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Why are mRNAs polyadenylated as opposed to any other polynucleotide?
During processing, the vast majority of mRNAs recieve a polyadenine (poly-A) tail. The function of this tail is not the subject of my question, but the reason it is specifically adenine, as opposed to any other nucleotide?
I have heard that adenine was the first nucleotide, and that's why it is chosen for this. This would also explain why ATP and NADP are preferred over other nucleotides for their roles (related), but it seems like a hollow explanation, after all, the RNA world hypothesis posits that RNA was the first nucleic acid, yet information is encoded on DNA in modern organisms due to RNA's unsuitability (Wikipedia).
Furthermore, other energy carriers, such as GTP exist, but a poly-G tail is, as far as I can tell, never observed. (related)

“I have heard that adenine was the first nucleotide”. From whom? How does he know? Citation please.

@David As far as I remember, it was my professor that told me that. However, I cannot find any sources to back it up.

Short Answer
As with many evolutionary ‘Why?’ questions, we do not  and cannot know.
General Possibilities
It is good to be aware of the general types of answer to this sort of question, as it avoids one assuming one type of explanation.

The selected alternative is functionally superior to the alternatives.

The selected alternative is the result of pure chance.

Evolution of the selected alternative used more abundant and/or pre-existing chemical intermediates or enzymes

Evolution of the selected alternative involved fewer new enzyme-catalysed reactions.

All one can do is see if any alternatives can either be eliminated or have strong support. My own approach in this respect is illustrated in two separate answers I provided to another question related to ATP.
The current Example
Regarding adenine and polyadenylation, there seems nothing to support explanations 1 or 4.
We do not know at what stage the polyadenylation reaction arose in evolutionary history, but it seems likely that it post-dated both the evolution of the other three bases in RNA, and the emergence of ATP as the prime energy carrier. If so, the concentration of ATP in cells would be much higher than that of other ribonucleotide triphosphates, and protein (or even RNA) modules that could bind ATP would already have emerged in enzymes.
Thus, I would tend to an explanation of type 3, although not being able to exclude 4. But as we do not know what form mRNA took in an RNA world, and when polyadenylation arose, we are whistling in the dark.


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Role of epigenetics in evolution and transmission of defects caused by drugs
In a documentary, they were saying that epigenetics changes caused by the environment in an individual can be transferred to the following generations. I have some questions on that:

How many generations are affected by an epigenetic change? can this be permanent?

Can drugs cause epigenetics changes in the current population that are visible in the following generations in the form of disease and birth defects?

Do epigenetic play any role in evolution? For example, is it possible that an epigenetic change becomes a permanent genetic change after a certain number of generations?

You may not be aware that you have stepped into a minefield. The term epigenetics has been subject to considerable hype (I would be interested to know what documentary you watched and what precisely was claimed), phenomena in insects extrapolated to humans, and association confused with causation. In order to separate fact from fiction here, one needs to be able to understand the basic science. Do you have the background to understand this article, for example.

Generally speaking, epigenetic modifications are not inherited as they are reset during embryogenesis. However, subsequent epigenetic modifications can be acquired during the period of pregnancy, which as a mechanism depends on the epigenetic state before the reset and on the physiological conditions of the mother including nutrition, health, stress, etc.. Obviously drug-intake years before pregnancy can still affect the mothers health-state.
Answering your first question: Epigenetic modifications generally cannot be directly passed, but indirect effects could theoretically pass through multiple generations without hard limit.

A major barrier to transgenerational epigenetic inheritance is germline reprogramming, during which histone variants and their modifications, as well as small RNAs and DNA methylation, are all reset. In mammals reprogramming occurs both in the germline and in the zygote immediately after fertilization. (Source: Heard & Martienssen 2014 doi: 10.1016/j.cell.2014.02.045)

2: The great potato famine is said to still have epigenetic effects, generations later. 3.: Epigenetic changes cannot directly "become permanent" as genetic changes, although hypothetically speaking, epigenetic states can lead to viability of certain mutations that would otherwise be lethal and can therefore in theory influence evolution.

"Epigenetic modifications cannot be directly passed" seems to be a bit of a controversial statement, as far as I know (as is the converse, that they can be directly passed), especially for humans. If you want to make that claim, it needs a reputable citation to back it up.

I agree, I added a source. Sorry! What I meant is that modifications are at first removed but then partly could be restored later. So it's not "direct". Given question 3 implies that the OP is no biologist, I didn't want to unnecessarily complicate things.

I think it would be helpful to be more specific about what "epigenetic modifications/changes" are. People tend to fixate on methylation/histones, but there are perfectly good epigenetic circuits set up that are based only on transcription factors/protein components. The heritability of the different kinds, that's a different question.

Much better. Thanks! The word "generally" adds a lot, too. I've made some edits to include the author names and made the DOI a link.

Epigenetic changes can only be passed directly onto the next generation when they occur in the cells that proliferate into the gametic cells (ovum and sperm cells).
There is some research with rat models that show the inheritance of epigenetic changes over several generations, so it´s possible.
(an example for cocaine-addiction: https://www.nature.com/articles/nn.3280)
The main protein family that participate in epigenetic regulation are the histone deacetylases (HDACs) and the histone acetyltransferases (HATs), which can modify proteins that bind to the DNA and thus control the expression and activity of genes, and these proteins can be influenced by environmental changes.
(Several types of cancer are thought to be caused/affected by the activity of HDACs that shut down tumor suppressor genes, and there are many medical studies focusing on chemotherapeutically inhibiting their function in cancer patients.)
This paper can give you a good overview: https://pubmed.ncbi.nlm.nih.gov/11420732/

Question 1: how many generations.
In one of the first description of transgenerational epigenetic inheritance, before any of the mechanisms were worked out, Woltereck found (my translation, caveat emptor) that he could find influences on both children and grandchildren of starvation in Daphnia (Figure 1).

Figure 1. Daphnia head morphology response to starvation. Left: control animal (fed normally, parents and grandparents fed normally). Right: successive generations of descendants of starved animals. 1. Gen: child, 2. Gen: grandchild, 3. Gen: great-grandchild.
How common such epigenetic changes are is a huge subject of debate. Nutrition appears to be the big one- see also the Barker hypothesis in humans, especially in re: the Dutch Hunger Winter.
Question 2: don't know.
Question 3:
It's a thorny question! Woltereck and similar people were already arguing about whether these observations might be evidence for Lamarckian inheritance, e.g. inheritance of acquired characteristics. We've pretty much gotten rid of Lamarckian inheritance in favor of vanilla Darwinian inheritance via DNA, but people still argue about it, as e.g. here.

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What websites biologists use to check what new plant or animal species have been discovered in the world?
What are the databases or websites that biologists use to check what new plants or animals have been found in the world? The service should list the location of the discovery, time of discovery, image of the new species, the name of the discoverer and other vital information

“The service should list…”. Is this an invitation to tender?

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Where can I download a list of all plant species of the world?
Where can I download a complete list or dataset of every plant species in the world?

If you download the tree of life 85mb file, it's updated often, although it contains all species of all living things. there are probably resources related to that, and sub sections with the different supergroups and kingdoms.

This website claims to contain all the plant species we know of (and also contains some statistics on the state of their collection). Keep in mind that there are many species that have yet to be found or assessed correctly. The world is a big place.
http://www.theplantlist.org

A web-crawler may assist in downloading the information for yourself - from this site :)

web-crawling, web scraping, maybe on kaggle there is a list too :)

@Andrew Interestingly, there is an option to download either your search result or per-family data in CSV format - for later machine processing

Fantastic, that is even better.


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Identification: creepy dangling spiderthing
Can anyone identify this creepy mess dangling from the cieling of my garage on a few strands of spidersilk? The thing is 5cm.

Should I burn down my garage and move to another country (Currently Belgium)?

I think I found it now. Have a look at this:
https://fireflyafrica.blogspot.com/2009/03/rain-spider-nest.html
it features a nest, large ("tennis ball" sized), hanging from threads, and they claim it is a "rain spider" nest, but rain spiders do not seem to span Belgium.
I am not familiar with what a 'Rain spider' is, so looking it up,'rain spider' is a genus of the Huntsman spider family, and there are huntsman spiders in Belgium. But huntsman spiders are known to carry their own (small pouch) egg sacs.
Looking up "rain spider nest" finds many photos similar to yours. But I cannot find any that live in Belgium or Europe.
This is probably on the right path, and you can try searching for various cousins or other relatives of the 'rain spider' that might be in Belgium.

Well, it's more pingpong ball sized, so I think it'll be the egg sack of a rather ambitious Tegenaria

Stored prey? for a couple of years?


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Why there is unusually big leaves on a single tree branch
I have a freshly planted katsura tree - in general it has leaves that are 1-2 inches in diameter.

But one single branch has grown disproportionally longer than others and leaves on this branch are up to 4 inches in diameter

Why is that? Should I trim it?

I'm not sure we can answer the bit about whether or not you should trim it (there is a landscape/gardening beta here which may be better). But what kind of 'why' answer are you looking for? One which explains it in terms of physiology / evolution / biochemistry / environment interaction?

With many plants, including Katsura, the juvenile foliage is different from the mature foliage. With Katsura the juvenile foliage has larger leaves.

The rest of new leaves are about the same size and structure as older leaves. Also no other branch has grew up THAT much - they added maybe a few inches but this one added 2 feet. I'm curios what may be the cause.


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Pectoralis muscles as push muscles vs pull muscles
Pectoralis muscles are the adductors, flexors of arm in addition to medial rotators  of arm. How does this action translate in to acting as helping in push ups or in bench press?
I am having trouble visualizing the primary actions helping in these compound movements.
I also have trouble understanding why this muscle being a powerful adductor does not work in pull up exercise?

