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Difference between crossover rate and recombination rate?
I am not a biology student and therefore, need clarification if crossover rate and recombination rate are the same thing. So if the text says 'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing? And if not then what is the difference? Also, is 'per base pair' and 'per locus' the same thing?

Let's start with the second question.

Is 'per base pair' and 'per locus' the same thing?

No, not necessarily. A locus (plur. loci) is a location in the genome. It can be of any size. A locus can be a single base pair or it can be 10 base pairs, or a whole gene or anything you want.

'recombination rate per base pair per generation' or 'cross over rate per locus per generation', is it the same thing?

Recombination rate and crossover rate are not exactly the same thing!
Let's define two loci. Here is a drawing of two haplotypes (the maternal one and the paternal one). Let's represent the loci on the maternal haplotype with capitalized letters and the loci on the paternal haplotype with lower case letters
---A---------B---

---a---------b---

Let's Let's say that between these two loci there are on average 0.2 crossover per reproduction. The crossover rate is therefore 0.2.
Let's draw the two haplotypes after crossover(s) in a case with...
... 0 crossover
---A---------B---

---a---------b---

... 1 crossover
---A---------b---

---a---------B---

... 2 crossovers
---A---------B---

---a---------b---

... 3 crossovers
---A---------b---

---a---------B---

... 4 crossovers
---A---------B---

---a---------b---

You might see a pattern here! If the number of crossovers is even (including 0), then the association between the two loci is unchanged. If the number of crossovers is odd (including 1), then the association between the two loci is changed.
The recombination rate is the rate at which the association between the two loci is changed. Let $P(n)$, be the probability that there are $n$ crossovers between our two loci. The recombination rate is therefore $P(1) + P(3) + P(5) + P(7) + P(9) + P(11) + ...$.
To make a long story short, the recombination rate is the rate at which the number of crossovers is odd.

Thank you for such a detailed answer. It makes a lot more sense now.


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stem cells divisions and normal cells division
I'm a beginner in biology, but I've read that stem cells replace the "worn out" cells or the dead cells. Well, I'm a bit confused - why do they do this?
Aren't there any cells nearby which are the same type as the worn out cells or the dead ones, that can divide and so on?

source: Stack Exchange

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

sort: votes


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How can I set micropipette volume with decimal separators, for example 109.5 in p200?

And how can I set:

150.1 in p200
871.3 in p1000
840.5 in p1000?

What is the brand and model of your pipet?

It doesn't make sense to set volumes of decimals of microliters with a P200, since usually the accuracy of these pipettes is in the order of a few microliters. So even if you set your pipette at 190 uL, you may still dispense a volume ranging from 187 to 193 uL. For a P1000, due to higher volumes the inaccuracy is of course higher, usually +/- 10 uL or more. Some brands are more accurate than others, like Eppendorf or Finnpipette. I suggest you check the specs of your pipettes and see how much accuracy you can achieve.

I think a fair take-home message here is you shouldn't, and with many brands you often can't. Rainin and Eppendorf P1000's measure to four places from 0100 to 1000, for example. The best bet is to use two different pipets, and use them in that fashion throughout the process to maintain consistency.

I would always use multiple pipetters in cases like that, but really the answer is that no pipetter is going to give you 4 sig figs of accuracy.  It's just not possible with the technology.

For p200 the smallest unit is the tenth of a ul (0.1) but the intervals go by 0.2 so to set 109.5 (assuming your pipette can be adjusted between intervals) you need to set the pipette so the pointer is equidistant from the 109.4 and 109.6 mark. For the p1000 the smallest unit is 1 ul so you cannot set it to 871.3.

Some brands of pipeters "click" at each allowed increment, so you won't be able to go between them.

Interesting. Thanks for sharing I didn't know that.

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What is the difference between optokinetic and vestibular nystagmus?
Optokinetic nystagmus is for stabilising the pictures we see when we are observing moving objects for example if we are rotating on an office chair. If we wear a mask while rotating however, the optokinetic nystagmus will not occur since we don't see. But I read that vestibular nystagmus will occur even if we are wearing a mask.
What is vestibular nystagmus exatly and how does it differ from optokinetic nystagmus?

The vestibular reflexes are the main cause for stabilizing eye movements. The labyrinth canals in the inner ear detect changes in head direction, movement and acceleration. This is important for balancing body and visual field. These are fast involuntary reflexes thanks to almost direct connections between the sensory hair cells in the ear and the eye muscle innervating neurons.
The optokinetic reflexes are complementing the vestibular reflexes for slow movements or visual field motions independent of head movement (source and further reading). It needs the visual input.
In my studies we actually did this experiment ourselves, measuring the eye muscle activity while rotating with opened or closed eyes. The results were basically the same in both conditions. With opened eyes you try to fixate something in the moving image for longer and have therefore larger jumps in the eye movements, but with closed eyes the saccades are still there.
Edit: The two senses can also be in conflict with each other. For example reading a book in a car (your vestibular system detects motion, while your visual field is steady) or watching a movie in the cinema (your visual system detects motion while your vestibular system doesn't). This causes motion sickness.


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How does alcohol interact with sympathomimetics to affect the cardiovascular system?
There is a fair amount of information on the cardiovascular effects of alcohol, and of sympathomimetics. How do they work? And how do their mechanisms interact?
We know that similar pathologies result from each. With alcoholics often experiencing mild left ventricular hypertrophy, mild diastolic dysfunction which preceeds systolic dysfunction, resistant hypertension; and a dilated cardiomyopathy - sympathomimetics leading to cardiomegaly, sinus tachycardia, left ventricular hypertrophy, and dilated cardiomyopathy #1.
An article notes that "alcohol competes with amphetamine for the metabolizing enzymes in the liver, therefore enhancing the bioavailability of amphetamine" #2. Are any effects of alcohol mediated by sympathomimetics/catecholamines, and if so which? Et vice versa.
[1] Chemical Cardiomyopathies: The Negative Effects of Medications and Nonprescribed Drugs on the Heart https://bit.ly/2AMU6eM
[2] Myocardial Infarction Associated with Adderall XR and Alcohol Use in a Young Man https://bit.ly/2SV4wQD
[3] Cardioprotection by regular ethanol consumption: potential mechanisms and clinical application https://bit.ly/2RRVVAQ
[4] De Musset's sign https://bit.ly/2HljluG


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Does blood clot reduce blood flow?
I read that blood clot reduces blood flow from few website and from doing an A level biology question; and if this blood clot is formed in pulmonary thrombosis, this can reduce gas exchange in lung.
However, how are we so certain this is true? If there is a blood clot, then blood pressure around that region increases I believe thus implying the blood will travel faster in that region? If so, then we can't firmly conclude blood clot will reduce blood flow as although blood clot will reduce the lumen of the vessel, the blood will also be travelling faster.

A blood clot can nearly completely or completely block an artery, in which case the blood flow will be reduced or stopped.
How do we know this?
Pulmonary Embolism (Merck Manuals):

Pulmonary infarction is when some of the lung tissue does not receive
  enough blood flow and oxygen and appears on imaging studies to die due
  to blockage of a lung blood vessel by a pulmonary embolus.

An embolus is a blood clot that usually develops in the leg veins in individuals with deep venous thrombosis, detaches and travels to a certain pulmonary artery and blocks it.
Similarly, atheroma (atherosclerotic plaque) that builds up within the artery and only partially blocks it, can reduce the blood flow to the target organ. For example, a partial blockage of a coronary artery can result in decreased blood supply to the heart and consequently in angina pectoris or myocardial infarction. It is then the investigation called coronary angiography that can show that a certain coronary artery is partially blocked.
When a clot interferes with blood flow (Harvard.edu):

In venous thromboembolism, a blood clot slows or stops the flow of
  blood through the veins...

Thank you for the answer, but I'm not sure if your last paragraph answers the question as I understand that decrease in cross sectional area can potentially decrease the flow rate (as there is a smaller cross section for blood to travel through) but this decrease can be compensated by an increase in fluid velocity thus the end result is that flow rate is not changed - this is the idea behind the continuity equation in physics. But I get your argument in the first few paragraph.

I deleted the last paragraph and added one new source. Also, look at the first image in this coronary angiography article and you'll see that a part of the coronary artery is narrowed, not completely blocked, so the flow of the contrast substance is not discontinued. But that narrowing results in decreased blood flow and hence in angina pectoris or myocardial infarction. So, it is a result from which you can conclude that the blood flow is decreased.

@BøbbyLeung This answer is correct. It looks like, though, you're looking for a physicsy physiology answer, though. I've supplemented this answer with some of the physiology in mine.

Given the context of your comment on @Jan's answer above, it looks like you're asking if the continuity equation, $\rho_1A_1v_1 = \rho_2A_2v_2$, applies to blood flow through a local vessel. The answer is that it doesn't, because the local vessel is not a closed system.
The continuity equation is derived from the principle of conservation of mass (see the earlier link) and requires that everything coming in at position 1 exit at position 2. Here, a blood clot, or specifically in your example, a pulmonary embolism, increases the resistance in one of a number of vessels in parallel. Blood flow is diverted to the parallel vessels with lower resistance, the ones without the clot. This is useful in a helpful clot at the site of injury as well as an unhelpful clot like a pulmonary embolism. Thankfully, a clot in an injured vessel has the ability to slow and finally stop the loss of blood. Again, this is allowed despite the continuity equation because there is an alternative path. Blood can either flow out of the vessel at the site of damage, or flow through the vessel.
The fact that changes in vascular resistance are met with changes in flow is a principle used to beneficial effect in normal physiology, not just the response to a clot. Arterioles, for example, regulate flow through vascular beds as needed, by increasing or decreasing resistance.
There is a case, a saddle embolus, where there is no parallel path. Here, though, flow still decreases because the pump fails (and pressure is lost). The rapid increase in resistance cannot be compensated for by the heart, and sudden death results.
Generally, when applying fluid dynamic principles to blood flow and the circulatory system, you have to consider whether the assumptions hold. Generally, you can apply the continuity equation to portions of the circulatory system in series (e.g., the cardiac output of the right heart has to equal the cardiac output of the left heart), but there are still caveats (vessel walls are not rigid -- they have a capacitance).
These principles are discussed in Costanzo Physiology Ch. 4.

