text:
Ambiguity about the relation between membrane potential and concentration gradient in neuron cells
I am stuck in an ambiguity about the equilibrium potentials of neuron cells. The following text is picked up from khanacademy website:
In one part it is said that:
We'll start out with K at a higher concentration inside the cell than in the surrounding fluid, just as for a regular neuron. (Other ions are also present, including anions that counterbalance the positive charge on K but they will not be able to cross the membrane in our example.)

If potassium channels in the membrane open, K will begin to move down its concentration gradient and out of the cell. Every time a K ion leaves the cell, the cell's interior loses a positive charge. Because of this, a slight excess of positive charge builds up on the outside of the cell membrane, and a slight excess of negative charge builds up on the inside. That is, the inside of the cell becomes negative relative to the outside, setting up a difference in electrical potential across the membrane.

As potassium continues to leave the cell, separating more charges, the membrane potential will continue to grow. Thus, the building membrane voltage is an increasing force that acts counter to the tendency for net movement of potassium ions down the potassium concentration gradient.
Eventually, the electrical potential difference across the cell membrane builds up to a high enough level that the electrical force driving K back into the cell is equal to the chemical force driving K out of the cell. When the potential difference across the cell membrane reaches this point, there is no net movement of K in either direction, and the system is considered to be in equilibrium. Every time one K leaves the cell, another K will enter it.

In another part it is said that:
The electrical potential difference across the cell membrane that exactly balances the concentration gradient for an ion is known as the equilibrium potential. Because the system is in equilibrium, the membrane potential will tend to stay at the equilibrium potential. For a cell where there is only one permeant ionic species (only one type of ion that can cross the membrane), the resting membrane potential will equal the equilibrium potential for that ion.
The steeper the concentration gradient is, the larger the electrical potential that balances it has to be. You can get an intuitive feeling for this by imagining the ion concentrations on either side of the membrane as hills of different sizes and thinking of the equilibrium potential as the force you'd need to exert to keep a boulder from rolling down the slopes between them.

I concluded the two following information from the above text:

The closer we get to the equilibrium state, the membrane potential
decreases because the concentration gradient decreases. (The steeper
the concentration gradient is, the larger the electrical potential
that balances it has to be)
The closer we get to the equilibrium state, the membrane potential
increases, because positive ions leave the cell.

How to solve this paradox?

Can you clarify your question? I think one of the issues here is understanding the difference between the membrane potential and the equilibrium potential. If positive ions leave the cell, the membrane potential becomes less positive/more negative. That is the only way positive ions leaving the cell will impact the membrane potential. The closer we get to the equilibrium state, the smaller the difference between the membrane potential and the equilibrium potential will be.

The closer we get to the equilibrium state, the smaller concentration gradient will be?

I interpret your question to be roughly: "the equilibrium potential is based on a concentration difference, but as ions move to create the electric potential, the concentration difference is changing. Why doesn't this in turn change the equilibrium potential such that the concentrations become equal and the potential becomes zero?"
If I'm correct...
The answer to your paradox is that very few ions have to move.
The number of potassium ions that would have to move across the membrane to establish the resting membrane potential is tiny. Electrical forces are very very strong. The imbalance in ions doesn't affect the concentrations inside and out appreciably.

For a typical cell, 1 microcoulomb of charge (6 × 10^12 monovalent ions) per square centimeter of membrane, transferred from one side of the membrane to the other, changes the membrane potential by roughly 1 V. This means, for example, that in a spherical cell of diameter 10 μm, the number of K+ ions that have to flow out to alter the membrane potential by 100 mV is only about 1/100,000 of the total number of K+ ions in the cytosol.

from Alberts, B., Johnson, A., Lewis, J., Raff, M., Roberts, K., & Walter, P. (2002). Ion channels and the electrical properties of membranes.
However, because membranes are also a little permeant to sodium, and because action potentials and synaptic transmission allow some additional ions to flow across the membrane, if you gave infinite time, eventually the ion concentrations inside and out would equalize, and the membrane potential would eventually be zero. The sodium-potassium pump solves this problem by continuing to keep potassium high and sodium low inside the cell.

Note that I also posted a very similar answer here: https://biology.stackexchange.com/a/57066/27148 but to a moderately different question that I don't think is really a dupe. I think that Q&A is good reading though for understanding how ions actually move in establishing resting potentials.

I think this answers a common question, but not the actual question/confusion the OP has. Take a look at the way the apparent paradox was worded, at the very end of the OP.

@DanHall Indeed I may have misinterpreted what they were trying to ask since I'm used to the problem I answered in students. Care to expand on your reading of it? I should add that my assumption was that they meant membrane potential increasing/decreasing to mean absolute value.

Take a look at my comment to the OP. It's hard to say for sure without some dialogue. I didn't phrase it as an answer. Since your the neurophysiologist here, I thought it best to leave it to you.

@DanHall Okay thanks. I've added an explanation of my reading of their question, so hopefully that will either help them realize I am answering their question or help them realize how to rephrase so I can answer their actual question :)

@BryanKrause I know that the concentration gradient is not necessarily zero in  equilibrium potential. My understanding from your answer is that: because very few ions leave the cell the concentration gradient does not change, right?

Correct! Basically you should take the concentration gradient to be whatever it is and don't worry much about it changing because of ions flowing. It only matters over a relatively very long time. :)

Your first deduction is wrong. The sentence actually means with a greater concentration difference at the initial condition, eventually there should be a higher electrical potential to satisfy opposite chemical potential. The dynamic of the system can be described by an exponential function. The closer to the equilibrium potential we get, the smaller the rate of approaching to the final state i.e. the rate of electric potential escalation will be.
Note that in reality this does not really affect the concentrations since a tiny amount of ion exchange can generate a considerable amount of electric potential.

You mean the last picture is showing the initial state?

The last picture demonstrates the final states for two systems with distinct initial concentration difference; Smaller for the right one compare to the left system.


text:
Energy metabolism in Cancer cells
The TCA cycle intermediate Isocitrate dehydrogenase commonly undergoes point mutations in cancers. This allows IDH to reduce a-Ketogluterate to 2Hydoxygluterate, causing a reduction in pVHLs ability to hydroxylate HIF-1a, and a subsequent accumulation of HIF-1a. This leads to angiogenesis via VEGF. If the cancer cell is converting its a-KG away form the TCA cycle, how does the cell make up for the loss of TCA function, and subsequent ETC function for energy production? Why would the cancer cell prefer to lose high yield energy production in exchange for low yield energy production?

Which IDH protein are you considering? Mutations are frequently found in IDH1 and IDH2. IDH1 is not even mitochondrial and clearly not involved in the TCA cycle. IDH2 is mitochondrial, but not NADH-coupled, and therefore probably not the main TCA cycle enzyme. Hence, it is not clear that there is any disturbance to the TCA cycle.

Two things...
Rapidly proliferating tissues (esp tumours) rewire their energy metabolism anyway to aerobic glycolysis where you have energy being produced by lactic acid fermentation even if oxygen is present. This is called the Warburg effect.Here's the thing about "low yield" though - glycolysis chucks out less ATP per reaction at the end, but you can crunch through a lot more ATP by just having more of it going on.
Secondly, hypoxia in a tumour is generally rate limiting, and therefore the shunting away of alpha-KG with the consequence of increased angiogenesis is good for the tumour.

the loss of function mutation of IDH does not necessary mean that the oxidative phosphorylation ceases. The supply of TCA intermediates can still be maintained if other pathways are upregulated, e.g. amino acid degradation. One has to keep in mind, that the TCA is not solely standing, but there is a highly dynamic network with many entry gates (illustrated in http://www.cs.cmu.edu/~blmt/Seminar/SeminarMaterials/kegg.gif).
If you are interested in, the group of Eyal Gottlieb (http://www.beatson.gla.ac.uk/cancer-metabolism-growth-and-survival/eyal-gottlieb-apoptosis-and-tumour-metabolism.html) is investigating the metabolomics in cancer cells with truncated ability to run TCA. For example the showed upregulation of Acetyl-Synthetase 2 allowing acetate usage for cancer cell growth under metabolic stress.
With best regards

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text:
Is there any alternative to cryopreserve cell lines without -80 freezer?
My university's -80 freezer just broke down and the repair will take 4 months according to the vendor. Is there any other way to preserve cells? Maintaining lot of flasks until the freezer is repaired is not viable option.
Is there any alternative to cryopreserve cell lines without -80 freezer?.

A tank of liquid nitrogen is not just an alternative, but a much better substitute, IMHO. The problem of gradually cooling inside a isopropanol container can be overcome by using a box full of dry ice (-79°C as I recall).

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What is Trypsin?
I am currently helping a PhD student in his research lab. We have been using Trypsin for the past couple of weeks but I am unsure of its purpose.
I was wondering how Trypsin functioned and what it was usually used for?
The Trypsin we had been using apparently had "gone bad" and therefore we have to start the experiment over again. What could have caused it to not function properly?

Welcome to Biology S.E.! If you have additional questions, please visit The Help Center

How do you know that Trypsin has gone bad, when you don't understand it's function in the protocol (no pun intended)?

@Chris You know because the grad student tells you after his cell cultures stop working right.

@user137 This can be one of the reasons.

I don't see how "bad trypsin" will spoil a cell culture. The only step that trypsin is used in cell culture is for detaching cells from the cell plate/flask, and if the trypsin is not working, the cells will simply not detach, and you will just either add more trypsin or use a different batch of trypsin.

