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When was the germ theory officially accepted?
Is there a specific year that marks the official acceptance of the germ theory? In the references, it is always quoted the work of Pasteur, Koch, and Lister, but their work is spread over decades and does not mean that their papers were accepted by the medical community.
Is there a watershed year instead? Perhaps a peculiar conference where the doctors wrote black on white that the new theory had become the new paradigm? Or a paper that encountered the agreement of all the peers?

Perhaps Max Plank's famous quote, "A new scientific truth does not triumph by convincing its opponents and making them see the light, but rather because its opponents eventually die, and a new generation grows up that is familiar with it.”  applies here?

Since this appears to be a historical question rather than one asking about biology as defined in the [help], I think this would be more appropriate on [HSM.SE]. If that is what you want, please delete your question from this site before reposting there because cross-posting is impolite. Alternatively, you can request migration of this question by flagging your post for moderator intervention and explaining what you want and why.

The decades long process apparently is still under way.

As in most sciences, there’s not really such a thing as “officially accepted” in Biology because there is no office and no officials who have that authority.  Rather, the usual term that I have heard is “generally accepted”.

I’m voting to close this question because it is asking for an opinion (judging whether something is "official accepted") as well as being off-topic for this site.

I don't think this is off-topic here as it asks for the process of the acception of a scientific idea.

@Chris — Even with that generous interpretation this still seems opinion based to me, as well as being focused on history rather than anything biological.

It was only after Darwin's 1859 theory of evolution sparked an interest in chemical evolution as an explanation for life that the germ theory was accepted. ref As a comparison theory, it took until the 1950's for a majority of scientist to agree that evolution was caused only by natural selection, a 90 year gap until consensus.
Pasteur published his germ theory in 1861. It took about twenty years for the most eminent international scientists (i.e. Tyndall) to give conferences on it in the UK and for Koch to evidence it in Germany. From the 1880s, Germ Theory was hugely influential, affecting nearly every aspect of medicine including public health, surgery, hospitals, training and treatments. In the 1950's we can find books like i.e. "Pasteur, plagiarist, imposter: The Germ Theory Exploded"
In France, Louis Pasteur was elected a free associate of the French academy of medicine in 1873, won the Copley medal of the Royal Society of London in 1874, medal of Grand-Officier de la Légion d'Honneur in 1878, and designed a vaccine for sheep in 1881.
Following France, Germany was one of the first to officially recognize germ theory:
On 24 March 1882 at the Berlin Institute for Physiology, Koch announced the discovery of the tuberculosis pathogen – with his lecture on the “Aetiology of Tuberculosis” he became world famous overnight. In the course of the 19th century, Roughly a seventh of the population of the German Reich died of the disease. Now Koch demonstrated that tuberculosis was triggered by the tubercle bacillus.
In 1885, Friedrich-Wilhelms-University in Berlin founded the Hygiene Institute, which was managed by Robert Koch.
In 1891, Koch agreed to direct the newly-founded Royal Prussian Institute for Infectious Diseases. ref
He was awarded the Nobel Prize in Medicine in 1905.
A famous epidemiologist, William Farr, working on cholera, published "a monograph" which showed that mortality was extremely high for people who drew their water from the Old Ford Reservoir in East London. Farr's work was then considered conclusive... Physicians were publicly denouncing germ theory in major newspapers 20 years later:
Irish physicist and science popularizer John Tyndall was superintendent at the Royal Institution in London and had published scientific works on heat, light and sound, as well as popular books. His ideas on germs became controversial in January 1870 after giving a lecture to the Royal Institution entitled Dust and disease. Here, he first reported experiments demonstrating that dust was mainly composed of organic matter, something he had not anticipated. He then demonstrated, using his light scattering assay, that air filtered by cotton wool was ‘optically empty’, meaning that the path of the beam appeared black, which he also saw with air that had been left to settle for long periods of time in a sealed glass chamber. Finally, he reported that his own breath, especially the end of his expiration, was remarkably free of floating matter. He had recently been taken by Lister’s methods for antiseptic surgery, which argued that infection spreads through the air due to the microbes contained within it and viewed his data as entirely consistent with these. Hence, Tyndall extrapolated his conclusions to make a strong statement in favor of the germ theory of disease; an idea which had not yet found acceptance with the majority of the English medical profession. Following Tyndall’s 1870 lecture, there was much criticism of his conclusions from prominent physicians who believed that ideas relating to the nature of disease ‘pertain most to the biologist and the physician’ and that a physicist should know better the facts of epidemic disease before delving into the living world. The pathologist Charlton Bastian confronted Tyndall directly in a series of letters to The Times, playing down the evidence supporting germ theory and discussing his own experiments which disagreed with previous work by Pasteur, Lister and the like. Bastian then published a 1,115-page book in 1872 describing many experiments that he argued proved that microbial growth could occur in conditions in which Pasteur argued...ref

A majority of scientists accepted evolution via natural selection as long ago as the 1950s? Damn, seems like the rest of American society is lagging very far behind. Did most of those scientists also believe in Human evolution?

87% of Americans with a science degree believe in the theory. https://en.wikipedia.org/wiki/Level_of_support_for_evolution#United_States

@TKoL I think you'll find that the general population lags behind scientific consensus in just about every field, and particularly in America where we seem to have a prevailing sense that the lay person is just as qualified to decide the truth of a topic as an expert is

@TKoL By the time Darwin published the Origin, evolution in the broad sense of "change over time" and life unfolding in a gradual process was already broadly accepted by scientists, the public, and influential clergymen who saw divine intervention in evolution as a crude view of God. By 1874 Tyndall could declare almost unchallenged that creation was a natural processes in which God played no scientifically detectable role. But prominent scientists had serious reservations about natural selection as the mechanism which persisted until the Modern Synthesis in the 20th century.


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Is there an equivalent to vertebrate endogenous retroviruses in invertebrates or microbes?
I know jawed vertebrates have a lot of junk DNA floating around coming from ancient retroviruses. Some of the DNA is important to mammalian evolution. The DNA also provides a useful means to study the evolution of viruses.
I wonder if similar things happen for other lifeforms. I know parasitic wasps have a very interesting story even if I don't know the details.
I suppose even if viruses inserted themselves into microbes that microbes have much more pressure to have less DNA and so they may have gained genes but the evidence of junk DNA would have long ago been lost.
I suppose I'm asking: did ancient viruses insert themselves into other life in a similar manner to the endogenous retroviruses found in vertebrates and would we have evidence of it today in a similar manner?

I would not say that they are “equivalents” of endogenous retroviruses, but there are two types of elements in bacteria that bear some similarity.
Prophages
As some bacterial virus (phages) can undergo lysogeny as well as causing lysis of the host (e.g. phage lambda) it is not surprising that there are traces of phages in almost all sequenced bacterial genomes, although it is not always easy to detect and/or identify them unequivocally. This was reviewed by Casjens in 2003 who considered its significance in terms of the evolution of both phage and bacteria.
Of course, the structure of such phages differs from that of endogenous retroviruses and is generally much more complex.
Insertion Elements (IS)
To some extent endogenous retroviruses can be considered as retrotransposons elements, and this is certainly the case for the related LINE (L1) elements. So perhaps the bacterial insertion elements — the IS transposons — are worth mentioning. The structure of one class is shown below.

(Source: https://commons.wikimedia.org/wiki/File:Composite_transposon.svg)

source: Stack Exchange

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

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Identify this bone found on beach
Does anyone have an idea what this bone is?
It was found on the beach in the Outer Banks, North Carolina, USA.

Can you show another angle or two? I think I know what it is, but would like to see the whole thing. I can only guess right now.

Im sorry having issues posting additional pictures on site.  I did take more though…. Ill work on figuring posting.

Imgur, our image repository doesn't seem to work well with Amazon shared photos, you can however upload direct to imgur from your phone/desktop through the question interface, that works best.

@anongoodnurse are you able to see the photos I posted?

Welcome to Biology.SE. All I see are bare links — one of the requirements for posts on this site is that they are self-contained. That means (among other things) that all photos must be uploaded to the site. Is there some reason you aren't able to follow the suggestion made by A Rogue Ant?

I think they are working now.  Will only allow me to post 2.

Great! You can add supplementary links to your post for the other pictures — it is just important that users don't have to leave the site to understand the question. (I see that I worded that unclearly before, sorry about any confusion.)

maybe a skate synarcual but that is a wild guess.

On the second pic i can see cellular structures in the well focused zone, I wonder if they give an idea of the family of the animal.

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


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Didehydro cysteine as a modification in unreduced/unalkylated proteomics
I am analysing proteomic data, some of which was digested with the Thermo SMART Digest Kit and some by in-gel digest. I am not a laboratory scientist, and have noted that the samples processed with SMART Digest Kit have very low proportion containing cysteine residues (~0.5% compared to 30% with in-gel digestion). We now have a belated realisation that the SMART Digest Kit does not reduce or alkylate proteins, and that thus disulfide bonds will largely remain.
In an aim to recover as much data as possible, I tried removing the fixed carbamidomethyl mod, however only a few unmodified Cysteines are found. I performed an open search on a small subset of data obtained with high fragment ion resolution, and identified a number of peptides determined to containing cysteine with a -2.0157 Da modification, labelled as "2-amino-3-oxo-butanoic acid" or "didehydro [cysteine]" (shown is -2H on https://www.unimod.org/modifications_view.php?editid1=401). [ed - I appreciate this is not a recognised modification of cysteine!].
If I undertake a fixed search with this as a variable modification I find many more cysteine containing peptides (up to 5%) with a majority with this -2H modification.
However, this modification doesn't seem to be a recognised one for cysteine, and I am no chemist. I wonder if anyone has come across this modification before and can explain it? Ed - I presume it's more likely to represent a different amino acid with a modification which gives a near-identical mass to cysteine -2H.
Incidentally, despite the claims that the SMART Digest kit has immobilised trypsin which should not auto-digest, we have very strong signal from trypsin auto-digestion products!

