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Is there any evidence that discards the possibility of an organism-aided evolution?
The theory of evolution of Darwin is mostly accepted nowadays, while Lamark theory has been abandoned. There are many experiments that show that experiences do not alter the genes or are passed to descendance (there could be some exceptions , see https://en.wikipedia.org/wiki/Transgenerational_epigenetic_inheritance but the inheritance is not clear)
Although genes are not modified by experiences, I was wondering if there is any evidence or argument that justifies that during the process of producing sperm, maturing ovules or the fecundation, the gene selection must be completely random. I mean, I question if there could species that chose from their own genes, those who had been more useful during their life and increasing the chance that their descendants had them since their conception.

Extraordinary claims require extraordinary evidence. If someone wants to claim there is an intelligence to evolution, they need to provide evidence in support of it, rather than asking others to provide evidence against it.

I am not making any claim. I simply ask if this issue has been previously studied or considerer and if it has been discarded for a given reason.

Note that there is a difference between GENS (a group related through male ancestors), and GENES, which is probably what you want to ask about.

I think the problem is the word "intelligent", which suggests you are referring to intelligent design, or the idea that evolution is controlled by some sort of superior being. That's clearly not what you are asking. Perhaps replace it by "organism-driven" or something like that.

I mean, I question if there could species that chose from their own gens, those who had been more useful during their life and increasing the chance that their descendants had them since their conception.

There are two kinds of argument against this - one from basic principles, and one from empirical evidence.
As far as basic principles, I think Dawkins makes very good arguments against Lamarckian evolution in his book "The Selfish Gene". Essentially he points out the example of muscles getting larger when we exercise, and notes that not only isn't this universal - plenty of structures get worn down with use, not strengthened - the fact that muscles specifically do this is itself an adaptation. And he points out there is no mechanism for this adaptation arising through Lamarkian evolution if it isn't already there. There's a basic bootstrapping problem involved that Darwinian evolution doesn't have.
When we consider your example the same issue arises. By what mechanism would an organism choose which genes to pass on? Can you? Of course the fact we don't have conscious control over the genes we pass on isn't necessarily dispositive, our bodies do plenty of things we don't have conscious control over. But not only would there need to be a mechanism by which some genes are selected to pass on and not others, you would need some way for the information about which genes to select to get back to said mechanism. Making this choice is an incredibly complex issue... The things you'd have to know about the environment, the ways genes impact the final phenotype, which phenotypes are truly optimal for the environment... We humans aren't at the point of doing this. Natural selection works out for extremely dumb reasons. You are proposing a system that does this in a smart way... We already know how evolution comes up with smart systems, that integrate information about the environment and infer general rules about how the world works and predict the best actions in consequence: it makes brains. The brains it's made so far that are best at this are ours, and "explicitly choosing which genes to pass on" isn't what we're using them for so far. That might come in future decades with genetic engineering, and when it does it will be an entirely novel form of evolution. It's incredibly implausible to suppose that other organisms have been doing this all along.
Now, could some genes or gene families happen to have some kind of positive feedback property that means they get selected more when they're useful and selected against when they're not, more than natural selection could predict? Maybe. It's not like organisms that use "meta-properties" of evolution, like tuning their mutation rates depending on the environment, don't exist (see this abstract on bacteria for example: https://pubmed.ncbi.nlm.nih.gov/16677295/). That could too. But it would apply to a few specific genes in those organisms, it wouldn't be a general evolutionary property.
As for empirical evidence, the thing is the "neutral hypothesis" can be tested, because random behavior has (paradoxically) very predictable properties. I think we can generally say that in everything we see about mutations appearing, the inferred mutation history seen in DNA patterns, in the evolutionary history of various phenotypic traits, that all those things point to mutations happening randomly with respect to usefulness. But one specific example I like very much is the Lenski experiments:
http://myxo.css.msu.edu/ecoli/
What happened is that Lenski ran a long-term experiment looking at the evolution of certain bacteria, by culturing them in a certain environment and, and this is key, freezing batches every few generations to have a replayable "record" of the state of the bacteria at various points. The most famous aspect of this experiment is how some of the bacteria evolved the ability to break down citrate, a completely novel and even definition-breaking ability for this type of bacteria. And here's the interesting aspect that's relevant to our discussion here: when they looked back at previous frozen generations ancestral to the specific bacteria that did this to figure out what happened, they found that if they cultured bacteria from before a certain point, almost none would develop the ability to break down citrate. But if they cultured bacteria from after that point, plenty would. Lenski deduced that the ability to break down citrate required several mutations, and one of those mutations was developed in the ancestor at that point. Hence, all the ancestors before that point were N mutations away from developing the ability to break down citrate, but those after it were only N-1 mutations away, and so they developed it much more readily.
Now how is this relevant? This difference between before and after the potentiating mutation would only happen if the mutations were occurring randomly, as opposed to "with the goal of developing the ability to break down citrate". If the bacteria were trying to break down citrate from generation 0, and acquired those mutations for that specific goal, then there would be no difference in which of the ancestors you looked at - they'd all be on the same path, and all equally likely to reach the goal. It wouldn't matter that the older bacteria were one extra mutation away from the adaptation than the later ones: they were planning on getting that mutation anyway. It's like, say you have a toddler and you want them to walk to a chair, but they don't control their walking very well; they're weaving all over the place, it's frankly not clear they even want to get to the chair to begin with. Where you set them down will make a big difference in whether they reach the chair or not: if you put them close to the chair, their random movements are quite likely to take them there, but the further away they are the more likely they are to just wander off wherever instead. Now say instead you have a hungry 6 year-old, and you put their favorite candy on the chair where they can see it. That kid is making a beeline for the chair, and it doesn't really matter where you set them down - if they're far away it might take them more time to get there, but not much, and they are as likely to get there in the end as if they'd been set closer.
The evolution of citrate metabolism in Lenski's bacteria behaved like the aimless toddler, not the focused 6 year-old.
ETA: Actually I kind of want to expand, add yet another element to the answer, which is: why this might not even be desirable. I see other comments have given examples of genes being transmitted non-randomly. I myself didn't exclude genes being transmitted non-randomly with respect to usefulness, but said it would be a property of specific genes in specific organisms, not a general feature of evolution, and I stand by that. I'll add that I don't expect this kind of property to be an important part of developing novel adaptations in particular, and that I expect big caveats on how smart these features are. I don't know what level of intelligence OP is considering, but I'd guess they're thinking, "wouldn't evolution work better if it chose adaptations more intelligently, like we humans would, instead of randomly?", mostly because it's what I myself would think. And that's the idea I want to challenge here.
I said earlier that natural selection works out for extremely dumb reasons. That's a weird thing to say, so let me explain: natural selection works because it's constantly testing things against reality. By definition; "natural" selection is "selection by nature". On average, things get passed on if they actually help, exactly insofar as they actually help. This is what makes evolution by natural selection so powerful, and come up with such innovative solutions that would never occur to humans: everything in reality is on the table (or at least, limited by the fitness landscape, not cognitive biases), and only things that work in reality are kept.
But that power is also a limitation. Because how is it that humans design that's different? We also test our designs against reality: we build them, check that they work, and keep them if they do. But "trial and error" is notoriously slow and inefficient. The power of our design process, the intelligence of it, is that we don't just test our designs against reality: we test them against imagined realities. We imagine how the world could be, we imagine different ways designs could interact with an abstracted mental model of how the world is. This is what allows us foresight and planning... which is something evolution by natural selection does NOT have, and which is why we can do things it can't. And I think that's the kind of intelligence people who ask "what if evolution was intelligent" are thinking of. But it's also a danger, because it means we can go full forward with an idea, and find out too late that it had awful consequences we didn't anticipate. It also bumps against the limits of our own imagination, which will never encompass the whole of reality. This is the big fear with genetic engineering, and it's why I'm not convinced that selecting genes for adaptivity would be as useful to an evolving organism as just blind natural selection would. You'd gain some things (speed, ability to cross fitness valleys) but lose others (reliability, ability to find fitness paths the foresighting system did not foresee). We might pull it off, but that gets to what I was saying earlier - we, as a species, are the smartest, best-at-planning-and-forecasting system nature has come up with yet. If we're barely, debatably at the point of being able to do this, what existing biological system could do better?

I agree with most of your comment. -however, I didn't want to ask if organisms could induce mutations, but if an specie could have to ability to determine from a given pair of genes which one had been more beneficial given its experiences, and transmit it more frequently to its descendance. I am conscious that it could reduce genetical variety and that it could be quite difficult to end up developing such a  mechanism, but there are a lot of species that have developed impressive mechanisms.

@zero-point I believe that is indeed the question I was answering...

The randomness of the assortment of genes was first shown by the experiments of Mendel in his experiments with pea plants, and demonstrated numerous times in different contexts in classical genetics.
There are specific instances where the assortment is not perfectly random. This is called meiotic drive. There are some genes that will skew the meiotic process so that a particular allele will be more likely to be transmitted to the next generation. These are the exception though.


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In what "space" does egg mature in Kiwi?
This huge egg here, is it sort of tethered to the ovary, filling up the coelomic cavity, and then exiting out of the infundibulum, or, where is it in the bird exactly? What "space" does it occupy?

I can't find the original source for your image, but it is likely an artist's rendition of an X-ray image, or is very edited.  Here is a real X-ray of a kiwi with its egg: https://www.audubon.org/news/why-kiwis-egg-so-big

In birds, eggs mature post-fertilization in the magnum and "shell gland", sometimes called a uterus.
I can't find anything to suggest a kiwi is any different, despite their large egg size. An exception is that kiwi have two functional ovaries (yet the join in one functional oviduct and the rest of the reproductive system is only present once) (Ballard & Cheek, 2016). Given this source mentions this specific difference, it seems unlikely they would have omitted any other important differences.
This course page may be useful for bird reproductive anatomy more generally: http://people.eku.edu/ritchisong/avianreproduction.html
Ballard, B., & Cheek, R. (Eds.). (2016). Exotic animal medicine for the veterinary technician. John Wiley & Sons.