Trypsin is a protease, an enzyme that cuts other proteins. It is used in cell culture to help lift cells from a plate by cutting the proteins that hold the cells to the plate and to each other. Trypsin can go bad because a trypsin enzyme can cut other trypsins, eventually destroying the batch's enzyme activity. This is why trypsin must be kept frozen. Of course you have to thaw it out to use it, so it's best to split the trypsin stock into small aliquots, so you don't have to thaw out the whole bottle everytime you split your cells.


text:
Using perceptual adaptation for enhancing realism of VR/other entertainment
I am quite a fan of the recent oculus rift VR glasses, but it does have several flaws over normal vision, most notably a much less wide field of view, the so-called screen door effect because of too low resolution (example 1, example 2) and often also a certain latency between head movements and corresponding view angle change.
Could one, in theory, create glasses which have these limitations to wear during everyday life to adapt to them, and later have the benefit of a more "realistic" experience?
I know making the glasses is not trivial, I'm just asking about whether the perceptual adaptation part would even work as intended, what timeframe I could expect to adapt in, and how stringent the wearing of them has to be (is waking up without them ok, or should sleep be blindfolded, etc).
Does anyone have experience/advice/knowledge on the subject, maybe even links to prior applications?

Very interesting question. Just for clarification: What do you exactly mean with: "Could one, in theory, create glasses which have these limitations to wear during everyday life to adapt to them, and later have the benefit of a more "realistic" experience?" This is your primary question right? Are you wondering, in general, if one could adapt to altered visual perceptions after a while? Or are you specifically asking whether electronic glasses exist that use this principle?

Both. I'm wondering whether this principle could be used in such a way, and if yes, whether someone has already done so. In the meantime I've learned that apparently combined nearsight/farsight glasses for elderly occasionally do something like this (left eye nearsight, right eye farsight, for instance), but I've never heard of limiting sight to enhance realism of "fake sight" (television, VR, etc).

Adaptation to altered vision is probably most well-investigated using prism-glasses. Prism glasses can shift the visual horizontally, for example by 20 degrees (Redding et al., 2005):

The use of horizontal shifting goggles has been investigated intensively to treat the symptoms of attentional neglect. Neglect occurs due to unilateral parietal brain lesions. For example, a lesion in the right hemisphere may induce left-sided neglect, where the left part of the visual field is seen, but simply not processed and neglected (Rosetti et al., 1998). Wearing prism goggles for approximately 6.5 hours/day, over the course of 2 weeks has been shown to reduce the symptoms of neglect significantly by as long as 17 weeks(!) after treatment (Frasinetti et al., 2002).
For the treatment of a neurological disorder such as neglect adaptation to prism glasses is great. However, treating healthy controls with comparable methods may induce unwanted side effects. 15 min of prism exposure has been shown to lead to several degrees of error in pointing tasks, for up to two weeks after the adaptation in normally sighted controls (Klapp et al., 1974).
To mention some studies closer to your question: in a virtual reality experiment subjects wore a head-mounted display that shifted the virtual position of their eyes. Their performance on a hand-eye coordination task first decreased by ~40% and then increased again with ~30% after adapting to the display. After taking the display off, there were transient after-effects, that impacted eye-hand performance (Rolland et al, 1995; Biocca & Rolland, 1998). In other studies wearing a head-mounted display longer lasting discomfort was reported in 5% of the subjects (Cobb et al., 1999) as well as binocular stress after removal of the display (Mark Mon-Williams et al., 1993).
Although the latter studies did not report serious after-effects, the more rigorously performed studies with the prism glasses have shown long-standing effects after visual adaptation. Hence, although the performance with virtual-reality head-mounted displays and comparable devices will undoubtedly increase after adapting to them, visual functions in everyday life may correspondingly be compromised.
So although this answer may not be addressing all your practical questions, I would say it is not advisable to let one actively adapt to head-mounted displays, or other wearable virtual-reality glasses that change visual function in the first place.
References
Biocca & Rolland, Presence 1998; 7:262-77
Cobb et al., Presence 1999; 8:169-86
Frasinetti et al., Brain 2002; 125:608-23
Klapp et al., Perception & psychophysics 1974; 15: 399-400
Redding et al. Neurosci Biobehav Rev 2005; 29:3, 431-44
Rolland et al., IEEE Proceedings of VRAIS 1995
Rosetti et al. Nature 1999; 365:166*9

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text:
Is radial cleavage (deuterostomy) ancestral to ecdysozoans?
Apparently Priapulids have deuterostomic development according to this paper:

Priapulids mostly reproduce by external fertilization, and the embryos undergo holoblastic radial cleavage, considered to be the ancestral cleavage mode in ecdysozoans.

Their conservative morphology might make them similar to the ecdysozoan common ancestor.
If Priapulids have deuterostomic development (radial cleavage), does that mean that:

The ELCA (Ecdysozoan last common ancestor) had radial cleavage and deuterostomic development
Insects and nematodoes have protostomy as a derived feature, not ancestrally inherited from the ELCA?

In the subsequent paper the authors make exactly this claim. I'm not an expert but deuterostomy is encountered in several unrelated taxa and I think it is more likely that deuterostomy in Priapulus and some arthropods evolved secondarily from ancestral protostomy (or amphistomy?), see Nielsen's review.

Note a related question here: https://biology.stackexchange.com/q/115095/22392. @alephreish based on the collection of data, it seems that deuterostomy (or deuterostome-like development) might be the ancestral condition, from which protostomy arose, and then deuterostomy re-evolved within some protostomes. Am I getting my ordering right? Not an expert!

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Was the deuterostome common ancestor a hemichordate, morphologically?
So it seems that the most accepted hypothesis now is that hemichordates are a sister group of echinoderms, not of chordates. Since acorn worms look to have a very basic, worm-y body-plan, how different would the deuterostome common ancestor have been from a hemichordate?
Additionally, since both hemichordates and chordates have gill slits and a post-anal tail, did the deuterostome common ancestor also have them?


text:
Why did worm-like lobopodians go extinct but polychaete worms thrive?
Obviously lobopodians are not extinct in the same way dinosaurs are not extinct (because of birds) - arthropods, tardigrades and velvet worms are all lobopodians.
But at the same time, there are no lobopodians occupying the marine worms-with-legs ecological niche - tardigrades are miniaturized, velvet worms are terrestrial, and arthropods generally have moved away from wormy shapes (maybe remipedes have undifferentiated segments).
At the same time, their ecological niche is obviously not defunct, but is occupied by polychaete worms. In fact, the old (and wrong) Articulata hypothesis comes because polychaete annelids look a lot like what arthropods should have evolved from - worms with stubby legs. And arthropods did evolve from worms with stubby legs, it's just that those worms were lobopodians instead of annelids.
So I guess my question is - similar to how today there are birds but not pterodactyls, why are there extant polychaete worms but no extant worm-like lobopodians - even though their body-type is essentially the same? Lobopodians were widespread during the Cambrian, did polychaete worms just outcompete them somehow?

No expert, but I'm not sure "Why" is answerable, other than with "Because they did" unless there's some direct evidence that there is a likely cause, such as with the Chicxulub impact and dinosaurs.

I assume polychates must have had some kind of an advantage. Another question is how long did lobopodians last - they are known mostly from the Cambrian but they might have lasted until the Carboniferous - https://www.sciencedirect.com/science/article/pii/S0960982212007427

In that case, there have been many mass-extinction events and we have lost quite a few whole lineages over the intervening time, including such long-lasting and abundant organisms as the artiopoda (which includes trilobites) and was around since the Cambrian right through to the Permian/Triassic extinction.

It could simply be that there's a paucity of specimens as the conditions needed to preserve them in fossils are relatively rare and as such we can't deduce much from the ones we do have.


text:
which enzyme phosphorylates sodium potassium pump?
I know that Na+/k+ pump possess atp-ase function; so the pump will hydrolyze ATP into ADP + Pi. And I see in a figure that the pump is phosphorylated but couldn't really find which protein catalyzes this.
Does the pump act as a phosphorylase??
Or is there a separate enzyme present nearby that does this?

What figure?  Go figure why a pump needs ATP, or read the associated text. Come back and post when you’ve researched your question better.

Also: Please add a link where you read this.


text:
Can MHC class I be used for presenting peptides of extracellular origin by non-professional APCs?
Wikipedia says that: "The antigens presented by MHC class II are derived from extracellular proteins (not cytosolic as in MHC class I)."
So does this mean that MHC class I cannot be used for peptides derived from phagocytosis by non-professional APCs? (i.e. peptides that of extracellular origin?).
For example, when non-professional APCs that can undergo phagocytosis (Eosinophil, neutrophil, dendritic cell) engulf bacteria, will they present their antigens using MHC I although the peptides are of extracellular origin? or will they not present any MHC at all? thanks!

when non-professional APCs that can undergo phagocytosis (Eosinophil, neutrophil, dendritic cell) engulf bacteria

Dendritic cells and probably neutrophils are professional APC, so this part of the question is a little confusing.
You're asking about cross-presentation, which is the process by which extracellular antigen can be presented to CD8 T cells on MHC class I.  Cross-presentation is mainly performed by certain sub-classes of dendritic cell. A number of other cell types have been shown to be capable of it, but it's not clear how important they are in vivo.
A decent review of cross-presentation is Understanding the Biology of Antigen Cross-Presentation for the Design of Vaccines Against Cancer.  A review of a related but somewhat different concept (MHC recycling) is Endocytic Recycling of MHC Class I Molecules in Non-professional Antigen Presenting and Dendritic Cells.


text:
How much oxygen does a human need to breathe?
So, I know that the title isn't very precise, but so is my current knowledge of the subject. It begs the question of what unit are we talking or maybe percentage? Let me explain the situation.
Earth's atmosphere consists mostly of 21% oxygen and 78% nitrogen. O2 is the compound we use to breathe, but nitrogen on the other hand is just a non-toxic gas and is not necessery. Well, it is as it increases pressure which is essential for human existance, BUT it can be substituted by other non-toxic gas like Argon.
On Earth's highest mountains oxygen percentage is on a similar level, but the pressure is lower. Hikers have to use oxygen tanks. If I deduce well, with lower pressure, human needs more percentage points of oxygen than in higher pressure.
Now I am writing a simulation of space ship, in which there is a security system, which controls oxygen in the cabin when pressure drops and it should always keep oxygen amount correct for any pressure given.
How can I calculate the perfect oxygen amount in air and what would be the actual unit of it? Any idea of a unit I have come with would be $\frac{kg}{m^3}$.

