text:
Storage DNA Condition
It is possible to store a digestion of cells with lysis buffer several days at -20 degrees and then proceed with the phenol chloroform isoamyl purification?

Strictly speaking your answer will depend on what you want from the sample and QA requirements etc - can you elaborate a bit?

Should be fine, but if I were you, I'd spare a few more minutes and carry on until ethanol precipitation (15 min of work at worst). Here's the protocol:
https://www.thermofisher.com/pl/en/home/references/protocols/nucleic-acid-purification-and-analysis/dna-extraction-protocols/phenol-chloroform-extraction.html
You can store it in -20 degrees for several days (extend the overnight incubation, that is the second step of ethanol precipitation) and you'll have the certainty that it will stay ok. In fact, freezing in most buffers, whether lysis buffers or extraction buffers shouldn't significantly hurt any nucleic acids. From my personal experience: I've frozen plant material in extraction buffer for RNA isolation (TRI-zol method) in -80 for a few days and got very high concentrations in most samples in the end. I was told freezing in -20 would impact quality but RNA is generally less stable than DNA.
If you had little to none material, you're better of doing the precipitation procedure and then freezing it. If those are minuscule amounts and/or you work with something sensitive like forensic evidence, following through with the procedure will be the most reasonable solution.


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When did the mammalian outer ear evolve?
All Eutheria and Metatheria have outer ears, and as far as I found out, monotremes once also had them, so they seem to be universal for mammals. Did other synapsids have them, too?
I know that soft tissue doesn't fossilize well, but isn't there any other way to find out, like muscle attachment? Has it something to do with mammalian ear bones?

Yes, it is believed to be linked to the mammalian inner ear bones. Since they act as amplifiers, the faint sounds gathered by the outer ear have a greater benefit. But really early mammals show many adaptations that they were relying very little on sight and a great deal on hearing. External ears just might not be beneficial enough unless you are really relying on hearing. The only other vertebrates that rely that much on hearing, the owls, also have external structures to help gather sound.
The fact that both developed at the same stage is circumstantial evidence that they may be linked as well.

source: Stack Exchange

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What is the heritability of brain gyrification?
Brains of mammals with a folded neocortex do not have identical patterns of folding in the same species.
Do two genetically identical individuals of a species have the same pattern of brain gyrification (i.e., folds/wrinkles)? Or are there other causes?

Not sure what happened to the comments here but the genetic basis of gyrification has indeed been of interest @Remi.b

@BryanKrause Indeed. I deleted this comment about 0.5 seconds after writing it :) I was hoping nobody had time to read it!

Short Answer:
Genetically identical individuals do not have identical brain structure.
Longer Answer:
The easiest way to answer your question is to look at "natural" clones: monozygotic (i.e. "identical") twins.
Brain morphology is of a lot of interest in neuroscience because differences in brain morphology are often confounding factors in human brain studies (for example those using MRI/fMRI).
I'll refer to a study by White et al., 2002. They studied volumetric and surface morphology measures in monozygotic twins. They found remarkably strong correlations in total volume (r values of .98-.99 for measures like total brain volume, cerebrum volume, cerebral gray matter/white matter, and cerebellum), and still strong correlations with different lobes of the cerebral cortex (r values from .69 to .97 for frontal/parietal/temporal/occipital gray and white matter).
However, surface measures: surface area, gyral and sulcal curvature, and surface complexity were more weakly correlated (r values of 0.49 to 0.69).
Of course, because these are monozygotic twins raised together, it's hard to know how much of the similarities are due to the shared environment as well as shared genetics. However, it is clear that brains of identical twins are not identical, and in particular their brains seem to differ more on measures of cortical surface structure rather than overall brain size. The authors write:

Many different types of nongenetic influences may contribute to the plasticity of the cortical surface characteristics, such as educational experiences, physical activity or social interactions. Furthermore, probabilistic events during the complex process of neurodevelopment [e.g. connections between neurons (Muller et al., 1997)], differences in gene expression either by chance or modulated by early-immediate genes (Abraham et al., 1993; Worley et al., 1993), or variability in cell–cell interactions (Fletcher et al., 1991) may also contribute to variability between MZ twins.

References
White, T., Andreasen, N. C., & Nopoulos, P. (2002). Brain volumes and surface morphology in monozygotic twins. Cerebral cortex, 12(5), 486-493.

You say "copying" (question has now been edited)
Welcome to Biology.SE. CC (stands for Copy Cat) was the name of a cloned cat. We never say "copying", we say "cloning".
Cloning in nature (question has now been edited)
Note that cloning is not necessarily a human process. Many animals (included animals that have a brain but excluding all mammals) clone themselves. See wiki>parthenogenesis
Rephrasing your question (question has now been edited)
We can rephrase your question as

What is the heritability of brain gyrification?

If it is unclear why this rephrasing of your question would be correct, then you'll want to have a look at this post.
Answer
There seems indeed to have genetic factors affecting gyri (White et al. 2010).  Typically, the Fibroblast Growth Factor (FGF)- and Sonic Hedgehog (SHH)-signaling pathways have been seem to affect gyri (Rash et al. 2013; Wang et al. 2016).

Sorry if my edit of the OP sniped your answer a bit. I do think the intended meaning of the OP was more "to what extent do genetic factors determine gyrification patterns" whereas your answer just seems to say "here are some signalling pathways that do" - I feel like that's not the best answer. It's obvious that some genetic factors are at play, but the question was regarding genetically identical individuals.

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Does the complimentary base pairing of rRNA with itself play a role in its transcription?
I have read that the termination of the transcription of mRNA involves a termination sequence in the form of a stem loop. As the structure of ribosomal RNA involves extensive internal base pairing, I wonder whether part of the mature rRNA provides the termination loop for its transcription.

Your question is unclear to me. You question appears to be about the termination of transcription of rRNA, although your title seems to be about rRNA structure that can be answered from any book or Wikiipedia. Your tag of reverse-transcription was certainly wrong and I have removed it. Please clarify your question, but first do some reading. A statement that "I know rRNA must come from a gene" suggests you might benefit from this.

As you haven't replied and as nobody else followed my vote to close this question I have rewritten it in a way that now makes some sense and may be what you meant. If not please edit it. I have reversed my close vote and will answer the question if nobody else does.

Summary
The process of the termination of transcription is still not well understood. It differs between eukaryotes and prokaryotes and between mRNA and rRNA. Although it involves stem-loop structures, such structures may be necessary, but are not sufficient for termination. The idea that the termination signal might be part of the mature functional transcript — especially for rRNA comes up against a number of problems, and turns out to be incorrect. Such problems include the extensive nature of the stem loops (which to use?) and the fact that the smaller stem loops emanating from the core conserved hydrogen-bonded skeleton, are not necessarily themselves conserved (reviewed by Brimacombe). In fact the large and small rRNAs are in a single transcription unit with other genes at the end of which are specific termination signals outside the region encoding the mature rRNA.
Prokaryotic rRNA transcription
This has been reviewed by Condon, Squires and Squires (1995). The structure of the well-studied rrnB operon of E.coli is shown below, with the promoters indicated as ‘P1’and P2’ and the terminator sequences as ‘T1’ and ‘T2’. (Adapted from Pfeiffer and Hartmann.)

This transcription unit includes the 5S rRNA as well as a tRNA.
Eukaryotic rRNA transcription
This has been reviewed by Goodfellow and Zoomerdijk(2012), from which the diagram below, of the mammalian rDNA repeat, is taken. The terminator elements are ‘T1–10’.

In eukaryotes the 5S rRNA is not in the same transcription unit as the large and small rRNAs (and the 5.8S rRNA). Indeed it is transcribed by DNA-dependent RNA polymerase III, rather than the DNA-dependent RNA polymerase I, which transcribes the rDNA repeat shown.

Transfer RNAs (rRNAs), ribosomal RNAs (rRNAs) all fold back on themselves and hydrogen bond to make complementary base pairs. So yes, this is common.

I think that, despite the title, the question is about termination of rRNA transcription, not rRNA structure. On reflection, he is probably asking if the transcription termination loop (if such exists for rRNA — I don't know) is part of the rRNA transcript and (perhaps) the mature processed rRNA.

Apologies, but I edited the question so that your answer is no longer pertinent. As it is just a two-liner, I trust it will not inconvenience you too much.


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What is the concentration/molecules per cell of iodothyronine deiodinase in a cell?
I'm trying to parameterize an in silico model and need the approximate concentration (M), or molecules per cell, of iodothyronine deiodinase type II (D2) enzyme in a human cell, ideally a glial cell.  I can only find specific activity values in the literature. Could anyone point me in the right direction, please?


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Are insects really strong or just small?
It's a common statement that insects are stronger, faster and jump higher than almost anything by mass.
However, this leaves out that compared to their mass, all large creatures are actually pretty weak and small creatures are usually strong.
Have there been any studies where the strength of insects and mammals, for instance, is compared directly rather than by this ridiculous "per mass" method? I'd like to have comparisons between creatures that are similarly heavy.
My goal is to figure out the differences in strength between insects, reptiles, amphibians, mammals, fish, etc while actually considering that strength doesn't scale as easily as mass.

How do you define "strength" ? You call the "per mass" method ridiculous, but what's a "direct" comparison? The most direct one I can think of is "how many grams can this creature lift", and I don't think you need a comparative study to find that hundreds of kilograms (what an elephant can lift) >>> hundreds of milligrams (what an ant can lift). Strength scales with mass, so a direct comparison of strength comes down to a comparison of mass. Strength does not scale linearly with mass, hence the flaws of "per mass", so the question is finding a better scale. So: "how do you define strength"?

