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What is the basis of the endocochlear potential?
I am learning about the endocochlear potential. According to different sources, the ionic composition of perilymph is about as follows (in mM): 150 Na+, 4-5 K+, 1.2 Ca2+, 1 Mg2+, 120 Cl−, and 20 HCO3−; and that of endolymph is 1 Na+, 157 K+, 0.02 Ca2+, 0.01 Mg2+, 132 Cl−, and 30 HCO3−.
This means (in a naive attempt to quantify ionic charges) that the sum of charges in perilymph is 150+4.5+2*1.2+2*1-120-20 = +18,9.
And in endolymph it is: 1 + 157 + 2*0.02 + 2*0.01 - 132 - 30 = -3,94.
From these numbers, it seems like perilymph contains more positive charges than endolymph. How is it possible that the potential of endolymph is highly positive (80-90 mV) compared to perilymph? Shouldn't it be the other way around?
I have searched the forum and the internet for answers, but my question seems so basic (or based on a very fundamental misunderstanding) that I can't find anything of help. The only explanation I keep seeing is that the high potassium concentration accounts for the potential. However, isn't that outweighed electrically by the excess of negative ions in contrast to the perilymph?

Not an idiot or stupid at all, please don't describe yourself that way - in fact since it is not true I will edit it out of your question :) You have a very common misconception for people studying this material, which is not realizing that the positive and negative concentration inside and out is effectively equal (you just don't have the full list). See if this previous answer: https://biology.stackexchange.com/questions/79619/why-is-the-resting-membrane-potential-of-excitable-tissue-not-affected-by-the-ex/79623#79623 helps out. If not, I can tailor a fresh answer here.

Hello Bryan!
Thank you so much for your nice reply! Unfortunately, I still don't quite understand it. As a matter of fact, I think I may be even more confused, and I'm not sure if I can put into words what exactly why. I will give it a try. First, if the charge concentrations are the same on both sides, shouldn’t the measurable voltage be zero? A potential of 90mV designates that an electric (not chemical) potential is actually measurable across a membrane, doesn’t it? Why is that if the electric net is the same of both sides?

My simplified understanding of electrochemical potentials used to be like this: if there is a concentration gradient across a membrane (for example of KCl), which is only permeable for K+ (but not Cl-), K+ will stream to the side of lower [KCl] to reach equal distribution. However, as no equal amount of negative charges follow (!), the charge concentrations will be different on either side and due to repulsion/attraction, an equilibrium between ‘chemical driving force’ and ‘electric driving force’ will be reached at some point.

If the charge concentrations remain basically the same on both sides, as you just said, how does the electric component exist at all?
Thank you!!

I am going to add follow-up question 3: in my example, the endolymph has a positive electric potential compared to the perilymph. If this does NOT imply more positive charges on the endolymph side, what does it mean at all?
If I misunderstood and you are saying that such a difference is there, but small; wouldn't that mean that the most important ions (in the original post) are not listed? Because the (even if slightly) more positive side can't have a more negative net charge, right? I think I am not getting this at all.

I think you're actually very close. I'll try to write up an answer in the next 24hr or so. This system is a bit more complicated than other membrane potentials because there is actually a third compartment involved, and the endolymph/perilymph do not share a permeable membrane.

Thank you a 1000 times in advance. I'm looking forward to your answer!

In the meantime check out: https://www.pnas.org/content/105/5/1751 and see if it helps at all.

About biological electrical potentials generally
Biological potentials on the order of tens of millivolts depend on very very few ions moving (about 1/100,000 of the potassium concentration, for example, for a typical neuronal potential).
Therefore, the sum of positive and negative charges in any compartment is always almost zero (to several decimal places and beyond measurement; if you say a ). Electrical forces are very powerful, and
Some previous answers that are related:
https://biology.stackexchange.com/a/57066/27148
https://biology.stackexchange.com/a/77925/27148
https://biology.stackexchange.com/a/81571/27148
The endocochlear potential in particular - this is really cool
Everything I said above basically can be summarized in a quick statement: you can't figure out potentials just by measuring ion concentrations and summing them up. If you counted all the ions (including charged proteins, etc), you'd get ~0 in any biological solution. Instead, you have to think about where the concentration gradients are and how particular ions are moving. Let's tackle the endocochlear potential... Hibino et al 2010 has an excellent diagram, adapted from their previous 2008 paper:

Let's walk through the key features here, focusing on panel (b). First, the general structure: there are three extracellular spaces, which are all electrically isolated from each other. Between these extracellular spaces, there are two layers of cells where all the business happens.
Between the perilymph and intrastria space, there are a collection of cell types all connected via gap junctions. We can treat them sort of like one big cell, I'll call it the syncytium. A sodium-potassium ATPase uses energy to pump potassium into the syncytium and sodium out (upper left of [b]). Additionally, because there is now low sodium in the syncytium, more potassium enters through NKCC channels, which are symporters that move 1 sodium, 1 potassium, and 2 chloride ions together.
Potassium  would accumulate in the syncytium, except there are Kir4.1 channels permeable to potassium on the other side of these cells, open to the intrastria space. So, potassium flows down its concentration gradient into the intrastria space. This also creates an electrical potential and makes the intrastria space very positively charged (shown as +90mV on the diagram; the syncytium would similarly get a negative charge from the flowing potassium, but that isn't shown).
Normally, not many ions would actually flow to create this potential (on the order of the 1/100,000 I mentioned above) and everything would stop there. However, there are another set of pumps and channels in the marginal cells. The marginal cells also pump potassium in, via the sodium-potassium ATPase and NKCC channels, keeping potassium concentrations in the intrastria space low, such that potassium continues to flow down its concentration gradient from the syncytium.
The marginal cells also have potassium channels on their opposite face, and these are open to the endolymph. The high concentration of potassium ions in the marginal cells and the positive charge in the intrastria space gives the necessary drive to push the concentration of potassium in the endolymph high.
Ultimately, there is a full circuit of potassium because potassium is flowing into hair cells from the endolymph, and then back out to the perilymph. The sodium-potassium pumps use energy in the form of ATP to maintain the imbalance between perilymph and endolymph.

Hibino, H., Nin, F., Tsuzuki, C., & Kurachi, Y. (2010). How is the highly positive endocochlear potential formed? The specific architecture of the stria vascularis and the roles of the ion-transport apparatus. Pflügers Archiv-European Journal of Physiology, 459(4), 521-533.
Nin, F., Hibino, H., Doi, K., Suzuki, T., Hisa, Y., & Kurachi, Y. (2008). The endocochlear potential depends on two K+ diffusion potentials and an electrical barrier in the stria vascularis of the inner ear. Proceedings of the National Academy of Sciences, 105(5), 1751-1756.

Hello Bryan, thank you so much for your explanation. I think I got a better idea now. There are just two things I'm still confused about.

You say that the sum of all charges is 0 in any biological context. Why do electrodes on either side of the membrane measure +90mV then? There must be more + ions that - ions on the more positive side for that to happen, or do I misunderstand the entire concept of voltage? 2) The K+ flowing into the intrastria space cause a positive potential. That made sense to me until I read they are effectively removed. Shouldn't the potential leave with them?

To clarify, I do understand the flow directions and the dependences on concentration gradients. It is the voltage measurements that throw me off. I don't understand how an electric potential is reconcilable with the same net charges on both sides, and why the voltage between syncytium and intrastrial space would still be positive after the positive ions moved on already.

@Jimmy Check out the first other answer I linked, I have a couple back of envelope calculations for how many ions are responsible for a biological potential. It works out to be something like 1/100,000. So although the concentration of positive to negative ions is equal out to at least 3-4 digits (well beyond any ability to measure actual concentration) it's that tiny little bit that makes the difference.

For the intrastrial space, potassium is getting pumped out but other ions are moving too between the marginal cells. Probably the better way to think about the +90mV is that if the space is less than +90mV, more potassium would flow from the syncytium and the potential would rise. +90mV is the voltage at which the net flow from syncytium to intrastrial equals the net flow from intrastrial to marginal. (same for the endocochlear potential itself)


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Is there benefit of use of red light over dim white light when interacting with rodents in the dark phase?
I've come across some "percieved wisdom" that rats and mice do not "see" red visible light and so use of this wavelength will allow humans to interact with rats in their active nocturnal phase without affecting their circadian rhythms.  Having gone to read the evidence for myself of this I can see evidence that red visible light does indeed impact rodent circadian rhythm (Dauchy et al J Am Assoc Lab Anim Sci. 2015 Jan; 54(1): 40–50) so is not a "fix" to allow us to see without the rodent being impacted.  What I cannot see is if there is any "benefit" to use of red vs white light if it has to be used or whether it just has the same impact and the only negative is the human can see less!!!!  Can anyone help ?

I propably can answer this qustion. But still i need to be 100% sure, what are you exacly want to know. Your question is: Why does chronobiologiest use in experiment red part of visible spectrum, but not whole light spectrum (white light)? Am i correct?

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Identify arthropod with many legs in Mumbai
Can someone please identify this ~5 cm long arthropod? I've been finding one of these every 2-3 days inside my apartment ever since rainy season started here in Mumbai (June).
The bulb portion is its head. The arthropod is capable of climbing walls.
Thanks.

Video of the worm (shot while brooming the floor. Hence the dirt)
https://i.sstatic.net/AB16p.jpg
By the way, I've seen it 6 times in the last 2-3 weeks. Except once when I saw it on the bathroom floor, all other instances were during night time. So perhaps this is some sort of a nocturnal creature?

It looks like a centipede. Can you confirm how does it move?