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What do the initial cell divisions look like in bird embryogenesis?
The germ disc in a bird (a disc because its a chordate) is a mystery to me. The ovum (yolk) is a huge mass of nutrients. It then gets impregnated. Then, what? What does the initial cell divisions look like (they can't be symmetrical since yolk is clearly pushed to one end of the whole thing. )

I'm pretty certain the ovum isn't the yolk. Ova are way smaller than that. Human embryos also have a yolk sac, and it develops during early embryonic development. According to wikipedia, in birds it's a specialized structure made in the mother's body and is part of the ovum in very small animals like some fishes or invertebrates, not birds.

I'm just interested in what is true. I've kept hearing the meme that the yolk in birds is a single cell, and it looks plausible but always sounded a bit weird. The human yolk sac isn't homologous with birds yolk sac, at all. It develops from the germ disc long after fertilization during the formation of the gut tube. Overall phylotypical stages in embryogenesis are hard to master because there is so much variation, one thing that looks identical is achieved by a completely different procedure, is common.

The yolk of birds may well be a single cell, but it doesn't mean that cell is the ovum. (actually I read down the wikipedia page, and it has a section on chicken eggs that explicitly says the claim you're describing is false "in strict sense". I know I know, wikipedia, there's a reason this is a comment and not an answer, but the citations might be useful). I didn't know the human yolk sac wasn't homologous to other yolk structures, thanks for that!

Overall, how the embryo gets to different stages differs a lot while the stages look the same. It's pretty confusing until you get that the processes aren't homologous. The mammal yolk sac is a part of the gut tube, it forms as the initial germ disc (that exists to conform to notochord organizational axis) bends into a cylinder.

Looking at this diagram and this one from this page, it looks like a small portion of the edge of the yolk develop a "cleavage furrow" which then develops into a multi-celled "blastodisc" or "blastoderm" that becomes a more differentiated embryo.

@Hypnosifl still a bit of a mystery. Since the unit those processes deal with are cells, if the yolk to begin is a single cell, the ovum, assuming the initial cell divisions are normal mitosis, doubling number of cells, is it originally undergoing an asymmetrical division where one cell takes the entire yolk and the other forms at one pole, and, does that other pole cell then continue from there to form the germ disc and all that?

This page also says that "The hen's egg consists of just a tiny patch of cytoplasm resting on the surface of a large ball of yolk" and that the initial cells during cell division have a plasma membrane on top and sides but not on the bottom, where "the bottom of the cell [meaning the cytoplasm I guess] is in direct contact with the yolk". Calls this "meroblastic cleavage", might google that term to find out more.

@Hypnosifl You should write that as an answer. I think using the contrast with frog development (where the yolk is more... 'intracellular') is probably also quite informative.

@Hypnosifl that sounds a bit contradictory, if the tiny patch of cytoplasm is continuous with the yolk, isn't it a single cell. Or do two cells partially fuse in the ovary?

@BryanKrause Do you know if the yolk is the same cell as the ovum and a single cell?

@IanMalcolm It is not controversial that there is one and only one cell present before post-fertilization devisions (which occur before the full egg is developed). What is a bit unclear is what you call a "single cell" after that in the early stages of development. I'm not an avian development (or any development) expert and people tend to pick up chickens as model organisms after the first day or so after many many cell divisions (frogs are much nicer models for the first few divisions), so the earliest steps of avian development are often left out of textbooks.

What I call a "single cell" is what you call "not controversial that there is only one cell present". No need to misrepresent my statements. @Oosaka thought the ovum and yolk were different cells (easy to think since the yolk is huge), I've heard that they're a single cell, although it is a bit counter-intuitive, but there are other examples of huge single celled structures. Main question is how that huge single cell does the initial cell divisions.

@IanMalcolm You can call that a single cell, but there is a lot of non-cellular material in a living organism as well. The majority of the yolk is kind of...in between. Hence the potential for controversy. "There is one cell" is not the same as "This is all one cell". Hypnosifl gave the answer already to "how that huge single cell does the initial cell divisions", though in a comment that should be an answer.

You call it "not controversial that there is only one cell present". If the material of the yolk is intracellular, is it not misrepresentative to point out that living organisms can have non-cellular (extra-cellular) material?

That's just it...it's kind of intracellular, kind of not. There isn't a lipid bilayer there from what I can tell, but it's also definitely segregated from the cytoplasm part of the ovum. It's also all material that originated in other cells.

@Bryan Krause - If you want to give an answer that repeats the points (or specific links) I mentioned in my comments go for it, I just found this much by googling and don't really feel I know enough to comment on the issue Ian Malcolm is interested in about whether the yolk itself would be considered a giant cell or more like "cell + giant blob of nutrients attached", I suppose this would depend on what definition of "cell" is most commonly used by biologists.

@Hypnosifl Alright, I'll take a stab at it later.

The point here is mostly that the yolk is often said to be a huge single cell. If its just material deposited by cells lining the follicles, then, it's clearly not a cell but extracellular, and the ovum is just enclosed in it. Grau and Wilson said so here, they also mention that most people believe the yolk is a cell. https://link.springer.com/article/10.1007/BF02146023

This is covered well in almost any text that talks of early embryonic development in birds. Basically, the cleavage divisions look roughly symmetrical if you look end-on from the animal pole. But, as mentioned in the question, the process is quite asymmetrical in profile, with the blastoderm being at one end and the huge yolk occupying the other.
The yolk later gets invested by a layer of cells (the splanchnopleure) to form the yolk sac while the blastoderm forms the embryo proper.
You could see this page for more details. (Not just this page, this site in general is an excellent resource for learning embryology.)

The question is based on the false belief that the ovum contains the yolk as a single cell. This is a belief that is very common, and often spread in the literature. Grau and Wilson said in 1963 in Avian Oogenesis and Yolk Deposition: The yolk of the hen's egg is often given as an example of a huge cell containing a food supply for the developing chick embryo. Current views hold that oocytes grow by removing nutrients from the blood and the follicle cells which surround them. Thus yolk deposition is thought of as primarily an intracellular phenomenon. We believe that this viewpoint is inadequate, and wish to propose the following alternative hypothesis.
Of course, if the yolk is not inside the ovum, then there is no mystery to the early cell divisions.

Hi, it's me, the person telling you the bird yolk isn't the ovum! I told you wikipedia confirmed, and I let it at that initially because it was just a comment, I didn't feel the need to do deep research, but I saw the question continued to spark debate so I actually went to look at wikipedia's sources. And from what I was able to read of "Atlas of chick development", a 2005 book, I'm thinking... the wikipedia page was maybe wrong and you were right all along? But also, the book is detailed enough (and chapters free to read on google books) that it might answer your questions regardless.

https://books.google.fr/books?id=JAjGAgAAQBAJ&pg=PA1&hl=fr&source=gbs_toc_r&cad=4#v=onepage&q&f=false

The yolk is both part of the oocyte and yet separate from the cytosol of the cell including the nucleus, mitochondria, and all the other normal cellular stuff. Grau and Wilson are merely arguing (without much evidence) that the oocyte doesn't play much of an active role in growing itself.

@Oosaka You were probably right, I always thought the claim that the yolk was a single cell seemed wrong. But it seems like a very common myth, myths are good at capturing attention so it took me a while to get that the yolk is extracellular and secreted by cells surrounding follicle lumen. That's what Grau and Wilson said, seem as credible as anyone else, and it fits with my own reasoning.

Bryan Krause opinion differs from Grau and Wilson. I think they seem credible, if anyone has strong evidence or indisputable evidence that they are wrong, feel free to present it in comment. If anyone has better answer, feel free to produce a separate answer.

To be supportive of differing opinions, here is the credentials of the author I cite, so that anyone may discredit his claim: Charles Richard Grau, Professor of Avian Sciences, Emeritus. https://senate.universityofcalifornia.edu/_files/inmemoriam/html/CharlesRichardGrau.htm
His claim supports Oosaka's initial comment, thanks for all comments and for making me understand what I wondered about. Everyone contributed to my understanding. It was also what my intuition was, but for some reason I trusted the popular myth. Shame on me.

@IanMalcolm Grau's credentials are great but that book being from 1963 less so; it's why I pointed out "Atlas of Chick development" being from 2005. I don't know if the sources actually disagree though, I would have to see what both say.

false. scientific theory does not disprove itself as a factor of time. most current scientific theory that still holds as fundaments much older than 1963, lots of good work from around that time as well. your initial comment was beneficial. anyone who has strong evidence Grau and Wilson were wrong may publish an answer.

@IanMalcolm Grau and Wilson are not claiming to prove anything, and they show no data. They're just publishing a hypothesis to motivate research. Their paper has only been cited a couple of times and none of those citations provide evidence for their hypothesis. The quote is from what is effectively a "letter to the editor" rather than a scientific paper.

Feel free to produce an answer that is the most accurate you can conceive of. That yolk is extracellular (see my answer, or your own comment, "a lot of non-cellular material in a living organism as well") resolves issue in initial cell divisions. If superior answer is provided, not a problem.

@IanMalcolm Um... scientific theories that are correct do not disprove themselves as a matter of time, no, but not all scientific theories are correct, if they were science would be finished. Plenty of old scientific papers still hold up, but when they do then the more recent review/consensus documents agree with them. "More recent sources are more likely to be more accurate" is a completely correct rule of thumb for figuring out what science says about a question.