The issue is that strength and mass are not in a direct relation. Increasing mass by 10x does not increase strength by 10x. The most direct one you linked is exactly what I want to find out, but for comparisons between different creatures.
The key is that the comparison has to be apples to apples. No comparing creatures of very different masses and assuming that they are equivalent.
Strength is pulling, pushing, lifting. Any application of force really, as long as it can be generalized enough that we can compare many different creatures on the same benchmark and that has studies.

Finding a better scale would perhaps be a result of this question. As long as we have good comparisons we can just plot them out on a graph and it should be quite informative about the exact relation between size and strength. Also about how they vary by type of creature.

"it should be quite informative about the exact relation between size and strength." We already know that: strength varies roughly as the square of linear size. Are you asking for an explanation of how this was determined?

Please quote a source with link for the "common statement" you refer to in your question, especially the "strong" aspect. Or else take responsibility for it yourself — e.g. "I believe that…" because otherwise it sounds as if you are setting up a straw horse to knock down.

As in the original question, what I'm looking for is actual measurements. I'm aware that the strength of muscles is proportional to their cross-section. The question is more specifically about how strong animals of different kinds are compared to each other, at the same weights. Clearly there are huge anatomical differences between insects and reptiles - how do they affect strength?
This is why I want to know about any experiments or other ways that creatures of similar mass have been compared in strength.


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Why can't Turner Syndrome occur in males?
In Turner Syndrome, one X chromosome is missing, meaning that the resulting egg or sperm has 22 chromosomes (without pair) and the 23rd chromosome is missing.  If this develops in an egg, and a normal sperm carrying a Y chromosome fertilizes that egg, then due to presence of a Y chromosome, can a male with Turner Syndrome develop?

Can you clarify what you're asking.  What is the chromosomal makeup of this proposed individual?

Because it is not viable to not have any X chromosome (non-peer reviewed reference).
The X chromosome is much bigger than the Y chromosome and carry a lot of essential genes (see here). A zygote just does not appear to be viable without X chromosome.

Why the tag markup for X and Y?

@arboviral clarity, I assume.

Tag mark removed. I did that in the past already. I suppose, it once was handy to not confound chromosome names with variables, with locus names or allele names.

I can't get it into my head and can't imagine it properly .Firstly ,if there is an egg containing 22 chromosomes with one chromosome missing and that is an x chromosome but an egg contributes only one x to zygote and other x or y comes from father  So,Can't that female contribute its other x chromosome to zygote as it has two x chromosomes?

@RabikJohn After production of the egg, there is no way for the female organism to "do" something about the chromosomes. If the egg or sperm was incorrectly built, the zygote develops as far as it can. And in case of no X chromosome that is not very far. Maybe you can read more about egg and sperm production processes to fully understand.

I think it maybe like that, egg has one missing chromosome which is an x one and if that egg is fertilized by a y chromosome carrying sperm, then there would be no further development of male because as remi has mentioned that without x chromosome  further development cannot takes place so essentially it would be a female with only one x chromosome and no male with turner syndrome develops


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What is the physiological mechanism for getting unconscious after a punch to the head?
It is the everyday life in boxing: One boxer gets a smack in the head, cannot do anything for many seconds and then: Victory of his opponent due to a Knockout!
What is the reason for losing consciousness for a short time by e.g. a strong smack in the head?
Are there any neuronal reactions that cause this?

Does this answer your question?

The answers are differing from each other; is it due to the Neuron compression or because the blood flow is truncated after a punch?

Yes, questions often yield different answers. Both answers may, or may not be correct. If the question is the same as yours, and you wish more answers, you can put a bounty on the previous question. I'm marking this as a dupe.


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Proteins folds: relation to splicing and post-translational modification?
Is the secondary structure pattern of protein folds related in any way to alternative splicing and post-translational modification?

"somehow related" is very vague - do you have some idea how they might be related?

Our prof.  in biochemistry basic seminary said, that diffrent kombinations of folds Is releted to diffrent function of protein. He didnt said anything that how Is this process regulated in Cell. So i thought that would be releted to alternative slicing. That one gene sliced to diffrent structure can have a simular pattern.

I see. So I don't think you mean 'secondary structure' - you probably mean domains. For example, see https://www.ncbi.nlm.nih.gov/pubmed/23562110 or this question https://biology.stackexchange.com/questions/13834/what-are-some-examples-of-genes-that-code-for-multiple-proteins


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Do hermaphrodites have more nerve fibers in their puendal nerve?
Recently I have been thinking, both the glans penis and the clitoris are the most sensitive parts of the body. They contain a lot of nerve endings. Do hermaphrodites share the nerve fibres between the two organs, or do they have double the regular amount of nerve fibers?
Also, at which point does their nerve branch out? Do they have two sets of dorsal genital nerves coming out of the pudendal nerve or does the same set of dorsal genital nerve go into both organs?

Short answer
The genitals of true intersex individuals are not duplicated. Instead, their external genital features are hybrid structures. In turn, it's not a matter of duplicated neural innervations.
Background
Hermaphroditic phenotypes in humans are nowadays preferably described as  intersex phenotypes. In humans they come in different flavors, dependent on the underlying genetic causes, which are often caused by mosaics of X and Y chromosomes. Dependent on the exact genetic underpinnings, various types of intersex phenotypes occur, with different internal and external phenotypes of the reproductive tracts.
To proceed to the most extreme case, namely the true intersex individuals - these people display both male and female external genital tissues. However, this doesn't mean they have fully developed male as well as female genitals.
Now taking a step back to the normal male/female situation - you have to realize the clitoris and glans penis develop from the same tissue (Fig. 1). In true hermaphrodites, the external genitalia are not duplicated, instead they form a hybrid, where it becomes unclear what exactly is present: a small (glans) penis, or an outsized clitoris (Fig. 2).
So in all it is not a matter of duplication, but a hybridization of similar feats.

Fig. 1. Male and female genital development. source: University of the Cumberlands

Fig. 2. Intersex external reproductive organs. source: ImageSlideShare

Hi, Thx for the answer and the edit. That also explains why a quick google search was unhelpful. Searching for "Intersex" revealed the required info much more quickly.


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Is there any mechanism that prevents DNA of an eaten entity's cell from affecting that of own?
When we eat food I heard that our digestive enzymes disassemble the DNA of the eaten cells so that the DNA cannot affect us. Then, is there any mechanism (that prevents the eaten cell's DNA from affecting us genetically) in cell-scale level? Or is it only in organ-system level(e.g. digestive system)? It seems that germs and viruses don't have the mechanism, as we manipulate them as genetic transferor. But I want to know if nucleate cells have the mechanism.

Possible duplicate of Do we consume dna, proteins of other organisms?

@kmm You may be right and your link has nice answers, but my question's key point is about cell-scale level, so I think it a bit diffrerent. But if nuclease and cell membranes are only mechanisms then my question can be duplicate either..

While not required for your main question: Viruses (and bacterial viruses) can have a stringent coupling of particle size and amount of DNA, which can prevent the inclusion of large pieces of foreign DNA (a practical problem for the early days of genetic engineering / cloning).

@tsttst I didn't know that! So your comment can be one way that primitive creatures like viruses use to prevent foreign DNA from interfering with its oen.

Cells have cell membranes and sometimes cell walls that keep random molecules from entering the cell. Only small, uncharged molecules can pass freely through the membrane. Complex structures of proteins embedded in the cell membrane regulate the passage of charged or large molecules. Pathogens like viruses or bacteria have had developed equally complex structures of proteins that can fool the proteins in the cell membrane to gain access to the interior of the cell. In other words, the cell membrane is almost always going to keep naked DNA from entering the cell, but viruses can get around this, by packaging their DNA in protein capsules that can compromise the cell membrane.
To create GMO, viruses are often used to transport the foreign DNA into the cell. Alternatively, the cell membrane can be attacked with chemicals, high voltages, or even mechanically punched holes, that allow DNA to pass through the membrane.
Bacterial cells will sometimes allow the passage of naked DNA, but this is very rare in plant and animal cells.

So you mean that it happens at digestive organ system level with nuclease?

I have no idea what you mean by that. All cells have cell membranes, it part of what makes them cells.

A ha, then outside of the cell the DNA is broken into smaller structures so that the cannot activate, and even unbroken DNA is blocked by cell membranes. Then can DNA injected by means you mentioned activate inside the cell's membrane?

@KYHSGeekCode Yes, it should. In fact that is how transfection works. Link - https://en.wikipedia.org/wiki/Transfection

@RoniSaiba I did well to adopt yours. Thanks!


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Is a gametophyte a spore?
The male and female gametophytes are pollen and embryo sacs respectively. I wondered if they are spores as their brethren are meiospores.

No.
But close.  Very close.  Basically, a gametophyte is a spore that has / is undergoing mitotic division.  Therefore, it is still haploid, having not undergone fertilization yet, but it is no longer a dormant, unicellular spore; it's passed into the new phase of gametophyte.
The gametophyte produces sexual organs which produce the gametes that will actually be used in fertilization.  Two gametes fuse, at which point, a diploid cell is produced (called a zygote, just as in animals).

The meiospores are the spores you see in the picture on the far left: they are dormant, unicellular, haploid spores, which will turn into the gametophytes.  (meio + spores; spores that have undergone meiosis)

Sources:

Meiospore, Biology Online
Gametophyte, Wikipedia
Plant Life Cycles, Developmental Biology, 6th ed.
Spore, Wikipedia


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What is the meaning of multicellularity?
I can't understand what multicellularity is. Wikipedia states that any organism having many cells is multicellular. By this definition bacteria can also be multicellular. For example, cyanobacteria can form filaments made up of specialised cells like spore cells and vegetative cells.
But aren't bacteria supposed to be unicellular only? I would appreciate it if someone could clear up my confusion.