Thank you very much for the detailed answer. If you have time, could you please elaborate on why is the local vessel not a closed system? A sketch of it would be helpful.


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Can an epileptic seizure start in the spinal cord?
My understanding of an epileptic seizure is caused by "invalid electrical signaling" in the brain. Can these start from the spinal cord  (outside the brain) and move into the brain and cause an epileptical seizure? (sorry for not using the right terms)

Can you clarify what you mean by "outside the brain"?

can you provide example of place "outside the brain"? is it leg/spinal cord? Space 2 feet away? I am serious

Yes, spinal cord


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Enzyme inhibitors against common cold viruses
Would some inhibitors of viral enzymes work against common cold viruses? Are there any studies? What could a treatment look like?
A lot of common cold viruses are rhino viruses which are picorna viruses. All picorna viruses contain two cysteine proteases, designated 3C and 2A according to Handbook of Proteolytic Enzymes
Volume 2, 2013, Pages 2402-2406
David S.Wishart Would it suffice to inhibit either of them?

Common cold seems like the most damaging disease of all. With on average two weeks sickness per year and person that equals to an annual loss of GDP by 300 billion EUR in EU.

A human enzyme involved in the production of rhinovirus capsids has been successfully inhibited.

Fragment-derived inhibitors of human N-myristoyltransferase block capsid assembly and replication of the common cold virus https://www.nature.com/articles/s41557-018-0039-2

The article also says that targeting a human enzyme could be more efficient since the risk of mutation is lower compared to a virus enzyme.

Pfizer has the orally administered Paxlovid which is the protease inhibitor nirmatrelvir in combination with its preserver ritonavir.

Can you please combine both answers into one by using the edit function?

Then there would be no way to vote separately, and the two solutions are basically different.  One inhibits a virus enzyme and the other a human enzyme.

These are two possibilies for the same problem. Please put them together, otherwise I will do it.


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What do chimpz/bonobos/orangutangs/gorillas feed their babies with?
I just read this question and it made me curious about what a more original baby diet would look like. So, at what age do our closest relatives in the animal kingdom start giving their offspring more solid food, in addition to milk, and how do they prepare it?

You are expected to show some attempt to answer the question on your own. go on google scholar and type in chimp weening diet.

@John I googled but it was hard to find relevant keywords.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3581971/


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Loss of antibiotic resistance due to long term storage
How possible is it for antibiotic resistant bacteria stored for a long time to lose such resistance?

What do you mean by "stored for a long time"? For example, do you mean "frozen in a laboratory"?

It is possible due to the fact that some antimicrobial resistance genes are induced by the presence of antibiotics themselves and are not promoted in the absence of a specific antibiotic, so the production of certain antimicrobial structures (enzymes, pumps, etc.) will be reduced once the bacterial medium is antibiotic free for enough time. This is sometimes refered to as "antibiotic pressure" referencing to some extent the genomic concept of selection pressure.
Take for example the phenomena reported in this paper's summary; they studied a patient hospitalized because of an infection by 2 K. pneumoniae strains. They knew beforehand that one of the strains was suceptible to carbapenems while the other one had a certain degree of resistance to this antibiotic. As the infection unfolded and a treatment with meropenem was administered, they took several samples and studied them via whole genome sequencing (WGS). They found out that the strain previously characterized as suceptible to carbapenems had acquired a plasmid (possibly by vertical transmission from the other strain) and hence now exhibited resistance to carbapenems, however when this strain was left in observation (and without being exposed to meropenem) it lost its previously acquired resistance.
In conclusion the sole presence of antibiotics induces resistance by different mechanisms in bacteria, but in some cases the lack of antibiotics in the medium can also revert resistance if this condition lasts for enough time. It is important to mention though that some resistance profiles will never be reverted no matter for how long the bacteria remains away from an antibiotic due to their nature. For example a gram-negative bacteria will always have instrinsic resistance to regular penicillin no matter what due to its cell structure itself (lack of a thick peptidoglican cell wall and presence of an outer cell membrane).


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How is Saccharomyces cerevisiae grown on acetate and ammonium able to produce TCA intermediates?
I am working with a metabolic model of Saccharomyces cerevisiae and I am studying its growth on acetate and ammonia. I am performing Flux Balance Analysis to compute the growth rate and then I am exploring the flux distribution over all metabolic reactions.
The flux distribution shows that acetate is uptaken and transported to the mitochondria, where it produces Ac-CoA, which enters the TCA cycle. But also some acetate remains in the cytosol and produces Ac-CoA, which is used to synthesize fatty acids and to enter the glyoxylate cycle.
My question is the following: if acetate is the only carbon source supplied and ammonia is the nitrogen source, how can initially Ac-CoA enter the TCA or the glyoxylate cycles? In both cases oxalacetate is needed, which cannot be produced directly from Ac-CoA from other alternative pathways.
My only guess is that TCA cycle intermediates are being produced somehow and keep the cycle running, but as the nitrogen source is not even an aminoacid, I do not understand where this whole thing starts.
Thank you very much for your help!


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why nucleosome spacing is longer in heterochromatin than euchromatin
Heterochromatin is defined as tightly packed form of DNA. But some experiments show that the average spacing of nucleosomes associated with H3K9me3 and H3K27me3, both heterochromatin marks, are longer than those with euchromatin marks. why packed DNA has longer spacing?
e.g in article :Genome-Wide Nucleosome Positioning Is Orchestrated by Genomic Regions Associated with DNase I Hypersensitivity in Rice. it says:"The average spacing of nucleosomes associated with H3K4me1 and H3K27ac, both euchromatin marks, are 178 bp and 179 bp, respectively. In contrast, the average spacing of nucleosomes associated with H3K9me3 and H3K27me3, both heterochromatin marks, are 205 bp"


text:
Why was cotton chosen to grow on the moon?
The choice of plants for the first lunar ecosystem is a bit unusual.
They are growing cotton, rapeseed and potatoes.
Why did the Chinese scientists choose them? Is it because of their ability to thrive in such an environment or because of their possible  contribution to sustaining life in long space missions?

China's state-run Xinhua News Agency mentions the reasoning for most of the species they sent:

Why were these species chosen?
Xie [the chief designer of the experiment] said potatoes could be a major source of food for future space travelers. The growth period of Arabidopsis, a small flowering plant related to cabbage and mustard, is short and easy to observe. Yeast could play a role in regulating carbon dioxide and oxygen in the mini biosphere, and the fruit fly would be a consumer of the photosynthesis process.

While this doesn’t mention cotton, it seems very likely to me that, like potatoes, it’s just a very useful crop.
According to another article, the goal for China is a moon research base:

“We’ll use the Chang’e-8 to test certain technologies & do some preliminary exploration for jointly building a research base on the moon,” Wu said.

Arabidopsis, yeast, and fruit flies are also model organisms.


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Is it possible to fuse DNA from two sperms into one sperm?
Is it possible to fuse the DNA of two genetically different sperms into one singular sperm? In theory, half of the number of chromosomes in a normal sperm would come from one sperm and the other half could come from a separate sperm. In return, the fused sperm could fuse with a healthy egg cell for fertilization.

It would be theoretically possible to engineer such a cell, but something very similar can occur in nature, two sperm cells can fertilise a single egg cell, resulting in a fetus with DNA from both. See here

Awesome, thank you! If it were to happen by engineering the cell, what process or pathway would theoretically be used to fuse the two sperms together?


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Species-ID: What is this thing attached to my wall (California, USA)
I found this thing attached to my wall next to my garden. I live in Simi Valley, California, USA.
At first I thought it was a caterpillar and I left it alone, but after 2 or 3 months I don’t think it is a caterpillar anymore. I touched it today for the first time and it moves. What is it?

What is the approximate size? Maybe 3cm?

It is About 1.5-2cm

This is very likely a chrysalis (or pupa) stage of a lepidopteran.
A similar looking example belongs to the giant swallowtail butterfly (Papilio cresphontes).

 Source: Bill Frank
P. cresphontes is found in southern California [source], so it would not be unreasonable to find it in Simi Valley.


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Does low gravity exposure to early stages of human fetus have potential to unloc unused genetic information from earlier stages of evolution?
The title seems quite self explanatory but let me elaborate.
New mutations do take a very long time and many generations to occure in the genetic code. But our genetic code already holds all the information gathered trough evolution process...even information that are older than mammals.
In case of start of pregnency in zero g or gravity of Mars (0,38 g)... there are many replications from the single cell egg to fetus couple month old...
Can gravity in this case has potentional to "open new variant" of genetic information gathered in our cells? Does diferent gravity has impact on metabolic processes on cellual level?

It seems like the question here is, "Does a reduction in gravity affect the way that biological macromolecules interact with one another in cells?" Specifically, does low gravity affect gene expression and metabolism? Is that what you're asking?

Yes. That is exactly it. Sorry if it was was not so clear. So is there any study about impact of different gravity?

I mean I do not expect that anyone know how exectly the gene expression and metabolism changes on cellual level due to long time in low gravity....I just wanted to understand the potencial of possible changes that can occure. What is the scale of potentional changes we might be able to observe during space clolonization.

No
The question itself does not even make sense, we do not hold onto much unused information, there is nothing to unlock. Unused genes mutate and get co opted for other purposes. We have about a hundred new mutation per generation. Much of so called junk DNA is actually just used for other purposes besides coding for proteins.
Will a colony evolve differently sure, any isolated population evolves along its own lines but it will happen at evolutionary speeds.

