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is there an assumption of homology?
Recently, i watched evolution vs creationism especially in islam view of evolution. There is one particular guy called subboor ahmad (he is muslim apologist). he claimed that there is an assumption of homology and that assumptions are being disputed by homoplasy. so i want to know if the statement of of assumptions of homology is actually correct or not? if not then how we can determine homology or homoplasy in first place?

That's a pretty broad question. You'd have to start with a pretty good understanding of evolution to have a more specific question. Both have occurred in evolution.

i have very basic understanding on evolution. my apologies for asking very broad question due to lack brief understanding on evolution . Thanks for sharing the info. Its very helpful for me

there is no assumption of homology, homology is a conclusion of comparing billions of features across genera, Homology not existing would require a breathtaking amount of coincidence, to not have homology it would be much closer to the tornado assembling a working 747 the creationists are always on about.

@John - Both homology and homoplasy (aka convergent evolution) have occurred (and homoplasy not even rarely.) If you want to say homology is not assumed but an absolute, that's an erroneous statement. Continued expression of lactase arose at least three times in different populations, and sight multiple times as well. This is a valid question.

@anongoodnurse I was referring to to the fact that homology exists, the apologist the OP is referring too claims the existence of homology is an unfounded assumption

@John - From my understanding, the apologist is stating that we (non-creationists) hold homology to be a given, and arguing that the existence of convergent evolution discredits homology. The answer isn't a sweeping condemnation of the apologist's take; the answer is that both have and are occurring, and that the existence of homoplasy does not negate homology. Your comment is unclear on that.

@Piee3.14 - How to determine which characteristics are a result of homology and which are convergent evolution is not simple, but it's easier now that we can do genetic analyses on samples, even old ones. And as I commented, there are examples of homoplasy even recently, such as the development of continued lactase secretion, which allows for milk to be a source of nutrition beyond infancy. This has evolved on at least 3 separate occasions in different populations, meaning it's not necessarily homologous. The page I linked to has many short articles which should be helpful.

I can´t remember to have heard of an "assumption of homology"; i studied (evolutionary) biology in Germany for several years. If I understand correctly, you are wondering how to tell homology and homoplasy apart? For morphological traits there are for example Remane's criteria (a german zoologist, he developed this in 1952), that can help to determine if a given structure (a bone or smth. like that) is a homologous structure. There is the 1. positional criterion (a similar position in a comparable system of features points to homology, i.e. how the front limbs of land vertebrates are structured and placed). The second one is the 2. structural criterion and the third one is the 3. transitional criterion ("Stetigkeit" = continuity) where you try to identify transitions/intermediate forms of a trait in different organisms. It is definitely not just assumed that similar traits are homologous, even though there are lots of traits that remain "unsolved".


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What is the evolutionary origin of euphoria and dysphoria?
What kingdoms from the three domains haven't evolved something like the reward system in us? Couldn't we feel neutral all the time and undergo an involuntary push towards the right behavior instead, without the need for joy or distress?

One question at a time, there are at least 4 separate questions here in only three sentences.

"involuntary push" towards certain behaviors to satisfy biological needs sounds like a reasonable description of mesolimbic system we do have. Like how else would such drives manifest in cognitive beings? We'd need to retain cognitive mechanisms for prioritizing conflicted drives in real time such that we don't just drop everything when we get a little thirsty or tired, but also so those drives can increase based on the severity of the need. Without varying degrees of discomfort and contentment, what would that even look like?

Perhaps it's best to equate euphoria with dopamine, because if it can be found to control sex, food choice and foraging of invertebrates, that a major piece of the puzzle:
Dopamine is believed to have evolved around 600-700 million years ago in simple organisms like bacteria. At this stage, dopamine likely had basic functions related to cellular signaling and regulation.
For worms and insects, dopamine played a role in various physiological processes, including locomotion, feeding, and mating behaviors.
In bacteria, it has pretty simple functions in several species like Escherichia coli (E. coli) and Pseudomonas aeruginosa. Although dopamine levels in bacteria are relatively low compared to those in mammalian systems, its presence suggests potential physiological roles.
Bacterial dopamine biosynthesis pathways are similar to those in mammals, involving the conversion of the amino acid tyrosine into dopamine through a series of enzymatic reactions. Key enzymes involved in this process include tyrosine hydroxylase, which converts tyrosine to L-DOPA, and aromatic L-amino acid decarboxylase, which decarboxylates L-DOPA to dopamine.
In E. coli, dopamine is produced in response to oxidative stress caused by exposure to reactive oxygen species (ROS). Dopamine acts as an antioxidant.
Studies have shown that dopamine can enhance the production and stability of the extracellular matrix, promoting biofilm formation in various bacterial species.
Dopamine can modulate flagellar rotation and affect the motility of certain bacteria. In Pseudomonas aeruginosa, dopamine has been shown to enhance twitching motility, a form of surface-associated movement.
in the honeybee (Apis mellifera), dopamine is involved in associative learning and memory formation related to foraging. Dopaminergic pathways are activated when the bee receives a reward, reinforcing behaviors associated with finding food sources.
in insects like fruit flies (Drosophila melanogaster), dopamine is involved in fine-tuning flight behaviors, such as wing movements and flight initiation, and also in arousal.
Dopamine contributes to reproductive behaviors in many invertebrates. It can influence courtship behaviors, mate choice, and mating success. For instance, dopamine affects mating behaviors and receptivity in the nematode Caenorhabditis elegans.
Nematodes are some of the simplest invertebrates, so their use of dopamine for sexual reproduction suggests that the evolution of mammalian euphoria could go back 570 million years ago.

This is kind of a  philosophical question in my opinion.
First of all, what is 'right' behaviour?
Something that may be right in one culture may not be right in another.
It highly varies from individual to individual as well.
For example if you think focussed and planned studying is a right behaviour and your brain is caught in some kind of a reward loop in a useless activity like browsing the social media which is causing you distress.
So the question arises that does studying give humans some kind of an evolutionary or biological advantage such that nature may try to evolve our minds in such a way that it is consistently able to focus on studying? I don't believe it does. We are basically same from the survival point of view whether we are browsing social media or studing as your body is surviving and functioning appropriately which is the entire point of evolution itself. If hypothetically studing gave you better survival instincts then maybe evolution could take place in that direction.
However lets take another case;
Lets suppose certain variations exist in genes coding for muscle enzymes and proteins such that some people have better stamina or strength. Over the course of evolution they are likely to be selected as it gives them some kind of an evolutionary advantage.
But the development of the complex human brain is a huge evolutionary accomplishment in itself. Maybe the development of this reward system is itself a beneficial thing and helps us to focus? It basically puts the brain on autopilot mode where we don't have to think much and keep doing things repetitively, it could have evolved to save energy and maybe nowadays we have created things that take advantage of this exact same thing.
It could be that this reward system was actually evolved for our benefit but we humans have themselves learnt to take advantage of this in other humans.

Reward is a natural process during which the brain associates diverse stimuli (substances, situations, events, or activities) with a positive or desirable outcome. This results in adjustments of an individual’s behavior, ultimately leading them to search for that particular positive stimulus.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992377/#:~:text=Reward%20is%20a%20natural%20process,for%20that%20particular%20positive%20stimulus.

If we follow along the lines of this definiton, then reward sytem development seems highly beneficial from the biological point of view.
It readily helps to distinguish between desirable and non-desirable stuff.
I strongly believe that evolutionarily it is in our best interests, it is we who are misusing it.
Another remarkable property of our brain is to get conditioned to what can trigger this response and what cannot.
Thank you.

It's not really philosophical. I wanted to ask what species did emotions like joy, sadness originate with. By "right behavior" I simply meant the things we naturally tend to do or avoid which increase our chance of survival and reproduction.

If you meant that by 'right' things then we are constantly evolving towards it. The development of senses of vision, hearing and smell and the development of reflexes are all directed towards it. Emotions are usually related with the frontal lobe and although other mammalian species and some other chordates feel emotions, humans are the ones with the most complex and complete set of emotions with the required capability and anatomical structures to express them as well. I would suggest you should read the development of frontal lobe, that will really help as well.

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What does bregma -4.36mm mean?
I am reading a journal paper. In this paper, they inject adeno-associated viruses into the brains of rats. In the below figure, there is something that I want to clarify:

In Figure A, I am not sure what is meant by "Bregma -4.36mm". I have read that bregma and lambda are two locations on the surface of the skull that allows for stereotactic identification of parts of the brain.

What is meant by the -4.36mm after Bregma? Any advice is appreciated.

4.36 mm anterior to (in front of) Bregma, it's the label for this coronal section of brain
If you look up a rodent brain atlas, the coordinates need some reference point; they typically use skull features, either Bregma or Lambda, for the anterior/posterior direction. They've likely taken their section, compared it to the atlas they have, and labeled it with the atlas page that looks most similar to the section.
The medial reference is usually the midline, so measured in mm left or right of midline. The dorsal ventral reference is typically a flat line between Bregma and Lambda, as well.

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Are all proteins translated by the RER ribosomes destined for the Golgi apparatus?
The proteins translated by the free ribosomes can fold in the cytoplasm and never go through the endomembrane system. But when the endomembrane system is described, it is always stated that the proteins are transferred from the ER to the Golgi and then to their destination. Are there any known proteins that skip that Golgi step? I've searched for a long time but could not find any information on this.


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Voltage-gated calcium (Ca2+) channels
My question is related to "voltage-gated calcium (Ca2+) channels". I don't really have a background in chemistry or biology other than basic elementary school knowledge so I'm a little confused about what kind of reactions need to take place (if any) to form the calcium cations that activate these channels. Do any calcium compounds that contain a calcium ion as part of the bond work to regulate the channels (such as the calcium found in milk) or do they have to be broken down into single calcium ions or form into specific calcium ionic compounds before they can be used for channel regulation?

