text:
Understanding entropy and the second law of thermodynamics as involved in metabolic processes
My AP biology textbook, (the 10th edition of Campbell Biology) states entropy as being the disorder or randomness of the atoms involved in any matter, but Khan Academy says that this example isn't quite right, and is too simplistic of a way of explaining the concept. And the TedED video I watched goes on talking about quanta and stuff ...
The online definition I was able to find of entropy on Wikipedia states the "The entropy of an object is a measure of the amount of energy which is unavailable to do work. Entropy is also a measure of the number of possible arrangements the atoms in a system can have. "
I'm confused how it's both at the same time and how they're related. And how does this even relate back to Biology again???

check this video https://youtu.be/8N1BxHgsoOw?t=63 and this: https://youtu.be/tFmJ4uVNX44?t=36 and https://youtu.be/Svvr5uF_FZ8?t=187 and some other vids :D https://youtu.be/9PGNeFmEFa8?t=1523 and https://www.youtube.com/watch?v=Ntdqft89_e4

If you want the concept of entropy explained, this is not on-topic for this site. In the general sense this is physics, but as it relates to chemical reactions, would be suitable for our sister site SE Chemistry. I would also suggest you read the account in Berg's Biochemistry. There are specific areas of biology and biological chemistry — not metabolic reactions, which are just chemistry — that raise particular problems in relation to the second law, but it does not seem that you are asking about these and that your question is off-topic.

It seems to me that the question you have that it relevant to this site, is not the definition of entropy, but why it appears in biology book in a section on metabolism. I do not own a copy of Campbell  so cannot check the section, but I can explain why it appears in the section of Berg et al. that I quoted in my other comment. It may be this is the reason it is mentioned in the less chemical Cambell. If you wish an explanation, could you please read through the section, accepting his definition of entropy, and tell us where it leads. Does it lead to the Gibbs Free Energy of coupled reactions?

2nd law of thermodynamics states that the overall entropy of the universe cannot decrease at any time. This can also be stated as the fact that the universe naturally falls towards the lowest energy state, or equilibrium. This becomes important in metabolic reactions. Reactions which seem to increase the state of energy, or perhaps the 'order' of the universe, have done so at the expense of another part of the universe, usually through the conversion of energy from molecules such as ATP or NADPH.
Think of the ATP Synthase on the cell membrane. It is creating ATP (Adenine tri-phosphate) molecules from ADP (adenine di-phosphate) and a phosphate group. This too seems like a system changing molecules from a low energy state to a high energy state. It is, but it can only do so by the natural flow of H+ ions which have accumulated on one side of the cell membrane and naturally flow from their high concentration to their low concentration on the other side. So while the ATP synthase molecule is making higher energy molecules (decreasing entropy) it is doing so as H+ naturally flows towards equilibrium, which increases the overall entropy in the universe.
In essence: things are always going towards a low energy state, i.e. equilibrium, i.e. maximum entropy. If any system goes against this, it does so via an outside energy source which has increased the entropy of the universe somewhere else.

+1 for describing entropy without using the word "random" and avoiding usage of "disorder".

I don't understand why you have to use the complex ATP synthase as an example. Surely any metabolic reaction would do, or indeed any chemical reaction as enzymic catalysis has no effect on the energetics.

(Pt. 1) I think I have a better idea of entropy now, my definition and example in my notes are as follows: Entropy is the measure of thermal energy in a system, thermal energy referring to the concentration of energy in bonds between molecules, this concentration naturally falls twords reaching equalibrium or the equal dispersion of energy between all bonds, when something is closer to equalibrium it cannot be used for work and carries less information.

(Pt. 2) For example, water is free flowing with energy bouncing between its molecules and is more stable then say, ice, which is structured and carries the information of it's structure, has fewer degrees of freedom for it's energy to flow, and want to melt into water to become more stable (spontaneously) It takes work to freeze water into ice (it's most natural ordered state) but work cannot be applied to water to make it anything more than plasma.

(Pt. 3) This is why it requires work (ATP) to create complex biological molecules, however life still increases the overall entropy of the universe because of the citric cycle and being "wirlpools" of moving matter becoming simpler forums

As tax money is no longer available for you payments, entropy is the tax of nature in that it is the energy taken (leaked) from your system, be it supplied or produced, that is no longer available for work.
You have to pay the tax (entropy) for every activity involving energy (money) other wise your activity will not be possible. If your activity involves lots of properties (number of particles or large size of the system, therefore higher degrees of freedom) you have to pay a higher tax ( termed entropic penalty). If your activity involves fancy properties (not so large number of particles but a highly flexible molecules in themselves, hence again higher degrees of freedom) again you have to pay a higher tax.
Carnot realized the concept of entropy when he was trying to design a perpetual motor.
He concluded that as long as the motor is made of material that consists of particles there will be leakage of some energy to the particles by means frictional dissipation and you cannot convince the particles not to do so. You can only minimize this leakage by choosing a system that has the least possible degrees of freedom.
This applies to literally every thing (every energy-involving activity or process) from biochemical reactions to electromagnetic radiation too (their particles are termed photons), and so it is a universal principle.

I am afraid this answer does not relate the concept of entropy to metabolism or even biology in general, so does not address the part of the question that is on-topic for this site.

Is it nearer to the topic now ? @David

By inserting “biochemical” in front of “reactions”?

Maybe, however, do you have any technical criticism for the answer?

My main concern with this question and answers to it is the relation to biology in general and metabolism in particular, as laid out in my detailed comment to the poster. This is so things remain appropriate for SE Biology. I will comment on answers if I think they are factually incorrect, especially if they have been upvoted, but otherwise I would not wish to discourage new contributors to the site. As for "technical criticism": you present a "tax" analogy that you think may help the poster. Only the poster can say whether or not it does so, although I personally would doubt it.

You doubt it because how much it relates to the question or because something in its essence?

The fact that I doubt it is unimportant here because it is a personal subjective opinion. I was just being honest with you. The basis of my doubt is a lifetime’s experience of teaching in higher education, together with my guess at the poster’s educational stage and requirements. I may be wrong.

I asked you for your honest opinion, so thank you.


text:
Quantifying the Genetic Basis of Complex Diseases
In general, there are 2 types of diseases for which we understand "causality" very well:

Infectious disease, where there is some etiological agent that causes the disease and
Monogenic genetic diseases (e.g. cystic fibrosis), where there are a set of mutations that make specific proteins that are very important non-functional.

My question is not about these diseases. Rather it's about the diseases like T2D (type two diabetes mellitus). Simply put, are complex, chronic diseases like this always traceable to genetic causes? For a given complex disease state, is there always a set of genotypes that leads to the disease? Large-scale GWA (genome-wide association) studies of course have upturned tons of disease-associated variants in complex conditions like T2D, most with tiny effect sizes.
But is it possible to get the disease with none of the disease associated variants (even assuming that you had a list of all disease associated variants; of course you don't actually have this list, but I'm just trying out an intellectual exercise)? If yes, what is the causal pathway for this way to 'get' the disease?
EDIT: To clarify my question as per comment suggestions: Do all (complex) diseases have a genetical background/causative mutation or can they arise for other reasons?

Welcome to the Biology StackExchange, if you haven't already take a look at the tour. I think you are asking a good, but also pretty difficult and potentially broad question. I think the core of your question is 'do all (complex) diseases have a genetical background/causative mutation or can they arise for other reasons' - if I'm right maybe edit this clarification into your question. Also, like David allured to, T2D is not a common abbreviation and you should explain it.

"what is the causal pathway" - very broadly: the environment. But, I think it would be impossible to find a disease that is truly only dependent on the environment: it's always a matter of degree, and there will be some genetic component that increases or decreases susceptibility. In some cases, this component may be trivially small in the extant population.

@Nicolai Thank you for your comment and apologies if I broke some rules. I agree the question is broad, but I figured I didn't know of a better forum to ask it since it's a basic question that I haven't seen directly answered in technical literature (textbooks and papers). Happy to delete the question if necessary. I also edited the question to fix the abbreviation and clarify the main thrust of my question.

I'm not sure what you mean by "complex", but many diseases are known to arise due to exposure to toxins or to an absence of essential nutrients in the environment.
Toxic metals:
A good example of this is exposure to some metals including arsenic, lead, and mercury.  See for example this information from the US NIH and the wikipedia article on metal toxicity.
In the case of arsenic, some of this poisoning is even "natural" — i.e. due to toxic levels of this metal in ground water that hasn't been contaminated by human activity.
Diseases that have been linked to such exposures include cancer, heart disease, diabetes, and anemia.1,2
Deficiencies:
Another class of diseases that are more-or-less purely environmental are those due to nutrient deficiencies — i.e. a diet lacking in minerals or vitamins.

References:

Byrns, M. C., & Penning, T. M. (2011). Environmental toxicology: carcinogens and heavy metals. The pharmacological basis of therapeutics. McGraw Hill, New York, 1853-1878.
Tolins, M., Ruchirawat, M., & Landrigan, P. (2014). The developmental neurotoxicity of arsenic: cognitive and behavioral consequences of early life exposure. Annals of global health, 80(4), 303-314.

source: Stack Exchange

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

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Why does higher venous volume increase atrial pressure?
If the cardiac output stays the same (hypothetically, although obviously it doesn't stay the same), then why does higher venous volume increase right atrial pressure? Shouldn't the flow rate be conserved (with a constant cardiac output) so that the venous return to the right atrium is no different than before, and therefore the pressure is no different?

