts called?
https://en.wikipedia.org/wiki/Floral_diagram

Please could you include a link to the source of your image. Thanks.

Because the background is now black rather than the white in the original diagram you've lost essential information. It also looks to me like a careful reading of the linked wikipedia page answers your questions. One hint that may help you is to think about how the cross-section of a stamen changes along its length. That will help you recognize structures you've circled in green. ——— Please also read the "homework" guidelines. (Note that "homework" can apply to questions even if they are not assigned as homework.)

ok i have corrected but I couldn't find any information about these pars


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Can we change the Eye/Hair color by knocking out the OCA2, HERC2 and MC1R genes using CRISPR in an adult human?
This paper seems to describe the use of a plasmid delivered by a gene gun to depigment rat skin;

https://www.nature.com/articles/3302264
Published: 27 May 2004
Seeing the gene therapy: application of gene gun technique to transfect and decolour pigmented rat skin with human agouti signalling protein cDNA

Could a similar technique using CRISPR and chitosan change the eye and hair color of an an adult?

Let's first breakdown this question

What is CRISPR?

CRISPR is a group of DNA sequences that play a key role in the antiviral defense system of prokaryotic organisms such as bacteria and archaea.
They are derived from DNA fragments of bacteriophages that had previously infected the prokaryotes.
These sequences are used to destroy DNA from similar bacteriophages for future infections.

What is CRISPR-Cas?

The CRISPR-Cas system is an immune system seen in prokaryotes that provides resistance to foreign elements such as plasmids and phages. This is a form of acquired immunity.
Some factors allow Cas protein which is an enzyme to recognize and cut foreign pathogenic DNA making them act like a pair of molecular scissors.

What are OCA2, HERC2, and MC1R?

Now we know we can cut a specific part (Gene) of DNA. What do we accomplish by cutting out the genes which Andrew mentioned? To answer this we need to know what those three genes do.

OCA2 (P-gene): Provides instructions for making a protein called the P protein. This protein is located in specialized cells
(melanocytes) that produce a pigment called Melanin.
Melanin is a natural skin pigment. Hair, skin, and eye color in people and animals mostly depends on the type and amount of melanin
they have.
HERC2 (E3 ubiquitin ligase HERC2): Protein ligase which helps in DNA repair regulation, pigmentation, and neurological disorders.
MC1R (Melanocortin 1 receptor): Proteins involved in regulating mammalian skin and hair color.

In short, these Genes affect the Eye and Hair Colour and Andrew is suggesting to us that by removing/modifying them using CRISPR we change the Eye/Hair Colours.

Can we knock out OCA2, HERC2, and MC1R?

Yes, it has been done before and there are sequences available to target these genes within the genome. An example would be the gRNA sequences developed by Sigma-Aldrich and Genscript. I'll provide links of articles which has knocked out the respective gene and links to the gene sequences.

OCA2: (Article: https://pubmed.ncbi.nlm.nih.gov/29555241/ | Sequence:
https://www.genscript.com/gRNA-detail/4948/OCA2-CRISPR-guide-RNA.html)

HERC2: (Article:
https://jmg.bmj.com/content/early/2020/06/22/jmedgenet-2020-106873 |
Sequence: https://www.sigmaaldrich.com/catalog/genes/HERC2)
MC1R: (Article:
https://www.genscript.com/gRNA-detail/4157/MC1R-CRISPR-guide-RNA.html
| Sequence:
https://www.genscript.com/gRNA-detail/4157/MC1R-CRISPR-guide-RNA.html)

Can we change the Eye/Hair Colour by modifying the above genes?

An Interesting article from MIT Technology Review called Engineering the Perfect Baby gives you a nice idea of what I am going to tell you.
In Theory: It's technically possible. We can put up a convincing theory and there is a huge chance that this can be successfully done.
In Reality: Well, Reality kinda sucks cause most of the genetic engineering breakthrough starts from failures. Killing a rat for scientific purposes won't make any big difference but what about killing a fetus? It's almost impossible to get the permissions required to use CRISPR to edit the human genome even if it is to find a cure for a deadly disease that would actually improve the human race significantly. Due to its obvious ethical questions, people always stand against it. I said "almost impossible" cause there are few people who actually got the permissions and there are indeed few ongoing trials experimenting with CRISPR on Human Genome.
A popular Example would be He Jiankui who gave rise to the first-ever gene-modified human babies "Lulu and Nana". He had to forged ethical review documents, misled doctors into unknowingly implanting gene-edited embryos into two women, and many more things which haven't come out yet. What are the consequences? He's bloody missing! May 2022 Update: He's been found.
The point is, there is absolutely no way they would approve the usage of CRISPR for modifying something as silly as Eye/Hair color.
I mean we all like our babies to look like Megan Fox but I totally doubt if anyone would dare to modify a human genome for changing mere appearance cause people would start protesting if they find out someone is putting all those innocent fetuses at unknown and uncalculatable risk for changing external traits.
We want people to use CRISPR for things like this - Scientists edit gene for blood disease in human embryos and not for things like this - The rise of the designer baby: Parents who paid $16,500 to choose the sex of their child.
TL;DR (Too Long; Didn't Read):

What is CRISPR-Cas?

Technique in which we can edit genes relatively more precise than before.

What are OCA2, HERC2, and MC1R?

Genes which control the color of Eyes, Hair, Skin, and has other purposes.

Can we remove OCA2, HERC2, and MC1R genes using CRISPR?

Yes

Has it been done before?

Yes

In Humans?

Nope cause we got all those ethics and stuff.

What are we trying to accomplish by removing those genes?

To change the Colour of the Eyes/Hair of a human being.

Can we change the Colour of the Eyes/Hair of a human being?

In theory, it'll work. In Reality, nobody would allow it. They'd be better off with Hair Dye and Contact Lenses than to risk the lives of innocent fetuses.

https://columbialawreview.org/content/would-you-like-blue-eyes-with-that-a-fundamental-right-to-genetic-modification-of-embryos/
Of clinics that offer PGD [...] 3% have used it to select for a disability common to the parent, like deafness or dwarfism.
Still, there is no outright federal ban on research on human embryos generally, meaning privately funded organizations could still conduct research in this field.

@AndrewM they could, except they don't, because of the enormous ethical implications. The vast, vast majority of biological researchers have very strong ethics, with the occasional exceptions of people like He Jiankui. Real life is not like the movies, with evil corporations conducting mass human experimentation behind closed doors for nefarious purposes.


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Why proprioceptive fibres (of CN V) have their cell bodies in mesencephalic trigeminal nucleus?
It's seen that GSA (General Somatic Afferent) fibres (of CN V) have their cell bodies in trigeminal ganglion. But the proprioceptive fibres' peripheral processes terminate at mesencephalic trigeminal nucleus, making it the only nucleus in CNS where cell bodies of 1st order neurons are present.
Why this is so?

if you are satisfied you may accept the answer for the future reference.

The mesencephalic nucleus of trigeminal nerve is involved with reflex proprioception of the periodontium and of the muscles of mastication in the jaw that functions to prevent biting down hard enough to lose a tooth. To subserve this reflex protective function, mechanoreceptive nerves in the periodontal ligament sense tooth movement and project to the mesencephalic nucleus.