Probably the term you are looking for is the partial pressure of oxygen.


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Is returning cholesterol to the liver really performed by HDL?
Various answers in biology SE, including two quite upvoted ones (1, 2) claim that (in humans) returning cholesterol to the liver is done by HDL.
If I understand correctly, Wikipedia's Reverse cholesterol transport page also says this is done by HDL.
However, this blog post (by Peter Attia) says:

Historically this process of returning cholesterol to the liver was
  thought to be performed only by HDL’s and has been termed reverse
  cholesterol transport, or RCT [...]
This RCT concept is outdated as we now know LDL’s actually perform the
  majority of RCT. While the HDL particle is a crucial part of the
  immensely complex RCT pathway, a not-so-well-known fact is that apoB
  lipoproteins (i.e., LDL’s and their brethren) carry most of the
  cholesterol back to the liver.  In other words, the “bad” lipoprotein,
  LDL, does more of the cleaning up (i.e., taking cholesterol back to
  the liver) than the “good” lipoprotein, HDL!

Which is right?

According to Reverse Cholesterol Transport: Molecular Mechanisms and the Non-medical Approach to Enhance HDL Cholesterol (Frontiers in Physiology, 2018), both HDL and LDL are involved in reverse cholesterol transport.

In short: HDL takes cholesterol from the blood (from lipid-laden macrophages) and delivers it to the liver 1) via scavenger receptors (SR-B1) or 2) via LDL and LDL receptors (LDL-R). (For a detailed explanation of the diagram, see the Figure 1. in the linked article. There's a similar diagram (Fig.1) in Journal of Cardiology.)
Petter Atti says in his blog (emphasis mine):

Historically this process of returning cholesterol to the liver was
  thought to be performed only by HDL’s and has been termed reverse
  cholesterol transport, or RCT [...]
This RCT concept is outdated as we now know LDL’s actually perform
  the majority of RCT. While the HDL particle is a crucial part of
  the immensely complex RCT pathway, a not-so-well-known fact is that
  apoB lipoproteins (i.e., LDL’s and their brethren) carry most of the
  cholesterol back to the liver. In other words, the “bad” lipoprotein,
  LDL, does more of the cleaning up (i.e., taking cholesterol back to
  the liver) than the “good” lipoprotein, HDL!

He says that LDL does "more of the cleaning" than HDL, which may be technically correct in the sense that more LDL than HDL particles may be involved, but this alone does not change the concept of good or bad cholesterol. In the image, you can see that the initial cleaning (step 2 and 3) is done only by HDL, so without HDL no cleaning might occur at all.
Low HDL and high LDL levels in the blood are known risk factors for atherosclerosis (NCBI Books, 2019). Not all LDL particles are bad, though, the most harmful are oxidized small dense LDL particles (Hindawi, 2017).

I don't think your quote of Peter's blog supports your claim, as Peter only said that more cholesterol is returned to the liver by LDL (than the amount of cholesterol that is returned to the liver by HDL, which is non-zero). The sentence before the one you quoted says, if I understand correctly, that LDL returns cholesterol to the liver..

@OrenMilman, I edited the answer completely.

Can you elaborate on the difference between uptake of LDL by either Scavenger-Receptor "SCR-B" or LDL-Receptor on liver cells. Must I read "the most harmful are oxidized small dense LDL particles (Hindawi, 2017)", first? Can you expand your answer, as most people I guess do not know that liver cells have the LDL receptors and have never heard of Scavenger Receptor on liver cells (me, only yesterday, before I read you excellent answer).

Great answer!  It's pretty much focused on the question, so why not elaborate more about the concept of "cleaning up": those words may not be used for LDL carrying  cholesterol that might become oxidized while being carried on LDL? Then, that would be the SCR-B, not the LDL-receptor on liver cells?

Re critique by Oren Milman above:
Your last link out, Hindawi, says: "Oxidized LDL is recognized by a number of receptors, including CD36 and TLR-4", thus "cleaning up" in a literal sense you apply seems not to be "done" by LDL. When LDL becomes messy from O2, it does not do any reverse transport any more - itself, needs to be cleaned up, by receptors presumably not located on the liver but on immunce cells. I think that's very interesting, why don't you elaborate. Quote is very difficult to find, as very relevant,  reading through the source you gave.


text:
Are gill slits an ancestral deuterostome feature?
Gill slits are present not just in vertebrates, but in hemichordates where they are used for filter-feeding instead of respiration. The only extand deuterostomic lineage that does not have them are echinoderms. However I came upon this when reading Wikipedia:

Intriguingly, extant echinoderms lack pharyngeal structures, but fossil records reveal that ancestral forms of echinoderms had gill-like structures

and this:

With the placement of hemichordates and echinoderms as a sister group to chordates, a new hypothesis has emerged-suggesting that pharyngeal gill slits were present in the deuterostome ancestor

Is it possible or likely that the deuterostome last common ancestor had gill slits?


text:
Did the last eukaryotic common ancestor (LECA) have meiosis?
I know that sexual reproduction - meisosis - predates multicellular organisms, but did it evolve only once, in LECA, or did it evolve once in a subgroup of eukaryotes, or did it evolve multiple times?
Did meiosis evolve only once? Is it ancestral to all eukaryotes (i.e. coming from LECA)?

This is a great question and the subject of a number of scientific articles, e.g. this review from 2015. Here is their one-line summary quoted:

In summary, long-term asexuality is rare, and there is growing consensus that meiotic sex was present in the LECA and remains so in all major eukaryotic lineages

Here's my longer summary.
Historically, answering this involved catching organisms 'in the act', phenotypically: observing meiotic, a.k.a., 'reductional' cell divisions (diploid -> haploid cells), or fusions of gametes, or fusions of nuclei, both also necessary components of eukaryotic sex.
A more comprehensive approach is to survey eukaryotic species genomically: by looking for genes involved in meiosis, cell fusion, or nuclear fusion, in the genomes of all known eukaryotes, or at least a set of species representative of the full diversity of eukaryotes. The answer so far is that all major eukaryotic clades have representatives with genes encoding these features, supporting the idea that sex is an ancestral feature and was probably present in LECA.
Note that some lineages of eukaryotes are entirely asexual, including some multicellular organisms - notably bdelloid rotifers . In addition many single-celled eukaryotes are facultatively sexual, i.e. can reproduce asexually for many generations, e.g. ciliates and many other protists. Either way, loss of sex (and the associated sex-essential genes) is likely a secondary event: looking at a tree of eukaryotes with presence/absence of sex, it is much simpler to assume that it was gained early, and subsequently lost in a few lineages, than initially absent, and subsequently gained in many lineages. This is called 'parsimony' in evolutionary/tree-based thinking.
Finally, note that only a survey of all extant (=currently living) eukaryotic lineages, including potentially lineages that have as of yet never been observed, can definitively answer this question: if we find a single lineage of eukaryotes that is highly-diverged from all other known eukaryotes (=has been around in this form since LECA), and shows no evidence of sex, maybe sex evolved after LECA. Indeed, while it looks like sex evolved concurrently with the first eukaryotic cell, exactly why remains unclear: why would the emergence of a eukaryotic cell (= having a nucleus and having membrane-bound organelles like mitochondria) and of sex co-occur?


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Are bilaterians well-nested in Cnidaria?
From looking at articles, it seems that all the major neurotransmitters - serotonin, dopamine and noradrenaline - are present in Cnidaria. This, in addition to the fact that Cnidaria have a nervous system which uses the same neurotransmitters, would raise the question of whether Bilateria arose from within Cnidaria.
My questions are:

Does Bilateria arise from within Cnidaria in the same way that birds are dinosaurs?
If so, would cnydocytes have been ancestral in Bilateria but lost?
Do Bilateria and Cnidaria share a common ancestor that is not shared with Placozoa, Porifera and Ctenophora?
If so, was this common ancestor similar to an Anthosoa, but lacking in cnydocytes?

Bilateria are most likely not nested in Cnidaria. Peterson and Davidson, 20001 and Medina et al, 20012 discuss the developmental history of the Bilateria with respect to other groups within Animalia.
It seems most likely that Cnidaria and Bilateria share a common ancestor, which explains the common gene groupings. As such, Cnidaria is a branch of the Eumetazoan tree, as is Bilateria. This ancestor would also have been an ancestor of Ctenophora, but seemingly not of Porifera, which may have diverged before the divergence of Cilateria and Cnidaria, though this is hotly debated. The following image from Peterson and Davidson, 20001 shows their relationships based on Homeobox gene evolution:

 Image attribution: From reference 1. Note the following text from image caption: This view of Hox cluster evolution devolves from studies of de Rosa et al. (33), Finnerty and Martindale (30), and others (see text). The adult enteropneust, the larval enteropneust, and the larval sea urchin photographs are from the authors' collections; the rest of the animal pictures are from ref. 40 [reproduced with permission from ref. 40 (Copyright 1980, Stanford University Press)]
Medina et al, 20012 reached a similar conclusion using ribosomal RNA sequencing, as you can see in the following image. Note the difference between the two maximum likelihood trees; on the left is the small subunit tree and the right has the large subunit tree.

 image attribution: from reference 2.
As you can see there is some rearrangement of the order of relatedness between the Cnidaria, Ctenophora and Porifera between the two RNA types. This sort of information has led to some controversy in the literature, with some studies supporting the Porifera-first tree and some disagreeing with this, based on ever larger data-sets including more genes and more organisms, as noted in the introduction of this review by Steenwyk and King, 20243 (see  section titled The Tangled Branches in the Tree of Life).
Refs:

Peterson KJ, Davidson EH. Regulatory evolution and the origin of the bilaterians. Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4430-3. doi: 10.1073/pnas.97.9.4430. PMID: 10781037; PMCID: PMC34315.

Medina M, Collins AG, Silberman JD, Sogin ML. Evaluating hypotheses of basal animal phylogeny using complete sequences of large and small subunit rRNA. Proc Natl Acad Sci U S A. 2001 Aug 14;98(17):9707-12. doi: 10.1073/pnas.171316998. PMID: 11504944; PMCID: PMC55517.