I've edited my post with a video link. Please check.

Welcome to Biology.SE! In the future please [edit] your post to include all essential information (e.g. size in this case) — comments are ephemeral and so should not be used to covey information important for understanding or answering the question. Also note that this is almost certainly a millipede rather than a worm. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I'm pretty sure It's a millipede from the Julida order, that includes 750 species distributed in the northern hemisphere.
https://en.m.wikipedia.org/wiki/Julida

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If due to some reasons a small portion of our neurons die, how does our body remake them?
There are various reasons such as intake of neurotoxins, and possibly traumatic injuries, that can cause neurons to die.
After several hundreds, or thousands of our neurons die, how does our body remakes them?

Evolution set us humans up to not regenerate our neurons on the whole, which is a pity since we can regenerate our liver cells, so it's not an impossible feat. If neurons die because you drank too much, banged your head, or just because they got old, they are gone. If this death is accelerated like in Alzheimer's disease, you can literally see holes in the brain autopsy. That said, we now know that in a few exceptional areas of the brain, neurons do regenerate. It's not many cells but it's something. The two areas known to date are the dentate gyrus of the hippocampus (DG below) and the subventricular zone of the lateral ventricles (LV). See the green zones in the image below.

From Ernst & Frisen PLoS Biology 2015 (CC-by)
In those areas, like elsewhere in the body, new cells are made from stem cells, that is infant-like cells that have the potential to become many cell types. If we could only understand why some cells regenerate and others do not, we might be able to promote this. Alas, our current understanding is woefully incomplete. We'll need more research # # # before we can dream of regenerating our neurons.

It's far from treatment-ready, but successful induction of adult neurogenesis from glial cells via gene delivery or gene silencing has been achieved in rodent models, as have been other promising preliminary results.

Please suggest some ways to accelerate the regenerating process. Like some fruits/veg which can help

Hi Ravi, if there were an easy fix with food, everybody would be doing it. Sadly, there is not.

Likely one of the big reasons that certain neurons don't regenerate is that the signals necessary for them to find their distant targets are only present during a narrow window in development. There are no appropriate guidance cues for, say, a LGN cell in thalamus to find V1 in cortex in an adult brain, and providing those cues would require quite a massive evolutionary change that just doesn't have much selective pressure. Of course there are some cells that make only local connections, but you wouldn't be able to rebuild any full region of brain tissue.

Disclaimer: I'm not an expert, but my recent reading on this topic is fresh in memory, so I'm typing up something of an answer.
The body does not remake any individual cells that die. In case of cells that regenerate, their place is simply occupied by cells which are newly born, or travel from elsewhere. Every individual cell is unique, with its own copy of DNA with its own unique epigenetic information, and unique (but typically similar to other cells) exact biochemical makeup. Once a cell dies, it can not be remade.
Neurons are also pretty special among cells - their function is extremely complex, and in adulthood, new neurons are only born in some specific areas - in the brain, the main exception being the hippocampus.
Majority of learning in the human brain happens as a consequence of what neurons we have being constantly reshaped, both physically - with dendrites, spines, synaptic terminals being constantly created, pruned, their molecular makeup changed, their gene expression regulated up and down.
Unfortunately, if a neuron dies, it is gone for good, and it will not be replaced. Instead, depending on area and degree of damage, other neurons will often pick up the slack, changing function and enabling the brain to re-learn some of the function it lost. In fact, the process of neurons learning to perform different function than they originally did is common in the human brain, e.g. the size of areas processing functions of individual fingers in a musician's brain will vary based on the instrument(s) they play and their experience with it.
That said, the situation is not as grim as it looks. A few thousand neurons, in most areas of the brain... isn't much, and probably won't impair your cognition much, and neurons aren't all that fragile either - it's possible for them to starve and lose function, becoming dysfunctional, instead of outright dying, which they can in many cases recover from. People are often capable of recovering almost completely from lighter brain damage, and cases of impressive recovery from more severe damage are also not unknown.

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@tyersome I see, thank you. I will keep that in mind for the future.

Please try to add supporting references

Neuroregeneration capability is rather limited, and patients that go through the trauma that you speak of usually require life-long assistance[1]. One treatment that has come to light in the past two years uses stem cell delivery to the brain[2]. When a cell dies, if it is replaced, there are stem cells that do it (google mesenchymal or skin stem cells and you will find that system). Damage like drinking doesn't kill cells, it just hinders them (by maybe effecting their protein production), and cells can rejuvenate or heal themselves and replace those dysfunctional proteins with an autophagic process[3, 4].
Overall, I am confused about your question. The body has limited capacity to replace neurons due to the way that this very specialized cell type develops with the body (among other reasons) and it comes down to there not being a stem cell close by, ready to undergo mitosis and differentiate. So your question assumes that the human brain has the great ability to regenerate these cells. Next time there is an assumption in the question you are asking it may be helpful to provide a citation or background information with citations.

Mayo clinic. https://www.mayo.edu/research/centers-programs/center-regenerative-medicine/focus-areas/neuroregeneration
Research sheds new light on how brain stem cells are activated. https://www.sciencedaily.com/releases/2019/06/190606133822.htm
Drinking. https://www.healthline.com/health/does-alcohol-kill-brain-cells
Autophagy. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2990190/

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I would like to add the point that only the neurons in the brain can't be replaced, if they died.
Olfaction and gustation have bipolar neurons which are replaced around 6 months ,over the lifespan of a human. Olfaction
So its not true to say that all neurons can't be replaced, some can be.


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Are all non-breeding naked mole rats the same sex?
In many eusocial species, all the non-breeding members are the same sex.  Honeybees are a good example, with only female workers.
Are naked mole rats that do not breed also all either male or female, or are they mixed?

Naked mole rat colonies contain individuals of both sexes, with one breeding female and one to three breeding males, and the rest non-breeding individuals of both sexes.
The other individuals in the colony have an additional caste system that seems to depend on size but not sex (i.e., there does not seem to be a hierarchical relationship between non-breeding males and females).
Non-breeding females, but not males, have suppressed reproductive tracts. In the absence of a queen, some non-breeding females' reproductive systems will begin to activate, until one becomes dominant and the others return to being non-breeders.
References

Clarke, F. M., & Faulkes, C. G. (1997). Dominance and queen succession in captive colonies of the eusocial naked mole–rat, Heterocephalus glaber. Proceedings of the Royal Society of London B: Biological Sciences, 264(1384), 993-1000.
Jarvis, J. U. (1981). Eusociality in a mammal: cooperative breeding in naked mole-rat colonies. Science, 212(4494), 571-573.

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What happens to the gamma motor neuron during too much contraction of a muscle?
Suppose a muscle is contracting too much, so we need a reflex to stop it from contracting too much.
Contraction of a muscle causes the muscle spindle to go slack, hence the Ia axons and II-axons do not fire action potentials. The Ib axon synapses with the alpha motor neuron via an inhibitory interneuron so that the muscle is stopped from contracting. But what happens to the gamma motor neuron? Is it also inhibited just like the alpha motor neuron is inhibited? If indeed, it is inhibited, is it the Ib axon that inhibits it? I mean if it was not inhibited, then it would activate the Ia axon and the II axon which would activate the alpha motor neuron. As a result, there would be conflicting messages sent to the alpha motor neuron (excitatory from Ia and II and inhibitory from Ib).
During stretching of a muscle, for example, during the patellar reflex, the Ia axon and II axon are activated, which activate the alpha motor neuron as well as the gamma motor neuron to get contraction and contraction over and over again until the muscle returns to its set point.
During stretching, is only the muscle spindle active?
During contraction, is only the Golgi-tendon-organ active?


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Can the mechanism behind changes in protein expression be inferred by the timing of those changes?
My question relates to the timing of protein expression changes, and whether there is a literature-based consensus as to how long changes in protein generally take.
For example, if protein changes 24h after a treatment, then its expression may be due to release of a translational block, whereas if a protein is expressed 72h after a treatment then it is being transcribed and translated rather than just the latter.
Or is this something that is too variable to draw general conclusions on?
Thanks in advance

I made some edits that I think clarify without changing meaning but feel free to edit again if that's wrong. "Gene expression" is a pretty broad term but I think you're asking about changes in protein.

NO. Science is about experiments to test hypotheses. Temporal associations are merely the basis for such hypothesis. And whenever zi hear the word “consensus” I reach for my  bro…  …omstick.


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What inhibits linkage between actin and myosin filaments
What is the mechanism behind the inhibition for cross-bridge linkage between actin and myosin filaments in the binding-tilting cycle? There are 2 possible ways that are in my mind:
a.  Tn-I (tropnin-I), binding to F-actin: when [Ca2+] falls below the threshold, Tn-C are inactivated. Therefore, Tn-I relocates and SOMEHOW this causes the cross-bridge to break (ref)
b.  ATP rebinds to the myosin head, forming ATP-myosin complex. This has a relatively low affinity towards binding the myosin-binding sites on F-actin (than myosin-ADP-Pi complex). Therefore, the cross-bridge break.
From my understanding, (a) is strange: when Tn-C is inactivated, it should cause Tn-T to change conformation so that tropomyosin covers the binding sites again. But I think I am wrong as otherwise, Tn-I is useless, but I really don't know how Tn-I exerts its inhibitory effect.
Thank you.