Welcome to Biology.SE. The link you give doesn't list that modification as being associated with cysteine (or with cystine for that matter) — can you clarify why you think 2-amino-3-oxo-butanoic acid is associated with cysteine? Also, didehydro should be followed by what is being modified — what is it? Please [edit] your post to clarify. Also please note that 'thanks' and 'signatures' are not used on SE sites, so I will edit your post to remove them.

Never mind about my previous didehydro question I reread your title. However, didehydro cysteine is not the same thing as 2-amino-3-oxo-butanoic acid ...

Thanks @tyersome - I am also unclear why the -2H modification is described as both didehydro and 2-amino-3-oxo-butanoic acid. Perhaps this is the residue that results when a specific amino acid is "didehydrated."  I don't know enough chemistry to to know if cysteine can be "didehydrated," and I wonder if it's more likely if I'm finding amino acid variants where cysteine has been replaced. No amino acids are constituted by C3H3ONS. The modified monoisotopic mass corresponds to 100.99354 which is closest to the mass of threonine (101.04768), but this is orders of magnitude above a 20ppm error.


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Difference between IC50 and Michaelis-Menten constant
I am new to biology, and getting to know the term IC50, I found that there is a connection between IC50 and Michaelis-Menten constant by the Cheng-Prusoff equation
$K_{i}=\frac{\mathrm{IC}_{50}}{1+\frac{[S]}{K_{m}}}$
where $\mathrm{K}_{\mathrm{i}}$ is the binding affinity of the inhibitor, $\mathrm{IC}_{50}$ is the functional strength of the inhibitor, [S] is fixed substrate concentration and $\mathrm{K}_{\mathrm{M}}$ is the Michaelis constant in the MM equation:
$\textrm{rate} = \frac{V_{\text{max}} [S]}{K_M + [S]}$
where $V_{\text{max}}$ is the maximum rate of reaction.
Suppose IC50 of the drug is $x$. From my understanding that means- the concentration needed to decrease cells viability by $50 \%$. Since Michaelis-Menten constant means the substrate concentration such that the reaction rate is half of maximum, it seems quite the same. What is  wrong in my view? Both seems to cause $50 \%$ of effictiveness

I have added a ref to Cheng-Prusoff.  I hope you don't mind. I was tempted to modify your opening sentence to "... Michaelis-Menten constant by the Cheng-Prusoff equation for competitive inhibition", but I was afraid I might change your meaning. In pharmacology, especially when dealing with receptor-agonist relationships, it is often assumed that inhibition is competitive (see here, for example). But there is the rub with IC50 values: how do you know that the inhibition is competitive?


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Calculation of solute, pressure and water potential
What would be the water potential (Ψw), solute potential (Ψs) and pressure potential (Ψp) at equilibrium when a cell with Ψs= – 0.7 MPa and Ψp= 0.7 MPa is placed in a solution with Ψs= – 0.5 MPa?  (Source)
a. Ψw= – 0.2 MPa, Ψs= – 0.5 MPa, Ψp= – 0.5 MPa
b. Ψw= – 0.5 MPa, Ψs= – 0.7 MPa, Ψp= 0.2 MPa
c. Ψw= – 0.5 MPa, Ψs= – 0.5 MPa, Ψp= 0 MPa
d. Ψw= – 0.3 MPa, Ψs= – 0.3 MPa, Ψp= 0 MPa
Water potential in the cell (before being placed in the solution) will be zero. But after it is placed, due to exosmosis water should move out thereby decreasing its water potential. But by how much does the water potential decrease (when the cell is in equilibrium) and what effect that might have on the cell's solute and pressure potential is what I am unable to calculate.


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Is the human mouth more burn-resistant than other animals which don't eat cooked food?
I burnt my mouth on some hot pizza and it got me wondering if we have been eating cooked food long enough to have evolved a better resistance to oral burns than other species. Have there been any studies on this?

Possible duplicate of https://biology.stackexchange.com/q/35532/27148 - to evolve a trait by selection it has to have some fitness benefit. For humans to evolve protection against pizza burns it would have to afford a survival/reproductive benefit, not just be a "nice to have".

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

Does this answer your question? Why do some bad traits evolve, and good ones don't?


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Inheritance likelihood of SNVs vs InDels
Suppose you have identified a couple of variants in a tumour sample. One of them is a deletion and the other is an SNV in the same gene. You have a familial history of prostate cancer and other cancers. The germline testing results are several weeks away but in the meantime how would you decide which one of them is inherited and which is somatic. They both could be somatic or inherited but for sake of curiosity let's consider they are different.

I don’t understand the question - are you asking whether there is a difference whether SNPs or indels occur on germline or somatic cells?

Welcome to Biology.SE. Thank you for taking the [tour], please also go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, your question: 1) isn't clear, 2) is overly broad, and 3) shows no evidence of prior research. Details: 2) among other things you haven't specified what gene(s) you are interested in. 3) you haven't said where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Please note all of these are reasons for down-voting and closure.


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How does Clostridium perfringens cause target hemolysis?
I am studying microbiology as a part of my course and I was studying Clostridium perfringens.
While studying its hemolytic characteristics, I came to know that it causes target hemolysis (i.e. zone of beta hemolysis due to Theta toxin surrounded by zone of alpha hemolysis by alpha toxin).
Surprisingly alpha toxin has a Phospholipase-C (PL-C) like action. Isn't PL-C supposed to be Beta-hemolytic? Since it will lyse the RBC membrane?
[Alpha-hemolysis is supposed to be conversion of hemoglobin to methemoglobin]


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Is there a term for fixation OR loss of an allele?
I remember reading a paper which used a term to describe either fixation OR loss of an allele via drift. Its definition is basically "the removal/fixation of a polymorphism in a population due to the action of genetic drift". An example of how it could be used in a sentence is:

The expected time to term is dependent on the effective population size of the population, $N_e$.

I can't for the life of me remember the term, or the paper, and it doesn't appear to be common in the literature as I haven't encountered it again. It's driving me insane! Does anyone know what this term might be?

It seems like “equilibrium” may work, though that is likely more general than the term you are looking for.

Also, I've heard "extinction or fixation" used in this context, re: The expected time to extinction or fixation is dependent on the effective population size of the population...


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is pepsin able to break down proteins into amino acids in human stomach?
I'm trying to find out if pepsin can break down proteins into amino acids after they are converted to peptides. Is pepsin able to separate amino acid monomers from the peptides?
can you please show me the actual reaction happening in the process?
I'm a 10th-grade student so please describe it as suitable for my knowledge.
thanks in advance.

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


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In enhanced chemiluminescence in western blots, will the horseradish peroxidase eventually get used up?
I am learning about enhanced chemiluminescence in Western blots. I have read online that in enhanced chemiluminescence that horseradish peroxidase (HRP) catalyses the oxidation of luminol to 3-aminophthalate, with this reaction resulting in the emission of light. I am using HRP-conjugated secondary antibodies on my Western blots, and applying the ECL reagent to the membrane to detect the signal.
I was wondering, in this chemical reaction, if the ECL reagent is left on the membrane long enough, will eventually all the HRP get used up (especially if you reapply the ECL reagent to the membrane)?

I’m voting to close this because it is unclear what you mean by "used up": Consumed as a reactant? OR Are you asking about the stability of HRP over time? In either case this seems like something you can easily look up so in addition to being unclear it is under researched. Finally, from the way this is currently phrased it appears you mean the first of these possibilities, which seems like "homework" — i.e. "trivial to biology professionals".

The HRP is an enzyme so it isn't a component of the reaction. By definition, enzymes only catalyze reactions but aren't an actual component of the reaction. As such they don't get used up during the reaction and are able to continually catalyze molecules until they run out of luminol in this case. The only thing to be concerned about is the membrane drying out and denaturing the HRP.
An anecdotal story, but I remember an intern dropped an extremely diluted microliter (~1/200k) of HRP conjugate into a liter bottle of TMB (A liquid that turns blue after exposure to HRP) and the entire liter bottle turned deep blue overnight. So a tiny amount of enzyme definitely didn't get used up despite a massive molar excess.


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

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

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

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

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

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


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Time required for DNA replication in E. coli
In a particular strain of E. coli, it was observed that DNA polymerase could add nucleotides to a growing chain of DNA at the rate of 600 per second. If the genome of this organism is 1.1mm long wherein a base pair occupies 0.34 nm, then how much time (in minutes) would be required for the complete replication of the chromosomal DNA molecule?
(Report the closest integer value.) {Source}
I solved this question using this method.
No. of base pairs: $ \frac{1.1  \times 10^{-3} \space m}{0.34 \times 10^{-9} \space m/bp} = 3.23 \times 10^{6} \space bp$
Time required for replication (in minutes by the DNA Polymerase) = $ \frac{ 3.23 \times 10^{6} \space bp}{(600 \space bp/s)\times (60 \space s/minute)} =89.86 ≈ 90 \space minutes$
The answer, however, is 45 minutes. What am I getting wrong?

Remember that E. coli has a single circular chromosome, and that chromosome is replicated bidirectionally. Hence, your calculated value (90 minutes) is exactly twice that of the correct answer.


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What options are available for high-throughput isolation and identification of microbes from soil?
I have a lot of experience with isolating individual colonies / species / organisms from the environment and then sequencing them for identification, but the process is slow and cumbersome.
My goal is to build an organism library so actually having the individual isolates is desired. The metagenomic approaches are great for screening a pool of organisms for something I'm looking for, but I still have to separate it out if I want to keep it.
I currently create soil dilutions, plate them, isolate colonies early on to create axenic cultures and then DNA barcode the microbes. This process is time-consuming and often biased towards faster growing microbes.
Are there any high-throughput methods of isolating and identifying microbes (mainly fungi and bacilli) from a mixed-substrate like soil?
A literature search on this subject doesn't reveal many options that are currently accessible. I'm seeing some research on microfluidic devices that may help, but I'm not aware of any microfluidic platforms that are available to consumers.
Aside from this technique and microfluidic techniques (not currently available to my knowledge), are there any other techniques to consider to improve throughput?