The functional significance of this anomaly is unclear, although there is a hint of special neural processing in the fact that, unlike DRGs and normal cranial nerve ganglia, MesV neurons receive synaptic input. Another hint is that while at spinal levels opposing extensor and flexor muscle blocks are roughly equal in size, in the orofacial motor system there is asymmetry. Jaw-closing muscles, the flexors, are massive and powerful with rich muscle spindle and Golgi tendon organ innervation. The jaw-opening muscles, the extensors, are small and delicate and lack muscle spindles and Golgi tendon organs

Reference

It is responsible for unconscious proprioception that stems from muscle spindles in the muscles of mastication and other muscles of the head and neck. It is thus essential in the process of receiving sensory information about tooth pain, helps prevent excessive biting that may break a tooth, receives information about stretch sensation from the muscles of mastication, and serves as the afferent limb of the jaw jerk reflex.
Reference


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Can elephants be allergic to peanuts?
Can elephants be allergic to peanuts? If yes, what is the reaction? Does the trunk swell up? I tried googling the issue but the only thing I found was a children's book about Eppie the Elephant. I realize elephants are not particularly fond of peanuts.


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Why does exhaled air still contain oxygen?
If the partial pressure of oxygen in the atmosphere is 159 mmHg and that inside human alveoli is 104 mmHg, and if these values are fixed or don't change very much, then why does exhaled air have oxygen in it? Or when we compress our lungs this value changes?
Oxygen should not move from a higher partial pressure to a lower partial pressure no matter what other gases are exhaled because when we inhale, the pressure inside the lungs becomes 1-3mm Hg lower than the atmosphere; then air starts to enter and at a point when it stops entering this is the moment when the total pressure outside and inside becomes equal, and oxygen and other gases diffuse in the blood and carbon dioxide in the alveoli; which is why the partial pressure in the alveoli is 104 mmHg. But when we exhale the lungs start to compress and thus pressure inside the lungs increases and air moves outwards. But how is it possible that only the partial pressure of oxygen doesn't change and the pressure of all other gases inside the lungs increases?
It should also increase because if our expired air has oxygen in it then it should also increase?

welcome to se.biology. I tried editing your question to make it more clear, but I struggled a bit with the second paragraph. I think you will get better answers if you try and condense the second paragraph into something more clear and focused. Adding more paragraphs, punctuation and only asking a single question might help.

A piece of advice in composing questions. Do what I generally do, which is write it in a word processor document first, edit it, and run an English spelling and grammar check. And English is my native language. And write short sentences.

You seem to be confused about diffusion versus bulk flow of fluid (air/gas).
In the lungs, there is diffusion between blood and the gas in the lungs. There is sufficient surface area that these equilibrate fairly quickly, and the partial pressure of oxygen in blood leaving the lungs is very similar to the gas in the lungs. Partial pressures are the best way to understand and explain diffusion of gases.
When you breathe out, a fraction of the bulk air moves out and mixes with outside gas. The partial pressures don't matter for this part, however, all that matters is that you have a big opening (as far as a gas is concerned) through the mouth/nose. Then again, when you breathe in, a fraction of bulk external air moves in and mixes with gas that remained in the lungs (you never completely breathe it out). This mixture will initially have more oxygen in it than the mixture that was exhaled, but it again quickly equilibrates with the blood via diffusion.
If you were to breathe in and wait long enough, eventually the partial pressure of oxygen in the blood would drop (used up in metabolism), and the concentration in the lung gas would also drop to match. However, you would lose consciousness far far before this would ever approach "zero".
The lungs are not a machine to pull all the oxygen molecules out of the air and provide it to the body. They are a gas-exchange surface to provide a massive surface area to help make the internal oxygen concentration as close as is possible to the external oxygen concentration. It never quite gets there, of course, but it gets relatively close.


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How do plants that reproduce with artificial vegetative propagation grow in nature?
How do plants that grow with artificial vegetative propagation grow in nature? Will they go extinct if humans stop intervening? e.g., Rose

Welcome to SE.biology! Your question seems to be on-topic, but it's expected that you show some evidence that you've tried to research the question before posting here. Please take a read of the help centre section on how to ask a good question and consider editing your post.

Downvoted because it could be answered by a minimal amount of research.

Rose species reproduce perfectly well in nature, by the normal means of seeds and suckering.  For instance, Rosa woodsii is found growing along streams throughout the western US: https://www.wildflower.org/plants/result.php?id_plant=rowo
The reason rose (and other plant) VARIETIES are propagated by various artificial means is primaily because they are selected for various factors, such as (in the case of roses) color, bloom size, number of petals, and (all too infrequently) scent.  But those characteristics don't breed true: just as with humans, plants grown from seed will be different from their parents.
A second reason is that these plants are often hybrids of different species, and so may not produce fertile seed. Vegetative propagation - sometimes to the extent of using tissue culture - is the only way to get more plants of the same kind.
With roses (and numerous other plants) there's also a matter of economics.  A rose hybridizer may grow hundreds or thousands of seedling roses to find one that might be a marketable new variety.  When such a variety is found, the most economical way to produce many plants for sale is to graft the plant onto a common rootstock*.
*This is why many gardeners think their hybrid tea roses eventually "revert" to a boring red color.  It's because they're grafted onto rootstock of the "Dr. Huey" variety, and the vigorous rootstock takes over if not properly pruned.


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Allamanda blanchetti fertilization mechanism
Here is an Allamanda blanchetti flower in my garden.
My question is based on the observation that the flower seems to be devoid of any reproductive structures, i.e., Stamen or Carpel, so how does it set seed? In the picture below it can be seen that the plant isn't sterile and successfully produces seed pods.

google lens app can recognize flowers 95% of the time.

Since the species identification portion of your question is a duplicate, I encourage you to  remove that portion. That will allow you to focus on a single question, which is important because each question should be posted separately. That improves the chances that you will get answers for each question and makes the answers more accessible for future users. ——— However, we expect you to do research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Start by looking up reproduction of this species. Thanks!

I have edited the question to be more specific about the fertilization process, since @Bryan Hanson has already pointed out a similar question for the species ID. But the question  as it stands now, edited, is different and not a duplicate.

Great, I've voted to reopen your question. This typically requires four other users to agree so it may take a few days. In the meantime I encourage you to dissect some of the flowers and see whether you can find out an answer yourself! A razor blade or sharp knife can be used to cut through the flowers to see what is inside — I suggest cutting along the long axis of the flower (slicing the "tube" at the base lengthwise). I think you will find this quite enlightening. However, it may lead to more questions, but that's good! (Also be careful to clean up the latex since it may be irritating.)

@tyersome sure! I will try it out as soon as possible. :)

There's now a followup question with dissection photos at What are these structures inside a cut open Allamanda blanchetti?

As far as the ID goes, this looks like Allamanda blanchetti.  See this question.

In the future I think it would be better if you just flagged the question as a duplicate of the other question (to which you gave a good answer).

I have looked up the reproduction of Allamanda genus on Wikipedia and other websites, but only taxonomy, distribution ,medicinal uses and the likes are listed. I am a high school student and don't really have much access to more scholarly articles. So please enlighten me on the matter.