I am not sure if you are referring to a mechanochemical cycle of "stepping" of a myosin molecule along an actin filament, or a cycle of contraction and relaxation of a muscle cell as a whole. These take place on completely different timescales and control the binding and unbinding of the two proteins in entirely different ways.
In the mechanochemical cycle, there are no proteins directly involved other than actin and myosin themselves, and the breaking and re-formation of contacts is controlled by the nucleotide occupying the ATPase site of myosin. ATP binding leads to a low affinity (weak interaction) state and ADP binding leads to a high affinity (strong interaction) state. ATP hydrolysis and nucleotide binding/unbinding "power" this cycle.
The cycles of contraction and relaxation of the cell occurs on a much longer timescale--each contraction involves many repetitions of the actin/myosin "stepping" cycle across many actin and myosin molecules, while relaxation involves slowing or stopping this cycle. This is where calcium and the troponin I/C complex come in--they are a "switch" that allows the stepping cycle to happen or not. So when the calcium is low and the troponin complex is bound, the actin/myosin interaction is continuously disengaged, whereas when calcium is high and the troponin complex releases, the cross-bridges form and release in a cyclical manner as ATP binds to myosin and is hydrolyzed.
As an analogy, think of a person walking across a room full of chairs. As the person is walking, his feet alternately make and break contact with the ground, and this is due to the coordinated movement of the legs. If the person sits down in a chair, then his legs stop propelling him entirely for a while and are still, and this is like when calcium is low in a muscle cell.

Thank you for the detailed explanation! Can I say like this: in my question, (a) is talking about muscle relaxation, (b) is talking about where muscles are contracting (isotonic tetanus - 'stepping' of myosin heads on actin filament)?

May I ask one more question? when Ca2+ returns to the sarcoplasmic reticulum (unbind Tn-C), how actually Tn-I inhibits the cross-bridge binding? Since I thought it is Tn-T that does the job by pulling tropomyosin back to covering myosin-binding sites. Thanks!


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What is the intracellular chloride concentration in rat T-cells or thymocytes
I'm modeling acid-base in T-cells as based on Grinstein J Gen Physiol 1984; 83: 341-369. I have an estimate of strong ion difference (SID), and Grinstein gives Na and K, but for SID to be true at 33 mM with K 147 mM and Na perhaps 20 mM Cl should be  (K + Na) - SID = 134 mM which is hard to believe but I could find no data on the subject.

Where is your estimate of SID from?

Felber and Brand 1982 estimate the intracellular T-cell chloride concentration to be about 30 mmol, which seems to me to be on the high end for intracellular chloride in mammalian cells (though my experience is mostly with neurons, I'm not as confident of intracellular chloride concentrations in other cell types; for a neuron I'd expect <10mmol). Still, that leaves a big anion gap for your SID estimate.
I think it is more likely that your SID estimate is simply wrong. The number you report sounds like an extracellular SID; Kowalchuk et al 1988 suggest intracellular SID is about 4X extracellular for muscle, which sounds about right for your situation as well.
Most of the intracellular anion contribution is provided by negatively charged proteins, amino acids, lactate, etc, rather than strong ions like chloride. Many of these are nearly completely deprotonated at physiological pH, though (for a typical amino acid the first pKa is ~2).

Felber, S. M., & Brand, M. D. (1982). Factors determining the plasma-membrane potential of lymphocytes. Biochemical Journal, 204(2), 577-585.
Kowalchuk, J. M., Heigenhauser, G. J., Lindinger, M. I., Sutton, J. R., & Jones, N. L. (1988). Factors influencing hydrogen ion concentration in muscle after intense exercise. Journal of Applied Physiology, 65(5), 2080-2089.

Thanks a lot - my estimate of SID was based on a buffer capacity of 25 mmol/l/pH as reported by Grinstein at pH 7 - for lack of other knowledge assuming a KA of 2e-7 like histidine gives from Van Slyke 1922 JBC equation 17 an estimate of ATOT , and from that using charge balance a value for SID.. But I can see you have to model the many negative charges on proteins in a different way. Thanks a lot for this help

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Is there something that makes flies slower at high altitudes?
At first glance, higher altitudes equal lower temperatures, which would likely slow down cellular metabolism.  However, while backpacking in New Mexico in ~90 degree weather, I experienced the same thing -- the flies were slow enough I was able to catch them easily in my hand, as well as with chopsticks.
Is this related to air density?  Why are these flies so much slower to react and move about in the mountains.

The atmospheric density may not be the only factor, but from a physics standpoint, flying animals should in general move more slowly at high altitude.
As an example, New Mexico's Wheeler Peak is at an altitude of ~4 km above sea level. For a back-of-the-envelope air density calculation, a good estimate of scale height is 10 km, i.e. $\rho(h) = \rho_{sea}*e^{-h/10km}$ , which means the air density at Wheeler Peak is about $2/3$ the density at sea level (other air conditions being equal).
For wing-flapping animals, the power required to maintain flight is inversely proportional to the air density. I'm not confident about how flies' wing movements would be affected (this is where an entomologist should step in), but in any case their air speed should be reduced at high altitude.

It may be influenced by inter-species differentiation in characteristics.  Were the flies larger or smaller than other flies?  If there were flies of different sizes present in the same location and under the same temperatures, how did their relative speeds compare?
To know the species of fly which one is examining is quite difficult.  It can come down to counting hairs on the fly's body under a microscope--literally.  But some species may simply have different habits when compared to another species.
Mosquitoes are in the same order as flies (Diptera), and in Southeast Asia there are many species of mosquitoes.  Some make a noise or hum while flying; some fly silently.  Some are quite fast; others are much slower to take off, making them easier to slap.  Some have an uncanny ability to sneak in and bite while one is otherwise occupied/absorbed in something, while others seem too eager and land in plain sight while one is watching.  Some are larger, with more painful bites; others are smaller and their bites itch longer after their deed has been done.
A consideration of these simple variables leads to the obvious conclusion that more information about the flies in question might be needed before a determination could be made as to why they seem slower.
Air densities might be a factor, in addition to gravitational forces.  I'm not knowledgeable about the relative impact of thinner air versus the amount of gravity to be overcome in flight, but I know large jet airplanes fly faster and with less drag (resistance) at higher altitudes, making high-altitude flight more efficient.

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What is the purpose of ethanol in a DNA extraction experiment?
We were doing a lab experiment in biology class in which we extracted DNA from a banana-detergent solution mixture.(The detergent solution was made of 100ml of detergent, 90ml of water, and 5g of salt.) We then added ethanol to the mixture.
I know detergent breaks down the lipids in cells and salt takes away the moisture from cells but how does ethanol affect cells?

In the case you describe the ethanol is not there to do anything with the cells but to make the DNA precipitate out of solution. DNA is very poorly soluble in 50-70% ethanol and it will precipitate out as a white sticky pellet. It works even better if the alcohol is kept very cold.
Ethanol does kill cells by denaturing proteins and disturbing the lipid bilayers but after you have added the soap, most cells will already have been disrupted.


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Why are there not effective pharmaceutical treatments to prevent weight gain?
Hunger is caused by signals from the brain, so is there a way to suppress the signal of hunger in the same way we suppress the signal of pain with painkillers?
If people felt less hungry, they would eat less and find it easier to lose weight, so why aren't there pharmaceutical hunger suppressants yet?

I think the problem here is with the assertation that "If people felt less hungry, they would eat less..."  Seems to me that most overweight people eat (and choose what to eat) for a variety of reasons.  Actual hunger is low on the list.

The two main factors are:

Hunger is more complex to treat than pain (more pathways, more potential targets), and I would argue against your suggestion that we are good at treating pain: despite the term "painkiller" we aren't great at blocking pain except for with local anesthetics that block all nervous activity (lidocaine for example). For systemic pain relief, there are lots of long-term efficacy issues with either opiates or NSAIDs, and that isn't even taking into account:
Side effects. Amphetamines are great for suppressing appetite. They also mess with the cardiovascular system, are habit-forming, and cause psychological issues. "Fen-phen" is a famous example of an anti-obesity drug that had major side effects leading to massive lawsuits. A more recent supplement, Ephedra, had many of the same problems and was banned by the US FDA for those reasons.

There are some drugs that are used to treat obesity, but many of these have come into regulatory issues with side effects and are only used in special cases like in diabetics or as an absolute last resort.

+1 DNP comes to mind. Pharmaceuticals are much more dangerous than diet and exercise which, in many (most?) cases, is a cure.


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Is a one ventricle heart feasible?
So this is derived from a lesson at Khan Academy.
The mind activity assumes that the one ventricle heart pumps blood to the lungs for oxygenation then rest of the body. However, the problem is that there is too much pressure at the lungs leading to bleeding.
This problem, however, can be solved if the lungs come before the one ventricle heart. This way, most of the pressure is used going through the body and pressure would not become a problem.
Thus, is a one ventricle heart that connects to body tissues first then lung feasible? If so, why have organisms not developed this way?

I removed the "evolution" tag because if this question could be tagged 'evolution', then really any question on this site could be tagged 'evolution'.