Read about stroke volume. Cardiac output is not fixed. It's an average.

Imagine the circulatory system is an amusement park ride.  The ride is the left ventricle and the arterial system.  After riding, people go around and get back in line to go again.  The line and the building housing it are the venous system.  Maybe the lungs are some sort of staging area where you get ready to get on the ride.
The right atrium is the end of the venous system.  Venous pressures are right atrial pressure.
When all is well the line is moderate and people wait a short time before riding again.  But now 100 more people arrive.  If the park workers can speed up the ride or loading rate to accommodate the extra riders then great.  But if the ride cannot go any faster then the line backs up.  If you imagine that it is raining out, all the people in line bunch into the building housing it.  Venous pressure increases.  It will stay increased unless the number of riders (blood volume) decreases or the heart improves its output to accommodate the load.
Congestive heart failure is a useful example.  The ride speed (cardiac output) cannot increase because the heart is weak.   If riders increase (blood volume) it backs up into the waiting line or venous system.  This increase in volume occurs if someone with CHF eats a salty meal – water follows salt and blood volume increases, which backs up in the venous system because the heart cannot increase its output to accommodate the increased volume.  These sick folks are said to be volume overloaded.  You can see increased venous pressure as the signs of CHF – for example dilated external jugular veins.
Among many adaptations to deal with increased venous pressure is atrial natriuretic peptide.  When increased venous pressure stretches the right atrium this peptide hormone is secreted which is a cue to the kidney to dump sodium, and with it fluid volume.

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Is mucus significantly affected by the presence of ions?
In mucus, there is besides water and the mucins (Proteins for mucus), there are Ions like $Ca^{2+},Na^{+}$, etc. I have read that These Ions can Control the mucus swelling, i.e. the volume that the mucus occupies. Moreover, I have heard that some polymers can be affected by the presence of Ions, These are called "electroactive polymers". Is mucus a substance that changes ist consistence dramatically, when Ions are added or removed (equivalently, if pH value is changed due to $H^+$ ions)?

Do you mean the mucus, or the mucins? By bringing up "electroactive polymers" it seems like you are thinking in terms of the mucins, but that need not have anything to do with the effects of ions on the volume/viscosity of mucus. In fact, I don't quite see the connection of electroactive polymer and ions, because the former is referring to sensitivity to an electric field, which ions don't necessarily need to be involved in (at least on anything but an atomic scale) due to the presence of other ions of opposite charge.

Yes.  Mucus is hydrated by the movement of ions.
Cells cannot move water.  Cells can only move ions, and water follows the osmotic gradient.  When hydrating mucus, cells move ions into the mucus and water follows.  A failure of this system is seen in cystic fibrosis.
Targeting ion channels in cystic fibrosis

CFTR, the protein that is defective in cystic fibrosis (CF), directly
  mediates the transport of chloride and other anions through the apical
  membrane of several types of epithelial cells [1], [2]. Therefore,
  mutations impairing CFTR function cause a severe imbalance in ion and
  water transport that leads to a variety of negative effects in various
  organs. In the lungs, impaired secretion of chloride and bicarbonate
  appears to have multiple consequences. First, reduced secretion of
  electrolytes, and consequently of water, causes dehydration of airway
  surfaces with impairment of mucociliary clearance [3]...

People with cystic fibrosis have a defective chloride channel, and it cannot move chloride into mucus.  They therefore have thick mucus with abnormally low water content, and much of the trouble they have with their lungs is because this thick mucus does not perform its functions well.


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What is the simplest way to demonstrate the germicidal property of UV light?
This is intended for a high school project. I am familiar with the one that studies growth of e coli over time in a petri dish but I a bit concerned about as to how safe a demonstration of this nature might be. also no idea as how one may obtain such e coli sample safely.

Welcome to Biology.SE! ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

You can make homemade bacterial growth medium.
https://www.madaboutscience.com.au/shop/science-extra/post/grow-bacteria-on-homemade-agar-plates/
Basically it is just nutrient jello: beef stock, sugar, gelatin to make a firm surface.  It would be nice to have all your cultures in uniform plates or cups.  You could order petri dishes or use what you have available.  I would consider an ice cube tray or you could cut off disposable Red Solo cups to make dishes.
Then forget e.coli.  Inoculate the dishes with random things in the environment.  Everything has microbial life.   Fingerprints from various people are fine. Tongueprints would be a good variation - the jello is not poisonous.   A paw print from an animal would be fun.  A stick from the yard.  A snail.  Label each one with a label you can see from above - maybe a piece of paper on the table next to it.
Each of these prints will grow a mixed bunch of germs and fungi.  You might want to keep them cool because they will grow fast.  Take pictures periodically over time.  Keep them covered so they don't dry out.
Each type of dish (for example, Ted's tongue print) will have one dish in the dark (under foil) one in the light and one under UV light.  If you make big dishes you could have a half and half: light side and dark side.
Count colonies that can be seen at each time period.  That is your hard number and you can graph it over time.  The lines will diverge which will be a great visual.
In addition to the inhibitory effect of UV you can discuss how it differs.  Suppose there are orange colonies which do not seem to be inhibited by UV in the same way as everything else.  You could smear some of the orange on a microscope and look it is.  Is it some resistant organism?  You could discuss the variety of colonies that appear depending on the inoculum.


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What are the differences between the margins of the lateral and medial condyles of the tibia?
During an osteology lecture about the bones of the leg, the professor mentioned that the posterior (i think it was the posterior at least, I didn't write my notes down very well) margins of the lateral and tibial platues at the articular surface are different; the medial one's is sharper, and the lateral one's is smoother, rounder, or, as he put it, "sloppier", and this helps give more motility to the lateral meniscus and makes its injuries less likely. It also apparently helps the motion range of the knee joint.
I can't seem to be able to find any article or book that talks about this (I've checked Snell's, Gray's and Grant's anatomy books), so I was wondering if this is really a thing.

The proximal end of the tibia is broad and flat known as tibial plateau. The intercondylar region crosses through the midline of this plateau, separating the medial and lateral condyles of the tibia.
The two condyles are in form of flat and broad surface for articulation with the medial and lateral condyles. The medial surface  is convex and subcutaneous. The lateral surface, also known as articular surface is smooth surface and somewhat concave, and articulates with the talus.
[Sources:
https://www.physio-pedia.com/Tibia
http://en.wikipedia.org/w/index.php?title=Medial_malleolus&oldid=240146811
http://www.bartleby.com/107/61.html ]

This doesn't really answer my question; my question was about the two proximal condyles, more specifically, their posterior margins. The bartleby article does mention the fact that the posterior of the lateral plateau is slightly convex, but makes no mention of what that's good for.


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Is there a difference between splice-site mutations, and non-stop mutations
I'm working on a bioinformatics project where a lot of the biology I've had to learn from scratch. From my current understanding, a non-stop mutation alters a stop codon such that the transcription continues, and a splice site mutation alters the region between introns and exons - where the sequence may include introns, or remove part of the exons from cancer.gov. I'm inferring therefore that these could be the same mutation type.
Is this understanding correct?

No, those kinds of mutations are quite distinct.  Also, you misstate the nature of a nonstop mutation; the change of a stop codon affects termination of translation, not transcription.  This is quite different from a splice-site mutation, which affects splicing, a form of mRNA processing that occurs between transcription and translation.

Great thanks for clearing that up


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Gene APOA2 SNP rs5082 alleles are A or G, but papers describe it with CC and TT?
rs5082 is a SNP in the APOA2 gene. It is associated with obesity and heart disease risk.
According to this article the alleles can be A or G
https://www.ncbi.nlm.nih.gov/snp/rs5082#frequency_tab
Why does this article only discuss CC or TT?  Where is the A or G?
https://academic.oup.com/ajcn/article/108/1/188/5036568

It is probably a matter of strand. Check which DNA strand authors of both papers refer to - forward or reverse.

The rsID letters are assigned based on the genome being the default "forward" direction while the researchers on that gene think of the nucleotides of the context of the transcript, (or in this case the promotor sequence) which runs backwards.


text:
How do mutations of viruses lead to drug resistance?
For instance, after starting zidovudine monotherapy against HIV, resistance develops against the drug because of a point mutation in the RNA transcriptase enzyme to which the drug binds.
So how does the virus ‘know’ to mutate this particular enzyme?

@David After your edits, the answers no longer make sense. Yes, the question was based on a misunderstanding, but the answers explain why that understanding was wrong.

@Barmar, I've restored the original title question.  I agree the changed title had reduced the value of the answers for little benefit.

@mgkrebbs — I think we can improve the question by improving rather than restoring a bad title. I have had another go. The essence of the misapprehension remains, but it is no longer expresses it as an assertion, which I have reintroduced in the body of the question.

@Barmar I don't think so, because a title is not a question, and the last sentence of the question still encompasses the misapprehension. However, I have had another go at the title and altered the last sentence to explicitly include the "know" that appears in the accepted answer.

Coming in from outside, after having visited this question once before, the new title makes the answers make no sense.

@probably_someone I have edited the title to capture the revised title without destroying the context of the top answers.

@James I regard that as unnecessary (the last sentence in the question includes "know") and retrograde. By retaining the original title you are propagating the non-scientific thinking of a question which should have been closed for the lack of research.

@David I appreciate your point and agree completely that we should not encourage the idea of sentient evolution (or whatever you want to call it). However, when asking a question, it is more helpful if the title is a question rather than a topic/chapter title. What do you think of this one?