Steenwyk JL, King N. The promise and pitfalls of synteny in phylogenomics. PLoS Biol. 2024 May 20;22(5):e3002632. doi: 10.1371/journal.pbio.3002632. PMID: 38768403; PMCID: PMC11105162.

Just to add - I think that Cnidaria and Bilateria are more closely related to each other than they are to Ctenophora. This is because Ctenophora does not have the other neurotransmitters - it uses only l-glutamate. Also, Cndiarians seem to have rudimentary eyes controlled by Pax6, but ctenophores do not.


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Separation of smaller DNA fragments and larger fragments without using gel electrophoresis?
For an upcoming experiment I would have two kinds of DNA fragments in a sample after a particular reaction step: First there would be fragments of a length of approx. 170 bps and then there would be Fragments of a length of approx. 270 bps or more.
I would like to maintain all fragments with a length of 270 bps or more and throw out all fragments with a length of 170 bps.
Of course, I could run everything on a gel and collect just those bands above 170 bps.
However, I am wondering whether there is something more elegant to reach that aim. For instance, we could use a filter that collects just those fragments with a size of 200 or 250 bps or more and those fragments with a smaller size flow through the filter.
Is such a thing possible and if so, how? Or would you suggest something else?
Many thanks for your support in advance!

One option is to use SPRI beads, like those sold by Ampure (Ampure XP beads) to separate DNA fragments by size. By adjusting the ratio of beads to sample, you can selectively bind fragments of certain lengths by excluding those of other lengths, as seen in the following image:

From this image, you might try using a beads-to-sample ratio of 0.7 to exclude fragments below 200bp, or a ratio between 0.7 and 0.6 to exclude only those fragments below somewhere between 200 and 250bp. The advantage to beads over a gel is the time it takes. Size selection by beads takes only around 10 minutes, versus maybe 30 minutes or more for a gel (including the extraction).
As with any molecular biology procedure, it's important to test it and make sure that it works for you. For instance, it might be a good idea to take aliquots of your samples and compare the lengths and yields that you get from a range of bead concentrations and/or to compare the yields that you get from using gel vs (in this case) beads.

Interesting, I didn't know about these.

In my mind, gel separation (using a fairly high percentage gel to separate the bands as much as possible) and manual excision is by far the best option. The problem with molecular weight cutoff filters is that the value they give (5000 Da, for example) is an average pore size, it is not exact. Therefore, any attempt to separate 270 bp from 170 bp oligos will end up with some of the shorter construct ending up in the final product, and some of the longer sequence in the flow-through. The chances of finding an off-the-shelf product that exactly meets your size requirements are also low. Only use these types of kits if you're separating a 300 bp PCR product from unused primers, for example.
You could do some sort of column chromatography using a size-exclusion matrix, but that's essentially the same thing as using a gel. The only advantage is it can be scaled, so if you have large amounts of PCR product to separate (let's say 5 or 10 ml), it would be easier to run a single column than to load that many lanes in a gel.


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ssDNA library amplification
Assume we are given approx. 80,000 dsDNA fragments of 40 bps length each.
I would like to amplify of each of the 80,000 fragments just one particular strand, such that I obtain amplified 80,000 ssDNA fragments of just 40 bps.
Also beforehand if could be helpful to amplify the 80,000 dsDNA fragments, so where the amplified fragments stay double-stranded.
If you could help me for both amplification steps, particularly the first one, I would be very delighted!
Many thanks in advance!

It is not possible (without any additional upstream steps). For example, how would you define which of the strand should be amplified?

Well I think of extending the fragment by say 10 bps upstream and downstream for each fragment, which is identical for all. Then I could selectively amplify a particular strand via the primers that match to the 10 bps each.

How would you add this 10bp sequence; by ligation?


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Why scientific names of animals & plants are made difficult to spell & remember?
Why scientific names of animals & plants are made difficult to spell & remember?
Mango: it is easy to spell.
Corvus splendens: it is difficult to spell

It's not difficult to spell if your an 18th century naturalist who speaks Latin.

Take the cat: felis domesticus - domestic feline. Take it to a slightly higher level, wolf: canis lupus - lupine canine("lupine" as an adjective ultimately originates from Latin).

I'm voting to close this question as off-topic because this is childish and not about biology in terms of SE Biology.

The reason scientific names are difficult to remember is because the scientific names are given in Latin. There are rules to be followed when naming a organism. That the name must be in the form of Genus species is one of those rules.
For a person who knows latin, it would be just as easy as the English names are for a English speaking person.
In earlier days, Latin was considered the language of the scholars. That was the reason Latin was chosen for binomial nomenclature. As scholars of all languages learned Latin, just hearing the name would give the hearer an idea of what the organism is even if (s)he had not seen it in person.

For more on scientific naming and rules while naming see:

https://en.wikipedia.org/wiki/Binomial_nomenclature
http://education-portal.com/academy/lesson/binomial-nomenclature-definition-classification-system.html
http://www.curioustaxonomy.net/rules.html

The thing is that there is such a language called Latin that is used to name species. During Linnaeus' times when he created the binomial naming system, Latin was the prevalent lingua franca among international scholars. Therefore, all the species names actually make sense, though only hardly so in English.
Names that make a little sense in English include:

Wolf: Canis lupus - Lupine canine
Domestic cat: Felis domesticus - Domestic feline
Wild horse: Equus ferus - Feral equine

These make sense because many English words originate from Latin, be it directly or through French.
Some of the words used in binomial names are Latinization of Greek words (that there are not such words in Latin itself), or valid Latin words that originally came from Greek, so some names would also make sense in Greek. Besides some English words also trace back to Greek.

Lion: Panthera leo - Latin word which originated from Greek
Megalania - Latinization of Greek neologism "mega"+"elaino" = "Great roamer"
Baker's yeast: Saccharomyces cerevisiae - Latinization of Greek "sacchar" + "myces" = "sugar fungus"
Penicillium chrysogenum - Latinization of Greek "chrysos" + "genos" = "Gold maker" as it produces a yellow(golden) pigment

Beyond those are names coined after locations and discoverers:

Flores man/hobbit: Homo floresiensis - Latinization of the location of discovery, Flores
Common kingslayer: Malo kingi - Latinization of the name of the victim, Robert King, whose death by the jellyfish's venom led to its discovery (note that the English common name also came from the name of the victim)

Some species are also named with Latinization of words in other "native" languages, such Panax ginseng, named after the Chinese name 人参 (I'm not sure exactly what dialect/topolect it is).

Beyond species names, Latin is also used in other parts of biology such as anatomy:

Biceps femoris: Two-headed muscle of the femur
Vena cava superior: Upper hollow vein
Corpus luteum: Yellow body (body as in object)
Ileum: Guts/intestines

Beyond biology, Latin is used in meteorology to name clouds, astronomy as the common name of stars (Bayer designation), and remains an official language of the Holy See (the authority of the Vatican) as well as the motto of many organizations:

Cirrostratus fibratus - fibrous layered cirrus(curly hair) cloud
Sirius: Alpha canis majoris - Alpha (number one) star of the constellation canis major
Old motto of USA: E pluribus unum - "Out of many, one" (signifying unity among states)

The question bares a resentment to awkward sounding Latin names. It is unfortunate, since there is surely logic in Latin nomenclature.., but admittedly  it is also unfortunately a steep learning curve to learning some Latin. Anyway, having one gold standard nomenclature, no matter how stupid it sounds, is a blessing for scientist of the field (it's coming from a genomics-ist dealing with alternative gene names on a daily basis where there is no Latin-like-gold-standard and alternative databases compete for rightfulness of their logic and nomenclature). I work on a protein called Mili, and in dozens of papers it is called so, but I cannot guess without googling how it is called in RefSeq or Ensemble power houses of genomic annotations


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What are the fibers and small droplets on the surface of dividing HeLa cells in the figure?
I did some literature searching but could not find any info probably because I did not know how people name them.

The figure is from the wikipedia entry HeLa

They are microvilli and blebs.


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Cell strength - why is an animal's body so strong?
A cell membrane consists of a double layer of phospholipids - to my mind a thin film of grease, if you will excuse my wildly unsophisticated understanding. It doesn't seem to be enough to convey the sort of mechanical strength that an animal body has, so why is, for example, the human body able to stay together rather than fall apart?

Possible duplicate: https://biology.stackexchange.com/q/88965/27148

Because the phospholipid membrane is augmented by other structures and materials created by the cells, such as collagen and keratin. Without these, you are indeed correct in that animals would just disintegrate.


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What is the function of smelly sweat in primates?
I remember one, sweltering day in Malaysia, I was climbing the very long staircase to a Buddha statue in a cave, when I suddenly felt enveloped in an overpowering smell of sweat. My first thought was that I must have forgot to wash, possibly for several weeks, but then I realised that I was in the middle of a troupe of monkeys.
And now I've come to wonder what the function is of this very characteristic smell. There seems to be connection to sexual maturity, since children don't start producing the smell until puberty, and the overwhelming base of evidence I collected that day, seems to suggest that this may be universal among primates.
Has any research been done into the function smell of sweat, socially or otherwise?

Why do you think it has a function?

It might not have a function. But maybe it's there as an indication that one should clean themselves to prevent disease. We similarly developed smelling dead bodies and excrement as foul to stay away from them because they can cause disease despite other animals like blowflies being attracted to these smells.

Sweat does not smell much on its own, its the bacteria that eat the sweat that smell.

@user438383 Well, mostly because it only really starts at puberty. The fact that other primates also smell strongly suggests to me that this an adaptive trait that goes several million years back; and although we in modern society find the smell rather offensive, it is not actually smell you connect with decay. I believe more in the idea that it signals adulthood and perhaps that you are ready to fight for your territory or group, which may explain why we now try to mask the smell with deodorant, since we live rather stressful lives in dense cities.

