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Apparent paradox in Glucagon action
Glucagon stimulates glycogenolysis and gluconeogenesis, thus increasing the plasma glucose concentration — so that tissues get enough glucose in the fasting state.
However glucagon also inhibits glycolysis. In this case, what is the point of having high blood glucose if it cannot be catabolized?

Hint: Are there some organs on which glucagon does NOT act (i.e. which do not have significant numbers of glucagon receptors)? Could these organs benefit from the increased glucose levels?

Summary
The apparent paradox is resolved by the fact that not all tissues possess receptors that cause them to respond to glucagon or, more generally, to the same hormone. Where different tissues do respond to the same hormone, the tissue response may differ because of differences between the pathways or particular enzymes within the different tissues. Tissues that use glucose in starvation generally do not have glucagon receptors. In the related situation of response to epinephrine, the glucose utilizing tissue, skeletal muscle, does not contain the particular enzyme isoform that is subject to cyclic AMP-dependent control in liver.
General principles of hormone action in the regulation of metabolism
Metabolism in simple, especially unicellular, organisms is regulated by supply and demand. The mechanisms underlying this are mass action and allosteric activation or inhibition of key enzymes. In more highly developed organisms with differentiated tissues serving specialized functions there are times when this intercellular control must be over-ridden to produce an integrated response to the overall benefit of the organism. This is the rationale for hormonal control.
An integrated response does not mean that each tissue responds in the same way. It means that each tissue responds in a manner that is appropriate for the organism as a whole, given the function of the tissue and its priority (e.g. for rationing of energy sources). A simplified example of how this is achieved is illustrated below.

Tissues 1 and 2 (e.g. liver and skeletal muscle) both contain pathway P1 (e.g. glycogen degradation), but only Tissue 1 responds to hormone H1 (e.g. glucagon) because Tissue 2 does not have the receptor R1, for H1. (SM is the second messenger involved in the signalling, e.g. cyclic AMP.)
Tissue 2 (e.g. adipose tissue) does have the receptor for hormone H1, but responds in a different way because it lacks pathways P1 and P2 of Tissue 1, but contains a tissue-specific pathway P3 (e.g. triglyceride breakdown).
Hormone H2 (e.g. epinephrine/adrenalin) affects Tissue 2 (e.g. skeletal muscle) as well as Tissue 1 (and 3), but the response is only partially similar in that although they share pathway P1, Tissue 2 lacks pathway P2 (e.g. gluconeogenesis).
Differential response to glucagon
Put simply, glucagon is a signal for starvation. Hence the appropriate integrated response is for those tissues (liver and adipose tissue) that can supply energy sources (glucose and fatty acids, respectively), and those tissues with greatest need for the scarcest resource (brain with its requirement for glucose) are supplied it, while those tissues that can manage with the alternative (fatty acid) are made to use it instead.
The brain has no receptors for glucagon (or insulin), so it can utilize the glucose made available by the liver. (Likewise the erythrocytes.)  The main factor preventing other tissues using glucose is that they have insulin-sensitive glucose transporters and the blood concentration of insulin drops in starvation. It is only liver where there is need to make sure that the glucose produced by gluconeogenesis is not glycolyzed.
But doesn’t the paradox remain if we consider epinephrine?
The function of epinephrine is to initiate the ‘fight or flight response’, which involves supplying energy metabolites for skeletal muscle contraction. This involves both the liver, which breaks down glycogen to supply glucose to the muscle through the blood, and the skeletal muscle itself, which breaks down its own stored glycogen. As epinephrine also acts through cyclic AMP, which inhibits glycolysis in liver, why is glycolysis not inhibited in skeletal muscle?
The answer to this is that cyclic AMP inhibits glycolysis by phosphorylating and activating the liver enzyme PFK2, which catalyses the formation of fructose 2,6-bisphosphate, an allosteric activator of phosphofructokinase. Skeletal muscle has a different form of FPK2 which is not affected by cyclic AMP, lacking the regulatory phosphorylation sites. (It is regulated by other metabolites.) Hence in liver, glycogen, through cyclic AMP, causes the concentration of fructose 2,6-bisphosphate to decline and, thus, the activity of phosphofructokinase (PFK) to be decreased, preventing glycolysis; whereas in muscle the concentration of fructose 2,6-bisphosphate does not change.

This regulation of phosphofructokinase by fructose 2,6-bisphosphate is described in sections 16.2.2 and 16.4 of Berg et al. (although they seem to have forgotten about skeletal muscle). However as the overall mechanism and details are somewhat complex, I have produced a simplified summary diagram of my own, above, in which the green lines indicate activation, and the red lines inhibition.


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What is the difference between fragmentation and true regeneration?
I read in my book that Planaria (flat worms) undergo true regeneration.
Fungi, filamentous algae and protonema of mosses multiply by fragmentation.
What is the exact difference between fragmentation and true regeneration ?

Regeneration is the ability of a creature to repair or regrow an organ after cutting it.
Not all creatures can regenerate.
If you cut a human hand it won't grow to a full human nor the human regrow a new hand
Some salamandras can regrow their tail if amputated but the tail itself won't becoma a salamndra
Planaria, Star fish, and plants can regenerate if the amputated organ has regenerative cells. The original organism will regrow the organ and the organ will grow a full organism.
Fungi, filamentous algae and protonema of mosses do not regenerate when fragmented in the sense that there is no real organ to regenerate. For example, the mycelia of Fungi is composed of many hyphea, creating new is independent of loosing them

Thanks for your contribution. You seem to address only the definition of regeneration, and not the difference it bears with fragmentation. Further, answers need to be backed up by sources, preferably references to papers from reputable journals, to allow others to background-read on your material.

source: Stack Exchange

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

sort: votes


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What is the best way to find which domains in a list of InterPro IDs are catalytic?
What is the best way to find which domains in a list of InterPro IDs are catalytic?
(In this case, we are looking at human enzymes and their domains' InterPro IDs.)
Thanks in advance!
Setz

Welcome to SE Biology. Please finish reading the [tour] to find out how this and other SE sites work. Your question may have a better response on our sister site, SE Bioinformatics, but in any case you should give an indication of the steps you have taken yourself to answer any question you posed here. Personally I would have submitted a ticket from the Interpro Help page. Some of these large web facilities have very good support (others less so).

In InterPro you can do a search "by text" and type in "catalytic". It gives you a list of IDs with description and you can download the list.

Thanks for your reply!

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


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Anyone can identify this moth?
Found on the ceiling of my flat.
Place: London, UK
Date: 9th of August
Size I would say slightly more than inch and inch and half (3-4cm) wingspan
Suspect on the photo:

That looks very much like a brown color morph of the Box tree moth (Cydalima perspectalis), which has been seen in the UK since 2008. The size is about right (around 4.0-4.5 cm wingspan).
This species is an invasive pest outside of its native range (Asia).

By Nagy Sándor (NagySandor.EU) CC BY 3.0, Link
According to the Royal Horticultural Society this species has been invading the UK from the southeast with London a likely place to find them.


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Slinky-like worm/leech identification
In my mulch bed today I came across a tiny red worm, between $\frac{1}{4}$ and $\frac{1}{2}$ an inch long. It moved across the ground by sitting upright on one end, waving the other end back and forth (presumably for some momentum), and then flipping over and standing on the other end. It did this motion flipping end-over-end, kind of like a slinky. Observed in the Chesapeake Bay region.
I haven't been able to find anything on this little creature through searches. An article about leaping nematodes is the only thing remotely in the neighborhood of what I saw but the motion described is different and these sound far too small to be the same creature. Any ideas what this is?

Welcome to Biology.SE! Can you get pictures of your worm — macro images in particular might be helpful for this identification. You might also want to check out iNaturalist — that site is much more focused on identifications and I think you are more likely to a definitive answer there.

Hi @tyersome, thank you for the feedback. Unfortunately I wasn't able to get a picture at the time or locate one again since then but will continue trying. I'll give the app a try I can get a pic. Thanks.

Did they resemble these "jumping worms" ? https://www.youtube.com/watch?v=jrGnUFDXuyQ  this video is not as red or as jumpy as I'm imagining yours to be

@JimN, very different. This was tiny by comparison to those, less than half an inch, and stood upright, never on it's side like a normal worm. Still have had no luck spotting again to get a picture.

@IPoiler how about this one: https://www.youtube.com/watch?v=AFkz-L4wNT0 (starting at the 25 second mark) or this one https://www.youtube.com/watch?v=xVk87DZB6NY (3:30 mark). Neither of these is red, though, but how does the size and shape compare?

@JimN, not quite but slightly more disturbing to watch (0.o). Looked a bit like a miniaturized single red/orange anemone polyp. Great work tracking down a potential hit in a video with less than 70 views though.

@IPoiler to be honest, I've spent a few hours on this :) which I don't mind. I've learned a lot along the way. I can't figure out what would match your description. But there are some parasitic worms/maggots that affect specific plants. I know you described your worms as being in your mulch, but did it seem like they were coming out of a certain plant? the roots? or concentrated around a certain something decaying in compost? Or was it around a particular kind of large tree?

@JimN after doing some reading on locomotion in different types of invertebrates, I'm pretty confident that what I encountered was some type of tiny leech. It didn't have quite the inchworm gait like the one in the video, seeming to instead flip from one sucker to the other like a slinky. It did mostly stand up on one end waving around similar to that one though.


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Does my reasoning about the first emergence of proteins make any sense?
In order to make proteins, a cell uses ribosomes, which itself is a structure made out of proteins. The first ribosome couldn't have been created with the help of ribosomes though, as the ribosomes weren't there yet! So where did the first proteins came from? Before the advent of ribosomes, which, when they arrived on the scene (in some primitive form), subsequently could be used to make increasingly complex proteins.