Alternative Heart Morphologies
Amphibians and some reptiles have a three-chambered heart, with 2 atria and a single ventricle. There are still separate circulatory pathways for the lungs and the rest of the body, but the oxygenated and oxygen-depleted blood mix in the ventricle, and are pushed at the same time to the lungs and body.
The disadvantage of this system is that it is less efficient at providing oxygen to the body than a four-chambered system, because the blood pumped to the body is a mixture of blood that has recently been to the lungs and blood that has not.
You seem to be suggesting another system, where there is just one serial pathway from heart to lungs to body, or from lungs to heart to body. This is more like the two-chambered heart of a fish: blood is pumped from the heart through the gills, and then to the body.
Lungs and body in series, and fluid dynamics
So why wouldn't this work for a mammal? It could, but gills and lungs are very different. The vasculature of the lungs requires a lot of pressure to get through, which is generated by the right ventricle.
Pressure is required to push fluids through a constriction (note that even a straight pipe is a constriction). After a fluid passes a constriction, there is always a pressure drop. That pressure drop is a function of the rate of flow and size of the constriction. If you give less pressure at the start, there is less pressure to "drop", and so you get a lower flow rate (note that this is nearly a perfect analogy with electricity, where flow is current, pressure is voltage, and the size of the tube is the conductance).
If you want to pass through a second constriction, you have to use pressure that is "left over" after the first drop: you can't use the pressure you started with because that was lost getting you through the first constriction. In reality, in a closed system, the total flow rate will be determined by the summed series resistance, so adding a second constriction slows the flow rate for the whole system, and you get a partial pressure drop after each.
If you put the lungs and body in series with each other, no matter which comes first, you need to have enough pressure left over when you pass one to get you through the next one, otherwise the flow will slow down. Blood in a human aorta has a mean pressure around 100mmHg, whereas back in the vena cava it is close to 10mmHg. That suggests you need about 90mmHg to get enough flow through the body's circulation. The lungs use a little less, but you still have a pressure drop of around 50-60mmHg. Therefore, you would have to increase the blood pressure by 50%-75% to get circulation through both lungs and body.
Higher pressures lead to more turbulent flow and take more effort to achieve. The four-chambered heart, with 2 ventricles, is simply more efficient.

@GerardoFurtado I'll edit to say some; only birds and crocodilians have a true fourth chamber, the other reptiles do not, though there is some separation compared to amphibians.

crocodiles actually have something bordering on a five chambered heart, it allows them to divert oxygenated blood away from non-essential organs during dives.

@John I agree that crocodiles have a more complex heart than mammals, although I think it's a stretch to call it five-chambered; I looked around and every source I can find describes it as a four-chambered heart and they note the second aorta that allows for diversion of blood away from the lungs.

there is this extended valve called the cog tooth valve that allows a one way diversion, it is just that that valve is right against the heart and is muscular, and it creates a one way communication between the aorta. hence why some call it five-chambered.


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Does introgression require interspecific hybrids to be fertile? How is this possible?
Wikipedia says that Introgression, also known as introgressive hybridization, in genetics is the movement of a gene (gene flow) from one species into the gene pool of another by the repeated backcrossing of an interspecific hybrid with one of its parent species.
Does this mean that the interspecific hybrid is fertile? But is it possible, that an interspecific hybrid is fertile?

Does this mean that the interspecific hybrid is fertile?

Yes

But is it possible, that an interspecific hybrid is fertile?

Yes
You might be confused by the idea that by definition two individuals from different species should not be able to interbreed. If so, then you should have a look at How could humans have interbred with Neanderthals if we're a different species?.


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Do mucous membranes surround visceral organs?
Wikipedia claims that:

A mucous membrane or mucosa is a membrane that lines various cavities in the body and surrounds internal organs.

The first part of that sentence is clearly accurate, but I cannot find any reference from Google Scholar or books that states mucous membranes surround internal organs.
The mucous layer lines the lumens of the body: digestive, respiratory,urogenital tracts, as well as cavities leading to openings such as the ears and nose, and forms the conjunctiva of eyes. The surfaces of internal organs don't fit any of these categories.
I think wikipedia is wrong about the viseral organ part, am I right?

You are correct.
"Serous membrane" might be what the Wikipedia editor was thinking of, for example the pleura of the lungs; other examples include the pericardium and peritoneum.


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Please identify hard hollow structure found on beach
This washed up on the shore in NJ last week. It looks like a molar but I cannot find anything similar
1.75” across about 1/2 high. It has a weird indent too

Most likely a shell. We would need some sort of scale for size and photos of other surfaces for full ID.

StackExchange works differently from other sites: the answer box is for answers only, it's not a forum with a string of posts replying to an original. If you need your accounts merged you can use the "contact us" link at the bottom of the page or https://biology.stackexchange.com/contact If you have new content to add use the [edit] feature.

Is it actually bone? all kinds of weathered junk washes up on NJ beaches

IT could be an old ceramic tube like a piece of a clay bottle, a weight for a net from an indian.

The most defining thing is the holes on one side, it has a hole in the top too. Use reddit or FB fossil ID or what's this fossil or fossil forums they specialize in weird beach finds.

https://www.reddit.com/r/fossilid/


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Why is a penis an organ?
According to Wikipedia an "An organ is a group of tissues with similar functions". I don't know anything about anatomy but it doesn't seem to me that a penis can be delimited somewhere to form a "group". Therefore  I do not understand why a penis is considered an organ.
Can you explain it to me ?

Organic = carbon based, thus teeth = organic

I though theeth were mineral

Frankly, that's a terrible definition by Wikipedia.
Merriam-Webster defines an organ as:

a differentiated structure (such as a heart, kidney, leaf, or stem) consisting of cells and tissues and performing some specific function in an organism

or

bodily parts performing a function or cooperating in an activity

The important defining feature of an organ is not that the tissues have similar functions but that, together, the tissues comprise a functional whole that achieves some end goal.
For the penis, it consists of multiple tissues with different functions:

(from https://www.ncbi.nlm.nih.gov/books/NBK525966/figure/article-20668.image.f1/ - original from Gray's Anatomy)
The different tissues pictured here: the fibrous envelope, the corpora cavernosa, the septum pectiniforme, the urethra and blood vessels, the nervous tissue in the skin: all of these tissues have different individual functions: structural, erectile, carrying urine or semen, etc.
The key that unifies them into an organ is that the functions of the penis at the organism level (principally sexual function) are not served by any of these tissues alone, but rather by their combination in a full structure: an organ.
Ultimately, organ definitions are somewhat opinion-based: people are lumpers and splitters, so you might find conflicting definitions for which groupings of tissues reflect distinct organs, but I think by most standards you would find the penis to be considered a distinct organ, affiliated with but distinct from the primary sex organs and associated glands.


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Why don't phosphatases both add and remove phosphate groups if enzymes catalyze reactions in both directions?
We know that Phosphatase is a type of enzymes that removes a phosphate group.
Why can't phosphatases add a phosphate group if we know that all enzymes reactions are reversible ?

@TheLastWord I think the question was quite clear - maybe you can explain better what about it you find unclear?

@BryanKrause I am just wondering if he meant to ask if Phosphatase enzyme can in itself add the phosphate group of if we can add it externally thorough some means or he is commenting on the reversibility of the reaction in general.

@TheLastWord Does my edit help? Maybe the 'it' in the second sentence was unclear, but I feel like this question addresses a fairly common misconception to biochemistry novices so I'm fairly confident I've extracted the correct intended meaning.

@BryanKrause That should be sufficient.

Enzymes make reactions happen faster in both directions. If the chemistry favours removing a phosphate an enzyme cannot change that. Only get there faster (or maybe slower too I guess.)

I think the description of enzymatic reactions as 'reversible' is potentially a bit misleading. It might be better to think of enzymes as agnostic to reaction direction.
The big missing piece is the difference in free energy of the reaction itself. Reactions that remove a phosphate group are energetically favorable in biological conditions. A phosphatase will effectively never add a phosphate group back because one would have to supply additional energy to make the reaction proceed in that direction.
Phosphatases catalyze a reaction that results in a free phosphate ion. However, kinases that add phosphate groups are catalyzing quite a different reaction, where a phosphate group is lost from a molecule of ATP which becomes ADP. This reaction is also energetically favorable, and the reverse reaction does not occur.

@MartinKlvana True, but the reversibility of the reaction depends on the free energy. The question is more about reactions proceeding in both directions rather than the reaction being feasible in at least one of the directions. If there is little difference in elevation between the two valleys, the reaction will go in both directions (or neither at all if the activation energy is too high); if there is a huge difference, one direction may be feasible and the other is not.

@MartinKlvana Right, but the difference in the reaction directions is critically dependent on the difference in energy between the products on each side of the reaction: that is what determines the asymmetry in reaction rates. The energy of the intermediate state is the same in either direction.

@MartinKlvana I know we are really talking about the same thing here and going in circles around each other. I think it's maybe important that I clarify where I am coming from here...for someone having trouble understanding these concepts, I want to avoid talking about differences in the activation energy because people are taught to think about the purpose of enzymes as reducing the activation energy, which they do, but that gets confusing then when you are talking about the two directions. I want to emphasize that the reaction won't go in a direction where the products are too high energy.

Not all enzyme catysed reaction are reversible reactions .reversible reactions are those which have free energy change between product and reactant sholud  approximately or exactly equal to zero. Phosphatase canot do the reverse of the reaction because if both the reactions where done by the same enzyme in both the direction then a cell will not be having the ability to decide weather forward or backward reaction that should actually take place at any given time.


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What is the function of dreaming? Does a particular hormone secretion interfere with dreaming? Why do some people dream more?
I'm really interested to know when we are sleeping how a series of stories come to our mind that we called this process dreaming. If you know a useful article on this topic, please tell me thanks.

Welcome. I see 3 different questions in the title, and a 4th in the main body. We encourage clear, focused questions, preferably 1 question per post. We also ask you to provide us with some background to narrow down the scope of the question and give us a lead in which direction you are seeking answers. So could you tell us your findings or thoughts so far investigating this topic? Have a look at the section on asking questions in the help center. Cheers.

Relevant xkcd. Researching & understanding sleep is hard, even without going into dreams. I'm not an expert, but my best guess is that a lot of this is just not currently known.