It has been known for some time that there are physiological changes associated with spaceflight- bone and muscle mass decrease, and the distribution of fluids in the body changes as well, all in response to the decrease in gravity. This is why astronauts ride exercise bikes when they are in space.
Perhaps the most accessible (and trustworthy) resources I have been able to find about the effects of low gravity on the molecular behavior of cells is from the NASA Twins Study, where one twin of an identical twin pair was sent into space for one year, while his brother remained on Earth. Before and after the year in space, the brothers were sampled and tested in all kinds of ways and interesting changes in gene expression and metabolism were found. For example, many genes changed expression levels in the brother who went to space, but they quickly returned to baseline after return to earth. However, a small number of genes remain at changed levels of expression, suggesting that long-term exposure to low gravity does change patterns of gene expression. It is important to note that these changes are not at the genome level; rather, they are attributed to changes in epigenetic regulation of the genome. You can see a summary of these results here.
My knowledge of evolutionary biology is too thin to comment fully on the part of your question that asks about unused genetic information from earlier stages of evolution, but I would expect that if gene expression and cell behavior changes in low gravity, that several generations of humans living entirely in zero or reduced gravity would be trending toward genetic difference from Earth-bound humans. You wouldn't necessarily see changes in an individual, but over time they could accumulate and cause different regions of the genome to be expressed in ways that humans on Earth do not experience.


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Can I ask tip for tissue measuring(especially for RNA preparation)?
I extracted RNA at mouse liver and human blood, but degradation occurs. I think, at mouse liver, too hard to measuring 50mg liver(I am newbie for animal tissue preparation) so spend several minutes. liver is soft but very small, and too hard to keep the weight. (human blood spend time for defreeze, but It degraded, too.)
for example, I want to weight 20mg mouse liver,
1. cut liver by scissors about 10mg after set zero point of scales with ep-tube.
2. cut liver almost 10mg, but it's exceed weight 2~3mg, so I have to cut it 2~3mg.
3. this scale is too small... so I spend for keep the weight for 20mg, like this: 10->23->19->19.3->19.8->21->19.8->20.
I want to ask for advice about how it faster animal tissue measuring and preparation. When preparation genomic DNA, is it OK so DNA is stable than RNA. but, when extract RNA, keep the weight fast and incubate sample at ice for prevent RNA degradation.

I do not have specific experience with liver tissue, but here I would do a couple of things. First, to get around your issues with weighing tissue, set an acceptable range around 20 (say, plus or minus 5mg, so ranging from 15 to 25mg) and then normalize your RNA yield to that starting weight. Second, look into ways to preserve the RNA in your tissue as you're processing it. You could try RNAlater solutions or other chemical means of stopping RNA degradation, or just snap freeze your tissue in liquid nitrogen. Good luck!


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How exactly is the sunflower seed pattern calculated?
I came across this https://www.mathsisfun.com/numbers/nature-golden-ratio-fibonacci.html
and the rotation simulator just below the first section says to type in a number for each rotation. But, it doesn't explain what it is actually calculating.
If I type a number, by what angle is it rotating each cell, how is it calculating the initial number of cells, and how is it scaling each cell with each rotation to look like a sunflower? This definitely has come up in natural phenomena before like the nautilus spiral and the fern, so I want to know the generalization behind this pattern.

For a general reference, look for L-systems (the L stands for Lindenmayer) or the book "The Algorithmic Beauty of Plants". (Available online as a PDF file.)

Too broad, I am looking for something that exactly describes the simulation. The question is general only to the same extent as the simulation's parameters.


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How does the blood of the veins in the legs get to the heart?
Does it have something to do with the valves? Thanks in advance!

You are expected to do some research on your own before posting here. That is the kind of question you ask google not here.

It has to do something with "muscle pump" and pressure in the right atrium. You can find out this from any decent explanation of the circulatory system...

The veins in your legs have one way valves. These prevent blood from flowing down, but do not actively push it up. However, normal muscle movement from walking etc will squeeze the veins to push blood through these valves, and so it will work its way up to where negative pressure in your heart atrium can begin having an effect. This does however mean that blood accumulates from long periods of standing without movement, and so exercises are needed to prevent fainting, for example, for soldiers on parade (see Pathophysiology, Homeostasis and Nursing
By Roger Watson, Tonks N. Fawcett, Josephine N. Fawcett)


text:
Is life deterministic in nature?
I am wondering, according to our current understanding, whether life is completely deterministic. To begin with, consider a single-celled organism, do we have any evidence of any single celled organism deviate from the law of cause and effect ? This, same idea applied to us raises the question, whether we have free will.

I'm voting to close this question as off-topic because it is a question of philosophy rather than biology.

If I understand your questions correctly, I would reframe it as whether life follows the laws of physics, in which case the answer is yes. Indeed, just how one defines life as opposed to other natural processes is still debated, see for example Erwin Schrödinger's "What is life?"
As to whether physics is deterministic, that depends on what you mean. Classical physics is precisely predictable if you have sufficient information, however, quantum physics has an intrinsic random component, and so could be said to be non-deterministic, although still following defined laws. As to questions about the nature of free will, I think that is better suited to a philosophy context.


text:
What is name of the red eyed rabbit or hare, found in Himalayan region?
Is it Rabbit or Hare?

The eyes are red in colour.
These animals are habitat of Himalaya.
The pictures are taken in Dowhill Park, Kurseong, West Bengal, India.

Perhaps a bit underwhelmingly, those are Himalayan Rabbits.
https://en.wikipedia.org/wiki/Himalayan_rabbit
The pure white fur and red eyes are usually a sign of albinos, but in this case it's actually a trait of the entire species.

[They] can only produce eumelanin under a certain temperature and they cannot produce pheomelanin at all.

Thank you for the identification. It's strange that the Wikipedia page doesn't have the classification. I have a question though, the article is saying a breed of rabbit. What does it mean? A species of rabbit?

It means a species of rabbit, yes. Of the genus Oryctolagus.


text:
What is the composition of a standard diluent buffer in a leptin ELISA kit?
I am trying to find the composition of the diluent buffer used for the dilution of a human leptin stock to be used in an ELISA assay. The manufacturer of the kit (https://www.thermofisher.com/elisa/product/Leptin-Human-ELISA-Kit/KAC2281) only indicates that the buffer contains 8mM of sodium azide, but I cannot find the precise composition of the buffer anywhere on the internet.

Simple reason: They want you to buy their buffer and not make it on your own.

Totally get that, but is there anybody who has found what those buffers usually contain?


text:
Difference in Basic Amino Structures
I'm having a hard time understanding why my slides in my biology course have two different representations of the "basic structure" of the amino acid:
1:

2:

The top one seem like what I would expect.  The bottom one, it looks like the amine group gained a Hydrogen ion and the Carboxyl group lost one.  Also, the center carbon gained an H.  I honestly don't know if this description is even correct or not.
I'm extremely new to this level of biology, so very simple explanations are much appreciated.  I just don't totally understand why there are two versions of the basic structure.
Also, I apologize if the tag is wrong, again, this isn't my major, so I'm very new to this material.

Ugly pictures in both cases :)

Your description is more or less correct, but so are both images. The bottom images shows the predominant form the amino acid would take at neutral pH (or any pH between ~2 and ~9.5). This is because the caroboxylic acid (-COOH) and amino (-NH2) groups are a weak acid and base and can lose or gain a proton (hydrogen cation), respectively. pH below the pKa of the functional group (~2 for carboxylic acid and ~9.5 for amino) favours protonation whereas pH above the pKa favours deprotonation. Also note that the "centre carbon" (the α-carbon) did not gain a proton in the second image, it's just drawn differently.
You could try this website for an overview of acid/base chemistry and perhaps these Wikipedia sections on zwitterions and isoelectric points with respect to amino acids, though there are many alternative sources of material available if you search for them. This question and answer may also be useful for you, at least eventually.

To expand slightly on this answer, this is valid for these sorts of chemical structures more generally in organic chemistry, too. When you see groups like these that act as weak acids/bases, you should think of them existing chemically in both forms, with the ratio dependent on the pH. People will switch back and forth between them freely because that's how the molecules actually exist, as well.

Thanks again for this, I now see the center H as just being drawn differently.  I must've been overwhelmed enough to miss that.

@joe_04_04 You’re welcome.


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ECG detection using minimal number of electrodes
Disclaimer: Hello, I'm someone from an electrical engineering background, so this question may sound dumb.
I wish to make a wearable ECG monitoring device for arrhythmia detection. Since the device is to be wearable, it has to be small and should not obstruct normal behavior (kind of like those ECG patch monitors).
My question is, which lead should I monitor for arrhythmia detection. I read that I do not need all 12 leads for this purpose. The leads should preferably involve electrodes close as possible to reduce area of contact with the body.

hi and welcome. Question is not dumb, but could you share what you've found on your own? That will help us to understand gaps, and answer better

First, let's talk about electrodes.
Background
What do the electrodes measure?
When we talk about ECG signals, we generally talk about leads - that is, difference of electrical potential between two electrodes. This voltage change comes from change in polarisation in the heart as the rise in electrical potential is created in SA node and travels to AV node before coming down and finally spreading to the ends of Purkinje fibers.

Conduction system of the heart (source)
Signal
The plotted signal you get from each lead will give you your PQRST curve, but note that even though the events are there, the plots look rather different.

Raw signals from a multi-lead setup (source)
You can see that if all you are interested in are the times and durations of the PQRST events, all you need is one lead. But which one is the best? In order to find that out, we need to talk about heart vector.
Heart vector
Heart vector is the sum of all the small depolarisations happening in the heart, and points roughly in the direction of where the most depolarisation is happening. During the heart cycle this vector changes in time.

Heart vector changing during the heart cycle (source)
You can see that the highest heart vector variation is on the subfigure B, which roughly lies on the line crossing an electrode on the right shoulder and the left leg.
But wait! Before you start working on your single-lead ECG patch, consider, that this will only give you the magnitude of a projection of the heart vector on the diagonal axis described in the previous paragraph. If you add one more electrode, you can build an Einthoven's triangle and actually find the heart vector (or rather it's close enough approximation).
Electrode placement
In Einthoven's triangle method, 3 electrodes are used - 2 are placed on the shoulders and 1 on pubis, or you can place them more distally - on arms and left leg.

Einthoven's triangle (source)
This gives you 3 leads, from which you can use any two to find the heart vector (guide here).
Number of electrodes
OK, but why is it so important, that we have found the heart vector? We had to add a whole electrode to our setup!
Averaging all heart vectors occurring during a heart cycle will give us (an approximation of) mean electrical axis, which can aid in diagnosing pathological hearts.
Setups with higher electrode and lead count can give you even more insight into the heart function, but I will omit them in this answer for the sake of brevity.
Similiar projects
3-lead ECG patch
Probably the closest to what you want to achieve is a 3-lead ECG patch described in the Quality of ECG Monitoring with a Miniature ECG Recorder (Janata, 2008). They compare the performance of a small ECG patch placed in 4 different locations to a Holter monitor for rhythm analysis. They find that the patch is useful, but there is some information lost compared to the Holter monitor. Not that the channels in the patch look really similiar compared to the ones from the Holter monitor, so placing the electrodes close together does limit the amount of information you will be able to gather.