The pectoralis major is not just an adductor and medial rotator of the arm. Its clavicular fibres also flex the arm at the glenohumeral joint. This is the action useful in performing push-ups and bench presses.
And yes, its adductor action also plays a role in pull-ups and climbing (along with that of the latissimus dorsi, another adductor).

References and further reading:

https://www.kenhub.com/en/library/anatomy/major-pectoralis-muscle

https://www.kenhub.com/en/library/anatomy/the-shoulder-joint

Romanes GJ. Cunningham's manual of practical anatomy. 15th ed. Vol 1, Upper and lower limbs. Oxford: Oxford University Press; 1986. (ELBS edition, 1989 reprint). 263 p.


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Does too much screen time really damage your brain?
So I was looking on the internet for articles to whether computers really damage your brain and I found that half of them say the do and the other half say the don't. Personally I don't think it does as majority of working people use computers in their day to day jobs and still have the same intelligence and cognitive ability after say, 10 or 15 years of using them.
So does anyone know wheter this sttement is true or not.
Thanks,
Ps. I'm not a biologist, I'm just a curious kid :)

"Damaging your brain" is far too vague a claim to be evaluated scientifically. If you can find a specific, notable claim, then skeptics.stackexchange.com is a good site for that question (check their Help to see what is on topic there). If you collect some background and have a specific question to ask about biology that can be asked here.

And of course it might depend on what you actually DO during that screen time.  Developing programs to solve problems in the sciences probably has different effects than say following social media.

JamesM, Rapidly moving images/cartoons/games for many hours per day modify the attention span and self control especially in children, and there is research for that area. It means that children can become confused when they don't have rapidly moving images and they are less able to focus on slow activities like reading, toys, etc. Perhaps read this, it's  a related scare article: https://time.com/5514539/screen-time-children-brain/ low self control i.e. when someone speaks to you and doesn't look calmly at you but looks around fast in all directions while thinking, can vary  with screen use.

@aliential: Interesting.  Perhaps that explains why I find rapidly moving images in video to be so annoying - I was never exposed to them in childhood :-)

Yes Garry Kasparov would not have had any chance of being a chess champion if he had cartoon network on TV as a kid. One study found that even 9 minutes of spongebob squarepants can shorten children's attention spans.


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Does our brain contain an innate function about closing only one eye?
I wasn't sure where to post this, but biology seemed fitting for me. Sorry if I'm wrong.
I was wondering why, when we close both our eyes and look at light, it is clear we can see the light even though our eyes are closed. We can identify where the light is too.
However, when you look at the light with only one eye closed, suddenly you cannot perceive this anymore and you can only focus on the open eye's vision. It's like our brain is ignoring the closed eye's vision somehow. What is triggering this "ignore vision"? Is it the closing of the eye?
I found this intriguing and wondered how this works and/or if there is any research about it.

Look up "Ocular dominance"

I'm only a 17 years old student but i guess this is the answer(its just what i guess, haven't seen it in any books or research):

This is a picture from the book Life.
When both eyes are working they send signals to brain.
signals from things on the left side are sent to right side of brain and signals from things on the right side are sent to left side of brain(coming from both eyes).
as you can see both eyes participate in sending signals to right and left hemisphere.
On the right side of picture you can see visual cortex of right hemisphere , it has signals coming from both left and right and makes the thing we see.
While seeing through only one eye (or when you cut optic nerve from one eye) there is still signals coming to visual cortex from the other eye and that makes image of what you see.(when you close one eye there is still little signal from it if you are facing a bright light source, but signal from the other eye has more effect as its more powerful( try it by closing one of your eyes and put a torch in front of only the closed eye, if the torch is bright enough you can see bright thing there))
when you close both eyes the signals coming from both eyes are almost the same and if you face a bright thing, you almost see it.
i just guess that's the mechanism :)

That's a nice explanation! But there is one thing I'm confused about. So, when closing only one eye: the optic nerve is cut from the closed eye? But when closing both eyes, the optic nerve of both eyes are open? Because when both eyes are closed, you can still "see" the light. But when only one eye is closed, you cannot.

no its not cut from the closed eye, i just meant it is like cutting it, when you close the eye, the signals coming from it become weaker and less as if there is no eye. its like comparing these numbers:1-both eyes open:10000-10000     2-one eye open:10000-10(0 if the nerve is cut)   3-both closed: 10-10  10000 is soo big compared to 10 so brain somehow omits 10.

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is this true to select 100 volume higher concentration of a drug test?
I am interested in knowing how to find/optimise the concentration needed for a drug effect in cell. and different organism
For example, if I use 1 micro molar for treating a cell. Should I use 10 nM when I use C.elegant ? how do you define or tune such a concentration ? Please give me reference too if there is any

Typically when working with compounds I come from two directions:
Does the drug appear in the literature and what concentration do they use?
I think a quick literature search is a wonderful thing because like many problems, often times someone else has asked your question (what's the right concentration?), and done the necessary legwork to find you a starting point. I don't think we can avoid this next part though, especially if your drug has never been used in your system/organism/etc.
Titrate your compound
For almost anything out there, even if the manufacturer has a number in mind you should always titrate for your own application. Things aren't simply going to work for you as they did for another investigator, in part, because you're never asking the same question as another investigator. A good literature search can help strengthen your finding, however.
In finding the working concentration for your compound you aren't going to be doing the optimizing. It doesn't make sense to find the best concentration when you don't know what concentration works to begin with. As a rule of thumb I try to make the range of titers broad enough that I can see where undesirable or no-effect is, so for example with a drug I'd try 100µM, 10µM, 1µM, 100nm, 10nM, 1nM, 0.1nM.
If you can pick out a good working concentration there, you can optimize by using a tighter criteria. For example, I find that 10nM works the best; now I know 100nM and 1nM are my respective maximum and minimum. May I'd try 40nM, 20nM, 10nM, 5nM, 2.5nM.
It's important to reduce technical variability by using the same starting materials such as cell number for each condition to get the best titer.

thank you so much for your message. This is definitely good. however, my main question is that is it normal that a drug with nano mollar works in a cell while with a 100 fold more work in e.g. C.elegant? or any other animal model? how can I justify that? do you have such an example?  for example when i use more than nano molar the drug will kill the cell imagine what will happen if I use micro molar . is this ajustable ? do you know of any paper with different concentration in cell and animal model?

I have no way of knowing without the identity of the drug.

for instance Rapamycin

So rapamycin as an example: I'd probably find my usage close to 10-20nm in cell culture, which I think is standard. However, I can find two references, immediately, that use rapamycin at 200µM and 100µM, respectively (ref1, ref2). Reference 1 makes an important point: higher concentrations are needed for C. elegans due to bioavailability.

Important to note is that different species have different kinetics to their usage of the same drug.

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Does evolution thinks?
I understand evolution as survival of the fittest rule , where its the nature and surroundings that shapes the life by extinction of species which are not fit to survive the nature at that period.
To me its analogy would be like soil passing though a net,where nature act as the net and the soil particles act as lifeforms. The particles whose shape and size are small (fit) will go through the net and live on while the bigger ones (unfit) will get stuck and hence go extinct.
Pretty clear so far.
However there are certain things that do not seem to make sense with this theory for me personally.

When we evolved from primates to humans why did we lose our body mass, muscles and hair? I mean sure we could be intelligent with the muscles and the
furcoat would keep us warm and hence more likely to survive.

The explanation I get for this is that we did not had any use of body hair and strong muscles over our intellect so we lost them, however how can WE make it happen ? Its not like intellect requires less muscles or something so how did we lose it from redundancy? whats the mechanism?
2.How does Genetical heritage evolve?
In a nutshell what I want to ask is does our actions (as a species) define our DNA in evolution? Apart from natural mutation and survival of the fittest is there anything that affects the biological evolution? It is believed that child of intelligent parent is supposed to be somewhat intelligent as well, is this linked to heritage or just the environment he grows in?

Pt. 2 of your question concerns the famous nature v. nurture debate; feel free to Google that, it's quite interesting. You said: "we did not have any use of body hair and strong muscles over our intellect so we lost them". That is wrong. Natural selection doesn't compare different traits within an individual and choose the ones among them that are the most "superior" (it doesn't "filter" body hair and muscles because we possess intelligence, unless intelligence somehow makes the former traits obsolete or if the traits are an unnecessary burden). Also, I suggest a title change for clarity

To answer the last question,  in my opinion,  genetically passed  intelligence is just a potenial.  However, the enviroment he grows  matters also. To be more clear,  intelligence just express itself based  on the "data" (static knowledge) in your brain.   Less data means less intelligence expression.  How google translate work ?  It is artificially intelligent.  However, its intelligence alone does not work well. Gtranslate continiously  read more and more  ebooks with the translations. So it can be more accurate.  Same intelligence, but different intelligence expression :)

Also, in addition to my previous post, I wanted to mention that species which are at a disadvantage don't necessarily go extinct, unless they are repeatedly at a disadvantage over long periods of time and therefore the allele frequencies dwindle to very small percentages, or because an environmental disturbance occurs to which they cannot adapt or recover from.

@ AleksandrH
Thats not my question. "we did not have any use of body hair and strong muscles over our intellect so we lost them" is what most people usually tell me.
"Natural selection doesn't compare different traits within an individual and choose the ones among them" is what I know as well, but what causes redundant features to be eliminated?

This is one of numerous other moments when I would love to downvote a few comments.

If I commented anything wrong, just let me know and I'll delete it.