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How do Human Skin Creases Vary?
I am studying human gross anatomy in order to produce an anatomically correct CGI model of the human body. As part of this, I'm attempting to understand the different features that define the topography of the skin. One class of features is the creasing of the skin, which appears to manifest both on a large and small scale (illustrated in figure 1 of [2]) with variation about the body. In my reading, I have found [1] which catalogues the major creases and only [2] which briefly discusses the smaller creases and cites paywalled articles. Since this topic seems particularly obscure, it would be good to have a definitive summary of this topic. Therefore:

What are the different types of skin creases?
Is there terminology that distinguishes the larger and smaller creases?
How are they distributed about the body?

[1]: Mallouris, Andreas & Yiacoumettis, Andreas & Thomaidis, Vasilios & Karayiannakis, Anastasios & Simopoulos, Constantinos & Kakagia, Despoina & Tsaroucha, Alexandra. (2012). A record of skin creases and folds. European Journal of Plastic Surgery. 10.1007/s00238-012-0774-3.
[2]: Wong, R., Geyer, S., Weninger, W., Guimberteau, J.‐C. and Wong, J.K. (2016), The dynamic anatomy and patterning of skin. Exp Dermatol, 25: 92-98. doi:10.1111/exd.12832


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Symmetry in Biology
It seems a curious fact to me that all organisms I can think of exhibit some definite symmetry on a large scale (much larger than molecules), and in particular mirror symmetry. Since it is so wide spread, I imagine there is some deep reason for it. One thing that comes to mind, is that it might take less genome to encode. Are there any such reasons?

Welcome to SE.biology! It's expected that you show some evidence that you've tried to research the question before posting here. Please take a read of the help centre section on how to ask a good question and consider editing your post. There is a whole wikipedia page dedicated to the topic which should be read before posting questions. Thanks.

please provide with some evidence that back you research


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What is this thing? It is hairy mostly a cocoon, and i saw a white worm pop out of it. It is spreading rapidly
I suspect it is originating from the mud. This has some plastic bits with it. They are spreading all over my walls. I think it is some  kind of cocoon for worm. Should it's rapid growth in terms of number be a matter of concern? found in Bangalore, India,

Bagworms?
https://en.wikipedia.org/wiki/Bagworm_moth
I don't know how destructive individual species are. They probably aren't more than an aesthetic concern.

Example: https://www.youtube.com/watch?v=H3o3lIVXANg

No, it doesn't seem like a bagworm.


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How can life survive in the water under the Antarctic ice?
If there is life in the lakes under the ice of Antarctica then how can those bacteria survive?
Where do they get energy from?
https://www.google.com/amp/s/www.livescience.com/amp/64501-buried-lake-antarctica-life.html
The dark waters of a lake deep beneath the West Antarctic ice sheet and a few hundred miles from the South Pole are teeming with bacterial life, say scientists — despite it being one of the most extreme environments on Earth.

Welcome to SE.biology! It's expected that you show some evidence that you've tried to research the question before posting here. Please take a read of the help centre section on how to ask a good question and consider editing your post.

I quoted a link now. Is that enough?

@JoeJobs The article you linked says "Scientists theorize that the bacteria in Lake Whillans — and possibly Lake Mercer — are surviving on deposits of carbon laid down by photosynthesizing organisms between 5000 and 10,000 years ago, when the buried lakes may have been connected to the open ocean." Can you explain where your question remains?

I knew Priscu and worked with some of his grad students at Montana State.
Here's one of their papers on the Lake Whillans project.
One of the more relevant findings is that many of the most abundant organisms (by genetic analysis of small subunit ribosomal RNA genes) were closely related to chemolithoautotrophic organisms. Basically, organisms that can obtain energy by oxidizing inorganic compounds. They found that there was sufficient chemolithoautotrophic carbon incorporation to support the heterotrophic demands of the ecosystem. They also found an abundance of organisms related to nitrifiers (organisms that oxidize ammonia into nitrite and nitrate), along with sufficient ammonia, suggesting that nitrification is a primary pathway of new organic carbon production in the ecosystem.
Source:
Christner, Brent C., et al. "A microbial ecosystem beneath the West Antarctic ice sheet." Nature 512.7514 (2014): 310-313.

How can oxidation of ammonia produce carbon?

Good question (guess I skipped over that part). The source of new carbon for most autotrophs is $\mathrm{CO_2}$. To my knowledge all nitrifiers fix $\mathrm{CO_2}$ using the Calvin Cycle, which is the same pathway used by by plants and most photosynthetic bacteria (photoautotrophs). The only differences is where the energy comes from. Photoautotrophs use light, and chemoautotrophs use chemicals. There are other carbon fixation pathways used by other organism as well.

BTW. I did not just have all that knowledge at the ready. I flipped open my copy of "The Physiology and Biochemistry of Prokaryotes" that I keep on my desk at work (By White, Drummond, & Fuqua). An excellent reference if you're interested in bacterial physiology.


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Can any molecule become a hapten?
Hapten are small-molecules, that can only become immunogenic when conjugated with a carrier protein. I was wondering if all small-molecules can become haptens (eg. by synthetic conjugation).
Given that lymphocytes are filtered by negative selection, I would expect that small-molecules that chemically mimic self-peptides would not work as haptens (at least not in the sense, that they could be detected by antibodies).
Are there any examples of small-molecules that have been tried as haptens but could not generate antibodies ?
Also is there any estimate of the ratio of naturally occuring haptens and synthetic haptens. I was investigating the IEDB (https://www.iedb.org/) as well as SuperHapten (http://bioinformatics.charite.de/superhapten/) but could not find a way to filter these two types of haptens.

What does this question mean? A Hapten is a molecule that exhibited a carrier response when bonded to a carrier protein. Not every molecule relates to the immune system so obviously no. If you are saying that any immune protein can be a hapten, then still no, because the point is that the response only occurs when bound to the carrier. This is how small molecules, which are precise enough to have biological action, can have an effect where needed. If the protein always has an immune response it will waste itself unnecessarily and the carrier is what brings it to where it needs to be to do its


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What spider is this? Is this invasive or dangerous?
Hi the picture below has been taken here,
I've never seen such a spider, is it an invasive specie or a dangerous one?

thank you

That appears to be a zebra jumping spider (Salticus scenicus). It is fairly widespread throughout North America. It does not post any kind of threat to people or to the environment:
Here is a map of iNaturalist observations for zebra jumping spiders.