Probably makes more sense to work on the background in chemistry and biology. In this case you want to learn what it means for an ionic compound to dissolve in water. Also voltage gated calcium channels aren't activated by calcium they are activated by voltage, that's why they're called voltage-gated.

Don't ions carry a charge? Where else does the "voltage" or potential difference come from? I'm assuming It takes a certain amount of charged ions to create the voltage levels necessary to open or close the gates.

You need a broader picture. I'd start with a neuroscience textbook like Purves Neuroscience or Kandel Principles of Neural Science. StackExchange is good for specific questions; it's not a good way to learn a topic backwards by starting with a question far from your understanding and working backwards to back fill.

If you explain why you're asking the question/what you're trying to achieve, it's possible someone can help you with that, but if you're trying to understand how neurotransmission works you should start from scratch.


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Datasets for Genetic Diversity of Species Across Geographical Distribution
I'm carrying out some research on applying machine learning methods to ecology and conservation. I'd like to know: are there some datasets on genetic diversity across geographical positions? Preferably:

Being well-established and trusted
Including multiple species

Information regarding any similar or related resources will also be highly appreciated. Thanks a bunch in advance, community!

To clarify; Are you asking for datasets that compare differences in genetic diversity between populations within the same species at different geographical sites?

@fileunderwater Not exactly, but I'm so desperate that it would do if there is one :-D

Ok, so what you are after are multi-species summaries of single/point estimates of genetic diversity in the different species, along with geographic location(?). Multiple estimates for each species from different populations are not necessary(?).

@fileunderwater just anything of the kind please

I’m just a bit confused, in the sense that different types of studies and reviews that contain some measure of genetic diversity shouldn’t be too rare or hard to find. If you are looking for more specific types of data, length of study periods or specific methods used that might be another thing. But your question is quite general at the moment. What about this paper or humans and primates; could this be useful to you? Osada, 2015, Genetic diversity in humans and non-human primates and its evolutionary consequences

@fileunderwater Thanks but are there larger datasets?

There probably is, but this isn’t really my area, so I don’t know. Doing some careful literature searches shouldn’t be difficult though. You best bet is probably to do some structured searches to find 5-10 studies of the type I linked and then combining the data from all of them for you training/review study.

@fileunderwater Understood. Thanks!

I'm not really sure what the scope of your research is, but if you are just trying to see if you can successfully apply "machine learning methods" to certain datasets, have you thought about just generating the datasets? Forgive me if I'm making wrong assumptions, but it just seems strange for relevant datasets not to be provided by whoever might interested in gaining real insights on "genetic diversity across geographical positions". Isn't your research overseen or financed by an institution? Just hard to believe that hunting for data would be a more significant part of your study than applying whatever machine learning algorithms are necessary.

Thanks. Sorry I didn't make the scope of my research clear. I want to use methods on REAL data instead of generated ones to evaluate their effectiveness in the task. In other words, the "real insights" you mentioned is the genuinely key part of our research.

Oh and regarding the institution part, our research is funded but they are interested in the methods. So WE need the results for validation, but the funders aren't so much interested in the detailed results of one single test.


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Reason for sorbitol synthesis in human body
Sorbitol has been proved to be a major contributor to development of complications due to chronic diabetes.
It forms in retina, lens, kidneys, peripheral nerves, ovaries and seminal vesicles by the action of aldol reductase on glucose. It only forms sorbitol when glucose concentration gets high as it has high Km.
It is seen that it accumulates in retina, kidney, lens and peripheral nerves as they lack the enzyme sorbitol dehydrogenase to convert it to fructose however ovaries and seminal vesicles have it so they are saved from accumulation.
Sorbitol accumulates and the membranes being impermeable to it, it results in drawing in of water by virtue of its osmotic activity.
I wonder why is it even being formed in the first place in retina, lens, kidney and peripheral nerves when it serves no function there?
I tried searching for any possible functions it may have in these tissues but apparently it has a role only in formation of fructose for sperms in seminal fluid.


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What's the fastest dinosaur? and what properties make it so fast?
I am a new user.
I was curious about the fastest dinosaur that existed during the Mezozoic era.
However as I researched, via Google, I was unable to find any precise information as few of them gave the title to, Troodon, other to Velociraptor, others refer to NanoTyrannosaurus. (According to my personal research, I find 3 dinos in the first place since the run at the same speed of approximately 80 kmph, Nano T-Rex, Troodon and Gallimimus as suggested in the comments, I don't think Velociraptor is classified as the fastest because they run at almost half the speed as the fastest ones. I was looking whether is there any better estimate of their speeds which keeps only 1 at the top)
So who is actually the fastest dino (including both  Saurischia and Ornithischia dinosaurs i.e regardless of hip structure. Also I want to know whether the fastest ones are generally bipedal or quadrupedal ,Probably Bipedal because the fastest dinos fall under the category of theropods?)?
Thanks!

On our current Earth, birds of prey stooping can reach up to 200 mph/320 Kph. We can measure that with scientific instruments as it happens. What kind of an answer are you looking for considering the time elapsed since any of these creatures were around? Also consider, estimates vary and experts disagree on what might have been possible.

@JiminyCricket. Thanks for telling me about that. I think that There should be some genes, that make a theropod so fast, like myostatin inhibits muscle growth, there must be some ancestor whose mutation caused the agility of theropods in the gene pool. I would like to know about that ancestor of current living dinosaurs a.k.a birds.

You should note that the earliest/oldest DNA we have been able to recover is about 2.4 million years old and is not from fossils, but frozen in permafrost. Dinosaurs became extinct 65 million years ago and all the remains we have are fossilized, which does not preserve DNA, not even promising amber samples (a la Jurassic Park) have been shown to contain DNA that is older than a few thousand years. This means no chance of working out genes!

@bob1 Thank you for telling me that. But I have a question: Would we able to study the fast dinosaurs by studying the fossils, maybe we have found, similar hip, leg structure for the fastest ones? Then perhaps we could trace the earliest dating source and compare living specimen, birds to find the gene?

Potentially yes, but it would take lots of modeling of locomotion of each species to work out speeds - paleontologists can't even agree on whether T-rex was an active hunter and speed or if it was a scavenger and slow walker, and that's one of the more studied species.

Ichnology, (study of dinosaur traces e.g. footprints) is one of the things being explored with technology, but some limitations are the few samples available compared with the totality of extinct life, and the uncertainty of CG models built on fuzzy data.

@bob1 So according to our current technological capabilities, we won't be able to figure out the speed of the fastest dinos? Will we able to estimate it in the near future?

We can refine the techniques we use to study the currently available data including comparisons to extant species, but unless we get a time machine to get first-hand data, we're still working with speculative (but informed) models based on a limited data set.

@JiminyCricket. Thank you for telling me that. So was ichology performed on theropods, and related species?

It's like detective work of a crime that happened hundreds of years ago and without any witnesses when the evidence has been trampled by elephants. We work with the traces available and it's the best educated guesses as to what creatures they belonged to. Footprints seem to match what we know of fossils - but it's not as if they conveniently own-up to who's footprint belongs to which species. That's why there's so much varying opinion between experts, the data is, as I said, fuzzy.

@JiminyCricket. Ok, Thanks for letting me know that. So, because of our technological capabilities we won't be able to find the neither the gene nor the ancestor who caused the mutation . Please don't mind my questions since I am a newbie in this field (I have just 1 last doubt), but can we estimate it using osteology, and skeletal analysis from their fossils just how we found for some theropods like troodon and Nano-TRex?

Let us continue this discussion in chat.

There's an interesting paper that might help you get an idea of the state of the art re genetic paleobiology: Ancient DNA and paleogenetics: risks and potentiality. It might help give you an idea of the limitations that are being worked with - notice that in the long-term, the DNA degrades by itself from thermal noise. Thermodynamics puts a limit on how long it survives, the length of fragments limits the ability of reassembly on a computer. This isn't the place for discussions (however interesting), but so dig into the topic.

question for a paleontology forum. gallimimus was allegedly about 80kph.

@JiminyCricket. Thanks. The paper is quite interesting, I will read it to get to know more about it

With many competing ways of reconstructing and estimating speed, combined with how many dinosaurs just have not been studied in this way this is unanswerable.


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What portion of the human genome is dedicated to the developement of the fetus?
I was thinking about how we don't know the function of a large portion of DNA and I thought maybe it's because it's only used during the development of the fetus

"Only used during the development of the fetus" fetus dev is pretty important, no? Depends a lot on what you mean by "dedicated to". Not much of the genome is "dedicated to" an artificial human concept. But this random paper estimates that in fish (a developmental model similar to humans), 5-10% of genes are not only used in but critical to development. This is a subset, and in humans there's more neural development, and genes != genome, but that's a start. (It's recommended to do a little googling before you ask a question.)

I'm guessing this question is coming from misunderstanding "junk DNA" etc and not realizing that there is no confusion about any DNA that codes for proteins that could lead to "missing" some because it's only used in development.


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Living in Singapore, what’s this bug? Found an identical one in my house on the floor

Hi! I’m living in Singapore (Southeast Asia). Found a small brown bug with a prominent dark stripe on its back like the pictured one, about the size of half a grain of rice. It was wandering around on my living room floor and I have no idea where it came from. I live in a high floor apartment.

This is a beetle. They typically have hard wings (so-called elytra) that distinguish them from many other insect groups. Globally, there are almost 200 described beetle families with more than 300,000 species - so, I can't even tell the family, sorry. But most likely, it was in your appartment accidentally.