Can you please provide more detail and focus your question a bit more narrowly as this kind of open ended question isn't a good fit for this site. (e.g. Do you really need to isolate and why?) ——— If I search for "soil genomics" the top two hits are articles from Nature Reviews Microbiology titled "Soil genomics" and "The metagenomics of soil". Have you read these and looked for more recent reviews and articles that reference them? Does this not allow you to find answers?

The question is very specific: what high-throughput methods are available for isolating and identifying microbes like fungi and bacteria? I don't know how to make it more specific than that. I stated what I want to do which is separate (isolate) the microbes and identify them (their species). I would like to know what high-throughput methods are available. The reason why has nothing to do with the question.

Have you looked into metagenome-assembled genomes? E.g. don't bother with isolation, just process everything together and rely on data analysis to pull the different genomes apart. This can be done with or without extra lab steps that add additional info (I once worked at a company that did this as a service: https://phasegenomics.com/products/proximeta/, so conflict of interest there). This is pretty routine at this point. You can also do it on standard shotgun metagenomes (e.g. https://www.nature.com/articles/s41587-020-00777-4), it's just slightly messier.

I'm building an organism library so actually having the individual isolates is desired. The metagenomic approaches are great for screening a pool of organisms for something I'm looking for, but I still have to separate it out if I want to keep it.

Do you now see why I suggested you tell us why you want to do this? SE sites get many questions that fall into a trap known as the X-Y problem, which means it is almost always a good idea to include "why" information in your questions. It is also best to include such information in the text rather than responding in comments — this is because comments are ephemeral and often overlooked. Finally edits should be incorporated directly into the text and not labeled — changes are tracked by the site anyways.

If your goal is just to get a lot of unique isolates, picking colonies from agar plates is pretty much a necessary evil. Colony picker robots can automate that part of the process. One potentially faster alternative to DNA barcoding is whole cell MALDI-TOF-MS, which can dereplicate isolates and potentially ID some of them with medium-ish throughput. I can pick and screen about 1000 colonies in a day without automation. Most of the ID libraries are geared for pathogen ID, so you'd probably end up sequencing still. But you can add your own spectra as your collection grows.

I've looked into MALDI-TOF but it seems like there are two big issues: one is that even if there is a strain of interest found in the results, I still need to go through the process of plating and isolating it and hoping I can distinguish it morphologically from the rest. The other is price. I'm an indie scientist and can't spend $20K on a machine like that. Curious to hear your thoughts on it though. Appreciate the info for sure.

@tyersome I can see your perspective clearly, yes. Can you understand how I might also see from my perspective that the question was clear? I don't think either side is all right or wrong. Clearly, SE admins/users/mods are trying their best to deal with an onslaught of low-quality questions. But as a long-time user, I am frequently met with downvotes and negative reactions for not asking a question in just the right way. It's a negative experience for both of us. I don't know the solution but I'm not alone in these thoughts.

@MikeyC I'd love to pick your brain more if you'd allow for it. Is there a way I can connect with you? I'd like to learn more about how you're able to screen 1000 colonies without automation. And what does screen mean exactly? (ID, assay, isolate, etc.) Thank you kindly.

@doremi No automation in the sense of robotic colony pickers or sample prep. It takes me roughly 30 minutes to spot 96 colonies onto a disposable MALDI target chip. The raw data is a peptide mass fingerprint (PMF), from which the software can generate IDs down to the species level, but only for organisms in the database. For colonies with no ID, there are dedicated Python packages for binning spectra into groups likely to be the same species. From there you could sequence as many isolates per bin as you deem necessary to confirm the identity of that PMF-type.

@MikeyC Got it. I'm hearing many folks warn about the limitation of the databases. That's  going to be a deal breaker for me since most of my target organisms are non-pathogenic and often only recently described. Thanks again.

Hard to know what you would consider "high-throughput", but it might be worth checking out the work by Kim Lewis at Northeastern University — see for example his 2020 Perspective in Cell1.
One of the tools his group uses is what they call the ichip, which allows them to grow "uncultivable" microbes2. This is done by placing the device in soil after sealing in 384 separate samples.
References:

Lewis, K. (2020). The science of antibiotic discovery. Cell, 181(1), 29-45.

Nichols, D., Cahoon, N., Trakhtenberg, E. M., Pham, L., Mehta, A., Belanger, A., ... & Epstein, S. (2010). Use of ichip for high-throughput in situ cultivation of “uncultivable” microbial species. Applied and environmental microbiology, 76(8), 2445-2450.


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Nondisjunction of chromosomes
Why is it that nondisjunction of chromosomes usually happen in the egg, followed by in the sperm, followed by in the embryo? Why isn’t there also a chance that it occur in any cell cycle at any point?
So, why does it usually occur during meiosis and not in any cell undergoing mitosis, except perhaps early in the development of the embryo?
And
Why usually the egg and not the sperm?
Non disjunction can occur in meiosis I,II, or during mitosis when chromosomes fail to separate during anaphase which leads to aneuploidy daughter cells or germ cells.
Most resources, including McMaster pathophysiology review, explain the mechanism of failure and remark that most occur during the formation of the egg, a few during spermatogenesis, and very few during mitosis leading to mosaicism.
I can not find any resources that explain why the probability of aneuploidy would differ between oogenesis, spermatogenesis, and mitosis.
Why isn’t it that the cell cycle can malfunction and produce cancers but I have never heard of a tumor of aneuploidy cells?

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

Haha. Ok. This is the first time I ever used stock exchange because I’ve always been successful finding the answers to all other questions. I just assumed this is where one goes when one had already exhausted all other avenues.

I think you mean "nondisjunction" rather than "disjunction".
From "Genetics, Nondisjunction" at NCBI,

Nondisjunction can occur during anaphase of mitosis, meiosis I, or meiosis II. During anaphase, sister chromatids (or homologous chromosomes for meiosis I), will separate and move to opposite poles of the cell, pulled by microtubules. In nondisjunction, the separation fails to occur causing both sister chromatids or homologous chromosomes to be pulled to one pole of the cell.

There's more info in the linked page.

Thank you for the article. It adds significant detail to my understanding. Is there any additional information as to why the nondisjunction occurs principally during meiosis and not mitosis and why it is more often during egg production and not sperm. I would have guessed that the probability of nondisjunction would be equally likely during any anaphase in any cell cycle.
And, thank you for the correction. I edited the question to correct “disjunction” to “nondisjunction.”


text:
Rapid generation advancement in Maize breeding
Maize (Zea mays L.) is one of the important crops and its acreage is increasing considerably especially in Asia and Africa.  The common production system in tropical and subtropical climates is rain-fed. From the “Mendelian era” of nineteenth century we have now reached the stage of “Genomics era” in twenty-first century where several new tools and techniques are available to understand the genetics of traits and accelerate the breeding process. I want to induce early flowering in commericially grown Maize to reduce the life cycle of the crop. Any method to fast track the generations of the breeding cycle in Maize. Is Rapid generation advancement method established for Maize crop? It will help to reduce the normal crop life cycle which is 120-150 days to 60-70 days so that in 1 year 3 cycles of the crop can be grown.

Depending on what you want, a 60-day generation for maize has been established with some lines suitable for research ("mini-maize"). I doubt that these lines are agronomically interesting, so if your goal is to breed these with the idea of developing germ plasm for production they may not be useful. If, however, your goal is to do research and determine variants useful for introduction into an agronomic background, then it may be useful. It looks like there are related strains optimized for gene editing.
If you are mostly just interested in traditional breeding in a fixed line, then there are a variety of environmental conditions that can accelerate flowering in most plants. The main issue is that these conditions may interfere with your phenotyping regimen or with desirable outcomes such as yield.
There is additionally significant natural variation among maize types (some apparently with <60d flowering time, which seems surprising to me). Possibly using one of those early-flowering cultivars as a starting point or founding parent could be interesting.


text:
Can a baby have a combination of traits transferred by the parents?
like: B=black color.
b=white color.
e.g.: one parent has genotype for skin color as (BB) and the other parent has genotype for the same trait as (bb).
can the child have the skin color which not too dark and not too white like brown?

Yes (I'm tempted to say "of course", as I would be surprised if you had not personally met families where the children had phenotypes intermediate between their parents' phenotypes ...)
This phenomenon is called incomplete dominance.  Now that you know the correct terminology you can easily do a web search and get lots more information ...

thank you, i have been stuck on this question for a while and your answer really helped

any particular reason for the downvote?

i didn't down vote you...

I know, I was addressing that to whoever downvoted ...

Can't speak for the down voter, but this does seem to the sort of question that we shouldn't be encouraging with answers — specifically from How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. This is "homework" since it addresses a basic biology concept that may seem trivial to biology professionals. I personally prefer to direct users who appear to have little or no background knowledge to Khan Academy.


text:
Validity of report of reverse-transcription of Covid-19 vaccine mRNA in cultured human liver tumor-derived cells
The following paper reports results suggesting that when Huh7 cells (severely karyotypically abnormal immortalized cells derived from a human liver tumor) were incubated with the Pfizer/BioNTech COVID-19 mRNA vaccine BNT162b2 the lipid nanoparticles were taken up. The paper argues that the vaccine mRNA was reverse-transcribed and suggests that the LINE 1-encoded reverse transcriptase activity might be involved.
Aldén et al. (2022) Curr.Issues Mol. Biol. 44, 1115–1126 “Intracellular Reverse Transcription of Pfizer BioNTech COVID-19 mRNA Vaccine BNT162b2 In Vitro in Human Liver Cell Line”
The clinical relevance of these results, if correct, relates to the possibility that the integration of viral cDNA may occur in human liver tissue following administration of the vaccine, that the integrated gene for the virus spike protein may be subsequently expressed and could therefore be responsible for some of the rare side-effects of the vaccine.
Question: Do the results really indicate reverse-transcription of viral mRNA and integration of the cDNA into the genome of this cell line? If so, to what extent is this relevant to side-effects of the vaccine administered in the clinic.
Footnote
The publisher of this journal, MDPI, has been classified as a borderline predatory publisher — hence my scepticism — although the subject is far from my field.