In prokaryotes, ribosomes are roughly 40 percent protein and 60 percent rRNA. In eukaryotes, ribosomes are about half protein and half rRNA. Ribosomes are usually made up of three or four rRNA molecules and anywhere from about 40 to 80 different ribosomal proteins.

Amino acids were abundantly present though before ribosomes came into existence. Most of them were left-handed as is life itself (look at the Softenon babies). You can compare this with the matter-antimatter problem in physics (which is not really a problem in my theory, but I won't bother you with that sh*t). A scenario to achieve is easy to come up with.
While competing-self-replicating molecules were present too, they could make good use of them. A rudimentary ribosome emerged (with earlier formed proteins, by accidentally combined amino acids so these proteins came first, actually).
Behold the creation of life! Once started life exploded, leading to us (some say that there is some kind of hyper evolution going on: the rise of the robots with no ticker, no tears, no feelings but a high calculating power).
Is my reasoning reasonable?

You raised what appears to be a similar point four years ago: Was there originally a non-ribosomal way of synthesizing proteins?. I am not sure what your actual question is this time. You do not seem to elaborate on your title and just state that proteins could have been formed from amino acids.

I'm asking now if they could have emerged by accident, just as amino acids did. Ain't it probable that in a soup full of amino acids these amino acids will react with each other to form a big collection of protein?

Before the question can be addressed I think you need to clarify or revise the statement “:…proteins, one of which could have been primordial life”. How can a protein be life?

@user1136 You can reduce and reduce, so the final question is: where did it all come from? Where there rishons, curved spacetime, inflation, singularities first? Where did they come from? Why is there anything at all? Why isn't there nothing?

If you wait long enough, amino-acids will combine to get the right proteins. Self-replicating molecules can use them.

@user1136 The answer can be connected with the fact that Nature (in physics) is left-handed. Only left-handed neutrinos exist. But I question this. It could be that the asymmetry originated just by accident. There are many scenarios to make this happen. Right hands don't fit in lefthand gloves.

Fred Hoyle thinks that matter is continuously created and the Universe is eternal, so no need for a cause. Panspermia, hmmmm....I would like to live there for certain! Maybe...

@user1136 You can see it as how the asymmetry between matter and anti-matter occurs in the early Universe,. For sure there is a similar mechanism is at work. between left and right-handed molecules of life.

Don't you mean "Lucifer's Legacy"?

why would proteins form without ribosomes?

@John Wasn't there an abundance of amino acids, prior to life? Amino acids were formed in a lab once. Why shouldn't proteins form?

Now you have changed your question to the merely asking whether a theory you propose is reasonable your question is clearly off-topic for this list and I have voted to close it on this basis.

@David Fair enough. But why am I not allowed to ask questions anymore? I did edit my questions, so is there still a reason for not being allowed to ask a question?

If you are being prevented from asking questions this must be a decision of one of the moderators. I am not a mod, just a list member able to cast a vote. You can ask on meta.

@David Good suggestion! Thanx. ;-}

I would also say that your "question",  though not a question, could be posted as your own answer to your original question. To amplify the reason I think it is not a question in terms of SE Biology, I would say that it comes in this category of subjective questions of the sort "…am I right?".

As their name suggests, the majority of a ribosome's structure and function come from ribonucleic acid (RNA), not protein. While ribosomes are about 35%-40% protein on average, a majority of ribosomal proteins are not essential for the catalytic functions of the ribosome, and none are in direct contact with the catalytic reaction site where peptide bonds are formed. Thus, it's hypothesized that the earliest ribosome analogs consisted entirely of RNA in what some might consider a pre-biotic RNA world.
In this "RNA World" framework, it is posited that other macromolecular structures, like proteins, DNA, and lipid membranes all arose after the existence of some primitive form of self-replicating RNA molecule.
References:
Khaitovich, Philipp, et al. "Characterization of functionally active subribosomal particles from Thermus aquaticus." Proceedings of the National Academy of Sciences 96.1 (1999): 85-90.
Nissen P, Hansen J, Ban N, Moore PB, Steitz TA. The structural basis of ribosome activity in peptide bond synthesis. Science. 2000;289(5481):920-930. doi:10.1126/science.289.5481.920
Davidovich, Chen, et al. "The evolving ribosome: from non-coded peptide bond formation to sophisticated translation machinery." Research in Microbiology 160 (2009): 487e492.

I think you will find a similar RNA world answer to the poster’s previous question. This present question is either a duplicate, and should be ignored, or deserves an answer either criticising the poster’s proposal or explaining the views of those who have considered the nature of early proteins. You may not be aware that there are some eminent scientists that argue against the RNA world, and even if you accept it there are problems about the appearance of proteins.

It's pretty obvious that the prebiotic world consisted of lf-replicating molecules. These molecules slowly merged with proteins to make ribosomes fit for producing proteins. Life got started!

Bacterial ribosomes stripped of their proteins still function. they are slower, more error prone, and breakdown faster but they still function. proteins are not needed for the creation of proteins. http://uu.diva-portal.org/smash/get/diva2:408601/FULLTEXT01.pdf

I edited fro upvoting so I could upvote and accept.


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Why are some protein sequences known but their 3D structure isn't?
Why are there some proteins that have a known amino acid sequence, but their 3D structure is not known? Wouldn't finding the former in a lab lead to the discovery of the latter? Please correct me if I have misunderstood something.

related https://biology.stackexchange.com/questions/85723/why-does-it-matter-to-predict-protein-structure

Protein sequencing is a nicely constrained problem: you have a one-dimensional sequence of amino acid members, which come from a limited set of options (made a bit more complicated by post-translational modifications, but not much more so). Because it's one-dimensional, it's a problem you can easily solve by chopping up a protein into little bits, using mass differences between amino acids to understand their constituents, and determining the order from that distribution. If a DNA (or mRNA) sequence is known, it becomes even easier - you can skip the protein sequencing process and get the amino acid sequence directly from the nucleic acid sequence and the genetic code.
By comparison, protein folding is an absolute nightmare to solve for. Chemical bonds between amino acids are not rigid, they can bend and twist in all directions. The conformation of those bonds also depends not just on adjacent amino acids (as in a 1-D problem) but potentially on any other amino acid in the sequence (not to mention external influences..).
In a large molecule like a protein there is a massive massive degrees of freedom problem. From Wikipedia, describing Levinthal's paradox, bold mine:

In 1969, Cyrus Levinthal noted that, because of the very large number of degrees of freedom in an unfolded polypeptide chain, the molecule has an astronomical number of possible conformations. An estimate of 3300 or 10143 was made in one of his papers[1] (often incorrectly cited as the 1968 paper[2]). For example, a polypeptide of 100 residues will have 99 peptide bonds, and therefore 198 different phi and psi bond angles. If each of these bond angles can be in one of three stable conformations, the protein may misfold into a maximum of 3198 different conformations (including any possible folding redundancy). Therefore, if a protein were to attain its correctly folded configuration by sequentially sampling all the possible conformations, it would require a time longer than the age of the universe to arrive at its correct native conformation.

Now, of course that's not the actual process that proteins use to fold (they don't iterate through all possible combinations, they settle through an energy landscape where only certain intermediate conformations are realized), and we can use that in computational models to solve protein structures more quickly than the age of the universe, but it's still quite a slow process. Projects like Folding@home have aimed to distribute the computational load among unused processing power in devices around the world, including idle gaming consoles and personal computers, but there are many many protein structures to solve.
It's possible to get a general picture of protein shape using imaging techniques like X-ray crystallography or cryo-EM, and for some purposes these techniques give a lot of information, but these techniques are also by no means simple and can be prone to errors.

Furthermore, the methods used to experimentally determine protein structure (e.g. x-ray https://en.wikipedia.org/wiki/X-ray_crystallography and cryo-EM https://en.wikipedia.org/wiki/Single_particle_analysis) are not one-size-fits-all solutions and are move effort-intensive than protein sequencing even in the best of cases.

You also don’t necessarily need to sequence a protein if you know its gene sequence.

@canadianer I kind of mentioned that, maybe I can make it more clear...

You did. I’m sorry I missed it.

I think you get more than a general idea of the structure from x-ray crystallography (!?), depending on resolution of course, I would even dare to say that you cannot possibly get more structural information anywhere else than you would from a high resolution crystal structure. Which is why some researchers are specialized x-ray crystallographers). CryoEM is also catching up, and NMR studies are good form small proteins and dynamics.

In my opinion, the focus on protein sequencing here is a bit 'pre-DNA-area', as we today nearly always do recombinant expression with protein sequences from DNA (i.e... we rarely isolate unknown proteins from natural samples and sequence them by chopping up the protein by hydrolysis).