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What are these semi transparent pill-shaped things in the Mediterranean Sea?
I was swimming with gopro in Sardinia, Le Bombarde beach in early November and today was reviewing footage - I noticed that water is full of semitransparent whitish "pills", see pictures below.
Any idea what that is, is it seasonal, has any implications to people taking a swim?
Jellyfish nearby should give approx idea of the size, seems something like 1-2cm long.

Quick guess based on your low-quality photo:
Reminds me of a pyrosome, a tube/rod-shaped, free floating colonial tunicate.
According to here, Pyrosoma atlanticum is the only species found in the Mediterranean.

 Image Credit: amutti; Source: inatrualist

 Image Credit: Megan Mariposa; Source: inatrualist
See iNaturalist,National Geographic and Project Noah for images of similar body shapes.

Unbelievable! Can you earn the ID badge twice?

@anongoodnurse :p. thanks! I should go earn it on Outdoors.SE ha! ;)


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Trying to find information about intraspecific allelic expression divergence in recombinant individuals due to changes in the cis regulatory regions
I am trying to find any research articles or resources that focus on differences in expression levels at the allelic level due to changes in cis regulatory regions in recombinant individuals. For example, when recombination occurs near a gene it can cause the promoter regions from the two parental alleles to swap places, which can then affect binding affinity so that one parental allele is preferred over the other and is thus over-expressed. I've seen work that deals with various hybrid crosses that show differences in parental allele expression. But I am curious if there is anything that shows how expression patterns can flip in a recombinant individual when compared to the expression patterns in the hybrid of the parental haplotypes. Further, I'm curious if this happens in a tissue specific manner, i.e. can the same gene have one allele that is overexpressed in Tissue 1 (the paternal allele can be preferred in this tissue), and then the same gene has the opposite expression where the maternal allele is overexpressed in Tissue 2. This is in a case where trans-acting factors are controlled for to ensure that differential expression is due to changes in the cis-regulatory regions. Hopefully my question is clear, if it isn't I can clarify. Thanks for any help!


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Building a better cell detection interface
First of all, i dont know if the following request is allowed within the guidelines of stackExchange, but i will post it and delete it if deemed necessary.
I am a student (computer science) who was tasked to build a program to count cells in an image. pretty straightforward. This task was given to me because imageJ was not accurate enough and because the researchers wanted to determine the ratio of cells that are in fibers and out of the fibers. you can see an example image normally that illustrates this (down below, not the same image as the researchers were working on, but from the internet, but analogous) .
Now, i was wondering if there's a great need for such a thing to make a website version of this program. It outputs an excel with the count of the cells and the ratio between the cells in and out of the fiber.
So , i wanted to ask people who are in this domain, if they would like to have such a program on the web. It uses deepcell as the model algrotihm. (the original website of deepcell isnt that great and doesnt distinguish between the cells in fiber and out of the fibers. )
if people do have a request for me to build something which imageJ lacks or something unrelated, i am glad to hear you out as well.

Note: the same question was asked in one of reddit's communities.
https://www.reddit.com/r/labrats/comments/14qlza4/building_a_better_cell_detection_interface/

I think a service like that would be generally valuable.  The problem I see is the variability that such a service would have to contend with: The cross product of the number of microscopes (and their settings), cell lines, culture conditions, and stainings is pretty big, meaning the service would get images that are very different on the pixel level.  Solving that task for one particular point in that space isn't so hard.  Solving it for the entire space may be.


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How long does it take for a gene to be switched on or off through the process of epigenetic expression?
I understand that in our lifetime, our experiences affect the expression of our genes. Some get switched on, while others switched off. Our experiences, diet, lifestyle etc. determines this expression of genes, but my question is, how long does it roughly take for such an expression to take place? Let's say you are a raging alcoholic suffering from chronic stress. Because of this lifestyle, certain genes get turned on. Then after a decade or two, you decide to change. You start eating healthy, you exercise, you change your lifestyle completely. How long would it now take for your new lifestyle to cause a different gene expression?
I realize this could be a silly question, but this is my understanding of how things work.

Have you Googled this question searching for an answer? One of this site's requirements is that the OP show evidence of searching for an answer (which usually means a quote with a link to the source.) Strange, maybe, for a Q&A site, but it helps us know where you are in understanding a topic. Not all epigenetic changes are alike; many are permanent, and some are even passed on to offspring!

If I had found an answer to my question, why would I be posting here? I'm sure the answer can be found somewhere, it's just that I don't want to read 100 pages of hard core research just to find a short 1 sentence answer to my question. Isn't that why Q&A sites exist? I still don't see the answer to my question in the link you provided. I also don't understand what you mean by being epigenetic changes being permanent. My question is not whether they are permanent, but how long does it take for such an expression to take place. Just give me some rough estimate.

"Isn't that why Q&A sites exist?" Not this answer site, obviously. And if you didn't find the answer in the link I provided, you can't have read it. It addresses your question about smoking exactly, and the other is easily inferred. There are few one-sentence answers in Biology. If they could be answered in one sentence, you should be able to find it very easily.

The smoking was just an example. I am mainly interested in chronic stress, and what genes could get expressed because of it, and if hypothetically your situation changes, how long would it take before bad genes get muted again.

Read the link!!!


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Database or model for plant nutrient requirements with respect to soil and climate?
Microalgae are organisms that can grow in aquatic environments and use light and carbon dioxide (CO2) to create biomass. Research showed that Microalgae biomass can be used as a bio-fertilizer.
My mission is: to find which plants in the world are best suited to arid climates and to arid soil that was treated using the Microalgae biomass.
With the help of a Reddit hero "CarverSeashellCharms," I was able to model which plants in the world can adapt to arid climate/arid soil based on a theory in biology named Species Distribution Modeling (SDM). This model takes in the geographic occurrences of a given plant in the world and based on the soil characteristics and climate variables, it can predict the probability of growing that plant (suitability) at any point in the world. The problem here is: this model considers only the soil characteristics and the climate variables without considering the Microalgae biomass (bio-fertilizer) effect.
So this is my approach to how to model the bio-fertilizer effect:
I'm into calculating a score that models the bio-fertilizer effect (effectiveness) and determining a new final score based on the suitability probability and the bio-fertilizer score.
Let's assume the following values:
Plant Nutrient Requirements:
Req_N = 0.3
Req_P = 0.05
Req_K = 0.2
Soil Chemical Characteristics:
Soil_N = 0.15
Soil_P = 0.02
Soil_K = 0.1
Fertilizer Chemical Characteristics:
Fert_N = 0.1
Fert_P = 0.02
Fert_K = 0.15
Step1: Calculate the nutrient deficiencies/excesses in the soil compared to the plant's requirements:
Deficiency_N = Req_N - Soil_N = 0.3 - 0.15 = 0.15
Deficiency_P = Req_P - Soil_P = 0.05 - 0.02 = 0.03
Deficiency_K = Req_K - Soil_K = 0.2 - 0.1 = 0.1
Step2: Calculate the nutrient contribution of the fertilizer to address the deficiencies:
Contribution_N = min(Deficiency_N, Fert_N) = min(0.15, 0.1) = 0.1
Contribution_P = min(Deficiency_P, Fert_P) = min(0.03, 0.02) = 0.02
Contribution_K = min(Deficiency_K, Fert_K) = min(0.1, 0.15) = 0.1
Step3: Calculate the overall nutrient contribution score (F):
F = (Contribution_N / Fert_N) * (Contribution_P / Fert_P) * (Contribution_K / Fert_K)
= (0.1 / 0.1) * (0.02 / 0.02) * (0.1 / 0.15)
= 1 * 1 * 0.6667
≈ 0.6667
Step4: Calculate the new score based on the suitability probability and the fertilizer score:
Let's say the suitability probability of the plant is 90%. w_s and w_f are 2 weight coefficients.
New Score = (w_s * S) + (w_f * F)
= (0.8 * 0.9) + (0.2 * 0.6667)
≈ 0.85334
The problem here is: To deploy and calculate this score I'm missing The plant nutrients requirements. How to determine the nutrient requirements (needs) of a plant (ex Indian fig, potatoes, ..) in terms of nitrogen (N), phosphorus (P), and potassium (K)... I mean how much nutrients a plant needs on average to grow. I know that the nutrient requirements of a plant can vary depending on factors such as soil fertility, and growth stage, but is there any database or any mathematical model that can model the nutrient requirements of a plant with respect to soil and climatic characteristics?
Note: I'm not a biologist, Just a data science Student. Sorry if the post is too long. I'm open to any biology/math resources and any other inspirations or approaches.

Not sure exactly what you're looking for, but I can at least suggest the following:
https://www.try-db.org/TryWeb/Home.php
TRY is a worldwide plant trait database providing free and open access to plant trait data.


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Masking tape for ELISA plate cover?
Has anyone ever tried using masking tape to cover their ELISA plates while shaking? Is this an acceptable substitute for conventional plate cover tape? I'm running hormone assays in a pinch and was just wondering!


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Weird Insect on Window, SW London
Insect is avout 5 cm long, antenna to tail, was on a windows. Tried to transfer to white paper, but it moved to a wall[

The overall appearance and shape points to a mayfly (in Ephemeroptera). However, I don’t know what species it is.


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Booger like things growing on my walls
Can someone help me dealing with this? They're constantly growing on my walls whether I clean them or not. They're very solid.

I live in Yerevan, Armenia. The place where these creatures are, is my apartment which was renovated before I moved here. They've been more than just these two, I removed them but they're still growing. The size is similar to booger size, some of them might be bigger, so 3cm+ and as for the photos, it's required to post no more than 2mb and I don't know how to post a better quality as I only have a phone.