@Oosaka I don't think you and I disagree. Anyone with an open mind understands that "if they were science would be finished", the problem is status quo bias, so many people lack an open mind. "scientism" is the belief that the present social agreement of what the world is, is somehow the perfect world view and the scientific process end state. This forum is not very open minded, so I see no benefit to you and me "debating", debate is just a fallacy based on instincts monkeys have to fight over territory, with ideas irrelevant but our monkey brains do not get that.

I'd be open to chatting over some other medium, but in this forum, I just wanted to sort out what I wondered about. Peace.

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What does this mean?
The phenotypic ratio of dihybrid cross 9:3:3:1 can be derived as a combination series 3 yellow: 1 green, with 3 round :1 wrinkled. This derivation can be writtenbas follows:

(3 round :1 wrinkled) (3 yellow: 1green)= 9 round,yellow: 3wrinkled, yellow: 3 round,green: 1 wrinkled, green

I only understand the phenotypic ratio but what is the above series mean?

The characteristic(or trait) which is visible in an organism is called its phenotype. The ratio of the phenotypes of the progeny produced in a cross of trait(s) gives us the phenotypic ratio.
A dihybrid cross refers to a cross in which plants having two contrasting characters are crossed with each other. For example, crossing round and yellow seeds with wrinkled and green seeds is an example of a dihybrid cross where the contrasting characters are as follows:
1. Round and wrinkled seeds (contrasting on the basis of the seed shape)
2. Yellow and green seeds(contrasting on the basis of seed color)

The above image gives us the perfect example of a dihybrid cross where two heterozygous parents (RrYy and RrYy) crossed with each other to form four new progenies:

Round and yellow (RRYY or RrYy or RRYy or RrYY)
Round and green (RRyy or Rryy)
Wrinkled and yellow (rrYy or rrYY)
Wrinkled and green (rryy)

We will observe that for instance if 16 progenies are produced, then 9 will be round and yellow, 3 will round and green, 3 will be wrinkled and yellow and only one will be wrinkled and green.
This brings us to the conclusion that the phenotypic ratio of a dihybrid cross is always 9:3:3:1 regardless of the number of plants progenies produced. For instance if there are 60 progenies produced then :

Number of round and yellow seeds will be - 9/16 of 60
Number of round and green seeds will be - 3/16 of 60
Number of wrinkled and yellow seeds will be - 3/16 of 60
Number of wrinkled and green seeds will be - 1/16 of 60

You can reach this site for further clarification

Great answer. It is important to mention that 9:3:3:1 are the odds of each phenotype occurring and not the actual fraction. We have statistical tests (like chi-squared) to see if a population is behaving in a mendelian form.


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About genomic imprinting
In the context of genomic imprinting, how does a human cell "know" whether a chromosome is paternal or maternal(out of a homologous pair), in order to silence genes?

What precisely are you referring to by “gene silencing”?  The only thing it means to me is ensuring the X chromosome of females (in man) only expresses genes to the same extent as in males. As far as I am aware this silencing of one gene copy occurs at random, without any reference to the parental origin of the chromosome. And please do not use the anthropomorphic “know” in questions.  You can phrase them in the passive voice, e.g. “how is it determined”. Sloppy phraseology leads to sloppy thinking.

@MaximilianPress. Once again. The question talks about gene silencing in a chromosome copy-specific manner. This is not equivalent to genomic imprinting, which is not mentioned in the question.

Deleting the answer-to-comment and my other comments as they seem to be problematic.


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How do viruses such as COVID-9 and flu return in the winter if they disappear in the summer?
COVID-19 is gone from the body after a short time, and the maximum time of exposure to showing the symptoms is two weeks. So if no one gets sick for two or three months, how would it return in the winter?
How can it survive so long? Nobody got sick from nowhere except the first one and that things happened once to a lot of years.

I think the first step in answering your question, is correcting part of it. Influenza does not disappear in the Summer. Infection rates decline, but people can still become infected in the off season. Remember, we live in a globally connected society. Summer in the Northern Hemisphere is winter in the Southern Hemisphere. Influenza also has a number of animal reservoirs and intermediate hosts, which can contribute to persistant survival.
As far as the seasonality of infection rates, there are a number of contributing factors. This article from Harvard University discusses a few factors:

"1) During the winter, people spend more time indoors with the windows sealed, so they are more likely to breathe the same air as someone who has the flu and thus contract the virus.
2) Days are shorter during the winter, and lack of sunlight leads to  low levels of vitamin D and melatonin, both of which require sunlight for their generation. This compromises our immune systems, which in turn decreases ability to fight the virus.
3) The influenza virus may survive better in colder, drier climates, and therefore be able to infect more people."

For a more exhaustive discussion of the underlying causes of influenza seasonality, here's an open access review article on the subject.
Some researchers suspect that the SARS-CoV-2 virus, the causitive agent of COVID-19 infections, may have a similar patern of seasonality, but it's probably too early to know for sure how influential each of these factors will be in the long term.

I see there is no  lockdown or test when there is Influenza  virus so it just keep going from heuman been to queman being but  for example in china every body has been checked so no way of second wave there?

+1, Summer in the Northern Hemisphere is winter in the Southern Hemisphere -- it's surprising how many "It disappears in the summer" arguments I've seen that have neglected this simple fact.

I'm not a public health expert, but I would probably never go as far as to say there's no chance of a second wave given any real-world circumstance. Presumably, most travel and lockdown restrictions will eventually lift. Even if everyone was tested, all testing has a finite limit of detection, and people shedding virus below this limit could remain undetected. And human to human transmission might not be the only concern. There is still the possibility of animal reservoirs. We already know that some animals can contract and trasmit the virus in a lab setting.


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BLAST, using Smith-Waterman in the last step and S-score
In my bioinformatics course we studied the BLAST agorithm. After finding the HSP's and joining the HSPs together that are close enough and in a correct diagonal trend, we perform a next step: namely a Smith-Waterman alignment. Why do we do this? Didn't BLAST already find the alignment by joinging the HSPs?
I also have a second question about BLAST. When calculating the E-value with the formula:
$E=K \times m \times n \times e ^{\lambda S}$
Which score is this S exactly? Is it the score found for the HSP with the used substitution matrix? What is the score if we have multiple HSPs in one database entry? Is the E-value, and thus the S-score, calculated seperatly for every HSP or is it a value for the entry in total?

You may be interested in bioinformatics.stackexchange.com

Please post your two questions separately.

The BLAST algorithm is a heuristic to find which the path through the matrices formed between a query sequence and a target sequences from the database is ‘best’. Such paths represent an alignment which is has a completely different basis to that of the Smith-Waterman dynamic programming algorithm. Not only is it ungapped, but it based on comparison of tuples with matches scored according to frequency, and then proceeds by trying to join those with certain relative scores.
The speed of the program is partly the result of rapidly discarding unpromising paths, storing and continually refining only the current best candidates. The alignments will not be Smith-Waterman alignments, but there is no point in performing a Smith-Waterman alignment on each high-scoring sequence pair as this is not the basis of inclusion in the pool of best candidates. Performing such an alignment would be a waste of time for those candidates that will ultimately be discarded.
Only when the run is complete is it appropriate to perform the Smith–Waterman alignment on the final top candidates to produce a gapped alignment from which statistics such as the E-value are calculated (using S, the raw score from such Smith–Waterman alignments).

I have revised my answer to include both points as the second is now readable thanks to @anotherHomoSapien, and happens to be related.


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DNA shared by octopuses and modern humans
What percentage of DNA do we share with octopuses? I tried looking it up but couldn't find the answer on the internet. Could someone enlighten me on the same? To make the question more specific, I am more interested in knowing how many genes humans share with octopuses, but answers regarding how different our shared genes are or even a metric of the entire genome alignment would be helpful.

Hi and welcome to Bio.SE! Where did you look it up already that wasn't satisfying? What sort of comparison are you looking for? For example are you looking for how many genes we share, or of the genes we share how different are they, or are you looking for a metric of the entire genome alignment?

@James, thank you! I did a simple Google search and did not find relevant results. Since they're three different questions and I'm obligated to keep this related to just one, for the purpose of this question, I'm looking for how many genes we share. However, I'd personally welcome answers regarding all the three degrees of analyses. Since expecting answers on all three fronts can perhaps be beyond the scope of this question, it'll be all the same to me if only the bit about how many genes we share is answered and I'm directed to different sources for further reading on the other two fronts.

I see the problem. There is a lot of sensational news stories calling them aliens, but very few quantifiable results! Good question.

Octopuses have more chromosomes and genes
Octopuses have 28 chromosomes, and 33,638 protein-coding genes (Albertin et al 2015).
Humans have 23 chromosomes, and 20,365 protein-coding genes (Uniprot).
Octopuses had an expansion of genes in only a few protein families
There is a large number of C2H2 zinc-finger proteins (C2H2 ZNFs) (~1800), interleukin-17-like genes (IL17-like), G-protein-coupled receptors (GPCRs), chitinases and sialins paralogues in the octopus genome.
However, there does not exist a comprehensive analysis of orthologous proteins in the octopus that I can find.
This means that although we can say that there are thousands of genes we only observe in octopuses, there is currently no study comparing orthologues that exist in both humans and octopuses.