This is molecular evolution and is completely undirected.
Mutations happen all the time, most of them disappear without anyone noticing, since they have no evolutionary advantage to permeate.
This is different when you treat the cells and put them under an evolutionary pressure. Under this conditions, mutations which affect the mechanism of the drug (as here with a single point of binding) pose a great advantage for survival and with subsequent generations all carrying this mutation. This mechanism is simply a statistical one as the numbers of viruses produced in the infection is really large. It is not a matter if such a mutation occurs, only when.
Such a selection of specific clones is seen in other diseases too, leaving to the deactivation of the drug or the activation of different signal pathways, avoiding the one which has been targeted.
If you want to read further on viruses and mutation rates/mutations, take one of the following articles.
References:

Mutation—The Engine of Evolution: Studying Mutation and Its Role in
the Evolution of Bacteria
Antiviral drug resistance as an adaptive process
Mechanisms of viral mutation
Why are RNA virus mutation rates so damn high?

It doesn't. Viruses don't "know" anything. Mutations occur at random. Most of them don't do anything, or have a slight negative effect on the ability of the virus to infect and reproduce. However, there are billions and billions of viruses. Once in a while a random mutation will offer a significant advantage like immunity to an anti-viral drug. The viruses that have that beneficial mutation will then massively out-reproduce the viruses that don't have it. Eventually the population of viruses will consist mostly of individual viruses that have that mutation.

Are you suggesting every mutation ever happened is just an accident?

Yes, exactly. It's just that there are billions and billions of them, so sometimes something useful crops up.

@user73023 The same is true for all the mutations in every species of bacteria, plant, animal, etc.

@BryanKrause Well, not all mutations are accidents. GMOs were created by humans.

@Jagoe: Well, humans are an accident :-)  And from a strictly linguistic point of view, the changes made to GMOs are not mutations.

@Jagoe Even mutations involved in creating GMOs are random. You try to target a specific piece of DNA, but what will you actually modify is based on chance. Same like throwing the ball on target. You are trying to hit the centre, but you might go off. Most GM process involve stage where you try to look at the thing you created and verify that the change occured at the place you wanted and that there are no side effects.

@Jagoe here's one (crude) way how some  GMOs were developed through random mutations - https://en.wikipedia.org/wiki/Atomic_gardening

@jamesqf Not really, if you look at the big picture. Genes are replicators that create vessels for themselves to spread. As part of those vessels, they managed to build brains, which themselves are capable of supporting their own replicators - cultural information, memes. Those memes hijacked the "plans" of the genes (oops!), just what happened probably a few times before (any parasite in the broad sense does the same thing). When you look at humanity as a whole, much of our progress is through the same mutation-and-selection process, just ridiculously faster than genes could ever do.

@Jagoe Except that GMOs have been created by nature over and over again. We just adopted the same mechanism, and tweaked it for our own purposes. Both selective breeding and "modern" genetic manipulation are things that happen in nature all the time. And it's not like humans are all that special; we've developed thanks to natural selection, just like every living thing on this planet. Retroviruses change genomes of other organisms (including ours) too; bacteria share plasmids; many plants routinely hybridize like crazy (wheat and citrus fruits are probably the most visible crazy hybrids :)).

Billions sound like greatly underestimated when this site claims there are hundred million virus particles in a single cough drop https://www.livescience.com/3686-gross-science-cough-sneeze.html  They wouldn't evolve nearly as fast if there were just billions.

The genetic changes in GMOs have been facilitated or caused by humans, hence they are not random in the sense that someone intended those changes to happen. And GMOs are in fact, artificially-induced mutants. By definition, there are no natural GMOs.

@jamesqf Not all humans are accidents. Many of us are born because our parents wanted to. Those resulting from unintended pregnancies are accidents in the sense of their parents not expecting them, not because they are something unfortunate.

@Luaan Humans have also developed thanks to genetic drift, gene flow and selective mating. Natural selection is not the only process in evolution.

@Jagoe Well, of course. When we talk about natural selection being important, we're talking about adaptive evolution, which is the buildup of complex systems piece by piece. Things like tails becoming longer can easily be due to genetic drift and such. But it still fits the general pattern - genes building machines to spread genes, and those machines not always doing what's best for the spreading of genes. I'm not sure what part of what I'm saying you're disagreeing with. What makes us human still developed through natural selection, even though it's not the only effect at play.

@Luaan I thought that you were using natural selection and evolution interchangeably.

@Colombo Yes and no. The problem with CRISPR-Cas9 is not that it misses its target, but that it introduces unintended changes in the same area in addition. It's certainly not the same kind of random as in atomic gardening.

@Jagoe: You completely misunderstood my comment.  I meant that human beings AS A SPECIES are an accident.  As for individual children... Well, the parents may have intended to produce A child, but until genetic engineering progresses a lot further, the particular child they get is still an accident.

Summary: They Don't.
Long explanation:
Mutations happen at random. A series of factors can lead to the perceived notion that the mutation was intentional.

The mutation can be harmful, beneficial, or neutral.

Harmful: We don't see the harmful mutations as these individuals don't proliferate. The mutant individual just dies off without passing their genetic material forward, or they die out after just a few generations.
Beneficial: To the virus' viewpoint, of course. The mutants gain a competitive advantage over the other strains, and proliferate. This advantage may be noticed (e.g., as in the case of developing drug resistance).
Neutral: Most of the time, the mutation won't affect the individual's performance. Due to the mechanism of codon degeneracy, changes in one base in the DNA code may not even cause a structural change to the codon's amino acid equivalent.

Most viruses are not successful in reproducing. Those that are make millions of copies of themselves. One successful mutant has the potential of creating a whole new strain.
Viruses too are subject to selective forces. In the case of drug resistance, the successful resistant mutant won't have to compete with the other strains as the drug already eliminated them.
Drug resistance is not immunity. However, a resistant strain can very well mutate again to develop a stronger resistance.

We only observe the final effect (a new virus strain that seems to be engineered) but not the intermediate steps. There was a lot of (random) intermediate and unsuccessful mutations in between.

Let me know if this is off topic, but as a developer, my eyes were opened when I learned genetic algorithms. While the mathematics are tangential to actual biology, I think it illustrates the mechanism of an environmentally directed evolution of random mutations. An example I have is here:
https://github.com/Jarrod1937/genetic-algo-example/blob/master/ga/Form1.cs
The mutations are random, but the fitness function defines when the mutation is beneficial. In the case of a virus, the virus successfully propagating is the fitness function, and thus those of a higher fitness are more likely to propagate more, thus you see the increasing adaption against things that prevent propagation. However, this isn't the virus knowing where or how to adapt, rather, it is a case of sample bias. Your sample of viruses are the ones that survived and propagated, you don't see all of the failures that came before.

Hi Jarrod - this is the same way biology works, as described in the existing answers by Charles, Chris, and Mindwin. The mutations are random; what makes certain mutations increase their prevalence in the population is selection (effectively, this is the fitness function), plus other random components like genetic drift (which has most effect for mutations that have no or a small survival cost or benefit). Genetic algorithms sometimes cheat a bit, though, and have non-random mutations or other algorithmic tricks in selection and 'mating' that are not accessible to biology.


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In theory, could a woman that has fathers and mothers cromosome identical, be able to live?
What Im getting at is something totally impossible, but im making some mental experiences.

Assuming I have a machine that can produce a living being just from a DNA code (like in the movie  The Fly). If I make a DNA sequnce, that has mothers and fathers cromosomes identical, would such a being be a monstrosity or a human being when it got out of the machine.
For such a person, when DNA recombination between 2 eqal cromosomes is done, it will just be creating clones if itself.
Now we introduce a new monstrosity, a male twin male version of the identical-cromosome woman, that only hase the Y Chromosome altered. His sperm cells too will all be the same.
when theese 2.people mate, it will produce a clone.

EDIT:
To clarify my question number one.. Chromosome pair 1 has 2 chromosomes, one from father, one from mother. If theese two would be identical.

There is no need to invent some fantastic machine to create genetically identical animals. This is done all the time in plant and animal breeding, just not with people. It's accomplished by inbreeding over many generations.. Animals are typically about 98.6% identical after 20 generations of inbreeding.
The danger in inbreeding is the hidden presence of recessive traits in the parents that will be fatal (or at least deleterious) in the offspring, since the offspring will get two copies rather than one. Breeders find parent stock that can withstand such intensive inbreeding by trial and error. Of course mutations continue to occur after a genetically identical strain has been created, so genetic drift is a problem for laboratories using identical strains of plants or animals.

Geneticaly identical organisms are possible.  Lab animals are bred to be genetically identical.  Animals are inbred, with culling of animals that show recessive traits. Eventually there are no recessive traits except any which might arise by chance mutation.    This is also routinely done with livestock - a bull with desirable traits might be mated (via frozen sperm) his daughters, granddaughters, great granddaughters etc, each time with the offspring animal having a greater proportion of the bull's DNA.
If you mate 2 genetically identical organisms, you will not have a clone.  Gametes are scrambled via meiosis.
https://en.wikipedia.org/wiki/Meiosis

No new genetic material is introduced, but the chromosomes are resorted in random ways which result in slight variations gamete to gamete, and in the resulting progeny.

hmm, perhaps i wasnt clear enough with the question.  If X is a chromosome ( and XX is a chromosome pair), ill call it XX=XleftXright. My question is, couldn an organizm that has Xleft=Xright survive?