Magnifying glass? Also, please [edit] your post to include your additional info. Thanks

@theforestecologist I don't have a magnifying glass. Do you have an email that I can send photos? I'm trying to take better quality photos with more than 2 megabytes that are not allowed here.

No email. You could try cropping them to reduce size.

Do you think these could be mold?

if you crop the pictures before uploading them they will fit,what type of material is in the walls,concrete,wood,stone?

@trondhansen it's mostly concrete covered with wallpapers. They're mostly growing on wallpapers and rarely on fabrics, however one time I saw it on my tv screen. I stripped that off from the tv screen and after 1-2 days I saw it's grown again the same place on screen. I removed that and cleaned the screen with alcohol and it never grew again.


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How can one use motility testing as a practically reliable test for organisms identification in bacteriology?
Background information:
The motility test is used to determine whether an organism is motile or non-motile. There are three types of bacterial motility *:

Active movement: true motility that we are testing
Passive movement: Drifting of the organisms in the same direction along the convectional current in the fluid
Brownian movement: It is an oscillatory movement about a nearly fixed point possessed by all small bodies suspended in fluid and due to irregularities in their bombardments by molecules of water.

* Sastry, A. S., & Bhat, S. K. (2017). Essentials of Practical Microbiology. JP Medical Ltd.
Question:
How can one use motility testing as a practically reliable test for organisms identification in bacteriology?
In other words, how to differentiate true motility from passive and Brownian movements?
Specifically, i'm screening for non motile bacteria.


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When an action potential reaches an axon terminal
I came across the following question in my study of action potentials in neurons:
When an action potential reaches an axon terminal:
A. Na+ channels close.
B. K+ channels open.
C. The interior of the cell becomes positively charged with respect to the exterior.
D. Options A and B are correct.
The correct answer is apparently C. But I want to know, how?
I know that action potential causes part of membrane of the axon to become positively charged with respect to the external environment, moving across the membrane (such that when it reaches another part, the previous part returns to its previous negatively charged state) toward the axon terminal.
This question seems (as far as my understanding goes) to refer to the repolarization of the membrane (as the action potential has already passed through the entirety of the axon, so it cannot to my knowledge cause a positive inner charge in the neuron anymore). If that is so, then the peak of depolarization has already been reached. In order for the neuron to reattain its resting potential, repolarization has to occur, which includes the closing of Na+ ion channels and the opening of K+ ion channels.
I might be mistaken, but I would say the answer is D.

You are mistaken. The question is asking you about what happens in the axon terminal when an AP arrives there.

Think about how neurotransmitters are released into the synaptic cleft. Whenever something is being released from the cell, think about increasing intracellular $\ce{Ca++}$ level similar to what happens with platelet release reactions.


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Are there any Bilateria directly able to photosynthesise? If not, are such feasible/possible?
I'm trying to think of a type of animal, easily understood, that does not (and never has) existed, but that could feasibly exist. As most non-bilateral animals are complicated for a child, I was considering merely bilateral, and thought that it might be possible for an animal to directly photosynthesise (even if only as a partial energy source).
My guess is that there are/could be symbiotic relationships that do exhibit photosynthesis, hence the qualifier 'direct'.


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Why am I getting a large horizontal band spreading across my native gel?
On every gel of this type that I've ran so far, I'm getting this large band interfering with my gel analysis no matter how much troubleshooting I've done. This is a Novex Wedgewell 6% Tris-Glycine Gel and in each well I've loaded 10ul of the Novex 2X Native Tris-Glycine Sample Buffer + 10ul of my sample. I ran the gel at 100V for 1hr at 4C. This image is from under a Fluorescein Blot filter.
I've troubleshooted the gel by pre-running it and also trying to load without any 2x loading buffer, but the band has still remained.


text:
What is the linear force in a bicep compared to the force at the hand?
So I know that like most joints, the bicep applies a force near to the pivot (the elbow) and creates a rotational torque in the elbow, this moving the lever, your forearm and hand. Due to the biceps close proximity to the pivot it at a considerable mechanical disadvantage compared to a downward force on the hand meaning linearly, muscle are a lot stronger than we think. Assume somehow you could take out a bicep, for example mine that has a max curl of 25kg dumbells, and hung it from an anchor point, removing the pivot. What would be the maximum linear force of that muscle? E.g. would it be 4x stronger than the torque in the elbow that's applied at the hand and therfore lift 100kg?
Sorry this question is a bit confusing. I really didn't know how to describe this hypothetical scenario. I hope you understand what I am trying to ask.

Are you essentially asking for the summed force of all myosin-actin cross bridges of an average bicep outside the context of the body?

Also, you must recognize that the strength of a person's bicep can vary greatly between different people -- wouldn't you expect such variability to also exist in terms of your question's scenario?

Lastly, given my two above comments, might I suggest you rewrite/rethink your question slightly differently? I suggest focusing on the pulling force of a single actin-myosin cross bridge. You could simply multiply whatever value that is upward based on some average number of cross bridges per sarcomere/myofilament/myofibril/fiber/fascicle

My answer is in the context of my comments posted under the main question. I tried scaling up forces throughout the muscle. I probably flubbed one or more things, so check my math and suggest fixes!!
TL;DR: The max linear force of an average male bicep is ~1600 Newtons.
The longer explanation:

VanBuren et al (1995) estimates ~0.2 pico-Newtons per cross-bridge.

In a direct comparison between smooth and skeletal muscle myosin, the average force per cross-bridge was 0.8 and 0.2 pN, respectively. Surprisingly, smooth muscle myosin generates approximately 4 times greater average force per cross-bridge head than skeletal muscle myosin.

The multiplication*:

Note: Muscle fiber anatomy has been detailed quite robustly: AL-Khayat 2013, Wang et al 2018, Mijailovich et al. 2019

Ojima 2019 claims each thick filament is formed of approximately 300 myosin heads. (though, I've seen less reputable sources [e.g., here] suggest as high as 500 without further support).

Ojima 2019 also claim each thick filament is ~15nm in diameter and 1.6µm long. AL-Khayat 2013 agrees on length, but suggests this could be as large as 30 nm in diameter. Szikora et al 2022 claims the length is consistent/conserved around 1.65μm across vertebrates.

We'll stick with the minimum suggestions: 15 nm x 1.6µm.

Also, note that AL-Khayat 2013 suggests actin filaments are ~10nm in diameter.

Higuchi et al. 1991 suggest myosin heads are 19nm long,while AL-Khayat 2013 suggests 15nm each.

Gerling & Brown 2013 found sarcomere lengths (at least in human latissimus dorsi) to have an average length of 2.7μm, while Dasbiswas et al 2018 suggests "The sarcomeres in relaxed human skeletal muscles are between 3.0 and 3.4 µm long, depending on the muscle sub-type." So, let's assume 3µm.

Previously, the force produced by a skeletal muscle myofibril was assumed to depend on cross-sectional area alone and not on the number of active sarcomeres (because of their arrangement in series). However, Mendoza & Rassier's (2020) results suggest that myofibril force is affected by intersarcomere dynamics and the number of active sarcomeres in series. As such, the total number of sarcomeres per volume of muscle is likely important.

AL-Khayat 2013 suggest vertebrate skeletal myofibrils are typically 1–2 μm diameter and 2–50 mm long.

Regarding Diameter:

Smith & Plowman 2007 note: "in regions where the thick and thin filaments overlap, each thick filament is surrounded by six thin filaments and each thin filament is surrounded by three thick filaments." If each thick filament is 15nm diameter, each thin filament is ~10nm in diameter, and each myosin head (i.e. space between filaments) is 15 nm, it would suggest each myosin and actin complex would be approximately 65nm in diameter. That would be a maximum of 15-30 actin-myosin complexes per diameter of myofibril. So let's stick with a conservative 15.

Regarding length:

If sarcomeres are an average of 3µm in length, 2–50 mm long myofibrils suggest an average of 667 - 16,667 sarcomeres per myofibril. The average is ~8600 sarcomeres per length.

Putting length and diameter together, this would suggest that each myofibril might contain 15 x 8600, or ~130,000 thick filaments on average.

130,000 x 300 = 39 million myosin heads per myofibril.

Chen et al 2017 state: "the number of myofibrils ranges from 50 per muscle fiber in the muscles of a fetus to approximately 2000 per fiber in the muscles of an untrained adult."

This would suggest 39 million x 2000, or 78 billion myosin heads per muscle fiber.

There seems to be a couple hundred thousand fibers in human biceps:

Klein et al 2003: "The estimated number of muscle fibers in the biceps ranged from 201,360–312,708 in the young men and 149,301–291,501 in the old men"

MacDougall et al 1984: "There was a wide interindividual range for fiber numbers in biceps (172,085–418,884), but despite large differences in muscle size both bodybuilder groups possessed the same number of muscle fibers as the group of untrained controls"

The average is around 280,000 fibers per male bicep.

280,000 fibers x 178 billion myosin heads per muscle fiber = 2.2 quadrillion (2.2x1016) myosin heads in a biceps.

This equates to 2x10-13 N per cross-bridge x 2.2x1016 cross-bridges possible, or 4400 Newtons.