And here is a gallery of photos you can view: https://inaturalist.ca/taxa/68901-Salticus-scenicus/browse_photos


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Does GABA enhance or inhibit negative effects of glutamate?
A study on NCBI studied the correlation between a depressive mood and chronic pain. I researched this because today I noticed unusual emotional volatility as a result of 2 days of acute back pain combined with acute muscle soreness (DOMS).
I am certain that the pain and difficulty sleeping (although I slept in on both days), and challenges with finding a sleeping position without pain, and continuous pain on most moving, standing, and sitting, that this has caused some emotional volatility on a physiological level. (Psychological effects as a direct result of temporary chemical changes in the body/brain due to acute pain; not due to neural pathways causing depression, of which I do not have, and I am a joyful person normally).
This question is not about alleviating pain, as it will go away on its own soon. The back is getting near healed by end of week and the sore muscles which have DOMS due to intense workout will also resolve on its own in a few days to a week.
Rather, my question is specifically concerning a particular phrase which I am unclear about:

Glutamatergic activity can be promoted through the breakdown of efficient inhibition of the actions of glutamate by GABA

I am unclear if this is stating that GABA reduces the effects of glutamate or if it enhances the effects.
There is no clear answer to my full [temporary] issue, since the study itself states that neither the corresponding pathophysiological mechanisms of chronic pain and depression nor their mutual correlation has been identified, so there is no pathophysiological scientific answer to the chemical workings, so I can only speculate.
The end result is I wanted to discover whether increasing or lowering GABA could have any effect on my mood as a result of my pain in the short term, which is easily experimented rather safely by either taking GABA or taking a supplement that inhibits GABA. It could have no beneficial effect - no problem. It's worth a try though. I've taken GABA before BTW.
To reiterate the particular question: With regards to the statement:

Glutamatergic activity can be promoted through the breakdown of efficient inhibition of the actions of glutamate by GABA

Does this imply that GABA enhances or reduces glutamatergic activity?
Note:
I think it's saying that GABA creates glutamatergic activity which inhibits the neuroexcitatory effects of glutamate. That is, taking GABA would decrease effects of glutamate. Let me know if this is correct or not.

It would be possible to rewrite this question without the personal medical details, but please don't use such an answer to do anything besides understand biology. In any event, it certainly is not as simple as eating GABA increases GABA in the nervous system (no matter what someone trying to sell you a bottle of GABA might say).

Glutamate causes an EPSP (Excitatory Post Synaptic Potential,) thereby making the neuron less negative depolarize) and closer to voltage required to cause an Action Potential (AP)  and thus fire.  GABA causes an IPSP (Inhibitory Post Synaptic Potential) making the neuron more negative (hyperpolarize) and further away from the voltage required to fire and cause an AP.  GABA & Glutamate receptors  are generally on different neurons that synapse with other interneurons & oppose each other, although neither one is generally the end neurotransmitter of the locus,  nor the only neurotransmitter of the neuron, so basically act as neuromodulators on the post-synaptic neuron. Glutamatergic receptors generally affect Sodium Channels &  GABA-ergic neurons generally  affect Chloride Channels. In theory, inhibiting an inhibitory neuron would be the equivalent of exciting an excitatory neuron, but since they primarily affect  post-synaptic neurons, the effect is cumulative, so the post-synaptic interneuron is basically adding up all the EPSPs & IPSPs to get a RMP (Resting Membrane Potential) & some additional stimulus must occur to get the neuron to fire (AP)

You might recheck what you've written here because a lot of this answer is incorrect or at least mis-written.


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Can bacteria be killed by purely physical trauma?
In a question over on Skeptics Stack Exchange, I half-jokingly listed "blunt force trauma" as a means by which a bacterium could be killed. That makes me wonder if it really is only a joke or whether such an assault is plausible. The webcomic xkcd also did an episode on the possibility of physically attacking a cell (though not a bacterial one).
There are plenty of resources on how bacteria can die from biological processes (e.g. infection with a bacteriophage, biological effects of antibiotics, etc.), chemical attacks (e.g. membranes getting lysed with bleach), temperature (i.e. cooking), and radiation, but have bacteria ever been shown to be vulnerable to a direct physical assault such as being hit with a hammer, cut with a knife, thrown onto a hard surface, twisted until they burst, or being drawn and quartered?
I do know that many common weapons that are generally effective against animal life (swords, axes, clubs, assault rifles, etc.) do not have the exact same properties at the microscopic scale, but does that mean that physically beating a bacterium to death is absurd or is there a known way to kill a bacterium using only physical force?
To be clear, I recognize that our normal means of killing unwanted bacteria - cooking food to prevent food poisoning, treating bacterial infections with antibiotics, cleaning hard surfaces with bleach, applying rubbing alcohol to wounds, etc., are probably effective enough that most people don't bother pulling out that old Wild West six-shooter they have in the closet or the antique sword hanging on their wall the way they might consider them if attacked by a bear or wolf, but that's not the question.

What's the limit of what you'd consider physical trauma?  Bacteria can be killed with sufficient centrifugation, which is reverse blunt-trauma in that they are smashed against a comparably-large and comparably-blunt tube bottom

Does a diamond knife count?

@Joshua Only if it's a blunt knife.

@Punintended That counts.  Blunt force trauma isn't really a vector quantity, it's the resulting state produced by the application of a strong force.  Humpty Dumpty doesn't really care which reference frame you pick - either way he's broken.

I guarantee that any bacteria that found themselves in the immediate vicinity of a supernova would be destroyed. So, yes.

Through google found a similar question on Skeptics.SE Is it possible to crush bacteria?

Borat eagerly awaits the answer to this question

My (limited) understanding is that it is quite hard to avoid killing some bacteria even with very gentle physical manipulation. On the other hand, it is quite hard to use physical force to achieve reasonable level of sterilization. Let's bring some examples with a few (hastily found) references.
Pressure
My guess is that most examples the OP mentions (hit with a hammer, knife) will exert their biggest effect on bacteria through a peak in pressure - bacteria are comparable in size to width of a moderately sharp knife edge and thus there will be more "crushing" than "cutting" even with a knife (Science of Sharp discusses that Chosera 1k - a very good stone - will sharpen a knife to 0.5 μm, Wiki has bacteria at 0.5 - 5 μm).
I recently collaborated on a project where initial interpretation of results was wrong simply because putting a glass slip over a sample to inspect it under a microscope caused around 10% of bacterial (B. subtilis) cells to die. Putting a small weight on the slip resulted in roughly 80kPa additional pressure applied and ~ 80% of the cells dying within 25 minutes. But 80% death rate won't do much to e.g. reduce risk of food poisoning - as long as there are nutrients, bacteria will regrow quickly.
As m4rio mentions in a comment to another answer, and in line with The effect of high pressure processing on the microbial, physical and chemical properties of Valencia and Navel orange juice you need to ramp up the pressure to 100s of MPa to achieve high efficacy. And even that may not work so cleanly - e.g., the linked paper mentions that after applying 600 MPa, bacteria regrew to detectable levels after 4 weeks of storage at 4°C. Killing all (or almost all) bacteria is just really hard.
Because it was fun, I'll also link to study showing that High pressure-processed guacamole (4 cycles, 689 MPa, 5 min each) is clean enough to not spoil for 30 days in 25°C.
Note: the two sources above were linked from a commercial vendor of high-pressure products and may thus be biased. While the exact numbers might be problematic, I think the main point is unlikely to be affected.
A review High-pressure processing – effects on microbial food safety and food quality mentions some limitations, e.g.:

Endospores tend to be extremely HPP resistant compared with vegetative cells, withstanding treatments of more than 1000 MPa

ascospores of heat-resistant moulds such as Byssochlamys, Neosartorya and Talaromyces are generally considered to be extremely HPP resistant

It should however be noted that it seems that high-pressure treatment is good enough to be semi-commonly used as the main sterilization for suitable foodstuffs - Current status and future trends of high-pressure processing in food industry reports high-pressure treatment to be FDA approved and USD 10 billion worth of food being treated as of 2015.
Pressure for killing cells previously briefly discussed at Can bacteria or other microorganisms be killed by applying pressure?
Ultrasound
While frequently used for cell lysis in lab, it also doesn't kill all cells. For example The Sterilization of Suspensions Contaminated with MicroorganismsUsing Ultrasound Irradiation reports that roughly 20-30% of bacteria (Bacillus) survived 60 minutes of ultrasound treatment.
Ball mill
This is probably closest to actual "physical trauma" - you put small beads and a suspension with microorganisms into a cylinder and roll it hard. A low energy process for the recovery of bioproducts from cyanobacteria using a ball mill discusses using this process to extract proteins from cyanobacteria. They don't report absolute number of cells killed, just that it varies considerably with the rotation speed, size of beads, .... My interpretation is that in most cases a non-negligible proportion of the cells survive while majority is killed (and their contents extracted for further use).