@j4nd3r53n thats fine, it's just always good to question whether a trait is really adaptive has a function or whether it's just a random byproduct of something else. Often things can appear to be adaptive when they are really just nothing :)

It's a tricky query to answer, so here's some prelim info and someone can be more specific from there:
Apocrine glands are a type of sweat gland found in certain mammals, including humans. These glands are responsible for producing a thick, odorous sweat that is involved in various physiological and social functions. Here are some key characteristics and functions of apocrine glands:
Location:
Apocrine glands are typically found in specific areas of the body, such as the armpits (axillae), genital region, and around the nipples in humans. In other mammals, they may be located in different regions depending on the species.
Odorous Secretion:
Unlike eccrine glands, which produce a watery and odorless sweat, apocrine glands secrete a thicker sweat that contains proteins, lipids, and other compounds. When this sweat comes into contact with bacteria on the skin's surface, it can lead to body odor.
Activation:
Apocrine glands are activated during emotional arousal, stress, and sexual activity. The sympathetic nervous system controls their secretion, and hormonal factors can also influence their activity.
Scent Communication:
One of the primary functions of apocrine glands in mammals is scent communication. The odorous sweat they produce contains unique chemical compounds that can convey information about an individual's identity, reproductive status, and social position to other members of the species. This is particularly important in social species where scent marking and recognition play a crucial role in group dynamics and hierarchies.
Sexual Signaling:
In some species, apocrine gland secretions may play a role in sexual attraction and mate selection. The distinct scents emitted by individuals can serve as cues for potential mates to assess each other's fitness and genetic compatibility.
Developmental Timing:
Apocrine glands are not fully functional until puberty in humans. Their activation and development are influenced by hormonal changes during adolescence.
Associated with Hair Follicles:
Apocrine glands are associated with hair follicles, and their ducts open into the hair follicle canal. This is in contrast to eccrine glands, which release sweat directly onto the skin's surface.
Here's a ref from nature stating that human primates may use sweat pheromones to communicate:
https://www.nature.com/articles/npre.2008.2561.1.pdf
Primates, especially those living in social groups, rely heavily on communication to maintain social bonds, establish hierarchies, and coordinate group activities. Scent plays a crucial role in primate communication, and sweat scent could have evolved as a means for individuals to convey information about their identity, reproductive status, and emotional state to other members of their group.
mate selection in primates can be influenced by olfactory cues. Scent signals emitted through sweat may allow potential mates to assess each other's genetic compatibility, overall health, and reproductive fitness.
the scent-marking behavior using secretions from sweat glands may serve as a way to establish territorial boundaries and prevent conflicts with neighboring groups.
The odor produced by sweat may play a role in avoiding predators. For example, certain primate species may produce alarm pheromones through their sweat, signaling danger to other group members.
Sweat scent in primates could be a remnant of their ancestral heritage, where scent communication was crucial for survival and reproduction.
incidentally, horses, dogs, deer, they also have strong pheromones.

Thank you for the article, +1. So it seems pheromones have an effect, even in the absence of smell. But evolution wouldn't have favoured sweat that would produce this characteristic smell when broken down by skin microbes, I think, unless the smell itself was important. Perhaps it amplifies the effect of pheromones?

To elaborate slightly on the existing answer in which mention is made of 'genetic compatibility', there are many compelling studies which indicate a strong preference for dissimilarity in class 1 HLA alleles between human mating partners, and that this dissimilarity is readily detectable in the body odour of respective individuals.  The link below 1 is to one such study; and the following paragraph is its abstract.

The major histocompatibility complex (MHC, called HLA in humans) is an important genetic component of the immune system. Fish, birds and mammals prefer mates with different genetic MHC code compared to their own, which they determine using olfactory cues. This preference increases the chances of high MHC variety in the offspring, leading to enhanced resilience against a variety of pathogens. Humans are also able to discriminate HLA related olfactory stimuli, however, it is debated whether this mechanism is of behavioural relevance. We show on a large sample (N = 508), with high-resolution typing of HLA class I/II, that HLA dissimilarity correlates with partnership, sexuality and enhances the desire to procreate. We conclude that HLA mediates mate behaviour in humans.

Interestingly, there are also allied studies which demonstrate that the use of oral contraceptive hormones disrupts this sensitivity, and one such example is cited by the study linked.
There is clearly a heuristic argument that this dissimilarity favours a broader range of immunological memory in any viable offspring; and this hypothesis is explored in the 'Wikipedia' articles on 'Major Histocompatibility Complex' and its subsidiaries on 'sexual selection'.
To address the comment inquiring upon a causative basis for this phenomenon in the relation between MHC or HLA type and body odour, the latter section of that 'Wikipedia' article makes the following observation and cites the relevant study.

MHC may be related to mate choice in some human populations, a theory that found support by studies by Ober and colleagues in 1997, as well as by Chaix and colleagues in 2008. However, the latter findings have been controversial. If it exists, the phenomenon might be mediated by olfaction, as MHC phenotype appears strongly involved in the strength and pleasantness of perceived odour of compounds from sweat. Fatty acid esters—such as methyl undecanoate, methyl decanoate, methyl nonanoate, methyl octanoate, and methyl hexanoate—show strong connection to MHC.2

I might add here that perhaps the most consequential determination of these sorts of studies is the finding that hormonal contraceptives such as the OC pill effectively inhibit any olfactory sensitivity to this potentially important dissimilarity in HLA type.
Consider for example the implications of less than optimal breeding matches arising under the influence of these hormones and of this manipulation of female fertility on a massive scale, the persistence of which culture in the face of such evidence -- arguably in order merely to sustain the putative bodily autonomy of women in the illusory form of a simple pill -- defies reason.  Common sense alone informs us that practices of this kind invite sociological and even biological calamity.
Influence of HLA on human partnership and sexual satisfaction
Infuence of MHC on odour perception of 43 chemicals and body odour

Does this have any relationship to the perceptible odor of sweat?

@Bryan Krause. The particular study cited rather correlates a preference for body odour between individuals in a mating couple with the dissimilarity found in their respective class 1 HLA types, than to attribute a direct effect of MHC type on such body odour.  However, there are other studies which demonstrate this effect, and I have amended the answer accordingly. to say that If it exists, the phenomenon might be mediated by olfaction, as MHC phenotype appears strongly involved in the strength and pleasantness of perceived odour of compounds from sweat.: fatty acid esters,


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What is an accessible book about plant evolution for a non-biologist?
I have an acquaintance interested in learning about the evolution history of plants. This person has a wide knowledge on botanics, from personal reading and taking care of plants, but E is neither a biologist or a biology student.
Based on this, which is an accessible book to non-biologist that can be used to learn about the evolution of plants?

Can you please provide additional details like: what extent of information do you expect, what topics should it cover etc. If a person is a non-biologist then they can simply start with a general book on evolution. There are many popular books for non-biologists (or even non-scientists). This website is also a good place to start. Unfortunately, the answer to your question would highly depend on the personal opinions of people. Unless you ask very specific recommendations, literature suggestions would be off-topic.

I have Fossil Plants by Paul Kenrick and Paul Davis, published by The Natural History Museum in London.  It takes the reader through a well-researched but accessible illustrated history of the evolution of plantlife from the beginnings to now.  There are photos of many key fossils, and artist's renderings of what the landscapes of the past would have looked like.

It is possible to download it as a pdf from researchgate. https://www.researchgate.net/publication/248686492_P_Kenrick_P_Davis_2004_Fossil_Plants_216_pp_London_The_Natural_History_Museum_Price_1695_paperback_ISBN_0_565_09176_X

@John, that is a review of the book, not the book.

So it is, my mistake, still helpful so I'll leave the link.


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Do Squirrels have 4 legs OR 2 arms and 2 legs?
Do squirrels have four legs, or two arms and two legs?
I first asked this question many years ago, and it has since unearthed a whole array of conundrums and questions that I have struggled to get a conclusive answer to.
See a squirrel (often described as a quadruped, 4 feet, which implies 4 legs) can stand on its back two legs and hold a nut in the paws of its front two legs - but those front legs are jointed in a very similar way to arms, look like arms and are being used as arms.
When a squirrel runs, it uses all four limbs - but then so does a gorilla, and that definitely has arms.
So in trying to answer this seemingly simple question I ended up lost in a world of definitions and further questions - questions like "what is an arm anyway?"  "what is the difference between a paw and a hand or foot?" - and after trying to find out the answers to those questions I ended up in a much stranger world.  Octopuses have arms, but no hands - bats have hands, but no arms (I will spare you one of the resulting conversations which wanted to know how long a nose has to be until it's a trunk, especially concerning anteaters).
I could be wrong but it seems to me that if your front paws are called hands, then you have two arms and two legs.  Koalas, for instance, are often described as having hands despite also being described as quadrupeds.  Perhaps the differences are merely linguistic choices rather than anything relating to the biological nature of these limbs.  I just don't know anymore, and at this stage, I am starting to wonder if I have given this question way too much thought, time and energy.
Can anyone help me out?

Very sorry if this question isn't appropriate here - if there is a better group for this question on Stack Exchange please let me know.

@fileunderwater that is specifically about human biology, and I want to know about squirrels/animals - humans have distinctly different arms and legs, however this is not the same with animals, so that question and it's answers won't help me here.

I disagree. That question is asking about the general case, and is referring to humans, cats and apes as examples. The answer is hardly ideal though, but that doesn't mean that it is a good idea to have overlapping and duplicate posts. Hopefully, somebody can add a better answer to the previous question, that answers both that question as well as yours.

In scientific text the terms, "forelimbs/anterior limbs" and "hindlimbs/posterior limbs" are used instead of hands and legs. Hands and legs are quite anthropocentric terms. So, I would say that this question is more about language than biology.

in litterature and science they generally have limbs.


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Why is this Sea Turtle yawning?
I found this video online of a Green Sea Turtle lying down on a sea sponge and letting out a big yawn.  Here is a screenshot of the video, just incase the link doesn't work:

As far as I understand, Sea Turtles breathe air like we do, and effectively hold their breath underwater.  Also, as far as I understand, yawning is common to most vertebrates and it is believed to be triggered by the brain when there isn't enough oxygen in the blood.
If all of this is true, why is this Sea Turtle yawning underwater?  If it's not breathing the water like a fish would, surely the yawning wouldn't have the intended effect of putting more oxygen in its blood?  Is my understanding here correct?  And if it is, can someone please explain the benefits of a Sea Turtle yawning underwater?