But, Mettikolla et al 2010 suggests only about 1/3 of cross-bridges are active at any time during isometric contraction:

These results imply that cross-bridges interact with actin in bursts and suggest that during active period, on average 36% of cross-bridges are involved in force generation

This suggests we should divide our above outcome, 4400 N, by 36%:
As a result, my math suggests ~1584 N per bicep

*MAJOR CAVEAT: Moo et al 2016 suggests that my above approach is faulty:

Sarcomere lengths have been a crucial outcome measure for understanding and explaining basic muscle properties and muscle function. Sarcomere lengths for a given muscle are typically measured at a single spot, often in the mid-belly of the muscle, and at a given muscle length. It is then assumed implicitly that the sarcomere length measured at this single spot represents the sarcomere lengths at other locations within the muscle, and force-length, force-velocity, and power-velocity properties of muscles are often implied based on these single sarcomere length measurements. Although, intuitively appealing, this assumption is yet to be supported by systematic evidence

We showed that sarcomere lengths varied substantially within small regions of the muscle and also for different sites across the entire [muscle]. Also, sarcomere elongations with muscle lengthening were non-uniform across the muscle, with the highest sarcomere stretches occurring near the myotendinous junction. We conclude that muscle mechanics derived from sarcomere length measured from a small region of a muscle may not well-represent the sarcomere length and associated functional properties of the entire muscle

This link I found answers my intended question fairly well and simply.
https://courses.lumenlearning.com/suny-physics/chapter/9-6-forces-and-torques-in-muscles-and-joints/


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Does binge watching cause sleep problems?
According to a study from 2017, binge watching is correlated with various sleep problems:

The people who reported binge-watching were 98 percent more likely to report poor sleep quality compared with those who watched one episode per sitting, according to the findings.

However, the study only showed a correlation and did not touch on causal inference:

The study authors did clarify that there were limitations to the study since they saw only correlation between binge-watching, and not evidence of causation, or that binge-watching definitively causes poor sleep.

Is there a study that investigated whether or not there is a causal relationship between binge watching and sleep problems?

Science cannot prove. That's neither the purpose of science nor is it a possibility. 2. You will not typically see causation discussed in scientific literature. Instead, we tend to discuss correlation,so a paper showing strong correlation is a good starting point. Keep your eye out for more papers demonstrating corraborative data/analysis to increase your confidence of this linkage (but always remain open/dynamic in your thinking as alternative trends may be later demonstrated).

Can’t causation be demonstrated by randomized controlled trials?

According to the national library of medicine: ‘Although no study is likely on its own to prove causality, randomization reduces bias and provides a rigorous tool to examine cause-effect relationships between an intervention and outcome.’ Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6235704/#:~:text=Randomized%20controlled%20trials%20(RCT)%20are,between%20an%20intervention%20and%20outcome.

I have to partially disagree with theforestecologist on their comment. It's true that Proof is generally the stuff of philosophers and mathematicians. But there is plenty of scientific literature seeking to establish and describe causal relationships, especially in medical research. Kochs postulates are one such approach that's been widely utilized for nearly 140 years for infectious disease research and frequently adapted to provide similar frameworks for different biological systems. Hill's criteria for causation are another example that's probably more relevant to this topic.

Should I modify my question to let the downvotes disappear?

The question if somethings that are correlated are causally related is definitely a valid question and prospective studies, for instance, increase the chances of deducing causation. So I also do not share all of the views expressed by others here in the comments.


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How are the muscles of some dead animals still able to function for an extended period of time without oxygen?
I found this video on youtube that features several butchered and sometimes cooked animals that are still able to move despite of this. Some of these animals have been dead for several hours already but they're still able to move, like this frog or this chicken filet. Other animals still display movement after they've been cooked in the oven, like this fish.
These aren't just random movements either. Some of the animals still seem to be able to respond to aversive stimuli as well. An example of this is the decapitated fish at 0:30 that only starts moving when its being sliced by a knife. Another example is this this dried fish at 1:21 that starts moving its mouth when a bit of water is poured
over it.
So how are these dead animals still moving without their muscles receiving any oxygen? I've looked up how long muscles can survive without oxygen. In humans this appears to be 60 to 90 minutes at most. Perhaps the same goes for many other vertibrate species. But the compilation even shows cooked animals still able to move. So how does this work?

Check out muscle metabolism.

@theforestecologist how is this an answer?

It's not. It's a comment. I think you'd benefit from reading about the different pathways/mechanisms of muscle metabolism. You might find particular interest in anaerobic glycolysis

Please take our [tour] and visit our [help] to further understand how the site works. Thanks


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Understanding infection rate of a complex network
Suppose we have a complex network of people and  the spread of a disease is modelled as a branching process (Diekmann et al. 1998)
The rate of infection of the complex network is:
$r = \tau(n-2)-g$
where $\tau$ is the infection rate of the disease through 1 person
$n$ is the # of people in the network
and $g$ is the effective # of people / sec.
What does $g$ mean exactly?

I didn't try particularly hard to find it, but I was not able to find the equation you include in the paper. Potentially you might need to share the exact source of the equation. After going through this (rather superficially) I think that you are mixing up the units and the definitions of your terms.
I'm not an epi person so someone with better credentials should feel free to fill in / correct.
Regardless, the paper does provide some definitions for a quantity $g$ in equations 4.2-4.5, and provides some motivation in the following statement:

We can use a branching process approximation to give a slightly more detailed description of the initial phase of an epidemic. Given ξ and given that the infective individual has k − 1 susceptible acquaintances, the probability that it will infect j acquaintances is equal to [Eqn 4.1, which is complicated]...

and then

The probability π that this process goes extinct when we start it
off with one individual can be found as the solution of the consistency condition

$\pi = g(\pi)$ (Eqn 4.3)
(see Eqn 4.4 as well)
$g$ is effectively a summation across that Eqn 4.1 with some extra decoration (including a term $z^{j}$ that they don't define very well but which I believe is the probability of not infecting any of $j$ individuals?), such that they then say

The conditions g(0) > 0 and g′(1) > 1 guarantee that 0 < π < 1. Note that for the present definition of $p_j$

$ g′(1) = (k − 1)Q = R_0$.
Where $Q$ is the overall probability of transmission, $k$ is number of individuals in a group, and $R_0$ is the familiar minimum viable reproductive rate.
I'm not going to stare at these equations any longer, but suffice it to say that $g$ appears to be a description of the now-unsusceptible (previously infected + immunized) population- when one more person gets infected, there is one less person who is susceptible (under this model, anyways).


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What is the exact definition of a "gene"?
(In this question, I'm only considering the molecular-biology notion of a gene, not the older Mendelian notion.)
Wikipedia defines a "gene" as "a sequence of nucleotides in DNA that is transcribed to produce a functional RNA", and an "allele" as "a variation of the same sequence of nucleotides at the same place on a long DNA molecule". Typically, one says that different alleles can be different "versions" of the same gene.
Taken literally, these definitions imply that both a "gene" and an "allele" are fully specified by their base pair sequences. But this contradicts that notion that different alleles can be different "versions" of the same gene - which implies that the notion of a "gene" is more general than that of an allele, since different alleles can correspond to the "same" gene.
The notion of "same place" in Wikipedia's definition of an allele seems to suggest that a gene is characterized by its location within a DNA molecule. I.e. two different alleles correspond to the "same gene" if they occur at the same locus on a chromosome.
So what exactly specifies the boundaries of a single gene, i.e. what specifies which alleles correspond to that gene as opposed to a different gene?
Put another way: what is the minimal amount of information required to fully specify a gene? It can't just be a base pair sequence, because that instead seems to define an allele. Is it a particular genetic locus? Or is it defined functionally, i.e. a set of alleles are instances of the "same" gene if they all code for RNA strands that are functionally similar/equivalent? If it's the latter, then is there a precise way to define "functionally similar/equivalent", or is there there some degree of subjective convention in demarking different genes? (If one allele leads to a healthy organism and another allele leads to a nonviable organism, then those seem very functionally different - so is it meaningful to say that those alleles are variations of the "same" gene?)
Or is the resolution just the empirical fact that the functional purpose of a protein is so well-correlated with the locus of its encoding DNA that we can be imprecise about specifying whether the locus or the function defines the gene?
(I've also seen the notion of a "gene" defined purely phenotypically, as in the older Mendelian framework. But my understanding is that in reality, quite few phenotypic parameters are directly controlled by individual genes - most arise from complicated polygenetic interaction effects. So it seems that in practice, a purely phenotypic characterization can't precisely demarcate individual genes.)
Yet another way to frame this same question: is "allele" or "gene" the more primitive concept?

Too many questions at once. Can you focus a bit?

I'm not following your reasoning. A dog is a dog. A Border Collie is a dog, as is a Poodle. And a Chihuahua, a Mastiff, and a Belgian Tervuren. Does that mean a dog isn't just and fully a dog? Does that mean more is required to define a dog? Does the fact that they are all so different mean that "dog" is an impossibly imprecise definition? If a dog is born with a heart defect causing death, was it really a dog? Or is it our quotidian way of thinking about dogs that allows us to be imprecise about what a dog is? This seems to be your logic. Please forgive me if I've misunderstood.

@alec_djinn There is only a single distinct question here, which I framed in several different ways in order to clarify what I meant to ask. Unfortunately, it doesn't seem to have worked.

@anongoodnurse You have misunderstood. Up to a few nuances, there is a simple characterization of whether two animals are the same species: whether or not they can interbreed. What is the corresponding equivalence relation that determines whether or not two alleles are the same gene?

@tparker And you have made the all-too-common mistake of assumint that, because I posit something contradicting you, that I "don't understand." I understand quite well, thank you. Two alleles are even more alike than two dogs.

@anongoodnurse You literally said "I'm not following your reasoning", thereby admitting yourself that you don't understand my question. This is not a criticism of you or your biology expertise; maybe my question was unclearly posed. But you are incorrect in assuming that I said "You don't understand" because I contradicted you; I said "You don't understand" because you said that you didn't understand, and then confirmed that with your subsequent sentences.

I was being polite. Instead of coming right out and saying, "This is really misunderstanding genetics," (which it is), I was deflecting to allow you to reconsider. My analogy stands.  Just as dogs which are different in appearance are still wholly dogs, genes coding for a specific functional protein but with differing base pairs are still wholly genes. You're reading too much into the whole thing; that's what the analogy shows.