In microbiology, the "ball mill" method of bacterial cell lysis is called bead-beating.

@user1136 I am not primarily a biologist - I did statistics on the project, so hope I am not messing up. What my colleagues did was use SYTOX green staining which "penetrates into the cells with compromised/permeabilized membranes where it stains nucleic acids and indicates cell death", so I think the cells were not completely broken (which is presumably why all cells were considered alive in previous work on the subject). You are welcome to check the methods and details at https://doi.org/10.1038/s41467-020-18800-2, primarily Figure 2.

There are plenty of physical or mechanical methods of killing bacteria, but most are used in conjunction with other agents and probably don't qualify as "blunt force trauma". For example, beer distributers might snake a brush through a keg line to disrupt any bacterial biofilms before flushing them out with disinfectant. Similar logic applies to rubbing your hands together when you wash them or using a brush to scrub biofilms off your teeth. We might not think of it as traumatic force, but it can be to bacteria.
Since you mentioned it, there is something that might resemble them being "twisted until they burst" (more like crushed to death). A device called a French pressure cell press (or just French press) used to lyse bacterial cells with purely mechanical forces. It basically compacts a culture of cells under high pressure, causing them the burst and release the cellular contents. Of course, it would require somehow gathering all of them together into a containment vessel and having an expensive laboratory instrument to put them in.

My understanding of how a French Press works is that the disruption is due to forces generated on the cells as they pass through the valve rather than the high pressure crushing the cells.

@tyersome Yeah, that's probably a more accurate description of the mechanism, though there are food safety applications that rely on pressure alone for bacterial killing.

The French pressure cell press idea is used today commercially. It doesn't have that name though. It's called HPP or high pressure processing. Hiperbaric is the company that sells and makes the machines. It uses up to 10,000 bar of water pressure in a container in order to kill bacteria. It's effective as long as the water activity of the food being processed is at a certain level. Also the pH matters as HPP cannot kill spores from sporoforming bacteria and has difficulty with molds. However it can kill E. coli, Salmonella, and Listeria in juices easily (I work with these machines).

@m4rio so to be clear, it’s used as an alternative to pasteurisation for liquid consumables!?

@Tim Yes. Most common liquid (or juice) pasteurizations include heat, UV, or HPP. HPP is the newest among the three and for companies who do not like to heat their product or UV it due to whatever reasons, be it they want it more organic, or it changes the flavor of the juice, HPP can be an alternative. It is the most expensive of the three but can give a good ROI if done in big bulk. As far as I know only big or big-ish companies use it. If you're doing HPP and you get a good CFU/ml reduction of bacteria as the FDA requires you can use HPP as your sole method of pasteurization.

Yes of course. While you can't swing a blunt object comparable in size to humans at something many orders of magnitude smaller to kill it. You can use something like an ultra sonicator, which swings a small blunt object at --you guessed it-- very high speeds to generate lots of shear forces in a liquid culture. Usually these instruments are not meant for killing cells, but even with my most gentle use for breaking up cell clumps, a look under the microscope would show ruptured cells with their interior spilled out.

I use a sonicator for making (mammalian) cell lysate all the time. But, I think you might be confused about how a sonicator works. It's not the force of the moving tip itself that does it - the extremely rapid motion of the tip produces very tiny vacuum bubbles in the fluid that almost immediately collapse, sending a strong shearing force through the liquid and disrupting whatever it comes into contact with. The principle is called ultra-cavitation.

@MattDMo Didn't I say shearing forces in liquid?

@Cell — The way you wrote your answer does sound like direct action by the tip — I encourage you to change your wording and ideally add the type of information mentioned by MattDMo. Your answer would also be improved by including references.

From a biochemical point of view, it is surprisingly difficult to break open a bacterial cell. A molecular biologist, for example, might want to break E.coli cells expressing a protein of interest, in order to purify the protien
Some of the methods employed are agitation with glass beads, griding with glass beads, sonication, and high-pressure cell disruption with the French Press.
In contrast, liver cells, or brain cells, may be broken by simple homogenization (for example in a Waring blender)

...cut with a knife...

Yes, freeze them.... slowly. <evil laugh>
Freezing causes ice crystals to form inside the cells. These act like little knives. The slower the freezing happens, the larger these ice crystals get. The larger the ice crystals, the more damage they will do by piercing the cell wall and other important membranes.
This is why if you freeze fruit in a home freezer it thaws out as a goopy mess; the cell walls have been punctured. This is also a key problem in cryogenics, the freezing and thawing process damages cells.
Flash freezing uses very rapid freezing to very low temperatures to prevent large ice crystals from forming and minimizing damage. Food which is flash frozen is less goopy.
Note that when done properly freezing can be used to reliably kill some microbes, freezing at home is not a reliable disinfectant.


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Is the diaphragm made of two muscles?
Is there a 'crural' and 'costal' parts of the diaphragm as suggested in this paper or is it just a single muscle?

@aliential so it's incorrect to consider there to be a 'crural' part of the diaphragm?

@aliential please do not answer in the comments; comments are reserved for comments, answers for answers. Comments are used to ask for clarifications or to suggest edits. Answers are there to answer the question. Placing answers in comments repels other users to generate a proper answer.

The delineation of muscles is often arbitrary. E.g., quadriceps femoris can be thought of as one muscle or four, depending on how you look at it. A debate over semantics is generally not useful in these situations. Understanding the crux of the matter is more important. In this particular paper, the crux is that the costal and crural parts of the diaphragms work somewhat independently in certain activities.


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Are specialized cells considered to have life?
A common definition of life, including the one in Biology SE Life requires physical entitites to have the capability of being able to reproduce.

A process defining organisms that grow and adapt to stimuli while
maintaining a state of organization and energy production and being
capable of reproduction.

Under this definition one could think that a specialized cell like a bone cell or a skin cell doesnt have life. But also, a common definition of cell, including the one here in Biology SE says a cell is

the smallest unit of life.

So, my question is, are specialized cells which dont reproduce supposed to have life? This question came up to me thinking of other living organisms which have tissues which seems to be inert and survive hundreds or thousands of years (ie, wood, bones, etc.)

I'm not sure if this belongs here and hence it might get closed, but 'life' has several meanings and 'a life' usually refers to an entire organism most notably humans, while cells are 'living' things or 'lifeforms', but it's not common to use 'a life'.