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Why is cognitive maturity related to organism lifespan in larger animals and mammals?
I am not a student of biology, so I should provide some context to me asking this rudimentary question. While doing a graduate-level course on Reinforcement Learning, the instructors focused on how we as mammals have such amazing intellectual potential and how we tend to learn by examples of outcome based on our actions. This set me thinking about the high disparity between different species of multicellular organisms in how we mature.
I would state a couple of examples to back my point, I am unsure if this list is conclusive or not.
Elephants(Average Lifespan: 60-70 years): Elephant babies tend to stick to their families until they generally mature.
Humans(Average Lifespan: 70-80 years): Human babies are generally dependent on their parents for at least 8-12 years before they start demonstrating some intellectual maturity, which is a good 10-15 percent of their average lifespan)
Birds(Average lifespan is species-dependent, but assuming a 10-year span): Bird offsprings are extremely fast learners and tend to veer off independently within months of their birth.
Fishes (Medium to short lifespan): Not an extremely well-publicized parenting method for their offspring. Fishes learn to swim and hunt for food at extremely young ages, which is a sign of cognitive maturity.
Insects (Short Lifespan): Generally parenting is related to feeding offsprings for a short while before they become entirely independent.
As can be observed, the general span for the attainment of cognitive maturity in such organisms seems to be an inverse function of the average lifespan of the parent, and I wonder, what could be the reason for it?
I absolutely apologize for any inaccuracies I might have cited because what I state is purely from a layman's observational perspective. I would be delighted to know what the bright folks here have to say on this matter.

This answer might not completely answer your question, since this just explains the case in humans, but I think you can give this a read while waiting for a more accurate one. I would recommend you to read this amazing paper.
Generally, across animal species, the longer it takes an organism to reach maturity, the longer it lives. How the timing of onset of maturity relates to longevity in humans, is still a matter of debate. In this regard, it is of special interest whether the onset of intellectual maturity is associated with longevity, as the brain and associated parts of the central nervous system comprise an organ system that is widely thought to have played a vital role in humans’ evolutionary success.
First, they talk about defining cognitive maturity:

It would seem intuitive to define intellectual development as that part of the lifespan in which ability increases and intellectual maturity as that part in which ability plateaus or decreases. In such a model, an inflection point or peak in ability would mark the onset of intellectual maturity. It is unlikely, however, that the multidimensional abilities of composing and writing reach their peaks when a composer's or writer's work is made public for the first time. Rather, we regard maturity as a state that is attained when a certain relevant threshold is crossed, regardless of whether ability increases after that point.

Looking into the case of humans, it may be either a genetic mechanism or plasticity that couples rate of development and maintenance and repair. In the former scenario, genes that alter the rate of development such that maturity is reached earlier, would have as a concomitant effect the downregulation of maintenance and repair, leading to a shorter lifespan. (This is a shortened version- please go through the paper for more detail)
They conclude stating that the onset of intellectual maturity is associated with longevity. So, you are right about cognitive maturity of an organism being related to its age, and it points out to a really interesting result- blooming composers and writers live longer than child prodigies- as pointed out in a paper in ResearchGate.
What could be the reason for it? American psychologist Jerome Bruner proposed the purpose of the period of immaturity as being a time for experimental play without serious consequences, where a young animal can spend a great deal of time observing the actions of skilled others in coordination with oversight by and activity with its mother. So, there is the obvious need for a period of immaturity and this varies amongst different mammals. (source)

This was indeed insightful!


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ID: Serated-leafed seedling
A seedling has popped up in one of my planters (acid soil; Toronto, Ontario).
What is it?

June 4, 2020:

June 20, 2020:

it's a kind of tree, perhaps a kind of oak. https://ask.extension.org/questions/332861

@com.prehensible The leaves look opposite. Are there Oaks with opposite leaves?

Yes i wasn't that convinced either that it's an oak, it just has a lot in common and also some differences. You could tell straight away from it's woodyness and toughness if its a tree by feeling it, if its twiggy its a tree, time will tell.

An extension of com.prehensible's comment -- your sapling could be a bur oak.  It is older than the seedling pictured below, but retains a similar cotyledon.  The range of this species includes Ontario.

bur oak seedling
Photo by Todd Dwyer, via Flickr
(please ignore the image artifact -- an effect of resizing)

Your photo appears to show the tree at a stage after the seedling shown above and before the more mature sapling shown here:

bur oak sapling
Photo by John T. Fowler, Alamy Stock Photo

Thanks! For what it's worth, an aquaintance had this comment: "...I don't think it's an oak of any species, since it has normal cotyledon (seed) leaves above ground. Oak cotyledons are modified to store food for the seedling, so they don't resemble leaves and usually don't emerge from the acorn. I don't think the example photo posted to Stack Exchange is an oak either." ... Food for thought?

Seedling emergence patterns - PDF: "...the cotyledons remain underground and the stem (epicotyl)
emerges above ground. This pattern is called hypogeous. Large seeded plants like
Kentucky coffeetree and oaks tend to have hypogeous germination."

..."the first photo is not an oak. The second one (the older plant) is an oak, but the bristles on the leaf lobes mean it's not a bur oak."

A diagram from The Woody-plant Seed Manual - United States Forest Service -- Google Books link here.

@Wilson it sounds like your acquaintance is quite knowledgable! I don’t suppose you can convince her/him to make an account on biology.SE? ;)

With regard to the seedling being an oak, just gently excavate around the stem - the acorn will still be there to identify. You can do this without hurting the roots.

The hairy stem and leaf pattern remind me of elms. Wikipedia has an example of american elm seedlings which look quite similar to what you have to me:


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Why do morning people have shorter biological clocks?
First of all, we all have a circadian clock than is run endogenously by differential gene expression and controls our change in awakeness, temperature, hormone levels, etc.. Circadian clocks are not exactly 24 h and they vary among people: some people have shorter clocks and other have longer ones. Apparently, people who have shorter circadian rhythms are morning people, and those that have longer one, are night owls.
How is this possible? In the following article "https://www.futurity.org/biological-clocks-sleep-disorders-protein-mutations-2289312-2/" it says that a 20-hour biological clock will make a person fall asleep earlier because they will get tired earlier and they will get awake also earlier. But for me, that would only be possible the first period or two if both cycles start at the same point time. Afterward, the cycles will get out of phase and that will not be true any longer.

Circadian rhythms are entrained by light via the suprachiasmatic nucleus, a part of the brain that receives signals from special retinal ganglion cells that are directly sensitive to (mainly blue) light.
However, light is not strictly necessary: the internal circadian clock is the result of shifting gene expression that proceeds without outside stimulus. Light is only used to entrain (or "reset") the clock each day.
When people talk about the duration of an individual's circadian rhythm, they are referring to what happens in the absence of a light cycle (that is, without entrainment).
https://en.wikipedia.org/wiki/Circadian_rhythm
https://en.wikipedia.org/wiki/Suprachiasmatic_nucleus
https://en.wikipedia.org/wiki/Circadian_rhythm_sleep_disorder

So the clock is reset each day, meaning that both periods will start at the same point every day, and since a morning person has a 20-h cycle then indeed, it will wake up earlier and go to sleep earlier than a longer biological clock, I am saying all that right?

@Laura That's the general idea, yes. However the circadian clock isn't everything and isn't the only factor in people being "morning people" or not. It's an influence rather than deterministic, like most biopsychology.

The Circadian Rhythms of humans is reset by light exposure cycles, but for a cycle to be reset it has to exist first.
Without light there are cycles created by protein production and gene inhibition.
In the relevant 24 cycle there is a is a gene complex that produces a set of proteins that react and decay into a product shuts down the gene's expression (protein production) as long as it is present. that stops the initial proteins production thus creating a cycle based on the proteins reaction and decay rate. So the gene is active and the protein is produced, over a roughly se amount of time the protein reacts and decays into a protein that shuts down the gene expression (inhibitor), Will say this takes time A, of course the gene was till produce the protein until the inhibitor stopped it so the reaction and decay continues for time A again until all the inhibitor is used up and the gene starts producing the proteins again. So you get a cycle of expression and inhibitor that resets once every times Ax2.
But as you can guess genes and proteins a small change in the protein can change can change how long it takes to react and decay. This is how you get some people with slightly longer cycles and others with slightly shorter cycles.
https://pubs.niaaa.nih.gov/publications/arh25-2/85-93.htm


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How does the energy we get from food transform into mechanical motion at the cellular level?
I am curious how, food broken down into glucose powers the movement of proteins in our cells (e.g., in muscle fibers for example).
Is the thermal energy converted to kinetic energy somehow?
As a mechanical engineer, I am just trying to visualize how the energy is converted to mechanical motion at the cellular level.

https://biology.stackexchange.com/questions/31323/how-is-atp-involved-in-muscle-contraction

I agree with a comment that your question is broad, but I think a good answer can be given anyway. That answer is essentially: ATP, Adenosine Triphosphate, also known as "the energy currency of the cell".
https://en.wikipedia.org/wiki/Adenosine_triphosphate
This small molecule has three phosphate groups, hence the name, and energy is released when one or two of those are separated from the molecule (creating ADP or AMP, Adenosine Diphosphate and Adenosine Monophosphate). This energy is what thermodynamically allows most endergonic reactions in the organism. The phosphate groups can then easily be added back, recycling the components back to ATP. This mediator, "currency" allows energy to be transferred from chemical reaction to chemical reaction: a reaction that "creates energy for the cell" really regenerates ATP, which goes wherever and is broken down in reactions that "use energy".
See for example this textbook describing how the breakdown of carbohydrates produces ATP:
https://opentextbc.ca/anatomyandphysiology/chapter/24-2-carbohydrate-metabolism/
And I will recycle Bryan Krause's link in comments to a question about how ATP is used in muscle contractions, which I believe is the final step of answering your question:
How is ATP involved in muscle contraction?