To answer why sequences are known before structures, it is worth highlighting the typical ‘workflow’ for a biochemical researcher. Briefly, sequence is always before structure because you need the sequence to determine the structure. As with everything else one would like to investigate, you have to start with the information that you already have. In modern sciences these are usually as following for protein research:
Workflow:
1. Isolate some bacteria or fungi from e.g. the ocean or anywhere else, and sequence their whole genome (DNA). This is very realistic to do, and not that expensive anymore.
2. Once you have the genome sequence, there is a lot of bioinformatic work to be done to annotate the sequence. This means, identify coding regions for e.g. for proteins. There are programs that are very good at this, because we already have a lot of information on what is encoded in living organisms (based on experimental data and years of research).
3. The DNA annotation programs can assign thousands of proteins in one genome. These protein sequences are then uploaded in relevant databases, for other people to view and work with. Note that these proteins sequences are NOT experimentally validated. They are however assumed to be correct with some statistical validity (which is usually correct now a days due to the overwhelming amounts of collected knowledge, and sophisticated software).
4. Scientists (i.e. biochemist and others) can then work with these protein sequences to find out if they actually are what the programs assumes. This involves the bottleneck of actually been able to produce and purify the protein of interest (which may be very difficult).
5. After experimentally assuring that the protein actually has the function you are interested in (by doing experiments), and being able to actually produce and purify it, one would typically want to determine its structure. This is because the three-dimensional structure of a protein can explain how and why it work the way it does. This is however difficult to do, experimentally (as well described by the other post answer).
Can you trust homology-models?
As a scientist working with protein structure and function, I would also note that (in my opinion) you cannot completely trust structures solved purely computationally (i.e. homology-models). These estimated homology-models are simply based on actually structures that are experimentally validated (e.g. crystallographic). Even though homology-models are very useful when you do not have a better structure, you can never be completely sure that they are correct (as they are simply assumed models of structural models; i.e. models of a models).
The active site of enzymes is of great interest to understand how enzymes catalytic their reaction. It is of vital importance to know how the catalytic residues are structurally placed/arranged in the active site to understand and even modify their catalytic behaviour. Even if you have a homology-model is 98% correct, the 2% error could be the structural placement of catalytically important residues. You also can not know for sure what the error is. One should therefore be very careful to put to much reasoning into a homology-model. In summary, if you don’t have a experimentally validated structure (which is difficult to get) you can never be completely sure of what is going on (or at least, you would be working in the dark - looking for effects).
Experimentally validated structures:
I would also like to add that x-ray crystal structures are, as of today, the golden standard when it comes to protein structure information (although cryoEM is catching up(!), and NMR structure give a lot of information about dynamics). You should check out the PDB database. If you have a high resolution structure, of e.g. 1.1A you are approaching atomic resolution and can even see the rings in the aromatic amino acid side chains (which is very cool!).
To answer your question in brief:
Sequence is always before stucture as you cannot experimentally determine structure without the sequence (also required to computationally model the structure). The protein sequences are simply assigned with complexed programs, from the DNA sequences. After you have the sequence you need to experimentally validate that the assigned protein sequences are correct. Only after all this work ca you start to determine its three-dimensional structure.....through a lot of hard work.


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Why are so many species reproducing late this year?
Hope this question is OK for this site, couldn't see where else to ask it.
We've spent a few days out in the countryside recently, and have been very surprised at how many species appear to have very young offspring so late in the season. I was always under the impression that the vast majority of animals and fish produced young in the spring (March/April).
For example, we saw tadpoles, fluffy (ie obviously very young) coots and weeny minnows. I would have expected that all of these would have been born/laid a good 3 or 4 months ago, and so would be more mature by now.
Caveat: We didn't do a scientific study, this is just a strong impression we got from days out in north west England.

It's hard to say without more information, but one substantial possibility is that you are mistaken that species are reproducing late - that's a problem with anecdotal rather than scientific data!
Additionally, species you mention like the common coot can attempt multiple broods where the season is long enough. Wikipedia specifically mentions Britain:

Eurasian coots normally only have a single brood each year but in some areas such as Britain they will sometimes attempt a second brood

The same could be true for species of frogs/toads and fish, so without knowing specific species it can't be known whether these are species reproducing again or species reproducing late.

OK, thanks for the reply. All makes sense.


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Germ cells vs. gametes
Naively, I thought that germ cells are diploid (in diploid species like human/mouse at least). Then, germ cells undergo meiosis and become haploid. I thought this was the critical change that defined these derived cells being named gametes (spermatozoon/ovum) rather than germ cells. However, I read that while XX mammalian germ cells undergo meiosis during embryonic development, XY germ cells don't go through meiosis until well after birth (puberty). This would mean that female gametes arise over a decade before male ones in humans. Is there an accepted definition of when germ cells differentiate into gametes and the terminology?

Your observation is right.

In females( having  XX mammalian germ cells), Oogenesis starts with
the process of developing primary oocytes, which occurs via the
transformation of oogonia into primary oocytes, a process called
oocytogenesis. Oocytogenesis is complete either before or shortly after
birth.(1)

The "germ cells" are called oogonia. Ovum is not a direct product
of meiosis I, the oocyte forms a primary oocyte in meiosis I, which
undergoes meiosis II after fertilization to give an ovum.

The ootid is the immature ovum formed shortly after fertilization, but
before complete maturation into an ovum. Thus, the time spent as an ootid is
measured in minutes.              ....(2)

(In oogenesis, the ootid doesn't really have any significance in itself, since it is very similar to the ovum. It matures into an ovum.)
This diagram sums it up very well:

Oogenesis in Eukaryotic Cells.(A) oogonium where the mitotic division
occurs (B) differentiation and meiosis I begins (C) primary oocyte (D)
meiosis I is completed and meiosis II begins (E) secondary oocyte (F)
first polar body (G) ovulation must occur and the presence of the
sperm penetration (fertilization) induces meiosis II to completion (H)
ovum (I) second polar body               ...(3)

It is commonly believed that, when oocytogenesis is complete, no additional primary oocytes are created, in contrast to the male process of spermatogenesis, where gametocytes are continuously created.

In males, again, as you say, Spermatogenesis is the process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testis. The germ cells here are the spermatogonia. But here, initiation of spermatogenesis occurs at puberty. So, males start producing sperm when they reach puberty, which is usually from 10-16 years old.(4)

(The process is almost similar to oogenesis, I would recommend you to start with the wikipedia page if you want to understand this in detail.)
Take away points:

The first haploid cell formed from a diploid germ cell is not an ovum/spermatogonia.

Ovum is formed after fertilization, whereas sperms are formed at puberty.

Oogenesis starts after birth, whereas spermatogenesis starts at puberty.

1- https://en.wikipedia.org/wiki/Oogenesis
2- https://en.wikipedia.org/wiki/Immature_ovum#Ootid
3-https://upload.wikimedia.org/wikipedia/commons/1/1a/Oogenesis.svg
4- https://en.wikipedia.org/wiki/Spermatogenesis

Thanks, i missed the distinction between meiosis I and II


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Is there an animal venom to which humans are naturally resistant?
Some species, no matter how poisonous or venomous, have natural predators that can withstand the poison/venom. Does human also have something similar?
This question came to me after I spent an hour observing my pet black widow and looking up related materials online. I realize that some species of wasps can neutralize the poison of the black widow naturally. Hence, I wonder if humans have something similar.

Humans are resistant to some natural compounds that can be (very) dangerous to other animals, for example caffeine and related molecules, but those are plant-based. We can tolerate doses of animal-produced toxins that are lethal to other, generally smaller, animals - for example, black widow bites are rarely fatal to humans, but can easily kill their natural prey.

@MattDMo Thank you! My question aims to ask specific natural compounds that other animals/plants/etc. use as their defense mechanisms that humans can neutralize it. For example, while the black widow's venom is rarely lethal for humans due mainly to our size, we do not have something that counters it effectively. On the other hand, the yellow wasp does.

what do you mean by resistant? death? damage? what kind of damage? Humans are not resistant to caffeine, nicotine or ethanol (for example) but we do not die from small dosages. Same goes for spider bites, snake stings etc. Even too much water can kill humans.

@Hachiloni no, we are not completely resistant to the things you mentioned, but we have functioning biochemical pathways that can metabolize those compounds. I was thinking specifically of the effect of caffeine on dogs - they are much more sensitive to its effects than humans, even taking into account differences in body weight, and can be poisoned by equivalent mg/kg doses that some people consume daily via coffee or energy drinks.

@MattDMo This turns out to be a lot less clear cut than I originally thought. It seems I would need a better definition of what I mean by "resistance" as well. But I lack the background to suggest a meaningful one. I guess originally my thinking was along the line of whether humans are natural predators of some other animals. If that is so and the animals produce certain toxins, then maybe humans are immune to those toxins, just sort of a evolutionary thing.

@Paichu I think an important point you might be overlooking is that humans are generalist predators, not niche ones. When you have a situation like a venomous black widow spider and a venom-resistant predating wasp, typically the reason is that they both co-evolved in the same ecological niche, which is how resistance develops. There is no relationship like that with humans and any of our prey - we don't occupy a single niche, and didn't evolve to specifically feed on any one thing, therefore no venom/resistance mechanisms have developed.

no venoms I know of, but humans are highly resistant to maillard compounds, far more than any other animal.  they are toxic byproducts produced by cooking food, mostly overcooking it.


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How do fish persist in the upper parts of mountainous rivers with waterfalls?
I was recently traveling in a remote mountain region and hiking alongside a very small river.
What caught my attention was the fish in the small ponds under the waterfalls.
These ponds were just a couple of square meters in size and each one housed between 5 and 10 fish.
The course (do you mean flow?) of the river combined with the waterfalls mean it was basically out of question that they could swim / jump upstream.
In such small mountainous rivers, how do fish remain in the upper parts over the course of hundreds of years.
I mean the size of the ponds and the amount of fish did not look to me like it could be sustainable for a population. And there should be the occasional one going down.
Are there examples or situations where the upstream population becomes extinct?

Welcome to Biology.SE! I edited your post, but please check to make sure I haven't changed your meaning. In your third paragraph you say that "... course of the river combined with ..." — did you mean flow. If not, can you clarify what it is about the river that makes you think it was impossible for fish to migrate upstream? Thanks!

@tyersome "Course of a river" is a common term. It refers to the path the river takes, including the path traveled across the surface of the earth, elevation changes, flow changes as a river goes through shallow/wide or narrow/deep sections, rapids, etc.

things to consider 1. some fish are very good at getting upstream and some can even climb the rock behind a waterfall 2 a rivers course now is not what it has always been, just because there is a waterfall now does not mean there was always one.