ECG patch used in the study
Single-lead ECG arrhythmia detection
If you really are limited to to electrodes, there has been some luck in detection of arrhythmia from a single lead signal using machine learning. An example would be Detection of Atrial Fibrillation from RR Intervals and PQRST Morphology using a Neural Network Ensemble (Khamis, 2018). However, keep in mind they used a proper lead I (LA-RA) setup, not a single ECG patch.

You could try to dig into the specs of the new/upcoming Withings ECG smartwatch for some insights https://www.withings.com/uk/en/move-ecg


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When we talk of functional macromolecules (e.g. proteins as enzymes, hormones, receptors, antibodies etc), towards what are they evolving?�
Actually this is a question which is given in a book and to be honest,it has baffled me.I'm not so much well versed with molecular evolution so my guess would be,say some sort of enzyme which could catalyse more than 1 reaction maybe coz then that 1 will be sufficient enough to do much more work,like it happens at organismic level,like reduction in legs of prawns and shrimps which has happened (earlier relatives has more legs but they were less effective as compared to their modern counterparts).So,my guess would be something like that but as I said earlier,I'm not so good in molecular evolution so please help me out.Or tell me about what were the characteristics or primitive macromolecules and those that occur today and via that,this question might be explained.Also,I've written the question as such given in the book i.e without any changes.

This is a nonsensical question akin to asking you to predict the future. Sure, further evolution of proteins etc may occur, but there is no “master plan”. Whatever TBH is should be ashamed of itself. I vote to close.

I'm voting to close this question as off-topic because the question is based on a false assumption.

Your question is not clear. Can you please [edit] it? Add more relevant details if necessary.

Well,can you explain that what are the changes that anyone have observed in the macromolecules of say the Proterozoic era or Palaeozoic era and the macromolecules that occur today.I guess that the book might be asking for this.........

"I guess that the book might be asking..." is not good enough. Please edit your question with a direct quotation from the book and naming the book, author and publisher. In addition please remove the non-unicode, non-isolatin character at the end of your title and explain what TBH is quoting from that (or delete any mention of it). As I have already commented, the question as you pose it is in my opinion based on a false assumption, namely that evolution is directed "towards" something. If this was only your interpretation of a book, then we can help you if we know what was written.

I think that TBH means to be honest,Read what I've written carefully,I've expressed my view that I myself was baffeled.Also,I've written the exact question of the book as such without making any changes i.e. the question has been copied word by word.The book is NCERT Exemplar problems and the chapter is evolution.I guess that you might be able to find a PDF of this somewhere on the internet.Also, isn't evolution is directed towards making us fitter for survival as quoted by Darwin in his book survival of the fittest.

So the title of your question (complete with dodgy character) is a quotation from a book of exam questions? This was in no way clear, and should have been stated in quotes in the question. What is clear is there is no reason for me to change my attitude to your question, or for you to spend any more time on such the flawed question in the book. One word of advice if you are approaching an exam. Use standard English (“coz” is not), divide your writing into paragraphs, and do not use text abbreviations. Unless you deliberately wish to antagonise the examiners towards you.

I mean I know this seems kinda wacky but this is the only explanation I could think of.Also,I'm kinda new on this website so can you give me some advice about posting question and writing the body please.


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How do mutations with very little fitness benefit get fixed?
I have one little issue with evolutionary theory that I have not been able to understand.
Suppose genetic mutations happen from generation to generation. Nevertheless, from one generation to the next the mutation will present very small changes (I don't suppose a giraffe's neck would grow 10cm). If this were the case, then the advantages one gains from this mutation would be very small. So shouldn't it be the case that the mutation in the case of the giraffe and every other mutation for that matter present very very little advantage so shouldn't transmission of genes at this stage be random? If this were the case I don't see how natural selection could take place?

In the long run (over hundreds or even millions of generations), small statistical advantages are bound to accumulate.
Even if a mutation gives only a +1% average reproductive advantage, it is still above chance and therefore this mutation is more likely to spread through the population.
(If you can code, I have found it to be an interesting exercise to write scripts that simulate generations of evolution.)
It is also not necessarily true that effects of mutations have to be small. Single mutations can be deadly, they can change colors, create large morphological changes, and so on. It just happens to be the case that most mutations that have large effects are deleterious, and therefore won't generally spread for long throughout the population. But some mutations will be beneficial and therefore have improved odds of being passed on.

Consider genetic drift: if a particular mutation is selectively neutral, it may persist indefinitely in the population, but it is subject to random changes in its frequency due to various non-selective influences.  As a result of the random fluctuations in frequency, the allele may be eliminated from the population or may become fixed in the population despite having no influence on the natural selection of the individuals of the population.
Now consider if rather than being neutral, the mutation is slightly deleterious.  Since its effect is only slight, it can persist in the population for a long time.  Still, like a neutral mutation, it is subject to random fluctuations in frequency and so can be eliminated or fixed in the population.  However since it is slightly deleterious, it is more likely that the fluctuations will eliminate the mutation.
Similarly, if a mutation is slightly selectively beneficial, it will still be subject to random fluctuations and can be eliminated or fixed, but in this case it is more likely to become fixed in the population.
One view of this process is formalized in the "nearly neutral theory of molecular evolution".


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What created the first ribosome
If a ribosome is made of protein, yet is used in protein sysnthesis, what created the first ribosome?
What created the ribosomal RNA?

This question has been asked before in several variations and has several detailed answers as I recall. I’m away at the moment with only my phone. Perhaps someone else could look up the actual question to mark it a duplicate.

@David yes, there are similar questions about DNA and DNA polymerase and ATP synthase. I didn't mark this as a dupe of them because it could be argued that ribosomes are different. However, we can mark all subsequent questions on this topic as a dupe of this one or the others

@WYSIWYG I’ll have a look when I get back this weekend. It would be good to have one or two definitive questions (the ribosome may require its own) with a selection of comprehensive answers. I have my own contributions to make, but would rather do so in a coordinated manner. Perhaps the way to handle it would be on meta.

@WYSIWYG — Found the previous question —  almost exact duplicate.

This is one of the "chichen and the egg" quesitons about early origins of life. The answer is: we don't know. There is a RNA world hypothesis which suggests that RNAs were the primary versatile biomolecules before proteins. This idea stems from the fact that there are self-replicating RNAs and ribozymes (RNA-based enzymes). Also, the fact that the catalytic center  (peptidyl transferase) of the ribosome is RNA, is also used in support of the the RNA world. However, this is still an idea and we cannot conclusively say that an RNA-world existed.

As the question is clearly a duplicate you might wish to migrate your answer to the original. I am considering writing a second answer (I already included a devil's advocate one) because I do not feel the current RNA world answer there is adequate.


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What do the acronyms in C.elegans neuron names stand for?
In this site, I see a variety of acronymic names for C.elegans neurons but what do these names mean (for example AVAL, AVAR)?

Listing all the names would not be possible and hence your question tends to be broad. However, have a look at this site.

Unfortunately, there doesn't seem to be a very systematic nomenclature. Some of the letters are acronyms while others describe a class of neurons. The letters V and D usually describe the ventral and dorsal counterpart of a pair of neurons. The same goes for L and R (left and right).
This list names all C. elegans neurons and you can see that, for example, the "ring interneurons" or motor neurons start with RI or RM. "Inner labial" or "outer labial" neurons are called IL or OL. Ventral cord motor neurons start with a V and their different classes are called VA, VB, VC and VD plus a number. The classes are determined by lineage origins or historic reasons ;) And there are a lot of exceptions to these rules, because their historic names remain even though we continue to learn more about these neurons.
The example AVAL/AVAR are ventral cord interneurons. They form a class with other ventral cord interneurons called AVB, AVD, AVE. So, the first two letters refer to the main class, the third letter to the subclass. The L or R refer to the left and right member of this pair.
Some friends working in C. elegans neuroscience told me that you basically just treat these letter codes as individual names for the neurons without bothering about their origin and meaning too much.

Quote : "Every C. elegans neuron name consists of either two or three uppercase letters indicating class and in some cases a number indicating the neuron number within one class. If the neurons are radially symmetrical, each cell has a three-letter name followed by L (left), R (right), D (dorsal), or V (ventral). "  link


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Could fish safely "breathe" pure oxygen in their water?
I've heard it said various times before that humans can't breathe pure oxygen, or at least not for very long, before it would kill us.  But during a discussion on Worldbuilding, the difference between air-breathing and water-breathing came up.  It made me wonder: what would happen to a fish if it had pure oxygen, rather than the ordinary gas mixture of air, dissolved in its water?  Would it be safe, or have the same oxygen toxicity problems as humans?

It can't be pure oxygen if it is dissolved in water. Also there are not tiny air bubbles in water it is dissolved gasses. You need to look up what dissolved means.

...huh?  I know exactly what "dissolved" means, and I didn't say anything at all about "air bubbles," tiny or otherwise.  I asked what would happen if the gas dissolved in the water was pure oxygen rather than air.

Pure oxygen is not dangerous because of a lack of other gasses it is dangerous because of the concentration, the amount of oxygen dissolved in the water will not be effected by whether the oxygen started pure or not.

Tropical fish are typically shipped with oxygen enrichment of the gas volume of the plastic bags. The oxygen is between about 30 and 90% depending on technique. There is also tranquilizer in the water. Local pet shops also inflate the bags ;I don't know if they use oxygen or compressed air.