Welcome to Biology.SE
Issues with the question

It is impossible to correctly answer this question as the phrasing is so fantastically unclear, wrong and misleading (no offense, really). I will give a few points here that may help you but the only thing you can really do to answer your own question is take some time to follow an introductory course to evolutionary biology such as Understanding Evolution by UC berkeley (online and free) for example.
You probably want to work on the format of the question as numbering lines that have different number of tags looks pretty bad.
You are asking 9 different questions (there are 9 question marks at least) that are all relatively unrelated! A post should always be reduced to one single clearly defined question.

A few simple definitions

Population: A group of individuals.
Locus: A position in the genome.
Gene: A functional unit at a given locus that codes for a protein.
Allele: A variant of two or more variants at a given locus. Simplified example: At the locus where stands the gene coding eye colour, there are 2 variants brown eyes and blue eyes.
Evolution: Refers to any change in allele frequency in a population through time.
Phenotype: The manifestation of a gene on the world. In short: It is how someone looks like.

Does evolution thinks?

It is always quite difficult to define what "thinking" means. But really here, we won't need to debate the detail of the terminology of what is a thought. Evolution is a process, it is not an organism, it has no brain and can not think. The answer is "no".

I understand evolution as survival of the fittest rule , where its the nature and surroundings that shapes the life by extinction of species which are not fit to survive the nature at that period.

This is wrong! "survival of the fittest" is just a quick and dirty expression for referring to the process called natural selection. Natural selection describes the fact that alleles conferring higher fitness (that is having lower chance of survival and/or higher fecundity) to individuals carrying the allele, raise in frequency in the population.
Natural selection does not necessarily decrease nor necessarily increase the probability of a population to go extinct.

Apart from natural mutation and survival of the fittest is there anything that affects the biological evolution?

Natural selection and "survival of the fittest" refers to the same process.
Yes, there are other forces that affect evolution (and are absolutely essential) such as mutations and genetic drift.

I want to ask is does our actions (as a species) define our DNA in evolution?

It is unclear what you mean by "define evolution" and you probably want to replace "species" by "population". Yes, the current state of population (including the behaviour of its constituent individuals) affect future evolution of the species.

It is believed that child of intelligent parent is supposed to be somewhat intelligent as well, is this linked to heritage or just the environment he grows in?

This is an interesting question. I wrote an introduction into the concept of heritability (incl. the role of genes and environment in shaping phenotypes) in this post.

When we evolved from primates to humans why did we lose [body mass and muscles]?

You will have to ask this question on a separate post. In this post, you will have to make sure that we indeed lost in body mass. Note that human shape is nicely adapted for high endurance (hunting large mammals over long distance and period of time)

When we evolved from primates to humans why did we lose [..] hair?

This question is a duplicate of this very interesting post. Have a look!
Recommendation
To the risk of repeating myself, I'd recommend that you have a look at a very introductory source of information on evolutionary biology such as Understanding Evolution by UC berkeley (online and free) for example.


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Can you naturally change your DNA that's passed to your offsprings?
Is it possible to change the genes that you'll pass on to your offsprings by natural activity and behavior.
For example if you do body building for quite a long time build strong muscles then would your offsprings have stronger muscle builds than average?
Or is random mutation is the only way DNA would change naturally?

No, this does not happen. This is the view of Lamarck on evolution which is wrong. The only natural way of changing DNA is by mutation.

@Chris Could OP be getting confused by epigenetics?

@user137 Possible. Then this question needs clarification.

Clarify your question please.

This is in between an extended comment and an answer.
What do you mean by "Natural"?
The question makes no sense as the term "natural" isn't properly defined. (I am voting to close as unclear).
For example, if you go to an area where there is "naturally" a high radioactivity, this will increase your mutation rate. Is this a natural way to change your mutation rate (even though you need a specific device to compare the level of radioactivity)?
As another example, some diets may potentially increase once mutation rate, but again you need a fair amount of research to figure out what diet does what.
Yet another example, a plant that is stressed tend to increase its mutation rate. This, I suppose sounds quite "natural".
In any of the above examples, the mutation are random in the sense that they do not have a foreseen impact on the phenotype of the offsprings.

if you do body building for quite a long time build strong muscles then would your offsprings have stronger muscle builds than average?

This sounds very Lamarckian. We've known for more than 150 years this is not how evolution works. If you are unaware of these concepts, you should have a look at Understanding Evolution (UC Berkeley) (or other introductory source of information) to get a notion of what evolution is about.
In the comments, one person talked about epigenetics. I think there is no point talking about epigenetics for the moment as it may do nothing but disturb the OP if indeed (s)he does not have some introductory basis to evolutionary biology.

Would a diet high in Cobalt-60 and nitrite salts maximize your mutation rate?

Yes, typically!

It's called the Manhattan Project Diet.


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Why is sex pleasure giving activity but not childbirth?
Asking from an evolutionary viewpoint.
Sex is a pleasure giving activity so that it encourages reproduction and spreading of genes. But childbirth ,the most crucial part of the reproductive process, is equally opposite and many times hazardous to the health or even fatal to the mother.
why is that so? Not enough selection pressure (low death rate than succesful delivery rate)?

Maybe since abortion wasn't always an option back then?!

It's definitely not an adaptive trait to feel pain when giving birth - your nerves as electrical alarms don't care what is the cause of the pain you need. This has nothing to do with the fact that giving birth can be fatal to the mother. Apart from that, reproducing is the most important life function from the evolutionary perspective.

@probably yes but what i meant is why giving birth causes potential trauma and suffering to human body?

Nerves are electrical alarms for any type of damage. How would they recognize the pain comes from actually a useful thing?

What I'm trying to say is why birthing is not evolved to a level where it's no longer damaging and potentially fatal to the mother

Because it can't evolve like that. There is a trade-off between the size of the head (brain!) of the child and the risk for the mother. The flexible skull (fontanelles) is an adaptation to that.


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How does human body keep track of its age?
How does the human body knows that it's time for a event that happens around a certain age like puberty or something that's periodic like menstruation or gestation time of 9 months?
Please note I'm NOT talking about day-night biological clock .

It's not clear what do you mean by 'how does the body know'.

this is still a very active are of study, the field is called chronobiology.
Epigenetic clocks which may be longest, there are several Horvaths being the most famous and is based on the DNA methylation. I don't know the details of how it functions however.

This is an interesting question, but as written now is broad and shows none of your own research. If you can edit to narrow down (e.g. only menstruation) and include some of your own research (what you found when reading about it), I'd happily remove my close vote and take a stab at the answer. Thanks!

@SanjuktaGhosh it's quite clear that it means how does human body triggers certain functions at certain age or period

@anongoodnurse I did search but nearly all result ended up on biological clock that regulates sleep. And that's not what I am searching for so I ended up posting a targeted question on SE

@anongoodnurse same here, also voting to close.

@user1062760 Please do not post such accusatory comments. What is there to be political about? There is no logic in favouring a certain user/group of users and discriminating against others. We don't even know anyone here in person. Posts are voted upon, not the users. Instead of taking things personally, why don't you consider the advice of experienced users and edit your post accordingly. Your question is interesting and others have said it too. However, it is also very broad. One can write a book or a big review on this topic. SE is not designed to handle questions like this. Pls understand

It doesn't always. Some people have an undistorted slown down aging. Jyoti Amge is over 18 and looks like an undistorted little girl. Yesterday, I saw a TV show that showed a 22 year old who looked like an undistorted 8 year old girl. There are also people who have distorted aging. People with progeria look like a distorted older person. I think nodoby has an undistorted sped up aging. Gabby Williams looked like a distorted toddler when she was 12. Nicky freeman from https://thewest.com.au/news/australia/forty-year-old-trapped-in-childs-body-ng-ya-220462 has a distorted bone structure of a ten year old boy and is all wrinkly. The girl in the YouTube video at https://www.youtube.com/watch?v=xoBetcKAxII&t=96s has the undistorted bond structure of a 13 year old girl and is all wrinkly.


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How do cells age and die if they are dividing into new cells?
If cells in our body keep on dividing into new cells how do they ever grow old?
The only cells to grow old would be defunct cells or those who won't divide into new cells like nerve cells.
What am I missing here?

Human chromosomes contain certain DNA regions called telomeres. These regions are shortened on each cell division and once they are gone, the cell cannot divide. Therefore an average cell in our body can divide only about 50 times.
There are indications that longer telomeres may increase lifespan, however this remains controversial. Telomeres are believed to be a method of higher organisms to prevent uncontrolled cell division and cancer, therefore artificially increasing telomere length may not lengthen but shorten lifespan because of increased cancer risks.
Also, ageing is not (only) caused by individual cells growing old. Often it is the organization between the cells that breaks down. Scarring is a good example for this. The wound is closed but the tissue inside the wound was not able to organize into functional skin tissue again but rather "patched up" the wound with comparatively unorganized tissue.
The brain is another extreme example of ageing by disorganization. It has been shown that even adult brains contain neuron progenitor cells (albeit fewer than other tissues) so even adults can regrow neurons in the brain. However, while the cell body of the neuron can be replaced, all its (sometimes thousands) of connections to other neurons are lost. Therefore, brain tissue can be regenerated in principle, but the information it contained cannot.

That makes it like a chicken and egg problem if division is limited then how do new cells form to take place of dead ones?

50 divisions per cell is plenty. That is a limit of 2^50 cells, which is tons of biomass. The cells that take the place of dead ones are called stem cells. They are spread throughout every tissue and are still able to divide and differentiate.


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Are plasmids found in eukaryotes?
There are some who says plasmids are found in some eukaryotes but is it like scientifically proven?