Bacteria are, as a general rule, unicellular.  However, there are some, like the cyanobacteria which you referenced, which are kind of border line.  Wikipedia's definition of multicellularity is a very broad sweeping definition, and its statement that bacteria are unicellular is also a broad sweeping statement.
The fact is, that as a general rule, bacteria are unicellular, but at times, like you said, they can undergo filamentation.  When they do, they end up with several connected cells which are generally considered functionally independent.  In certain circumstances, however, the cells can be dependent on each other for survival, and because they didn't separate completely, it's hard to define whether we're looking at multicellularity or symbiosis.
It is generally accepted that cyaonbacteria are truly multicellular.  In order to be multicellular, an organism generally has to fulfill 5 basic requirements:

More than one cell
Cells stick together
Cells communicate
Cells are dependent on each other
Cells are differentiated

By these requirements, some cyaonbacteria technically are multicellular bacteria, defying frequent claims that all bacteria are unicellular.  That said, wikipedia isn't totally wrong, since as a general rule, bacteria are unicellular.  Cyanobacteria are an odd (debatably) exception to the rule.

Sources:

Bacteria with bodies - multicellular prokaryotes, Gould, S.E.
Multicellularity in Cyanobacteria, Paleontology Podcasts
Introduction to Cyaonbacteria, University of California Museum of Paleontology
Wikipedia: Multicellularity, Cyanobacteria, Filamentation

At least on the page "multicellular organism" Wikipedia does not claim that all bacteria are unicellular in contrast, wikipedia specifically mentions cyanobacteria as being multicellular.

Yes, fair enough.  I just wanted to go into why the definition at the top didn't apply for cyanobacteria.

Another species near that border line is the trichoplax that has differentiated cells but can survive being split up into single cells, and can reassemble

The Wikipedia article you mention actually gives cyanobacteria as an example of a multicellular organisms. So yes, there are some (primitive as they may be) multicellular species in the bacterial domain. This should not come as a surprise since a domain in biology is the highest taxonomic rank meaning that it encompasses a huge variety of different species. However, the misconception that all bacteria are single-celled is quite common because it is true for the vast majority of bacterial species.
Furthermore, it is quite common in evolution that similar traits evolve separately (for example flight evolved independently in bats and birds and the claw of the mole and the mole cricket look similar but evolved independently) this mechanism is called convergent evolution. In fact, multicellularity evolved independently at least 46 times in eukaryotes.

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How to find the age of a memory stored in the brain?
Is there any way to find how old one's memory is?
One can find the age of stones, plants, animals, etc. So why not find the age of a memory stored inside one's brain?

Are you referring to previous lives O.o ? Regardless, the question is unclear and should be revised if OP wishes an answer on it.

The fundamental problem here is that we don't even really know how memory is stored.  Even if we did, how do you distinguish a memory from a memory of a memory?   For an analogy, say I stored a file (memory) on my first hard disk, back in the '80s.  For nostalgia's sake, I look at it every year or so, and copy  it to each new machine I buy.  Is it still the same file today?

We are only barely beginning to understand how the brain works, including memory. We do know that it is a very complex thing. There are many different kinds of memory; many different processes are involved in creating and recalling memories. One factor that plays into a naïve concept of "how old a memory is" is that "remembering" does not seem to be a passive activity; instead, every time we remember a memory we re-create it.
Having said that I don't see a theoretical reason why there wouldn't be a way to determine the age of a memory... but we currently don't know it.
Consider that we don't magically know the ages of stones, plants, or animals. We learned to figure it out from studying those things, seeing how they change over time, and deducing ways to use that knowledge to guess their age. For example, people discovered that in many climates trees alternate a growing season and a dormant season, and this results in the trunk having "tree rings" for each year they've lived. They've also seen that animals have specific life cycles and look different (if only in size) depending on their ages, and they can use that to roughly estimate an animal's age. Obviously this depends completely on the animal in question; different animals grow in different ways and we can tell their ages in correspondingly different ways, and not always to great precision.
For most of human history we were completely unable to tell the age of stones. Only the discovery of radioactivity, and that the atoms inside stones transmute into other elements over the millennia and that this allows us to tell how long it has been since the stone crystallized (i.e. the atoms got stuck where they are), enabled radiometric dating.
Similarly with memory, it is completely plausible that once we understand very well what a memory is, what its exact correlates in the brain are, and how those correlates change over time, it will be possible to tell how old a memory is. But we aren't there yet (see some articles at the end for where we are).
And while it's plausible that we'll be able to know the age of a memory once we understand it well enough, it is by no means inevitable. To give a counter-example, there is absolutely no way to tell the age of, say, a water molecule. We understand water molecules extremely well. They form and can be destroyed, so for every water molecule there is a certain amount of time since it formed, i.e. it has an age. But a water molecule is just an oxygen atom linked to two hydrogen atoms; its properties are dictated by chemistry and don't depend on how long it has existed. There is no way to tell the age of a given water molecule just from looking at it. Similarly, computers give a timestamp to a file when they create it, but if they didn't do that I don't think we could tell how long a file had been on the disk just from examining the disk itself. So it is certainly theoretically possible that once we understand how memory works, we'll find that we can't, in fact, know the age of a memory.
Here are some papers on memory to give an idea of what neurobiologists are looking at these days:
The Regulation of Transcription in Memory Consolidation
http://cshperspectives.cshlp.org/content/7/1/a021741.short
This paper looks at the role of DNA transcription in the consolidation of long-term memory (as such consolidation apparently requires new proteins being created)
Structural Components of Synaptic Plasticity and Memory Consolidation
http://cshperspectives.cshlp.org/content/7/7/a021758.short
This paper (more or less the same authors) looks at the structural factors involved in consolidating memories by strenghtening synapses and creating new ones.
The many faces of working memory and short-term storage
https://link.springer.com/article/10.3758/s13423-016-1191-6
This recent (2017) paper discusses "Working memory" and how the field doesn't have a single, coherent definition of that concept yet.
Functional neuroimaging studies of encoding, priming, and explicit memory retrieval
http://www.pnas.org/content/95/3/891.short
This 1998 imaging study looks at what regions of the brain light up in various memory-related tasks, and suggests such imaging studies can be useful to investigate brain function. They were right, but notice how general the areas they see are, and how they only can guess at what might be going on there.
The Molecular Biology of Memory Storage:
A Dialog Between Genes and Synapses
http://teachline.ls.huji.ac.il/72336/sphira/Kandelnobellecture.pdf
This is a very long lecture from 2000 from one of the authors of the above papers, summarizing their life's research on the molecular and synapse-level mechanisms of memory. These paragraphs give a historical overview of how scientists have thought memory works:

In his Croonian Lecture to the Royal Society of 1894, Santiago Ramo´n y Cajal
  proposed a theory of memory storage: memory is stored in the growth of new connections[16]. This prescient idea was neglected in good part for half a century as students of learning fought over newer competing ideas. First, Karl Lashley, Ross Adey, Wolfgang Köhler, and a number of Gestalt psychologists proposed that learning leads to changes in electric fields or chemical gradients, which they postulated surround neuronal populations and are produced by the aggregate activity of cells recruited by the learning process. Second, Alexander Forbes and Lorente de No proposed that memory is stored dynamically by a self-reexciting chain of neurons. This idea was later championed by Donald Hebb as a mechanism for short-term memory. Finally, Holger Hyden proposed that learning led to changes in the base composition of DNA or RNA. Even though there was much discussion about the merits of each of these ideas, there was no direct evidence to support any of them [reviewed in 17].
We were now in a position to address these alternative ideas by confronting
  directly the question of how learning can occur in a circuit with fixed neuronal
  elements. Kupfermann, Castellucci, Carew, Hawkins, and I examined the neural
  circuit of the gill-withdrawal reflex while the animal underwent sensitization or habituation, a form of learning in which the animal learns to ignore an innocuous stimulus to siphon when given with monotonous repetition. (We later also extended these studies to an examination of classical conditioning [20].) Our studies provided clear evidence for Cajal’s idea: learning results from changes in the strength of the synaptic connections between precisely interconnected cells [6, 7]. Thus, while the organism’s developmental program assures that the connections between cells are invariant, it does not specify their precise strength. Rather, experience alters the strength and effectiveness of these pre-existing chemical connections. Seen in the perspective of these three forms of learning, synaptic plasticity emerged as a fundamental mechanism for information storage by the nervous system, a mechanism that is built into the very molecular architecture of chemical synapses [95]

Notice how twenty years ago, this person was saying we can finally begin to answer century-old questions of what form memory storage takes in the brain to begin with.
A Putative Biochemical Engram of Long-Term Memory
https://www.sciencedirect.com/science/article/pii/S0960982216311393
Exciting 2016 article: they've maybe found one place where one memory might be stored! First line of the abstract:

How a transient experience creates an enduring yet dynamic memory remains an unresolved issue in studies of memory.

Same idea in the first line of the abstract of this 2016 article on associative memory:
Neural ensemble dynamics underlying a long-term associative memory
https://www.nature.com/articles/nature21682

The brain’s ability to associate different stimuli is vital for long-term memory, but how neural ensembles encode associative memories is unknown.


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Blackgram leaves. SDS page. Phosphate buffer method

I am doing protein analysis in blackgram leaves by using phosphate buffer method. But I cannot get proper bands on my SDS-PAGE. What should I do to get proper bands?