It won't be safe. Typically there is a limit to how much oxygen can be in the water due to the physics of solubility. However, there are some circumstances where the water can be temporarily supersaturated with oxygen. For instance, near a waterfall, dam/thermal discharge, algae bloom etc.
If a fish were to remain there, they may contract gas bubble disease. Mortality of young salmon and trout has been observed after 3 days at 120% oxygen saturation.
You can read more about it at --- Fondriest Environmental, Inc. “Dissolved Oxygen.” Fundamentals of Environmental Measurements".

the saturation rate of oxygen will not be affected by whether the oxygen starts pure or mixed with air. So this does not actually answer the question.


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Apart from nerve cells and muscle cells, what types of cells do not undergo mitosis in adult man?
Neurons and muscle cells in adult humans do not have the ability to divide by mitosis, so they can not repair themselves and their cell cycle remains in the interphase. I’m looking for more cells with this feature. Are there other cells with this inability to undergo mitosis in humans or in plants?
In an adult human:

Do nervous cells ever undergo mitosis?
I wonder if all muscle cells do not undergo mitosis or if this inability only applies to cardiac and skeletal muscle cells.

As I understand no specialized cells undergo mitosis, not even epidermal cells. The difference resides in that certain tissues like epidermis maintain a pool of undifferentiated cells that undergo mitosis and trough this, generate new cells that differentiated into the specific specialized cell. Such a pool exist in certain brain areas like the hippocampus, where it's possible to observe the appearance of new neurons in the adult.

To answer the numbered questions:

In general, neurons never divide by mitosis. However, I believe you may have unintentionally misphrased your question; there are functional neural stem cells in the adult human brain as well, and these are believed to give rise to new neurons throughout the lifespan of an individual. They have only been found in specific parts of the brain, though, such as the SVZ and the subgranular zone of the hippocampus (Gonzales-Perez 2012; Behnan et al. 2017). It also bears noting that following an external insult (such as DNA damage, oxidative stress, hypoxia), even terminally differentiated neurons can re-enter the cell cycle and go as far as to replicate their DNA, but this tends to result in apoptosis or arrest at the G2/M phase; such aberrant re-entry into the cell cycle is more frequent in brains afflicted by neurodegenerative diseases (Frade & Ovejero-Benito, 2015). In addition, the possibility to induce neurons to proliferate and form cancers has been demonstrated in retinal cells in mice (Ajioka et al. 2007).
Correct; as with neurons, muscle cells (myocytes) lack the ability to undergo mitosis. But again, I believe what you really want to ask is whether or not muscles maintain a pool of stem cells that can replace lost cells. The answer to this is yes—there are stem cells within skeletal (Wang, Dumont & Rudnicki 2014)  and smooth muscles (Majesky et al. 2011) that proliferate in response to damage. According to some studies there are stem cells in the adult heart as well, although their regenerative capacity appears to be very low (Bergmann et al. 2009).

If your intention was indeed to ask about which cells are unable to undergo mitosis, then the answer will likely be a very long list, as no terminally differentiated cell type undergoes division under normal circumstances. This would, for example, include all different blood cell types (erythrocytes, megakaryocytes, neutrophils, eosinophils, basophils, B-cells, T-cells, natural killer cells, mast cells, macrophages), most skin cells (e.g. keratinocytes, melanocytes), epithelial cells (such as those that form the intestinal lining) and such. This would likely include most if not all of the cell types listed here that do not have the "(stem cell)" note next to the links (although I did not confirm this by checking the literature on them).
References:

Ajioka, Itsuki, et al. "Differentiated horizontal interneurons clonally expand to form metastatic retinoblastoma in mice."
Cell 131.2 (2007): 378-390.
Behnan, Jinan, et al. "Identification and characterization of a new
source of adult human neural progenitors." Cell death & disease 8.8
(2017): e2991.
Bergmann, Olaf, et al. "Evidence for cardiomyocyte renewal in
humans." Science 324.5923 (2009): 98-102.
Frade, José M., and María C. Ovejero-Benito. "Neuronal cell cycle: the neuron itself and its circumstances."
Cell cycle 14.5 (2015): 712-720.
Gonzalez-Perez, Oscar. "Neural stem cells in the adult human brain."
Biological and biomedical reports 2.1 (2012): 59.
Guo, Dayong, and Lynda F. Bonewald. "Advancing our understanding of
osteocyte cell biology." Therapeutic advances in musculoskeletal
disease 1.2 (2009): 87-96.
Majesky, Mark W., et al. "Vascular smooth muscle progenitor cells:
building and repairing blood vessels." Circulation research 108.3
(2011): 365-377.
Wang, Yu Xin, Nicolas A. Dumont, and Michael A. Rudnicki. "Muscle
stem cells at a glance." (2014): 4543-4548.

Yes, nervous cells never undergo mitosis coz they lose their centriole thereby they are present permanently in G0 phase of cell cycle in which a cell doesn't divide,rather it just carries out it's day to day metabolism.
As far as plants are concerned,they have meristematic cells which are capable of regeneration.But if you know a little bit about plant anatomy then you can say that primary xylem and primary phloem do not divide throughout their lives.
I hope this helps.

Though neurons do not possess the ability to divide in adult humans, glial cells do, and in case of injury or disease, tend to fill up the gaps created by loss of neurons.
Most muscle cells lose their ability to divide after maturation. There are a few cases however, like those in disease or damage, when cells that are lost may be replaced. These are discussed below:

Skeletal muscles:
Each skeletal muscle fiber arises by fusion of multiple myoblasts during embryonic development. Once fusion occurs, the ability to divide is lost. However, a few myoblasts do persist in mature skeletal muscle as satellite cells, which retain the capacity to fuse with one another or with damaged muscle fibres to regenerate functional muscle fibres. So even though our muscle cells cannot divide, they can, in some cases, be regenerated.
Smooth Muscles:
Certain smooth muscle fibers, like those in the uterus retain their capacity for division. Also, new smooth fibers can arise from pericytes, stem cells
present in association with small veins and blood capillaries.
Cardiac Muscle:
These fibers are unable to divide on their own. However, there have been studies related to this, and it was shown that bone marrow stem cells could be used to regenerate damaged heart tissue.
(Refer: Cell transplantation for cardiac regeneration: where do we stand? Neth Heart J. 2008 Mar; 16(3): 88–95.)
I hope this answers the question.
I read this in Principles of Anatomy and Physiology, 12th Edition, Tortora, G. J., Derrickson, B.


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Difference between vacuolar and symplast pathway
what is the difference between Vacuolar  Pathway and Symplast Pathway ? Is the symplast pathway does not take into account the vacuole to vacuole movement?

The vacuolar pathway involves the movement of water between vacuoles of neighbouring plant cells. The symplast pathway, on the other hand, involves the movement of water from the cytoplasm of one cell to the cytoplasm of a neighbouring plant cell without it entering a vacuole inbetween, so the symplast pathway has no vacuole to vacuole movement.


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Why is there a layer of moist lining the inner walls of alveoli?
I'm taught that the walls of the alveoli are moist, so gaseous oxygen molecules can dissolve into this water. This then allows the dissolved oxygen (liquid state) to diffuse faster from the alveoli into the bloodstream through the basement membrane.
However, why is it faster for gaseous oxygen to first dissolve in water (transitioning into liquid state) then diffuse through the basement membrane and dissolve into the blood stream than for gaseous oxygen to directly diffuse through the basement membrane and then dissolving into the blood stream?
The second mechanism would eliminate the need for the moist layer lining the alveoli wall.
Is there some physical or chemical explanations to this phenomenon?

The fluid in the alveoli contains phospholipoproteins that act as pulmonary surfactant, which keeps the alveoli open during breathing.


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What does hypolithial mean
I'm writing a thesis in biology and my supervisor asked me to find literature about beetles living under rocks - specifically she wants me to find something about hypolithial diversity. However Google doesn't even recognize the word 'hypolithial' so I'm kind of stranded without any references on where to start searching.
I know that hypo lithia comes from ancient greek and means below stones, but nobody mentioned it like that in the literature.
Has anybody heard of this term or knows a similar one which I could use for my research?

Google for sublithic or hypolithic.
You'll find lots of things like (https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-11274-4_767) with further references and links

Scholar provides some useful results..


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What is the evolutionary relationship between heme, chlorophyll and other tetrapyrroles?
As a non-biologist, I have searched the Internet and found dozens of papers discussing the similarity between the structures of heme and chlorophyll molecules, but I could not find any discussion of their evolutionary relationship.
To be more specific, I would like to know whether the use of tetrapyrrole in the blood and in photosynthesis can be traced to the earliest organisms in which tetrapyrrole had some function, and then the molecule evolved to be capable of the different functions it currently performs in animals and plants.

The general subject of your question is certainly on topic here, but a simple reference request is not, and at present it is unclear what your question is. Your title refers to evolution, yet the answer you say that you will probably accept says nothing about evolution. Is your question one of chemistry — why is the tetrapyrrole ring found in different functional molecules and how does it perform different functions? Or do you wish to know which tetrapyrrole is the most evolutionary ancient and whether others evolved from it? Please edit your question so that it asks a precise question.

@David Thank you, your second suggestion is the correct one. I tried to explain this but I certainly lack expertise to do it properly. Please edit the text accordingly if it contains any inaccuracies.

I have edited the question as you suggested, trying to condense it to its essentials to clarify it. Let me know if there is anything you object to.

@David Thank you very much! No objections, on the contrary, I think you improved the question a lot.

I've finally posted an answer of sorts. If you are a non-biologist, I assume that you have some chemistry. In any case answers on SE are not necessarily aimed at the poster, but at the question. However, if you wish clarification, do comment on the answer.

Preamble
I found this question interesting, so that, despite my general ignorance in this area, I have attempted to address the question of the evolution of tetrapyrroles rather than answer it. Additional contributions are welcome as comments. I apologize for the large graphic, which I feel is indispensable to my answer, however I have included a summary above it, so readers can decide whether they wish to read further.
Summary

There are four main types of tetrapyrrole associated with proteins
They share a common pathway from 5-aminolevulinic acid to uroporphyrinogen II
The unresolved question of which subsequent pathway evolved first is discussed in relation to their antiquity and complexity.
The possible evolutionary relevance of the two different pathways for the synthesis of  5-aminolevulinic acid — found in different organisms — is also discussed.