HuH-7 cells are an immortalized cell line derived from a hepatoma (liver cancer), and while they can be used as a surrogate for hepatic cells in some assays, they are different in many ways. Beware of papers that purport to show unexpected results using only one cell line.

I’ll note that there are many pairwise statistical comparisons (t-tests) in the paper, yet no mention of a multiple-test correction. Though that’s not a critique of the science, per se

See some... other kinds of evidence: https://pubmed.ncbi.nlm.nih.gov/34344759/, esp. relating to the integration into human genome, and note that there is an incredible conflict of interest in this paper's authors. They have a good reason to scare monger.

I do not wish to answer this question, which I felt was unclear and for which I do not have the expertise. However, because of the interest shown in it I have rewritten it. I have made the title meaningful, described what the paper reports and replaced the ambiguous "is this serious" by precise questions. I have deleted the reference to another publication quoted in that work because any questions on its validity belong to a separate question (assuming that the purpose of this list is to post-review papers). If the poster thinks I have changed the meaning, please explain rather than roll back.

"Is the claim for integration of spike protein mRNA into the DNA of this cell line valid?" - Explicitely, if hidden, the authors do not claim integration, they claim retro-transcription.
If so, to what extent is it relevant to side-effects of the vaccine administered in the clinic.

"Is the claim for integration of spike protein mRNA into the DNA of this cell line valid?" - Explicitely, if hidden, the authors do not claim integration, they claim retro-transcription only: “At this stage, we do not know if DNA reverse transcribed from BNT162b2 is integrated into the cell genome.”
"If so, to what extent is it relevant to side-effects of the vaccine administered in the clinic." I think that edit over-does the question as there is no restriction to "significance and validity" of that study (nor others, no study claims to have found causality for side-effects).

Further to my edit of the question. The original referenced one specific paper and asked only “Is this serious?”. Hence my reversion to this one paper. The purpose of this site is not to re-referee papers, so the interest in this one must indicate that people think it has biological importance in relation to the vaccine mentioned in the title. I tried to specify the results reported that might be important, and why. This is open to improvement.  An alternative general question might be about integration of vaccine mRNA copies into human DNA after inoculation, but I think that has been asked.

@PeterBernhard — The reason for invoking integration into the genome is that the preparation in which the reverse-transcribed virus DNA was detected was “purified genomic DNA”. This is certainly the implication, and the context in which the paper was written. However I now notice that they write "At this stage, we do not know if DNA reverse transcribed from BNT162b2 is integrated into the cell genome" so I will modify my edit accordingly.

Great answer, thanks for making me feel appreciated. The "foregoing study" Nogoodnurse linked to did a subsequent study using available "paper work", i.e. data. Now, that data seems reaped in looking for RNA, neither DNA nor RNA that might have been transcribed from retrotranscribed m-RNA. Can you dig? They used data not produced searching for "chimeric transcripts". What they were rebuked for, then, was a adapation work. - What is the reason why this study did not undertake what they say is needed in the future? (long DNA-, not RNA-,  sequencing)

Re: Intracellular Reverse Transcription of Pfizer BioNTech COVID-19 mRNA Vaccine BNT162b2 In Vitro in Human Liver Cell Line by Alden et al. (  Curr. Issues Mol. Biol. 2022, 44(3), 1115-1126; https://doi.org/10.3390/cimb44030073 )
Regarding the question: "Question: Do the results really indicate reverse-transcription of viral mRNA...?" They provide results suggesting this, but missing key additional data (see Figure 5 comments below).
Regarding the question: "Do the results really indicate ... integration of the cDNA into the genome of this cell line?" No, they provide no evidence of that (see Figure 5 comments below).
Regarding the question: " If so, to what extent is this relevant to side-effects of the vaccine administered in the clinic." As they fail to convincingly show the above points, and are working in a cell line system of questionable relevance to normal human cells in the body, this paper seems to have no real relevance to side-effects of the vaccine administered in the clinic. See below comments.
This paper is NOT reliable. A non-exhaustive list of problems in no particular order appears below, but first let's consider their Results:
Figure 2: Yes, they show that BNT162b2 vaccine mRNA enters the cultured cells. However, all their statistical comparisons except for those against the controls are invalid -- see pt. 2 below.
Figure 3: They fail to show that BNT162b2 affects LINE1 mRNA levels. First, the control plots are visually not different from those of the vaccine-treated samples. Second, essentially all their statistical comparisons seem to be invalid -- see pt. 2 below.
Figure 4: Fluorescence always makes pretty pictures, but this figure again seems to fail to show anything useful. First, the LINE1 protein antibody used binds to the LINE1 ORF1 protein, which does not have reverse transcriptase activity, rather than the ORF2 protein, which does contain reverse transcriptase activity. An anti-ORF2 Ab is available, but they did not use it. Also, from Fig. 3 we see no significant difference in LINE1 RNA levels, so LINE1 protein levels would be unlikely to vary. Finally, the statistical comparisons shown are likely to be invalid -- again, see pt. 2 below.
Figure 5: This section claims to detect reverse-transcribed BNT162b2 in DNA preps from buffer-washed cells previously exposed to BNT162b2. Maybe they have, but key controls are missing.
The one piece of evidence shown is successful PCR amplification of a segment of the vaccine sequence. They do show some useful controls, such as lanes for cells not treated with the vaccine, but miss other essential controls such as cells treated with a different mRNA vaccine not containing that amplicon, and DNA from relatively karyotypically and morphologically normal cultured cells treated with BNT162b2, another mRNA vaccine, or nothing. It's all too easy to have a few stray molecules of a DNA fragment present in the lab (like the BNT162b2 PCR amplicon) contaminate other samples and lead to false positives after lots of cycles of amplification. They also provide no evidence any reverse-transcribed BNT162b2 is integrated into the cells' genomic DNA.
As for the paper's significance to BNT162b2 influence on actual normal human cells, there really isn't any because of how abnormal this immortalized liver tumor-derived cell line is in terms of of genomic stability and of gene expression. It's sort of like using Godzilla as a model organism for humans.
The promised non-exhaustive list of problems:

It's clear they don't understand some of the features they discuss, such as LINE1 elements, calling LINE1 "endogenous reverse transcriptase" when they are actually transposons. They also seem to think there is just one LINE1 gene, not understanding that they are present in thousands of copies throughout the genome (having "jumped" into many genes).

It's clear they don't understand how to do statistics properly. If you just do more and more comparisons between different experiments, eventually you will find a difference just by chance. To correct for this, you must reduce your significance threshold to take into account the number of comparisons you make. An easy way of doing this is called "Bonferroni correction" and there is no evidence they used it or any other such correction.  As far as I can tell, after the Bonferroni correction is applied, essentially none of their meaningful comparisons end up being statistically significant.

Their main "control" consists of no vaccine, rather than a dummy/different vaccine. Effects associated with vaccine presence could for example be due to the lipid nanoparticles or modified RNA -- that is, they could be non-specific responses.

The fundamental flaw: as a stand-in for human cells, they use only a highly chromosomally abonormal cultered liver cancer cell line Huh-7. According to a description of the line, "The majority of Huh-7 cells show a chromosome number between 55 and 63 (mode 60) and are highly heterogeneous." (normal cell count is 46) In addition to "...containing many mutations and INDELS, it is worthy to note the Huh7 cells have a point mutation in the p53 gene."

The LINE1 protein they image likely appears in tumor cell lines (like the Huh-7 line they use), but not in normal cells. From "Methods Mol Biol. 2016; 1400: 261–280.
doi: 10.1007/978-1-4939-3372-3_17 ""Using immunohistochemistry, we found nearly half of human cancers stain positively for ORF1p, with immunoreactivity in some common cancers approaching 100% of cases. No staining was observed in the cognate normal tissues"

The Zhang et al. (PNAS May 25, 2021 118 (21) e2105968118; https://doi.org/10.1073/pnas.2105968118 ) paper mentioned in this paper is discussed in my answer to a Medical Sciences StackExchange question: MedicalSciencesQuestionAboutZhangPaper
The summary of my answer to "can the SARS-COV-2 RNA modify our DNA[based on this paper]" is "The short answer is maybe, but rarely, and the whole Covid virus has never been seen to integrate into the cell's DNA intact. Any integration requires "helper" molecules not found in the Covid virus, and only very rarely found in a normal cell."

Comments are not for extended discussion; this conversation has been moved to chat.