Can you please exactly describe what you have done? At the moment this is not possible.

You should de-stain your gel longer. I can see at least one thick band at the top, but without de-staining longer you are probably missing other fainter bands.
Also, please explain what you mean by "proper bands". The top one looks fine to me. There might be others but we cannot see them.

There are other bands below; definitely destain. But perhaps the OP is referring to the frowning?

In protein analysis lots of bands can be seen in the gel bt I got only one band. That's why I am asking what should I do? Can you send a proper protocol to me. My mail I'd mohanlal0606@gmail.com. please help me by sending detailed protocol.. Thank you all for your comments..

@Mohanlal seeing a single band might be a good result, depending on what you are trying to achieve. For example, if your goal is to purify a protein, it's very good news when a single band shows up on an SDS-PAGE (assuming this is the correct protein, of course). I don't think you need to change anything to your electrophoresis protocol, except de-staining longer. You might need to change whatever you are doing before the SDS-PAGE if this single-band result is not what you want.


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What does the placenta consist of?
It includes the basal plate, the pool of blood between the chorionic plate and the basal plate and the chorionic plate, what else?

Why isn't anyone giving an answer

Possibly because the question seems like it could be easily answered via Google, and because you haven't demonstrated that you've made any effort to answer it yourself yet. Putting it another way, what do you think the answer is? What is blocking you from researching this yourself?

You could’ve easily googled this, but anyway...
Placenta is a composite structure made of embryonic and maternal tissues.
The placenta is composed of: The chorion, which is the embryonic-derived portion of the placenta. Chorion contains the trophoblast cells (cells that make up the outer cell layer of the blastocyst). finger-like structures called chorionic villi are also present in the placenta. Lastly, the space in the placenta that surrounds the villi and the maternal blood is called the intervillous space.
Source: https://study.com/academy/lesson/the-placenta-and-the-fetus-structure-and-function.html


text:
Are there biological ratchet cycles that are small in number?
I recently came across the strange factoid that all animals that can jump do so to roughly the same height (within an order of magnitude).  The argument was that the work done by muscles in a single contraction is proportional to their mass, and the amount of energy required to jump is also proportional to their mass.  The secondary issue of power could be solved by an approach like the click-beetle uses, where they store the energy in their shell slowly, then release it quickly.
I'm an engineer, so my first thought is that a ratchet could be used to circumvent this sort of limit.  If I could cycle a muscle 2-3 times and use a ratchet to store that energy, I could release 3x more energy and jump higher.  As an engineer, it seems like a no-brainer.
But I can't seem to find any biological example of such a ratchet.  The closest I could find was the muscle proteins that cause contraction in the first place.  But that didn't fit the image of the structure I cared about because it was literally millions of these ratchets and the result felt "too smooth" for the concept I was searching for.
So my question is whether biology has a structure that operates like:

Powered by a muscle that gets to contract multiple times (or another chemical process which cycles a small number of times. 2-10 is fine, 10 million is not)
Stores the energy of each contraction
Releases that energy in one burst.

Mentally I'm thinking of a ratchet that I could crank down with 3-4 pulls of a lever, and then release all that energy at once, but I'm open to other biological structures which meet the above requirements.

It's a very interesting concept, the only thing I can think of that's at all similar is neurons, which slowly gain charge, then release it when they transmit the signal.

Do contractions for giving birth count? :)

@Armatus It's not quite what I had in mind, but it sure is darn hard to argue that it doesn't count =D  As I commented on your answer, I was looking at jumping heights and the rapid explosion of energy needed to jump higher, but contractions certainly are using a ratcheting like motion... just to gain mechanical advantage rather than storing power!

First I would in return ask why the actin-myosin coupling should not qualify - the many repetitions of this contractile unit never contract at exactly the same time, and their combined contractile force certainly accumulates in a ratchet-like fashion across the microsecond time scale (with other units contracting before previous units have relaxed). Just because it's a lot of them doesn't make it less ratchet-like :)
With this restriction though, and looking for a "macro-scale" example, I am not aware of anything fitting your description. If I think about it as follows, it also seems intuitive that this wouldn't evolve.
A ratchet as you describe, let's say able to store up x contractions of a muscle for instantaneous release, can also be thought of as a series of x muscle contractions coupled in series across time. It would be equivalent in output to coupling x muscle contractions across space and executing all of them simultaneously. In other words, growing x times the muscles achieves the same benefit.
When it comes to the probability of evolving, what's more likely: an entirely new mechanism to store mechanical energy across time and allow building up, or a simple duplication of the same tissue? The currently existing muscles answer this question: duplication. This can be seen in the different structures that muscles have across living species (muscles in animals, similar contractile mechanisms elsewhere).
The smallest contractile unit in muscles are myosin heads coupled to actin filaments. Duplicate this unit (repeatedly) in two dimensions of space to obtain a myofibril. Multiply the myofibril many times and you reach a single muscle fibre. In fruit fly larvae, this is where it stops - each muscle consists of a single fibre. By the time you're at the adult fly though, the muscles that power the wings consist of a handful of packed parallel fibres. As you go down other routes along the evolutionary tree towards the mammals, you end up at muscles that consist of masses of fibres packed into fascicles, of which many are packed into an individiual muscle. As described above, at each level you have a "many-ratchet", because fibres and fascicles don't contract at exactly the same time everywhere.
So yes, you could evolve a ratchet. Or you could just evolve a bigger muscle. If many animals happen to stop evolving more muscle at around the same absolute potential jump height, that to me suggests that this is a universally beneficial jump height to evolve for terrestrial animals regardless of body size.

Even the fastest striking animals we know of (mantis shrimps) don't use a ratchet mechanism. They do have to 'lock' their muscles though (with some sort of spring mechanism) in oder to release all the energy build up by muscles in a minimised time window. https://www.nature.com/articles/428819a

The reason I don't count actin-myosin is because my particular interest is in jump heights.  The maximum jump height for an animal turns out to be constant, whether you are a mouse or a cheetah.  It's limited by how much energy a muscle contraction can bring to bear divided by the mass of the muscle.  I'm looking at how to store mechanical energy in other forms that could escape this limit.

Even with a constant maximum power output per gram of muscle (which is basically the limit imposed by the nature of actin and myosin as a contratile mechanism), there should still be the ratio of jumping muscle to remaining body mass as a limiting factor that could be tweaked to evolve higher jumps.


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Evolution as a directed graph exploration?
First of all, I am not biologist, nor good in chemistry/physics.
Secondly, I am really eager to understand.

So I think of a "life" (of a certain whatever being) as a space of somewhat properties. Having a wings is a property. Being tall is a property. Ability to speak as humans do is a property as well.
Properties can be combined. Nearly like Lego blocks do combine: one can build both: a) quite elegant structures, b) total absurd of those blocks. Like with Lego, not necessarily each block can be composed with each block. There are some (probably extremely sophisticated!) rules, defining what can be combined with what; thus set of all properties you might get in future depends upon all the properties you already have. In other words, you present defines all the possibilities of your future.
There is at least one measuring system: it takes a set of properties as an input and maps it to a, let say, number (or something else, which obeys ordering; number feels like the most simple example) denoting how "good"/"bad" this particular combination is.
As a natural consequence of all above-mentioned, there is a directed graph, where: A) vertices represent all possible sets of all possible (respecting rules) combinations of all possible properties; B) directed edges represent the possibility to "evolve" from one concrete set of properties to another one concrete set of properties.

Based on those assumptions, I am going to define what "evolution" is:
Evolution becomes nothing but a finding a shortest path in that unbelievably huge directed graph. I assume most of the readers don't understand algorithms, so brief remark: "shortest-path" problem is one of the hardest even known; roughly saying, it takes "infinite" time and hence is impractical for humans; however, this perfectly explains why evolution takes billions of years - indeed, it's not that hard to define graph, which can't be solved faster than that.
But in order to find shortest path, which is known well from algorithmic theory, you have to be as broad as possible. You try to explore as many vertices, as possible, which means you're creating creatures with all those properties (see #2) and measure their "goodness" with help of your metrics (see #3). The problem here is that you have to track/memorize all the paths you have tried already; especially those, which are proved to be deadends: otherwise your graph exploration will never terminate: you will cycle over the routes you've seen already, but forgotten.
The other thing of great importance, is how expensive your computation is. It runs billions of years and thus you have to guarantee that it's defended properly, can't be lost because of stupid mistake or unexpected circumstances; and the best known way to do this is to copy information about entire process (since very beginning) to each and every Life-being you ever create. The more copies you got, the more reliable entire system: even if you loose all of them momentarily and exactly single creature will survive, it will be sufficient to continue your computation (to continue evolution) relying on the information it accumulates.
Taking into consideration the dimension of the graph we're talking about, that "backtracking" requires enormous amounts of memory. Hence, you need perfect compressing technique to pack your data in the most compact way. And it seems to me that DNA is exactly for this reason (probably not only for this, but this one is definitely important).

What I'd like to hear, is how logical entire thinking I've demonstrated, ignoring numerous details (which I even not aware of)? Could it work like a dramatically simplified representation of evolution? Did I define the DNA's role correctly then? Can you extend this "graph analogy" with fresh details? Am I missing something really big and fundamentally important?

UPDATE:
1) @IMil:

Evolution becomes nothing but a finding a shortest path in that unbelievably huge directed graph.

What makes you think that evolution followed the shortest path?