Welcome to SE.biology. Please take a look around the help center on how to ask a good question. In particular, it's expected you show evidence of prior research on your question, and also include links to information you cite, rather than just 'there are some who say...'. Thank you.

These resources may help.
This book, “Plasmids of Eukaryotes”, explains that...
“The possession of plasmids was for a long time recognized only in the bacteria. It is now evident that plasmids, or replicative forms of DNA structurally and experimentally comparable to bacterial plasmids, exist in eukaryotic organisms as well. Such plasmids are in fact common among fungi and higher plants.”
Also, this website (ScienceDirect) explains that...
“Most plasmids inhabit bacteria, and indeed around 50% of bacteria found in the wild contain one or more plasmids. Plasmids are also found in higher organisms such as yeast and fungi. The 2 micron circle of yeast (discussed later) is a well-known example that has been modified for use as a cloning vector.“


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bunsen vs meker for best sterile field
I need one bunsen and i have a friend that sells me a bunsen-meker burner.
I see that bunsen-meker burners have more flame diameter, so should have more diameter of sterile field, but i dont know XD
Is good for sterile field? or i should buy a typical bunsen?
thanks.

Can you maybe explain what you plan to work on?

I need to prepare culture media to inoculate with spores of my mushrooms. Isolate the mycelium and inoculate liquid media for later inoculation in solid media for medium-scale production.
Until now I used a homemade still an air (SAB), with good results, but uncomfortable and unpredictable.
Now I want to buy a lighter to have a sterile field as large as possible, so I would like to know if the bunsen-meker that I have available to buy is correct or do I need a common bunsen burner, which I It would be more expensive as it is not second hand (the meker is brand new).

Bunsen was a person. Give him a capital in your title at least, even if you have an aversion to titular norms.

The difference in flame diameter between a Bunsen and Meker (or Fisher) burner really isn't that much, so I'm not sure how much larger the sterile field would be. On the other hand, Fisher burners can be tuned to be much hotter than standard Bunsen burners, so that may impact the size of the field as well. But, at the same time, they use more fuel, so you have to think of that as an additional cost.
If you're just sterilizing inoculating needles/loops, flask necks, etc., a Bunsen is perfectly fine. However, if you're trying to create a larger "sterile" field, there are too many variables to make a definitive recommendation. Are you setting up in an area with relatively little airflow, or are there cross-breezes? How large of a field do you actually need - what is the area where you'll be working with open containers of sterile media?
All in all, to be safest, you'd probably want the Fisher burner, but I don't know what the cost differential is and what your budget is. If you're careful with media manipulation and have a good still area to work in, a Bunsen should be fine, though.

thanks! This info is so useful!

@JaumeEscaleCamps glad to help. If this answer addressed your problem, please consider accepting it by clicking on the check mark/tick to the left of the answer, turning it green. This marks the question as resolved to your satisfaction, and awards reputation both to you and the person who answered. If you have >= 15 reputation points, you may also upvote the answer if you wish. There is no obligation to do either.


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What is the difference between a myofibril and a myoblast? (In skeletal muscle)
I read that a muscle fibre (myofiber) is formed when myoblasts fuse.
https://teaching.ncl.ac.uk/bms/wiki/index.php/Skeletal_muscle#:~:text=The%20multinucleate%20feature%20is%20established%20in%20myogenesis%20where,cells%20%28each%20muscle%20cell%20is%20one%20muscle%20fibre%29.
On google I saw that a muscle fibre is formed from many myofibrils.
https://biologydictionary.net/myofibril/#:~:text=Myofibrils%20are%20long%20filaments%20that%20run%20parallel%20to,are%20made%20up%20of%20repeating%20subunits%20called%20sarcomeres.
Does that mean that myoblasts and myofibrils are the same thing?

Myoblasts are the embryonic precursors of myocytes (also called muscle cells). Myoblasts differentiate into muscle cells through a process called myogenesis.
A myofibril (also known as a muscle fibril) is a basic rod-like unit of a muscle cell. Muscles are composed of tubular cells called myocytes, known as muscle fibres in striated muscle, and these cells in turn contain many chains of myofibrils.
So, to answer your question, No. These two are different and one is the precursor of the other.


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What is the difference between a dermatome and a sensory neurone?
I read that a dermatome is an area of skin supplied by a single spinal nerve but that this is sensory information? Why do spinal nerves supply the skin? I thought it was the other way round- sensory information is carried by a sensory neurone to the spinal cord.
Please could someone explain this in simple English because I am really confused.

This is just a confusion of English.
"Supplied" is a bit of a weird term to use, I agree, due to the direction of information flow, but feel free to substitute in just "connected to". It seems pretty common to use this word, for example Wikipedia says:

A dermatome is an area of skin that is mainly supplied by afferent nerve fibres from the dorsal root of any given spinal nerve

and I see similar phrases elsewhere (not sure which is your original source). Afferent nerve fibers, as you describe, are those carrying information into the central nervous system from the periphery, so yes, the information is coming in from the skin.
If you interpret it instead as the spinal nerve providing the connection rather than information flow, then it makes a bit more sense to say "supplied". I suspect the phrasing is borrowed from blood supply since nerves and major vessels tend to develop and travel together. I also suspect the phrasing comes from anatomy, which is sometimes not particularly interested in function which can lead to some confusing results. You'll also see similar phrasing in standard English in other contexts, like roads, even when movements of goods or people are two-way. Merriam-Webster also provides a definition addressing exactly this circumstance:

to furnish (organs, tissues, or cells) with a vital element (such as blood or nerve fibers)

So yes, a given spinal nerve is "supplying a single dermatome with nerve fibers", even if the information ultimately moves the other direction.


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How do Human Skin Creases Vary?
I am studying human gross anatomy in order to produce an anatomically correct CGI model of the human body. As part of this, I'm attempting to understand the different features that define the topography of the skin. One class of features is the creasing of the skin, which appears to manifest both on a large and small scale (illustrated in figure 1 of [2]) with variation about the body. In my reading, I have found [1] which catalogues the major creases and only [2] which briefly discusses the smaller creases and cites paywalled articles. Since this topic seems particularly obscure, it would be good to have a definitive summary of this topic. Therefore:

What are the different types of skin creases?
Is there terminology that distinguishes the larger and smaller creases?
How are they distributed about the body?

[1]: Mallouris, Andreas & Yiacoumettis, Andreas & Thomaidis, Vasilios & Karayiannakis, Anastasios & Simopoulos, Constantinos & Kakagia, Despoina & Tsaroucha, Alexandra. (2012). A record of skin creases and folds. European Journal of Plastic Surgery. 10.1007/s00238-012-0774-3.
[2]: Wong, R., Geyer, S., Weninger, W., Guimberteau, J.‐C. and Wong, J.K. (2016), The dynamic anatomy and patterning of skin. Exp Dermatol, 25: 92-98. doi:10.1111/exd.12832


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Why is there not an immune response to injected immunoglobulins?
When you inject immunoglobulins as a treatment for certain diseases, the immunoglobulins are a foreign substance.
I can appreciate that maybe the constant region would be similar to the hosts as it is from another human and these don't change a lot.
However, in the variable regions, wouldn't there be the possibility that the antigen receptor region could be the complement to the patient's own antibodies? Wouldn't this trigger an immune response and destroy the injected Ig's? Yet we seem to do this procedure, so why doesn't this process occur?

Does this answer your question? Why does not the host produce any immune response to antiserum antibodies?

No, it mainly discusses animals not human antibodies. Also, it doesn't explain why human to human transplant of immunoglobulins doesn't create a reaction

If a head-to-head "match" between antibodies from two different people was to occur, a similar match would most likely have occurred already in the donor. People have the same tissues after all.
But in the donor; the B lymphocytes producing the antibodies had to go through the processes of "central tolerance" and "peripheral tolerance".
This would weed out the cells producing autoantibodies.
Theoretically, nasty autoantibodies in the recipient could react with innocent antibodies in the donor though.

Intravenous immunoglobulins (IVIG) are human blood products purified from the plasma from many healthy donors.
These are natural proteins that your body normally makes to help you to fight infections and to serve other functions for the immune system. In addition, all immunoglobulins are screened to eliminate the possibility of carrying pathogens or other diseases 1. Since the body's immune response is activated by the recognition of T cells to the antigen, these naturally produced, screened IVIG will not trigger an immune response against them.
However, IVIG are not 100% safe. Injection of immunoglobulins can cause some adverse effects, such as fever, headache, chills, etc. These adverse effects are usually transient and mild, but there are few cases of severe side effects. You can find more details in this paper.
Resources

https://www.rheumaderm-society.org/ivig/

Guo Y, Tian X, Wang X, Xiao Z. Adverse Effects of Immunoglobulin Therapy. Front Immunol. 2018;9:1299. Published 2018 Jun 8. doi:10.3389/fimmu.2018.01299

Re: "these naturally produced, screened IVIG will not trigger an immune response against them." In rare cases, they may indeed do so. Screening has no effect on this, rather it would be sequence differences in the Ab genes between the donor and recipient. In practice, such sequence differences are minimal enough between humans that no effect is normally observed.  For animal Abs injected into humans, a reaction is more likely, so such Abs are often first engineered (before or after antigen selection) to replace much of the molecule with human sequences (see "chimeric" or "humanized" Abs)

Screening of IVIG is very good, but not perfect, in identifying pathogens, and so there is a quite small risk of infection for the recipient.