I've also commented this on your Medical Sciences SE question: Highly relevant to this question:  "Host-Virus Chimeric Events in SARS-CoV-2-Infected Cells Are Infrequent and Artifactual"

The paper may be reliable in its finding that
"BNT162b2 mRNA is reverse transcribed intracellularly into DNA in as fast as 6 h upon BNT162b2 exposure",
however, the authors   apparently refrained  from trying to find integration into the genome of the hepatitic cells. They do not claim to have found integration into the genome.  They say,
"(f)urther studies are needed to demonstrate the effect of BNT162b2 on genomic integrity, including whole genome sequencing of cells exposed to BNT162b2, as well as tissues from human subjects who received BNT162b2 vaccination."
In that context they do not  refer to a previous study which - before the question had been edited anew -  had been linked to: Zhang et al., Reverse-transcribed SARS-CoV-2 RNA can integrate into the genome of cultured human cells and can be expressed in patient-derived tissues. Interestingly, this study did not use tissues from human subjects who received vaccine (or had been infected), however in their setup used whole genome sequencing to detect recombinded virus-host-DNA. This study did not.
Isn't  whole genome sequencing easy to do these days? Was there a   lack of "tissues from human subjects"? In fact, mentioned previous study by Zhang et al. (on virally infected cells) recurred to existing RNA-analysis (existing data) when trying to find out about normal  cells, after they had examined artificially LINE1-upregulated cells in vitro.   That may hint  to what does not go without saying,  which neither the study challenged by question nor its  co-study mentioned above explains and elaborates on,  and  only to experts seems obvious and apparent:
The study  questioned did not undertake to prove whether retrotranscribed DNA - which was  undebatedly found  - is of host cell genome origin (post integration) or of viral origin  (post retro-transcription).
Both studies do not speak of "free viral cellular DNA". That  may be  some blunt way to describe the issue, however, first, the technique of recombinant DNA vaccine shows very cleary (and very unexpectedly)  that DNA in cells may exist without being integrated into the genome of the host cell. Adenovirus vector  technique is  based on viral DNA in cells  not being integrated into the genome (There is no  finding of vaccine recombinant DNA  being retro-transcibed into the genome (after transcription to m-RNA)).
Second, it is accepted knowledge that several virus species persist latently in host cells in so called episomal form. E.g. herpes virus DNA is known to persist episomally  in the nucleus without  integrating into the host cell's genome. The following quote refers to adeno associated virus (different from Adenovirus used in vaccine): "Although AAV vector genomes can persist within cells as episomes, vector integration has been observed in various experimental settings, either at non-homologous sites where DNA damage may have occurred or by homologous recombination." Deyle and Russell, Adeno-associated virus vector integration; see also, e.g., Chong et al.Transfection types (...): "Stable transfection refers to (...) integrating foreign DNA into the host nuclear genome or maintaining an episomal vector in the host nucleus as an extra-chromosomal element (...). The transgene may then be constitutively expressed even with the replication of cells (...). In contrast, transient transfection does not require integrating nucleic acids into the host cell genome (...)"
This shows that retrotranscription as a first step may very well be distinguished and proved independently from integration into the genome.
The study in question here proved retro-transcription of vaccine m-RNA. Different from Zhang et al. they did not do any "whole genome sequencing" to find out about integration. The authors do not give reasons.  In case of positive findings, we still wouldn't know if CoV-DNA integrates  in normal tissue.
Whereas the first study  searched for
"chimeric transcripts"
i.e. DNA sequences that comprise quote "partial (...) subgenomic RNA sequence that was flanked by a duplicated host cell DNA target sequence" to lay proof of integration into the genome, the study challenged here did not. You will not find the word "chimeric transcript" being mentioned in the description of the methods employed:
"Genomic DNA was extracted from cell pellets  ... PCR was then performed using primers targeting BNT162b2 (sequences are shown in Table 1) (Remark:no chimeric sequences among)  ... Bands corresponding to the amplicons of the expected size (444 bps) were cut out and DNA was extracted ... The sequence of the DNA amplicon  was verified by Sanger sequencing."
However, it seems unanimously accepted that chimeric transcripts are  valid proof of integration - if validly found. The latter had been questioned by peer review in respect of the study by Zhang et al.
To sum up: There is no reason given for not using "long sequencing" technique that might have found chimeric transcripts. Alternatively, the study might have given reasons why chimeric transcripts cannot be accepted as proof of integration. The study questioned here seems to self-restrict itself in significance and reach.
It may be some biased opinion to think of the previous study having been reviewed as technically not valid in respect of its findings of  chimeric transcripts as a reason why the study challenged here refrained from long sequence technique (Remark: mentioned previous study did not either in respect of tissue from patients, in its non in vitro follow up,  as it then used pre-existing data that resulted from RNA, not DNA search and sequencing which in my opinion might explain the artifacts they were blamed for).
Final remarks: Merits of this study may lie in the use of nano lipids in combination with cancer cells. It had been shown before that any cell can possibly uptake the nanolipids; however, in respect of the previous study by Zhang et al., this study results in some strong argument for LINE1-expression not being dependent either on artifically induced over-expression nor - as it used nano lipids - on viral infection  (host-virus membrane fusion or receptor mediated endocytosis). Natural infection may very well appear as a prerequisite for upregulation of LINE1.
Still, any study might be challenged for  not being "reliable" or "serious" (quote pre-edited version of this question), in my opinion, as long as  the mechanism of LINE1 activation, of inducing LINE1, remains unknown.
There are no known side-effects of LINE1 integrating DNA, and they have not been searched on by the study questioned nor are there any other studies up to date on effects of CoV-DNA integration. It is beyond the scope of this study to offer cues  that hint at chimeric transcripts (integration) coresponding (not to side-effects but) to severity of disease  (Zhang et al.: "...in some patients-derived tissues ... a large fraction of the viral transcripts could have been transcribed from SARS-CoV-2 sequences integrated into the host genome.")

Comments are not for extended discussion; this conversation has been moved to chat.


text:
Do some plant proteins have no domains?
I've always been under the impression that all proteins consist of at least one domain (with the exception of intrinsically disordered proteins). However, I've come across some things which challenge that while reading some papers and I'm not sure how to understand it. From one paper (https://doi.org/10.1016/j.tig.2006.09.003);

We determined the tendencies for individual protein functional (Pfam)
domains to occur among duplicates or singleton genes (see the
supplementary material online) resulting from independent GD events
that occurred 60 and 70 MYA in the lineages of Arabidopsis (a) [15]
and Oryza (r) [16], respectively. Analysis of Pfam domains as the
experimental unit also permitted us to compare these angiosperm events
with GDs in yeast [20] and Tetraodon [21]. Between 1334 and 1704
domain types were found in the four organisms, with duplicated genes
containing an average of about one domain and singletons averaging
0.15–0.40 domains (see Table 1 in the supplementary material online).

If the average singleton in the genomes of the organisms under study here have 0.15-0.40 domains, that means the majority have no domains. Checking the supplementary material confirms this. In a second paper (https://doi.org/10.1016/j.gpb.2016.06.003), Figure 6 shows that both rice and humans have a substantial number of proteins without any domains.
What is the meaning of this? How can these proteins have no domains? The best explanation I can come up with is simply that this data is a possible artifact resulting from simple lack of detection by domains were based on the specific database being used (Pfam in one case and InterPro the other), but I'm not sure if this is the correct understanding of this.

I suspect you are confusing two different things — from your quote it seems likely that the paper is talking about the subset of domains that are defined in the Pfam database. My understanding is that most proteins have never been studied and their existence is inferred from DNA sequences. This means that unless the inferred proteins have detectable homology to a characterized protein they won't have a defined domain. This is not the same thing as them not having one or more structural domains ...

Makes sense. So, in this context, is there a clear significance to that singletons have a lower defined domain frequency than duplicated genes?

Hard to see what it might mean, but since I don't have time to read the paper I'd be unwilling to say that it didn't mean something. Could be just that duplicated proteins are by definition more common and thus more likely to have been studied, but there may be something deeper like them being (on average) less essential (due to the duplicate) and so easier to study/recover mutations ... if you are sure (based on rereading the paper) that the interpretation in my first comments is correct, you could [edit] this question to focus on what you just asked and see whether anyone has an answer ...


text:
Is double-stranded DNA denatured to single-stranded DNA in retorted canned tuna?
A PCR reaction has a cycle of about 55°C annealing, 72°C extension and 95°C denaturing with short time spans. Retorting canned tuna heats the tuna to 115°C to 121°C for 30 minutes to 2 hours depending on steam temperature and can size. So, much of the DNA is degraded into short segments of less than 150 to 200 bp long.
Has the DNA at that temperature been degraded to single-stranded DNA as well, or is is just short segments of double-stranded DNA?

Citations for heating causing shorter DNA fragments in processed meats:

Ebbehøj, K. F., and P. D. Thomsen. 1991. Species differentiation of heated meat products by DNA hybridization. Meat Science, 30(3), 221-234.

Şakalar, E., M. F. Abasiyanik, E. Bektik, and A. Tayyrov. 2012. Effect of heat processing on DNA quantification of meat species. J Food Sci. 77(9): N40-N44.

Retorting fragments mtDNA in any meat product. More than 3 dozen papers on retorted tuna DNA alone.

Welcome to Biology.SE. Your second paragraph sounds like a conclusion, but isn't obviously based on the preceding paragraph. Are you claiming that 'retorting' fragments the DNA? If so, can you provide a citation or other reference that supports that? ——— It would also be helpful if you could say why you want to know this seemingly random factoid. ——— Please take the [tour] and consult the [help] starting with [ask] for details about site usage and expectations.

Ebbehøj, K. F., and P. D. Thomsen. 1991. Species differentiation of heated meat products by DNA hybridization. Meat Science, 30(3), 221-234.  https://doi.org/10.1016/0309-1740(91)90068-2

Şakalar, E., M. F. Abasiyanik, E. Bektik, and A. Tayyrov. 2012. Effect of heat processing on DNA quantification of meat species. J Food Sci. 77(9): N40-N44.  https://doi.org/10.1111/j.1750-841.2012.02853.x

Retorting fragments mtDNA.  in any meat product.  More than 3 dozen papers on retorted tuna DNA alone.

Great, please [edit] those into your post — comments on this site are ephemeral and often overlooked, so they should only be used to discuss the post not to amend it. ——— You may be best placed to answer this question. In a typical molecular biology context I would hazard an answer, but I'm not sure how relevant what I do know will be for a complex, non-aqueous material like tuna. In solution, DNA that has 'melted' (strands are separated) will reanneal, but the rate of that reannealing depends on the complexity of the sequence — see: Cot curves.