Typically when you have maternal twins the X chromosomes (and all the others chromosomes) are essentially identical. There is  nothing pathological per se about having an identical pair of chromosomes. It just depends on the presence or absence of recessive alleles.

To further elaborate, since my knowledge is limited in this topic:clarify:   Chromosome pair 1- has 2 chromosomes, one from father, one from mother. If theese two would be identical.


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Detect differentially expressing cells
I have data (RNA expression values, obtained with in situ hybridization) collected from 1mio human cells. For each cell, I have the expression value of a negative control (non-human RNA) and single-cell measures for different RNA species. I know that the values from the negative control correlate in a linear fashion with all the other RNA species. For example, when a cell has a high expression value of the negative control, the signal for all other RNA species will also be high. I now want to detect the cells that express an RNA without having a high negative signal, e.g. the "real" expressing cells.
One thing to have in mind is that some RNA species are abundantly expressed in many cells, other are very rare and have a low expression value.
I tried to do this with a linear model (for each of the RNA species, negative control vs. single RNA), computing z-scores, infer p-values and correct for multiple testing. For some RNA species, it works just fine. As soon as I have many cells expressing a certain RNA, the thing gets more tricky because the slope of the linear model doesn't reflect the linear relationship of negative control vs. RNA species in non-expressing cells because it is more shifted towards the "real" expressing cells.
To visualize the problem, I attached two plots. One plot showing high RNA expression many cells (left plot) and one from an RNA species which is expressed on a very low level in few cells (right plot). Blue colored dots are considered as expressing cells according to the linear model. As you can see, for the scenario shown on the left side, many "real" expressing cells are not detected.

Any ideas which statistical model would better fit to detect those cells?
Thank you for your suggestions!

Have you tried just substracting the values for the negative control from each RNA species X? I think that should both improve your actual measurement and make it easier to detect with cells have non-detectable levels of the RNA.

good point @Nicolai, I will try that.. but how would you then define expressing cells? with a manual cut-off? I have to say that I'm not a big fan of manually defining things for such analyses because I think that will just introduce an unnecessary bias.

You can try linear mixed effects model. I'm not 100% sure if it would help but the cell to cell variability of the slope/intercept can be modelled as the random effect.

Welcome to Biology.SE! This question seems like it might be a better fit for the Bioinformatics site.

@tyersome may be a better fit at [stats.se] but this isn't really a bioinformatics question.

@tebiwankenebi is the negative control and the expressed genes measured in the same cell (i.e. a two color FISH or something)? If not, you cannot simply subtract the negative control values. In that case, it is really not possible to differentiate a high false signal from a low true signal. However, if you consider each cell as a replicate population then would have to do some kind of two sample test or LM fit (using the expressed gene and negative control as predictors). LM may be less stringent than t-test or Mann-Whitney. Can you provide some more details on how you fitted the LM?

@WYSIWYG thanks for your answer. Yes, the expressed genes are measured in the same cell (it is actually multi-channel ISH). The linear model I use models Y = "mRNA of interest" ~ "negative control", assuming a linear correlation between the negative control signal and mRNA signal. I don't know if my approach is valid because I know that there is no linear correlation in real expressing cells (high mRNA, low negative control).


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How to get a list of kinases that phosphorylated a particular protein?
I am analysing the protein SF2 (also named as SRSF1). In the database, it is shown that this protein is often phosphorylated at the 189th tyrosine residue.
I want to know which proteins could have phosphorylated the protein at this site. Is there a way to figure this out using databases? What about getting a list of proteins that phosphorylated SF2 at any site?

I use PhosphoSitePlus too. I use it in combination with ELM as it finds linear motifs and generally gives a good generic candidate.
The literature if not. Checking all close homologues sometimes pays off.
Checking protein protein iteraction databases such as StringDB or IntAct may help too, but that gets very iffy —XL-MS (a smoking gun) is rare and does not pick up low concentration enzymes like kinases.
(A note: this question ought to have been asked in bioinformatics SO)


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Why does opening of the Ca-channels trigger the release of neurotransmitters?
I understand that the opening of the Calcium channels trigger the release of stored neurotransmitter in granules, but what is it about the flow of positive ions that makes the vesicles fuse with the cell membrane? Does the vesicle itself carry a charge or concentration gradient?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, have you looked at the related Khan Academy material? ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

I am not sure if this response is autogenerated, but I don't see how my question does not follow the guidelines. Synaptotagmin is not mentioned in any explainations I have read about action potential.

You'll note I didn't downvote (or flag) your question and I'm not claiming your question violates the guidelines. This was just intended as friendly encouragement to do some research on your own since this information is readily available online. ——— For example, when I did a search with keywords from your question ("neurotransmitter release calcium") one of the top hits was the Khan Academy video I linked to, another was this review, which does include details of the molecular mechanism ...

Ok I understand now, thank you for the clarification.

Synaptotagmin is a protein that is part of the synaptic release machinery. It binds calcium specifically, which leads to a conformational change that encourages vesicle fusion with the membrane, therefore the ultimate release mechanism is not via voltage or charge but by calcium itself.


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Why are nutrients from food absorbed more efficiently?
It seems to be common knowledge that micronutrients such as vitamins are more easily absorbed by your body when in your diet versus supplements such as pills.
I am wondering what the reasons for this are.

Does this answer your question? Is there evidence to suggest that nutrients in vitamin capsules are not as readily absorbed as the same nutrients in whole foods?

Welcome to Biology.SE! Note that "common knowledge" is often unreliable and this sort of claim should be referenced. We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, the "Related" links on your post include a very similar question on this site.  ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

magnesium in veg and bananas is in molecules like Chlorophyll, which is better to eat than: Magnesium chloride. ...
Magnesium sulfate.
Magnesium citrate.
Magnesium oxide. There are billions of micro-nutrients from many elements. When the source is already, previously metabolized by another organism, the nutrients probably exist in a less concentrated matrix and in less strongly bonded organic forms than synthetic lab-nutrients. Laboratory and rock-sourced nutrients are often more concentrated and have not previously been metabolized, in molecules like globin and chlorophyll.


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Who were the first authors to talk about local adaptation?
I was curious to read about what Darwin had to say about the existance of locally adapted subpopulations. I discovered to my surprise that the expressions and terms "local adaptation", "spatial heterogeneity" (or just "heterogeneity" even) and "environment" are completely absent from On the origin of Species. The expression "local conditions" was found 12 times but I could not find a place where he would suggest subpopulation of the same species could be locally adapted to their environmental conditions.
Who were the first authors to talk about subpopulations being locally adapted to their environmental conditions? Who were the first authors to understand the role that migration plays in reducing local adaptation?

Darwin mentions adaptation and coadaptation ample times in The Origin. All adaptation is local, I submit. The word adaptation comes to us from natural theology as Chambers showed in a later edition of Vestiges of Creation.

“… ‘second, of another impulse connected with the vital forces, tending, in the course of generations, to modify organic structures in accordance with external circumstances, as food, the nature of the habitat, and the meteoric agencies, these being the 'adaptations' of the natural theologian’." 10 ed. Of Vestiges of Creation, quoted by Darwin a later ORIGIN


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Can Huntington's Disease be homozygous dominant?
Can Huntington's Disease be homozygous dominant? I am not sure whether the individual who is homozygous dominant for Huntington's Disease will survive into adulthood, or die when they are infants or fetuses. I cannot find any good information on that topic.

It's a one gene defect AFAIK.

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Yes, but it's relatively rare.
The disease progresses more rapidly in homozygotes than in heterozygotes.1
Reference
1: Ferdinando Squitieri, Cinzia Gellera, Milena Cannella, Caterina Mariotti, Giuliana Cislaghi, David C. Rubinsztein, Elisabeth W. Almqvist, David Turner, Anne‐Catherine Bachoud‐Lévi, Sheila A. Simpson, Martin Delatycki, Vittorio Maglione, Michael R. Hayden, Stefano Di Donato, Homozygosity for CAG mutation in Huntington disease is associated with a more severe clinical course, Brain, Volume 126, Issue 4, April 2003, Pages 946–955, https://doi.org/10.1093/brain/awg077
Sourse: Homozygosity for CAG mutation in Huntington disease is associated with a more severe clinical course; Ferdinando Squitieri et.al. Brain, Volume 126, Issue 4, April 2003, Pages 946–955, https://doi.org/10.1093/brain/awg077

Welcome to Biology.SE! Good job on providing a supporting reference, but in the future please include the complete reference information since links can break. Also, do you have a reference to support the rarity of homozygotes and what that means? Are they less common that would expected for the prevalence of heterozygotes in the population? Underrepresented in the children of two heterozygotes? Thanks!


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How can the symptoms of ovulation (pms or pmdd) occur if one is menstrating?
Even if your period is lasting overly long. Wouldn't starting to ovulate end menstrating?

Does this answer your question? Can ovulation and menstruation occur simultaneously?

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What's the meaning of the label MRE and a number like 162 or 600 in the names of bacteria?
I've stumbled across labels like E. coli MRE 162 or E. coli MRE 600 for different kinds of E. coli bacteria.
What's the meaning of MRE and the numbers like 162 or 600 in this context?

Interesting, I think it must be a strain/isolate designation, but I couldn't find any listing that mentions whatever collection "MRE" stands for ...

Have you checked out my answer? If it answers your question satisfactorily please accept it. If it does not, please indicate what is lacking.

MRE is an acronym for the Microbiological Research Establishment at
  Porton Down, UK.