Evolution does not. In order to find one, you have to try all of them (i.e. all possible paths starting from all existing vertices), measuring "shortness" according to a particular metric system you've accepted. Thus, "try them all" becomes an iteration over all possible properties in all possible ways (see #1 on the top of OP). Some of them clearly better than the other one (already known, seen in past and memorized somehow); but that does not discover the "best" path yet: there are, generally saying, unknown number of vertices you haven't visited yet, haven't measured yet, haven't tested out yet.. So, imagine you do not memorize what you have seen; what's than? What will happen if your metric system will get changed one day? - You'll have to start from the beginning rather than re-measure known subgraph (which is much more faster).
2) @Cort Ammon:

"There is at least one measuring system ... denoting how good/bad a combination is." This may be true telelogically, but we have no clear indication as to whether such a measure exists in a physical sense. Personally, I find it's more effective to think of there being at least trillions of measuring systems, each doing its own thing, which may or may not even be associated with evolution directly, such that the gestalt of all of those systems gives the behavior we see. While we can think of systems as "striving for good," we can also think of them as "just doing their own thing." Both approaches model nature quite well, with their own quirks.

I can't agree with you here. Having any positive number of metrics does not contradicts to the statement "there is at least one"; as well as having a "superposition" of any positive number of metrics does not.

So what we end up finding is that your definition is akin to saying "A written language is nothing more than a construct which admits finite sequences of letters".

Exactly. What I am saying, is that there exists an enormously huge graph of all possible combinations of all the letters. If you allow you letter sequences to be infinite, than graph itself becomes infinite as well; however, since it takes place in Nature those must be physically limited like everything else. Some of those letters indeed unite into words, which do make sense; the other sequences are just nonsense (with respect to the given metric system: hence, there might be cases, when one metric system disagrees with another one, it's OK). Then evolution becomes a process of searching for the greatest novel ever written (once again, according to the preferable metric system - even if it itself is some kind of "summary" of millions/billions/trillions of factors we're not aware of).

As a programmer, you probably have already heard of evolutionary algorithms and esp. genetic algorithms used for optimization problems.

One thing you are leaving out is that evolution takes place in an environment, and the environment is always changing, sometimes drastically. Retaining information about previously helpful adaptations wouldn't necessarily be helpful in the long run, since changes in the environment may have negated their utility.

a) Finding the shortest path in a graph is not a particularly hard problem - Floyd-Warshall is O(V^3). b) Modelling evolution as a path in configuration space is theoretically neat, but leaves out almost all the details.

I am afraid this is not a question about biology is defined by SE Biology, which is a question and answer site, but an attempt to initiate a discusion. Any supposed "answers" will only be matters of opinion, which is why I am voting this off-topic.

You may want to look into something called fitness landscape which sounds like the basis of your model and one thing we know about it is evolution is crap at finding the shortest path, it often locks itself out of the best path even, it is all about finding the local high. https://en.wikipedia.org/wiki/Fitness_landscape

@John actually I might post an answer along those lines if the question was "what is a good conceptual model for evolution using examples from computer science or statistics" - if you equate a fitness landscape with a likelihood surface, then a particle filter arguably does something suspiciously evolution-like.

But in order to find shortest path, which is known well from algorithmic theory, you have to be as broad as possible. You try to explore as many vertices, as possible, which means you're creating creatures with all those properties (see #2) and measure their "goodness" with help of your metrics (see #3). The problem here is that you have to track/memorize all the paths you have tried already; especially those, which are proved to be deadends: otherwise your graph exploration will never terminate: you will cycle over the routes you've seen already, but forgotten.

Evolution is an optimizing algorithm, but it isn't necessarily the best optimizing algorithm of its type. For example, genetic algorithms used by humans often have certain features that biological evolution doesn't, like carrying over the best solution from generation to generation. Biological evolution doesn't do that: if by chance you're fitter than any of your kids, tough you'll die anyway.
In that spirit, biological evolution doesn't go out of its way to explore as many vertices as possible, or to avoid "cycling over routes you've seen already" (impossible in practice because not many evolved traits can be reversed exactly. But when such reversals are possible we do see them happen. Many lineages have seen gains and losses of limbs, of flight, or moving in and out of aquatic life like ping-pong balls...). And in fact evolution has no memory of the past. We can make inferences about the past when looking at current organisms, but the only thing evolution acts on is the organism that currently exists.

It runs billions of years and thus you have to guarantee that it's defended properly, can't be lost because of stupid mistake or unexpected circumstances

You mean, like the Permian extinction? Those guys were pretty much lost I'm afraid. Same with all other extinctions.

Hence, you need perfect compressing technique to pack your data in the most compact way. And it seems to me that DNA is exactly for this reason (probably not only for this, but this one is definitely important).

What evidence do you have for DNA being the most compact form data could possibly take?

What I'd like to hear, is how logical entire thinking I've demonstrated, ignoring numerous details (which I even not aware of)? Could it work like a dramatically simplified representation of evolution?

Your basic idea, that mathematics, computer science and the field of optimization algorithms in particular can inform our understanding of evolution is sound. But finding the shortest path along a directed graph doesn't strike me as the best metaphor. Think more of finding the fitness peaks in a traits landscape, such that finding them is an NP-complete problem. Here are different algorithms that are used in this kind of problem:
https://optimization.mccormick.northwestern.edu/index.php/Heuristic_algorithms
Note that your requirement to remember past solutions is akin to the Tabu Search, but that's only one possible algorithm. Most heuristic algorithms don't do that.

Did I define the DNA's role correctly then?

No, you didn't. DNA enables the hereditary transfer of certain traits, which allows biological evolution to run as, um, well, an evolutionary algorithm. That is its role in the optimization process that is evolution. It does not copy the entire history of the evolutionary process; it just copies the molecule at hand, and the fact that it contains traces of what happened to previous copies is an epiphenomenon. And in fact it does not allow Evolution to re-create previous iterations of itself.

Can you extend this "graph analogy" with fresh details? Am I missing something really big and fundamentally important?

It seems to me you are treating evolution teleologically, imagining how you would design an ideal optimizing process to generate life and seeing if evolution matches. As this and other answers have found, it doesn't match (as an aside, I'm not sure the ideal optimizing process you envision would even be better than evolution. Tabu search isn't the best of all the heuristic algorithms). But more fundamentally, the assumption that evolution must be the best possible process for doing... what you think evolution is supposed to do, is unfounded. It might be true, it might not. It is generally more productive when looking at evolution to focus on what it does, and not on what we think it intends.
This is not to say teleological thinking has no place at all in evolution, insofar as one can argue that if something is optimized in some way, because it was created through an optimizing process that was optimizing for some specific characteristic(s), then it isn't absurd to use teleological language like "wings are for flying". They are, not in the sense that somebody wanted birds to fly and so made them wings, but in the sense that every characteristic of wings is what it is because it makes them good for flying. Because bird ancestors reproduced or not partly on the strength of their flying abilities.
In other words, if something was fine-tuned by evolution, then we can talk about it being "for" something. It's very possible that DNA is one such thing; maybe some traits of DNA are there to make evolution work better in some way or another(ETA: note even there the primary purpose wouldn't be "to make evolution work better", it would be to promote the reproduction of the organisms carrying that DNA. But if "evolution working better" in some way promoted that, then sure). But evolution itself isn't such a thing. At least I don't think there is evidence that it is.

Your theory is based on many false assumptions.

Evolution becomes nothing but a finding a shortest path in that
  unbelievably huge directed graph.

What makes you think that evolution followed the shortest path?

The best known way to do this is to copy information about entire
  process (since very beginning) to each and every Life-being you ever create

DNA doesn't intentionally store information about the evolutionary process. Some genes get lost completely, and mutations are, in general case, irreversible. That should be obvious in case of viral DNA/RNA, where there is simply no space for historical data. Many species, and groups of species, become extinct, and since the fitness of any species is determined by how well it fits in the ecosystem, extinction of dinosaurs makes "backtracking" of mammals impossible.

Can you add sources to your answer?

you really should expand on the shortest path comment as well, as it stands it is not informative.

As for the shortest path: I'd say the burden of proof lies on the author. Evolution is driven by random mutations, and if you draw imaginary paths from, say, last common ancestor of chimps and humans to us (or chimps), there is no reason to believe that the actual path was the shortest one.

Thanks for your answer. Please, see UPDATES at the bottom of the OP.

You can prove your model trivially if you start from the assumption that all evolution consists of altering DNA.  I think the general consensus is that that's a good place to start, but there may be more as we discover.
Now the issue is that, from this model, we can show that your graph approach is trivial.

A node in the graph is associated with one sequence of DNA
Edges between them represent changes that may occur in DNA.

Thus I simply redefined "Property" to be "the presence of a particular sequence of nucleotide."
Generally speaking, we recognize that there is some conversion function from this sequence of nucleotide into "properties" we care about.  This means the graph I described above is isomorphic with the graph you were looking for.  Of course, as you noted, that function is extraordinarily complicated.
"There is at least one measuring system ... denoting how good/bad a combination is."  This may be true telelogically, but we have no clear indication as to whether such a measure exists in a physical sense.  Personally, I find it's more effective to think of there being at least trillions of measuring systems, each doing its own thing, which may or may not even be associated with evolution directly, such that the gestalt of all of those systems gives the behavior we see.  While we can think of systems as "striving for good," we can also think of them as "just doing their own thing."  Both approaches model nature quite well, with their own quirks.
So what we end up finding is that your definition is akin to saying "A written language is nothing more than a construct which admits finite sequences of letters." (That's the definition of a "formal language," by the way).  While technically true, it misses out on basically all of the nuance of language.
And there's also the concept of epigenetics which studies ways gene expression changes which don't involve changing DNA.  This is an open field.  We still do not fully understand what is going on there.  But it certainly does appear to play an role, and it does not immediately fit into the simple mapping from DNA to properties.