Thank you sir.  the Cot curves site is very helpful.  My question has not practical significance for us, except it is very helpful to exactly how things are working, in the PCR reaction.  Again, thanks very much for your help.

What does the word “retorted” mean in this context? The only definition I can deduce is from the chemical apparatus, retort. Please clarify by editing your question.

It is ssDNA. At retort temperatures (110C - 135C) the hydrogen bonds are broken and the DNA is single stranded. From what you wrote the size of the DNA fragments also changes based on temperature. If however you let the DNA sit for some time and cool after exposure to these temperatures some fragment can reanneal.


text:
Question about using Mendelian inheritance to reverse-guess the parent genotype
I would like some help with a question about Mendelian inheritance, based on the following information (I assume this is autosomal and not sex linked):
-- Start of information --
"As flatfish (Pleuronectiformes) develop, they lose their bilateral symmetry. One of their eyes migrates across the top of the head, so that both eyes end up adjacent on the same side of the head. As a result, the adult fish is able to lie flat on its side on the sea floor with both eyes facing up. In some species of flatfish the right eye migrates to the left side of the head (they are left-eyed); in other species the left eye migrates to the right side of the head (they
are right-eyed).
In one species of flatfish, the starry flounder (Platichthys stellatus), different populations have different proportions of left-eyed and right-eyed individuals. Off the west coast of the USA the population is evenly divided between left-eyed and right-eyed individuals. However, in the north Pacific, midway between the USA and Japan, 70% of the population is left-eyed and in Japanese waters all the starry flounder are left-eyed.
Consider the following hypotheses (I – III) about the starry flounder. The hypotheses assume that a single gene locus determines the final location of the eyes on the head.
I. The Japanese fish are homozygous for a dominant left-eyed allele (LL), whereas west coast fish are homozygous for a neutral allele (ll) and have an equal chance of developing into either left- or right-eyed individuals.
II. The Japanese fish are homozygous for the left-eyed allele (LL), whereas in the west coast fish both left-eyed (L) and right-eyed (R) alleles occur in equal proportions. Heterozygous individuals (LR) have an equal chance of developing into either the left- or right-eyed form.
III. There are three alleles of the controlling gene: the left-eyed allele (L) is dominant to both the right-eyed allele (l) and the neutral allele (l’). Further, the right-eyed allele is dominant to the neutral allele. Fish that are homozygous neutral (l’l’) have an equal chance of developing into right- or left-eyed individuals."
-- End of information --
Question:
The question says: When a left-eyed mid-Pacific female and a right-eyed west coast male were crossed and the offspring were all kept in standard laboratory conditions on the west coast of the USA, 50% of the thousands of offspring were right-eyed and 50% were left-eyed.
Of the following this result completely rules out:
A hypothesis I.
B hypothesis II.
C hypothesis III.
D none of the hypotheses
The 3 hypotheses only talk about Japanese fish and west coast fish, there is no mention of mid Pacific fish, and, if it is talking about the North Pacific fish, the info state that "However, in the north Pacific, midway between the USA and Japan, 70% of the population is left-eyed and in Japanese waters all the starry flounder are left eyed."
From this we infer that:

the 70% part refer to the non-Japanese fish due to the word 'and'
the non-Japanese fish must be the north Pacific fish since there are no other fish mentioned.

So:

What are mid Pacific fish? And what are their genotypes/alleles?
Some fish have equal chances of being left or right eyed, so that specific genotype represents 12.5% and 12.5% where each square of a Punnett square is 25%. So you add 25% + 25% and + or - 12.5% or 25%. Therefore the closest thing to 70% is 50+12.5 = 62.5% or 50+25% = 75%, either under or over, when trying to determine how to get the mid Pacific fish.

So I can't get the 70% and still don't know what mid Pacific fish are.
I know how to do Punnett squares. But my issue is the wording of this question. It says "left-eyed mid-Pacific". None of the genotypes mentioned in any of the hypotheses mention Mid-Pacific.
Unless it means midway between Japan and USA, which the question info state is NORTH Pacific.
So my question is, do we need to and if so how, to reverse-guess the female North Pacific fish' genotype. Or if we don't, how to do this question.
My reasoning is, the only way Hyp 1 can create a right eyed fish, as opposed to Hyp 2 (which say R is right eyed) is if I take each hyp 1 as it is (ie, the available alleles are LL for homozygous dominant left and ll for homozygous neutral where there is a 50:50 chance of being either left or right), without trying to figure out what a Mid Pacific fish is (I believe if a Mid Pacific fish is a cross between a West Coast fish and a North Pacific fish, then we need to look at all the possible combinations of this, in which the result is 70 left eyed. There are 2 problems with this, one this is a practise exam question where you have 1.5 minutes per question, and 2, there is no way to get 70 from adding or subtracting 12.5, 25, and 50.) then, Hyp 1 says LL and ll. A cross between that is 100% Ll, which is 100% Left, ruling it out instantly since we want 50% left and 50% right.
However, the answer was D, no hypothesis is ruled out.
This is a Punnett square I did for each combination listed in the 3 hypotheses, based on a West Cost male and a Japanese fish.

(So, in total we have 4 fish types, the West Cost male and a Japanese fish mentioned in the hypotheses, the North Pacific fish mentioned in the information and the Mid Pacific asked for in the question.)
Can someone help explain this?
Thank you.

Homework questions are usually closed here, but you certainly have given it the appropriate amount of thought, so +1 from me. :)

@anongoodnurse Please clear me of confusion, is the biology stackexchange closed to homework questions? This question is actually not homework nor homework related but it is the closest tag I could find, and, I have asked other questions here that are 'homework'.

If you had enough rep to close vote, you'd see that the second reason (of 5 possibilities) is that it's a homework question. But as I said, I think you've been very diligent in your thinking and explanation of same. I wouldn't worry about it, but do take the "Homework help" out of the title.

This is found on Course Hero (can't see it because I haven't signed in). I'm not saying that this is a HW question - but I was looking for it because I wondered where it came from; since it seems that a lot of the problem has to do with interpretation of the question, the best thing to do would be to go back to the person who asked it ... can you give any more context about why you're trying to solve this particular Q?

Also: https://www.coursehero.com/file/pc9ee9i/offspring-F1-of-many-crosses-between-Japanese-starry-flounder-and-randomly/

@BenBolker This is a GAMSAT practise question so a lot of people would ask it, and, there is no way to ask the person who asked it.

First of all, let's distinguish between the three populations. The Japanese fishes are all left-eyed, midway between the US and Japan the population is 70% left-eyed, and in US (or the west coast) the population is 50% left-eyed.
Let's take a look at the US population. I want to emphasize on the point that this trait is genetically determined. That is, it does not have environment factors influencing the phenotype. Next, let's look at this logically. In order for the entire population to be 50% left-eyed, the trait needs to be 50%. That is, every fish needs to have (roughly) equal chances of producing an offspring with left eyes as well as an offspring with right eyes. This does not strike me as following the dominant-recessive pattern, since that will ensure 75%-25% phenotypes. On the contrary, I'm thinking off a heterozygous genotype which will result in a random phenotype. However, we don't have proof for this yet. All we know is that the population is 50% left-eyed.
Moving on, the Japanese population needs to all be left-eyed, so any newborn fish will be left-eyed (or so we can assume, for simplicity's sake). The genotype of this population ensures left-eyed fish.
The population midway between the US and Japan is trickier. Since they are 70% left-eyed, the eye position is not controlled by chance. However, if they were like the US population, then they would all be left-eyed. Hence, we can safely assume that this population is a mix between the US population and the Japanese population. This assumption is not only based on the location (midway between both the populations), but also based on the information that they give us. Since a single gene determines the location, you cannot have a population with 70% having one phenotype. You rightly mention this when you say:

So I can't get the 70% and still don't know what mid Pacific fish are.

This is because only genetic factors determine the phenotype (given or assumed from the question). Hence, I'm thinking of an approximately 50-50 mix between the Japanese population.
50 Japanese fish + 50 US fish = 100 fish
Since 50% of the US fish are left-eyed - 25% of the total fish are left-eyed (50% of 50%)
Since all the Japanese fish are left-eyed - 50% of the total fish are left-eyed (100% of 50%)
Adding this gives us 25 + 50 = 75% of the 100 fishes are left-eyed.
This is very close to the 70% that we have been given.
Now let's look at each hypothesis in turn.
Hypothesis I
If the Japanese fish are homozygous dominant LL, that means that they will all be left-eyed. On the other hand, if the US population is neutral ll, then they have an equal chance of being left-eyed or right-eyed. Since this is what we have observed, this hypothesis could be true.
Hypothesis II
This hypothesis states that LL individuals are left-eyed, RR individuals are right-eyed, and LR individuals have an equal chance of being left or right eyed. The Japanese fish are LL, so all of them are left-eyed. The west coast fish are LR, and hence the population is 50% left-eyed. Again, this agrees with our observations, so this hypothesis can be true.
Hypothesis III
Since the L gene is dominant to both l and l', fishes with at least one copy of the L gene must be left-eyed. Hence the Japanese fish must be LL, Ll or Ll'. However, since all newborn fishes are left-eyed, the population most likely carries the LL gene. Moving on, the US population must have the l'l' genotype since they are 50% left-eyed. If they were Ll' or Ll, they will be almost 75% left-eyed (or even more because the l' gene gives a random phenotype). On the other hand, if they were ll' then they will be 75% or more right-eyed. However, the l'l' genotype works without a problem. So this hypothesis is plausible too.
Notice that I said that these hypotheses could be true. We don't know for sure that they are true, since as you noted, the hypotheses do not talk about the midway population. There are also multiple possibilities, and we don't know for sure which one is correct. However, none of these are incorrect based on the information given. Since the question asks for the false hypothesis, the answer is None of the above. Hope I made this clear!