Tetrapyrroles in proteins — Diversity and Chemical Rationale
Although the cyclic tetrapyrrole structure looks complex, it appears to be very ancient, presumably because of the greater chemical versatility of its complexes with metal ions in proteins, compared with simpler proteins that contain metal ions. The ring provides a precise four-co-ordination which can be held in position to provide two additional co-ordination sites (at right angles to the plane of the ring) which can interact with protein side-chains or other molecules (such as oxygen). The combination of ion, substitution of the tetrapyrrole and interaction with the protein allows fine-tuning of the redox properties of the ion.
The diagram below (adapted from Zappa et al.) shows the four main types of tetrapyrrole in proteins and how their biosynthesis is related. The two mentioned in the question are actually both derivatives of protoporphyrin IX: chlorins, such as chlorophyll — with its role in photosynthesis — and haem proteins — with the examples of the cytochromes of the electron transport chain being more widespread than that of haemoglobin in eukaryotes. In addition, however, are the corrins — most notably in Vitamin B12 with a role in methyl transfer — and sirohaem — which occurs in certain sulphite and nitrite reductases.

Which tetrapyrrole is oldest in evolutionary terms?
How can we address the question of which tetrapyrrole was first to arise? This question is, in fact, which synthetic pathway — which series of enzymes — was first to arise. In my review of the literature I (like the poster) find this an area which angels are fearful of, but, being foolhardy, I suggest two criteria. The first is what we consider the relative ages of the functions the proteins subserve, and the second the relative complexity of the pathways needed to synthesize them.
The first criterion is subject to dispute. Unfortunately the easy comparison between haem as an oxygen carrier in eukaryotes and chlorophylls as ancient prokaryotic photosynthetic proteins is complicated by the more ancient role of haem in cytochromes. One might argue that cytochromes are a feature of aerobic metabolism that followed the emergence of oxygen generation by photosynthesis, but unfortunately the electron transport chain exists in anaerobic organisms, where the terminal electron acceptor may be nitrate, nitrite, ferric iron, sulphate or carbon dioxide. Given this, and the greater complexity of the pathway from protoporphyrin IX to bacteriochlorophyll a compared with that to protohaem (10 steps compared to one), one might argue that chlorins emerged after haems.
But what about the other tetrapyrroles? One approach to relative ages is to consider the biochemical processes that might have been present early after the emergences of life. One such analysis of this was made by Weiss et al. in a paper published in Nature Microbiology (2016) 1, 1–8, entitled “The physiology and habitat of the last universal common ancestor”. They drew the conclusion that the Last Universal Common Ancestor (LUCA) was an anaerobic autotroph that existed in a hydrothermal setting and obtained energy using a Wood–Ljungdahl pathway with hydrogen as the electron donor and carbon dioxide as the electron acceptor. The two types of tetrapyrroles that they postulate would have been present in the LUCA are corrin (as cobalamin for methyl group transfer) and sirohaem for sulphur metabolism (sulphite reductase) in the hydrothermal environment.  No mention of porphyrins! Given the complexity of the 16 step pathway to corrin, compared to the one-step pathway to sirohaem, one might suggest that the latter evolved first.
Synthesis of 5-aminolevulinic acid — evolutionary implications?
5-aminolevulinic acid (frequently referred to by its old name of δ-aminolevulinic acid) is the precursor of uroporphyrinogen II, the common tetrapyrrole precursor. However there exist two pathways by which this can be formed, of which, as I understand it, only one is present in any organism. One of these (at least to my thinking) could have evolutionary implications. These pathways are shown below in a figure adapted from a paper on prokaryotic haem biosynthesis by H. Panek and M.R. O’Brian (2002).

The intriguing aspect of this is that one of the pathways (the C5 pathway) involves reduction of glutamyl-tRNA, whereas the other (the Shemin pathway) is a conventional synthase reaction with substrates glycine and succinyl-CoA. Arguments supporting the RNA world hypothesis include catalytic RNA, and the presence of nucleosides in molecules such as NAD where there complexity belies the simplicity of their function. So, putting my head over the parapet again (to vary my metaphors), I would suggest that the use of glutamyl-tRNA for the synthesis of this ancient and important intermediate might be another fossil of the RNA world. (Perhaps not what the poster had in mind in posing his question.)

Note the molecules are not that similar, only one portion is similar.
The similar portion in each molecule is a cyclic tetrapyrroles. Cyclic tetrapyrroles and porphyrins in particular are a fairly common structure in biology they have several functional uses and are fairly easy to construct from existing simpler biological molecules. The fact that they are functionally good at binding metals makes them a reoccuring solution, although not all Cyclic tetrapyrroles bind metals. Many many biological molecules contain Cyclic tetrapyrroles.
Many biological molecules have similar structures to other molecules, especially ones that perform similar tasks, there are only so many shapes you can make with carbon atoms, the shape of a molecule affects its chemical properties and that shape is simple and has useful properties. Heme itself is a functional component of many proteins called hemoproteins, basically whenever they need to bind iron. Another cyclic tetrapyrroles would be cobalamin otherwise known as vitamin B12 which binds cobalt.
Its the same reason hammer handles look very similar even in very different cultures, just attaching a stick is a simple easy to discover solution, so it is the one that gets found most of the time. Functionally that is the shape that works. Or to put it another way they are only so many shapes you can make a wheel.
https://www.sciencedirect.com/science/article/pii/S0167488912001000
http://www.org-chem.org/yuuki/porphyrin/porphyrin.html
https://www.cpp.edu/~lsstarkey/courses/CHM-Lab/PorphyrinBasics.pdf
https://www.mdpi.com/journal/molecules/special_issues/porphyrin_chemistry
To address the updated question. I honestly don't know if they share an evolutionary origin. But given that they are synthesised in different organelles (mitochondria for heme and chloroplast for chlorophyll, I would guess no.

Many thanks for explaining this, and most probably I will accept your answer, but the references you provide hardly mention any evolutionary issues. In light of your answer, - could you possibly add a reference discussing earliest known occurrences of porphyrin in living organisms?

Also, could you name examples of other biological functions, aside of in blood and in photosynthesis, that porphyrin rings have?

Chemically you are incorrect. The similar portion of each molecule is a tetrapyrrole  — in one case a porphyrin, in the other a chlorin. If the question is about the relationship betweeen structure and function in tetrapyrroles, then I suggest it needs extending, but I would wait until the poster clarifies things first.

@მამუკაჯიბლაძე the earliest known occurrence would be an entirely different question.

@John I agree. Still, I believe telling about it in the answer would be relevant for the existing question, as it would provide some information about possible common precursors of hemoglobin and chlorophyll. Note that, as David points out, I should talk about tetrapyrrole rather than porphyrin in that comment of mine.

@David Yes your right, They are both cyclic tetrapyrroles, I forgot about that little extra ring on chlorophyll. I will correct this. But to be clear many paper still identify them as porphyrins

One more thing - it is true that only the tetrapyrrole portions are similar, but they are the main functional parts, performing metal binding, which is crucial both for photosynthesis and for oxygen transport in blood.

And also, I want to apologize for the unclear question. The word "evolutionary" was only mentioned in the title, not in the text. According to the suggestion by @David I have now added second paragraph trying to clarify the question.

@მამუკაჯიბლაძე I did mention that

authors: მამუკა ჯიბლაძე


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Why do some foods do not taste good when eaten together that eaten separately would taste great
The way I understand it, 'good tasting food' is evolutionary concept e.g to be able to distinguish between high nutritional value foods and ones that have no nutritional value whatsoever.
So if well-prepared fish tastes well and so does some other food (birthday cake/[put food that would not go along]) on its own why then when mixed together they might taste bad. The mix has the same nutritional value, same proteins carbs, and fats, but they just don't go along.
Why do some foods do not taste good when eaten together?

Here are a few recipes: Orange tilapia, Honey orange fish filets, Baked Fish in Parchment with Orange and Olives, White fish à l'orange, and fish with spices and orange juice. I am VTC as primarily opinion based.

Here is a list of surprising food pairings that people actually enjoy.

@Remi.b fish was just a (bad I suppose) example...

Can you find good examples?

@Remi.b I don't intend to... the question is not about some specific case. Also, your argument is defeated by yourself (by providing the link) as if some foods 'go together' that means that others don't...

My goal with this link was to show that even combinations that seem unintuitive might actually go well together. This link does not suggest that some food items fundamentally don't go together. I think that the fact that it is hard to find a good example shows that it is mainly a matter of culture preference and preparation. There is maybe nothing more fundamental than that. To me for example, sugar and meat were really the things that would be impossible to pair. My mind was changed when I started to travel a bit.

Your link is the other side of same coin... if something goes 'well' that can only mean that something does not...

If you could just come up with a few examples, that would clear up the argument. In all case, I'm done arguing on that matter. Good luck with your post.

Conditioning almost certainly plays a large role. Think of young children. Some are willing to put almost anything in their mouths (having been unconditioned), while others refuse to eat all but a select few foods until they're older (i.e after they've become conditioned either culturally or by what's available).


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do platelets cytoplasm contains DNA?
I'm a 12th-grade student and I have an entrance exam this year.
I have a question in biology. I would appreciate you if you help me <3
as we thoroughly know platelets are multiple pieces of a big cell which is called megacaryocyte so they do not have any nucleus. so I wanna know if they cytoplasm contains any type of DNA or not? I'm sure that without the nucleus there can't be any linear DNA but I doubt on the cycle DNA.
thank you


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Do four-leaf clovers have some disadvantage in reproduction?
As far as I understand, four-leaf clovers are caused by genetics, so when reproducing, they should produce four-leaved children. I haven't found any disadvantages of four-lead clovers (e.g., infertility or worse survival capabilities), so I wonder why four-leaf clovers are so rare. Do they have any competitive disadvantage that makes them less likely to reproduce?

Neutral selection could mean that the probability of fixation is simply very, very low... A complement to the question: based on a (non-quantitative) examination of photographs of four-leaf clovers among wild type clovers, it seems to me that the area of individual leaves is the same, meaning that four-leaf clovers could potentially be better at harvesting light (?) so I'd be curious to have an answer too

I don't think that Neutral selection is a concept! Do you mean absence of selection (hence a probability of fixation of $\frac{1}{2N}$, where $N$ is the population size).