Note that your first quote used the word "organisms," while your second one used the term "life." Are specialized cells in the body alive? Yes, by most definitions they are living. Would a culture of skin cells in a petri dish be considered a viable organism? Probably not. But definitions in biology can sometimes get fuzzy around the edges. The Philosophy stack is probably a more suitable place if you're looking for an in-depth discussion of this question.

It has to belong here, because if Biology deals with life, you can't do science over something that doesnt have a definition. The requirement for doing science over something is to be able to test it, and to be able to test it you need a definition

Life is defined in many ways.
Common definitions are usually simplified definitions. Under some definitions it would be "life" under others it would not be. But it doesn't matter. The problem you are having is thinking definitions of life are anything more than artificial categorization. Really there is no difference between living things and the rest of chemistry, or at least there is a smooth gradient connecting them, but we humans can't easily think that way, so we create descriptive but imperfect definitions to help our thought processes. There is a lot of gray area for any definition of life, and you have found one.

If we use definitions to identify similar properties and the common nature of entities, and be able to build knowledge over it, how is it that it doesnt matter? For example, can I expect a wood cell to biological age? How about a skin cell? How about Taxonomy? There are 103 million entries in Google talking about this branch of Biology, it doesnt seem it doesnt matter to classify living things. I think there should be more discussion on the definition of life if some unidentified definitions are being used to build knowledge in Biology

All of those things can be asked without ever deciding whether the thing is "life" many living things do not age and many do. The difference between life and non-life are arbitrary, a hold over from when we though life was special. Its only useful at the most simple level but once you are talking about biology in any detail the definitions become counterproductive, as can be seen in your original question.

The short answer is that Yes, specialized cells are considered to have life, as are sterile ants that serve the colony but do not themselves reproduce. The definitions that are given for life are attempts to characterize a phenomenon that people are already capable of recognizing. Specialized cells arose out of a reproductive process and they do other life-y things like metabolizing. So they are alive.
If the definition given in a book seems to imply that specialized cells aren't alive, then the definition is ill-formulated, misunderstood, or both.


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What is the difference (if any) between an Intrinsically Disordered Protein and an Intrinsically Disordered Region
The wikipedia definition of an Intrinsically Disordered Protein is a protein that lacks a specific 3D structure.  An Intrinsically Disordered Region is similarly defined.  Why are they often listed separately?  Isn't an Intrinsically Disordered Protein just a protein that has at least one Intrinsically Disordered Region?
Just a couple examples:
https://doi.org/10.1002/pro.3680

In contrast to structured proteins, intrinsically disordered
proteins and regions (IDPs and IDRs)

https://doi.org/10.1146/annurev.biophys.37.032807.125924

There are a number of significant differences between the amino acid sequences of IDPs/IDRs and those of structured globular proteins and domains.

This is surely just plain English. Assuming the explanation in the Wikipedia article is that generally accepted, an IDR is a  disordered region within an IDP, which may have have ordered regions as well as disordered regions (as in the animated illustration). I don’t see your problem. A region is a part of a larger entity. If the whole protein is disordered, then all its regions are, but you can’t talk about the whole protein as a region. (I assume from your name that you are a native English speaker.)


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What is a function-triggering antibody?
I am reading a journal paper on the effect of a neural cell adhesion molecule on neuronal development and in the abstract of this paper I have come across the following:

The autophosphorylation and activity of Pak1 were enhanced when
isolated growth cones were incubated with NCAM function triggering
antibodies, which mimic the interaction between NCAM and its
extracellular ligands.

In this paper, the NCAM protein becomes activated when it is exposed to NCAM function triggering antibodies. I understand that antibodies are molecules produced by the immune system and bind to antigens. However, I am not sure how incubating growth cones with NCAM triggering antibodies would actually trigger/activate the NCAM protein itself.
Isn't the purpose of an antibody to bind to an antigen  so that it can be removed from the body? I am not sure how exposing an antigen its respective antibody would trigger its function. I have read several other papers about neural cell adhesion molecules where antibodies were used to activate their function. I have searched function-triggering antibodies on Google but I have found no useful results regarding this. Any insights are appreciated.

The term "function-triggering antibodies" is not standard, these are more widely known as cross-linking antibodies. As you may know, an antibody has multiple "arms", with the antigen binding region or Fab (Fragment antigen binding) at the end. IgG antibodies have 2 arms, IgM can have 10. The Fab portion is generally identical on all the arms, although it's possible to engineer them differently. This allows the antibody to bind to multiple antigens at the same time, drawing them close together.
NCAM is a homophilic binding protein, with an extracellular domain that binds to other NCAM molecules, both on neighboring cells and on the same cell. That binding induces structural changes in the intracellular domain which promotes the binding and activation of kinases, proteins that phosphorylate (and thus activate or inhibit) other proteins. This starts a signaling cascade that induces changes in the cell, typically by controlling the activity of transcription factors in the nucleus.
Receptors are generally not spread out evenly over the surface of the cell, they often exist grouped together in membrane structures known as lipid rafts. When drawn close enough together, NCAM molecules can begin their signaling cascades on their own, as adapter proteins bound or recruited to the intracellular domains get activated – the kinases and their substrates are in close proximity as well. To induce this type of signaling in the lab, cells can be treated with cross-linking antibodies that draw the receptors together. This in effect triggers the function of the receptors, beginning their downstream signaling.

Source

Thanks for your reply. You stated that receptors are grouped together in lipid rafts located in the membrane. However, I just want to clarify whether NCAM binds to receptors in lipid rafts, and that it is the close proximity of NCAM molecules that can initiate signaling cascades?

Yes. NCAM is a homophilic receptor, meaning that one of its ligands is itself. Cross-linking receptors brings them close together and stimulates internal signaling, including p21.

Antibodies can function as enzymes (see https://en.wikipedia.org/wiki/Abzyme).
If you use the right monoclonal antibody, the variable end can be the right shape to bind to the site you mention.

This is incorrect. The antibodies in question are not abzymes, they're simply cross-linking antibodies that mimic the binding of a ligand to an extracellular receptor.


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What are these structures inside a cut open Allamanda blanchetti?
As suggested by @tyersome in my previous question on the same topic which I posted yesterday, I have cut open few flowers of Allamanda blanchetti
in order to observe if any reproductive structures could be found.
I took 2 buds in different stages of opening as well,if they had some kind of bud pollination. But it seems there is no difference in the bud and bloomed flower.

then I found these  yellow long stiff hairs all stuck together, with some transparent secretion on them,no pollen. I think that these hairs cluster together to form this small star shape projection inside the flower we usually see when it is in bloom.

and this small green bulb like thing with a thread like extension to attach it to the base of the pedicel.
and then on further extending the incision this small swollen part almost like a ovary. But on its transverse section I didn't observe any ovules or placenta inside.

I don't have microscope or other high resolution equipment, I tried looking at it with a magnifying glass but no new details appeared.
So what are these structures? Do they enable sexual reproduction for the plant? Links to related reliable websites are also welcome.

+1 for the dissection and photos. Good work!

This is great — I'm glad you got a good answer. If you have lots of flowers, you might want to try dissecting them at different times (e.g. over a number of days after the flower first opens to see how the fruit develops). You can also try some experiments to see whether these flowers are self-pollinating (e.g. enclose a flower in a bag before it opens) and see whether it makes a fruit.