Scope of this Answer
This answer attempts to summarize the principles involved in biological energetics, with only the most minimal reference to particular molecules or systems. It is directed at those approaching the subject for the first time, particularly from a physical science or engineering background.
Energetic processes in biology
Energetic processes in biology involve chemical energy — essentially the energy embodied in the chemical bonds between the atoms of molecules.
In considering biological processes involving energy transfer, it is usual to adopt a thermodynamic approach in which the change in (Gibbs) Free Energy is considered. Chemical reactions are energetically unfavourable if they involve an increase in free energy, but are energetically favourable if they involve a decrease in free energy. In reactions of the latter type occurring in isolation, the chemical bond energy is converted to thermal energy (heat). In biological chemistry, however, processes that involve an increase in free energy are made possible by ‘combining’ them with such energetically favourable processes so that, rather than being released (lost†) as heat, the free energy is used to achieve an overall negative free energy change.
Such a ‘combination’ of two reactions (generally termed ‘coupling’) is, in effect, a different reaction (or succession of reactions), although the overall free energy change is the same as the sum of the separate ones. The coupling  requires specialized protein macromolecules (enzymes), which actually participate in the reaction (naïvely speaking, direct the flow of electrons from one bond to another) and help lower the activation energy of the reaction that prevents it occurring spontaneously at ambient temperature.
The process of acquiring energy from food consists of a series of energetically favourable oxidation reactions that eventually result in the bond energy of the initial food molecule (carbohydrate, fat etc.) being used to form bonds in a ‘form’ that is useful to the cell for driving energetic processes. This ‘form’ is predominantly the phosphodiester bonds of a molecule entitled ATP, which not only has a high negative free energy of hydrolysis (which breaks these bonds), but for which a plethora of enzymes (and other proteins) have evolved that can facilitate the transfer of this bond energy to form bonds in other molecules.
This explains in principle how the energy from oxidation of foodstuffs can be used to sythesize other complex molecules required by the cell — chemical energy being both donor and recipient. What about the conversion of chemical energy to mechanical energy?¶ In general in these cases the hydrolysis of ATP is coupled to a change in conformation of a protein and its points of interaction with other proteins, resulting in their relative movement, as in the case of the actin and myosin components of muscle fibres. Proteins are molecules with three-dimensional conformations determined by the most energetically favourable combination of many non-covalent chemical interactions (mainly hydrogen bonds and hydrophobic interactions). Often there exist alternative structures with only small difference in free energy, so that a change in structure (or the point of interaction with another protein) can be effected by coupling this (although energetically unfavourable) to the hydrolysis of ATP.

† Thermal energy generated by metabolic processes can not be used in the directed manner implied in the question. Its only use for the organism would be to maintain body temperature (and indeed the specialized brown fat cells exist for that purpose).
¶ The question refers to kinetic energy, a term that is not much used in biochemical energetics, except in relation to the random movement of molecules. Although a protein moving along a filament will, I suppose, possess kinetic energy (à la billiard ball) this is a consequence of the changes in interaction of molecules, rather than from a direct ‘cue stroke’ from ATP hydrolysis.

Beyond the Principles
To go beyond the principles, one must read the book, as it were, and get to grips with the molecules. In my original answer I gave links below to some relevant sections of Biochemistry by Berg et al. the fifth edition of which was then available on NCBI Bookshelf. This is no longer the case, presumably because the edition is 20 years old. However as a basic introduction for the cash-strapped student who is not going to specialize in biochemistry, a second-hand copy of this edition is generally to be had on ebay for the price of two cups of coffee. The relevant sections are:

Free Energy, chemical reactions and ATP
Thermodynamics of redox reactions
Enzymes
Glycolysis, the Citric Acid Cycle and ATP synthesis
Motor Proteins

I think the question is far too broad to answer in detail — the poster needs to read a book on biochemistry to understand the problem properly. But by confining this answer to principles, I hope to provide something of some general use. Suggestions for improvement are welcome.


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What is the name of this spider I found in The Netherlands?
This spider is smaller than 1 mm and fast.
The spider has tiny hairs on orange coloured legs. The backside of the spider is dark-brownish and has a small red stripe in the middle. I have taken pictures magnifying 25x using a lens of some watchmaker glasses. As a reference the lens of the lamp shining on the spider is 6mm.
Found inside my house on the second floor on the attic.
The location is North-Brabant, The Netherlands, location on maps.
I have searched all over the internet but I keep coming back to mites which this specimen doesn't resemble.
Unfortunately the camera isn't as good as my eyes, although a little zooming is possible.

The spider skittered around again today and I managed to take a picture, unfortunately not a zoomed one but maybe some characteristics will be recognized.

I think it is indeed a mite - have a look at genus Anystis or Tetranychus.

@JimN Yes that is it! I never thought to search for spider mites. Would you like to write an answer so I can accept it?

I believe you are looking at a spider mite of the genus Anystis or Tetranychus. Both of these have The Netherlands in their range.
Here is an info page on the two genuses, includes a map of observations and a gallery of photos that you can even filter to only view images from a certain range. You can also filter the gallery to group photos into species categories.
Anystis: https://inaturalist.ca/taxa/249515-Anystis
Tetranychus: https://inaturalist.ca/taxa/203334-Tetranychus


text:
Has a primate species ever weighed the average mass of a tonne (1000 kg)?
I ask because primates are mammals from the euarchontoglires superorder. Most mammals that weigh a tonne are laurasiatherians (except for elephantids and their ancestors) (elephantids are afrotherians). The only mammalian species from the euarchontoglires superorder that I know that weighted a tonne is Josephoartigasia.
So, I wonder why there was possibly never a primate species that weighted the average mass of a tonne.

Biggest one known was 500kg. the biggest bear is 750 kilos. primates are best adapted to forests, and forest animals tend to be smaller than high plain and grassland animals big apes have existed for 20,000 years, it's about one ice age.

There is no specific reason why a primate couldn't weight a metric tonne. You can look at mammals evolution and notice that the primates belong to the clade Euarchontoglires which also contains rodents, treeshrews or rabbits. So basically these species most likely had a common ancestor that was very small.

Primates are currently the biggest animals of that clade. Great apes are the biggest primates. Gorillas at about 150kg on average are the biggest (by weight) currently non-extinct great apes. Chimpanzees, Orangutans and Humans are approximately equals at 75kg. The biggest known primate, now extinct, is the Gigantopithecus which was probably a sort of giant Gorilla twice the size of what you know as Gorillas (200-300kg), so still well short of a tonne. The biggest non-extinct rodent is the Capybara (you can see one at the Cosmocaixa in Barcelona). But the biggest known extinct rodent was the Josephoartigasia and did weight 1000kg.
Euarchontoglires sister clade is Laurasiatheria which does contain many animals bigger than 1000kg, such as Bisons, Rhinos, Girafes, Orcas, Walruses... These 2 clades belong the Boreoeuthenia clade, whose sister clade Atlantogenata also contains many animals heavier than 1000kg (most notably elephants). So evolutionarily primates would have had plenty of time to become as big as rhinos, but it looks like this group found its ecological niche in staying relatively small (although humans and chimps are not that small as compared to rodents or rabbits). Getting big is not always smart as we know from mammals surviving the Cretaceous extinction thanks to their tiny size.
Evans et al. (2012) tried to estimate the maximum rate of evolutionary body mass increase in mammals (through natural selection, it is likely you could force this process to be much much faster). They found that it took about 1.6 millions generations for body mass to increase a 100-fold in terrestrial mammals. So a back-of-the-envelope calculation tells you it would take about 30 million years for current primates to reach 1000kg. They also point out that the aquatic cetaceans grew much faster than any terrestrial mammal, suggesting that being terrestrial strongly limits growth rate. They also point out that macroevolutionary growth rates are far slower than what would be predicted from microevolutionary rates, for reasons still unknown.
https://en.wikipedia.org/wiki/Mammal
https://en.wikipedia.org/wiki/Gigantopithecus
https://en.wikipedia.org/wiki/Josephoartigasia
Evans, A. R., Jones, D., Boyer, A. G., Brown, J. H., Costa, D. P., Ernest, S. M., ... & Harding, L. E. (2012). The maximum rate of mammal evolution. Proceedings of the National Academy of Sciences, 109(11), 4187-4190. https://www.pnas.org/content/pnas/109/11/4187.full.pdf


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A balanced diet with the minimum carbon footprint
Many studies shows that 1 kg of non-vegetarian food as 3-4 times more carbon footprint than 1 kg of vegetarian food. I think that does not represent the complete picture food from animal sources are rich in some nutrients. For example pound for pound fish will be much richer in protein than normal vegetables to so get the same amount of protein as from fish, we will have to eat lot more vegetables. So at the end of the day, the net carbon footprint of our protein requirement might be much closer between veg and non-veg food. Similarly for carbohydrates, cereals may be the most carbon efficient than any animal source.
Question: I am interested in a balanced diet with the minimum overall carbon footprint. Any reference or studies on what is the minimum carbon footprint with which we can get say 100 g of all the essential nutrients such as carbohydrates, proteins, vitamins, omega acids, saturated fats etc.

Can you provide a link to one or two of the studies you refer to so they can be evaluated for trustworthiness? Thanks.

I’m voting to close this question because I think it is concerned with dietary advice rather than Biology in the terms of SE Biology.

@David Sure but can you recommend any other stack-exchange site where this question could be more appropriate? Also, question is not a dietary advice which are everywhere but rather I am asking for a balanced which minimizes carbon footprint.

@anongoodnurse This link has a lot of details: https://ourworldindata.org/environmental-impacts-of-food

The carbon footprint really depends on non-biological factors, such as how your food is grown or harvested, processed, and transported to you.  If you eat fruit & vegetables grown in your own garden, or fish you catch yourself, there really is no carbon footprint.  If your fresh fruit is shipped in by air from another continent, and your fish is caught by a factory trawler working the Southern ocean, then the same diet has a very high carbon footprint.