@v6ak As far as I understand, four-leaf clovers are caused by genetics After a quick look, it seems that the question of whether there is a genetic based to this phenotypic variation is not resolved. It might just be a rare phenotype caused by some developmental instability or specific micro-environmental conditions. Do you have any reason to think the opposite? Note that some clover can have five leaves.

An allele does not need to be at a selective disadvantage in order to be rare. Using that logic, one could say that anything that does not exist would be at a selective disadvantage (as something cannot be more rare than if it does not exist).

I haven't said that there must be some competitive disadvantage, just there might be some. And I am curious if there is some.


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Why might a cell have no respiratory reserve capacity?
I am trying to understand why a cell might have minimal respiratory reserve capacity in the presence of unlimited substrate supply. This essentially means that the oxygen consumption rate (OCR) of the cell does not increase from its basal rate when oxidative phosphorylation is uncoupled — i.e. the reactions of the electron transport chain are uncoupled from ATP synthesis. What factors might conspire to cause this? I am thinking specifically of the photoreceptors1.
I am interested in all logical possibilities here e.g.
(1) mitochondrial ATP production is barely meeting demands at basal level.
(2) oxidative phosphorylation may already be physiologically uncoupled.

Is this a question about trouble shooting an experiment, or a theoretical question?

Welcome to SE Biology. I assume that you are trying to understand the results in the paper you cite. I do not wish to be discouraging, but few people will read that paper (questions here should be self-contained), and the key term it uses — respiratory reserve capacity — is one that I, as a biochemist, am unfamiliar with, and find difficult to understand from a brief perusal of the paper. If you understand it yourself it would be helpful if you could edit your question to expain it.

Thanks for the responses. It's a theoretical question, the answer to which I was hoping might shed some light on the Warburg effect in the retina. I have some experience with metabolic assays but was hoping someone more experienced might be able to enlighten me.


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Pentaploid genotype frequencies
I know that if I am dealing with a diploid case, and I have 3 alleles, then I can have 6 possible genotypes. I am doing this by adding up all the numbers from 1 to 3. $$1+2+3 = 6$$
But if I want to generalize this, say for a pentaploid, how do I effectively compute the number of distinct possible genotypes? (Assuming perfect HW equilibrium)
I want to say this is just a simple problem of combination with replacement, but I'm not sure if the biology allows me to make this statement.

I want to consider the case where there are 3 alleles and it's a pentaploid species.

Ploidy number vs number of alleles
You seem to be confounding number of alleles with ploidy numbers. You rightly figured the number of possible genotypes for a diploid individuals when there are 3 possible allelic states.  When you ask for a pentaploid, are you many alleles are you wiling to consider?
Pentaploids are very rare
If I am not mistaken, species with an odd ploidy number are very rare. Tetraploids and hexaploids, while still rare are much more common than pentaploids.
General case
It is indeed a simple math problem. Let's answer to the question in the most general case. If the ploidy number is $P$ and there are $S$ possible alleles, then the number of possible genotypes is
$${P+S-1 \choose S-1} = {P+S-1 \choose P}$$
, where ${\choose }$ refers to the binomial coefficient. For a pentaploid organism, with 3 possible alleles, there are therefore 21 possibilities.
More information
You can have a look at this webpage that offers much more info about the combinatorics of genotypes.


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Finding specific genotype occurrences given allele frequency
So let's say I have a tetraploid species and I have 4 possible alleles for a particular locus. I have found that I can have 35 total possible genotypes and I know the allele frequencies for each of the 4 alleles, that I will randomly set as $$F_a = 0.2, F_b = 0.3, F_c = 0.4, F_d=0.1$$ for the sake of the example.
However, I am having a hard time wrapping my mind around how to calculate the number of occurrences of a particular genotype, $abc$, in a population of 1000 people.
I understand the allele frequencies, for instance, in the population of 1000 people, given all 1000 observed genotypes, 40% of them had allele $c$. But these are individual values and I have no information on how likely they are to be linked. (I am supposed to assume HW principle holds, but not sure how this helps).
How do I calculate the number of occurrences of the genotype $abc$ in the population?

Under Hardy-Weinberg conditions, the frequency of the genotype abcd (in this particular order) is simply $F_a \cdot F_b \cdot F_c \cdot F_d = 0.24\%$.
If we don't consider the order, then we must ultiply the previous probability by 24. There are indeed 24 (=4*3*2*1) ways you can get this particular combination. The probability of abcd in any particular order is therefore $24 \cdot F_a \cdot F_b \cdot F_c \cdot F_d = 5.76\%$.
You might want to have a look at the post Solving Hardy Weinberg problems

But that's only for that particular permutation of that genotype, correct? Hence, we'd have to take into account how many different ways that genotype can occur

Or is that, since the allele frequency already account for those things, we can ignore the other permutations?

@Jonathan Good point, I should have made that clear. If you are interest in the fraction of abcd genotype (in any particular order), then you have to multiply by the number of ways you can get this particular genotype.

But that doesn't fully answer the question either, because then we would double counting if you just did $4!$. Hence, it would have to be the number of ways to get that particular genotype plus some constraint. Maybe for abcd it's straight forward. But if it was $a^2b^2$, then it wouldn't be.

Could you please update your answer to include this? It would be very useful key point for everyone else with the same question.


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Selection coefficient of gorillas
I've been reading about selective sweeps. And I found a case study that talks about drosophila and how their selection coefficient is between 0.0001 and 0.005.
I want to know what it'll be like for gorillas? That is what would be the selection coefficient range for them and why? Also, I was told that N*s of gorillas is between 100 and 10000 where N is the current population size and s is the selection coefficient.
Help would be really appreciated. I do not have a biological background therefore, it's taking some time to wrap my head around these things.

I found a case study Whether it seems to matter or not, please always link to your source.

A selection coefficient is not so much specific about a species as much as it is specific to a given mutation. What mutation are you talking about in gorillas?

Do you mean mutation rate? Per site mutation rate is 1.5e-08

No, I did not talk about mutation rate. A specific mutation has a selection coefficient. A species does not. It makes no sense to ask "What is the selection coefficient in gorillas?", it only makes sense to ask "What is the selection coefficient of the p.P252R mutation in gorillas?"

It's not a specific mutation. I want to simulate sweeps in the genome. I have all the parameters I need but I am struggling with the selection coefficient. I've edited the question and have added the parameters so you can see.

There are no correct answer then. If you simulate a selection coefficient of 0.3, then you will likely simulate something that is very rare. If you simulation a selection coefficient of 0.0001, then you won't even really have a selective sweep. Just pick a number in between. But there are no right or wrong.

ok. So what is usually the range for a strong selection? It'll be close to 1?

I would personally consider anything above 0.01 as being strong selection. You will likely never find a new beneficial mutation with a selection much higher than 0.1. On a side note, you might be interested in the Distribution of Fitness Effects of new mutations (DFE; although in general such distributions are only estimated for deleterious mutations as they are much more common).

On another side note, you might be interested in the post Sequence evolution simulation tool


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Why is the V/Q Ratio 0.8 not 1?
According to: https://en.wikipedia.org/wiki/Ventilation/perfusion_ratio the ideal V/Q Ratio would be 1.0 because 1 L of blood can hold about 200 mL of oxygen and 1L of humidified air has about 200 mL of oxygen.
However, the actual ventilation/perfusion ratio for the entire lung is described as 0.8. I understand there are regional variations due to gravity, but on the whole, shouldn't the average V/Q ratio be 1?
One thought I had was that because it takes time for O2 to diffuse across the membranes and bind to Hemoglobin, that could explain this loss in efficiency.


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Who created the codon wheel chart (not as a table)?
I'm trying to find out who created or first used the codon wheel chart as far as we can know.
I don't mean the tabular format.

Perhaps better asked on the History of Science & Math StackExchange.

I am Rosemarie Swanson, still alive, and yes, the Gray code representation  of the codon wheel was my idea.  I was trying to develop a linear similarity scale for amino acids.  On Thanksgiving of 1977, I suddenly realized that instead of a linear scale, a circle gave a better representation of the similarity of amino acids.  Later, I thought to look at codons.  When I realized that a 2-bit gray code representation of codons approximately matched my amino acid similarity circle, I was excited.  I worked very hard on writing up the idea, but had a hard time getting it published, until the editor of Bulletin of Mathematical Biology said he would like for me to submit the manuscript in 1983.

Amazing. What made you look into circular representation?

It is very difficult to answer this one for certain but I think the codon wheel representation is sometimes attributed to Rosemarie Swanson who represented the amino acid code using Gray code (or reflected binary code).
Swanson's work actually went quite a bit deeper than the simplified codon wheels you find in ordinary textbooks (ordering by size of the amino acid and position within the chain as well). You can have a look for yourself here in her 1984 article A unifying concept for the amino acid code in Bulletin of Mathematical Biology.
DISCLAIMER: I do not claim that I know the answer to this question for certain nor can I. However, I cannot find official publications earlier than Swanson's 1984 paper showing a circular representation of the amino acid code.

Even if she was not the originator, your answer takes this back far enough to deserve upvoting.

Nice but as you say it still does not mean it is her idea. I wonder if she is still alive and can be asked

 This answer *pre-dates* the others' focus on Rosemarie Swanson

The German Wikipedia article for the "code-sun" credits this circular diagram to Carsten Bresch and Rudolf Hausmann1.
 1. Bresch, C. and R. Hausmann. 1972. Klassische Und Molekulare Genetik. Springer-Verlag, Berlin / Heidelberg / New York 1972, ISBN 3-540-05802-8.
Below is a screenshot of page 243 from a supposed 1970 edition2 of the text that introduces the "code sun":

Interestingly, this source is 14 years earlier than Swanson's paper3 (and even 7 years earlier than she claims to have come up with her version (which, for those who have not clicked on the link to her 1984 paper in Johnny's answer, looks quite different)).
What remains unclear to me (due to the lack of availability of additional pages of an online version of this text and my own lack of access to other versions):

if this idea in Bresch and Hausmann is original or from an alternate earlier source.
whether this wheel (or "sun") was depicted in earlier versions of this text (e.g., first version was in 1964)
how this version relates to Swanson's ideas years later...