Thank you very much!

Re: 1: "mid Pacific" is just a short way of referring to "in the north Pacific, midway between the USA and Japan".
Re: "what are their genotypes/alleles" Yes, that is what they want you to consider. For each of the 3 stated hypotheses, you should be able to come up with possible genotypes and rough genotype frequencies for the mid Pacific fish of different eye phenotypes.
Re: 2: Consider the genotype frequencies of the mid Pacific parental fish under each of the 3 hypotheses.  A Punnett square only represents 2 specific parental genotypes. If multiple parental genotypes are present in a population, you will have to make a Punnett square for each different combination of 2 parental genotypes, and adjust overall resulting offspring genotype frequencies according to the proportion of that combination.
From comment: "Ultimately my question is how do you determine the genotype of that "70% left eyed J-WC mid-Pacific hybrid"?"
Since the 70%... is a population, there may be more than one genotype among them.

If mid-Pacific refers to midway between USA and Japan, then, the hypotheses only mention pure Japanese and pure West Coast. This means I have to cross a pure Japanese that according to Hyp 1 and 2 have only LL, and a pure WC which is neutral L and R. As I mentioned in my question, the hybrid J+WC mid-Pacific fish are known to have 70% left eyed. That means you need to somehow combine the possibilities of the alleles with 12.5%, 25% and 50% to get 70%, how do you do this? (Eg 50% LL left and 12.5% LR since LR has equal probabilities of producing either left or right)

"If multiple parental genotypes are present in a population, you will have to make a Punnett square for each different combination of 2 parental genotypes, and adjust overall resulting offspring genotype frequencies according to the proportion of that combination." I know this, that is not my question. Ultimately my question is how do you determine the genotype of that "70% left eyed J-WC mid-Pacific hybrid"? So that I can then use this to cross with a pure right eyed WC to get 50:50 left and right?

It seems like you are assuming there is only one genotype represented in the "70% left eyed J-WC mid-Pacific hybrid" population. If so, why?

My reading of the hypotheses is that they do not all specify each of the Japanese and West Coast populations as having only a single genotype.

I interpret the hypotheses as, the J and WC fish have only 1 genotype - and the hypotheses are there to try and figure out which genotypes they have. That's why it is a hypothesis and not the fact.
To answer your question about why I assume there is only 1 genotype for the 70% left eyed hybrid fish: Since 1), and since there is nothing to suggest the 70% left eyed fish are made of anything else, and, since they specifically mention that some genotypes gives a 50:50 chance of either, I believe this is there to tell you that one genotype can have more than one phenotype, so, one genotype.

I'd re-evaluate your assumption of always one genotype and try seeing if more than one genotype in a population makes things work better.  Remember, "absence of evidence is not evidence of absence" - just because they don't say the 70% population has multiple genotypes doesn't mean that isn't the case. Just for fun, what would you expect to see in terms of phenotypes if the mid-Pacific population were 1/2 Japan genotypes and 1/2 West Coast genotypes?

So what is the answer and what is the correct interpretation? No one has answered my question.


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Why are some plants naturally yellow?
Some plants are naturally yellow. Or rather, they have yellow leaves. This is shown in the following picture, taken from my neighborhood.

I found a Quora article that explains why, but since that is not a reliable source (as far as I know), I would like to have more evidence to this claim. In short, the article claims that plants are yellow due to artificial selection (they look good, so we breed them more). Is this true? Or is there a more plausible answer to why plants are naturally yellow?
In the case of this particular plant, it is not looked after very much, and perhaps only watered once in a while. Won't the lack of chlorophyll affect the plant's ability to perform photosynthesis? I have an alternate theory as to why this plant is yellow, but I'm not sure if that is correct. This plant is very close to a backwater which is highly contaminated with pollutants (the green in the background of this photo is actually weeds and algae in the river). Could that be a valid reason why the plant is yellow?
I was not able to find any other links to this question (they were all about dying plants no matter how I phrased my Google search), but I will edit the question if I get anymore links.

The plant in your photo seems to have plenty of green. It seems that perhaps the new growth is more yellow/green, but without a clear closeup photo of the leaves it's hard to tell much.

Looks like a privet, which often has yellowish young (and old) growth for entirely different reasons.

There simply can't be one answer to this question, especially since I couldn't identify the plant from the photo. However, looking at the different possibilities can be helpful, even if it's just scratching the surface of a very large topic.
Introduction
First of all, why are the plants green? It is common knowledge that the photosynthetic pigment, chlorophyll, gives this color to leaves. This substance has maximum absorption in the red and blue parts of the spectrum, so the spectrum of light transmitted and reflected from the leaf is dominated by the green part of the spectrum. In most plants, the amount of chlorophyll present is far bigger than the amount of any other pigments, and hence we perceive the leaf/plant as "green". However, some plants have other pigments that is the dominant pigment in their leaves, and this causes the leaf to be a different color, "yellow" in this case. Let's take a look at some hypotheses as to why this can be the case.
Hypothesis 1
It should be remembered that chlorophyll is far from being the only pigment found in leaves. For example, carotenoids - which give yellow and reddish colors - are present in plant leaves. There are many carotenoids (according to Wikipedia there are over 1100 known, but that number will continue to grow). The biological roles of these carotenoids are also varied. In the course of the question, we may be interested, for example, in the photoprotective role of carotenoids. They are involved in the deactivation of reactive oxygen species (ROS). ROS can be formed during photosynthesis and can potentially be harmful to cells. Therefore, in conditions of excess solar radiation, plants can increase concentrations of carotenoids to prevent oxidative stress. It has already been pointed out to you in the comments that younger leaves look yellow - this is a common occurrence. The leaf is a very expensive organ, in the sense that the plant invests a lot of plastic substances in its development. So it makes sense that young, growing leaves get extra protection. That is, a young leaf that has not yet formed all the necessary structures (thick enough cuticle, efficient conductive system, etc.) is less efficient in terms of photosynthesis and therefore more susceptible to negative  processes of photodamage. Increased concentrations of carotenoids, among other things, can reduce such risks. If you add to this the small thickness, it is understandable why young leaves often look more yellow.
Hypothesis 2
I have already said that leaves are expensive organs. They have a high protein content, which is very valuable to the plant. If a leaf is damaged or aged, there is a threat of irreversible loss of protein, which would be a great waste. Therefore, in such cases, plants trigger complex processes of removing valuable substances from the leaves. In particular, chlorophyll begins to break down, and the decomposition products are transported to the more durable parts of the plant. This is the reason why leaves change color in the fall, before defoliation. When the concentration of chlorophyll decreases, other pigments, such as carotenoids, increasingly affect leaf color. That's why damaged and old leaves often turn yellowish.
Although, I doubt that in the case of your plant, this process is often the cause for yellow leaves.
Hypothesis 3
Again about photodamage. We have to remember that the capture of photons by chlorophyll is only the beginning of a very long chain of chemical transformations needed for photosynthesis to take place. If the plant is under unfavorable conditions (low or high temperature, lack of moisture, etc), the biochemical cycles can be disrupted. In this case, chlorophyll will continue to absorb photons and enter the excited state, but it will not be able to release this energy further into the cycle. This can be due to many reasons, like the depletion of the plastoquinone pool for example. Under such conditions, the threat of heat shock (if the captured energy is released as heat) or oxidative shock through the formation of reactive oxygen species (ROS) increases. Some plants have developed interesting mechanisms to prevent such adverse effects. In particular, mottled leaf coloration, where green areas alternate with meteolated (chlorophyll-free) areas. Such meteolated areas act as a kind of buffer storage of substances which can be used when the resources of the green areas are exhausted (I am speaking in a very simplified manner here; in fact, these mechanisms are very complicated and it is not quite correct to describe them simply as storage of substances). What is important to answer the question is that some plants can purposely form areas of tissue without chlorophyll, including yellowish coloration. In general, the leaf may look "more yellow."
Hypothesis 4
Before that, we were talking about chemistry. But leaf color is also influenced by anatomical structure. The evolution of the leaf was aimed at maximizing its efficiency as an organ of light capturing and transformation. For example, in the structure of a typical broad-leaf, we can distinguish (conditionally) 4 basic layers of tissues: upper epidermis, columnar tissue, spongy tissue, lower epidermis. All these histological layers contain cells of different shapes. When light passes through the cells, it refracts. That is, each cell acts as an optical lens. For example, the upper epidermis can focus scattered light. Columnar cells often act as photoconductors (similar to an optical cable). The lower epidermis can also act as a reflective layer (so the underside of the leaf often looks lighter than the top). In this case, the light that has passed through the upper epidermis, columnar tissue, and spongy tissue is reflected from the lower epidermis, and is forced to pass through the spongy tissue again. Then it can reflect again from the lower edge of the columnar tissue. In general, geometry and optical properties of leaf cells are also very important for effective light energy absorption. It is important that, passing through the leaf, light is repeatedly refracted and reflected. We know that photons with different wavelengths refract and scatter differently. Therefore, the very anatomical structure and shape of the leaf cells may have an effect on how different parts of the spectrum will be reflected or transmitted by the leaf. One (potential) consequence is, the leaves of some species may be more likely to reflect the yellow portion of the spectrum (and hence be perceived as yellow).
Hypothesis 5
Selection. Indeed, leaves with unusual coloration are perceived as more ornamental. Therefore, artificial selection is often aimed at selecting plants that exhibit unusual leaf color. We have already looked at several natural mechanisms that give yellow leaf color. If artificial selection (by humans) was aimed at intensifying such mechanisms, you could very well get plants with bright yellow leaves. The same applies to mottled and variegated leaves.
Conclusion
The hypotheses I have described are only the tip of the iceberg. Even though it requires a lot of research and investigation to get an accurate answer to your question, I hope these hypotheses have provided you with a general intuition as to why some plants have yellow leaves.