Hi @Zahra - normally we strongly encourage edits to improve questions, and I like many that you've made, however they change your question a little too much for one that already has an answer. I'd strongly encourage you to both A) Edit this question along the lines of AliceD's suggestions, without disrupting the central point of the original question, and B) Ask a new question along the lines of your edits - I think that second question will be a good one. Thanks!

Thanks for your guidance AliceD .I will regard these points in my future questions and in this case l tried to explain more in the body and I have changed my question too.

Thanks Bryan for your points. I changed my question . whats your idea about this new one?

@Zahra Hi, sorry for the confusion - I've rolled your question back to a previous state, because the edits you made invalidate an existing answer - it changes the meaning of the question too much. I think your new question can be a good question but you should ask it as a new question please.

Dreams are hallucinations that occur during certain stages of sleep. They’re strongest during REM sleep, or the rapid eye movement stage, when you may be less likely to recall your dream.
Research is yet to reveal the true reason of dreams. But we know for sure it is not one reason.
Speculated Reasons:
1. Dreams as fight-or-flight training
One of the areas of the brain that’s most active during dreaming is the amygdala. The amygdala is the part of the brain associated with the survival instinct and the fight-or-flight response.
One theory suggests that because the amygdala is more active during sleep than in your waking life, it may be the brain’s way of getting you ready to deal with a threat.
2. Dreams as memory aides
One widely held theory about the purpose of dreams is that they help you store important memories and things you’ve learned, get rid of unimportant memories, and sort through complicated thoughts and feelings.
Research shows that sleep helps store memories. If you learn new information and sleep on it, you’ll be able to recall it better than if asked to remember that information without the benefit of sleep.
How dreams affect memory storage and recall isn’t clearly understood yet.
3. Creative times!
One theory for why we dream is that it helps facilitate our creative tendencies. Artists of all kinds credit dreams with inspiring some of their most creative work. You may have awakened at times in your life with a great idea for a movie or a song, too.
Without the logical part of the brain working, emotional and illogical thoughts take over your mind!
Eectroencephalography (EEG), electro-oculography (EOG), and
electromyography (EMG) are used to monitor neurological data from the brain to reveal information about neurological activities in the sleeping brain.
Here is a scientific literature (pdf) you can go through for in-depth study ( this link leads to ResearchGate page, you can read it there or download the pdf) :
https://www.researchgate.net/publication/281071308_The_Role_of_Dreams_in_the_Evolution_of_the_Human_Mind

Thanks alot Navoneel.


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Can a bacterium express a virulence gene and not produce toxins and what may be the cause of this?
I am preparing a seminar on viable but non-culturable (VBNC) state in bacteria, mainly foodborne pathogens and I just saw this line in a journal article by Lothigius et al that "the expression of the virulence gene in VBNC cells does not necessarily indicate the cells will produce toxins". Any explanation on what this statement means?
Lothigius, Å., Sjöling, Å., Svennerholm, A.-M., & Bölin, I. (2010). Survival and gene expression of enterotoxigenicEscherichia coliduring long-term incubation in sea water and freshwater. Journal of Applied Microbiology, 108(4), 1441–1449.

Where in the article do you find the quoted sentence? Or is it an interpretation of yours from the article as a whole?

To expand a bit on @Mohamed's answer, there are several mechanisms by which virulence gene products can be up- or down-regulated without changes to mRNA expression.
Post-translational modifications
Adenylate cyclase-hemolysin (AC-Hly) is a toxin produced by the Bordetella pertussis, the causal agent of whooping cough.  There are very few amino acid differences between the AC-Hly of B. pertussis and closely related Bordetella species.  Palmitoylations of lysine residues on the C-terminus of the B. pertussis AC-Hly are necessary for its specific cytotoxic activity.  [Bouchez 2017]
RNA secondary structures
After transcription, mRNAs can form secondary structures by base pairing, preventing ribosome binding and translation.  For some pathogens, virulence gene mRNAs forms these structures, which melt at human body temperature, allowing for fast production of toxins without the need to increase virulence gene transcription. [Narberhaus 2010]

Gene expression means making mRNA and then translated to protein. Their might be many steps unders regulation in this path where a gene makes mRNA but then that mRNA is not translated (like degraded or inactivated).


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What animal does this foot skeleton belong to?
I found an articulated foot skeleton. Sun bleached. What animal is this likely from?

Where was it found (in the world; there are people here from many different countries), what sort of environment (hill, beach, river etc.) and some sense of size will help with ID

Please see the species ID guidelines to improve your post: https://biology.stackexchange.com/tags/species-identification/info


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What are the differences (if any) in brain activity when hallucinating versus perceiving a real object?
I was wondering if there is difference in brain activity when someone is hallucinating an object, say a giraffe compared to when someone is genuinely observing a real giraffe?


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Can anyone identify what type of bug this is?
Can anyone identify what type of bug this is?

Hi, @Correo. Can you tell us where this bug was found please?

From a rummage around Google images for "black and red striped bugs", your insect looks a bit like:

Mylabris syriaca

Hycleus ornatus, although yours has different antennae.

The antennae do not match Hycleus, and it is definitely not Pyrrhocoris (Hemiptera). It does look like a blister beetle, as is Mylabris.

looks like Mylabris syriaca to me..

I'll take a wild guess and say that this is Mylabris quadripunctata


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Can you please identify this beetle? (Rajasthan)

I thought that it was dangerous and kept it under a polythene at my home, in Rajasthan.
Is this insect harmful, rare or common? If the pic is not clear, I would like to mention that it is green, six-legged and its body is separated in two from the neck.

This looks more like a true bug than a beetle, and may be a member of superfamily Pentatomoidea; the photo isn't as clear as I would like.  If I'm right as to group, species range in habit from predator to agricultural pest (and North American members of similar appearance are closer to the latter).

I agree. Not a beetle, but a Pentatomidae.

Not harmful to people but some species in the family are agricultural pests. Common name is "stink bug", named for the defensive scent it gives off when threatened.

I also agree. Looks like some species of stink bug (also called a shield bug) in the Pentatomidae family. As Karl said, these are often agricultural pests. Other than a fowl odor when crushed, these insects pose no direct danger to you.

@Karl I think you can make an answer out of your comments. There will probably be no need to ID that organism down to the genus level.


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How do elk know how long their antlers are?
They fight to compete for females, particularly those with similarly sized antlers. How would an elk know that its antlers are similar in size to another elk's if they can't see how long their own antlers are?
"The stag with the biggest antlers asserts dominance by showing them off and occasionally fighting with them."
Source: Natural Curiosities Ep. 4

Why do you think they can't see how long their antlers are?  I don't know about elk specifically, but most grazers have a very wide visual field.  Also, if they didn't somehow have an idea of their width, they would have trouble going throught the forest: picture one trying to run between two trees that are closer together than the width of the elk's antlers :-)

For comparison humans can't see what hat they're wearing. Elk have a wider field of vision but I doubt they have a field of vision tall enough to actually see their antlers, which extend very much behind their heads (example: https://elknetwork.com/wp-content/uploads/2016/09/bull_elk.jpg). To navigate through the woods I imagine they have a kinesthetic awareness and don't stray much beyond that. But to compare antler sizes requires some visual acuity -- my reasoning with this is that I wonder if confidence rather than perfect accuracy might play a role in this form of competition.

Maybe they make sense by weight.

I think you anthropomorphise in your question going by how you have worded it. It is an ongoing debate but so far only a limited number of animals have been shown to have a sense of self-awareness. Without self-awareness and a notion for length, the question of "who's got the longest" becomes irrelevant. It probably just so happens that the biggest animal (which also happens to have the biggest antlers) is a little stronger and thus asserts more dominance.

@Jamie: Without some data on the elk's visual field (and I couldn't find any in a quick search), we're both just guessing.


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DNA fingerprinting
About a month ago i performed a DNA fingerprinting lab and now i have a small lab report due in about two weeks.
Questions:
What are some possible errors that can happen during the process of DNA fingerprinting?(non-human errors)
My research:
One of the errors that can happen during the process of making DNA fingerprint is when the microcentrifuge tubes are open air particles can get inside it. The air itself has many things especially bacteria that can possible get into the microcentrifuge and can cause false results.(Can someone confirm this)
Thank you

This should be a comment

The most common causes of failures related to the laboratory process
were contamination and human error. Most human errors could be
corrected, whereas gross contamination in crime samples often resulted
in irreversible consequences. (article)
In DNA fingerprinting work, it is well known that, although fragment
lengths of a sample are uncorrelated, measurement errors of fragment
lengths are correlated. Unless the fragment length is very large, the
measurement errors are directly proportional to fragment lengths. In
the currently practiced matching procedures for forensic
identification, these facts are ignored or inadequately used. Some of
these issues are addressed in this study. (article)

You should provide more information about the method(s) you used. Further you found:

One of the errors that can happen during the process of making DNA
fingerprint is when the microcentrifuge tubes are open air particles
can get inside it.

This is error is not a specific DNA fingerprinting error, based on this I would suggest to read something about "DNA extraction/purification errors" like:

foreign DNA in your sample
Wrong phenol-chloroform ratio (I don't know if you used this --> reason why you should tell something about your methods)
PCR errors
etc..


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Is sex linked inheritance independent of dominance?
I have a little challenge with what my lecturer said in class. I disagree with explanation but don't know how to convince myself. Please review and tell me your opinion.
Eye-color in drosophila is a sex-linked trait in which a white eye male was crossed with a red eye female. The F1 generation consist of 54 white eye and 49 red eye female; and 47 white eye and 50 red eye male. Explain.?
He said and I quote

"the white eye male will transfer the white eye allele to the F1 female generation while the red eye female will transfer her red eye allele to the F1 male generation"

I disagreed because his explanation didn't account for the red eye f1 female generation and the white eye f1 male generation.... I proposed that the female parent was heterozygous for the eye color trait..... Hence a cross shows that the phenotypic ratios for either eye colors for any sex is 1/4...In response he acclaimed there's no dominance since it's a deviation from medellian principle.

please dont post text as pictures.