It is a great answer, many thanks! I update OP, please checkout the very bottom, there is your name. BTW, do you realize how close your statement to the Godel's theorems? I omitted this question in the OP, but still... question seems to be extremely important. If one show how this idea isomorphic to somewhat formal language... ;)

@SerejaBogolubov I love Godel's incompleteness theorems, and Tarski's undefinability theorem, but few people appreciate their implications.  And, of course, when it comes to systems that are really operating in the world of real numbers rather than integers, they don't imply quite as much as we might like.

@SerejaBogolubov As for your edit, I agree that "trillions of metrics" is "1 or more."  My point of that was to show just how inordinately difficult it is to use that "1 or more" phrasing, except in brutally abstract settings (such as with Godel's incompleteness theorems).  Those metrics also most definitely do not superpose in a meaningful way.  Biological systems are notoriously nonlinear.  At some point, I think those issues start to add up, and the fact that modeling life as just an abstract representation of DNA starts to fall through long before you get the opportunity...

... to raise enumeration issues.  I could see drawing an analogy to coin flips.  You might have some theory like Gambler's Ruin which says that after some countable number of coin flips, the gambler must lose, but failed to model the probability that the real coin lands on its edge instead of heads or tails (1:6000 for a US nickel), and how that influences the game.  (I "won" a DnD game by rolling a die so that it landed on an edge instead of a face.  The DM was a big fan of a comic in which the only way to win that game was to roll a die on edge)


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Is it possible to extract tissue-culture material from a seed?
Here is the problem: Tissue culture is cloning, and all plants from the same mother plant are identical. On the other hand, plants grown from seed are all different. If parent plants are genetically diverse (not inbred), growing from seed is the best thing in the long run.
The problem starts when some plants have a low germination rate, or are difficult to grow from seed. We want to grow a large number of plants as fast as tissue culture does, but we want diversity. Suppose the plant can produce a large number of seeds or at-least can produce them easily.
Can we extract cells from the seed and grow them via tissue culture? Which part of the seed should be used, and how different it is from using vegetative parts such as the apical meristem?

Yes. It's quite common, to the degree that it's done by some hobbyist plant breeders. See en.wikipedia.org/wiki/Embryo_rescue  However, AFAIK (I'm not an expert), it wouldn't be done for raising multitudes of plants, like tissue culture.
Rather, it's used in hybridization, where you hope to produce hybrids from plants that don't readily hybridize.  You would typically rescue a number of embryos, grow them on until mature, then perhaps use tissue culture to mass-propagate the ones that have interesting characteristics.

Can you add some more references to this (i.e. not just a Wikipedia page)?


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Spider identification please

Can someone tell me which spider this is please? I've found a few of them in my home in North-London, are they poisonous?

Can you please add where you actually live?

Im North London. Also this one is yellow/brownish with black markings but I have found others with a darker purple back..

I have taken to color correct your image so the spider can be identified easier.

@Chris your color correct makes the spider look green on both of my screens. I'd suggest having at it again :p

It think this spider is a Tegenaria domestica also known as the barn funnel weaver in North America and the domestic house spider in Europe. See here or here (picture taken from the first link):

They are not poisonous and usually avoid confrontations, but can bite.

That's really informative, thank you for your help.

Does this species ever have a greenish hue to it, or are you putting that down to the OP's lighting?

@rotaredom I think this is due to the image. I have corrected the color already, have a look into the edit history to see the original version.

Ah, gotcha. Looks like you've got it nailed, then.

I'm not convinced this is the same species, actually.

Its my fault with the colour, i captured it in a red plastic pot but tried to get a bit of white paper inside for the pic.  It was a yellowish/brown with dark black markings

Hi, I'm afraid this definitely is not a Tegenaria and definitely is a Scytodes.  Look at the long, spindly, almost delicate legs, and the very odd carapace.  The 'Rohrschach Blot' markings on the carapace are quite different from the wavy lines on the Tegenaria carapace as well.  Scytodes are slow-moving spiders of closets and quiet areas, rather like their distant cousins the Recluses.  Quite harmless, though, as far as I know.

Very nice, indeed!  This is a Spitting Spider (one of the Scytodes species, but I'm not sure which is most likely over in the UK).  That's a good photo, by the way.  This spider is easily told in the wild by its odd-shaped, domed carapace, with the 'Rohrschach-blot' design around the edge, and the spindly, banded legs.  It's a slow-moving, very mild-mannered spider, with one of the more fascinating methods of catching prey:  basically it spits a sticky saliva in zigzags that restrains the potential food, then rambles up and bites it.
I include a photo and a couple of links for your enjoyment - using a familiar species from the US, Scytodes thoracica.
https://bugguide.net/node/view/3347
https://www.youtube.com/watch?v=LaP52uKg2pU


text:
Question regarding stop codon
I just wanted to ask that in a given RNA, If there is a start codon and no stop codon, is it still considered mRNA, I mean can it be translated to a protein ?

Possible duplicate of Mutation That Loses Stop Codon

@Adrian …and then again possibly not a duplicate, as the poster has given a single tag of DNA sequencing. Are you asking about interpreting the results of DNA sequencing? When you ask about a given RNA, do you mean mRNA? And are you talking about an actual case or a homework question or what? You have already attracted two close votes. If you want an answer I would edit your question quickly, before I add my vote as "unclear what you are asking".

Yes, this is still considered mRNA. A lack of stop codon is usually due to a so-called readthrough mutation, where DNA sequence changes within the stop codon and after transcription it can no longer be recognized by release factors. But yes, ribosomes still recognize the mRNA molecule and start synthesizing abnormal proteins, usually until the ribosome stalls on the 3' end of mRNA and can neither go further nor detach. There are various mechanisms converting this "stalling signal" to a chain of intracellular reactions that lead to degradation of that protein and that abnormal RNA.
Bacteria for instance have a very curious mechanism of solving that problem, namely a tmRNA molecule that is targeted to a stalled ribosome by some specific proteins and acts as an aminoacyl-tRNA as well as mRNA template. It resumes translation, allowing addition of a peptide tag to the malformed protein, which will serve as a marker for degradation. More on that here:
https://en.wikipedia.org/wiki/Transfer-messenger_RNA
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3358797/


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snail motion and snail tracks
I took a picture of a snail whose tracks are not continuous. What is the reason? Does the snail lift itself from the ground during its motion?

something to do with a rythmic organ contraction?

During particularly dry weather some snails will only touch the ground with part of their "foot" at once. In effect moving more like a desert snake in the image below. They do this to reduce moisture loss. Even though it is still a continuous motion it leaves a discontinuous trail. the same number of these points of contact are present the entire time at no point does it leave contact, think of it more like high stepping. This behavior is sometimes called "jumping" even though it has nothing to do with actual jumping.

http://www.molluscs.at/gastropoda/index.html?/gastropoda/morphology/locomotion.html

thanks, do you know of any videos showing these different types of motion?

sorry no I don't


text:
Which statement is incorrect for Rubisco?
My question is this:
Which of the following is NOT correct for rubisco?
a. It is the most abundant enzyme
b. It catalyzes two different reactions
c. It is involved in photorespiration
d. It is not used by CAM plants
e. It is not efficient in fixing CO2
My issues with picking one are because:
a. It is the most abundant enzyme due to its inefficiency
b. It catalyzes both oxygenase and carboxylase
c. It binds O2 meaning its responsible for photorespiration
d. Malate eventually provides a molecule of CO2 to the calvin cycle where it is bound to rubisco, meaning it is used by CAM plants.
e. It only fixes 3 molecules of CO2 per second, making it inefficient. The only reason why this doesn't matter is because of the abundance of rubisco.

@RozennKeribin, the problem he has is that all five choices seem to be correct (for the reasons he provides in the second list), and thus none of the five choices seens to be NOT correct, and thus the multiple choice question has no solution (as far as he can see).

d) is "it is NOT used by CAM plants". In your following text you say it IS used by CAM plants. Seems incorrect to me.

Your justifications for your answer need rethinking. (a) It is either abundant or not. You are not asked to give a reason, and your reason is contentious. (e) Efficiency is not the same as speed. Again, focus on what efficiency actually means, not on why you think it doesn't matter. You need to state clearly whether you think each alternative is true and then say why.

David, I didn’t have to give reasons, just needed to choose an answer. I was just showing my thought process on why I was stuck.

Rozenn, somehow that literally went right over my head. I was reading it wrong and didn’t even realize I answered the question already. Doh. Thanks.

Short answer
D
Background
A. Is correct, as it is the most abundant enzyme on land, and probably also in marine environments (Raven, 2013).
B. Is correct, as Rubisco catalyzes the carboxylation, or oxygenation reaction depending upon the molecular concentration of CO2 or O2 (Sudhakar et al., 2016).
C. Is correct, as it reveals the inefficiency of Rubisco, as CO2 and O2 compete for the active site. Fixation of O2 during photosynthesis oxidizes ribulose‐1,5‐bisphosphate into 3‐phosphoglycerate and phosphoglycolate - which is basically a waste of energy.
D. Is incorrect and hence the answer to your question: Rubsico is present in CAM plants.
E. Because of the photorespiration described under B & C, Rubisco is indeed regarded to be inefficient.
References
- Raven, New Phytologist (2013); 198(1): 1–3
- Sudhakar et al., Phenotyping Crop Plants for Physiological and Biochemical Traits, 2016


text:
Does Pasteur's experiment contradict an origin of life?
To my understanding, Pasteur’s experiment demonstrates that life is only made from life. If this is true, then how could origin of life (aka. abiogenesis) ever have happened?
It seems to me that Pasteur’s experiment and the theory according to which there is abiogenesis contradict each other. Do they?