@BryanKrause — I am familiar with that usage, but in the context of that sentence (using "combined with") it appeared to me that the OP might mean something different, which is why I requested clarification ...

Sorry, my bad, I'm not a native English speaker :) @Bryan Krause is right


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Absorption of glucose in small intestine
During the absorption of glucose in the small intestine, glucose enters the epithelium by Na+/glucose co-transporter by the concentration gradient of Na+. The gradient is generated by pumping 3Na+ out each time and the entrance of 2K+ by Na+/K+ pump. The K+ is then removed by the concentration gradient via the potassium channel protein.
My question is is it more favorable to use a Na+ channel protein to pump Na+ out of the cell to generate the concentration gradient? Or there are some biological significance for K+ to enter the cell and leave again repeatedly (e.g. maintain stable charge distribution in and out of the cells? Thank you.

Na+ channel proteins would not be able to generate a concentration gradient, as they are passive transporters, not pumps. They essentially can only facilitate diffusion of Na+ down a gradient. The Na+/K+ pump is ATP-driven, providing active transport needed to establish or maintain a concentration gradient.


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Why do ion leak channels exist?
I've recently learned about ion leak channels in the context of membrane potential and action potentials. Neurons have ion pumps that require energy in order to maintain the resting membrane potential and concentrations of K+ and Na+, yet the K+ and Na+ leak channels seem to directly oppose this purpose. It seems like, if left unopposed, the ions would eventually diffuse across the membrane such that there would be equal concentrations on both sides and a membrane potential of 0.
If the ion pumps spend energy and store it in an electrochemical gradient, don't leak channels let that potential energy dissipate back across the membrane? Wouldn't it be more efficient to tightly seal ions into their respective sides until the energy is released during action potential?
Am I missing:

An important function of leak channels directly involved in maintaining membrane potential or causing action potentials?
Some broader evolutionary purpose of leak channels that help ensure a cell's health in other ways?

Additional clarification requested: Would it be correct to say that leak channels function in facilitating changes in membrane potential (and return to "baseline") until the threshold, at which point the voltage-gated ion channels allow for a much larger influx/efflux?

Check the parameters that go into the Goldman equation... it shows that permeability of ions is as important as their concentrations. If the permeability is zero, there is no potential. Because other conductances are mostly closed at rest, the leak channels are almost entirely responsible for the resting membrane potential (there is a minor component, a couple mV, supplied by the sodium-potassium pump itself, that is missed by the Goldman equation). If there were no leak channels, there would be effectively no resting potential, and certainly no useful one.
Additionally, there would be no return to "baseline" after a signalling event.
Leak channels are entirely integral to nervous system functioning (and the function of other excitable cells, including muscles and immune cells) - a system without them would be nothing at all like what we actually observe in any biological nervous system. The membrane potential massively amplifies the concentration differences into an electrical signal, such that large changes in voltage occur merely by opening and closing channels: very few ions need to move for this to happen, making a very efficient signalling system, requiring only the maintenance of ion concentration gradients (which change very slowly).
I would say it's correct to say that the role of leak channels is quite diminished during an action potential, since voltage-gated conductances ultimately overwhelm the leak conductance. You can see this from the Goldman equation, too. But they are quite important in setting threshold itself, and in returning to rest after an action potential. However, even during an action potential there is very little actual ion flux. Electrical forces are very strong, so not many ions need to move (see again the answer I linked above).


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Gene of interest number of copies in transformed K. pastoris
When transforming a K. pastoris strain, is there a way to predict how many copies of the gene will be integrated following the homologous recombination? More specifically is it something that a molecular biologist is able to control in a simple way, or, is it usually left to the chance (and determined afterward using gene sequencing)?
Alternatively : if I want to transform an electrocompetent wild type strain such as Pichia X33 using a plasmid vector, is the multiple integration an iterative process I control or is it random?)

Edit: Thank you all for the answers. Finally if I understand well the process is pretty random but you can control it to some extent. @gaspanic: I keep the idea of using fluorescent reporters and FACS for that ;)

Do you mean if you target the same locus in a diploid/polyploid species or do you mean off-target integration?

Yes if I am targetting a same locus in haploÏd or diploÏd specie.

I only worked with with S. Cerevisiae and as long as you use 50 nt flanking regions it should only go to your region of interest unless your background has defective DNA repair mechanisms etc. In my lab we typically don't do whole genome sequencing just to verify a transformation. With conventional transformation techniques you only target 1 site in a diploid because the efficiency is so low, but with the cas9 enzymes you could integrate in both loci of a diploid.

Also your schematic won't work because the background will already have zeocin resistance.

Out of curiosity, is there a specific reason for not verifying systematically the transformation of final clone by sequencing? Apart from cost and time reasons? It is not the first time I see that. I guess yes, in the future CRIPR would be more used. (You are right about my schematic, it was only for illustration purposes)

I should mention we always verify the correct integration with PCR and gel electrophoresis. It also depends on what you're doing. For simple gene deletions in my lab we didn't do it. That's because the transformation efficiency is so low and using 50 nt homology flanks is so precise for targeting that the correct integration was likely the only recombination event. Also with yeast you can easily and rapidly test many independent transformations so rare events wont contribute much. But if you have a mutant with modified heterologous gene expression, whole genome sequencing would be important.

Thank you very much for all these precisions

To predict the number integrations is probably not possible, but you can favor multiple integrations, if that's what you are after. At least in Saccharomyces cerevisiae integration of a first plasmid appears to stimulate the insertion of additional plasmids at the same site (1). It is therefore possible to favor multiple integrations (2) by increasing the DNA-to-cell ratio in the transformation, thereby increasing the chance that any competent cell receives more than one copy of the plasmid, which could then integrate in tandem. The easiest way is to simply use more DNA, but depending on your cell competence you might need to compensate this increase by using less cells for your transformation (or simply plate less cells on each plate) as you will probably also increase the overall colony yield.
One way to actively select for multiple integrations is to use a competitive inhibitor for the selection marker. Again, in Saccharomyces cerevisiae transformations with HIS3 selection can be combined with 3-AT (3). This allows you to inhibit HIS3 activity just enough to only permit the growth of cells that have integrated a desired number of copies of the plasmid. Of course, this method is far from fool-proof, as you might also select for mutants that have increased HIS3 expression for other reasons. Edit: I actually found one paper doing this in K. pastoris (4).
Finally, if your implementation allows it you can facilitate the screening for multiple integrations by including a fluorescent protein-expressing cassette in your plasmid. That way you can easily screen for different numbers of integrations by fluorescence microscopy or FACS.
Sources:

Orr-Weaver et al. (1983): https://mcb.asm.org/content/3/4/747
Plessis and Dujon (1993): https://doi.org/10.1016/0378-1119(93)90172-Y
Wikipedia (retrieved 15 Aug 2020): https://en.wikipedia.org/wiki/3-Amino-1,2,4-triazole
Menéndez et al. (2018): https://doi.org/10.2144/00295rr05

Welcome to Biology.SE! How would using less cells compensate for having more DNA — did you mean more cells? This looks like a good answer, but answers are much more likely to receive a favorable response if you [edit] to include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thanks!

Thanks for your comments! I clarified the text a bit and added links to relevant papers. If you still think I should clarify it better, please let me know!


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If coral didn't exist, would jellyfish not exist either? (Or vice versa)
Is the evolution of corals, sea anenomes and jellyfish intrinsically linked to the point where if say corals did not evolve, neither would jellyfish? Or vice versa.

Hello and welcome Jefferey. How did you come to the conclusion coral & Jelly fish are reliant on each other?

They both evolved around the same time and are part of the same phylum. Do they have a common ancestor? I'm not saying their reliant per say.

Poor wording on my behalf. But is seems although the relationship is not clear. https://www.britannica.com/animal/cnidarian/Evolution

Welcome to Biology.SE! I don't think I understand your question — can you clarify what it is that you are asking?. Are you thinking that different lineages within a group are somehow dependent after they've separated from each other? If so why? If not, then why would the extinction of corals (or their failure to ever form a separate lineage) have any effect on jellies? ——— As an analogy, does the failure of the hominid lineage to form trolls have any effect on humans or the other great apes? What does that question even mean?

I was a little tired when I wrote this. I think the answer provided understood what I was getting at, though even in hindsight I can barely grasp what 1AM me was getting at. Heh, sorry for the confusion.

I found this article with phylogenetic trees of Cnidaria answering your question.
You should note that phylogenetic tress are statistical models based on sequencing. They may change depending on the methods used, the organismed sampled and the genes used for comparison
I translated the groups you mentioned to the following biological names:
Corals - Hexocorallia and Octocorallia
Sea anenomes - Actinaria (Hexocorallia)
Jellyfish - Medusozoa
(Not the same levels)
Judging by Figure 3 (don't know if I'm allowed to post the figure to this site)
And my limited knowledge in the subjet they each group could've evolve seperatley with a higher linkage between jellyfish & corals(octocorallia) than to sea anenomas.
Sea anenomas and corals(hexocorallia) are very closly linked and sea anenomas appear at the first junction of the tree which means that if sea anenomas did not exists neither the rest of the group.


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How do genes determine facial features?
What is known about the genes responsible for inherited facial features — the family resemblances that are so recognizable? Take for example a particular shape of nose: which gene or genes make it snub or Roman?

If you read the [tour] you will see that this is a site for "biology researchers, academics, and students". Now I am afraid that although it is sometimes possible to answer questions from laymen in common language, this is not the case here. First, the answer is complex because many genes come into play, second if you don't study biology you will not be familiar with the molecular genetic language and concepts. When you can say that you have been reading some elementary genetics, you may be able to frame a suitable question (however old you are). (But please run a spelling check next time.)