Ok. Thanks for the correction. It's been taken. But any idea on the question.

Welcome to SE Biology. The feedback from Ebbinghaus indicates that an edit will improve your question, the picture should be removed and the text added to your question. Including an explanation of why you disagree with your lecturer will also improve your question. The chance of attracting good answers increases in conjunction with the quality of the question.

Drosophila follow the same sex determination as in humans, XY for males, XX for females. The eye colour is sex linked, that is, the genes for eye colour are only carried on the X chromosone in this case, not the Y (there are other linkages that are only carried on the Y, but that's not the case here). The wild-type colour, red, is dominant over the white eye colour. When speaking of inheritance of eye colour in drosophila males specifically, you don't need to consider dominance or recessiveness as males only get one copy carried on the X - either the wild type red, or white, there is no interaction between alleles. The dominance and recessiveness only comes in to play with the eye colour of females, as they get two copies, one on each X they get from the parents, in which case the heterozygous will appear red eyed, as will the homozygous for the red eye allele.
For the image: In this cross we have a heterozygous red eyed female (XWXw) crossed with a white eyed male (XwY). In the offspring you see that half of the females would be heterozygous for red eyes, thus presenting as red eyed, and half would be homozygous for white. In the males half would be red eyed and half white eyed as there is no dominance or interaction between alleles as they only have the single copy on the single X chromosome they have inherited.
Hope this makes sense!
With all that in mind, you are right, you will only get white eye males in the F1 generation if the mother in a cross is heterozygous for the eye colour trait.


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Book on the history of Darwin's discoveries and development of his theory
This question is a book request. I am wondering if there are any books with these elements:

Tells the history of Darwin's discoveries.
Captures Darwin's changing views of the origins of species, because of his discoveries and his thinking on the subject.
Is a modern text but incorporates some of Darwin's writings (e.g. from the Voyage of the Beagle, etc).

Note: I am not asking for a book that is just explaining the process of natural selection, rather I am looking for a historical book about Darwin's discoveries and the inception and development  and eventually his publication of his theory of natural selection.

On your second point, for the most part, Darwin's views were fully formed within a few years of his return from the Beagle. They didn't really slowly change. But he was slow to publish for a variety of reasons.

@KarlKjer While that is somewhat true, I think there is a lot of nuance missing from that description, and Darwin certainly wavered on things and shifted his views prior to that time; the slow publication is only one aspect of the story.

I'm not certain it fills every element of your question, but I really enjoyed Michael Ruse's "The Darwinian Revolution: Science Red in Tooth and Claw."
It's especially good for setting up the collection of worldviews that predated Darwin, and the influence on him by both biologists/anatomists as well as very crucially geologists like Charles Lyell (Darwin really thought of himself more as a geologist; the long time prior to publishing Origin was largely because he was trying to build up some scientific chops as a biologist).
The aspect it is most likely to lack is references to original source material from Darwin. While it certainly draws on such writings, I don't recall it actually containing reproductions of those writings, at least not on a substantial basis.
Importantly, however, this book is not a biography - it is a history of the scientific community at the time, centered around Darwin and Origin and placing them in relevant context.

Thanks a lot (+1). To not discourage others from answering, I will wait some time before accepting.


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Is the occurrence of a particular enzyme in a given subcellular location a random phenomenon?
Enzymes occur in different subcellular locations. Some are specific to a given subcellular location, whereas others are heterogeneously distributed. What evolutionary decisions influence the occurence of enzymes in particular compartments?. Are the locations species-specific?

Some trace their evolutionary origin in the ancestral organelles (such as mitochondria and plastids) and therefore they are localized in those organelles. Can you add more details to make your question more specific?

I have edited the question above. I wanted to know more about this. Thanks

You have changed your question completely. What's more it is now nonsense: "What evolutionary decisions..." Evolutionary decisions indeed! And If you have to ask about enzyme locations being species-specific I suggest you ask yourself why enzymes are in particular organelles and whether organelles are species-specific. Do some reading about organelles yourself, instead of wasting our time.

Dear David, First of all, you edited my question. I just re-phrased it.This was the same question I was asking from the beginning. I respect your comment. If you don't understand the question, you cannot comment on the question being non-sense. As you know more than me or anyone in this group, I'm just asking you the same question "Why do enzymes occur in specific locations? And What evolutionary decisions influence the occurrence of enzymes in particular compartments?" This may sound a very general question. I just want examples. A review article that explains this question might be useful.

Also, there have been many proteomics studies in related species of bacteria, parasites, etc. where the same enzymes can be found in different subcellular location. I'm just adding to their observation my question as to why they might occur in different locations and also why they are species-specific. If I could not clarify my message still, then its worthy to close this question totally. Thanks.

There are various methods for targetting proteins to subcellular organelles or membrane locations. In general they depend on ‘tagging’ or ‘signal’ sequences in the proteins. Such tags or signals are recognized by specialized proteins that are able to conduct the protein through the membrane barrier to the particular location.
The individual processes for different target locations vary, so I do not think it appropriate to provide details here. You can read a summary of them in this Wikipedia article. For more extensive treatment you can look at the relevant chapters in Lodish et al.  or in Alberts et al. on-line (old edition).
(Please consider donating to Wikipedia, if you use it.)

It might be too broad a topic to be explained here, but you should at least describe some part of it (even if introductory) lest this is too short to be an answer.

@HomoSapien — It may be better to close it as too broad. I looked to see if it were answered previously. I'll add another sentence, but more than that...

Yeah, but that is another point. I meant that just giving some references would be appropriate for a question, especially if its too broad.

@HomoSapien — I think the two book refs are ok. They give a breakdown of the chapters for different locations (nucleus, peroxisome, membrane etc.) That seems to me a good entry point for a novice.

Yeah, they are. +1 for you mentioned donating for wikipedia ;)

Enzymes occur in different subcellular locations. Some are specific to a subcellular location. Some are heterogeneously distributed. Lets take the example of metabolic enzymes. The location of an enzyme in a particular subcellular location may dictate the flow of metabolites through different compartments. I wanted to ask "what evolutionary decisions influence the occurence of enzymes in particular compartments?. Are the locations species-specific?". A review article, book or research article that explains this question might be useful. I'm editing the questions too.


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Can the Quarternary Extinction event be linked to the spread of mankind around the world?
Evidence is presented in a variety of media by Paul S. Martin as his 'Overkill hypothesis', particularly in Twilight of the Mammoths.
The internet describes this idea as 'controversial.' Other than the works of Paul Martin, what evidence has been presented supporting this hypothesis?

Please provide more information for your question. Do you have a source that presents this hypothesis or some other reason to believe so. Please indicate some evidence of prior attempts to research/answer your own question

@theforestecologist I have read Paul Martin and generally agree with him. However, I haven't found any other semi-credible popular science books that agree with him. I asked the question in the general sense to see what other evidence was out there, preferably in readable summary forms.

Mr. Martin has forgotten one glaring problem with this hypothesis--TIMING.

extinctions rarely have a single cause however humans could very well have been a contributing factor. Intelligence makes for some destructive hunting methods like setting a grass fire to kill a herd of animals or driving half a herd off a cliff to eat only a few of them.

Mammoth much like elephants are believed to be particularly vulnerable, the breed slowly and have few natural predators, the introduction of just one new species of predator (and in humans case a very successful one) can be devastating to a species like that.

Only in islands can this hypothesis be supported.  But islands are NOT continents, and that raises problems with the hypothesis.  The most inconspicuous of which is timing.
In Australia, the gap between man setting foot on Australia and the extinction of Australia's megafauna was 17,000 years. Too long.
Man left Africa and set foot in Eurasia more or less than 50,000 years ago, yet the extinction of Eurasia's megafauna happened 10,000 years ago. Too long.
The oldest discovered American, "Eve", was discovered in a cave in Mexico's Yucatan Peninsula and dated to be 13,500 years old, 500 years older than the supposed time that man crossed Beringia. This could imply that man crossed Beringia at a far earlier date, yet the dating of the extinction of America's megafauna coincided with that in Eurasia. Too long.
There's also into consideration the Younger Dryas climate chaos phenomenon, which did coincide with the extinction of the 30 genera of Pleistocene megafauna, a handful of microfauna and plants, not to mention the Clovis culture itself.
If man was the cause of the extinction event, the gap between man setting foot in new lands and the megafaunal extinction would've been a few generations, not a few millennia.

Do you have any concrete evidence or citations to support your answer? I confess I know nothing about the hypothesis being described, so I can't judge the validity of your answer. As it stands now, the answer is completely opinion-based.

http://www.bbc.com/earth/story/20161102-what-really-happened-to-mammoths-and-other-ice-age-giants?ocid=fbert  http://www.sciencemag.org/news/2016/08/climate-change-not-humans-killed-giant-camels-and-sloths-south-america  https://en.wikipedia.org/wiki/Younger_Dryas

why only a few generations? do you think humans would instantly fill the land mass? A lag is to be expected since humans need to reach semi-isolated areas and hunting an organism to extinction is not going to happen instantaneously, it took humans many generations to cause even the uncontroversial extinctions. Then you have to consider whether humans are the final cause or just so severely weaken the population than something else can easily take them out. Saying it took too long is just misleading unless you can quantify how long it "should" take.