If I may, your goal should not be to try to convince your friend but to understand whether the meaning of Pasteur's experiments on evolutionary biology.

@Remi.b Well yes, that is what I thought. It's not my primary goal to convince my friend, but to understand where I misinterpreted it

Please describe briefly Pasteur's (note the apostrophe) experiment. Without it your question is meaningless and you cannot start thinking logically about what his experiment demonstrated (I presume that the cause of food spoiling by bacterial growth is not due to "spontaneous generation"). You can only argue about science with someone if you understand and define what you are talking about.

@AyyLmao I've edited you post to try to highlight your interest and not the argumentation you're having with your friend. Feel free to roll back if you don't like the edit.

@David yes, I think in the popular culture "Pasteur's experiment" came to refer to the fermentation experiment that offered an evidence against the prevailing idea of spontaneous generation (see description here on wikipedia)

@Remi.b — I would advise the use of plain English in editing unclear questions such as this. Abiogenesis is not a word I had encountered previously, which suggests to me that 90% of the readers of this page will be in a similar position.

@David Good point. Re-edited

Related: Why did abiogenesis only happen once?, Do we see protocells forming in nature today? and Is it possible there were multiple origins of life?

Pasteur's experiment does not demonstrate that life is only made from life (even if he might have thought it did).  It simply demonstrates that life does not arise under the conditions of his experiment, during the short time available.  You might also note that if he'd had some thermophiles https://en.wikipedia.org/wiki/Thermophile in the flasks, he might well have gotten different results :-)

Pasteur’s experiments demonstrated that the appearance of living matter in spoiled food (soured wine and the like) was not due to so-called spontaneous generation of living organisms, but due to the multiplication of pre-existing but invisible micro-organisms, which could be eliminated by sterilization of the food containers — hence the term pasteurization used (in Britain, at least) for the sterilization of milk.
No more, no less. His experiments say nothing about, and were not concerned with, the origin of life on earth. They related solely to the vitalist misinterpretation of everyday observations in 19th century France. As far as I am aware, Pasteur never concerned himself with Darwin’s theory of evolution. French and British science (and Pasteur and Darwin) had different philosophies and emphases at that time, and contacts were limited.
One may ask what is the difference between abiogenesis and spontaneous generation. The former envisages a slow series of chemical processes leading over millions of years to the first self-replicating molecules and subsequently to simple single-celled organisms — an idea that only really gained traction after the Miller-Urey experiment. The latter involves fully developed organisms appearing out of nothing in a couple of days — a sort of arbitrary non-Christian version of creationism.
The scientists who developed the the idea of an origin of life from inorganic matter were well aware of the significance of the work of Pasteur. They were also aware of the subsequent progress of chemistry and biochemistry. It is worth mentioning that Pasteur was so concerned with repelling the vitalist viewpoint (a sort of irrational superstition akin to belief in magic) that when Büchner demonstrated glucose metabolism in yeast extracts containing no living cells he wrongly rejected this. (The word enzyme means in yeast.)
You can read about Pasteur and Spontaneous Generation here, and Büchner and the Liebig–Pasteur dispute here. There is also a long Wikipedia entry on Pasteur — the French version is even more extensive. You can read about his supposed religious views here if you are interested, but you should remember that the views of a scientist, however famous, are only of scientific value if they are supported by his experiments.

Consider the context. In Antiquity and the Middle Ages from Aristotle on, people thought that many living things (from microbes to mice) would arise through spontaneous generation. Seemed sensible enough; if you don't pay close attention to animals getting somewhere, and you have no knowledge of anything microscopic, it can easily look like animals just come out of the environment. After the Enlightenment scientists got better understandings of reproduction on the one hand, and made many experiments showing that under certain conditions (like keeping meat sealed so flies couldn't get to it for example), life didn't, in fact, spontaneously generate in the way it was previously thought it did. At this point the idea that all living things come from the reproduction of other living things of the same species became increasingly accepted.
Pasteur's experiment was more or less the death knell of the spontaneous generation hypothesis; some previous experiments had shown microbes growing after a flask was supposedly sterilized, or kept the flask sterile by keeping air out (which opened one to the argument that spontaneous generation required air). His showed microbes not growing in a flask where air could flow but dust did not settle because of its shape, and immediately growing when the flask was tipped and dust fell in.
Pasteur's experiment didn't so much "prove that life only comes from life", as disprove a specific other hypothesis that existed at the time. And in that sense it is still consensus biology: No biologist today thinks that snakes, mice, microbes, or even viruses can arise directly through abiotic processes. If you replace "life" with "modern life", the principle is true as far as we know.
Now biology has advanced a lot, and there is a different context, with people asking different questions and advancing different hypotheses to answer them. The question of the origin of life is one such question, that has nothing to do with what Pasteur was trying to prove. And that's where the "modern life" caveat becomes relevant; while all modern living things are too complex and specific to arise directly via abiotic processes, it doesn't follow that the same is true of the first living things. We know that living things used to be different from how they are now; and in fact when looking into the past via the fossil record and genetic evidence we find clear patterns of gradual development of the modern biosphere's diversity and complexity from simpler and more generic ancestors. While it is harder to find evidence for the evolution of early cells, because the genetic evidence is muddled by the time scales involved and the fossil evidence near-nonexistent for obvious reasons, it is sensible to figure that similar patterns would occur there, and that the earliest cells were as different and simpler than a modern cell as a Precambrian worm is from us.
Here is a video of Nick Lane talking about a promising hypothesis on the origin of life. It sort of illustrates how different, and simpler, those primordial living things could have been compared to current organisms.
https://www.youtube.com/watch?v=gb7pZyks_HE&t=1151s

Pasteur proved that modern lifeforms can't form from non-living things.  That doesn't prove that there is some hard and bright line that prevents a micell containing enzymatic RNA from changing a bit into something we would recognize as "life".
Does your friend know about Friedrich Wöhler?  Who synthesized urea in a test tube, proving that the chemistry of life is not fundamentally different to the rest of chemistry?


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What is the X-chromosome responsible for?
I understand that the X-chromosome is responsible for certain disorders, like red-green colorblindness; but besides disorders, what do the genes on the X-chromosome determine?

The number of genes on the X chromosome approaches 1000 and thus your question is too broad for this site.

@canadianer Could just give some general things that these genes would be responsible for, or is it too broad?

"besides disorders" - it's not a complete answer, but for info it's not really helpful to think of genes as 'coding for' a disorder. Any gene that does anything useful can get broken, and when it does the severity of the consequences depends on how important its normal function is.

Can you explain a bit more of your thinking here, and show what research you have done before asking?

@arboviral I agree with what you have said. I phrased the question that way because I had only known that genes on the X-chromosome were responsible for certain disorders until that point.

@CMK My point was more that it's more accurate to think of them as responsible for whatever's broken in the disorder. So the lack of a properly functioning gene for [...] results in a disorder. Otherwise some people are bound to think "hey, why don't we just delete the gene and then nobody will get the disorder".

@arboviral Thank you. That makes a lot of sense.

Here is the list! There are about 900 protein coding genes and about 500 non-coding transcribed sequences. It is not going to be feasible to explain you the function of every single one of those genes. Your question is hence too broad.
You will find here on wikipedia a small subset of those ~900 genes.
If your question was

Are all genes that are on the X chromosome related to sex?

Then, the answer is "no". Most of them have nothing to do with gender specific traits.

Where did the quoted section in your answer come from? (I agree it sounds like that is the misapprehension that prompted the question, but I don't see it anywhere.)

Thank you for your answer and for the links, although I would he lying if I said that I understood what they were saying. However, concerning the genes involved with sex determination, what do those genes determine, in fact?

I have changed "sec determination" with "gender specific trait". That was a typo. In humans, there are only one gene affecting sex determination, it is SRY (coding for TDF) present on the Y chromosome. I don't know much else about eventual gender specific beneficial genes on the X chromosome.

Somewhat related: Do males of all sexual species have Y chromosomes?

@Remi.b Thank you for your response. What is your opinion on this article, which says that there is more than one gene that affects sex determination? https://genderedinnovations.stanford.edu/case-studies/genetics.html#tabs-2

I only just read the first few sentences. I am not so surprised that with severe medical intervention such as a gonadectomy or large injection of male hormone in females, you can masculinized or feminize the individuals. In principle, it is completely possible that several loci affect sex determination (it is the case in many species), I just had never heard such claims in mammals.

I would like to start the answer by mentioning that I was fortunate to attend a lecture by Jenny Graves, a scientist working on X chromosomes recently.
In her lecture she mentioned the genes on X-chromosomes as "brain and balls" genes. As Remi.b has already added a list you can go through it to find a few of these genes. I am highlighting a few of them as follows:-

Androgen receptor (AR) - Required for prostrate formation in males. Mutations may lead to muscular degeneration and loss of motor control (Kennedy's syndrome).
AIFM1 - An inhibitor of apoptosis. Mutations may lead to neurodegenerative conditions like Charcot-Marie-Tooth disease 4.
MeCP2 - Heterozygous female MeCP2 mutants suffer from Rett Syndrome. It is almost exclusively seen in females because male mutant embryos die during pregnancy.
BEX1, BEX2 and BEX4 - Brain-expressed X-linked (BEX) proteins

Also regarding sex determination - the mammalian XY sex determination is Y centered i.e. the SRY gene on the Y chromosome is the gene responsible for determining maleness. Interestingly some species not using the XY system have evolved female specific sex determination genes. I will add relevant citations when I have time.