@Andrew several studies (see my answer) suggest the the heritability of facial morphology is between ~60-90%, so it's inaccurate to say the environment is 'large responsible'

As there is one good answer to your question, I have edited it to a form that I think acceptable (if still a bit broad and showing no research). You may or may not be able to understand the answer, but it is appropriate to this site.

So some genes from diffrent peoples just decode for slightly diffrent protein?

First, it's been estimated that the narrow-sense heritability of facial morphology is about ~60-90% (Martinez-Abadias et al 2009, Weinberg et al 2013, Liu et al 2012), so genetics is likely to be a greater influence than environment. But actually, the molecular genetic understanding of cranio-facial morphology is quite poor relative to other quantitative traits.
There's a list of genes from Wu et al (2019) which have been implicated and replicated across studies, but it's likely that there is a substantial amount of population specific differences in the effect size of different genes. The most replicable gene is PAX3 (which encodes a transcription factor).
As for the actual molecular genetics, it's complicated. Here are some quotes from a review (Weinberg et al 2018):

As with most common traits [61], the implicated variants from the
above facial GWAS tend to reside in noncoding (regulatory) regions of
the genome. Many variants at the 15 aforementioned facial loci were in or near
enhancers known to play a role in human craniofacial development.

An important finding from this study was that the effects of genetic
variants on facial morphology tend to be highly specific, even within
a single structural component like the nose. Another important finding
was that variants at these 15 loci tended to show preferential
activity in human cranial neural crest cells—a critical cell
population for building the face.

As for a more specific example, Adhikari et al (2016) peformed a GWAS on admixed Latin Americans and identified a significant association in the EDAR gene (well studied and known for being at high frequency in East Asian populations and influencing ear wax type, follicle/gland type and teeth formation). EDAR has a general role in the development of ectodermal tissues (such as the skin).
They found that the variant in EDAR was associated with reduced chin protrusion. Other studies have also shown that EDAR variants influence the cranial morphology in mice (using knockout studies). Functionally, they propose that:

The impact of the Eda pathway on mandibular morphology has been
interpreted as resulting from epithelial–mesenchymal interactions
during mouse craniofacial developme

References

Martinez-Abadias, N. et al. Heritability of human cranial dimensions: comparing the evolvability of different cranial regions. J. Anat. 214, 19–35 (2009).
Weinberg, S. M., Parsons, T. E., Marazita, M. L. & Maher, B. S. Heritability of face shape in twins: a preliminary study using 3D stereophotogrammetry and geometric morphometrics. Dent. 3000, 1 (2013).
Liu, F. et al. A genome-wide association study identifies five loci influencing facial morphology in Europeans. PLoS Genet. 8, e1002932 (2012).
Wu, W., Zhai, G., Xu, Z. et al. Whole-exome sequencing identified four loci influencing craniofacial morphology in northern Han Chinese. Hum Genet 138, 601–611 (2019). https://doi.org/10.1007/s00439-019-02008-6
Weinberg, Seth M., Robert Cornell, and Elizabeth J. Leslie. "Craniofacial genetics: Where have we been and where are we going?." (2018): e1007438.
Adhikari, Kaustubh, et al. "A genome-wide association scan implicates DCHS2, RUNX2, GLI3, PAX1 and EDAR in human facial variation." Nature communications 7.1 (2016): 1-11.

It would be nice if you could actually link to the articles. It’s a pain to have to search for the paper — even more so on a phone.


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a biochemical pathway for evaluating the effect of 3' to 5' exonuclease on the proofreading activity of DNA synthesis
Can the following oversimplified biochemical pathway for DNA synthesis serve as a model for evaluating the degree of the effect that the 3' to 5' exonuclease affinity for mismatched base pairs can have on the degree of the fidelity of dsDNA synthesis? Is this idea basically correct to model the relationship?

Thank you for your attention

What do you think, and where specifically are you stuck? Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. "Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning.

@MattDMo — It doesn’t sound like homework to me, but neither does it sound like a question in terms of SE Biology. More like someone with a more numeric training starting out in Systems Biology and soliciting comment on his schema.

No, it is not a homework. I follow a course on DNA replication and had a lecture on the role of the 3' to 5' endonuclease domain of the DNA Polymerase. It was said that the activity of the endonuclease alone improves the error rate of dsDNA synthesis. I wondered if a biochemical model can demonstrate that or even quantify the effect of the endonuclease. So my question is thinking in terms of a pathway makes sense. I think of implementing a model in MATLAB to see if just by changing the exonuclease's affinity for the mismatches improves the fidelity of the synthesis. I appreciate any comment.

well I tried to implement this pathway in MATLAB and it seems to me that it makes some sense. Here are two versions of the reaction progress simulation, one with low and the other with high affinity of the 3' to 5' exonuclease domain for the mismatches. The violet curve of the simulation corresponds the amount of synthesized dsDNA and the green curve corresponds to the error-free amount of that dsDNA.
The next figure shows that with low affinity of the exonuclease for the mismatches, the error rate is high (12%).

The figure below shows that the dsDNA synthesis error rate decreased with the increase of the affinity of the exonuclease for the mismatches.

The MATLAB code of this simulation is provided
https://matlab.mathworks.com/users/mwa0000016879211/Published/x551/x551.html
Your comments and suggestions are most appreciated.
Thanks,


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How can we determine which chromosome came from which parent?
In this article there is a graph (figure 1) describing different levels of methylation in the maternal and paternal chromosomes after karyogamy.
How can the researchers identify which chromosome originates from each parent?

That article is a review, and cites two other reviews for this figure.  The more recent one is freely available and looks fairly thorough, with more direct references to primary publications.

A straightforward way to identify which chromosome came from which parent would be to use sequences of known fragments of parental chromosomes or to use SNP arrays. I hope that I did not miss your question completely.
Regards,

is that the common way? I learned this subject in a course where they also spoke of sequencing techinques including SNP arrays but they said that teaching how to recognize chromosome origin is out of scope so I assumed there is another way.


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Is there a chemical reaction that blocks two cysteines by reacting with a third molecule?
The idea is to block the two cysteines so they can't react in the future. We need the reaction to remove the -SH groups of the two cysteines, or modify them.
Also important, the reaction should not make cross-link between the two cysteines.

To explain briefly my motivation: I am a PhD student and I do optical tweezer experiments. We can hold and manipulate two micrometer beads in two optical traps. We have a process to tether one protein using two DNA linkers to the two beads. I need to block two of the three cysteines of my trimer to properly couple the protein to both beads.

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, I've voted to close this question because it is primarily about chemistry rather than biology. While this might be a better fit for [Chemistry.SE], please don't repost (instead request migration). ———— In addition, we encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). I would start by looking into peptide synthesis. Thanks!


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Can phylocode classify viruses?
Can phylocode classify viruses? Based on what I found this system began in 2019, so there is not much information about it.
I know that the Linnaean classification system cannot classify viruses, but what about this new classification system (phylocode)?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, please add links and references about "phylocode" and why you think it might be useful compared to existing viral classifications. Thanks!

PhyloCode is not a new system but it isn't popular yet and actually quite opposed by some.
It overlaps with the ranked based systems but does not nullify them, meaning that even if PhyloCode becomas popular the ranked systems will still be needed.
One might understand from your question that virus have no classification system, but they have. The common one is called ICTV.
PhyloCode can classify virus and there is already a classification for virus (ICTV)


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What are "intrinsic hypothalamic fibers"? (From an article on neuronal mechanisms of sexual desire)
I came across the phrase intrinsic hypothalamic fibers which I cannot understand. What is meant by intrinsic - that these fibers (long myelinated axons?) start in the hypothalamus? Or that they start and end in hypothalamus? Or something else?
The article is "Pathways of Sexual Desire" by James Pfaus (2009).

Figure 8 Brain opioid systems overlaid on opioid binding regions (high density of receptors indicated by red to yellow, lower density in green to blue). Three systems exist: the pro-opiomelanocortin (POMC)-derived opioids such as р-endorphin, which arise from the same population of projection neurons that produce the melanocortins; the interneurons in the cortex, limbic system, hypothalamus, and brain stem, which produce enkephalins and dynorphins; and the intrinsic hypothalamic fibers, which contain endo- morphins. These systems are activated at orgasm in humans, at ejaculation in male rats, and during paced copulation in female rats. They shut down hypothalamic regions associated with sexual arousal and desire, thereby inducing refractoriness. However, opioids are also released in the VTA during phases of sexual arousal and desire and help to disinhibit DA neurons and, thereby increasing DA release in mesolimbic terminals. This is an important mechanism by which experience with sexual rewards sensitizes sexual excitement once the inhibitory effects of refractoriness and satiety wear off. VTA = ventral tegmental area; DA = dopamine; mPOA = medial preoptic area; mPFC = medial prefrontal cortex; NAcc = nucleus accumbens; PIR = piriform cortex; MeA = medial amygdala.

"Intrinsic hypothalamic fibers" are fibers instrinsic to the hypothalamus; so yes, these are fibers either projecting from somewhere in the hypothalamus to somewhere else in the hypothalamus, or locally in the hypothalamus (the hypothalamus itself is a pretty complex structure containing many distinct nuclei). The paper you reference specifically mentions the medial preoptic area, mPOA, as a target:

Infusions of mu opioid receptor agonists to the mPOA inhibit sexual behavior in male rats

and

infusions of a mu antagonist to the mPOA, but not NAcc, block sexually conditioned place preference

"Fibers" does not necessarily refer to myelinated axons, just axons of any sort.