Folks were identifying genes for 75 years before we understood the role of DNA in heredity. Originally genes were defined as the unit of heredity from back when Mendel posited that the mechanism of inheritance was pairs of indivisible particles, each pair acting in combination to control one heritable trait.

In this question, I'm only considering the molecular-biology notion of
a gene, not the older Mendelian notion.

That's where it begins to get confusing. It's not like we discovered DNA and then went back and re-worked all of our thinking about genetics to be in terms of DNA sequences rather than Mendel's abstract gene. People still do a huge amount of classical genetics: looking for interesting traits that breed true. They may eventually start looking for the underlying DNA sequence responsible for the trait, but that can still come very late in the game. That means people still often use the term 'gene' in the purely Mendelian sense: the unit of control for a heritable trait.
Of course the discovery of the role of DNA changed things. At the crudest level the model went from
One gene determines one heritable trait
to
One gene determines one protein
As the model became richer and we became aware of things like alternative splicing and lncRNA that was modified to
One gene determines (at least) one protein or one non-protein-coding RNA that has a structural, regulatory, or catalytic function.
Part of your difficulty may be that you aren't appreciating how subtle and complex simple concepts like "the same" or "similar" are when applied to biology. Two proteins or two DNA sequences may be considered "the same" without being amino acid for amino acid or base for base identical. It usually means "indistinguishable for the context in question". If we talk about a "gene for hair pigmentation", we care that the protein generated by the gene controls the color of the animal's hair, but we don't necessarily care whether the hair comes out as blonde or brunette. At other times that subtle difference is exactly what interests us, and we'll talk about the blonde allele or the brunette allele.
You can find plenty of formal definitions for the gene in references and text-books. However in actual usages people are pretty careless about what they call a gene.
My own take is that a real definition of the 'gene' is multi-level:
A gene is the unit of control of heredity  which is implemented as a    sequence of DNA bases which directs the synthesis of a particular    protein which has a particular biological function. Said sequence is    typically located at one or more specific locations in the host    organism.  In actual usage, people may use the word 'gene' when referring to  a structure at any level of the definition without    regard to the properties of the other levels.

I found a dedicated paper about the definition of what is a gene. Their short definition is:

“a gene is a discrete genomic region whose transcription is regulated
by one or more promoters and distal regulatory elements and which
contains the information for the synthesis of functional proteins or
non-coding RNAs, related by the sharing of a portion of genetic
information at the level of the ultimate products (proteins or RNAs)”

To your individual questions:
Speaking of the human genome, different sequences on the same locus are called alleles. It is thereby the locus that is most important for the definition. The phenotypic definition of genes is outdated. You cannot have different alleles on different loci. It is thought that gene duplication is an important mechanism of evolution; you have the same sequence on different loci so that they can evolve without functional pressure, but those are then considered different genes.
Example of paralogs, genes that are related through duplication

The genes encoding myoglobin and hemoglobin are considered to be
ancient paralogs. Similarly, the four known classes of hemoglobins
(hemoglobin A, hemoglobin A2, hemoglobin B, and hemoglobin F) are
paralogs of each other.

Although similar, paralogs are considered different genes.
Addressing comments:
There were comments asking at which similarity two sequences are considered the same gene and someone implied this is a grey-zone and analyzed with computational tools.
Here topics were mixed up! What is done computationally is the evaluation of the probability that two genes are homologous. Even with 100% sequences identity, two genes of different species or at different loci within the human genome would not be considered to be „the same gene“. These would be called homologos (orthologs or paralogs).

I'm not a geneticist, so that must be taken into account in this comment. Reading from the National Human Genome Research Institute website, the gene seems to be the important thing, the locus is simply like a home address, a place where a gene is located. It would be nice to have input from a geneticist.

Thank you. It makes sense to me that a gene is specified entirely by its locus within the genome. I can't think of any other definition that I can understand.

@anongoodnurse Suppose I gave you two different sequences of base pairs, without specifying their locuses within the chromosome. How would you know whether they are two alleles for the same gene, or alleles for two different genes?

Because they would be far more alike than different, @tparker. And I would take the definition by the National Human Genome Research Institute over a 2007 opinion piece. An address is simply an address. It's who lives there that counts.

@anongoodnurse So your proposed definition of a gene is "a set of alleles that are far more alike than different"?

@tparker - Not at all. You're putting words into my mouth, which is a poor form of rebuttsl, and isn't very educational. Did you read the link I posted?

@anongoodnurse: The word locus means location, nobody is arguing against that and a gene is a functional unit on the DNA. I am not saying, that the words gene and locus are interchangeable in any way, the OP presented conflicts between 3 aspects of the definition of a gene (locus, sequence, phenotype) and my answer was that locus is most important, given paralogs exist.

@tparker It'll be a lot easier to learn biology if you don't constrain yourself to think of definitions as things that can be condensed to a single pithy statement. That's just not how people use terminology in the real world.

"So your proposed definition of a gene is "a set of alleles that are far more alike than different"?" That's actually a decent working definition since it also covers the case where there are multiple copies of a gene occurring in different locations. Definitions in biology are not like mathematical definitions and are frequently highly dependent on context. Sometimes it's the location that's important, sometime the general biological function, sometimes the specific sequence, and sometimes a combination of all the above.

@BryanKrauseisonstrike I certainly understand that terms in biology cannot be defined as precisely as they can in (say) physics. My issue is that I truly don't understand in the slightest how different genes are distinguished or considered identical. By locus? By sequence (I don't think it can be that, because that's "alleles")? By function?

@BryanKrauseisonstrike There are specific databases of genes whose construction requires people to make decisions about which alleles constitute one gene vs. different genes. Are there patterns or rules of thumb for these decisions? Or is each one just a separate accident of history?

@CharlesE.Grant Thank you for constructively responding to my honest request for clarification instead of resorting to ad hominem attacks. Your comment seems to somewhat disagree with answer above, so I suggest making it a separate answer (and I will upvote it).

There are two levels of sequence you have to think about: the DNA sequence and the amino acid sequence. Two DNA sequences may differ quite a bit and still produce the same protein, which moves the debate to when are two proteins the same. There are a whole bunch of computational and experimental tools for quantifying how different two DNA sequences or protein configurations are. And people do argue violently over where to draw the line sometimes.

@CharlesE.Grant Thank you, this is very clarifying. So a specific gene is characterized by the protein that it codes for? Two genes are the same if they code for the same protein, and they are different if they code for different proteins? And so the challenge of delineating different genes simply boils down to the challenge of delineating proteins?

@CharlesE.Grant This seems to imply that the exact same (protein-coding) base pair sequence occurring at two completely different loci of the genome would could as the same gene, since they would necessarily code for the same protein.

@tparker I'd expect such a database to have some rules, sure, but those rules don't determine what a gene is for all biology, they are decisions of convenience for that specific database, and yes in some cases the rules applied may be ad hoc or inconsistently applied to respect history and consistency of terminology with the literature.

The topic can always be made more complicated. Even synonymous sequences (coding for the same peptide sequence) can lead to different proteins (by structure). So I would side with Bryan Krause and suggest not to dwell too long on definitions.

I edited my answer.

There are other good answers already, so I'll give an overview of the ways genes are used.

Biology paper gene: string of DNA that encodes for a some unit, often a protein, with some function
High school biology classroom gene: the above definition, but also any monogenic variation which gives rise to a phenotypic change (used as synonymous with allele or SNP)
Laymen gene: any hereditary factor, including overall polygenic predisposition, to some phenotype. This would probably be in "using the word incorrectly" territory.


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Micro-intradermal spasms in the legs after exercise
Heyo !
When i'm doing physical effort that involves and then rest, I feel small and suddle of what feels like contraction all over my legs (but not feet); It stops by itself after a few minutes and there's no pain at all, just a strange sensation. It's like having pin and needle when coming and ending, but it's less "noisy" and more precise in each "contraction" and can it really feel things are moving/contractiong/whatever but I can't see anything with my eyes.
The things, they are so small in "size" and strengh and too shallow to be muscle while being too deep to be skin. From the sensations, my best guess is blood vessels exploding but don't have any bruises. My other hypothesis is dermis doing some folky things but yeah, no idea...
Thus my question: What is this thing ?

Pins and needles are different from tiny spasms, which are called fasciculations. In either case, it's certainly not caused by exploding blood vessels, which would leave a mark resembling a bruise, as RBC's and the heme group from RBCs can migrate through tissue pretty easily and, more importantly, blood vessels aren't given to exploding like that. Read about fasciculations and discuss it with your doctor. Sometimes there is a medical cause.

Thanks ! Can you put your comment as an answer so I valide it ?

Sorry, I misunderstood before. No, I cannot put it as an answer because we don't provide answers to questions seeking medical advice. Note I only gave you a term to research, and reassured you that blood vessels aren't given to behaving as you wondered about.

I wasn't seeking medical advice, I just wantd to know what were these...

i was resting and looking at my leg the other day, and there were little muscular contractions in the thigh muscles, i thought they were a heartbeat at first and actually they were just random little movements inside the thigh.

Has commented by @anongoodnurse, it's called fasciculation.


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optimal spatial arrangement (distribution) of plants
Microalgae are organisms that can grow in aquatic environments and use light and carbon dioxide (CO2) to create biomass. Research showed that Microalgae's biomass can be used as a bio-fertilizer.
My mission is: to find the optimal field patterns . I mean the optimal spatial arrangement (distribution) of plants in a given area. To elaborate more, I need to consider if I plant a given land in raw (strip) pattern or rectangular pattern or maybe hexagonal or circular pattern, can this boost the crop yield or optimize the bio-fertilizer or the water management.
Note: I'm not a biologist, Just a data science student. I'm open to any biology/math resources and any other inspirations or approaches.