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How do G proteins move?
G proteins consist of an alpha subunit and a beta/gamma subunit. These proteins are involved in various cellular signalling process.
From what I have understood, the alpha and gamma subunits have covalently bound lipid tails. That is, they seem to be directly connected to the cellular membrane. If this is the case, how do these protein subunits move?
I understand that the cellular membrane is flexible but I'm currently imagining a flying fox type scenario. This is where the alpha subunit is covalently bonded to one phospholipid and is now gliding down a cell membrane. I kind of find this hard to believe because it seems ridiculous (but fun!).
How do alpha and gamma protein subunits move if they are covalently bonded to the cellular membrane?

Interpretation of the Question
The question asks how the G-protein α- and βγ-subunits move, but does not state the context or circumstances of the movement. I assume that the question is, in fact:

How do the G-protein α- and βγ-subunits move apart and migrate
from receptor to target enzyme when their interaction is prevented by
the binding of GTP to the α-subunit?

False premise in the question
The problem envisaged in the question is that as the α- and γ-subunits have lipid moieties covalently bound to their amino acid chains, they are somehow part of the lipid cell membrane. This non sequitur may arise from a misunderstanding of lipid chemistry: the cell membrane is a bilayer the main constituent of which is individual molecules of phopholipids containing two long fatty acid chains and one polar organic phosphate (e.g. phosphatidyl choline) attached to a glycerol backbone. Other hydrophobic molecules (cholesterol, proteins with hydrophobic amino acids on their surfaces) can interact with these phospholipids.

The lipid moieties attached to the G-protein subunits are, in contrast, single palmitoyl or myristoyl fatty acid chains (in the case of the α-subunit) or farnesyl or geranyl (substituted fatty acid) chains (in the case of the γ-subunit). So the idea that they are somehow equivalent to the membrane phospholipids is incorrect.
How do they move?
As the lipid bilayer is fluid, its constituents can move within it, like ships on the sea. A review by Wedegaertner discussing G-protein trafficking illustrates this as shown below:

When the interaction between the subunits is prevented by GTP, they are free to drift apart in the membrane, like a boat cut loose from a ship at sea. The illustration shows them attached to the membrane by a single line representing the lipid group, but also considers evidence that they may move away from the membrane, presumably because the interaction is weakened on dissociation. Their movement is presumably random thermal motion in each case, as is that which leads to their reassociation after the GTP is hydrolysed.
However, as @BryanKrause mentions in his comment, it should be emphasized that the ability of the subunits to ‘float’ through the membrane (rather than ‘sink’ into the cytoplasm) facilitates their mode of action. They must first associate with the hormone/agonist receptor to receive the initial signal (or first messenger) and then move to interact with the target enzyme/protein which transmits the signal within the cell (e.g. through the second messenger cyclic AMP produced by the enzyme adenyl cyclase). See, for example, this Nature Scitable article.


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Why do more complex DNA strands take longer to anneal?
My textbook and several websites told me that more complex DNA strands take longer to anneal because it is harder to find the correct sequence. A simpler, repeating sequence like ATATATATA would be faster to anneal since it would be really easy to find a spot to reanneal.
I kind of get the logic here. Yet, this wouldn't always produce the exact complement strand. Consider the following:

The point is to illustrate that there could be matching of strands without correctly pairing the whole thing (i.e. there is a shift of the strands).
This means that if you want to fully anneal the strands, you need to find the correct spot in the second strand to begin annealing - which is no better than if these were completely random strands.
So then, why is annealing more complex strands slower? I've tried searching it up on the internet but all I get are people telling me it is true, and without much of an explanation.

What is meant by complexity?
This is the crux of the matter. As is often the case, confusion arises from not defining one’s terms. In this case the three possibilities we have to deal with are:

The extent to which a sequence is not homogenous. e.g. ATATATAT is more complex than AAAAAAAA; ATGCATGC is more complex than ATATATAT; ATGCTCAG is more complex than ATGCATGC. This would seem to be the definition assumed by the questioner (and also in another answer).
The length of the sequence. This is the definition given in the article quoted in the question: “Complexity - the total length of different sequences”. However it is not one that would have occurred to me on encountering the expression.
The extent to which a length of DNA (especially a chromosome) has regions present in multiple copies. This seems not to have been considered in the question, but is historically what was meant be genome complexity deduced from annealing experiments. This is shown in these extracts from a venerable text on nucleic acids, long out of print:

In human cells unique DNA has a Cot1/2 value of 1000 (moles nucleotide seconds litre–1)…Repetitive DNA includes all of the rest of the DNA. Among the repetitive DNA is a fraction which reanneals with a Cot1/2 value of between 100 and 1000…thought to be those [genes] coding for proteins which form major structural components of the cell… [some examples given of multi-copy genes like tRNA]…At the other extreme DNA with a Cot1/2 value as low as 10–3 consists largely of satellite DNA.

Explanation for Case 3 (complex because of multiple copies)
As the article quoted in the question correctly states, “Renaturation, or duplex formation requires random collisions between two single-stranded molecules”. However such experiments are performed with fragmented DNA in solution, not whole chromosomes, so the two molecules that must collide are gene-size or smaller in length. The more copies of geneX or sequenceX there are in the DNA, the greater the number of targets there will be containing geneX or sequenceX, hence the faster fragments containing such genes will anneal.
Explanation for Case 1 (complex because less homogeneous)
Assuming that one is comparing single-copy genes of different degrees of homogeneity, one can imagine that for something like ATATATAT there will be more ‘hits’ that give partial overlaps that may be detected as double-stranded:
A T A T A T A T A T A T A T A T
        T A T A T A T A T A T A T A T A

Alternatively, once bound imperfectly, there may be a greater chance of perfect binding after dissociation because of proximity.
However, it is also possible that writers are confusing or amalgamating this with Case 3, as simpler DNA may actually be present in more copies in a genome.
Explanation for Case 2 (complex because longer)
The explanation here is trivial. If you perform reannealing experiments with two geneomes — E.coli (4.6 Mbp, c. 4000 protein-coding genes) and Carsonella ruddii (0.16 Mbp, 182 protein-coding genes) — employing the same amounts of DNA as 300bp fragments, the fragments from the smaller genome will be approximately 20x more likely to make a random collision with a complementary fragment.

You are correct that this won't produce the correctly complemented strands 100% of the time, indeed that's what the experiments outlined in the link you provided are aiming to measure... how much DNA is duplexed over time after a single denaturation. Simple sequences will be so alike that an approximation of 100% can anneal fairly quickly, as measured by the sensitivity of the experiment (A260/A280 is not sensitive; these things are done much differently these days).
The information that you are missing is that if those bits in the middle don't match then the DNA there won't anneal - it will still exist as single-stranded or partially duplexed strands and so will show up as not 100% annealed in the assay. To fully anneal you need full complementarity of the strands, and given that you have a single denaturation, the chance that 100% will anneal in any given aliquot is low, so in a rate equation it will take a "long" time.
I'm no chemist or physicist, so if someone has a better answer, please feel free to chime in.

From physics point of view, annealing is about finding the lowest energy configuration of the two DNA strands. The configuration space of two strands has many minima, and after every annealing cycle the strands settle in one of them, which is not necessarily the lowest. One then reheats the DNA to allow it to explore teh surrounding minima and hopefully settling in the one of even lower energy. In a sequence containg many identical elements, such lower energy minima a readily available - in the OP language it would be really easy to find a spot to reanneal. On the other hand, if the sequence elements are very different, a large deviation from the current configuration is required to find a more favorable configuration.


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Why don't we dribble tears through our nose?
Basal tears are tears produced by the lacrimal gland and they lubricate the eye. They are then funneled into the lacrimal sac and then from there into the nose eventually.
If this is the case, why don't we constantly dribble out tears from our nose? Where do the tears go?


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Why don't we bleed interstitial fluid?
Interstitial fluid is the fluid between cells in tissues - forming the medium between cells and capillaries. From what I gather, the typical human has 5L of blood and 11L of interstitial fluid. This raises an interesting question. If I get cut, why do I not bleed interstitial fluid?
When humans are cut, generally their capillaries open and blood comes out. But this should also allow the interstitial fluid to come out - so why don't we see it?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). In particular, I'm almost certain your assumption that interstitial fluid doesn't escape is wrong — I've had (and seen) many injuries where clear fluid leaked out around the wound. ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

For fluid to flow from a wound there needs to be a significant pressure gradient between where it is now and the outside of the body. Your skin generally does not have a strong compressive effect, which is why a deep cut exposing fat will not lead to the fatty tissue being expulsed from the body any more than the interstitial fluid is.
Blood, however, flows. For it to circulate there needs to be a pressure gradient between where it is now and where it is going. Since veins (including the vena cava, which channels blood back into the heart) do not have vascular walls strong enough to create a suction effect (i.e. lower pressure than the surrounding tissue), you can conclude that the pressure of blood vessels is always higher than that of surrounding tissues, and thus higher than the pressure outside of your body. This is why all blood vessels, including veins, will bleed, whereas less pressurized systems such as interstitial fluid will not.

Or, as my biology teacher used to say: just because the bucket is missing its cover doesn't mean the water will jump out.