The purpose of yawning is not clear, the "triggered by the brain when there isn't enough oxygen" explanation is just one and doesn't have much supporting evidence. It's also unclear to me whether this turtle is actually yawning or not, and I certainly don't think that can be assumed. Possibly someone else will be more familiar with sea turtle behavior, though.

@BryanKrause It does look like a yawn to me, but then again you are making me wonder if I am anthropomorphizing this turtle?

Bored with trivial questions on SE Biology?


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Observed to Expected CpG
Observed to Expected CpG is calculated as below :
Obs/Exp CpG = Number of CpG * N / (Number of C * Number of G)   where N = length of sequence.

I also don't understand the expected CpG which is:
Expected =  (Number of C * Number of G)/ N

Can someone give an example or intuition for the above formula ?

First, count the number of each nucleotide in the sequence, and divide that by the total number of all four nucleotides in the sequence.  For the C. elegans genome these frequencies will be approximately:
A = 0.32
C = 0.18
G = 0.18
T = 0.32
These frequencies should sum to 1.00.
If you select one nucleotide at random from that DNA sequence then those frequencies become the probabilities for selecting a specific nucleotide at that site.  So very roughly you would be twice as likely to get back an A or a T (compared to a G or a C).
Next count the number of each of the 16 possible dinucleotides (e.g., AA, AC . . . TG, TT) in that DNA sequence and divide the numbers by the total number of nucleotides in the sequence.  That will give you the observed frequencies of the dinucleotides. CG (or CpG in your post) is one of these.  If CG occurs proportionally to the frequencies of C and G then if you picked a random dinucleotide from the sequence you would expect the probability to be 0.18 * 0.18.  You can do this same calculation for all of the dinucleotides in a genomic sequence and compare the observed frequencies to the expected frequencies.
If every site is truly random in the sequence then the observed dinucleotide frequencies should be identical to the expected frequencies, and this would be a zero order Markov chain.  In fact, genomic DNA is usually not accurately modeled as a zero order Markov chain.

According to you explanation, shouldn't  there be N^2 in the denominator for expected CG ?

Technically, I believe the denominator should be THE TOTAL number of dinucleotides that can be formed by the genomic sequence.  For the purposes of this example that number is not very different from the total number of nucleotides in the sequence.  There is no component of the calculation that  requires squaring the total size of the genome (that would be a very large number).


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Can rigor mortis change the anatomical position in which a person died?
I've been told as an undergrad in anthropology that the flexed position of the body in which some Neanderthal skeletons were found indicates that they were deliberately buried. Apart from the good preservation of the remains, one of the arguments for deliberate burial was that if the individual had died in this very flexed position during sleep, rigor mortis or post-mortem bloating would have caused the body, if not already buried, to extend (see e.g. Villa's [1989:325] comments to Gargett 1989). Barring sudden death by rockfall and ceiling collapse, this suggests that the body was completely buried before rigor mortis set in, or was deliberately placed in this sleeping position after rigor mortis faded by those that buried it.
But I thought I had heard in a biology course that rigor mortis stiffens the muscles, but does not contract them (see e.g. Faux et al. 2006). If someone died during sleep, could rigor mortis really straighten a highly flexed death position?

rigor mortis doesn't cause any movement so the body remains in that position stiffly.

Rigor mortis does not cause movement. It causes rigor (Latin for stiffness.)
This is only a comparison, but think of it this way. Superglue doesn't shrink or change the shape of the connection of the two things glued together; it just holds them there with powerful 'stiffness'. So imagine that at death, part of our muscle cells exuded superglue. You would get stiff (the muscle to bone/fascia connections would not change) but you would not move. Immediately after death, some muscles relax; most obviously the eyelids open partially, the mouth, hands, and sphincters relax (you won't have to pry a gold coin from someone's dead hands like in the movies.) But aside from general relaxation, you very closely stay in the position you were in when you die.
Physiologically, this is roughly how muscles work: muscle cells are filled with filaments, actin and myosin (I'm leaving out tropomyosin and  troponin for brevity.) Contraction occurs when the myosin can bind to the actin, break the bond and reform it on the next spot on actin, and repeat, like crawling along the actin. ATP and Calcium ions are necessary for this crawling movement. In death, ATP is quickly depleted (aerobically then anaerobically), whereas Calcium floods the cell, and the bonds within each muscle cell which were formed when death occurred become stable. The muscle does not contract any more; it just stiffens. But since stiffening requires contraction in life, it's called contraction in death.
As a parallel, touch your fist to your shoulder. Without resistance, there is some contraction there. Now keep it there while someone tries to move it; that requires much more forceful contraction, but the position of your arm doesn't change (remember, you're keeping your fist to your shoulder.) All this is thanks to the number and stability of those tiny bonds between actin and myosin. Those tiny bonds develop and stabilize in death. But they don't last forever, hence rigor reverses.
Rigor mortis has been studied extensively for an astonishing number of reasons including forensic studies and how it affects the meat we eat.
I have seen a lot of death; one of my duties was to "pronounce" people dead. Sometimes when someone died during the night in a nursing home, a nurse would wait until morning to call - what difference did it make, anyway? - and I saw bodies in rigor. They were not all drawn up as in a fetal position. The nurses would usually straighten the patients out before rigor set in to make it more dignified and easier to transport the patient. If rigor caused movement, they wouldn't be straightened yet stiff  (rigor is something one needs to document, as is lividity.)
Rigor Mortis

Excellent answer! I realise that you're writing from experience and know what you're talking about, but might you have a source for this? I had indeed seen the word "contraction" been used in a rigor mortis context but it was not clear the word had another meaning. I'm really curious, could bloating change the position if it were originally flexed? This bloated pig does not look in a normal position: https://bugwitch.files.wordpress.com/2013/05/img_4276.jpg

@TheThunderChimp - The Link explains it better than I did. Once rigor passes, many things can change the position the body is in, such as gas, etc.; for example, drowning victims are usually face down bottom up in the water, whereas scuba divers are found face up, bottom down.

But if someone died in foetal position in a locked, clean room at normal temperature, would the remains still be in foetal position 1 month (or 100 years) later?

@TheThunderChimp - Yep. Absolutely.

Thanks @anongoodnurse. If you had a source to the effect that bloating does not change position I'd be delighted

@TheThunderChimp - I'm sorry, I don't have such a source. Bloating isn't something I see very often in humans, thank goodness.

This timelapse video here suggests the limbs move outwards during bloating if the individual is on its back (warning graphic stuff): https://www.liveleak.com/view?i=5bd_1306689849


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When is strict sterile technique necessary? Cloning vs. protein expression
Background: I have previously worked with RNA, and then we use laminar flow hoods for any work where we do plating or inoculation of cultures while applying sterile technique. I am now working in a biochemistry lab. I'm told that I can work on a lab bench, while doing basic cloning for production of plasmids in E.coli, and don't need to use a Bunsen burner as long as I apply sterile technique (and in most cases I don't see people sterilizing the bench with enthrall prior to work). However, if I do any work which relates to expression of proteins - then I should use the Bunsen-burner while applying sterile technique.
Question: Is it really so that you don't even have to use a Bunsen-burner while plating (normal E.coli: XL1-blue cells)? in this case, why? Are there not always something in the lab which can grow on kanamycin plates? We don't use white/blue screening, we simply spread XL1-blue cells onto LB plates with kanamycin - then pick a averaged sized colony to make a LB-culture. It seems to me that we are just lucky that we usually pick the right colony (which we do confirm by sequencing after mini-prep).

As answered you can do without the flame just fine for stuff that you do not want to store for an extended period of time. In my experience if you open a kanamycin plate for a couple of minutes, only 1 in 10 plates will have some kind of contamination, almost always some sort of fungus. Yes, there's stuff that will contaminate your plate, but there's just not that much.

Short answer is it never hurts to practise thorough aseptic technique.
My general rule of thumb is, if I'm opening a culture of bacteria (plates, eppendorfs, tubes etc.) I do it under a bunsen - the exception being if I plan to lyse the cells anyway.
For protein purification, sterile technique is important if you plan to store the sample for a while. Proteases in the environment and on your sample/self can make short work of destroying all your hard work.

Never trust your antibiotics fully. For one thing, they often won't stop fungi, which will ruin your samples even in the presence of some pretty nasty chemicals. If you're using some of the crappier antibiotics (Ampicillin is a prime example), the antibiotic degrades over time. B-Lactams in particular are an issue, as the B-lactamase is secreted in to the media. By day 2 of a culture, there will basically be no ampicillin left!

The ampicillin is a very important point. I once had to train some people who always had their maxiprep fail. After going through every step many times, I saw that they had made many frozen solutions of ampicillin and kept them at -20 for 6 months or more. I never use frozen ampicillin older than 1 month, keep it as dry powder until you need it.

For most plasmid preparation, strict sterile technique is not necessary. The antibiotics in the media will select for bacteria which carry a resistant plasmid, so you don't usually have to worry about other organisms getting in.
However, when you're using several types of plasmid, you do need to be careful to avoid cross-contamination, because each plasmid is resistant, so bacteria transformed with plasmid A will live just fine on plasmid B's plate. When plating your cells, be sure to pass your cell spreader through a flame. It doesn't have to be an official Bunsen burner, I used an alcohol burner just fine.
If you make a big bottle of media and use small aliquots at a time, then the bottle should only be opened inside the hood.

that sounds rational, however, how about protein expression? because you also use antibiotics there, but I have heard that e.g. bacillus is a very common lab bacteria that a gets everywhere and grows quite fast even with antibiotics? I mean, there is a good reason why media is autoclaved before use even though you use antibiotics. Why should I not take the same consideration with protein expression using e.g. rosetta as with basic cloning using XL1-blue ?