@John  Look no further than the damage done in the 19th and 20th centuries with modern megafauna like bison, rhinoceros and antelope.

none of which are extinct, even with firearms, so even under perfect circumstances it is not fast, unless the starting populations are tiny.

@John  What matters is the crash itself.


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Non-Lifestyle related diseases
Given the obvious importance for global health, I've found it easy to track down lists from Google of the top lifestyle related causes of death (like heart disease, lung cancer etc), but as a consequence it proven difficult to find a source of the opposite, the leading causes of death which have no (or very little) relation to lifestyle choices (like smoking, obesity etc).
What I'm interested in is those chronic and generally quite fatal disease which just happen for either genetic or spontaneous reasons, or perhaps due to environmental causes which are so ubiquitous as to be unavoidable.
I'm not looking for an exhaustive, or even very large list, the top five to ten would do, and I understand that there's no clear distinction between lifestyle and genetic factors, but obviously health organisations make some estimate of what is mainly the cause otherwise lists like these would not be possible. I just want the opposite list.
To clarify in the light of some answers, I'm looking for diseases which one might contract in adulthood (this could include pathogens) which could in a normal healthy person living within reach of modern medicine still present a more than 50% chance of being fatal. Basically I'm after a risk figure (my field of research) which would act as a baseline presuming a safe, healthy life.

Getting impaled by a giant metal rod might leave you pretty deadish

Fair point, have edited the title to specify diseases. Mind you standing precariously above sharpened metal rods might well be considered a lifestyle choice.

I think it's somewhat fallacious to equate all heart disease to lifestyle choices. The heart of someone living a very healthful life will eventually give out. Cancer is not always caused by something we've done. So there's plenty of overlap.

@anongoodnurse I quite carefully did not relate all heart disease to lifestyle choices but put it  (quite uncontroversially) in a list of diseases which are "related" to lifestyle and then go on to specify that I'm interested in differentiating disease by what is "mainly the cause". Having already specified in the question that "I understand that there's no clear distinction between lifestyle and genetic factors" I'm not sure what to make of your contribution that "there's plenty of overlap".

So the CDC has a list of total leading causes of death
https://www.cdc.gov/nchs/fastats/leading-causes-of-death.htm

Number of deaths for leading causes of death
  • Heart disease: 614,348
  • Cancer: 591,699
  • Chronic lower respiratory diseases: 147,101
  • Accidents (unintentional injuries): 136,053
  • Stroke (cerebrovascular diseases): 133,103
  • Alzheimer's disease: 93,541
  • Diabetes: 76,488
  • Influenza and pneumonia: 55,227
  • Nephritis, nephrotic syndrome, and nephrosis: 48,146
  • Intentional self-harm (suicide): 42,773

Cancers can be further subdivided into types which may or may not be related to lifestyle. There are lung cancers and skin cancers that are not linked to smoking or skin damage respectively. Cancer is very complicated.
Most of the causes on this list have lifestyle or environmental components to them. Influenza and pneumonia have less to do with lifestyle and more to do with the immune system either being too robust or not robust enough but the immune system is influenced by lifestyle as well.
To get a list of diseases that are the leading causes of death and not influenced by lifestyle or environmental, you'd probably be looking at genetic diseases like cystic fibrosis for example.
The WHO has a list of these monogenetic diseases. These are diseases that are caused by a single gene (either one or two copies of the gene depending on the disease) and are independent of lifestyle and environment.

Thalassaemia
  Sickle cell anemia
  Haemophilia
  Cystic Fibrosis
  Tay sachs disease
  Fragile X syndrome
  Huntington's disease

You can read more about these diseases here: http://www.who.int/genomics/public/geneticdiseases/en/index2.html

Thanks, that's something like what I was looking for although I failed to specify in my question (my mistake) that I'm looking for causes of death which would not be apparent within early childhood, something which could just happen and you'd have no way of reasonably avoiding it.

If the main goal is trying to avoid death, then living a healthy lifestyle, going to the doctor for checkups and getting blood work done regularly are your best bets to identify diseases early on and hopefully prolong your life.

I'd think even influenza &c could be said to be lifestyle-related.  After all, you catch them from other people, so if your lifestyle is such that you spend a lot of time in crowded places, you're probably more likely to get them than if you're a hermit living in the wilderness.

As I've specified in my edits I'm not looking for medical advice, I'm a statistician, my interest is in risk perception, I'm trying to establish systems for communicating risk that are more accurate than Lifetime Risk (which gives the misleading impression that your risk would be zero if you avoided whatever factor is being discussed) but more meaningful than Odds Ratios which most laymen cannot relate to. I have access to mortality statistics, but in order to extrapolate the data I need to know which causes of death would give the best indication of a "random, unavoidable" cause.

I'm getting the distinct feeling that the information I need is tantalisingly there but not being specified, you mention in your previous comment "living a healthy lifestyle, going to the doctor for checkups". If the only diseases not influenced by lifestyle are monogenetic ones then what are you going to the doctor's regularly to get check for? This is exactly what I'm asking, you seem confident that a person leading a healthy lifestyle should still visit the doctor regularly for check ups. If you could just list the things a healthy person might need checking for, that would be my answer.

This is a list of the top ten most common genetic diseases.
This is a link to a list of the 'worst' genetic diseases
This is a link to some fatal genetic diseases
I hope that helps, I think genetic diseases are the only ones that would not be considered a lifestyle disease. Other diseases would be caused by a pathogen; I have never heard of one arising spontaneously (although I could be wrong about that).

The OP asked for causes of death. Some on your list are not fatal. Also, diseases arise spontaneously all the time that are unrelated to lifestyle. Many cancers come to mind.

@anongoodnurse Could you perhaps list some of the many cancers that come to mind or point me to a reliable source. This would be pretty much what I'm looking for, but whilst it's easy to find a list of cancers broadly related to lifestyle (lung, skin, colon etc) I've found it harder to get a list of ones which really aren't.

@Pseudonym - That's a matter of taking all cancers and subtracting those that are influenced/caused by lifestyle. Too many to list.

@anongoodnurse I presume from your comment that you personally cannot supply me with an answer, but for the sake of any other experts potentially willing to help, l'm only asking for the top few, not the entire list, just ten of the highest risk cancers that are not strongly connected to lifestyle factors would do, even one would be a good start.

@Pseudonym - I can supply you with an answer, but believe in the value of working to get what you want (seriously. I didn't become a physician by asking other doctors for help all the time.) I gave you a formula to find the answer: google the top, say, 10 cancers and delete those with known lifestyle causes.)

@anongoodnurse I am certain that Biology.SE is not the primary source for any of the information given in its answers and so all of them could be deduced by Googling eventually. I have mortality statistics ordered by coroner's code numbering in the several hundreds of causes. I could re-sort them all in order of mortality, and Google each one to see if it's lifestyle related but it seemed eminently sensible to first see if any one had already done this. A simple "no, I don't have that information to hand" will suffice, I don't need to be chided like a child who hasn't done their homework.

http://www.slate.com/articles/health_and_science/science/2014/02/deadliest_cancer_chart_shows_mortality_and_incidence_rates.html Here is a detailed chart for the deadliest and most common cancers. However, they don't mention how many of these are related to lifestyle so additional research may be needed for that.


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How does the tRNA recognise the first methionine during translation?
The process of translation starts with the initiator tRNA identifying the codon coding for methionine (AUG). However, my textbook also says that there are various untranslated regions present on the mRNA. It was then that this question had occurred to me. How does the tRNA actually differentiate between the regions that are ought to be coded and that are not? One may say that translation always start with the methionine, but my question is different. For example, if the code is
5'...GUAUGCAUGAUC...3'
then when the tRNA arrives, it reads from which of them? Does it leave the first two nucleotides and read it as AUG CAU GAU and so on or does it leave out the first six nucleotides and read it as AUG AUC and so on?

I suggest you read further in your text book or consult a better textbook if necessary (look at NCBI Bookshelf on line) before posting here. Be advised that the answer is different in prokaryotes and eukaryotes.

There are different processes for recognising the initiator site in prokaryotes and eukaryotes.
In prokaryotes the process relies upon the Shine-Dalgarno sequence, this is a well conserved sequence throughout prokaryotes found upstream of the start codon. It interacts with the 16s ribosomal RNA to place the initiator codon in the A site of the ribosome.
In eukaryotes the process is somewhat more complex and relies upon a large protein complex which assembles on the 5' cap of mRNAs. This complex mediates an interaction between the mRNA and the ribosome, the ribosome then scans (using GTP for energy) 5' to 3' to detect the start codon.
One final process which is unusual but does occur is cap independent initiation mediated by internal ribosome entry sites (IRES). These are sequences which form structured loops which can mimic the interactions usually formed by the cap complex. These sequences appear in viral mRNAs allowing viruses to bipass anitviral mechanisms in cells.
You will need to do some reasonably extensive reading if you want to uderstand fully these processes and how they may be manipulated by cells to alter expression.

To explain this to a beginner, rather than encouraging him to do some more reading, I would leave out IRES and instead correct your description of eukaryotic initiation, which does not involve placing the AUG in the correct position but involves scanning from the cap to the first AUG in a suitable context.

@david I have adjusted as suggested I felt that introducing scanning left the obvious question, how does the ribosome know when it has reached the start codon? However upon your advice I have altered the answer. I have included IRES as these are important in viral infection and will point the reader to literature which could help understand the regulation of eukaryote initiation.


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What is the protein with the highest affinity to lactose?
I was wondering: What is the protein with the highest affinity to lactose? Are there some databases with values for affinity?