I'd argue that in something like a graze, you can see interstitial fluid "bleeding" (it's the clear fluid that forms on the surface. It's just that a) it's not pressurized, and b) mixed with blood, it's totally eclipsed by the heme. You'd have to be under fairly specific circumstances to see it without blood present

Besides the answer by TheChymera, there's also the "problem" that interstitial fluid can't really flow freely.
Blood runs in veins, allowing to quickly circulate through your entire body. And if you cut yourself (and cut one or more veins), there is a direct path for the blood to take.
Interstitial fluid, however, has to creep through all kinds of small openings, not having a free path. Compare driving on the highway (crowded though it might be) and crawling through houses in a crowded city. Sure, if you're an experienced parkour-athlete you can get through. But if everyone wants to get out of a city, getting out over the highway will be the fastest.
By the way, there is one situation where you may "bleed" interstitial fluid: in a blister.
Here, the waterproof (and interstitial-fluid-proof) part of your skin detaches, and the fluid can accumulate. But it will do so only slowly, creeping through some small openings.
And the fact that it comes in slowly is also what makes a blister a problem, as it also means it can't flow back quickly. So if you press on it, it feels like some trapped fluid, even though you could in principle keep on applying pressure and push it back.

This is a very good addition, as it also explains — with respect to the bigger picture — why veins will “bleed” more than capillaries, even though the pressure at that point in the vascular system is lower.


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Does night sleep provide more energy-regain than sleep during the day?
After reading this, I know that sleeping is an universal function, and that basically everything with a brain has the need to sleep.
However, I am still confused to what extent it is necessary to sleep at night to regain energy, or if some rest during the day provides a sufficient energy-regain?

The circadian clock is entrained to sleep-wake patterns. (Sun)Light has a strong capability of adjusting and resetting that clock. Hormonal balance and other functions in the body, in turn, are synced to it. Hence, your question will depend much on whether you are aksing what happens after acute reversal of the sleep/wake cycle, or whether you mean what happens when you revert it for prolonged periods of time. Also, what do you mean with 'some rest'? Of course powernaps during the day can help. I vote to close because it is unclear what you are after.

I think the reason is primarily, that it is more quiet (the chance is very low that other people are disturbing your sleep) in the night as well as it is also dark. Keeping in mind, that the brain "gets tired" due to some proteins (melatonin) and in contrast, being more awake during the day, it seems to be just logical that the sleep in the night is healthier, thus providing more energy.

And isn't the production of melatonin controlable by outter conditions such as illumination and noiseness? Or do you think the biological clocks can keep going in the time undependent environment?

Of course, but it needs some time until it can rise high enough, sufficient for deep sleep at night, where your immune system can regenerate. Some people get health problems such as high blood pressure or weight gain when their sleep at night is insufficient. Found e.g. with shift workers. However, a "quick nap" (about 20 min) at daytime will provide you new energy, as you just rest quickly and don't get to relaxed, where your muscles feel weak, such as after a longer sleep.

i would like to know what happens exactly when you sleep? if you can answer me! (thanks by the way, your answer was a logical and brief one)

A couple of quick google searches would tell you that the important part of sleep is the REM (Rapid Eye Movement) sleep.
REM stands for rapid eye movement. During REM sleep, your eyes move quickly in different directions. That doesn't happen during non-REM sleep.
Usually, REM sleep happens 90 minutes after you fall asleep. The first period of REM typically lasts 10 minutes. Each of your later REM stages gets longer, and the final one may last up to an hour. Your heart rate and breathing quickens.You can have intense dreams during REM sleep, since your brain is more active.(1)
During an eight-hour sleep pattern, the average adult only spends approximately 1.5 hours (or 20% of total sleep time) in rapid eye movement (REM) sleep. REM sleep is important because it is the restorative part of our sleep cycle. Typically, you begin the sleep cycle with a period of non-REM sleep followed by a very short period of REM sleep. The period of non-REM sleep is made up of stages 1 to 4. Each stage can last from 5 to 15 minutes. A completed cycle of sleep consists of a progression from stages 1 to 4 before REM sleep is attained, then the cycle starts over again.
However, if your REM sleep is disrupted even one night, your body won’t follow its normal circadian sleep cycle (“inner clock”) progression. Instead, you will slip directly into REM sleep as a result of not getting the right amount of sleep the night before. You will also go through extended periods of REM sleep until you “catch up” on this stage of sleep. Poor sleep cycles can cause grogginess, a lack of concentration and more.(2)
During day, brain might not get enough time to restore itself as one can hardly sleep for 2-3 hours during day. Though your body might get refreshed after this, your brain might not. Also, as @TheGreenOne says, there are lot more chances of day sleep getting disturbed than night sleep. Another thing is that the brain is habitual to sleep at its normal time (night) (see SCN), so it won't be very easy to get in/out of the habit to sleep during day.
References:

http://www.webmd.com/sleep-disorders/guide/sleep-101
https://www.azumio.com/blog/health/rem-sleep

there's some great information up there, thanks


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What is the disadvantage of circular DNA?
I have searched online and there is little information about the disadvantage of a circular DNA. Since I know that with chromosome arrangement like human, we have telomere that held the DNA strands together, which loosens as the organism ages and the cell divides. With circular DNA there is no need for telomere and the number of times for the cell to divide is greatly increased. Then comes my question, does circular DNA has major disadvantages? And if a multicellular organism has circular DNA arrangement, does it have a longer lifetime?

This question is similar to a previous one — What is the advantage of circular DNA in bacteria? — so I suggest that you refer to that.

@David, that question asks about advantages, not disadvantages, and the answers there address that question, not this one.

@mgkrebbs — Oh, come on. It’s all a single question about the relative occurrence of the two types of chromosome. Whether it has been answered properly is not the point. The question is poorly expressed and there is no reason to regard its wording as sacrosanct.

@David, they are obviously related, but the concern of the questioner is different in the two cases, and the direction of the answers should specifically address the particular concern, as the two sets of answers do.  I would also suggest that the concern expressed in your comment below, "the interesting question is why eukaryotes have linear chromosomes", deserves its own separate SE.Biology question.

@mgkrebbs — I do not flag a lot of duplicates, but the policy seems to support my attitude. The question was poor and the poster accepted an answer that was not very informative (imho), so it doesn’t matter too much whether it is closed or sinks into oblivion on its own.

Does this answer your question? Is there an advantage to linear chromosomes?

Per se, there is no disadvantage of one type of DNA over the other. They evolved for different reasons, and the fact that both are still present indicates that they fulfill their role(s) satisfactorily. There is no competition between the two types of DNA. Even multicellular organisms (eukaryotes) have circular DNA within their mitochondria, and both genomes cooperate for a proper functioning cell (and there's even gene transfer from the mitochondria to the nuclear DNA, and there is also translocation of mitochondria). Most multicellular organisms have chromosomes instead of circular DNA, although there are some multicellular bacteria with circular DNA, so these would not 'suffer' from the shortening of the chromosome ends, but take into account that aging is due to many factors (oxidation, protein degradation, membrane degradation, etc), so it is not the sole responsability of telomeres to extend the lifespan of an organism.

I see. Thanks for the excellent answer.

The interesting question is why eukaryotes have linear chromosomes.


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Does there exist a reagent that can only be precipitated by Haemoglobin and nothing else?
I recently read Sherlock Holmes and in the book A Study In Scarlet, Holmes says to Watson that he has discovered a reagent that can only be precipitated by Haemoglobin and nothing else. I know about the Guiacum test but is there any other test like I have discussed above as the Sherlock Holmes test.

This very point is well addressed by Laura J Snyder in Sherlock Homes: Scientific Detective (a great read) where the author challenges the view that Conan Doyle is the 'father of scientific crime detection' and argues that the new science of forensics actually influenced Conan Doyles' writing, rather than his novels being the inspiration for the new emerging discipline.
Furthermore, not all his claims were scientifically valid, and the 'infallible test for bloodstains' is a good example.
The relevant passage is as follows:

Let us examine, for example, the ‘infallible’ test for bloodstains Holmes is presented as having ‘invented’. By1887, when A  Study  in  Scarlet was published, many researchers already shared the desire for such a test; this desire was not satisfied until the turn of the 20th century,when the spectroscopic method was developed.
A modern chemist has noted that the method Holmes describes – one which would precipitate a brownish dust and change the color of blood in water to mahogany – would need an acid to increase the oxidation rate, as well as a material to be oxidized. By examining the possibilities for the ‘few white crystals’ and the ‘drop of transparent fluid’ that Holmes uses, this chemist suggests that the ‘Sherlock Holmes test’ would probably have had a sensitivity similar to the guaiacum test that Holmes derides as being ‘clumsy and uncertain’[15].
Moreover, Holmes’ test does not distinguish between human blood and the blood of animals– a problem that, by 1887, was considered an even larger concern than the sensitivity of the blood tests currently in use. A solution to this problem did not arise until the work of Paul Uhlenhuth in 1901 [16].

The two references quoted in the above passage are:
[15] Gerber, S.M. (1983) A study in scarlet: blood identification in 1875. In Chemistry and Crime: From Sherlock Holmes to Today’s Courtroom (Gerber, S.M. ed.), pp. 31–35, American Chemical Society (Columbus,OH, USA)
[16] Thorwald, J. (1965) The  Century  of  the  Detective (Winston, R. and Winston, C. trans.), Harcourt, Brace and World


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What decomposes the decomposers?
Decomposers feed on dead organisms. What feeds on them? In particular:

What decomposes mold?
If fly larvae feed on animal dung, what eats their dung?
Are all fungi eaten by animals? If not, what decomposes them?

Just think of it like scavengers but at the microscopic level. Microorganisms can scavenge each other just like larger animals can.

Maybe your thinking on a "food chain" paradigm. So, who eat the specie that are at the end of the chain?. In a "food web" paradigm there is not such a problem.

Probably (1) "fungi and other decomposers", (2) "fungi and other decomposers", (3) "fungi and other decomposers".
If you're interested in precise answers ("exactly which taxa are responsible for the decomposition of some particular type of dead tissue?") you probably won't get an answer. In general the answer is "detritivores chew on it, break it down, extract some of the useful material, poop it out; then a broad spectrum of other decomposers (fungi, bacteria, protozoans) do the rest of the job".