@CuriousTree I've never done much protein expression, but I think part of why we can get away with less than ideal aseptic conditions with plasmid prep is the time. We never let the bacteria grow longer than 24 hours, then we lyse and purify the DNA. Longer than that and the antibiotics aren't reliable. How long are your protein cultures grown for? Do you keep the cells frozen? Do you plan on thawing them out and starting new cultures with them?

degradation og antibiotics is a good point, we normally grow the cell from the morning then express our protein overnight before harvesting, and don't re-culture them. All in all they grow about 24 hours, in presence of kanamycin and chloramphenicol.

That's only true if Plasmid A and B are different but contain the same basis of resistance. A kanamycin plasmid won't survive on chloramphenicol and vice versa.

@JoeHealey There aren't that many antibiotic resistance genes, so it's common to have two different plasmids with the same gene. The labs I have been in also tend to use the same vector for all our genes, so they all have the same resistance.

Yes I agree, it's important to be mindful of your samples genotypes. There are additional confounding variables as well, for example, kanamycin and neomycin have the same basis of resistance, so cannot be used to kill off one another ;)


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Is SCNT possible with only the nucleus of a somatic cell (rather than a whole somatic cell)?
The following figure from Life: The Science of Biology (11th edition) explains how SCNT (somatic cell nuclear transfer) was used in the cloning of Dolly:

(The original paper about cloning Dolly - Viable offspring derived from fetal and adult mammalian cells)
Note that an enucleated oocyte and a whole somatic cell were fused, i.e., the nucleus of the somatic cell wasn't isolated from the somatic cell.
Another example in which SCNT was used successfully is the cloning of the monkeys Zhong Zhong and Hua Hua. In this case, fetal fibroblasts were fused with enucleated oocytes, as explained in the paper Cloning of Macaque Monkeys by Somatic Cell Nuclear Transfer.
However, one can find various explanations and figures on the internet that explain that in SCNT, only the nucleus is transferred into an enucleated oocyte.
For example, the following figure is used in Wikipedia's SCNT page:

Though it is noted alongside the figure:

The diagram depicts the removal of the donor nucleus for schematic purposes; in practice the whole donor cell is transferred.

So my question is:
Has anyone ever successfully used SCNT while using only the nucleus of a somatic cell, without the whole somatic cell?
(My guess is "no, the nucleus alone won't do", basically because of the importance of the centrosome, along with the following quotes from the paper From Zero to Many: Control of Centriole Number in Development and Disease:

Centrioles are essential for the formation of microtubule‐derived structures, including cilia, flagella and centrosomes. [...]

  Notably, oocytes and spermatozoa lose parts of the centrosome in a complementary manner. Centrioles, but not centrosome proteins, are lost in the oocyte. On the other hand, in sperm, the PCM material is lost, but not the centriole/basal body, which is necessary for flagella formation. Fertilization brings together the basal body from the sperm, which becomes a centriole within the zygote, and the PCM from the egg.

)


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How does the phosphorylation state of 4E-BPs affect translation of nuclear-encoded mitochondrial transcripts?
A 2020 review paper about mTOR (ref. 1) says:

because biomass accumulation demands vast reserves of energetic currency, mTORC1 enhances translation of nuclear-encoded mitochondrial transcripts through 4E-BP1 to expand the ATP production capacity of the cell

The above quote cites a 2009 paper (ref. 2) that says:

Upon DR mitochondrial protein density increased 25% in control flies, while in d4E-BP null mutant flies there was no change

(DR stands for "dietary restriction", which is known to inhibit TOR, which is an inhibitor of d4E-BP, if I understand correctly.)
These two really confuse me, as it seems to me that ref. 1 cites ref. 2 but says the opposite.
To spell it out: It seems that everyone agrees that active (i.e., non-phosphorylated) 4E-BPs inhibit translation, but ref. 1 claims that the inhibition is strongest for nuclear-encoded mitochondrial transcripts, while ref. 2 claims the inhibition is weakest for these transcripts.
As far as I can tell, the claim by ref. 1 is also supported by two other papers: A 2012 paper (ref. 3) that says:

gene silencing of 4E-BP1 up-regulated the protein expressions of all RCs and the action of 4E-BP1 appeared to be specific to these mitochondrial proteins.

And a 2013 paper (ref. 4) that says:

Whereas 4E-BP1/2 depletion did not affect polysome distribution of β-actin mRNA (Figure 6B, upper), it prevented the Ink1341-induced shift of TFAM and ATP5O mRNAs toward lighter polysomes (Figure 6B, lower). Therefore, 4E-BPs act as major mediators of mTORC1 on translation of TFAM and ATP5O mRNAs. Accordingly, asTORi decreased ATP5O and TFAM protein levels in control, but not in 4E-BP1/2-depleted cells

Finally, I found a 2017 paper (ref. 5) that seems to make a claim similar to the one ref. 2 makes. It says:

cold inhibits translation in general, but the synthesis of proteins destined to the mitochondria is selectively preserved, resulting in a cellular enrichment of these molecules.

and:

4E-BP can be phosphorylated at multiple sites but phosphorylation of Thr37/Thr46 by the mammalian target of rapamycin (mTOR) acts as a priming event required for further phosphorylation. Cold exposure increased the proportion of nonphosphorylated protein, largely at the expense of the primed fraction [...] Taken collectively, our observations suggest that reduced ambient temperature induces a physiological state comprising posttranslational modification of 4E-BP—resulting in a lower proportion of the phosphorylated isoform primed for inactivation—and a switch from global protein translation toward mitochondrial metabolism and efficiency.

So my question is:
Is it really that refs 1,3,4 say one thing, and refs 2,5 say the opposite?
If yes: Has anyone offered an explanation to resolve the seemingly contradicting results?
References

Liu, Grace Y., and David M. Sabatini. "mTOR at the nexus of nutrition, growth, ageing and disease." Nature Reviews Molecular Cell Biology 21.4 (2020): 183-203.
Zid, Brian M., et al. "4E-BP extends lifespan upon dietary restriction by enhancing mitochondrial activity in Drosophila." Cell 139.1 (2009): 149-160.
Goo, Chong Kiat, et al. "PTEN/Akt signaling controls mitochondrial respiratory capacity through 4E-BP1." (2012): e45806.
Morita, Masahiro, et al. "mTORC1 controls mitochondrial activity and biogenesis through 4E-BP-dependent translational regulation." Cell metabolism 18.5 (2013): 698-711.
Carvalho, Gil B., et al. "The 4E-BP growth pathway regulates the effect of ambient temperature on Drosophila metabolism and lifespan." Proceedings of the National Academy of Sciences 114.36 (2017): 9737-9742.


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If bond break absorbs energy, why ATP hydrolysis releases it?
We know that bond formation releases energy and bond break absorbs energy. I still don't figure out why ATP hydrolysis (that breaks a bond between oxygen and phosphorous) releases energy, and it releases a LOT.

Please note that this off-topic for biology (it is a chemistry question) and has already been answered on Chemistry.SE.

This is well within the realm of biochemistry in my opinion.

ATP synthesis is actually an endergonic process, hence the need for oxiditative phosphorylation to drive the formation of ATP. Although the P-O bond releases a large amount of energy, the reverse of this process is not occurring in ATP hydrolysis. During hydrolysis, the ATP is broken down into two products, with the addition of water, these products are more thermodynamically stable, so energy is released. Breaking of the P-O bond does require energy, but because more energy released by adding the water in, the overall reaction releases energy. ATP is a thermodynamically unstable molecule (bond breakage releases free energy), but is kinetically stable (bond breakage has a high activation energy). I am not too sure what the exact reasons for ATPs hydrolysis being exergonic are, textbooks state it is because the major sources of the free energy associated with the P−O bond dissociation are the relaxation of the electronic repulsion, increased resonance of the products and the stabilisation of the solvation free energies of the relevant species after the hydrolyses. However, this paper (DOI: 10.1021/acs.jpcb.7b00637) claims that the solvation effects upon hydrolysis actually destabilise the products, but I am not sure of the validity of this paper.


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Genetics and Heredogram - Proving the teacher is wrong
I want serious help here. I'm in first year of medical school and I jut had my second test in Genetics. One question of the test gave us a heredogram and asked us what was the most probable type of genetic disease the family had. There were 2 types of disease that would fit the heredogram. Recessive autosomal and Dominant X-linked. I put both and explained why both them fit. But a lot of my colleagues put only one of them. He said after that he wanted X-linked, because the heredogram had more trends of X-linked diseases. I just don't bite that. This is not the way we calculate probability. For example a autosomal disease can happen in 44 out of the 46 chromosomes while the X-linked only in the X chromossome (1.5 in average). Also, what if recessive diseases are more common than dominant. What if most of the people with X-linked diseases are infertile or if most of them dies. All of these reduces the chance of a given heredogram being Dominant X-linked. We can't say something one based on the trends.
The heredogram is the below.

Do you agree with me? I really need some opinions of other people so we can contest the teacher. Otherwise half of the classroom will get a zero.

This site does not exist to give opinions so people can contest their teachers. It exists to provide objective answers to problems of biology which are of general importance and interest. The title shows a particular petty arrogance which is more likely to antagonise people than gain their sympathy.

I think you are making this too complicated. You don't have enough data from this diagram to make any sort of rigorous statistical judgement. You are just looking for clues.
Note that in the first generation offspring of the affected male founder, all the female offspring are affected and none of the male offspring are affected. This is exactly the pattern you would expect for a dominant X-linked trait.
For an autosomal recessive trait, you'd expect roughly equal numbers of male and female offspring to be affected in the first generation where once parent is affected and the other is a carrier. This is true regardless of all the red herrings you raise about the number of autosomes, fertility, and lethality. So this is a little odd looking for an autosomal recessive trait. It's a tiny sample size, so not impossible, not definitively ruled out, just a little unlikely.
Diagrams like this don't usually give you a definitive result, but they can indicate where to start looking.