The third photo gets to the heart of the matter. Here's an enlargement:

The gold-colored areas are the anthers of some of the stamens, the filaments of which are fused with the tissue of the petal.  (This is typical of the Apocynaceae, the family to which A. blanchetti belongs; they have epipetalous stamens, that is the stamens are "adnate" i.e. fused with the petal.) This is the male part of the flower; the anthers have the pollen grains which the plant is trying to get transferred to another flower.
Above the knife is the style.  This part of the female structure is a hollow tube which runs from the openings in the stigma (the out of focus green blob) down to the ovary (not in photo). The central part of the fourth photo is presumably the ovary (missing its style). The ovary contain the ovules which will become seeds after fertilization from pollen which sticks to the stigma and grows a tube down the style.

So the fertilization occurs just like any other flowers[like a hibiscus]? because the anthers and stigma seem hidden .

@AmarylisVaselaar, yes, much like other flowers. Some of structure tries to route the pollinator to the stigma first, then the anthers, for out-crossing. See  1, 2,

Great research articles I couldn't have found them out myself.


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What are the ants underneath leafs in my garden doing?
So a few days ago I spotted a couple of ants underneath some leafs of a major branch of a tree in my garden. Yesterday I had the impression the amount of leafs being occupied by ants has increased a lot what then made me curious. So I spent quite some time yesterday observing one of the minor branches the ants had been very active on by that time. What I figured so far:
Underneath each leaf the ants are gathering, is an insect that looks sort of similar to a fruit fly (gonna call it fruit fly for simplicity, despite it certainly is something different).
Around that insect are varying amounts of dots, which could be eggs or larvae. The ants seem to collect something from the larvae and also seem to be interacting with the fruitfly.

At some point I spotted on the far end of the minor branch 2 living fruitfly. They seemed to be not capable of flight despite having wings. So I concluded they must just have been hatched. They seemed to try escaping the branch, as they pretty directly were just running up all the branch. Having almost made it from the minor to the major branch, the 2 fruitfly came across an ant, which immediately attacked both of them on contact. I was expecting the ant to carry them away then. While being attacked, both fruit fly tried to hide in the attatchment point of a leaf. The ant was circling around the attatchment point of the first fruitfly I was wondering why it did not carry that fly away, since it could clearly geto to that fly. After roughly a minute the ant turned back to their hide, having fully ignored the second fly, after attacking it once, and also leaving the first fly motionless at the attatchment point it was trying to find cover in.
But what happened a few minutes later is what left me astonished.
A few minutes after the 2 fruitfly had been attacked, roughly at the same time, they started moving again. But different then before (kinda looked as if they had been injured but not killed by the ant). They did not seem like trying to escape the branch anymore. But just slowly moving to the next leaf in range continuing for 1 to 2 centimeters going underneath the leaf and then stopping there. Pretty much being in a position, as a fruitfly is positioned underneath the other leafs, where the ants are gathering .
After like 4 or 5 hours 1 ant for the first time scouted the leaf these 2 flys went on. And in fact, other than attacking them again, this ant interacted with the 2 fruitfly1 like the ants under the other leaves interact with the fruitfly positioned on those leaves.

By now (over 12 hours later) the 2 fruitfly are still there I just checked and the small fruitfly that was only being attacked once, disappeared. The other one still being at the very same spot it moved to yesterday, tho. I would consider them being dead. But I am not even sure about that.
So what exactly are the ants I observed there doing?
If any other pictures would be helpful ask for it, I can take them later today.
Also I have a speculation what it could be that was going on here, but not sure if that would anyhow improve this OP.
Oh, since I can't identify the species, it might be useful to know at least: this is happening in Bavaria - Germany

1 well with 1 of them, the other that had just been attacked once, was simply being ignored

From what you described, it seems to me the "fruitflies" are aphids and the ants are farming them. This is a widespread and common phenomenon known as ants-aphid mutualism.
P.S.
I elaborate a bit. Aphids feed on plant sap, rich in sugar, which they don't digest completely. The excretions (poop) are thus still rich in sugar (you may have noticed how your car windows get sticky sometimes under tress - that's aphids poop, I believe). Some ant species co-evolved with particular aphids and collect their excretions, a valuable sugary energy source. In turn, ants protect aphids from predators and they move them around to cover other good plant spots for aphids to suck sap and even move them to different plant individuals. This mutualistic interaction between aphids and ants is quite common and causes a lot of economic losses to the agriculture sector.
The behavior you observed of an ant attacking aphids was probably more the ant checking them and trying to evoke a pooping response. Sometimes they get them between their jaws and carry them around. Aphids also have quite complex social structure, with an optimal spatial organization. Hard to say if ants are moving them around to reach this optimal "farm density" or for other reasons.
TL;DR ants farm aphids as humans farm cows. When ants interact with aphids they are mostly checking them and trying to get their sugary poop.
/Emilio

Yeah, I can Identify the "fruitflys" as one of the kinds being found in that wikipedia article you linked. But could you please elaborate a bit more on what is going on there? I.e. where were those individuals coming from that had been attacked in my observation and i.e. why had they been attacked? And why the attack seemingly caused a change in their behavior?


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CML (Chronic Myeloid Leukemia) and blast cell percentage
I'm trying to understand the oncogenesis of CML. I have a question about CFC cells and blast cells. Are those the same? I know that in the chronic phase of CML there is a blast percentage of 1-10% of blast cells in the blood. Considering that the total amount of WBC is around 1x10–11 cells/l. That means the blast cells should be around the same order of magnitude. Looking on research articles I found that the amount of CFC (which contains according to my understanding all of the blast cells) are only 1x10–8 cells/l. Thus comprising around 0.1% of the blood count.
What cells can be considered as blasts? Only the myeloblasts? Are all blast cells CFC cells?
I also know that the average value of CFC cells in the bone marrow is around 10–5 cells, so how can they be 10–9 cells?
Reference:
https://pubmed.ncbi.nlm.nih.gov/9922073/

Not to be rude, but are you sure you read the article?  Figure 1 describes the CFU ontology and defines CFC as experimentally-determined CFUs.  Table 2 describes the relative number of each CFU per 10$^5$ marrow cells.  Those numbers are much closer to your 0.1% figure than the 1-10% value expected during chronic-phase CML.  Re: your final question, leukemia is pretty much defined by immature cells leaving the marrow, which would elevate the PB levels.  Ta-da!

I did read the article, but I'm learning about leukemia to make inter-disciplinary research, it's not my field of expertise. I am pretty confused about the percentages. If the CFC build up <1% of the cells in the bone marrow and immature blast cells are contained within the CFC compartment, how can they be present at 10% in PB? The only possible solution for me is: The 10% blast cells compromises not only the CFC but other types of cells. Which other types of cells? It seems that every article assumes a definition of blast cells I just don't find anywhere. Thank you for your help.


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What species is this colourful caterpillar?
What species is this colourful caterpillar found on a road in Central Europe?