It was applied to Escherichia coli strain MRE600 as that was where the strain was first deposited, according to this paper.
I tracked the answer down in an article by Chris Morris on the Culture Collection Page of Public Health:
“My association with Porton Down, the current location of the European Collection of Animal Cell Cultures (ECACC), started at an earlier date than the inception of ECACC, and was when the site was known as the Microbiological Research Establishment (MRE), part of the Ministry of Defence.”
The numeric portion of the strain designation (600 etc.) that follows MRE is presumably just a reference or accession number within the institute, with no biological meaning.
(As a matter of interest, Porton Down had a certain notoriety in Britain back in the ’60s as a secret military establishment.)


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Does a breastfed infant gain immunoprotection due to intramuscular vaccination of the breastfeeder?
There is a claim that infants gain immunoprotection from breastfeeding.  I am especially interested in specific protection against pathogens the breastfeeder (not necessarily the mother) has been vaccinated against intramuscularly.
While I know, that IgA and IgM may be present in breast milk and provide passive protection against foodborne pathogens, it is unclear to me, whether there would be any synthesis (and transport to breast milk) of those antibodies without contact between the pathogen and a mucosal membrane of the breastfeeder.  Answer to my previous question suggest that there would be no IgA production as signals received by B-cells in a muscle will lead mostly to IgG synthesis.
I am not asking about the transplacental transport of IgG, only about breastfeeding.

Vaccinating the mother or a breastfeeder to provide immunization for the baby through breastfeeding is not proven nor recommended by health authorities.
If a mother is vaccinated intramuscularly or any other route, it will anyway pass IgA and IgM, and to a much lesser extent IgG antibodies to the baby through breastmilk but it is not proven to confer specific immunity against all pathogens.
And as per your other question, a child from a mother who hasn't had any infection/vaccination with Hepatitis A and hasn't passed any IgG through the placenta will not be conferred immunity against Hepatitis A even if it is breastfed from a woman who had the infection or was vaccinated against Hepatitis A.
There are other ways a mother's breastmilk can induce immunity (cell immunity) this is currently under research and it has been proven to confer immunity in animal models in recent studies but is still not a medical recommendation in humans (studies in pups regarding passing immunity through foster breastmilk for candida albicans , tuberculosis and helminth infections).
What is already proven is that breasfeeding and vaccination of the baby does provide with a more robust vaccination response so that is why breastfeeding and vaccination to the baby at the same time are encouraged.
Maternal Milk T Cells Drive Development of Transgenerational Th1 Immunity in Offspring Thymus
Pre-conception maternal helminth infection transfers via nursing long-lasting cellular immunity against helminths to offspring

May you point me to the source of the claim that intramuscular immunization leads to transport of specific IgA/IgM to breastmilk? The answer I linked in the question suggests there is no synthesis of specific IgA.


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Evolution of multicellular eggs
Which animals where the first in which ova were not simply released, but instead provided with some additional nutrition and/or protection in the form of a larger egg?

What animals are you talking about? Unless I am mistaken, eggs are, by definition, single cells.

@kmm the term 'egg' is also used for the vessel surrounding the ovum. I don't know if there is any other term for what we commonly call the egg (for example a chicken egg).


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Using autoclaved store-bought distilled water for labwork?
I'm a high school student who's working on a molecular biology project in my school's lab. I need pure water for making culture media, buffers, running a BCA protein assay, running digests, cleaning glassware, etc. I don't have easy access to any professional lab equipment, so I'm looking for an easy way to get "lab-grade" water.
Ideally I'd go to a university and fill up a carboy using a lab's milli-Q system, but this is not easy for me. I also don't want to shell out $$$ to buy ultra-pure water from online suppliers.
Will autoclaving store-bought distilled water (NOT mineral or spring water), suffice for microbiology labwork that needs pure water?

Yes, distilled water would be absolutely fine for your needs. You really don't need ultrapure water except for the most sensitive of applications. You also don't need to autoclave the distilled water before making things like media/buffer/etc; instead you would autoclave/filter them after you make them.
You can take a look at this document for an overview on different grades of water.

Distill your own.
A great excuse to build a distilling apparatus in your high school lab!  Distillation is a valid scientific endeavor it itself, and you can generate fresh distilled water as you need it and be sure of its purity, lack of plastic / metal contaminants etc.

This sounds like a cool project but I doubt I have the time to build and maintain a proper apparatus. More worrying is the amount of contaminants that are in our old, neglected glassware. I need to find a practical protocol for cleaning glassware on a budget...


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How many times have the cells in a human body divided?
Every single cell in a multicellular organism can in principle trace its "ancestry" back to the zygote through a continuous chain of cell divisions. How many divisions have occurred in a typical cell in an adult human body since the zygote was fertilized?
Obviously the answer depends on the organism's age and on the type of cell (as different types of cells divide at different rates). To be concrete, what is the average number of cell generations from the zygote across all the cells in, say, a typical 25-year-old human?
(Or any other age, if that's more convenient to estimate. I'd also be curious about the approximate minimum and maximum number of divisions, and which types of cells they occur in. If it's too difficult to estimate these statistics over the whole organism, I'd be interested to know if there are any specific types of specialized cells for which it's possible to estimate the "generation number".)
To be clear, I'm not asking about the maximum number of times that a cell can divide. I'm asking about the average number of times it has divided at a given point in time.

As a starting point for further exploration, Fig. 1 of this paper shows an association between different cancer types and the lifetime total divisions for the stem cell subtypes from which those cancers are derived.  The authors give their derivations of the replication rates for each subtype in the supplement (PDF download).

What type of cell?  For instance, AFAIK red blood cells don't divide at all, they are produced by other cells in the bone marrow.  I would expect the same is true of other kinds of cells, such as sperm cells.

What research have you done on the subject? this is something you could google.

E[MAX(X(t))] of the sampling distribution is the not the same as the largest value in the support for X(t)'s distribution function. It is a sensible to similarly wonder about the maximum number of times it has divided at a given time point $t$.

The supplemental material of the paper that Dirigible references in a comment to my question gives a rough estimate of these values. If I understand their simple model correctly, then we can estimate the average number of times that the stem cells in various types of tissues have divided over an 80-year lifespan from Table S.1 by finding the row corresponding to a cancer of that tissue, and then calculating $\log_2(s) + d$, where $s$ and $d$ are given in the table. (For specialized cells, I guess you'd add 1 more to capture the final cell division that produces the specialized cell?)
I haven't done the math out, but glancing over the table, it looks like the generation number varies widely between tissues, from a low of about 27 for some brain cells to a high of almost 6000 for cells in the colon and rectum.

Please [edit] your post to include the actual citation of the paper. It's not clear what paper you are referencing. Thanks

@theforestecologist - The paper is Variation in cancer risk among tissues can be explained by the number of stem cell divisions. The supplementary material is found by clicking on the link near the end of the article.

The supplementary material says epidermal stem cells divide about every $48$ days, typical stem cells divide about every $5$ days, oral mucosa stem cells divide every $14$ to $20$ days, etc. Some cells seldom divide. Carcinoma cells tend to divide much more frequently than average cells.


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To what extent does loss of neurons in the substantia nigra affect movement?
There is a substance known as MPTP that is capable of crossing the blood-brain barrier. Once it does so, it is metabolized into a toxin called MPP+, which then selectively destroys dopaminergic neurons in the substantia nigra pars compacta of the brain, causing parkinsonism. This effect of MPTP was discovered when drug users were poisoned with it in the 1980s.
How much of an effect does this destruction of neurons have on movement? Were these patients completely paralyzed as a result, or did they retain some ability to move voluntarily?

Great questions!  Here's some quick answers, but I'll give an additional little recommendation at the end if you're interested:
How much of an effect does this destruction of neurons have on movement?

Answer:  A large effect.  The key term here is "Parkinsonism," meaning that the symptoms resemble Parkinson's disease. This often involves motor symptoms like shuffling gait, tremors, rigidity, and bradykinesia (which means slow movement).  While they typically don't result in total paralysis, these symptoms can be debilitating and require treatment, such as L-dopa.

Were these patients completely paralyzed as a result, or did they retain some ability to move voluntarily?

Answer:  Generally, these patients were still able to move, but they greatly struggled with controlled movements.  As stated above, Parkinsonism/Parkinson's disease is marked by many motor symptoms, but these do not result in complete paralysis.  Rather, they make voluntary movements more difficult and slower.  According to a paper entitled "The MPTP Story (doi: 10.3233/JPD-179006)" it appears that at least one patient was nearly (if not totally) catatonic and exhibited very little voluntary movement.

If you'd like to know why this is the case in Parkinsonism and Parkinson's disease, I'd encourage you to look up the direct and indirect pathways of the basal ganglia online.  There's likely a good lecture with helpful visuals on how these pathways work to facilitate (direct) and inhibit (indirect) movement by their effects on the thalamus and motor cortex.  Alternatively, you can let me know you're interested via a reply and I'll do my best to explain those pathways on here.  Hope this helps!