Thank you for the link. I, too, found some interesting (and seemingly reliable) support for your initial statement.

This question may be on topic at the Sustainable Living site. https://sustainability.stackexchange.com/


text:
Biological Calculations
(a) At the moment of fertilization a female egg is about 100μm in diameter. Assuming that each lipid molecule in the plasma membrane has a surface area of 10-14 cm2 , how many lipid molecules are there in the egg plasma membrane if 25% of the surface is protein?
(b) Each fertilized egg cell (zygote) divides 30 times to produce all the eggs that a female child will need in her lifetime. One of these eggs will be fertilized giving rise to a new generation. If lipid molecules are never degraded, how many lipid molecules have you inherited that were synthesized in your grandmother? Assume for calculation purposes that the lipid molecules synthesized by your grandmother is equally divided between the daughter cells at each cell division.
My answer:
 (a)  Given, a female egg is about 100μm in diameter.  Radius = 50μm
           Each lipid molecule in the plasma membrane has a surface area of 10-14 cm2.
           25% of the egg surface is protein and 75% of the surface is lipids.
           Therefore, Surface area of egg is = 4π(radius)2
                                                                                =  4*3.14*2500*10-12
                                                                      =  3.14*10-8 m2
                                Area for the presence of lipid molecules = 3.14*10-8 *3 / 4
                                                                                = 2.355*10-8 m2 = 2.355*10-8 * 104 cm2
        Number of lipid molecules in egg plasma membrane = 2.355*10-4/10-14 = 2.355*1010 molecules
(b) Each fertilized egg cell divides 30 times into 2,4,8……230 cells. Assuming that the lipid molecules     synthesized by our grandmother is equally divided between daughter cells at each cell division.
•   After 30 divisions we have 230  cells synthesized in grandmother
                      Initially the zygote has 2.355*1010 lipid molecules from above calculations.
                      Therefore, each cell has 2.355*1010/230 = 21.93 molecules.
•   After mother takes birth, she inherits lipid molecules present in zygote, that is a single cell
Number of lipid molecules that is inherited from grandmother by mother is 21.93 molecules.
This zygote undergoes division for 30 times.
Thus, each cell inherits = 21.93/230
                                          = 2.0424*10-8 lipid molecules from zygote
•   Finally, a single cell in mother undergoes the zygote formation that leads to our birth.
Hence, we have 2.0424*10-8  lipid molecules inherited from our grandmother.
Can anyone please confirm it?

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I think almost everything is correct except for the last part.
The reason one may easily overlook that part is that we inherit the complete 22 molecules from our mother who inherited the whole 2.35 * 10^10 molecules from her grandmother zygote. Grandma gave the whole thing to her daughter and that that number was distributed in all the cells in mom's body, which is 22 per cell. These 22 lipid molecules would be inherited by us from our mom, so the answer seems to be 22 logically.
This can be understood easily as given below:
2.35*10^10 -> From granny to mommy
22 -> From mommy to us
Hope this made sense... Thanks!


text:
Can you identify these ants?
I think they could be carpenter ants, but not sure.

Welcome to Biology.SE! Identifications questions should also include: 1) the location (e.g. country and region — the more specific the better) where you observed this organism; and 2) an estimate of the size of the organism. Please [edit] your post to include this essential information. ——— In addition, we don't provide advice about pest treatment (especially regarding safety), so I've deleted that part of your question. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


text:
Protein structure prediction from amino acids sequence
Information given at this resource https://predictioncenter.org/ is close to impossible to digest (as with everything in this field), so if anyone could tell me what is the accuracy we can predict tertiary protein structure now - I would be grateful.
Also would love to hear your thoughts on 'why a cell can make exactly the same protein structure thousands of time using known to us physical laws, but we have to guess it using machine learning'? Why is it difficult?

"using known to us physical laws" — Do you mean that we know the laws of Physics or that we know that the laws of thermodynamics determine that a protein folds to the lowest free energy possible, or that we know how a protein actually progresses to its thermodynamically favoured state? If you tell us what you think we know and what precisely you think the "it" is we need to guess, we may be able to explain why "it" is difficult. At present your question lacks the clarity needed to help you effectively.

@David yes you're right, I had too simple image of the process, after more studying I understand why you're objecting

what is the accuracy we can predict tertiary protein structure

That depends on the protein.  If the primary sequence closely matches the sequence of a protein for which the structure is already resolved, then template-based methods to model 3D structure can be used (a.k.a homology modeling).  These methods tend to be accurate, as assessed by template-modeling score, though crystal structure confirmation is only available for a minority of models (1%, per this 2010 paper).
For proteins without structurally-resolved homologs, ab initio folding is often used, which relies on molecular mechanics assessment of iterative peptide chain folding to find structures that minimize the Gibbs free energy. Popular software for protein molecular mechanical modeling include CHARMM and AMBER.  Ab initio methods are computationally intensive and are more difficult to validate.

'why a cell can make exactly the same protein structure thousands of time using known to us physical laws, but we have to guess it using machine learning'? Why is it difficult?

It's hard to know all the cellular factors present when a particular protein is synthesized and how those factors affect the folding of the protein.  What is the temperature and pH proximal to the ribosome?  Are chaperone proteins involved?  Is the lowest-energy structure the true structure, or does the native structure fall in a local, stable minimum with a functional potential selected by evolution?  A good discussion of that last point can be found on Quora.

Thanks +1! There are many good points for further research in your answer :fire:

The predictioncenter.org runs an open contest every two years - Critical Assessment of Structure Prediction (CASP).  CASP 14 is underway now.
The best programs for ab initio folding are highly augmented molecular dynamics with machine learning and a bunch of predictive algorithms aggregated to create a structure.  Look at David Baker's Rosetta software. More recently Google's DeepMind beat out Rosetta and a gaggle of others.
predictioncenter.org/casp13/zscores_final.cgi
Deepmind is a Deep Belief driven network https://deepmind.com/blog/article/AlphaFold-Using-AI-for-scientific-discovery

We trained a neural network to predict a distribution of distances between every pair of residues in a protein (visualised in Figure 2). These probabilities were then combined into a score that estimates how accurate a proposed protein structure is. We also trained a separate neural network that uses all distances in aggregate to estimate how close the proposed structure is to the right answer.

The problem of protein folding is known as Levinthal's paradox: a typical protein of a few hundreds amino-acids can fold into an astronomically big number of configurations, all of them consistent with the laws of physics (e.g., having the same or nearly the same energy). Yet the actual protein in a cell (nearly) always folds in the same structure and all the known proteins fold in about a thousand well-defined structures (moreover, sometimes proteins with little sequence similarity adopt exactly the same structure).
For those who want to know more about the physics behind, a rather readable introduction is Huang's Lectures on statistical physics of protein folding, whereas the other answers in this thread have already given a rather good review of the methods used in practice  - note that these are not necessarily relying on the machine learning, as the OP suggests, although the ML has been used for this purpose for a few decades already, e.g., see this book.


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VPg priming of the replication of RNA viruses
I'm doing a presentation on the replication of SARS-CoV-2 for my chemistry class, and I found that to replicate its RNA, the virus uses RNA-dependent RNA polymerase, which is primed by a VPg primer. Since the presentation is for a chemistry class, not a molecular biology class, I would like to know the chemistry behind the way that primers work.
I've tried searching the information on the internet, but could not locate the information I need.

Can you clarify what it is that you are looking for? What is it that you need that resources like the Wikipedia page on base pairing do not provide?

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I have edited your title so that it is clear you are talking about the specific VPg primer for the replication of RNA viruses like coronoviruses. It would helpful if you could tell what you know about the chemistry of RNA polymerase already so that I (as an ex-chemist) can an answer your question appropriately from a chemical standpoint.

Search for Subissi papers on the CoV RdRp, he did several in-vitro experiments, mixing directly some nucleosides, oligos, nsp7,8 and 12 in a test tube and looking at what was synthesized. https://pubmed.ncbi.nlm.nih.gov/25197083/

Although this question should probably be ruled off-topic as unresearched homework, I fancy that not all readers will be familiar with the VPg primer for viral RNA replication. I shall therefore suggest some of the chemical aspects of this process that might be include in a presentation, and comment on the process itself.
Some Chemical features of VPg-primed viral RNA replication

The chemical reaction. This is no different from many other reactions involving an RNA polymerase. It involves the reaction of an NTP with the 3’OH of the ribose on a growing RNA chain, forming a phosphodiester bond, thus extending the chain. The growing RNA chain is termed a primer because it is required to start the addition in many cases, however in the case of many single-stranded RNA viruses the actual initiation of a new strand uses a primer composed of a small peptide to which to U residues have been attached. Simple diagrams of this process are generally presented for DNA-dependant DNA polymerase and can be found in standard texts, e.g. Berg et al. Figure 5.22
The reaction mechanism.  This reaction is catalysed by an enzyme which participates in the reaction. The mechanism of catalysis is summarized on the EBI facility (where diagrams can be found) as:

RNA polymerases catalyse the nucleophilic attack of a bound nucleoside
  5′-triphosphate by the 3′-hydroxyl of an RNA primer, resulting in the
  incorporation of a nucleoside monophosphate into RNA and the release
  of pyrophosphate. This is thought to occur using two-metal catalysis.
  In RNA polymerase II, two magnesium ions are coordinated by four
  aspartates (3′OH of RNA also proposed to weakly coordinate to Mg2+A).
  Mg2+A is proposed to lower the pKa around the attacking hydroxyl while
  Mg2+B is there to stabilise the negative charges during transition
  state…

The thermodynamics of the reaction. The breaking of one phosphodiester bond and the formation of another means that the reaction is more or less at equilibrium (no change in Gibbs Free Energy). One reason that it is thought not to reverse is because the pyrophosphate produced is hydrolysed in the cell to orthophosphate, which is irreversible as the free energy change in this reaction is lost as heat.
Hydrogen Bonding to the template.  The reaction involves copying a template strand, and the basis of this specificity is Watson–Crick hydrogen bonding between template base and incoming NTP. However, specifically for the VPg primer, there is hydrogen bonding of the two U residues to the end of the template strand. (Diagrams of AU hydrogen bonding should be easy to find.)
The chemical linkage of the VPgUU primer. The uridylic acid residues are added to the VPg peptide at the hydroxyl group of a tyrosine residue in a reaction that is catalysed by the viral RNA polymerase. It is worth noting that although many amino acid residues of proteins are chemically inert, the hydroxy amino acids have reactive potential, most notably in being phosphorylated.