Just by its appearance and location, that’s maybe a Pale Tussock (Calliteara pudibunda), a kind of moth found in Central Europe.
You can find some observations of that species on iNaturalist: https://www.inaturalist.org/taxa/205294-Calliteara-pudibunda?locale=en-GB


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What does it mean for a protein to be dominant-negative?
I am reading this journal paper, which investigates the interaction of the NCAM protein and the Pak1 protein. In this paper I have come across the term "dominant-negative Pak1" and "constitutively active Pak1". I am not sure what exactly is meant by a protein being dominant-negative. I have searched online and found that dominant negative refers to a mutation whose gene product adversely affects the normal wild-type gene product within the same cell (with this occurring if the product can still interact with the same elements as the wild-type product, but block some aspect of its function).
Would I be correct in inferring that dominant-negative Pak1 is a mutated version of the wild-type Pak1 and interferes with the normal activity of wild-type Pak1 in cells? Any insights are appreciated.

You've got it. A DN not only doesn't have the desired catalytic activity, but it also binds to or otherwise inactivates WT enzymes, in effect "knocking out" that particular enzyme in the cells. The protein itself is still there, it just doesn't perform its normal function.


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Can the extinct Chinese Paddlefish be revived?
I learned that a rare and unique giant Chinese Paddlefish recently became extinct. I'm wondering if samples of DNA were collected by scientists to allow reviving of the specie in the future.
My quick Google check only revealed one paper that studied DNA of the fish 15 years ago - so there is a possibility that some DNA information exist out there. But is it enough to restore the species?
I'm interested in learning about any organisations or projects that would systematically collect genetic material of all endangered species. Is there a way to ask them about this specific fish?

Informally speaking, there is no real/good way to bring back extinct species. Especially sexually reproducing species; you'd need to revive a male and a female at the very least, and these are markedly different genomes due to unique sex chromosomes.
Some 'bad ways' exist though; in principle, if you found a perfectly preserved nucleus (the organelle that holds genomic DNA of most eukaryotes), it may be possible to insert this nucleus into a sibling or sister species (e.g. wooly mammoth nuclei into denucleated elephant zygotes). This would be the cloning approach. However, you then run into practical issues. You have to guarantee that this embryo will implant itself, which itself is not always the case. The nucleus and chromosomes must also be intact enough (which may not be the case after storing them, e.g. in ice, which may require thawing which often damages cellular structures) to create a rather healthy, fertile organism that will breed at a sufficient rate to restore a stable population. These and many more complications will reduce your chance of rescuing an extinct species to near-zero. Even then, one could argue that it is an incomplete de-extinction because you've only substituted the genomic DNA, and not other parts of the genome (e.g. chloroplast or mitochondrial genomes) which are part-and-parcel of the genetic signature that makes a species a species.
Alternatively, you can create hybrids where fragments of DNA from extinct species are brought into the genomes of similar existing species, by molecular methods such as recombination using CRISPR/Cas9. Here though you are only creating hybrids, not reviving extinct lineages. The extent to which you could do this is also limited and you would have to increasingly troubleshoot why a hybridization didn't work the more host genome you replaced with the extinct species' genome. Transgenesis using individual genes (say, transfering an enzyme into a new organism) is quite plug-and-play, but replacing entire chromosomes would be near impossible to pull off, not least because you would have little insight into why things aren't working - only that they aren't.


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What does Δcys mean after a gene name?
I am reading a paper and I have come across the following statement:

"Plasmids encoding full-length NCAM140 and NCAM140Δcys, intracellular
domain of NCAM140, and the NCAM140ID729–750 fragment were as
described".

I know that NCAM140 is an isoform of the NCAM protein with a molecular weight of 140kDa. However, I am not sure what Δcys means in NCAM140Δcys. Any insights are appreciated.

When describing mutations, $\Delta$ usually stands for deleted sequences. In this case it means the exchange of 4 cysteine residues in the NCAM protein by serines to disable palmitoylation and the association of the protein to lipid rafts. If you search for this specific mutation, you will find the paper from Niethammer et al., 2003, which describes the mutation. Figure 2a (below) shows a schematic view of the locus and is described as following in the caption:

Mutation of NCAM140 palmitoylation sites abolishes NCAM140 raft association.
(A) Schematic diagram of the structure of NCAM140 and
NCAM140Δ. The plasma membrane is indicated by the pair of vertical
lines. The semicircles represent the five Ig-like domains. The two
fibronectin type III–like domains are shown as black boxes. The
expanded segment shows the NH2-terminal sequence of the cytoplasmic
domain and the four cysteines that were mutated to serines in the
NCAM140Δ construct to remove all sites for palmitoylation.


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Are the controls for RT-PCR the same as those for RT-qPCR?
I am searching for negative and positive controls for RT-PCR but all the results seem to point towards RT-qPCR. Are the controls the same for both?
I have found

-RT control
No template control
exogenous control
endogenous control
no amplification control

Do they apply for both or just RT-qPCR?

Those acronyms get slung around a lot with slightly different definitions.  RT = reverse-transcription and q = quantitative?

@Punintended yes, that's what they mean to my knowledge. but since the steps differ in both these methods I was wondering if the same controls applied to both.


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Meaning of “gene expression heterogeneity” of embryonic stem cells
What does it mean if a gene has a heterogeneous expression? Does it describe the differences of patterns of expression of that particular gene in a population of cells that are identical? The papers I have found did not really elaborate on what it meant, and I do not know where else to find the definition.
In particular, I want to understand heterogeneity in the context of stem cells. In the paper by Angarica and Sol, 2016, it reads:

“Experimental studies at the single-cell level have revealed that embryonic stem cells (ESCs), and more generally pluripotent stem cells (PSCs), exhibit significant gene expression heterogeneity.”

“Single-cell studies have allowed gene clustering, depending on the levels of heterogeneity in the gene expression landscape in PSCs.”

Does it have more to do with the variation of its expression in the population?

“In mouse ESCs genes exist that are uniformly expressed in most cells and exhibiting a unimodal distribution (Oct4, Rest, Tcf3, Sal4); other genes exhibit bimodal expression and are expressed in some populations but not in others (Nanog, Rex1, Tet1, Esrrb), and yet another group of genes display sporadic expression (Neurod1, Klf4, Otx2, Pax6) and are undetected in most cells but highly expressed in some speciﬁc subpopulations.”

Reference:

Angarica and Sol, 2016, Modeling heterogeneity in the pluripotent state: A promising strategy for improving the efficiency and fidelity of stem cell differentiation.

Heterogeneity is a noun meaning:

the fact of consisting of parts or things that are very different from each other

In scientific use the context determines what is differing.
The context here is gene expression in individual embryonic stem cells (presumably single-cell RNASeq). Here the heterogeneity in expression would be for the genes

…(Neurod1, Klf4, Otx2, Pax6)

for which the expression is

…undetected in most cells but highly expressed in some specific subpopulations.

The conclusion is that although the embryonic stem cells may appear to be a homogeneous population (all alike) and do show similarities in many genes that they express, they must, in fact be a mixture of two (or more) types. (This makes the generally accepted assumption that the basis for distinguishing cells is the genes they express and the proteins they make.)
Thus the idea, expressed in the question, that the cells are identical is incorrect. I know little about stem cell differentiation, but I would assume the implication is that the subpopulation will differentiate on a different path to the rest of the population, or that it has already started to differentiate, or something of the sort (which I imagine is discussed in the paper).