In my opinion, we cannot say autosomal recessive is more unlikely. Consider the first and second generation only for example. An affected father, a non-affected mother, 3 affected daughters and a non affected son. Given the disease is Dominant X-linked the chance of the parents have that children is (1/2)^4=1/16. While if the disease was autosomal recessive (1/4)^4 = 1/256, that is 16 times less. But consider an Dominant X-linked disease is 23 times less common than an autosomal (what could be completely true given the number of chromosomes). Than now autosomal is MORE LIKELY than X-linked.

@JoãoMaldonado No, you are miscalculating the likelihoods. The likelihood of the data given the Dominant X-Linked model is exactly 1. For the first generation of offspring for an affected father and unaffected mother, the female children are necessarily affected, and the male offspring are necessarily unaffected. No other pattern is possible.

For the autosomal recessive model, the father must be carrying two copies of the recessive mutation and the mother must be a carrier, with one copy of the recessive mutation. The status of each of their offspring is essentially a coin flip depending on which copy they inherit from the mother, so the likelihood of the observed 1st generation is (1/2)^4=0.0625. You may have a point that somatic chromosomes outnumber sex chromosomes, so that might boost the likelihood a little (this is called a prior), but it isn't going to be as simple as multiplying the likelihood by 23.

I’m not saying it is that simple. Just that it is not correct to say that X linked is more likely for sure. Also, you misunderstood the probability I calculated. The question is: what is the probability that an affected father and a non-affected mother have 4 children, 3 females affected and one male not affected.

If the disease is Dominant X-linked there is a likelihood of 50% of a random children be a female affected and 50% of the children be a male not affected. So the probability of that couple have 4 children with the pattern said above is 1/16. If the disease is recessive autosomal there is 25% of a ta from children be female affected, 25% female not affected, 25% male affected, 25% male not affected. The probability of the couple have tha 4 children as I said is 1/256

Also. If we have the statistic # people in that community (or the world considering the distribution is uniform) with autosomal recessive diseases divided by # of people with X linked dominant diseases and we consider and we consider both types of diseases live the same, have the same probability of finding a couple or having a fertile child etc. Then it would be as simple as multiplying this number to the 1/16 we calculated. Of course it is not like this. People with X linked diseases could be more or less fertile or find more or less couples or having more or less fertile children and etc.

My point is that no one can say that one disease is more likely than the other or ask that in a test. Inferring the mode of disease is something extremely complicated and by what I searched is only done with algorithms and computers, that calculate an error of the estimate, because neither them can say for sure what it is. So asking that in a test is very questionable, what he could have asked is to say what types of diseases would fit that heredogram or ask for only one of them, considering that more than one are possible to answer.

"The question is: what is the probability that an affected father and a non-affected mother have 4 children, 3 females affected and one male not affected" No, you're calculating the wrong thing. All we're interested in here is the probability of observing the disease or not given the inheritance model. The genders of the offspring are treated as a given for the purposes of this estimation.  I'd suggest that you review this material with your professor, because you're working from some fundamental misunderstandings.

I really doubt I’m misunderstanding statistics, I can be misunderstanding genetics. I’m already graduated in bot Mechanical Engineering and Math. The point for me using the sex into consideration was t standardize the ratio. I’m not concerned in the probability of that heredogram being autosomal recessive, but the ratio of the probability of it being autosomal recessive divides by the probability of it being Dominant X linked, i.e. how many times it is more likely that the given disease is autosomal recessive considering to the other option, based only on that heredogram

And as we HAVE to use the sex when we thread X linked diseases, we also have to use with the autosomal to calculate that ratio. If the sex weren’t important they would just vanish when the ratio is calculated. I’m not concerned with the 1/16 or the 1/256. But with the ratio (1/256)/(1/16) = 1/16 (by coincidence). You calculated the same ratio as I.

If you really want to understand why I calculated that way consider just a couple with an affected male having only one child, female and affected. Let’s make the question: What is the chance of this heredogram be referring to a Dominant X linked disease. Answer: Probability of the disease in the male population multiplied by the probability of males with that type of disease find a couple, multiplied by the probability of couples with an affected male with that disease have a living child, multiplied by the chance of that child be female, multiplied by the chance of that child be affected.

Then you divide trust  by the Probability of all genetic diseases in the male population multiplied by the probability of males with an type of genetic disease find a couple, multiplied by the probability of couples with an affected male with any genetic disease have a living child, multiplied by the chance of that child be female, multiplied by the chance of that child be affected with the same disease

Sorry but you are misunderstanding statistics at least as involved in interpreting the diagram. In formal terms we're using the diagram to do a maximum likelihood test to choose between two models. You assume one model, calculate the probability of the observed pattern of disease given model, then assume the other model and calculate the probability of the observed pattern of disease. The probability of the observed pattern of disease given a model is called the likelihood. You choose the model with the greater likelihood. No need to take ratios.

You are introducing a host of complications that are unneeded for this question. Given two models we're simply asking which model "better" explains the data right in front of us.  Check out any text on statistical genetics and really, please talk to your professor.

You can do that, you can calculate the probability only based on the disease model or pattern. But as I said, there are more things involved. A more complete estimation is the one I presented above, where we have to know many other things beside the disease pattern . If you calculated 2 likelihoods and both of them are 50% the you would say they are equally likely? No.  What you can say is: Considering both diseases are equally frequent in the population and all affected have the same life standard and life expectation and all other important things, then now they are equally likely

But if the frequency of one disease in the population in greater than the other than the chance of that heredogram being refereeing to this disease is greater as well.

You are introducing a host of complications that are unneeded for this question. Given two models we're simply asking which model "better" explains the data right in front of us.  Check out any text on statistical genetics and really, please talk to your professor. I hate to engage in credentialism, but you started it: Me: MS Applied Math and 15 years working as a bioinformatics programmer, and of course your professor is presumably a trained geneticist, so they "outrank" us both. Of course, I could be wrong, but so far it's two against one. Seriously, consider that you may be wrong.

I think neither one of us are wrong, we are just calculating different things. You calculated which model fit better. You did that 100% right. But the question was not which model fits better but whic disease type is more likely. These are different things. Let’s finish this topic with me presenting you a different question. Suppose we discover another type of genetic disease model that affects only 7 people in the role world. All the affected are female and they have only female daughters. All the daughters are blond, blind, have septum deviation and die before 30 years ild

On a pragmatic basis, statistics is the art of making decisions in the face of uncertainty. Many of the complicating factors you added are simply unknown, or even unknowable. Faced with a patient in the clinic you have to do the best you can with the limited facts you have: the pattern of inheritance in the family tree. As I said, it's not a definitive test, but it gives you a place to start looking.

Then you as a geneticist see a random heredogram. There is an affected mother, a non affected father, and 4 female daughters that are bold, blind, have septum deviation and died at 20 years old. By what you said I would say the new X disease model is the one that fits the best right? But is it more likely?


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Barr body in mitosis
In early embryonic development, some female cells pass through a process called lionization and one of the X chromosomes get condensed and began to be called Barr body.
What I don't understand is how the Barr body behaves during mitosis. Specifically, if a cell had condensed a paternal X chromosome, all of its children will have a paternal Barr body. But aren't  the barrbodies supposed to decondense to be able to be copied during mitosis? If so, when they recondense, why isn't the choice of which chromosome will condense random?
Thank you!

X inactivation is mediated by several epigenetic marks on DNA that cause condensation into heterochromatin. These include DNA methylation and histone modifications:
https://en.wikipedia.org/wiki/X-inactivation#Silencing
As you suggested, a newly copied DNA strand would be free of the epigenetic marks that mediate heterochromatin condensation. Yet epigenetic modifications are inherited, along with DNA molecules, by the daughter cells during cell division. That is, cells have ways of copying these modifications from the old DNA strands to the new ones. These mechanisms are not all known, and are the subject of much research.
In this fashion, each cell division produces two cells that inherit the X-inactivation status (i.e. heterochromatic state) of the parental cell.
This cycle of epigenetic inheritance only ends when the chromosomes are reactivated in primordial germ cells before meiosis and the production of eggs or sperm. The embryo of the animal's offspring can then make that initial, random X chromosome inactivation that is inherited by all of the cells in its body.


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How does Liebig's law affect the growth of specific characteristics on a plant
I am familiar with the law of minimum, that is that the growth of the plant is dependent on the least available nutrient/resource.
I visited a farm in which they purposefully shaded tabaco plants to guide the growth of the plant (e.g. to make the plant grow taller and wider leaves with better concentrations of nicotine). I am wondering if this applies to other nutrients/plants. Example: Does deficiency in nutrient X guide the growth of spinach with Y% more iron?


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Clarification of method notation in yeast cultivation method
I'm reading a paper about yeast culture and in the methods, it says:

Then $5$ ml of sterile $M/15\ KH_2PO_4$, was added to the slant,

What is the meaning of $M/15$?

Can you add the paper itself? or a screenshot of the relevant section?

The only interpretation I can think of is a concentration of (1/15) M, i.e. 67 mM. But I've never seen anyone write it this way.

@VictorChubukov That's what I thought, thanks

@VictorChubukov. That's what it is. I just verified. I don't know much about the history of that though but it is an old notation that is no longer used. Can you please post an answer?


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What is omicron squared in genetics?
Saw this equation in the conext of epidemiological genetics:

I have never seen it before and I don't know what variable it represents. Help?

Please always link to where you found this equation. It might well have been an equation that is not common enough to be recognized without the original reference. By chance, it is a very easily recognizable equation, one that has nothing to do with biology.
What your showing is an equation to compute a variance. It is not omicron but sigma ($\sigma$). In statistics, $\sigma$ is the standard deviation and hence $\sigma^2$ is the variance. $\mu$ is the mean and $n$ the number of elements from which these statistics are being computed.


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Identify mystery insect found in Boston, USA
This insect is approximately 2.5mm.  It was recently observed in a Boston USA shower.  Do you know what type of insect this is?

This is a spider beetle (Coleoptera: Anobiidae: Ptininae); the focus does not let me go deeper at this time.