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When cancer is detectable, how many sub-clones are there at that stage?
I have read somewhere that cancer is detectable when the number of cells reaches $10^7 - 10^9$, which probably varies according to the specific tumor. At this early stage, what is the expected number of subclones of the tumor? Any references would be super appreciated!
p/s: To answer this, I tried running a simple code for a birth-death process, but my laptop freezes at $10^7$ cells. :(

Is this in humans? What is the form of detection? There are over 100 different types of cancer, so maybe pick one?

@Andrew Any example in human cancer would be sufficient. Thank you for pointing out the confusion!

How do you define subclones?

It is impossible to define subclones. But is is possible to define when metastasis. Thus, this question may be unanswerable.

@MattDMo I apologize. I was under the impression that this is a well-defined concept. I have seen some phylogenetic trees for keeping track of cancer mutation, which is why I assume they are what biologists consider subclones.


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Why does our visible range not include infrared or UV radiation?
As the radiation peak of the sun is in the UV region and since at around room temperature materials emit radiation at IR, I wonder why our eyes are not capable of using these wavelengths.
I guess there is a reason why we exactly only see the region between these intensity peaks?

some quick googling showed that there are lots of easy to understand answers around (https://www.ceenta.com/news-blog/why-cant-i-see-infrared-or-ultraviolet-light), (http://scienceline.ucsb.edu/getkey.php?key=3019)

The first link isn't revealing any information, just physical basics about light. The last two answers from the second link are, in return, quite interesting. Particularly, I wonder why visible light offers the possibility to notice (sharp) boundaries..

Usually we don't ask why in biology because the explanation is always the same, it was good enough for survival. But here are a couple of explanations.
The radiation peak from the sun is in the visible range of the spectrum, between 400nm-700nm with the highest point around 550nm as can be seen here or calculated from Wien's law and the sun temperature.
That's why photosynthetic pigments use the visible spectrum and following them the rest of the ecological system.
Our retina blocks most of the UV light and water absorbs the lower part of the IR, illustrated very nicely in this article, figure 1.
It is true that materials on earth emit more radiation in the IR than in the UV-visible spectrum due to their temperature but:

most objects have the same temperature approximately
the soil emits a lot of radiation
the radiation from the sun in the IR is high compared to the radiation of earth. This is the best graph I found, emphasizing the great difference between sun & earth intensities
in the IR range there isn't a lot of variance in the wavelength intensity and therefore it is less useful.
Notice how uniform the IR reflection is from this leaf spectral signature

To summarize:

UV light is dangerous so we filter it out and not use it
IR light is uniform and not useful
Visible light is the peak of sun emission and therefore the most efficient range to use

Crystal clear answer. Thanks a lot!

The first sentence is good, the following explanations not so good.  It doesn't explain why many birds & reptiles are tetrachromats and see in the ultraviolet (and some insects in the infrared), or why most mammals - primates being the exception) are dichromats, and don't see much of the red portion of visible light.

@jamesqf the question was about our, human vision. The topics you mention are interesting but out of scope in my opinion. I'd answer them in depth in a separate question if you post it.

@Hachiloni: Human vision is not qualitatively different from that of other animals.  The fact that many other animals DO see in IR and UV ranges is sufficient to demonstrate that your answer is not correct.  Also note that photosynthesis does not use all of the visible spectrum, otherwise leaves would be black, not green.

Also re your point #2, IR light is most certainly not uniform.  For instance, it's fairly easy to take infrared photographs with a modified digital camera.  (You remove the built-in IR blocking filter, and install a visible light blocking one.)  A search for "infrared photography" will give numerous examples, e.g. https://petapixel.com/2016/10/27/introduction-digital-infrared-photography/

@jamesqf if human vision was not different from other animals we wouldn't have this discussion. Photosynthesis may use the whole spectrum in different intensities, check this (https://www.simply.science/images/content/biology/cell_biology/photosynthesis/conceptmap/Photosynthetic_pigments.html) for point #2 you might be right but: 1. check the long exposure time required, that is not usefull in a biological context. 2. I was thinking of the landscape existing when vision was developed. That's why I added the leaf spectral signature. I enjoy this but please edit my answer or post a question


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What exactly is "lateral septum"?
I came across the phrase lateral septum and I can't seem to find the precise definition online. Is it "the areas roughly to the right and the left of the septum pellucidum"? Or is it the parts of the septum pellucidium itsef? I'm confused.
If it is near the septum pellucidum (to the left and right), does it include particular nuclei?

Brain pathways for sexual excitation involve the activation of incertohypothalamic and mesolimbic DA transmission in the mPOA and NAcc that focuses attention on incentive sexual stimuli and engages motor patterns of approach and consummation. Collectively, the behavioral patterns stimulated by those systems and the subjective feelings that accompany them constitute the epiphenomenon referred to as sexual desire or, when mixed with genital and sympathetic arousal, “libido.” The core of this pathway includes the mPOA and its outputs to the VTA, which contain DA cell bodies that project to various limbic and cortical regions, such as the prefrontal cortex, olfactory tubercle, NAcc, ACC, lateral septum, and corticomedial amygdala.

The article is "Pathways of Sexual Desire" by James Pfaus (2009).
I have read the Septal area article in Wikipedia but still cannot get it.

It is confusing.  The septum pellucidium is a thin membrane separating the left and right lateral ventricles.  It contains white matter (nerve fibers), blood vessels and a few neurons.  It has traditionally been thought of as just a separating membrane, but the fibers running through it connect to the hippocampus and hypothalamus and so it is probably a relay to those structures.
Lateral to the septum pellucidium are the septal nuclei. The septal nuclei are NOT considered part of the septum pellucidium (or vice versa).  The septal nuclei are traditionally divided into two major subregions, the medial and lateral septal nuclei.  As you might have guessed, the medial nuclei are immediately adjacent to the septum pellucidium.   As the septum pellucidium is quite thin, the right and left medial nuclei appear to compose a single midline nucleus with the septum pellucidium running through it. The lateral nuclei are the ones a bit further out and it is these that are called the lateral septum. The septal nuclei may be further divided into caudal and ventral regions.  Many neuroanatomists group the most posterior parts of the septal nuclei into a third group, the posterior septal nuclei distinct from the lateral and medial divisions.
This is part of the problem.  Structures in the brain were named based of where they were and what they looked like since their functions were unknown. For example the hippocampus was given this name because it looked like the tail of a seahorse (genus Hippocampus), and the locus ceruleus ('blue place') looks blue. As we have learned more, some neuroanatomists have divided regions into subregions or sometimes lumped regions together based on their models of the proposed physiologic functions or neurochemistry of those regions. The subcortical 'limbic' nuclei, including the septal nuclei are among those most subject to these changing definitions,.  And as you might guess, different neuroscientists often disagree about these divisions.  Being human, they sometimes behave as though their definitions are THE definitions, or gloss over differences between sometimes unclear definitions.  Ideally, people splitting nuclei into proposed subregions try to propose clear definitions, but this is not always the case and these proposed definitions may not be accepted or used.  This can make it difficult for experts to know exactly what regions are being discussed, let alone people not long immersed in the field.  Over time however, fields tend to come to a consensus on terminology though for many brain regions this consensus remains elusive.  I hope this discussion makes the topic of the lateral septum a little more comprehensible, if only by validating your sense that the topic is confusing.
Here is a readable overview about the septal nuclei and septum pellucidium:https://www.neuroscientificallychallenged.com/blog/know-your-brain-septum
Check out the first reference here to discussing the neurochemistry of the medial septal nuclei from a chapter by Risold in the Rat Nervous system https://www.sciencedirect.com/topics/neuroscience/medial-septal-nucleus
In contrast look at the introduction of the following paper regarding the lateral septal nuclei:
https://bio.biologists.org/content/8/7/bio043554
"Whole-brain mapping of projection from mouse lateral septal nucleus"
And if you have access, you may be interested in
https://onlinelibrary.wiley.com/doi/abs/10.1111/ejn.13746
"Differential and complementary roles of medial and lateral septum in the orchestration of limbic oscillations and signal integration"
And here is a paper that describes development of the posterior nuclei as being different from that of the lateral and medial nuclei
https://www.nature.com/articles/s41598-018-30020-9


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Mariana Trench fish "how they can thrive under that extreme water pressure is still a mystery"
New Mariana Trench species is the deepest-dwelling fish in the ocean

Exactly how they can thrive under that extreme water pressure is still a mystery for now, but these creatures have been sighted regularly at depths of around 26,200 ft (8,000 m) and down to a record-breaking depth of 26,830 ft (8,178 m), as captured on video by Japanese researchers earlier this year.

I often see comments like this, but I have not seen any explanation why extreme water pressure would be a problem. Is there a reason?


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Identify this black dragonfly with bluish coloration along its flat top, yellow on it's mid-body and green on its head
I took these photos around noon in late July in Hsinchu county Taiwan. This particular stick in this particular pond is visited by many dragonfly species. I have seen this kind of dragonfly very regularly, in different nearby ponds, they seem to me to be far more active than other dragonfly species in the same area at the same time.
Its body is about 5 cm long and mostly black. However it has light "power blue" to white markings on the flat top surface of its "tail" and "mid" sections and the front part of its body before the head, and it seems to have some smaller yellow bands on the sides of its fore body and greenish markings on its head.
Wings are mostly transparent but are tinged orange or brown near the body.
Question: Is it possible to identify this particular species of dragonfly?

This species of dragonfly is Brachydiplax chalybea. Colloquially known as blue dasher.
General information
More information

can you confirm that it's not this instead? https://biology.stackexchange.com/a/94939

The colour and placement of colour - blue and it is located on the dragon fly thorax. Also the dragon fly in your link has a distinction of where the colour ends, unlike your image and the blue dasher. Whereby the colour is 'smudged' along the abdominal segments.

Care to try another? Identify these two big, beautiful dragonflies in Taiwan?