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Examples of animals who 'forget' their offspring
Occasionally on the news I read about young children dying in hot cars on a sunny day. Usually the article reports that the parent(s) 'forgot' about their children still being in the car.
Obviously natural selection would select against a trait where parents forget about their dependent offspring or their whereabouts. However, I can imagine that under certain circumstances and on the fringe of the bell curve for offspring-caretaking, this occasionally happens.
Are there documented examples of animal species (preferably mammals or birds) who truly sometimes 'forget' about taking care for their dependent offspring, or forget their whereabouts?
Disclaimer:
I'm aware of possible anthropomorphism in this question. With 'forgetting' I don't mean behavior such as abandoning offspring at the age where they need to become independent, or accidentally being separated from their young.
Here's an example of what I would file under forgetting:
A parent feeds their young every two to three hours. One day, they go out to find food, but get distracted by something interesting (let's say a mate). They spend a day frolicking around with the mate, and eventually return to their young. On return, they find out one of the young has died due to starvation, and they are visibly surprised / startled / upset about this.
Edit:
To respond to Tyersome's comment: I have done plenty of searching and research. I haven't been able to find anything, neither in the scientific literature nor pop-culture websites / books. When you Google 'animal parenting' you'll find plenty of examples of various species who abandon their young (such as harp seals or rabbits) or who don't care for their own young (such as cuckoos), but these are 'deliberate' actions across an entire species, not examples of accidentally forgetting.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, when I searched for "animal parenting" I got many hits including a freely available article that appears relevant? ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Do you make a distinction between “forget” and “overlook” in responses to this question? The only thing you can observe in animals other than humans in behaviour. The latter is fairly common in birds, e.g in feeding of young.

@fileunderwater: yes, I would exempt the 'deliberate' overlooking of feeding certain young (by birds) from this question, since that seems to stem from some sort of choice for one or two offspring, not randomly forgetting a different one each time.

@YoupT With e.g. birds I think it is hard to make that distinction. Again, what you can see in feeding situations is behaviour. If certain weaker young are not fed because stronger siblings are more active and monopolize the feeding situation, and the parents do not observe this and actively feed the weaker young, you will end up with an forgotten/overlooked offspring which may eventually die. Was this chick forgotten or deliberately ignored? How would you make the distinction? It would certainly not be random, but I find it hard to label it a deliberate decision to choose one offspring.

I'll add a better description of 'forgetting' in animal behavior.

If the action of forgetting the offspring is accidental, and thus with a random frequency, how do you expect us to know if some species are more lenient then others to randomly "forget"?


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Nuclear vs Cytoplasmic Fluorescence
When staining transciption factor proteins with fluorescent antibodies (Alexa, etc.), why are the fluorescence signals stronger in the nucleus as compared to fluorescence signals in the cytoplasm (in context of transcription factor-activation?)
Is it simply spatial localization, that more fluoresence-marked proteins are at the same place, or are there other factors related?

Can you please clarify what you want to know. —— Do you find a strong signal in the nucleus surprising? Given their function, where would you expect to find transcription factors?

Yes, your hypothesis is correct. There are more of them.
A few terms need clarifying here, just in case...
First, fluorescence is due to the property of a dye that can be conjugated to the antibody. Different fluorophores have different properties, some are more efficient than others. Some display strong "solvatochromism", i.e. they are happier in the hydrophobic environment (brighter and red shifted).
Second, DNA is stained not with an antibody but with the UV fluorophore DAPI, which shines brighter in DNA —same thing with ethidium bromide and Sybr Safe.
Now, if you are labelling a TF and they ought to be in the nucleus you definitely will have a brighter signal as you suggest. There will be a way-ever-so slight difference as the environment is less aqueous, but the nucleus is not that packed as on pictures.


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What is the role of the pyrrolidine/piperidine moieties in fagopyrins?
Fagopyrins are phototoxic compounds that cause fagopyrism. They are chemical compounds related to hypericin and pseudohypericin. Some variations lack one or both methyl groups, which I think is to streamline the molecule so it better fits in membranes and so increase damage. The main difference from (pseudo)hypericin though is the presence of pyrrolidine or piperidine (or both) moieties, which may come from L-proline and L-piperidine-1-carboxylate (in turn from L-lysine) respectively. So, what is the function of those moieties in the fagopyrin molecules? Does it render fagopyrins more toxic than (pseudo)hypericin?

Radical generator
Looking at the molecules they are highly conjugated —must be dark red or similar!
And the disease is photosensitivity. Aromatics + UV? That is a standard UV radical reaction. It may be enough as a catalyst, but you'll get more will a cyclic amine, such as pyrrolidine or piperidine. If you want to go technical confer: Hofmann–Löffler reaction.
The radical will be passed on to other molecules, such as oxygen (generating peroxide), which will damage DNA and will raise an alarm biologically ultimately attracting neutrophils, which are expecting some attack (not poisoning), thus causing local inflammation, which manifests as skin irritation.
Demethylation
With the caveat that secondary metabolism is highly promiscuous and that some modifications are more accidental that anything else, let's look at the methylation and membrane permeability.
Promiscuity and secondary metabolism evolvability
This figure I found has the methylation patterns. A first glance I have assumed it was the usual C-methyltransferase action adding methyl groups, but instead it is a removal twice in the case of fagopyrin B and once in C and D. Specifically, fagopyrin is clearly two condensed anthraquinones molecules (emodin?) —which is a rather interesting non-standard change, I have not looked but so hope that someone has found the enzyme responsible! As you point out an anthraquinone is made by polyketide synthesis: the last acetyl-CoA results in a methyl group on the aromatic structure, which is occassionally oxidised to a carboxyl group (e.g. rhein) and in this case decarboxylated —I do not think a C-methyltransferase can remove groups even with pushed stoichiometries nor do I believe I have heard of one. But anyway. The anthraquinone condensing enzyme may not be able to tell apart the standard and the demethylated metabolites, which is otherwise meant for another pathway, i.e. it could just be promiscuous.
Membrane
Let's calculate the effect on solubility (python3 w/ RDKit).
Wikipedia has the SMILES string for the main fagopyrin and it's easy to spot the methyl groups.
from rdkit import Chem
from rdkit.Chem import AllChem
from rdkit.Chem.Draw import SimilarityMaps
# let's make the molecules
normal = Chem.MolFromSmiles('O=C1C2=C(C3=C(O)C(C4CCCCN4)=C2O)C(C5=C6C(C)=CC(O)=C15)=C7C(C3=C(O)C(C8NCCCC8)=C9O)=C9C(C%10=C7C6=C(C)C=C%10O)=O')
demeth = Chem.MolFromSmiles('O=C1C2=C(C3=C(O)C(C4CCCCN4)=C2O)C(C5=C6C=CC(O)=C15)=C7C(C3=C(O)C(C8NCCCC8)=C9O)=C9C(C%10=C7C6=CC=C%10O)=O')
# no need to orient them as the indices are the same. Whoohoo
img=Chem.Draw.MolsToGridImage([normal, demeth],
                              molsPerRow=2,
                              subImgSize=(200,200),
                              legends=['w/ methyls', 'w/o methyls'],
                              useSVG=False).save('/Users/matteoferla/Desktop/mols.png')

Now let's calculate logP (Partition coefficient).
    print('w/ methyls', Descriptors.MolLogP(normal))
    print('w/o methyls', Descriptors.MolLogP(demeth))

w/ methyls 6.71
w/o methyls 6.0

They are really soluble in octanol and insoluble in water. The unmethylated version is less hydrophobic.
Let's look at what is causing the difference by looking at the Crippen contributions to logP. Using the BluePurple colormap (suggestions welcome for best colormap for this descriptor), so that purple is hydrophobic while light blue is hydrophilic. Note that this is not partial charge (Gasteiger).
for mol, name in ((normal, 'meth'),(demeth, 'demeth')):
    AllChem.Compute2DCoords(mol)
    contribs = Chem.rdMolDescriptors._CalcCrippenContribs(mol)
    fig = SimilarityMaps.GetSimilarityMapFromWeights(mol, [x for x,y in contribs], colorMap='BuPu', contourLines=10)
    fig.savefig('/Users/matteoferla/Desktop/'+name+'_crippen.png', bbox_inches='tight')

The difference is a result of the methyl groups, being slightly more electron withdrawing than hydrogens making the carbon between it and the hydroxyl/ketone more hydrophobic. But overall does not change the polar sides, so is in effect unlikely to have an effect on its high membrane permeability.

The methylated fagopyrins are in fact the first fagopyrins, from which the unmethylated fagopyrins derive. The methyl groups are in the aromatic structure and in fact derive all the way from the first polyketide synthetized in the pathway (which leads in St John's wort to hypericin and pseudohypericin, which also have methyl groups (two in hypericin and pseudohypericin having one, the other being hydroxymethyl)). My conjecture regarding membranes is from extrapolation from how cholesterol fits better in membranes than its precursor lanosterol, which may be faulty reasoning.

I had mistakenly though they were extra added in addition. My bad. I have expanded that part of the answer —although it is a bit off topic now. The radical generator paragraph is satisfactory, though?

Yes, it's sastifactory enough.

Great. Don't forget to mark the question as solved then.


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static versus dynamic equilibrium when bending over
When a person stoops/bends over, is the equilibrium functioning static equilibrium or dynamic equilibrium? I am not sure, because on the one hand the person is not moving (static), however, his/her head is moving (dynamic).
Thank you!


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What does it mean that the transcript is enriched?
I think I don't get the meaning of "enriched" in the context of genes.
What's the difference of gene being "enriched" and "expressed" in the cell?

Welcome to SE Biology. It would be far better if you cite an actual example of the use of "enriched in the context of genes" that is unclear to you (with a link if possible). That way we would be able to clear up any misunderstanding, for example whether it is the gene that is enriched or its transcript. See the Help on Asking Good Questions.  (In general when one has a problem it is good to explain it in detail: often that helps one see logical flaws or questionable assumptions.)