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Does destroying a virus envelope make the virus inactive?
Some viruses have a lipid envelope around their protein capsid. The envelope can be dissolved with soap, but does that still leave the capsid and interior genetic material intact? If so, is the virus still active?

Enveloped RNA viruses will get inactivated quickly without a membrane. RNase is a ubiquitous enzyme that would quickly digest any exposed genetic material.
Via https://www.neb.com/tools-and-resources/usage-guidelines/avoiding-ribonuclease-contamination:

RNases are found in all cell types and organisms from prokaryotes to eukaryotes. These enzymes generally have very high specific activity, meaning tiny amounts of contamination in an RNA sample is sufficient to destroy the RNA. The major sources of RNase contamination in a typical laboratory include:

Aqueous solutions, reagents used in experiments
Environmental exposure, RNases are in the air, most surfaces and dust
Human contact with hands and skin

Without a membrane (and any associated receptor-binding proteins), the genetic material of an enveloped virus would not normally have a way to get incorporated into and infect the host cell, in any case.
Your question is about enveloped viruses, specifically, but there is an interesting exception of a kind, so-called viroids that infect plant cells. These have no capsid or protein envelope, but are still infectious.


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Why does more melanin means harder vitamin D production if melanocytes lie deeper in the skin than keratinocytes?
From my Googling, I understand that keratinocytes are primarily responsible for generating vitamin D from UV rays, and melanocytes are for producing melanin to block UV rays. However in lots of skin diagrams I've found, such as this one, melanocytes lie deeper in the skin than keratinocytes. Wouldn't it follows that no matter how much melanin you have, it shouldn't be any more difficult for you to generate vitamin D, given that keratinocytes are more superficial than melanocytes, so vitamin-D making with keratinocytes should happen before UV blocking with melanocytes?

In your googling about melanocytes have you also read what happens to melanine after it is produced in melanocytes?

@BagiM There's this sentence, "Once synthesized, melanin is contained in special organelles called melanosomes which can be transported to nearby keratinocytes to induce pigmentation." (https://en.wikipedia.org/wiki/Melanocyte#Melanogenesis). But what does that mean? Does melanin transported to keratinocytes "cover" them up, preventing them from making vitamin D or something?

Now that you noticed term melanosomes, you can google images with "melanosomes" to see how are melanosomes distributed in skin cells. Searching for "melanosomes racial" should give you some images highliting differences in melanosomes distribution between skin types. Sadly, many general skin section diagrams show melanine distribution in caucasian skin as default, so you need to be a bit more particular/persistent in your search.


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Why don't all cells have active telomerase?
If telomere degeneration plays a role in aging, and extending them is biologically possible with telomerase, why isn't it active in all cells? Humans use it in their germ cells, so why not all somatic cells too?

We don't want all body cells dividing indefinitely. When that happens we call it "cancer".
Telomeres are one of many ways to regulate cell division and prevent runaway growth in a last-ditch manner where a cell becomes non-viable after dividing too many times without telomeres. From Wikipedia:

With telomerase activation some types of cells and their offspring become immortal (bypass the Hayflick limit), thus avoiding cell death as long as the conditions for their duplication are met. Many cancer cells are considered 'immortal' because telomerase activity allows them to live much longer than any other somatic cell, which, combined with uncontrollable cell proliferation[46] is why they can form tumors. A good example of immortal cancer cells is HeLa cells, which have been used in laboratories as a model cell line since 1951.

and:

Telomerase activation has been observed in ~90% of all human tumors,[48] suggesting that the immortality conferred by telomerase plays a key role in cancer development. Of the tumors without TERT activation,[49] most employ a separate pathway to maintain telomere length termed Alternative Lengthening of Telomeres (ALT).[50] The exact mechanism behind telomere maintenance in the ALT pathway is unclear, but likely involves multiple recombination events at the telomere.


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Mesh formation in the wells of SDS PAGE. How to solve it?
I casted 10% resolving gel and 4% stacking gel and every time a mesh like structure ( polymerisation) in the wells are formed.How to avoid this from happening and how do i get clear wells? If someone has any idea about it, it will be a great help. Thank you

Have you tried rinsing the wells with buffer? Do you have an image of this problem? How old are the chemicals you use - especially TEMED and APS?

Is the comb the right thickness for the spacer you’re using?

This issue is driving me crazy too. Although I haven't identified the exact cause, here are the steps I've taken to minimize mesh formation:
(1) Prepare your gel on the same day you plan to perform SDS-PAGE. Do not store your gel in the fridge overnight.
(2) Allow the stacking gel to harden for a longer period (>40min). I suspect that the mesh forms when the stacking gel hasn't hardened sufficiently.
(3) Switch out the comb. It's possible that mesh formation is associated with a specific comb. Mark the comb number and monitor any mesh formation.
(4) Prepare more gel than you actually need. In my experience, some gels with mesh formation occurred while others did not. By making a few extra gels than needed, I was able to select the gels without mesh formation for my experiments.
All these steps are based on speculation; nothing has been proven yet. Good luck and please share your experiences if you get any improvements!


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Bacterium fixed nitrogen transfer mechanism
As it is well known, Rhizobium and other bacteria have the capacity to fix Nitrogen and thus perform a crucial role in the natrual nitrogen cycle.
I am trying to find a reliable source on how the origin of the nitrogen that the bacteria fix, for example inside the nodules.
Most sources simply explain how nitrogenase converts N2 (in gaseous form) to NH3. But I have not found a source explaining the origins of N2 in the soil environment.
I don't see how the N2 could be diffused in the soil from the atmosphere (it would need impractical large time for such diffusion, and morever that would negate the soil aeration in general)
An agronomist pinpointed the N2 relased in the soil during decomposition, but that N2 would not be a net general fixation (from the atmosphere to the soil as a biological useful nitrogen)
The solubility of N2 into water could explain some net transfer on atmosphereic N2 into the soil, but it is relatively small amount (20mg/L)
So my question is where does the N2 in a plants root environment comes from?
Do the plants transfer N2 to the roots dissolved in the phloem?
I would appreciate and insight and/or any sources.

related to your question,your bacteria replaces the ammonia step in this cycle  https://en.wikipedia.org/wiki/Nitrogen_cycle

What sort of structure do you think soil has? Is it a solid mass like a lump of plastic or metal, or does it have pores/holes/granular structure?

air contains 78% nitrogen(N2),bacteria converts this to nitrate that the plants can use.https://en.wikipedia.org/wiki/Soil_gas

Thanx for all the comments. The answer to my question seems obvious now. My assumption on the diffusion time is not correct, due to the pore structure of the soil.


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How do Action Potentials travel in Cardiac Muscle Cells?
From my reading, the action potential is generated by pacemaker cells within the SA node and the conduction system of the heart carries the action potential to the cardiac muscle cells. I was just wondering whether the action potential travels through gap junctions or along the sarcolemma? It would need to travel along the sarcolemma to activate L-type calcium channels during muscle contraction, but how does the action potential actually travel from the SA node to the membrane of the cell? How does it just 'jump' to the surface of the muscle cell?
In addition to that inquiry, when do action potentials travel through the gap junction then? Does the action potential travel through both the sarcolemma and the gap junctions?


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T-tubules in Muscle Cells
I understand that T-tubules are common to striated muscles such as skeletal and cardiac muscles (with smooth muscle cells having caveolae) but what precisely (if any) is the difference in the T-tubular systems of skeletal and cardiac muscle cells?

The Wikipedia article T-tubule describes the differences.


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Membrane Potential Question

Hello, I've come across this question and am slightly confused. The question states that for this scenario the membrane is only permeable to K+, thus would the membrane potential in this state just be the equilibrium potential of K+? If this is not the case I would not know how to calculate the resting potential. I've tried finding the individual equilibrium potential of the ions and finding the potential difference but this gives a value that would not be correct given the circumstances in the question. Anyone have any idea how to proceed?

Please do not post text as graphics. It discriminates against those with visual problems — especially those using screen readers — and it prevents questions being indexed.

Usually we use the Goldman Equation when calculating membrane potential with multiple ions and the Nernst equation for calculating reversal potentials for individual ions.
Try out the Goldman Equation with all these ions, setting the permeability of the ones that are zero to zero. Try the Nernst equation for potassium. You'll find that when you set the permeability to zero of all ions but one the Goldman Equation algebraically becomes the same as the Nernst equation for a single ion.
https://en.m.wikipedia.org/wiki/Goldman_equation
https://en.m.wikipedia.org/wiki/Nernst_equation


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How difficult is it for wild birds to find food?
This question came to my mind when I was wondering if my parrots would have it better on the outside than with me. Also, is starvation a significant cause of death at different stages in a bird's life cycle? Obviously, this is an open ended question due to the many species and different habitats, but I wanted to know what the answer is in general.

If you live in the Costa Rica rainforest then your parrot may be better off living outside in the jungle.If you live in downtown New York City then your parrot is better off living inside with you.Starvation , predation and accidents(especially in urban areas) are three main causes of early death in many species.


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Do endocrine cells always lie adjacent to capillaries?
The circulatory system transports plasma contents to the body via the interstitial circulatory system, reabsorbed with the lymphatic system. Cell metabolism "waste products" are transported into the blood via this "sewer system", to for example be excreted by the urinary system. The lymphatic system provides a basic route for interstitial fluid to return into the blood stream. The endocrine system has to be relatively fast, and, lymphatic transportation is relatively slow. Do endocrine cells always lie adjacent to capillaries so that hormones are secreted directly into the blood stream?