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Identify this thin and strangely-shaped dragonfly, and understand why the shape looks so weird
I took these photos around noon in mid August in Hsinchu county Taiwan. I've seen many dragonfly varieties but I've never seen anything like this before.
Its body is about 5 cm long and very thin compared to the ones shown in the related questions below. The midsection looks strangely shaped to me, as if it is bent upwards in the back and suddenly ends, and a very thin "tail section" was then added below it.

This dragonfly damselfly is from the species Pseudocopera ciliata. Dragon fly anatomy changes between species and there is not definitive answer for why it looks like that, the best guess i can give is that it may assist the female as she tries to find the hookup point for mating.
General Information
More Information(Pay-wall)
This is in Chinese but confirms presence in Taiwan: http://gaga.biodiv.tw/new23/s3-37.htm

Thank you for that. :)

I added an image that addresses the peculiar shape, feel free to change it. Thank you for the very speedy species identification!

Fantastic, thank you for that. I have been to Taiwan and I think it is a very beautiful place. No worries.

If you can say something about the "...and understand why the shape looks so weird?" part of the question that would be great.

Sure, I did some research and tried my best (check the answer). Remember to click the tick, approving them definitivel answers :)

yep, I've accepted several thousand answers across multipe SE sites, I usually give it at least a few days for comments and additional answers to accumulate.

No worries, I'm new.

I've added a supplemental answer

Thanks to @Andrew's answer for identifying the genus and species, but there's an important point to be made.
I showed this page to a friend and they immediately said "Oh, that's not a dragonfly!!"
It is not a dragonfly, it's a damselfly!

...why the shape looks so weird?

While this doesn't explain exactly why it looks so "weird", it does explain why it would look weird if it were thought to be a dragonfly!
There are four ways to identify the difference between the two. The categories are

Eyes: relative sizes and distance between them
Body shape
Wing shape
Position of the Wings at Rest

For more see:

Reconnect with Nature: What's the difference; Dragonfly vs. Damselfly
Treehugger: How to Tell the Difference Between a Dragonfly and a Damselfly
Damselfly Insects – Are Damselflies And Dragonflies The Same Thing?
US Fish and Wildlife Service Facebook: Dragonfly vs. Damselfly Guide

And these two excellent videos:

All About Dragonflies and Damselflies
The difference between a dragonfly and a damselfly

Example of a Damselfly, cropped from Ischnura heterosticta: Female common bluetail damselfly. Taken in Swifts Creek, Victoria:


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nontechnical understanding of a mammalian expression system
I just started working as an intern in the pharmaceutical industry. My background is in economics and I have pretty much zero knowledge of biology/chemistry. I am trying to build a basic understanding of some of the products I work with to better understand their place in the market. One (the most important) such product is a mammalian protein expression system. My questions are the following:
As I understand it the "output" of such a system is a protein, the "input" is DNA and the system itself is a cell, is this correct?
In the context of producing pharmaceuticals, would this system be used primarily for R&D, manufacturing or both?
I have read that an expression system consists of host cell lines, vectors, media and know-how. Would it be possible to explain in layman's terms what each of these elements is, and how they fit together?
Thanks

If you are talking about a commercial product, it would help if you could give us the name on the label, and a link to it. If it is a the name of a system assembled in some laboratory, could you give us details. I ask this because, not being familiar with a commercial product of that name, all it indicates to me generically is a system where protein is the output and mammalian describes either the origin of the machinery that makes the protein or the protein itself.

The general principle of the expression system is simple: it is a biological machine that uses cell media as its input (i.e. a broth of simple nutrients, including the protein building blocks) to generate its output, a specific protein of interest, according to its "settings", if you will, which is the DNA plasmid that describe which protein will be made. The cogs of the machine are carefully engineered mammalian cells that both create protein from nutrient, and multiply themselves to increase production capacity.
In a perfect expression system, there would be no need to know the underlying biology of the system: just provide the specified broth with a correctly formatted DNA plasmid, let it simmer for a specified duration at a given temperature, and voila!
The value proposition of a commercial system for its users is being as close as possible to this perfect system, i.e. not having to "roll your own" from first principle (after all, the general processes underlying protein expression are covered in an undergrad biology education) which would entail a great deal of effort and expenses. In some way, this is similar to the business model of cloud providers like AWS: abstract the low-level sysadmin-type stuff to provide a reliable platform for applications.
This is useful in both an R&D context (you can iterate on the protein and specific process steps for your product, not on the expression system) and a production context (you have a reliable expression system, that conform to regulatory requirements, with vendor technical support).
However, even the vendors have not entirely abstracted the biology of protein expression, and the specific working of the system is part of the differentiating features of a specific commercial product versus other products in the same line, and competing solutions from other vendors. You have asked clarification on a few technical terms:

host cell lines: The carefully engineered mammalian cells, which have been tuned to product protein in great quantity, while maintaining quality (e.g. avoiding aggregates) and, typically, specific requirement on post-translational modifications necessary for the application the protein was designed for. It must be easily to culture in large batch. There cells are a blank slate in which the DNA plasmid will be inserted to start useful production. A vendor's expression system will feature a cell line that tries to fulfil these something conflicting requirements.
vectors: How to format the DNA plasmid (= protein recipe) and get it into the host cell line. For mamalian system this will typically be viruses that can infect the host cell line to deliver the plasmid. The reliability and ease of use of the vector system, as well as compliance with regulatory standards in a pharmaceutical environment is also a differencing feature of an expression system.
cell culture media: Specific cell line will have different "nutritional requirement", as such vendors will have specific "recipes" for the nutrient broth in which to grow the cells of the system. This is more or less directly dependant on cell line, so less of a differentiating factor per se.
know-how: Biological processes tend to be messy, so some troubleshooting is expected even in commercial systems. Documentation as well as expert technical support can be an important selling point.

Ultimately you will need to understand to some degree the biology underlying the particular
expression system to be able to compare it horizontally to competing solutions from other vendors,
and vertically to other methods of producing proteins (e.g. prokaryotic expression system, cell-free systems), and, if you are in a customer-facing position, to be able to answer some domain-specific question on the spot. Here is an overview, here is another from a different vendor. I would suggest asking more specific question after perusing these.

Vector is based on a plasmid which is covalently closed circular DNA that can naturally exist in the host cell.
The plasmid has its origin of replication and a promoter, both of which are recognized by the host cell.
In order to express your mammalian gene in the host cell (e.g. in E.Coli bacteria), you must insert the gene of the interest downstream of the bacterial promoter of your plasmid. The bacteria will express the gene, without caring that the expressed protein has nothing to do with its own functions.
You also must insert into your plasmid another selectable marker, which is also a gene that will allow the cell to survive in the selectable media (chosen by you). For example, you can have a penicillin resistance gene.
Now when your vector is ready, you can add them to your cell culture. The bacteria will engulf these vectors (almost most naturally) and will start expressing the genes present in the vector.
But you are not sure yet which bacteria engulfed your vectors and which not.
In order to select only the cells that succeeded in engulfing your vectors, you must plate your cells on a selectable media. In our example a media containing penicillin. The cells that did not succeed in engulfing the vectors will die. You will have only the cells containing the vectors, and therefore the cells expressing your mammalian protein.
Grow the cells. When the cells divide, the vectors (little plasmids), will divide with them. So you can establish a production. Lyse your cells after creating a large enough population and purify your mammalian protein through the biochemical purification steps.
Hope it helps.


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Can below-threshold potential changes of neurons convey information?
In neuroscience we learn that when the membrane potential of a neuron reaches a threshold (typically around -55mV) it "spikes": That is, it actively propagates a signal. I have two related questions with this respect:

The spike initiation zone is typically (e.g. for mammals) at the axon hillock - from there the action potential is actively (opening of ion channels..) propagated through the axon. But what happens then at and after the (chemical) synapse? Is the propagation after the synapse to the postsynaptic cell passive?

Newer imaging techniques (e.g. calcium imaging) can capture sub-threshold changes in the membrane potential. How are these sub-threshold potentials relevant for information processing? Are they propagated to postsynaptic cells, albeit again only in a passive manner?

For an interesting reversal, check out C. elegans neuroscience. In C. elegans most communication occurs by sub-threshold potentials, and detection of action potentials is rare 2008, 2018 and controversial. Not my field, but it might be worth checking out C. elegans neuro-transmitter release absent action potentials.

This type of passive conduction (sub-threshold) is called electrotonic conduction. When an action potential reaches the axon terminal (pre-synaptic knob) it induces Post-Synaptic Potential (PSP), through chemical or electrical synapse. Now if there is EPSP (i.e. excitatory) generation, then in the post-synaptic neuron there will be electrotonic potential, that will move towards 'axon hillock'.
Upto the axon hillock, the conduction is mostly electrotonic and hence we need this type of conduction to actually generate Action Potential.

In theoretical neuroscience this electrotonic conduction along dendrites is computed by using Cable Theory. It will eventually die out with distance as$-$
$V(x)={V_o}\, e^{-\frac{x}{\sqrt{r_m/r_i}}}$ ; standard notations used.

ref article:
https://www.sciencedirect.com/science/article/pii/B9780123971791000178

Hence we can conclude that for information transmission, sub-threshold potentials are extremely important.

If these are subthreshold, does that theoretically also means that they can travel both way (as closed ion channels do not prohibit that)?

Theoretically yes. If there is potential gradient it will flow.

All voltage perturbations can propagate in both directions. Usually, they are called orthodromic and antidromic if propagation is from dendrites to axon or viceversa respectively.

@heracho what then actually hinders the current flow in the dendrites, stemming from an action potential, do reverse direction? In axons we know that channels close to hinder exactly that - but how about dendrites?