About what kind of affinity are you thinking? Binding of the sugar? Or do you think about specificity of enzymes?

Galectins 1&3 perhaps

Did you make any attempt to find out the answer? If yes then please add that to the question. It is not appreciated that you ask others to do literature search for you.

Yes, I did some research. I found that galectin 1 & 3 had very high affinity but there were not specific to lactose. I found this website: http://www.bindingdb.org/bind/index.jsp


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What is the correct value of Neuronal Resting Potential - is it -65mV or -70mV?
Some books show the resting potential of neurons as -65mV, such as Neuroscience: Exploring the Brain, Fourth Edition (2016, published by Wolters Kluwer).

However, a majority of internet sites, including Wikipedia, show the resting potential as -70mV.
Which one of these is the correct value, and why is there this small difference?

This seems a rather specialized question. Why are you concerned about what you admit is a small difference? Does it have any practical relevence to your work? We would be interested to know.

@David I  was just reading about the resting potential of the neurons in the book mentioned above.The book uses -65mV in all the pages ,when i checked the internet ,it is -70mV everywhere.So i was curious.

@David Why are you concerned about what you admit is a small difference?  I am new to the field so i was confused.  ** Does it have any practical relevence to your work?**  No,I am not building anything,just reading only

Neither is incorrect. Neuronal resting potential is a function of the internal and external concentrations of ions and the conductance of the membrane to those ions via ion channels. Different neurons exhibit a range of resting potentials.
You can calculate the resting potential for a given cell using the Goldman Equation.


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How many nutrients do trees process daily?
Is this tree fact below that I have found on social media sites true? I don't know the source of the quote. It's pretty amazing. I'll be glad if someone can provide the source too!

Natural Wonders
Every day, a 40 foot tree takes in 50 gallons of dissolved nutrients from the soil, raises this mixture to its topmost leaves, converts it into 10 pounds of carbohydrates and releases about 60 cubic feet of pure oxygen into the air.

There are 1000s of tree species that all vary in anatomy, morphology, & physiology; so, this type of generalization seems inappropriate & misleading. 2 trees of the same size but of different species would surely absorb/process nutrients at variable rates & in varying quantities. Further, even 2 trees of the same species would not experience consistent nutrient uptake & processing if environmental conditions (e.g., temperature, water availability, humidity, soil type, etc.) varied b/w each. Finally, trees of the same size aren't necessarily the same age, & age would impact these processes, too

I don't know much about trees, but I was very skeptical about this post at first. If this web page is correct, then the post is actually not so far-fetched.
Trees are amazing. According to the page, the average tree absorbs 10,000 gallons of water and uses 1000 gallons, evaporating the rest. 24 gallons of water contains one pound of dry matter. That means that the average tree would accumulate almost 42 pounds of dry matter in a single day.
Now, I certainly cannot vouch for the credibility of the website, but it was difficult to find a page that showed the numbers, so take it with a grain of salt and try to find other sources that back it up or counter it.
Here's the link: https://www.thoughtco.com/process-of-using-water-by-trees-1343505

We found the following link when search on the quote, the information is cited there:  http://gibneyce.com/tree-stats---classics.html
Cristina Hubbard, Executive Director
Forest Web

It's vague and hyperbolic.
The USGS water page says that a big oak tree can evaporate 40,000 gallons per year, that's 400 gallons per day for the growing season.
This page also disagrees with the quote, giving less than half the figure, about 400 gallons per day for a 40 foot tree.
A 10x10 meter square of forest gains about 4 tons of weight per year, 11kg per day, so that fits in with the quote's estimate of 10 pounds per day.
So there is some truth to the quote for a hot day, it's overly generalized and vague.


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What does it exactly mean to sequence the genome of a species?
Since all organisms are different from each other - that is, we all have different alleles, some SNP, microsatellites, etc. -, what does it exactly mean, for the genome of a species, to be sequenced? I understand what it means for an organism's genome to be sequenced, but I don't really get what it means for a species.
I'm quite confused about this. Thanks in advance for the help!

Sequencing a "species" builds a reference genome that is considered to be a good "representative" of the species. Of course there will be genetic variation between the reference and healthy specimens in practice (usually SNPs), however it should be minimal.

+1 for a concise answer, but saying the variation is "minimal"...


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How Ants can eat Chili peppers also?
I captured a picture where ants feeding on Chili peppers also, I was shocked.

Actually this peppers is one of the best way to get rid of ants is to prevent them from ever considering from home.

What exactly is your question?

@BryanKrause I edited my question, still is it unclear?

Yes it is still unclear you seem ask why the ants eat the pepper then state it repels them instead. Since I have never heard of chili peppers as an ant repellent, a source fr this claim might help. Are you asking why insects can eat chili peppers with no problem? The answer is capsaicin only works on mammals and possibly fungi.


text:
Identify these hinged barbed bones
My daughter Stella and I found these bones on the shore of Port Phillip Bay, Victoria, Australia.
The smaller, barbed bone is attached by a hinged joint that allows it to move through just over 90 degrees. The photos show it at its two extreme positions.
The photos include an Australian 20 cent coin for scale (29mm diameter).
Can anyone identify what kind of bones these are, and which species they come from?

Looks like one of the scorpionfishes.

I think it is part of a Australian trigger fish skull. check the pictures below, unfortunately someone sawed off most of the spine on the skull photo, but you can see the base of it, it is probably not the exact same species, but it is certainly part of a triggerfish skull. There are a half dozen species in Australia.

Cool find.


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What is the genetic explanation for gall forming in erythrina by gall wasp?

http://www.cabi.org/isc/datasheet/46220
Gall wasp  layed egg in the stem of the erythrina variegata,  the larva make gall, I like to know how the gall formation occurs in erythrina variegata


text:
Understanding mRNA vaccine for COVID
As I've learned, mRNA helps us to produce virus spikes proteins to induce learning of the immune system.
But then, I remember to have read that the coronavirus has some trick to pretend to be "food" to our cells, that is it has some lipid element. So it can entry the cell easily. But this was not same part as the spike protein, right? (otherwise it would have been contradictory with the mRNA approach?)

You have it wrong. Coronaviruses are part of a family of viruses that are called "enveloped viruses". These all have an "envelope" comprised of a lipid layer derived from the host cell as the virion exits. The envelope is distinct from the spike. The spike protein is produced by the virus during replication and is not found naturally in a host cell.
This does not pretend to be "food" at all, but it can help evade host immune responses by hiding the other virion capsid proteins.

thx this was the missing bit if information


text:
Misuse of DNA leaks to create your clones, or children
Recently, sequenced DNA data leaks have been reported.
The linked article discusses possible risks like blackmailing based on health related data.
However there could be one more misuse, at least theoretically, therefore this question. For not specialists, actually good to know.
Is it by current state of the art technically possible using this DNA data to (given you have fully sequenced DNA of an individuum):

clone this individuum?
engineer artificial gametes to breed his/her children?

I voted to close because this is science fiction, not present-day science, which should answer your question: We are not remotely close to being able to do what you suggest.

I don't understand, why this question gets down and close votes for basically asking "Is this science or fiction?"

As @iayork mentions in their comment, creating a human clone from a sequenced genome is still in the realm of science fiction. Also, DNA testing companies like MyHeritage don't sequence the client's entire genome. They typically analyze the client's DNA with a SNP Chip that compares the client's DNA to known reference sequences at several thousand position with well known variations in the human population.


text:
Does human DNA code for enamel multiple times?
Given that DNA provides instructions for multiple parts of the body as a general representation, how is that about the number of teeth with regards to the enamel code?

there are 32 teeth but they are referenced as a "shape" that is there is no such a thing like "number 32" in our genetic code
is then the enamelin gene encoded 32 times in all corresponding places, or just once  and referenced somehow?

Morphogenesis doesn't work in either of the ways that you propose.
To understand better, let's shift the focus from teeth to something that's easier for me to explain and visualize: extra fingers, also known as polydactyly. This is a surprisingly common condition, appearing in approximately 1 of every 500 births, and for many people the extra digits are fully functional. More importantly, the causes, even when genetic, are subtle and typically involve very tiny changes in DNA code.
In the embryo, the hand starts out as an undifferentiated blob of tissue. At a certain point in development, it starts patterning and splits into fingers. When the patterning goes wrong, the split happens too often (polydactyly) or not enough (syncdactyly). Once those splits into "stuff that will become fingers" has occurred, however, then the "make a finger" system encoded in the DNA starts running in each and does its best to make a finger, leading to the final outcome.
Thus, the genetic code doesn't need multiple copies of the "make a finger" system or multiple independent invocations of the "make a finger" system: it just needs a system for making a pattern. The specifics for teeth (and any repeated structure) will be different, but the general principle will typically hold (with some caveats; evo-devo is complicated)
If you're a computer person, you can think of it as (very) loosely analogous to calling "split" on a string, then using "map" to apply a function to each of the components that comes out.

thank you: indeed the split can be referenced by computer persons to be an invocation in parallel thread execution. So be it a "split" into 5-fold fingers either 32-fold pre-teeth areas (which activate later, after birth), is there anything like genetic code capturing the actual number, for fingers, "make 5 fold split"?

@J.Doe To the best of our understanding, there is generally no encoding of a numerical value as a number in natural genetic materials. Number can be tightly or loosely controlled by a large variety of other mechanisms, however, and in some cases there are literal duplications of genes. The relationship of any of these things to the count of large-scale morphological features, however, is typically complex and indirect. I suggest reading up on evo-devo to start learning about it in more depth.