A broader point for reflection
One question that this raises is why the need for a protein — VPg — as adjunct to a nucleic acid primer. Reading further on the subject will reveal this protein actually interacts with different parts of the viral RNA in the course of acquiring the Uridylate residues and selecting the AA where it should bind. The chemical interactions with RNA and other proteins here are the weak non-covalent interactions — hydrogen bonds, van der Walls interactions and some ionic interactions — that are typical of proteins. Rather than their weakness being a reason for considering them unimportant, such interactions are crucial to the chemistry of life because their very weakness means that they can be both broken as well as made. The interactions are reversible, leading to the very dynamic property that typifies life. They are worthy of a chemist’s attention.

Nucleic acid synthesys can occur two ways, with a template or without. In most biological systems the template synthesis is the one that occurs since it is the only way to replicate genomic information. For template based nucleic acid synthesis in biological systems (being of DNA or RNA) the enzymes performing the reactions can use single stranded material (in the case of virus ssDNA or ssRNA virus) however they still need a small region of double stranded nucleic acid to bind and start polymerizing, otherwise synthesis could start anywhere in the template strand which wouldn't be particulartly useful, hence the primers, the polymerases bind to the double stranded region and start polymerizing always adding new nucleotides to the 3' end of the primer strand that are complementary to the nucleotide in the template strand. Usually in living cells the synthesis of new RNA molecules won't occur with an RNA template (there is usually no RNA dependent RNA polymerase, there are exceptions but they are usually result of previous viral infections), but only with a DNA template to procuce messenger/transfer/ribossomal RNAs. In the case of COVID and othe + strand RNA virus, the virus has to encode the RNA polymerase and also produce a primer that will create a double stranded region that will allow RNA synthesis to occur.

Hello @lint, and welcome to Biology.SE!  Yours is a good explanation of the reasons for using primers and their importance in guiding polymerase amplification.  You clearly explain the molecular biology of PCR, but OP is explicitly looking for a chemistry perspective -- perhaps one that includes a discussion of the hydrogen bonding involved in primer specificity and the catalysis of DNA polymerization.

I don't think there are any biochemical reasons for the requirement of primers. The need for a primer in the synthesis relates to the requirement ofhaving a double stranded region that guides where in the sequence the process starts, otherwise you would have an entire population of molecules with different sizes and start sites. There are cases where primers are not needed for nucleic acid synthesis from template like RNA transcription and DNA replication start, in this case the specificity of the start is  given by the recognition of specific sequences by the machinery.

@lint — The need for a primer is tied up with ensuring the ends of a linear genome get replicated. Easier than for a double-stranded chromosome, but still an important consideration. It's not that there will be a population with different sizes of RNA that is important, it's that the genome would get shorter and shorter.


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Insect with long neck—what is it?
I found this insect in Fish Haven, Idaho (right next to Bear Lake) in June and think it’s absolutely fascinating:

If you can’t tell from the picture, it’s a few centimeters in length—very thin with a pair of transparent wings that extend straight backwards past the end of the abdomen. The thorax is brown, and past the point where the wings connect it is long and neck-like, leading to a black head with two long antennae. Can anyone identify this insect?

That appears to be a species of snakefly and the lack of a long needle-like ovipositor indicates that this specimen is a male.
The "kite" rather than rectangular head shape suggests it is in the Raphidiidae.
From the location I think it could be in the genus Agulla and might be the Idaho Snakefly (Agulla adnixa), but I don't know if that is the only species from this group in that area.
Reference image (Copyright © 2007 by Hartmut Wisch) from BugGuide.net:

To identify a snakefly: Texas has the prettiest cicada, green with dark shiny eyes. The first time I saw a snakefly it was like a horror movie. It's as of nature added a neck and head on a cicada's face! Eeeek! (Nature is amazing, sometimes downright astounding.)


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Question regarding the number of alleles
Why is it that in biology we often say that a gene has two alleles? When we analyze allele frequencies (e.g. using Hardy-Weinberg Equilibrium), formulas are often generalized for two alleles of a gene.
Given mutations, isn't it quite likely that a population will have more than two alleles for a gene?

The two-allele scenario is often used in genetics teaching because of its simplicity. However, quite a few genes have more than two alleles. Some examples that readily come to mind are:

The ABO gene in humans: This determines ABO blood group, and has six common alleles. Many more rare alleles have been described [1].
The human leukocyte antigen (HLA) genes: These are well-known for their allelic diversity. One of them, HLA-A, alone has over 6,000 alleles [2].

Reference

Seltsam A, Hallensleben M, Kollmann A, Blasczyk R. The nature of diversity and diversification at the ABO locus. Blood 2003; 102(8):3035–3042. https://doi.org/10.1182/blood-2003-03-0955
Robinson J, Halliwell JA, Hayhurst JD, et al. The IPD and IMGT/HLA database: allele variant databases. Nucleic Acids Research 2015; 43:D423-431. http://hla.alleles.org/nomenclature/stats.html

Depending at which level you are defining an allele. As @Adhish described, at the molecular level there is no theoretical limit on the number of alleles of a given gene. The presence or not of more than 2 alleles depends on evolutionary factors such as population size, fitness change, genetic drift, etc. Hardy-Weinberg Equilibrium with two alleles is easier to understand but is possible to extend the genotype predictions for multiple alleles in the equilibrium. Also remember that the Hardy-Weinberg Equilibrium is theoretical and requires assumptions that are never really met in nature, so is extremely hard for multi allele systems to ever reach the equilibrium.


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Identity of strange bird with fish net tangled around one foot

This bird was photographed at a small beach in Rio de Janeiro, Brazil.
What kind of (ocean?) bird is this??

Where was this photo taken? Also, great pic!

When asking for a specific species, you should give more contextual details like the country / region it was taken and the season (the question is not always related to the same time you took the pic).

Welcome to Biology.SE! In the future, please [edit] your posts to include all the relevant information in a visible format! Thanks!

This could be an immature black-crowned night heron, Nycticorax nycticorax.
Lines of evidence:

pale yellowish bill
thick neck
hunched back
orange eyes
head feather patterning consistent with "black crown" in adults

See these photos and captions published by the Cornell Lab of Ornithology:

Juvenile Black-crowned Night Heron
Thick-necked heron with a thick bill. Juveniles are brown and streaky overall. Note pale yellowish bill.
© Evan Lipton

Immature Black-crowned Night Heron
Immature birds have a mix of juvenile and adult plumage. This individual has faint streaking on the chest, a dark gray cap, and a nearly complete dark gray back.
© Alex Lamoreaux

Adult Black-crowned Night Heron
Stocky and compact heron. Often tucks neck into its body creating a hunchbacked look. Adults have a black cap and back that contrasts with its whitish to pale gray belly and gray wings.
© Jeff Timmons

Note the fishing line tangled around the adult bird's feet.  Must be a common trait!

Thanks for the replies. First, it took this photo from about 60cm distance to this bird with a 50mm prime lens. The bird did not move and i tried to speak calmly to it while robbing loser and closer, hence the pretty crisp image that looks almost like taken with a tele lens. Second: in my post there was some text box in which i entered the location - but once posted i did not observe this particular info was not visible. It was shot at a small beach in Rio de Janeiro, Brasil!

The tip with "Crowned Night Heron" seems to be accurate, the stocky slightly odd physiology is certainly spot on. The coloration of these birds seems to change according to age, that is somewhat confusing. I thought this particular bird looked already erh "old and wise", but judging by the colours it was only somewhere between juvenile and immature??

@RudMe — I think this is the correct id since this looks like a Black-crowned Night Heron, which is a common heron with a worldwide distribution. I encourage you to acknowledge Dirigibles work by accepting this well written answer. ——— Please also take the [tour] and then go through the [help] pages for more information on how to use this site effectively. Thanks!

Okay, done (i think). Did indeed not know about this as it is not obvious like it would be with some plain text link


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What plant is this? I can't identify

Please help me identify this plant. This was shot in the assam-meghalaya region of india.


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Vitamin A Deficiency
I have a quick question regarding Vitamin A deficiency.
The photoreceptor molecules in both rods and cones have the same general structure which is retinal which is bound to a protein called opsin and depending on the photoreceptor opsin changes but the retinal is always the same. And it is the retinal that makes the opsin light sensitive and so it is highly important.
My question is, why is it that when researching the symptoms of vitamin A deficiency one of the most common ones is night blindness. I understand that if not enough retinal is formed not enough rhodopsin is formed and so the patient would suffer from night blindness but wouldn't it also mean that the patient wouldn't be able to produce enough of the other photoreceptors as well and so doesn't only suffer from night blindness but from complete blindness?