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How exactly does DNA polymerase III detect a mismatched base?
How exactly does DNA polymerase III detect a mismatched base? I know how it removes it, via exonuclease activity, but how does it 'detect' it molecularly in the first place?


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Where do biologists get information about mouse genes?
From this article https://ui.adsabs.harvard.edu/abs/2005Sci...308.1909S/abstract
“We created transgenic mice that overexpress human catalase localized in the peroxisome, nucleus, or mitochondria (MCAT).”
How exactly do such changes occur step by step? Those. how did they find which genes needed to be changed in order to get the result in overexpression of catalase and in mitochondria?
I am new to biology, and although I understand, for example, how CRISPR works, it’s not clear where people get such data "this gene in the mouse is responsible for the expression of catalase in mitochondria. "Where to find such data?

When looking at the scientific literature, it's often helpful to looks at the Methods section to figure out how people did specific things. Unfortunately some journals aren't great about making the methods obvious, but for your paper it is accessible here: https://science.sciencemag.org/content/sci/suppl/2005/06/23/1106653.DC1/Schriner.SOM.pdf. Look at the section **Generation of Transgenic Mice **.

Hi Potion and welcome to Biology Stack Exchange and biology in general!
To answer your questions, these changes do not occur. The authors of the publication have engineered "new" genes (also called transgenes in this context).
They have done so by fusion a portion of a of another gene (also called domain) to the beginning or the end of the sequence of the catalase gene. If your gene of interest is localized to a given organelle (for example mitochondria), you can also swap the domain which is responsible for the targeting to this particular organelle with one from a different gene you know goes for let's say peroxisomes.
If you want to know more details for this particular work I encourage you to check the supplementary material here: https://science.sciencemag.org/content/sci/suppl/2005/06/23/1106653.DC1/Schriner.SOM.pdf
Hope that helps!


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At which point does the physical change in evolution occur?
So you go from homo erectus to human for example. At which point do the actual physical changes take place. Does it happen in the embryo, is it only a change in DNA at a very early stage in the new animal or does it happen when the animal is growing or has fully grown?
And which body parts change first, what is the order of sequence?

You've essentially asked, "Which came first, the chicken or the egg?" Obviously reptiles laid eggs, so eggs. But the first chicken egg, was it laid by a chicken? Chicken first? Or did the not-quite-a-chicken ancestor lay the not-quite-a-chicken-egg that became the first chicken? Egg first? The point is, either way, the two of them, the ancestor and the chicken, had to be extremely, exceedingly, unimaginably similar in appearance. That's the point at which physical changes in evolution take place.

It’s not clear to me what you are asking. Changes in DNA are required for changes in the organism, which goes through an embryonic stage. Are you asking at what stages or tissues a mutation in DNA can occur that will produce a heritable change in an animal? And the answer to the last question surely depends on the nature of the overall evolutionary change and even then can vary. And please finish the [Tour] to find out how this site works, and the Help on asking questions.

@anongoodnurse "Had to" is a tiny bit too certain.  Punctuated Equilibrium events do happen occasionally.  It's just sort of like winning the lottery.  More like "the two of them, the ancestor and the chicken, were so likely to be extremely, exceedingly, unimaginably similar in appearance that we can basically assume they were in any case where we don't have evidence to the contrary."

@Jeremiah - I agree that some changes occur suddenly, but those are so rare as to easily allow a "had to". The difference between the red jungle fowl and a domesticated chicken is that one gene changed enough to allow a harder shell. Look at a picture of the red jungle fowl and tell me it doesn't look like a handsome rooster to you. The mutation, btw, occurred several times in different locations. No one is recorded to have exclaimed, "Omg! A CHICKEN!"

@anongoodnurse Yeah I'm not really commenting on the chicken in particular.  The thing is though that a red junglefowl is just a wild chicken.  Domestic chickens are a subspecies of Gallus gallus.  They diverged from junglefowl solely as a consequence of domestication.  There was never some species of wild chickens unless you are talking about junglefowl.  Now, could the green and red junglefowl have gotten their different colored feathers all at once?  Yeah.  Color changes are one of the more common single generation shifts so it's totally feasible.  Did they?  Probably not.

@Jeremiah - I believe you and I are pretty much in agreement overall. I agree about feather coloration, but (always a but) having raised many breeds, especially rare breeds, of chickens, those feathers don't look at all different from some of the chickens I raised, especially the crosses.

I'm not sure where any of the "buts" are coming from if I'm being honest. I wasn't attacking your comment even from the start, just pointing out that punctuated equilibrium events occur and that evolution isn't always totally gradual. Like most species, the chicken probably has some stutters and jumps in its history if you go back far enough. An egg probably did hatch at some point that looked very different from its mom.  What this change was and whether it was in a junglefowl or before is kind of immaterial. I don't think we really disagree on anything. I was just clarifying a generalization

It's somewhat unclear what this question is asking, but it seems like it assumes that evolution is some sort of linear process, which it isn't.  You may as well be asking "at what point did latin turn into french".  People tend to overthink evolution, largely due to intentional efforts to obscure its simplicity by certain groups and individuals, but it's a very simple process at its core.  Evolution is just the name we give to the change that happens when selection acts on variable populations with transmissible traits.  If you have a mechanism for generating variability, like mutation and crossover, a mechanism for allowing traits to persist across generations, like heritability, and a selective mechanism, like natural selection, the population will change over time as new traits are generated and the ones that are selected against are pruned off while those that are selected for increase in frequency.
This isn't limited to biological systems.  Languages evolve over time, and are even mapped out using the same cladistic methods that biologists use.  Genetic algorithms like differential evolution are used to find the optimal solutions to complex optimization problems.  Even internet memes undergo a diversification and selection process that maps quite well onto biological evolution.  Any time you have diversity, transmission, and selection, you get the process we have come to call evolution.
Looking at it like this, you can see that it doesn't make sense to ask "what changes first" because that will be radically different from instance to instance.  The diversity generation processes in biological evolution are random.  Nonrandom selection will then prune that down, but what it gets to work with in what order is largely down to a roll of the dice.
There are some general tendencies in this regard.  Changes effecting non-vital systems, for example, are less likely to be deleterious in a way that would cause them to be selected against than more drastic changes, and so more "good" ones would likely pop up before a "good" change happens to show up for something easier to break.  Polygenic traits that are impacted by a number of different genes are also more prone to drift, since a change in any one of those factors will likely not break things too much when others can pick up the slack.  So one could predict that, say, changes to a polygenic, largely aesthetic trait like hair or skin color, would happen more often than something more impactful like a change in skeletal structure or an organ moving to a new spot, not because the mutations themselves are necessarily any more likely but because they are less likely to be selected out when they happen if they aren't immediately beneficial.
This doesn't necessarily help when talking about what changes happened "first" in the transition from one organism to another though.  This is partly because defining when such a change starts is usually very fuzzy, since evolution is generally a very slow, smooth process.  However, there are those occasions where a population diverges very rapidly into something that it makes sense to differentiate into two different species, sometimes in one generation.  On these occasions, it does make sense to talk about a "first" change in the evolution of that species.  The problem is that sudden, all at once changes that actually benefit the organism are extremely rare, and so are the exact opposite sort of "first" changes one would predict using the statistical logic above.  If the new species diverged from it's parent species slowly, but experienced some incidence of punctuated equilibrium during that process, that instance of punctuated equilibrium, statistically, probably happened later than a bunch of smaller mutations.  However, if that punctuated equilibrium event is what caused the speciation event to occur, then the least likely mutation to be first is, in fact, first.
Humans do have evidence of punctuated equilibrium events in our history.  One especially well documented one is the fusion of human chromosome 2, changing our chromosome number from the 24 seen in chimps and our common ancestor to the 23 we have today.  The markers of this fusion are very obvious (it has 2 centromeres) and this simply couldn't have happened gradually.  At some point, a parent with 24 chromosome pairs had a kid with 23, and that kid was probably distinctly different from their parent, though we don't know how.  If that led to a speciation event (actually pretty likely since it would problematize breeding with the parent species) that would be the "first" mutation in that new species history.  If it didn't, then there were probably a million virtually undetectable changes to stuff like fingernail growth and nose hair texture before anything big like that happened.

Human chromosome 2 doesn't actually have 2 centromeres. It has what appears to be remnants of a centromere, and genetic material identical to telomeres in the middle, whereas in "normal" chromosomes, the telomeres are only at the ends, suggesting a fusion (along with banding patterns). But this is a nice explanation, much better than my comment.

Good call.  I didn't really mean two functioning centromeres, but that's definitely worth clarifying, as two actual functional centromeres would make the chromosome nonfunctional and I don't want anyone repeating stuff that is going to get them hammered later when some creationist drills down into the details.  Thanks!

Pedantically, selection is not necessary for evolution to occur, though it is sufficient when combined with heritable differences in fitness and in most cases the more "interesting" contributor to evolution.

True, and I actually find nondarwinian mechanisms of evolution to be plenty interesting, but I thought diving into the weeds of genetic drift and spandrels and heffalumps and woozles was going to be more confusing than helpful when someone was asking a question like this one. Maybe the blue jolly ranchers are gone because they are your favorite, or maybe it's just because you happened to grab all the blue candies, but if someone still doesn't accept that a bag can be cleared of blue candies through random grabbing if you put the non-blue ones back, the second point just muddies the first.


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Why do we use klenow fragment in pyrosequencing?
Why do we use klenow fragment in pyrosequencing instead of polymerase

The Klenow fragment is a polymerase. Are you asking why the fragment is used instead of the full polymerase?

Yes exactly right