@TestGuest As I understand, the voltage perturbation propagates passively through the dendrites. This is because they don't have the Sodium channels (or another) necessary to actively propagate the signal. To be more precise in your comment, it's Sodium channel inactivation (not just closing) the mechanism that hinders the action potential to propagate antidromically in the axon.

Electrical synapses (Gap junctions) can generate current to other cells without the emission of a spike. This sub-threshold interaction is proven to have functional implications in neural activity (eg. Retina).

Thank you, that is good to know, though I was also interested in this property wrt chemical synapses.


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Evolution: what were we doing for 100.000 years?
I'm not a biologist/anthropologist but there is a question that comes up again and again and which I couldn't find any deeper thought, even not a speculation. As far as I understand it, according to modern evolutionary science, the anatomically modern Homo Sapiens Sapiens exists since about 100-300.000 years. Lets be conservative and take 100.000. However, human's ability to build a culture, a society, a civilization that uses the rational mind, an analytic thinking that gives birth to philosophies and, even more recently, to science and technology showed up only very late compared to the human's history. Lets say with the Sumer civilization about 3.000 BC. Now, this implies that, despite having anatomically a fully developed brain, for about 95.000 we were doing not much with our intelligence other than hunting, surviving, develop very rudimentary tools, migrate and not much more but without any cultural development which one should assume is proper of a human brain such as thinking, developing increasingly sophisticated tools, develop philosophies, religions, arts, music, sciences, math, technologies, etc. The latter even not much developed before the scientific and industrial revolution in the last few centuries.
This doesn't make much sense to me. One might argue people were busy with surviving, there was no education and we couldn't develop our IQ, there were no books for cultural transmission, etc. This might be part of the answer explaining a stop of cultural evolution for some centuries, even some thousand years, but for 100.000 Years? This doesn't look to be the fully picture.
So, my question is if there is something (article, book, etc.) of someone who pondered on this aspect in more detail? Is there a possible explanation why evolution produces a brain without using its full capacities for 95% of its existence so far? Are we 100% sure that the brain humans had 50.000 ago are the same we have nowadays?

If you think hunter gathering does not fully utilize the brain I suggest you try it for a month, if you survive I think you will understand just how much thought needs to go it survival. I also suggest studying history to see just how slow technological progress was before the advent of science. this question is one big misunderstanding of a person in a very privileged position in time and location.

This question contains potentially interesting aspects (although I think there are several false presumptions in the post - for example, go and look up the Lascaux cave paintings), but I think it's off topic for biology. Biology can't give you the answer to the question you have.

I’m voting to close this question because it's not about biology.

If you gave paleolithic people some neolithic age F1 crop choices, corn/potatoes/sheep/beef/wheat, they could have enough food for thousand strong tribes, and civilizations 45000 years ago. Just imagine giving aborigines and papuans some cows, melons and corn and letting them form civilizations.

I can think of two factors that could explain why a civilization took so long to appear despite humans having fully developed their capabilities.

Civilization is built into previous achievements: this generates an exponential growth in technologies making it easier to improve or create technologies giving that you already have the tools to create it. Think about a simple light bulb, how long it would take you to build one from scratch having to build any tool you use? Having this into account is not surprising that a fully articulated language could take thousands of years to be built from scratch.
Population size: 100-10K years ago the human population was a fraction of what it is now. This would slowdown civilization if we consider that development is proportional to the population.

The measures and reasons for the evolution of behavioural modernity https://en.wikipedia.org/wiki/Behavioral_modernity?wprov=sfla1 have generated many theories, like for the FOXP2 gene that works on human speech.
Biologically we can consider the evolution of crop species and their yields and docile livestock as a non-human evolutionary change which has massively boosted human culture into civilizations i.e. wheat, potato, corn, grape yields
If you study "the evolution of stone tools", there are theories of the full planning and workflow to shape difficult stones into fine craftmanship, which give an intuitive grasp of cultural and biological increments in technology. The crafted tools of humans changed gradually and radically over the last 70k years. That study doesnt overlap much with biology though, because of sparse biological evidence.
There are also mathematical formulas to chart the evolution of intelligence / noogenesis as a sum of the total synapses in many individuals communicating together, something that changed exponentially recently when humans made tribes of many thousands.
Tribal humanity becamy civilization. Aborigines and Maori and Papuans and tribal north Americans and Eskimo all represent different cultures of technologies and tribes.
There seems to be a synergy of many synapses communicating, when tribes group into civilized cultures of 1000ds of humans, further boosted by emergent technologies like agriculture, which is represented in indus valley/egyptian/mayan cities, which accelerates the technologies in a confusingly exponential way.


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Alleles and Ploidy
I was recently studying inheritance and variation and came across a sentence:

A diploid organism can show only two alleles

How is this possible?

@Andrew Thanks I got it. Should I need to delete this question. Or leave it as it is

"In a diploid organism, one that has two copies of each chromosome, two alleles make up the individual's genotype."

Source

Human is a diploid organism. We have 23 chromosomes. Every body cell has 46 chromosomes, one set of 23 chromosomes from mom another set of 23 chromosomes from dad. There is one chromosome number 1 from dad another chromosome number 1 from mom. Each chromosome contains in average 1000 genes. Each gene encodes a protein. For example half of the hemoglobin (the protein of red blood cells that transports oxygen) is encoded by the gene that you had from your mom, the other half of the hemoglobin is encoded by the gene that you got from your dad. In both cases you are encoding the hemoglobin, but the exact structure of the molecule can be different. These differences are representing the allele. The idea is generalized to all other 20'000 genes of the human genome encoding other proteins (such as insulin, hair, skin, retina proteins).
There are slight exceptions to everything I said which you can ignore at this stage (for example some cells do not have chromosomes, because they destroy them, and reproductive cells have only 23 chromosomes instead of 46).
Hope that this helps


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Insect Identification question: Is this a flea? If yes, what kind?
I live in the pacific northwest and I found these insects in the carpet and comforter. I suspect them to be flea based on my image search. But I would like to confirm. Can you also tell me what kind of flea is this?
1
2
3
My apologies for the grainy pictures. These are my attempts at capturing the photo from the microscope's eye piece using my smart phone.

This may be indistinguishable, thus better images may need to be taken.

It does look very much like a flea though.


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Bougainvillea flowering problem
My bougainvillea plant hardly flowers and only at the tips. It has one very long vertically growing stem(if I may call it so).

Is this an example of apical dominance.
If so how is it to be corrected?
Do I have to cut the long step?

what is the water regime? what is the climate (day length and heat)? how much sun does it get?

@Hachiloni Everyday a lot of water is added to it. It receives continuous fresh air, but direct sunshine for nearly 3 hours in the morning. In August, days are long with rain as it is monsoon here in India.

This question and others like it are much better suited to [gardening.se].

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, I'm voting to close this question because it would be a better fit for [Gardening.SE], but please don't repost (instead request migration). Thanks!

bougainvillea is a qualitative short day plant meaning that it needs long, uninterrupted nights to flower. Most flowring accours when it gets 8hrs of light (=16 hrs of night).
India is a huge country so you need to be more specific or tell us how many hours of light the plant gets. Note that if it's exposed to light from the house/street it may not flower as the light intensity for photoperiod is much smaller than that of photosynthesys.
Flowering requires a lot of energy, even if all conditions are met not enough sunlight might prevent flowering. bougainvillea loves sun, give it as much direct light as possible.
According to fao, Paclobutrazol shortens the time to flowering in long day conditions, meaning that GA might delay flowering. Another way to prevent GA synthesis is to stop watering the plant. Once the leaf start to fall give it water again.
Don't water too much:

these plants need full sun & well-drained soils. After establishing,
minimal watering is needed. Two or more irrigations with 3/4 – 1″ of
water per week would provide too much water for the bougainvillea to
bloom well.

What to do:

Give it more sun
Give it less water
Induce water stress to prevent GA synthesis
shorten the day, you may cover the plant with a dark cloth from the late afternoon to the morning

Yes, too frequent watering is what I have seen stopping flowering. I have seen them flower even growing with only indirect light. The gardening and landscaping SE is also a good place to ask. If your plant has been grown from seed, that may account for slower flowering also.


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Shrinking size of Y chromosomes
I read on the web that the size of Y chromosomes decreased in earlier period of time and the picture below tells that it is still occurring.
So basically I want to know what caused  this shrinking and if it has stopped now then what caused this break ??

you can find at least the beginnings of the answer on Wikipedia: https://en.wikipedia.org/wiki/Y_chromosome#Degeneration

@Ben Bolker what about the second part ?

Welcome to SE Biology. As a new user, you should finish reading the [tour]. Please do not post text as graphics, which discriminate against people with visual deficiencies and which cannot be indexed. Rewrite it as text.


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How do platelets produce proteins (if they do)?
I'm aware that platelets don't contain a nucleus, but do contain mitochondria (so have mtDNA) and rough endoplasmic reticulum / Golgi. Since platelets require many important cell surface proteins (such as aIIb b3 for ECM binding), are these proteins (1) synthesized de novo in the mitochondria using mtDNA, and then somehow shuttled to the ER / Golgi for secretion, (2) remnants from proteins that were synthesized in their megakaryocyte precursors and not actually created anew, or (3) synthesized via some other mechanism I'm not aware of? Online sources weren't clear on this question. Thanks!

it seems that megakaryocytes, while nucleated, create a large dormant reserve of mRNA and ribosomes, which can be used by platelets later, upon their activation. So platelets can synthesize only certain proteins already transcribed by their megakaryocyte predecessors. The reserve of mRNA decline with the platelet age.

Specific references would really improve this answer.

Please include references; even the best of answers are useless without resources to allow other users to background-read on your topics