Good question! As you write Vitamin A is quite important vision as it is an integral part of the light sensitive rhodopsin protein. Rhodopsin is necessary for a type of photoreceptor, the rod. It is located in outer segment of the photoreceptor. Vitamin A is also required to other opsins that are needed for the cones to function.
When someone has Vitamin A deficiency it does not mean that they have no Vitamin A. For example instead of having i.e. 100 Vitamin A you only have 30 (arbitrary numbers!).
In the retina, you have the very light sensitive rods and the less light sensitive cones. Rods need a lot of rhodopsin (and hence Vitamin A) as they have to detect small levels of lights (it is thought that a rod can detect a single photon!).
Cones, on the other hand are not so sensitive to light. During the day there are tons of photons*. Since you need less Vitamin A for cones to function, you will see the symptoms of Vitamin A deficiency later compared to rods.
Hence, when you still have a bit of Vitamin A but not enough (e.g. 30 instead of 100) you will first notice it in systems that need Vitamin A the most. It turns out that this are the rods. And yes, if you had 0 Vitamin A you would be blind. But since Vitamin A is needed for many other processes, you will probably be dead at that point.
*Personally, I find it hard to grasp just how large the difference in Illuminance (and hence photon numbers) is for example between day and night. See here for a comparison. As you can see, our visual system has to deal with an enormous dynamical range of illuminance. The fact that we usually don't even think about these differences in light intensities in everday live is testament to how fantastic our visual system is in dynamically adapting to the huge differences in input.

Thank you for your answer! You explained it perfectly, sometimes people explain things in a really complicated way and I need a dictionary just to go through the answer but yours was really easy to understand and I appreciate that.


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Century old trees and evolution
We always think of natural selection as occurring at the level of populations not individuals. how about century old trees where germline is being produced from constantly dividing cells. Are all meristems in an old tree sharing the same genetic material, or enough mutations occur that different meristems have a different genetic background and are being selected differentially? Do different cells in a tree behave evolutionary more like different populations?
Added Note: The point I was trying to make is that for multicellular organisms in which the germline/somatic separation does not occur early in life, maybe Lamarck was not that wrong. In school we always learn to ridicule Lamarck with the giraffe story. But maybe in some instances Lamarckism makes at least as much sense as Darwinism.

The population of cells within a single tree can definitely be subject to selection. It still remain that it is a population of which selection is applied, you just shifted the level of selection. See evo101 > The hierarchy of selection for a quick introduction.

Note btw that this concept relates to formation of cancer.

Yes, indeed, somatic mutations can and do occur on different branches of a plant. Here is a recent study exploring this concept in an annual herb (rather than an old tree), and showing that selection is active in filtering these mutations during growth of the plant. From the end of the abstract:

These results support the hypothesis that somatic mutations accumulate during vegetative growth, but they are filtered by different forms of selection that occur throughout development, resulting in the culling of expressed deleterious mutations and the retention of beneficial mutations.

Interesting. In mammalian systems you can also get heritable, but non-permanent modifications on DNA such as methylation as a result of environmental factors. These presumably have some influence on selective fitness too. Any idea about this in plants?


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my way of solving the biology question
Pure-breeding tall and pure-breeding short pea plants in the P generation were crossed as shown below. Based on the diagram below, one can assume that
a)short plant height is the dominant trait.
b)the F₂ generation will all be tall in height.
c)the alleles for plant height do not segregate during meiosis.
d)tall plant height is the dominant trait.
My answer: The answer is D becasue tall plant is the dominant trait because  A dominant trait is an inherited characteristic that appears in an offspring if it is contributed from a parent through a dominant allele

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In particular, you are required to use the "homework" tag for "homework" questions. (Note that "homework" can apply to questions even if they are not assigned as homework — for example because it "addresses a basic biology concept that may seem trivial to biology professionals".) ——— Thanks!

can you help me if your good in biology,if my answer is correct ?@tyersome

and thanyou for the welcoming message,im glad to  join :)


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16S sequencing: pooled or individual samples?
I am planning to run 16S sequencing on a set of individuals to explore microbial diversity. The question I am facing is: should I sequence them individually or I pool them (for example 5 individuals = 1 sample)?
I was just thinking on advantages and disadvantages of both methods:
1) individual. I can get the diversity of each individual, in that way I know the proportion of individuals which have a particular species of bacteria. The cost are higher since I need more samples with respect to the pooled way, but the reads/sample needed should be lower (since this number increases with the microbial diversity).
2) pooled. I have only a general proportion of diversity in the pool (I can't assess how many individuals have a peculiar becterium). The cost are lower due to small amount of samples, but reads/sample should be higher due to more than one individual pooled (?).
Can someone help me? Are my assumptions right or I am missing something?

It would help if you shared more about the type of questions you are interested in answering, types of samples you're working with, and sequencing platform. Generally speaking, there's no scientific reason for pooling samples if sequencing them individually is an option. Most next-gen sequencing platforms generate enough reads that pooling is almost never necessary, especially for 16s amplicon sequencing.

Sure, so I have to sequence insects from 5 countries to explore their microbiome. I will use MiSeq sequencing to sequence V3-V4 region. I would like like to know if my thoughts are right and why I should use individual instead of pooled. or viceversa

By pooling samples one loses a lot of information (it excludes any possible analysis of beta-diversity)... but, yes, it is cheaper.

Ultimately, it depends on what insights you are trying to glean from your sequencing data, but from a purely scientific perspective, there's almost never a reason to pool samples in the the way you described. You pro-con list is not far off, in terms of information lost or gained, but I think it overlooks some of the down-stream consequences of losing that information on your analysis. For one thing, pooling limits your ability to make biologically or statistically meaningful comparisons. For example, if your individual samples are pooled by country of origin prior to sequencing, you have no way to estimate varation within those pooled samples. Because of that, not much can be said about any observed difference between countries beyond simple descriptions of richness and taxonomy. Treated as individual communities, you can look for differing trends, make meaningful beta-diversity comparisons, and actually analyze them with statistics. If you have environmental data, you might even be able to do some meaningful ecological analyses.
Second, as you mentioned, a pooled sample should theoretically have more diversity than the individual samples it was pooled from (at least it should have no fewer unique sequence variants than the richest of the pooled communities), but pooling could also mask community diversity. If one of the pooled samples has a particularly high abundance community that is dominated by just one or two organisms, it could create the appearance that some organisms at moderate abundance in other more diverse communities are actually vary rare, or non-existant. Even at a much greater depth of sequencing, diversity metrics accounting for abundance lose value, since any outlier sample could skew pooled results, creating a false impression of overall community profile.
Lastly, all of the cost-savings assumptions in your post are going to depend on the sequencing center you use and how they bill samples, so there isn't really a straight answer to give. But I will say that the per-sample cost of Illumina 16s amplicon sequencing is pretty cheap (especially compared to the cost of collecting insects from 5 different countries). And because of how sequencing is performed, pooling samples might not even save you much money. Sequencing is often billed per sequencing kit or per lane of sequencing used, not per individual sample you send. So, unless you have someone to share your sequencing run, it's possible that you'd pay roughly the same amount for 5 samples as you would for 95, with only minimal cost savings on library prep and extraction kits.
To summarize, pooling samples reduces your effective sampling effort and limits your potential scope of inferrence. The only valid reason I can think of for pooling samples in such a way would be if you cannont isolate enough bacterial DNA for sequencing from any one individual (which could be the case, depending on what type of insects you're working with). Like I said at the start, though, it really depends on what you want to learn from your 16s data. If the microbiome comparison is crucial to the outcome of your study, I'd suggest sequencing as many individual communities as possible, or at least a subset of individuals from each country (depending on how many you collected). If you don't plan on doing much analysis beyond describing microbial richness and maybe some taxonomic classifications, maybe pooled samples are sufficient for you needs.

Thank you so much MikeyC for your very clear answer!


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Does using CRISPR/Cas9 knockout need to add donor DNA in the process?
I am new to this technology and don't quite understand how it works. Hope someone can give some suggestions! Thank you.

Short Answer:
No, for CRISPR/Cas9 knockout you do not need to add donor DNA.
Little bit more detail:
CRISPR/Cas9 allows you to cut at a given position (defined by the gRNA). This will lead to double strand breaks (DSB).
If you do not add any donor DNA, the cell's DNA repair mechanism will try to repair the double strand break. Since these CRISPR/Cas9 mediated DSBs usually have a blunt end it is really hard for the DNA repair mechanism to fix it. If will often introduce an error, for example by missing a basepair (or several) leading to a frame-shift mutation. This DNA repair mechanism is called Non-Homologous End Joining.
If you do add donor DNA it will contain both the sequence you want to introduce (say a green fluorescent protein) and homologous sequences on both sides of the double strand break. In other words, if you want to cut the sequence ATCGCA exactly in the middle you will get ATC and GCA. You want to insert AGA. The donor plasmid must then have the sequence ATCAGAGCA. As the cell now has the homologous regions, it will use the Homology Directed Repair mechanism.
The sequences are for illustration only - in reality a gene is usually several hundred basepairs and it is recommended to have much longer homology regions.


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What species of spider is this? Could anyone help

This image was taken in assam, India. The size was around 1cm. Could anyone help identify?

can you add an estimated size? 5 mm? 5 cm?

This is a male Carrhotus sannio (the females are brown/grey). The white dorsal stripe on the cephalothorax is right beneath the outside eye; the upside-down v-marks on the back of the abdomen point to two white lines (sometimes broken) which run parallel to the length.
Gallery of males:
https://inaturalist.ca/taxa/334660-Carrhotus-sannio/browse_photos?quality_grade=any&term_id=9&term_value_id=11

It looks like Adanson House Spider, Hasarius adansoni. From the eyes, it's definitely a salticid, and the reported 8mm size for females is close to the 1cm you estimated for yours. Here's an image from spiderid.com with similar markings:

Pattern of white strips and dots is different in both images. It is definitely Jumping Spider (salticid), but not Hasarius adansoni.