Is your mission to find the optimal pattern or for somebody else to find it for you? Also, can you please [edit] your post to clarify your specific question? Thank you.

yes it is my mission to find the optimal pattern. and my question is exactly : how to find this pattern for a given plant. thank you for your response@theforestecologist

Do we assume all "leaves" are on a flat surface? I.e., no height/leaves above other leaves.

we can assume that plants are planted at the same time so we can expect the same growth rate.  So yes we can assume that no height/leaves above other leaves. Sorry for my late response. @BigMistake

Perhaps the only way to find this out is to try different things and see what works.


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Models of evolution by positive versus negative selection
I am making a program for simulating natural selection. Now, I have discovered an interesting difference between positive selection and negative selection.
Positive selection occurs when the population size is limited by resources.
Take bird territories as an example. Assume that there are not enough suitable
territories for all the birds of a generation.
The fates of the individual birds are interdependent in the following way:
Every time a bird finds a territory and successfully defends it, the chances for the remaining birds are reduced.
In other words, the chances for each bird of finding a territory depends
on how successful other conspecifics have already been.
Now assume that there are two different phenotypes with different fitnesses.
A rare mutant has higher chances of finding and defending a territory than
the wild type.
The probability distribution of the mutant after selection is described by
the little-known Wallenius' noncentral hypergeometric distribution
(see Wikipedia: https://en.wikipedia.org/wiki/Wallenius'_noncentral_hypergeometric_distribution )
Now consider negative selection. This occurs when the population size is limited by predation. Assume that the birds are hunted by predators and that the predators have a limited appetite or limited time and energy for hunting, so that the number of surviving birds is fixed. The fates of the individual birds are also interdependent under negative selection: Every time one bird is caught by a predator, the chances for the remaining birds are increased. Assume that the mutant birds have a higher chance of escaping predators. The Wallenius distribution now models the number of birds killed rather than the number of birds surviving. The distribution of surviving birds under negative selection can be called the complementary Wallenius distribution.
The difference between positive and negative selection only applies when the fates of the birds are interdependent. Under positive selection, the birds are selected for survival, one by one. Under negative selection, the birds are selected for elimination, one by one.
I have simulated these distributions and discovered that positive selection has the strongest effect when the overall survival rate is high, while negative selection has the strongest effect when the overall survival rate is low.
The difference is shown in the following graph. The graph shows the expected number of surviving mutants after positive versus negative selection. The initial population has 10 mutants and 990 non-mutants. The fitness ratio is 5.

The green line indicates positive selection and the red line indicates negative selection.
The grey line indicates the situation where the fates of the individuals are independent. We can observe that both positive and negative selection have stronger effects than when fates are independent.
Independent fates means that the chance of survival of each individual is independent of what happens to the other individuals. Independent selection can happen in the following cases: (1) Unrestrained growth. (2) Feeding, when food is plentiful, but difficult to find. (3) Predation, when predators have unlimited appetite, but limited success in hunting the species in question. (4) Diseases: The ability of one animal to survive a disease has no negative effect on the other animals.
The total number of survivors is not fixed under independent selection, but determined post factum.
The difference between the effects of positive and negative selection can be explained most easily by the number of individual selection events. A selection event under positive selection is a bird finding or winning a territory. The number of such events is higher when the survival rate is high. A selection event under negative selection is a bird being caught by a predator. The number of such events is higher when the death rate is high and the survival rate is low.
Now, here comes my question:
I find it hard to believe that I could be the first one to discover the statistical difference between positive and negative selection, but I cannot find any literature describing such a difference. Can you please direct me to any literature describing the difference between positive and negative selection in terms of the mathematical/statistical effects.

I don't think that you are using the same definition of positive selection as other people. Positive selection is usually more considered to be the outcome of innovation that allows competitive advantage; the rate of new innovations is positively related to the summed population mutation rate. There are many descriptions of positive/negative selection behavior in terms of gene frequencies, but it seems that you are assuming perfect heritability of different phenotypes and seeing what happens rather than doing pop genetics.

Thank you for your comment Maximilian. You are right that the terms positive and negative selection are often used in a different meaning than here. The concepts I am adding here are not described anywhere in the literature, as far as I can find. For lack of better terms, I am calling them positive and negative viability selection. I am open for other ideas if you have a good suggestion. My models are described in this preprint: https://www.researchgate.net/publication/375029380_Statistical_models_of_different_selection_mechanisms

I skimmed this question and the preprint again and I think that the main stumbling block here has to do with vocabulary. For example your "positive viability selection" is very close to "negative frequency dependent selection", though I suppose you can make some definitional arguments for a difference. Similarly "positive frequency dependent selection" looks a lot like your "negative viability selection". I am not an evolutionary ecologist though. I added the ecology tag to your question since I think that's more appropriate.

I have a hard time to understand exactly what and how you are modelling your scenarios, so it is difficult to answer the question. For one; are you modelling survival rates of individuals under different scenarios, or are you modelling actual evolution across time (e.g trait or allele frequencies across time)?
However, I think (as also suggested in the comment by @maximilian) what wording and language plays a role here. For instance, your framing of territorial competition (and the predator-prey scanario) are very similar to what is used in evolutionary game theory. You should look into theory in that area for inspiration and similarities.
You should also look at density dependent selection since theory in that area also deals with similar issue that you mention. For instance “K-selection” in crowded environments with fixed resources or territories. One recent paper you might find interesting is Bartram & Masel. 2019. Density-dependent selection and the limits of relative fitness.
I’m not sure that you will find what you are looking for here, but it might provide a couple of starting points

Thank you for the reference. You ask if I am modeling survival rates. I am modeling the statistical distribution of individual selection events as a function of phenotype. How many birds of each phenotype will find a territory? How many rabbits of each phenotype will avoid predators? These are statistical distributions. The statistical distributions get complicated when the fates of the animals are interdependent. The survival rates of birds of one phenotype depends on how many birds there are of a different competing phenotype. That's what I want to model.


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Relation between the number of children and maternal telomere lengths
I've read multiple papers with contradictory findings. Some suggests a strong negative effect by birth-giving on telomere lengths. Others disagree. However, none of them establishes causal relations in my humble opinion.
Which study is the most credible?

I think the first study should rather measure the change in average TL before and after rather than measuring just the after and comparing it to a control because the apparent difference could just be the variability we already normally have. The second study doesn't state how it was carried out. TL increases in dividing cells. For example, cancerous cells have longer telomeres.  It would be a good idea to look at hormones that control cell division and how pregnancy might affect their levels. It can also require multiple births to have a significant effect since pregnancies don't last much.

@user7777777 Cute analysis! So, none of them are very credible, statistically.


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How to quantify and measure phenotypic variation?
It is easy to quantify and measure genotypic variation, because genes are digital, like the 1's and 0's of a computer. You just check how many places the gene "letters" A,C,G,and,T differ. But how does one quantify and measure phenotypic variation? The reason I am asking this question is because there are several species, like dogs and also us humans, where their genotypic variation is very small, but, at least intuitively, the phenotypic variation is large compared to their genotypic variation. Humans of different races look very different from one another, and different breeds of dogs look even more different, despite, in both cases, being extremely genetically similar. Has any book or paper or text proposed a rigorous definition to quantify and measure phenotypic variation?

It depends on the phenotype you're quantifying. If you want to quantify height, for example, just measure it and record the number. However, you seem to be implying "overall" phenotypic variation of all phenotypes. You may be interested in looking up "PheWASs," or phenome-wide association studies. You may also be interested in the correlation of every phenotype to every other phenotype and every phenotype's variance.
Also, phenotype extends beyond how something "looks" to disease susceptibility, protein expression, behavior, and internal organ structure. You'd have to take all of this into account, which would be difficult. Perhaps something analogous would be studies of protein expression: search for "transcriptome -wide association study."
Lastly, you have a misconception about the genotypic variance of humans and dogs. It's correct that small genotypic variation can lead to large phenotypic variation. However, humans have a large degree of genetic diversity between us, and dogs also have a decent amount. You are not alone in asking this question. One authors said "The domestic dog displays greater levels of morphological and behavioral diversity than have been recorded for any land mammal" (See also: "Behavioral Phenotyping" section of that link, and a related paper). Here are FST charts from Google showing the impressive genetic diversity of our and their species:

(Of course, FST is a poor measure and much of the variation exists outside the way it is shown/defined in these graphs.)


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How are the "cartoon" images made and what is their "proper" name?
How are the "cartoon" images made and what is their "proper" name?

How do people create these cartoon-style images? One option I found is BioRender, but it seems expensive.

Is there any other -proper- name, besides "cartoon"?

Example image from https://sites.tufts.edu/opioidpeptides/pathways-and-receptors/general-opioid-signaling/

You can draw them in Illustrator or any other vector graphics program.

You can use BioRender for free with slightly limited utility. I would call this an illustration or schematic.

they are called illustrations or diagrams and traditionally they are drawn by hand.


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Why don't each of T and B cells make two different TCRs/antibodies, except for the class switch?
I have not been able to find any literature that clearly states this, but if I understand correctly, T and B cells are diploid.
If so, there are two sets of genomes, and if both are TCR/VDJ reconstituted, it would seem that one cell would have two different TCR/antibodies. In other words, there will be a TCR/antibody produced by TCR/VDJ rearrangement of a patternal chromosome and a TCR/antibody produced by TCR/VDJ rearrangement of a maternal chromosome.
Why doesn't that happen?