In the context of transcriptomics the term 'enrichment' is usually connected to differential analysis:

If a transcript (or some/all transcripts of a gene) are detected in a given sample that transcript is expressed
If a transcript is detected at (statistically significant) higher levels in sample  (or condition) A compared to another sample B, that transcript is enriched in sample A.

In some cases one might compare two cell types, where only one expresses a given transcript, in this expression and enrichment in that cell line (compared to the other one) would be almost the same.

Thank you so much! Totally makes sens now.

In most cases (i.e. assuming there is no aneuploidy) a gene won't be enriched, however, the transcript from a gene may be enriched. A synonym in this case would be overrepresented. In other words, you find relatively more of the transcript compared to other transcripts.
Since you seem to confused about the difference between transcripts and genes, I highly recommend working through the material on a site like Khan Academy. This will help you understand the basic vocabulary and concepts of molecular biology. There are also a number free online textbooks available at NCBI where you can get more in depth information.


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Photolysis in the Light Reactions of Photosynthesis
I'm a bit confused concerning photolysis. During the light reactions, photons are used to excite the chlorophyll molecules so they are passed to the primary electron acceptor. The electrons initially come from a split water molecule. Is water split by the photons?

Does this answer your question? Photolysis of Water?

@tyersome the post you link to is about photolysis, but that post is about the chemistry of the process. Another post, Photosynthesis: What Powers the Splitting of Water?, appears to also ask about photolysis but from the perspective of the role of ATP. This current post, though related to the aforementioned posts, seems to be -- at least in my understanding -- more focused on the mechanism involved. I have provided an answer below that reflects this interpretation of the OP's question.

Regardless, the OP should sufficiently have received a response to their question from any of these three posts which are now linked as being related. Thanks.

A catalytic site on a subunit of Photosystem II is responsible for splitting water via photo-oxidation. This site, called the Oxygen-evolving complex (or OEM), uses energy from sunlight (which is converted to electrochemical potential energy in the photosystem's reaction center) to accomplish this task.

 Source: Wikimedia
See Barber (2012)1 for an explanation. The abstract (my emphasis):

The oxygen in our atmosphere is derived and maintained by the water-splitting process of photosynthesis. The enzyme that facilitates this reaction and therefore underpins virtually all life on our planet is known as photosystem II (PSII), a multisubunit enzyme embedded in the lipid environment of the thylakoid membranes of plants, algae, and cyanobacteria. During the past 10 years, crystal structures of a 700-kDa cyanobacterial dimeric PSII complex have been reported with ever-increasing improvement in resolution--the latest at 1.9 Å. Thus, the organizational and structural details of its many subunits and cofactors are now well understood. The water-splitting site was revealed as a cluster of four Mn ions and one Ca ion surrounded by amino-acid side chains, of which seven provide ligands to the metals. The metal cluster is organized as a cubane-like structure composed of three Mn ions and the one Ca2+ ion linked by oxo bonds. The fourth Mn is attached to the cubane via one of its bridging oxygens together with another oxo bridge to an Mn ion of the cubane. The overall structure of the catalytic site provides a framework to propose a mechanistic scheme for the water-splitting process and gives a blueprint for the development of catalysts that mimick the reaction in an artificial chemical system as a means to generate solar fuels.

My understanding is that we are still not totally certain how this actually works...

Cady et al. (2008)2 wrote a review in 2008 of various functional models trying to explain the chemistry of the oxygen-evolving complex of photosystem II.

A quick Google Scholar search reveals plenty of proposed mechanisms published since.

Most currently proposed mechanisms do, however, incorporate the 4 oxidation steps proposed by Kok et al. (1970)3 (now referred to as the Kok Cycle, or Kok's S-state cycle).

From Kern et al. (2013)4:

The oxidation equivalents generated by the absorption of four photons by the PS II reaction center are stored in the four consecutive redox states of a Mn4CaO5 cluster, known as the Si (i=1 to 4) states. The accumulated energy is used in the concerted oxidation of two molecules of water to form dioxygen (1) returning the catalyst to the most reduced S0 state in the Kok cycle (Scheme 1).

 Scheme 1 from Kern et al. (2013) explaining states of Kok Cycle.

You can learn more here.

Works Cited:
1 Barber, J., 2012, January. Photosystem II: the water-splitting enzyme of photosynthesis. In Cold Spring Harbor symposia on quantitative biology (Vol. 77, pp. 295-307). Cold Spring Harbor Laboratory Press.
2 Cady, C.W., Crabtree, R.H. and Brudvig, G.W., 2008. Functional models for the oxygen-evolving complex of photosystem II. Coordination chemistry reviews, 252(3-4), pp.444-455.
3 Kok, B., Forbush, B. and McGloin, M., 1970. Cooperation of charges in photosynthetic O2 evolution–I. A linear four step mechanism. Photochemistry and photobiology, 11(6), pp.457-475.
4 Kern, J., Alonso-Mori, R., Tran, R., Hattne, J., Gildea, R.J., Echols, N., Glöckner, C., Hellmich, J., Laksmono, H., Sierra, R.G. and Lassalle-Kaiser, B., 2013. Simultaneous femtosecond X-ray spectroscopy and diffraction of photosystem II at room temperature. Science, 340(6131), pp.491-495.


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Why did isopropyl alcohol not work as a disinfectant for E. coli in this experiment?
I recently performed a lab to test different concentrations (20-99%) of isopropyl alcohol and its inhibition of E. coli growth. My control was an antibacterial disk, and what I did was I dabbed the disk in each concentration and put it on the agar with the E. coli. I dabbed it enough so it wasn't soaking wet but it still had some liquid.
Unfortunately, I had no results at all from the alcohol-soaked disked, but I know the experiment should work because the antibacterial disks for all Petri dishes worked.
I don't know why the alcohol did not work at all though, especially since it is proven to be effective as a disinfectant at least for E. coli.
If anyone has a link with this exact lab being tested, or something similar (isopropyl alcohol and effect on zone of inhibition in bacteria labs) that would be amazing.
Concentrations 20,30,40,50,60,70,80,99%
-Disk diffusion, I put the bacteria by streaking across the quadrants
-I dipped the disks until it was soaked then dabbed enough to make sure it wasn't dripping
-Negative control:sterile disk In the middle, positive control: antibacterial disk on quadrant A
-I was going to measure zone of inhibition but there was none produced for all 12 plates except for quadrant A containing the antibacterial disk.

At 70 - 80% EtOH should work for sure. Can you give us details of the concentrations EtOH used, the  kind of plates/medium used, the method of plating (colonies or smooth surface of evenly distributed growth), the contact time of EtOH, the way EtOH was removed (evaporation/drying/etc), the strain of E.coli, and so forth, the study design (what was your negative and positive control), and last but definitely not least, the outcome measure used to determine the #cells left after treatment?

Just a thought: isopropanol is quite volatile and might just evaporate from the disk rather then diffuse into the agar, especially at 37C. I'm not sure the disk diffusion method is appropriate for testing microbial sensitivity of volatile liquids.

@AliceD This is all I know:
-Concentrations 20,30,40,50,60,70,80,99%
-Disk diffusion, I put the bacteria by streaking across the quadrants
-I dipped the disks until it was soaked then dabbed enough to make sure it wasn't dripping
-Negative control:sterile disk In the middle, positive control: antibacterial disk on quadrant A -I was going to measure zone of inhibition but there was none produced for all 12 plates except for quadrant A containing the antibacterial disk.
Thank you for your fast reply, I didn't expect there to be an answer so I'm sorry this is late

@canadianer I am thinking the same but do you know any references I can cite? I have to evaluate my procedure but I have no way to cite any of my assumptions :(


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Frameshift Mutation
With regards to LMNA frameshift mutations further downstream in the tail region, specifically (p.Arg455Gln fs*5) which has yet to be found/recorded in any medical literature...Does anyone have any knowledge regarding frameshift mutations (esp. concerning LMNA)? Is it possible that this is a "background mutation" and of little consequence?

Check in gnomAD. It is not in the population. It truncates the protein and the protein has a pLI of 1. So it does not tolerate LoF mutations. This mutation removes the lamin tail domain.


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Assembly of polypeptides expressed from different chromosomes to make a fully functional protein
In case of human beings, the whole genome is divided in 23 pairs of chromosomes in somatic cells. It has been observed that in case of many proteins (e.g. immunoglobulins, hemoglobin) different polypeptides are assembled together which are expressed from different chromosomes. My question is- what guides them to assemble them for the making of a fully functional protein??

They have complimentary interfaces on their surfaces and it is energetically favourable for them to stay together once they have found each other by Brownian motion. Often they are highly unstable alone. So it is simply thermodynamics and a decrease in Gibbs free energy.
This happens across life. Enzyme complexes in bacteria are on the same operon, especially in thermophiles, because they come together at a faster speed. In Eukaryotes it makes no difference as the mRNA needs to be processed etc.


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What is known about major events of pre-LUCA evolution?
All organisms share many common biochemical features (including 20 amino acid genetic code) and are believed to have a common ancestor (so-called LUCA). According to wikipedia article, this common ancestor was quite complex organism with advanced biochemistry. Are there an knowledge about evolutionary events occurred during pre-LUCA era? Namely, which of biochemical pathways already present in LUCA were evolved earlier than anothers?

There is an awful lot of literature and debate about what happened before LUCA consequently here are some key words to read more about, first on Wikipedia, then on review papers and then on the many papers...