I added a few relevant citations because someone downvoted without providing a reason.

Thank you for your answer. So, does this mean that the X+chromosome contains genes that direct the formation of part of the male reproductive system?

Yes. Since, the size of the Y chromosome is much smaller than X chromosome it does not contain many genes. Most of the genes on Y are only involved in early determination of sex. Information regarding organ development is still encoded by X.

@CMK Also consider upvoting if the answer satisfies your curiosity.

Thank you. I would upvote, but my reputation isn't high enough. I'm sorry about that. But, just to be clear, the X-chromosome does direct The formation of the male reproductive in part?

@CMK Yes, it does. The androgen receptor (AR) being on the X is a clear indicator of the fact. If you take a look at the list Remi provided i am sure you will find a few more genes involved in male development. I will go through the lis and let you know if I find a few as well.

Okay, thank you for this. It has been extremely helpful. Would this, then, mean that female is not the default gender as many people say, or is this conclusion gratuitous based on this fact? Thank you.

Female is called the default gender because in absence of SRY gene all embryos develop to be females. Loss of function SRY mutant XY genotype gives rise to female babies. Although these individuals require hormonal supplements for proper development during puberty. Link for syndrome - https://en.wikipedia.org/wiki/XY_gonadal_dysgenesis

I understand. However, I read elsewhere that there are genes which required to suppress male development and promote female development. It's found in this article. https://genderedinnovations.stanford.edu/case-studies/genetics.html#tabs-2


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Reversal of cross-linking in ChIP-seq
Chromatin immunoprecipitation (ChIP) is a type of immunoprecipitation experimental technique used to investigate the interaction between proteins and DNA in the cell. A summary of the protocol for ChIP is here. Briefly, the steps are:

DNA and associated proteins on chromatin in living cells or tissues are crosslinked;
The DNA-protein complexes are  sheared into ~500 bp DNA fragments by sonication or nuclease digestion;
Cross-linked DNA fragments associated with the protein(s) of interest are selectively immunoprecipitated from the cell debris using an appropriate protein-specific antibody;
The associated DNA fragments are purified and their sequence is determined.

After step 3 (immunoprecipitation of the protein-DNA complex), it is my understanding that the protein–DNA cross-link is reversed and proteins are removed by digestion with proteinase K.
Can anyone tell me if during this step the DNA at site of cross-linking is included in further sequencing step or is washed away with the protein itself?

Welcome to Biology.SE! I've tidied up the question a bit - hope the edits are okay.

So you want to know if in the crosslink reversal step the DNA gets lost?

Yes. More specifically at the point where protein & DNA is attached.

After the crosslink reversal step, you still have some DNA connected to protein fragments.
So at that step, instead of doing a normal DNA purification, we also need to use a phenol-chloroform extraction or special columns to seperate DNA from protein fragments.
Thermofisher usually gives really good explanations too.
Please let me know if I didn't understand the question correctly! :)


text:
dbSNP clarification
I am currently going through this paper - link.
In their methods section the authors have described they have used dbSNP for checking biallelic expression of genes. I would like to know if dbSNP contains SNPs for intergenic regions i.e. for non coding RNA regions.

Yes, dbSNP is in no way limited to coding SNPs.  One example, an intergenic SNP I found in ensembl.org:
https://www.ncbi.nlm.nih.gov/SNP/snp_ref.cgi?searchType=adhoc_search&type=rs&rs=rs542978047

Thanks a lot. I am currently trying to learn as much as possible on the topic.


text:
What makes white phosphorus toxic?
What makes white phosphorous toxic?
I mean it causes liver and kidney damage, and altered blood coagulation, but it is hard to find anything about what biochemical mechanism this poison uses to kill liver and kidney cells and why the liver is not capable to neutralize it even in a 50mg/kg dose (LD50 in rats). It would take just a simple oxidation to convert it to phosphate, which is commonly used by living cells.
conclusion:
I think the main cause that white phosphorous is so toxic that it is not something common in the environment, so there was no evolutional pressure to adapt to it. The human body can deal with it relative fast, but it damages cellular organelles and causes possibly fatal liver and kidney damage in hours. Some of the metabolites are even more toxic and they can cause arrhythmia and disturb the CNS. Because the molecular mechanism of toxicity is still mostly unknown and there is only a short time to treat people before liver and kidney damage, currently I think there is no way to save somebody exposured to a high dose of white phosphorus.

There seems to be some difference on the development of symptoms depending on the route of uptake, but eventually poisoning with white phosphorus leads to kidney and liver damage.
Oral uptake leads to gastro-intestinal problems like abdominal cramps, nausea and vomitting, if you take up low doses chronically, this may lead to phosphorus laden stool (also called "smoking stool syndrome").
Since white phosphorus will ignite when it comes in contact with air, skin contact often leads to severe chemical burns. White phosphorus is also highly soluble in lipids and is therefore suspected to cross through our skin rather fast, leading to absorption in the body and subsequent poisoning by liver and kidney damage.
See reference 1 for a short overview and reference 2 for extensive information.
Regarding the exact molecular mechanisms is surprisingly little known and published. It is clear that poisoning with white phosphorus causes Triglycerides to accumulate in the liver, causing the fatty liver syndrome. Depending on the source it is also speculated that carbohydrate and/or protein synthesis in the liver is also affected (see for example here or here). Mostly this is explained by the high reduction potential of the phosphorus, which disturbs the fine balanced metabolic pathways. Finally this seems to leads to liver failure (see also reference 3).
According to the toxicology profile (reference 2) the damaged protein synthesis in the liver leads to fatty liver very fast.

Liver damage in animals exposed to white phosphorus progresses
  rapidly. Four hours after receiving a single oral dose of white
  phosphorus, minimal fatty changes in hepatocytes were observed; by 12
  hours fatty changes were extensive (Ghoshal et al. 1969). Exposure to
  white phosphorus has been shown to damage the rough endoplasmic
  reticulum and cause a disaggregation of polyribosomes (Ganote and Otis
  1969; Pam et al. 1972). This damage results in impairment of protein
  synthesis, in particular, a decrease in the synthesis of the
  apolipoprotein portion of very low density lipoproteins (VLDL), which
  are required for the transport of triglycerides. A significant
  decrease in protein synthesis has been detected as early as 3 hours
  after oral exposure (Barker et al. 1963). The smooth endoplasmic
  reticulum is also involved in the formation of the VLDLs, and damage
  to the smooth endoplasmic reticulum also impairs the formation of
  VLDLs. The net result of these ultrastructural changes is an
  accumulation of triglycerides in the liver (Ghoshal et al. 1969). This
  results in steatosis and fibrosis, which is one of the mechanisms
  involved in the hepatotoxicity of white phosphorus. The mechanism
  behind the damage to the endoplasmic reticulum is not known; also, it
  is not known whether white phosphorus itself or a metabolite of white
  phosphorus is the damaging agent. In addition to these damages, white
  phosphorus or a metabolite causes damage to the mitochondria and
  nuclei in the livers of animals orally exposed to white phosphorus
  (Ghoshal et al. 1969). The damage to the mitochondria may impair the
  cell’s ability to produce ATP, thus resulting in necrosis of the cell.

Another possible (and additional) toxic effect may be traced to the (possibly enzymatic) generation of phosphines from phosphorus and water which are highly toxic to the central nervous system (here my source is only german, you can find it here). According to reference 4 phosphines are interfering with the COS gasotransmitter signaling. They can cause cardiac problems by this mechanism. Phosphines smell garlic like, this is an observation often made, when victims of white phosphorus poisonings are authopsied.
References

White Phosphorus Exposure
TOXICOLOGICAL PROFILE FOR WHITE PHOSPHORUS
Biochemical changes associated with acute phosphorus poisoning (in
humans)
Sulfurous Gases As Biological Messengers and Toxins: Comparative Genetics of Their Metabolism in Model Organisms

Nice, altough if I understand the answer correctly I am surprised. Isn't breath the most dangerous&important route of uptake ?

While this is all true, the question is about how it causes liver damage. Probably I should rephrase my question if this was not obvious.

@inf3rno Yes, that would be good. It wasn't clear to me. I will have a look into this, too and edit the answer. But this will take a day or two.

Hard to find anything in the topic, but this might be interesting: https://books.google.hu/books?id=xZf-CAAAQBAJ&pg=PA195&lpg=PA195&dq=white+phosphorus+hepatotoxicity&source=bl&ots=yoiD7rlE8e&sig=--hsfvTfuc-Zth98NnR2qJPywEI&hl=en&sa=X&ved=0ahUKEwiK-oLrvPHZAhUzyaYKHZr7CzkQ6AEIUzAF#v=onepage&q=white%20phosphorus%20hepatotoxicity&f=false

It references this article: https://www.sciencedirect.com/science/article/abs/pii/0014480072900354

@inf3rno Interesting link. Since this paper is quite old, I will see who cites it, maybe some other useful papers will come out there. But this is nothing I can do from home, here I need the journal access in the institute.

Okay. I have already checked, there are a few relevant articles on the list after 2000, but I have read only the abstracts. Maybe the fulltext contains more about the mechanism.

@inf3rno I have now updated the answer, after I went through the articles. Still, there is little hard data on this, most likely due to ethical reasons (who wants to poison experimental animals simply for finding out why this is poisonous) and also due to handling hazards. Additionally to the toxicity, white phosphorus is also pyrogen, I wouldn't want to work with it.

Phosphines might interfere with the COS gasotransmitter. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216388/ Probably that's why they are so toxic.

@Chris Added some extra info to your answer.

@inf3rno Thanks. I would have looked at the paper tomorrow.