This is a great answer! Thanks for taking the time and effort to post  I will give you my replies to your hypotheses down below:
[1 of 6]

This is very possible. I live in a very tropical climate, and especially since the plant had very tender and soft leaves, the excess radiation would be a very plausible reason for the plant to have yellow leaves.

[2 of 6]

Not much of a chance, but thanks for the info  We don't have autumns here, so virtually all plants are evergreen.

[3 of 6]

Although this is plausible because of the high temperatures, I don't think this is the reason. The plant looks yellow throughout, and there aren't any patches of green like you mentioned, so I don't think this is the real reason.

[4 of 6]

This is very interesting! However, there isn't any way of finding out if this is true (unless you actually try refracting light through the leaves). I didn't know about this before, so thanks a lot for mentioning this

[5 of 6]

This could or could not be true. This plant was certainly not selected for or against, but the whole species could have been used for artificial selection years ago. Anyways, thanks a lot for your information, and I really appreciate it

Thanks for the edits, English is not my first language. I will try to add some links soon to make the answer "complete".

Sure, that would be great


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Movement of Common Jelly Fish
Among the different types of movements in the bodies of various organisms, the movement exhibited by jelly fishes are very unique and peculiar in some ways. I can't understand how to classify the type of movement for jelly fish.
Its movement is also similar to octopuses and squids, but they have proper propelling arms which they use to propel themselves forward. Whereas Jelly Fishes don't have such structres in them, then how are they producing such movements?
Also they outer structure (often known as "bell" or "hood") is made up of an external epidermis and an internal gastrodermis (containing nerves but no muscles) and their bodies are mostly water, so how are they able to produce such movements.

Welcome to the site! Questions without evidence of a search in an attempt to answer are off-topic. (E.g. did you google "how to jellyfish swim"?) Please take the [tour] and carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question.

I obviously did the research and I have noted my inferences in the description of my question. I also mentioned what I don't understand particularly and so I asked them as I didn't get any satisfied on Google. If there was a way to just get all the answers from the web then I wouldn't use this site. If I google how jelly fish swims? do you really think that will aswer my question, Put some thought into it. I didn't ask this doubt particularly here for no reason, if I just could have got my answers on Google.

Also it is a not a question about species identification or something, I don't know what kind of "evidence" I have to submit to ask a question on concept.

It's not obvious that you researched it because we see no sources. You must wonder what kind of Q&A site this is, being asked to show your search results; shouldn't we just answer your question? Actually, no. We're expected to help if we so choose. We're scientists or people interested in science, a lot of us teach, practice, or research some aspect of Biology. We expect some meaningful degree of research (show a source + a quote); not a ton, but not nothing, either. Consider this kind of like a classroom, not a chat room. You'll get a (better) response with a better effort on your part.

Also, I googled "how do jellyfish swim" just to see what was out there, and my first hit answered the question. Usually with multicellular organisms like jellyfish, movement involves muscle tissue. There are lots of ways to move in the ocean, but clearly jellyfish propel themselves, so... muscle.


text:
What is a gain-of-function assay in neuroscience?
I am reading this paper and I have come across the following statement:

"We sought to test whether exogenous Kirrel3 expression induces synapse formation via a gain-of-function assay... Because most CA1 neurons do not express Kirrel3, we used this in
vitro specificity to our advantage and tested whether exogenous
Kirrel3 expression in CA1 neurons could induce ectopic DG-to-CA1
synapses".

In the above statement, I am trying to figure out what is meant by a "gain-of-function assay".
I have searched online for a definition for gain-of-function, and all the search results talk about it in the context of virology, e.g. this paper states:

"Gain-of-function (GOF) research involves experimentation that aims or
is expected to (and/or, perhaps, actually does) increase the
transmissibility and/or virulence of pathogens"

I was wondering, in the context of neuroscience research, what is a gain-of-function assay? In this context, does it simply refer to the fact that the researchers overexpressed Kirrel3 in CA1 neurons (which normally do not express Kirrel3)?
Any advice is appreciated.

The function in this case is the formation of synapses.

Nothing special is meant here except the standard English meaning of these words.
The second half of the quoted passage explains what they intend to do:

Because most CA1 neurons do not express Kirrel3, we used this in vitro specificity to our advantage and tested whether exogenous Kirrel3 expression in CA1 neurons could induce ectopic DG-to-CA1 synapses

To find out what Kirrel3 does, they're going to add Kirril3 ("exogenous...expression") and see what happens, and use that to infer something about the function of Kirril3. The cells that don't normally have Kirill3 are gaining its function. The opposite approach would be to remove Kirril3 from someplace that it normally is, which you could call "loss of function" - that might be a knockout animal, RNAi, use of an antagonist or other pharmacological manipulation, etc.


text:
Please explain to me the difference of molecular weight in g/mol versus dalton
From my studies i thought so far that:
1 NA * Da = 1 * NA  mu = 1 g,
However since 2019 SI says that one dalton is only approximately one gram per mol
1 NA Da  ≈ 1 g/mol
This makes sense if I consider the definition of :
1 Da as 1/12 Mass of Carbon-12
while MW of 1 * C 12 is 12,0107 g/mol
However this leads to differences in mass calculation for molecules:
lets say for ssDNA PhiX genome of a length of 5386bp I calculated 1664042 g/mol but 1664051 Da MW leading to a difference of ~ 9 Da
so my question is how should i calculate and report molecular weights from now on to not include errors resulting from the change made by the International System of Units
can anyone explain to me or hint me to a publication or similar on how to correctly do mass calculation ?

This is a chemistry question and should be moved to SE Chemistry.

For practical purposes, the answer is that it doesn't matter. The example you give corresponds to a relative difference of approximately 0.00054 %. Depending on your pipetting skills, the volume you are trying to pipette and the pipette you use, your accuracy will be at best within a few percents of the intended volume.
If this helps convince you, try calculating the volume you need to pipette with both molecular weights: the difference will show only after several decimal places, that you would need to round anyway because the pipette only goes to two decimal places (assuming you are using a typical 10 uL pipette).
In addition, you can consult the Gilson Guide to Pipetting, section Tips for Mistake-Free Pipetting (page 23 in the edition I got at the time I wrote this), to learn about common causes of inaccuracy when pipetting and, more interestingly, how much variation they incur. You will see that they all amount to a lot more than the inaccuracy incurred by using an approximate molecular weight in your calculations.

Yes in actual practical terms this wont make a difference, even in microvolume work >0.1μl. However my question is more aimed at theoretical ideas, and if there is any guideline or strong opinions on how to use Da or g/mol in the future..


text:
Help Identifying this small spider (Tennessee)
This small spider, about .75" when legs spread, has a distinct "teddy bear" image on its cephalothorax. Help with identity please.

Welcome to Biology.SE. Please [edit] your post to include as much of the following essential information as possible to improve your chances of getting a good answer: 1) photos from multiple angles if possible; 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information; and 4) any behavior you observed. Detailed tag info page. ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site.

This is a ground crab spider from the family thomisidae. The general identifiers for this family are that the front legs rotate outward (crab-like), the two hind legs are much shorter than the front two legs (about half the length), and there is a fairly distinctively wide eye arrangement, which is hard to make out in this photo.
I don't know if anyone will be able to narrow it down to genus from this pic alone... from its features and the geography, the possible genera are: Modysticus, Ozyptila, Xysticus.
You can browse some galleries of these here: https://bugguide.net/node/view/1957/bgpage


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Vero cells and Influenza
I am currently reading a paper regarding Influenza. In the paper they describe a mutant and a WT, and the differences in replication. They grow the two strains in Vero cells (kidney epithelial cells). Why do they grow them in Vero cells, when it is a respiratory disease?
Link for article: https://pubmed.ncbi.nlm.nih.gov/9878611/

In addition to @David's answer, the viruses in this paper were specifically grown in Vero cells because of their lack of interferon expression1,2, which the authors were looking at for examining functions of the NS1 fragment from influenza.
Normally, influenza viruses are grown on MDCK cells for propagation or (more commonly) in embryonated chicken eggs.  The authors propagated the viruses in eggs in this paper, as explained in the Materials and Methods. The authors also used HEK293 cells for transfection, which are used in co-culture with MDCK to generate genetically modified influenza viruses.
1: Diaz, M. O., Ziemin, S., Le Beau, M. M., Pitha, P., Smith, S. D., Chilcote, R. R., & Rowley, J. D. (1988). Homozygous deletion of the alpha- and beta 1-interferon genes in human leukemia and derived cell lines. Proceedings of the National Academy of Sciences of the United States of America, 85(14), 5259–5263. https://doi.org/10.1073/pnas.85.14.5259
2: Mosca JD, Pitha PM. Transcriptional and posttranscriptional regulation of exogenous human beta interferon gene in simian cells defective in interferon synthesis. Mol Cell Biol. 1986 Jun;6(6):2279-83. doi: 10.1128/mcb.6.6.2279-2283.1986. PMID: 3785197; PMCID: PMC367773.

@bob1 provides a specific reason for the use of Vero cells in this case, where the study concerns the behaviour of these cells in response to infection by influenza virus. However, it is worth pointing out that the implicit assumption of the poster — that one should grow a virus in the cells it infects in the wild — is questionable.
The problem has been historically that the cells a virus infects in the body cannot generally be grown in tissue culture — some kind of immortalized cell is needed. Originally — before tissue culture had been developed — viruses were passaged by inoculating eggs, and an answer I provided to another virus question goes into this area in more detail.
In summary, if you want to grow a virus to obtain large quantities of virus or its components you choose the best system available for doing that. If you want to study its pathology you inject it into a suitable animal model, or if you want to study how tissues respond to it, you choose a suitable cell line (as in this case). But the two things are generally quite different.

What about A549 human lung epithelial cells? I think that was the OP's point. A549 grows Influenza as well. Look at the link, and you'll see why they chose Vero.