According to the Oparin-Haldane hypothesis life formed from an abiotic primoridal soup.
These abiotic building blocks were formed by lightning, meteorites, UV or other processes (see Miller–Urey experiment and the Murchison meteorite)
Not all metabolites we know today existed and many that do not have a use today existed (non-proteogenic amino acids on Wikipedia is an article/list on the topic).
The genetic code is a frozen accident (Crick), but many believe it went in waves and was rather promiscuous (e.g. 3rd position pairs came later) and may have included ornithine and norleucine, which were "usurped".
Ignoring the temperature/location aspect, from a chemical point of view, life arises from a hypercycle process and requires gradients.
DNA did not form as is. The ribose may have been glycol and the nucleobase glycine: many metabolites in nucleotide metabolism are able to base pair.
The RNA world came first, then DNA with chromosomes came later. This has an odd effect in that early enzymes had to be highly multifunctional.
To have evolution, you need compartmentalisation.
Tar is gloop that forms easily abiotically. Tarrification is a threat to early life, but could have helped with compartmentalisation.
Montmorillonite clay can act as a scaffold for DNA polymerisation.
Ribozymes are RNA enzymes. The most core cellular processes is still RNA operated: the ribosome and tRNAs.
Many cofactors are primordial and are attached to riboses, e.g. NADH, FADH and arguably cobalamins.
Proteins came later, but still today the catalytic power of protein comes from their cofactors or from a single amino acid (e.g. cysteine as a nucleophile).
Once you have potentially RNA-encoded proto-enzymes you can start building more of the useful compounds that were available in the primordial soup but were depleted. Most pathways will therefore form by retrograde pathway evolution.
Enzyme activities can only be evolved if there is a pre-existing activity to select. Luckily accidental activities happen, called promiscuous activities (this term a century ago had no sexual meaning and used mean "being muddled").
Modern enzyme are highly specific and evolved to work at a high turnover (fast) and work at physiological substrate concentrations. But still have promiscuous activities because the substrate chemistry is similar. If the enzyme has never see a given compound the enzyme will not be evolved to not act on it and maybe the activity has no detrimental effect (neutral). When an enzyme evolves into a new activity an intermediate form is seem with higher promiscuity. These are often argued to be primordial-like.
Many pathways have a common origin, for example the Krebs cycle and the branched chain amino acid pathways and actually experiments in E. coli have found that the enzymes can rescue "deficiency" (auxotrophies) in the other pathway albeit slowly. Therefore, as enzymes could act on different similar substrates a set of overlapping pathways arose (patchwork hypothesis).
LUCA is the last common ancestor. It was likely thermophilic and lived in thermal vents as seen in every documentary. If life started there is debated.
Early enzyme were like very unstable, very very slow and may have often broken good metabolites in a futile manner. Given the problem of segregating with a chromosome and the need for high promiscuity, they had to be multifunctional. Not to mention that similar-ish amino acids were used interchangeably —isoleucine and valine say are hard to tell apart to modern tRNA synthases, go figure for the early ones.
Enzymes generally fall under a few families, which share a common ancestor. Rossmann fold enzymes for example bind NADH. TIM barrels are a ubiquitous fold.

So to answer your question, between the RNA world and LUCA, enzymes were slow and were selected upon to remake the more complex metabolites in the soup and then the simpler ones and thanks to their poor selectivity a patchwork of pathways arose. Once simple core pathways started and all metabolites could be made, more complex compounds that cannot arise abiotically such as the amino acids tryptophan and arginine were made. The enzymes became more selective and stuff like straight chain hydrophobic amino acids were selected against and the genetic code was fixed. Then you can make stuff like chromosomes and everything happens fast and efficiently.
Caveat. Early life was messy, really not efficient (it had no competition) and happened a long time ago. As time machines are physically impossible, all this is conjecture (sensu Popper), but the words theory and hypothesis are used happily in the field of origin of life.

Nice and broad answer. Can you provide a reference for review/paper dealing with hypothesis of inclusion of ornithine into early genetic code? Or any recent (scientific) review about the genetic code evolution?

1970s paper asking why no homoserine, ornithine, citrulline etc.
nice paper on early code
re-analysis of Miller experiment with modern tech
norleucine
a very recent review of the different hypotheses.


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Which sample type is more proper for whole genome sequencing in AML patients? Peripheral blood or bone marrow?
I intend to perform whole genome sequencing in AML patients in order to find genomic abnormalities, particularly translocation and gene fusions. However, I am not sure whether it is better to obtain peripheral blood or bone marrow or if there is no significant preference between them.
Please, provide me with scientific resources to refer to.
Thank you in advance.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). You also need to specify why you are doing this and what you mean by "proper". I would also guess that this is going to depend on many factors including what is already known about the patients and the resources available. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

In particular, note that bone marrow biopsies are painful and carry a non-trivial risk of infection (and other negative outcomes) for the patient. Consequently, I double any responsible institution is going to let you get that kind of sample unless you can come up with a compelling reason for doing so (from the perspective of the patients).

Thank you immensely for taking your time and guidance. Regards


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CD spectra of Porin molecules?
Can anyone please help me how will the CD spectra or graph of porin molecule look like. Porin molecule has 14 beta plated structures joined by some random coil, but it's very confusing to draw it. Can anyone please help me?

Welcome to Biology.SE! First, please define abbreviations (i.e. CD). Second, we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For example, if I search with your title I get numerous hits to papers including this.——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

CD (circular dichroism) spectrum of porin will look like CD spectra of most beta-sheet-reach proteins. You can look, for example, paper on PorB protein (Minetti et al, JBC, 1998) where authors present CD spectra of one of porines:
Circular dichroism spectra of recombinant PorB class 3 protein as a function of SDS. Standard solutions of PorB rclass 3 protein (1.0 mg/ml) dialyzed against a buffer comprised of 10 mM sodium phosphate and 0.05% zwittergent 3-14 and incubated with varying concentrations of SDS (0-1%) at 25.0 °C for 24 h prior to spectroscopic analysis. Far UV CD spectra are recorded for rclass 3 in the absence of SDS (solid circles) and at the following SDS concentrations: 0.15% (open triangles), 0.25% (solid squares), 0.30% (open diamonds), 0.40% (solid triangles), 0.45% (open circles), 0.50% (solid diamonds), and 1.0% (open squares).


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Which theory has more evidence, humans appeared in Africa 200,000 years ago, or there were already humans in Europe at least 210,000 years ago?
This theory
Modern humans originated from a woman who lived in modern day Botswana
says

Every person alive today descended from a woman who lived in
  modern-day Botswana about 200,000 years ago

And this finding states
Piece of skull found in Greece ‘is oldest human fossil outside Africa’

A broken skull chiselled from a lump of rock in a cave in Greece is
  the oldest modern human fossil ever found outside Africa, researchers
  claim.
The partial skull was discovered in the Apidima cave on the Mani
  peninsula of the southern Peloponnese and has been dated to be at
  least 210,000 years old.

Which certainty these findings have? Which one are we supposed to believe?
The question of the topic is, which theory has more evidence, humans appeared in Africa 200,000 years ago, or there were already humans in Europe at least 210,000 years ago?

I don't necessarily see a contradiction in both quotes: There were humans in Europe 210'000 years ago, but their female offspring do not/little contribute to todays human gene pool.

Considering even your linked article says the skull piece date is only preliminary results that have not been independently confirmed I would say it is the weaker one.

Mitochondrial Eve https://en.wikipedia.org/wiki/Mitochondrial_Eve does not mean "first woman" or first humans. "Every person" refers only to the matrilineal line. See also "pedigree collapse" by which everyone before a certain point will either be the direct ancestor of everyone or the ancestor of no one.

I voted to close this as "needing details or clarity", because the question as asked is entirely based on a misunderstanding as noted in comments. Revising the question ask more broadly for an explanation would solve this.

I disagree with the close-voters. I think this post should remain open. The main question (the one in bold) seems perfectly legitimate regardless of the comments (which are somewhat tangential given the main bolded scope of the OP's question). The OP has demonstrated prior research, has formatted the question decently well, and has asked a question that can receive non-opinion answers. The bolded portion of the question is not unclear (as close-voters are suggesting) and can be understood regardless of the context of the question or comments.


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What are the sizes of individual cells of the cyanobacterium Nostoc spheroides?
In this article Nostoc spheroids are described as edible blue-green algae, but they are mostly named cyanobacteria, which are prokaryotes.
In the above and other articles about Nostoc spheroids only sizes of the colonies are mentioned and i couldn't find the individual cell sizes.
Can the sizes of individual cells of Nostoc spheroids, and other cyanobacteria like Nostoc commune and Nostoc muscorum be found somewhere on the internet ?

We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and edit your question accordingly. Thanks!

@tyersome  If you read my question well, i did some research. I thought this is a very straight forward question. It's not my fault if it can't be answered !

You may have done some research, but IMO posting a link to Wikipedia page notifying us that there is no such page isn't convincing. 2) Lack of interest in searching out trivia for you isn't a sign that the question can't be answered. ——— If you really care about this information I encourage you to either write a convincing argument for why this is interesting or spend the time to find out the answer yourself.

If you have a question about a bacterial species. Bergey's manual is your friend: it is the definitive manual for bacterial morphology. Most universities have it as a pdf —I am unable to speculate on whether it is also available on say sci-hub (a paper pirating site). Check out figure 810.78 on page 576. Their shape can vary a large bit, but it is in the 1-3 µm range, so the usual size for diderm bacteria (2 µm is the length of an E. coli).