I searched for this question  and obtained the answer, which I will expand on.
There is a mechanism called 'allele exclusion' (allelic exclusion),
which means that when one of a pair of immunoglobulin/TCR genes is successfully reconstituted and
becomes a functional gene, the other one ceases to function.
Eventually, only one or the other is expressed.
For more information, search for "allele exclusion" or "allelic exclusion".
https://en.wikipedia.org/wiki/Allelic_exclusion
https://pubmed.ncbi.nlm.nih.gov/12707333/


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Must RNA and DNA be the way it is?
We're carbon-based based life form with (mostly) iron-based oxygen transportation for apparently good reasons.
Is the same true for why life on Earth developed using nucleotides, amino acids, RNA and DNA: "the chemistry" just works easiest that way?
For example, are A, C, G, U the RNA bases for some "good chemistry reason", or would any C-N ring work?  I'm dubious about that, since dinitrophenol is also a C-N ring, and it's highly toxic.

Unclear what you're asking. Are there other imaginable configurations? sure. RNA could be made of 4 different bases that aren't A, C, G, U, or maybe 5. DNA could never have been used in genomes I suppose. I can come up with lots of superficially plausible ways for life to happen. But the only way to really know for sure is to "replay the tape of life" and see what happens next time, or go look at other planets where life has developed. Alternate proposed configurations (e.g. arsenic instead of phosphorus in DNA) have generally been debunked.

@MaximilianPress "arsenic instead of phosphorus in DNA) have generally been debunked" is the kind of thing I'm looking for.  As for "imaginable configurations"... we can imagine a lot of stuff that doesn't really work.  To clarify: are A, C, G, U the RNA bases for some "good chemistry reason", or would any C-N ring work?  (I'll edit the question to add that.

Yes, exactly. There are many superficially plausible (not merely imaginable) biochemical configurations for life. See the field of exobiology/astrobiology, and alternative biochemistries. Trivially, there exist synthetic nucleotides. Ultimately, the only test is that of empiricism: you have to go find / build biology that uses these systems to know whether it works, and that has only been successful for rather minor variations.

@MaximilianPress your link to alternative biochemistries is the exact same as what I mentioned in my question.

If you've read that page then I'm not sure why you're asking the question, honestly. It didn't occur to me to look at it when it seemed to be a reference for us being carbon-based life, which was not really under dispute.


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What is health?
I was studying human health and diseases in a book and first it defined general health as: “The overall complete physical, social, and mental well being.” It further went to say that health is being efficient, devoid of negative thoughts, etc.
The word complete is throwing me off, here. Isn't that the definition of an 'ideal' health that is impossible to achieve?
To some extent, we can have complete physical well being, but that is not the case for mental and social well being. We are humans, and it's in our nature to have negative thoughts and things like that, and that makes us human. But, that means that the definition of the health I read isn't true. How would you define health?
(Or,it might just be me who's overthinking all this.)

Complete here means "considering all these attributes together" rather than independently. Complete doesn't mean ideal, health is a spectrum.

That's not a good definition of health, even though it is used. One can be in good health, poor health, excellent health, average health, good physical health but poor mental health, the opposite, etc. There may be people in perfect health, and many people might claim to be in perfect health, but I'm very skeptical it exists and I've never seen a physician's report state that someone was in perfect health unless "perfect health" was clearly defined before hand (e.g. Air Force fighter pilots have very specific requirements, including height.)

Then, instead of defining health as perfection, or "completeness" in all the aspects, which are practically unobtainable, wouldn't it better if we defined health as a 'balance' between all those things?

Health is one of those things we don't have a good single definition for, health is contextual kinda like species.

The sentence does not indicate unobtainable perfection, you are inventing this. Just remove the word complete from the sentence and it still means the same thing, the word is just there to make clear that it involves all those things.

So the book invokes individuals with low levels of psychopathology and negative thought. They have very high scores in psychometric health tests.
Yes most of us have average symptom levels of mental disorder, and there are those with very high and very low levels of mental disorder.

This refers to health strategies:

Psychology used to be associated mostly with illness, maladaptive practices and negative thoughts, so in 1998 the term positive psychology became popular.
Mental health can be defined by positive or negative outlook, self-belief, judgement, good sleep, efficient organization, mental energy.
Negative views of the past, of oneself, of others, of society, sometimes nightmares, bad daydreams, and poor logical processing.
It is possible for someone in very good mental health to have very few of those types of negative thoughts.
Positive psychology and the absence of negative thoughts can be measured using various psychometric instruments and assessments:
Positive and Negative Affect Schedule (PANAS): A questionnaire measures both positive and negative affect, capturing the presence of positive emotions (e.g., joy, enthusiasm) and the absence of negative emotions (e.g., fear, sadness).
Satisfaction with Life Scale (SWLS): This scale assesses an individual's overall life satisfaction, reflecting their cognitive evaluation of their life as a whole.
Flourishing Scale (FS)
Resilience Scale (RS)
Self-Esteem Scale
Positive Psychotherapy Inventory (PPTI)
I have heard people described as being "almost completely devoid of complexes", i.e. they are very rare and fortunate to have a can do attitude about everything, social confidence and no particular secrets or conflicts with themselves.

It would be cool to be the human on the left. To clarify what you questioned: Those who are especially well-balanced may not be very wise or performant in other psychometric scores for knowledge or life skills, for example, it just means that they sleep well, wake up feeling good and ready for the day, don't worry much, enjoy their lifestyle, feel socially confident and optimistic to achieve what they want, they enjoy a lot of things in life, have few subjects that they find embarassing or complexing, deal with challenges well, have few bad memories or social hangups, are very satisfied with themselves, and enjoy themselves... The other end of the scale is often people with trauma, they have mood-swings, depression, possibly agression or argumentative cycles, out of control thoughts patterns which torment them, negative views of society, family, contemplate suicide, often dwelling on memories, have nightmares at night, bad sleep, strong ego, judgement... Most of use are somewhere in between those two extremes. The scientific way to measure it is psychometric tests.


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Why do pollen grains tend to remain in the 2 celled stage in most angiosperms?
In over 60% of angiosperms, pollen grains are shed off at 2-celled stage (Vegetative cell and a generative cell) and in the other 40% it is shed off at 3-celled stage (Vegetative cell and 2 male gametes). During the pollen pistil interaction, if the pollen grain is 2- celled, it divides to form a 3-celled stage during the growth of pollen tube in the stigma, while as the 3-celled directly goes into the ovary/ovule. I don't understand the need for the pollen grains to remain in the 2-celled stage if, ultimately, they convert into a 3-celled stage. Why don't the pollen grains remain in the 3-celled stage from the very beginning? What is the advantage of being in the 2-celled stage before pollination?
Source

This is an interesting question and I've upvoted it. It would be better if you could provide a source for your claim, so that you don't send someone (like me) on a wild goose chase. Thanks!  :)  (I like to find the answers to interesting questions, as it's fun to learn new things, but I'd like to know I'm spending time on something that's a fact.)

@anongoodnurse Thank you for the upvote. As for the source of my claim, I read that in the textbook issued to me by my school, and you can find that here. It is on page 7 and 17 (to save you some time :>).

Thanks for providing a link! As you're new here, you might not have understood that the source, a link and a quote should be edited into the question. That insures that the question is self-contained. Again, though, thanks! That chapter discusses things I never knew.

Thanks for letting me know. And, you're welcome. :)

Since, the topic itself is under research i would refrain from making bold assumptions but my hypothesis (based on evolutionary benefit; extra nutrient availability in pistil) is plausible enough and helpful for understanding your topic, but before that let me explain to you some prerequisites since you would need that understanding to think beyond as well. (Your answer is in last 2 paragraphs.)

PPI: Pollen Pistil Interaction:

As the pollen lands on the stigma (which is relatively moist) pollen absorbs some of moisture and it's metabolic activity is triggered resulting in pollen tube growth (obviously there are intermediate steps like reorientation of pollen, which in itself involves many extra cellular messengers (ECM) generaly sucrose gradient or some other peptide gradients and they trigger intra cellular signals which is the area of focus in your answer).

PT : Pollen Tube:

Consider it like a Big Long Tube (not hollow but contains actin filaments/shank actin filaments and its mechanism of extension in pollen tube is like reverse-fountain cytoplasmic streaming don't be afraid of the term it's simply like that - at axis/center of tubule its convoluted into itself while extending forward at the peripheral portion thus pushing ahead into the pistil.
Pollen tube isn't like shoot hair which is often misunderstood as similar (shoot hair is continuous projection of single cell with no blocking in between, but in PT there is callous deposit to prevent back flow) for images and further explanation refer this https://www.frontiersin.org/articles/10.3389/fpls.2020.589712/full

Progamic Phase: It is the phase between pollen landing on pistil and fertilisation. That is Period of Pollen Pistil Interaction & Pollen Tube Elongation.

Does cell while moving into pollen tube derives any nutrient from pistil? In my opinion it is very unlikely and there are rarely any conclusive research papers out there to confirm or discard that entirely BUT it might be dependent on some signaling molecules for his maneuvering and metabolic activities and it is strongly established.
Now, coming to your question

Your question is like that:
Why pollen's spermatic/generative cell divides in 'progamic phase' instead of already divided beforehand during the 'gametogenesis' phase itself.
Answer could be sought in Evolutionary benefits, why to spend so much of energy and resource in dividing all pollen cells into 3 celled stage when most of them are ultimately not going to succeed thus leaving this for the progamic phase to do so.
Also, to keep pollen 'effectively' light weighted this is beneficial, since loading pollen with vegetative cell will increase its survival time under outside environment we can not compromise on that part, thus if sperm cell is divided into the parent body itself it will lead to increase in overall weight. (Read last paragraph again).
Availability of nutrient in pistil - such hypothesis is dependent on point number 4 in prerequisites list. I could not conclude it immediately but it could be turning point to the answer.