 1. Bresch, C. and R. Hausmann. 1972. Klassische Und Molekulare Genetik. Springer-Verlag, Berlin / Heidelberg / New York 1972, ISBN 3-540-05802-8.
 2. Bresch, C. and R. Hausmann. 1970. Klassische Und Molekulare Genetik. Springer-Verlag, Berlin / Heidelberg GmbH 1970, ISBN 978-3-662-23449-5.
 3. Swanson, R., 1984. A unifying concept for the amino acid code. Bulletin of Mathematical Biology, 46(2), pp.187-203.

Interesting. I also asked ChatGPT and it claims that the codon wheel was developed by a team at the University of Wisconsin-Madison in the 1970s. I couldn't find a source though.

@JonathanSisam do yourself a favor: don't ask ChatGPT questions. It doesn't actually know the answers

@rosemarie-swanson, can you comment on the similarities/differences/history comparing your representation and that of Bresch  & Hausmann? Thanks :)


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If mammals evolved to be nocturnal, then how did we get so staunchly diurnal in such short time?
Much of human health revolves around sleeping well through the night.  We know about circadian and body temperature rhythms which make us sleepy at night, peak melatonin production in the middle of the night, deep sleep phases, sleep disruption from light at night, and high cancer rates among people who work the night shift.
Clearly, we are built to sleep at night.  You would suppose, then, that we must have evolved to be diurnal long ago and descend from a long line of diurnal animals.
Yet, the evolutionary legacy of mammals is predominantly nocturnal.  Mammals started out as nocturnal (to avoid the reptiles) and most mammals today are still nocturnal.
How did we get so staunchly diurnal so quickly?

You think 65 million years is a short period of time?  Part of the answer is that the extinction of the dinosaurs left a lot of daytime ecological niches for previously-nocturnal mammals to fill.

jindeed, a short enough time to turn an pig into a blue whale isn't a short time.

The Nocturnal bottleneck for mammals as it's called was assumed 'til recently to have only ended at the Cretaceous–Paleogene extinction event 66 million years ago.

At the basis of the nocturnal bottleneck hypothesis lies the idea that
Mesozoic ectothermic reptiles (including dinosaurs) would be
restricted to daytime activity at times when the sun can help to heat
up their body to operating temperatures.......

The arguments against:

include:

(i) presence of insulating proto-feathers,

(ii) fossils of breeding dinosaurs in cold regions

(iii) raised body posture

(iv) fibrolamellar bone structures

(v) presence of nasal turbulate bone structures

(vi) stable growth rate (isotope deposits in bones and teeth)

(vii) possible ‘mass homeothermia’ or ‘inert homeothermia’ in large dinosaurs

(viii) the occurrence of small dinosaurs in cold regions

(ix) the existence of potential external thermoregulatory structures in some dinosaur species (e.g. dorsal boney plates in Stegosauria).

Recent molecular analyses have added to the doubt of the original theory:

saurischians are now generally believed to have had partial
endothermia, allowing them to incubate their eggs and inhabit colder
regions......
Independently, parallel evolution in Synapsida led to partial
endothermia in therapsid reptiles (250 Ma, Late Permian) and full
endothermia in mammals

Nespolo RF, Bacigalupe LD, Figueroa CC, Koteja P, Opazo JC. 2011. Using new tools to solve an old problem: the evolution of endothermy in vertebrates. Trends Ecol. Evol. 26, 414–423
The implication being that the pure nocturnal adaptation in mammals would not be a completley effective strategy for predator evasion.

In a large comparative study [Roll], divided 700 species into classes of
dominant temporal activity niche: nocturnal, diurnal or both (mostly
crepuscular). They used an existing phylogenetic construction to
reconstruct the evolution of diurnality in rodents, which are thought
to have diversified after the K/T boundary. The reconstruction of
temporal niche usage within rodents led to the conclusion that rodents
shared a nocturnal ancestor that existed before the K/T boundary.
Subsequently, diurnality evolved through secondary evolution at least
seven times independently in Rodentia.
Using the molecular phylogenetic construction of [Huchon et al],
we constructed the temporal niche phylogeny within the full therian
subclass using the nocturnal, diurnal and
crepuscular/arrhythmic classification of [Roll et al.]. The most
parsimonious interpretation leads to a minimum of 16 changes of
dominant temporal niche.

Bolding mine.

Most subdivisions of Theria are indeed nocturnal, but many changes and reversions occurred, and different interpretations may be
possible, especially when higher-quality data on activity patterns in
more species become available.

Conclusion.
It apears that mamals may have been chased by the saurischians throughout the day, night and twilight hours and that many adaptations and reversions may have occured over a period (possibly) much longer than the 66 million years previously thought. Research is ongoing.
Bolded references:
Roll U, Dayan T, Kronfeld-Schor N. 2006. On the role of phylogeny in determining activity patterns of rodents. Evol. Ecol. 20, 479–490
Huchon D, Madsen O, Sibbald MJ, Ament K, Stanhope MJ, Catzeflis F, de Jong WW, Douzery EJ. 2002. Rodent phylogeny and a timescale for the evolution of Glires: evidence from an extensive taxon sampling using three nuclear genes. Mol. Biol. Evol. 19, 1053–1065

Another point against strictly diurnal dinosaurs is that birds evolved from their dinosaur ancestors long before the K-T extinction event.  While most modern birds are diurnal, there are exceptions, notably the owls.  Although owl fossils only date back 30-40 million years, there doesn't seem to be any obvious reason why earlier birds, or their dinosaur ancestors, couldn't have evolved a similar lifestyle.

@jamesqf 250Ma ago, in fact.There was a bit about sexual selection and owls in the study (I linked to under the word "argument") that you might find interesting: "highly enhanced scotopic vision (e.g. owls), or other senses (e.g. echolocation in bats), may negate such disadvantages. In this respect, it may be hypothesized that the complex sexual selection mechanisms that have arisen through diverse and vivid feather coloration may be the main drive for a diurnal lifestyle where an acute colour visual sensory system would be an advantage."

Interesting, yet I wonder if predator evasion is a really a satisfying explanation.  After all, many small mammals today are preyed on by birds (among other creatures): hawks in the daytime, owls at night, yet don't seem to be in danger of extinction.  (At least from non-human causes.)  And many small mammals are burrowers, which means they'd encounter low/no light conditions in daytime.


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Does the brain have a clock and can it be sped up?
Before i start, I'm an engineer and have very limited knowledge on biology and neuroscience. My question is, does the brain have a clock like a computer where it has a set processing speed?
Clocks in CPUs can be overclocked to increase processing speed and I am wondering if the brain has something similar. The average human reaction time is around 0.25ms, Is it possible to react faster to stimuli and not only react but perceive surroundings faster than others. What I mean is while everyone perceives 1 second to be 1 second long, Is it possible to focus and stretch 1 second out mentally to 3-5 seconds and move/think/react faster as a result?
How could this theoretically be achieved too? BCI headset, Chip implant in the brain, serum or chemically?

It's not true that everyone perceives one second as one second.  It's subjective, of course, and I have no idea how you might actually measure it, but if you've ever been in a seriously dangerous situation, you might have experienced time slowing down.

You have to keep in mind that every generation finds analogies between biology and the 'hot' mechanical technology of the time. Back in the 19th century people would make analogies between living organisms and steam engines. At a high level, this can be useful: steam engines and living organisms both employ feedback systems. Once you get down in the details though the analogies break down: living organisms don't boil water to make steam. In the same way, living organisms certainly have periodic cycles in their biological pathways, but nothing like a cpu clock that synchronizes all activities.

Try to read something about suprachasmatic nucleus and circadien rhythm. Might help.

While the brain is often compared to a computer (sometimes even rightfully), one key aspect people often overlook is that the brain is inherently analog, whereas computers are inherently digital:
All a computer really does in any single operation is to combine 0's and 1's really really fast - and the faster it's able to do that, the faster it will generally be.
A brain however, fundamentally works by combining a multitude of signal inputs with varying strength's and each single operation (encoded by a single neuron) will give output depending on the weighted sum of all inputs.
Such a 'single operation' in itself is reasonably fast, whats make a brain 'slow' is the propagation of the signal to next neuron/operation: Brains are orders of magnitudes bigger than computer chips and instead of metal/wires they use concentration gradients to propagate the electrical signals. Of course it's possible to increase the speed on individual connections between neurons by insulating them, which nature already does.
However, you can't just 'overclock' the whole brain, because there's simply not enough space to add 'full insulation' to every single connection between two neurons (of which there a lot: ~100 billion neurons, with a couple thousand connections each) and because electrical signal propagation by concentration gradients will always be slower than by wires.
I guess if would replace all neuronal connections with metal wires and some concentration gradient to power/voltage/frequency converter using nanobots, you could potentially speed up the brain - or just built cyborgs instead.
Also, not really what you asked  -  but there IS a clock in the (mammalian) brain and changing it speed, will seriously mess with your day/night or sleep rhythm.

The answer to your question could be yes or no, determining how you define "clock speed".
First, the title of the question is partially misleading since when you talk about a biological "clock", most people will assume you're referring to sleep/wake, night/day, or melatonin-related (daily cycle) activity. (Turns out your question is about speeding up neural processing power).
Brains (neural networks) are a highly parallel asynchronous architecture (as far as the research suggests). There's no centralized "clock" - every input-to-output chain reaction happens at the speed the hardware supports. It's well known that this architecture imposes some fundamental limits on humans, the easiest example being reaction time (you can confirm this with a few quick searches). In this regard, the answer to your question would be "no".
Think of a neuron as being a machine with n inputs and 1 branchable output (see https://www.reddit.com/r/askscience/comments/2yl5jh/how_does_one_neuron_with_multiple_synapses_decide/ on how axons implement a single output which can be branched). The neuron's architecture is event-driven on the inputs. This produces 2 main limits: the calculation step (how quickly the neuron handles the event and sends an output signal on its axon), and propagation speed (how quickly the signal travels).
This leaves 2 clear options: optimize the neuron cell for a faster calculation step, or optimize the propagation speed (think of this as upgrading all your 10/100 Mbps cables to 1/10 Gbps).