text:
Why would it be impossible for gram-positive bacteria to store sulfur as gram-negative sulfur-oxidizing chemolithotrophs can?
I have a question that I am not sure what is the correct answer on <<Brock's Biology of Microorganisms>>
When the book introduces "Cell Inclusions", there was a mini-quiz that contained a question asking "Why would it be impossible for gram-positive bacteria to store sulfur as gram-negative sulfur-oxidizing chemolithotrophs can?"
I understand that gram-positive bacteria have a thick proteoglycan (consisted of a net of glucosamine and amino acids bonds together covalently) cell wall whereas gram-negative bacteria only has some lipid membrane.
I also understand that sulfur cell inclusions are usually elemental sulfur wrapped up in PHA (poly-beta-hydroxyalkanoate) polymer.
I just cannot put the two facts together to answer the quiz question?
Thank you in advance for your generous hint!

I also understand that sulfur cell inclusions are usually elemental sulfur wrapped up in PHA (poly-beta-hydroxy alkanoates) polymer.

This is not correct! It is true that most PHA producers generally belong to the Gram-negative group of bacteria. However, PHA is not used to store sulfur. PHA is there to store excess carbon and energy. Though, this energy can come from sulfur metabolism!
From Brock Biology of Microorganisms 14h edition I cite:
"The oxidation of sulfide is linked to the need for electrons to drive either reaction of energy metabolism (chemolithotrophy) or CO2 fixation (autotrophy). In either case, elemental sulfur from the oxidation of sulfide may accumulate in the cell in microscopically visible granules [...] Interestingly, although sulfur globules appear to reside in the cytoplasm, they are actually
present in the periplasm [...]"

"Why would it be impossible for Gram-positive bacteria to store sulfur
as gram-negative sulfur-oxidizing chemolithotrophs can?"

The as here is very important. Because some Gram-positive bacteria are perfectly capable of storing sulfur but not in the same way as Gram-negative bacteria. As we know, in Gram-positive bacteria the periplasmic space is found between the inner membrane and the peptidoglycan layer which – I assume so – is not suited to "hold" or produce these granules in a similar fashion.
To give a bit more context:
Sulfur oxidation and sulfur reduction are two different processes that involve the transformation of sulfur compounds. Certain Gram-negative as well as Gram-positive bacteria (e.g. Desulfotomaculum) are able to do so. Some strains are even able to do both reduction and oxidation! In either case, for both types of bacteria, there are strains with sulfur metabolism involving the storage and usage of sulfur for energy production, just in different manners.

Sir, is it because only gram-negative bacteria have periplasm, so only gram-negative can accommodate end products of sulfur oxidation?


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Why is hydrogen to oxygen ratio used to compare energy storage efficiency?
I came across an article that says that lipids are more efficient energy storage molecules compared to starch because lipids have higher “hydrogen to oxygen ratio”.
I do not understand how “hydrogen to oxygen ratio” equates to more efficient energy storage.
I am guessing that since energy production have to do with reducing NAD+, so “hydrogen to oxygen ratio” is a measure of the ability to reduce NAD+. And since NADH is then later used in oxidative phosphorylation in mitochondria to produce energy currency ATP, “hydrogen to oxygen ratio” is a measure of the potential amount of ATP the molecule is able to produce. And thus it is a measure of energy storage efficiency.
Is this correct?

Answer
In my opinion:

The original poster’s overall interpretation of the statement in the article (as
reported) is most likely correct.

Problems with original statement
Although the statement may be clear in context, I would rephrase it because of two specific objections I have to it. These are:

“Energy storage efficiency” in isolation is ambiguous. It is not clear whether it refers to storage per unit mass or per unit volume, both of which may be considerations for living organisms.
“Hydrogen to oxygen ratio” is an imperfect heuristic for the reduction state of the carbon backbone.

I would also be specific in naming the lipids involved in ‘energy storage‘ — there are other lipids (e.g. steroids) that are not used as energy stores.
So my restatement (adapted from Berg et al. ‘Biochemistry’) would be:

Triacylglycerols are more concentrated stores of metabolic energy than
polysaccharides such as starch or glycogen because they are more
highly reduced. The energy yield per gram from the complete oxidation
of triacylglycerol is over twice that from polysaccharides (38 kJ/g
cf. 17 kJ/g).

Comments on restatement

I have avoided the use of the word ‘efficiency’ for reasons of lack of precision,
already mentioned. In general I deplore its use in biology, partly
because it is seldom defined, and partly because it generally
involves the implicit assumption that the most ‘efficient’ is the
‘best’. If this were so in the current case, potatoes would be bags of oil.
There are other factors that contribute to the concentrated nature
of triacylglycerols for storage of metabolic energy. These include
dehydration and lack of branching (important for reducing the
volume).
It is important to talk in chemical terms — i.e. about oxidation and
reduction. I reproduce below part of a diagram I used to use for teaching
which summarizes the relationships between metabolic intermediates
of different oxidation states.
The above diagram shows the limitations of the heuristic of
“hydrogen to oxygen ratio”. The pair on the left (which might be found in
saturated v. unsaturated fatty acids) both have the same H:O ratio
(infinity) but are in different states of reduction.
It may be better (at least in abstract) to consider carbon atoms as the basis on which to
compare the oxidation states of different metabolites, rather than
weight, which is influenced by the oxidation state itself.

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The nitrogen cycle
As I understand it, bacteria absorb nitrogen from the air, and deposit nitrates in the soil. These are absorbed by plants which use them to build complex molecules such as proteins. This enters the food chain. Eventually an organism dies and decays, and nitrogen is released into the atmosphere again.  This is called the nitrogen cycle.
Am I correct so far?
My question: what percentage of atmospheric nitrogen is involved in the cycle per year?
Background to the question: On another forum I was involved in discussing the old statement that every breath we take contains a molecule of Caesar's dying breath. We raised the point about molecules being ripped apart, and created by biological processes. One person said that the nitrogen cycle is so slow that virtually all the nitrogen molecules from Caesar's time still exist unchanged. That statement is one I found surprising.  Is it correct?

Welcome to SE Biology. This is a question and answer site, not a personal  proof-reading site as you will see if you finish reading the [Tour]. Please do so. We work on the basis of one question per post. What is your question? Initially it appears to be about the percentage of atmospheric nitrogen fixed each year — a consideration that is hardly at the forefront of modern biology, but must be of interest to somebody. However then it seems to morph into astrophysics, in relation to the conservation of nitrogen on earth, together with the speed of the cycle — whatever that may mean.

I thought my question is perfectly clear: "what percentage of atmospheric nitrogen is involved in the cycle per year?"  The rest is merely stating the reason why I'm asking the question.   I don't see what proofreading has to do with it, nor astrophysics.

Proof-reading: "Am I correct so far". Astrophysics: "all the nitrogen molecules from Caesar's time still exist unchanged" suggested loss from the earth's atmosphere.

Not proofreading. It's just establishing if I've understood the basic premise correctly.  You can ignore that line if you wish. As for astrophysics, it's not about losing from Earth's atmosphere,  it's about chemical reactions destroying molecules, and creating different molecules.  I thought I made that clear.

OK, OK. You could have found the answer yourself — simple queries, first page of answers — but I've done it for you.

Mass of Nitrogen in Atmosphere
ca. 4 x 1018kg (Wikipedia page on “Atmosphere of Earth”)
Nitrogen fixed by natural, nonagricultural organisms per annum
ca. 2 x 1011kg (“Global Nitrogen: Cycling out of Control”)
Atmospheric nitrogen fixed per annum
ca. 0.5 x 10–5 %
Conclusion
If we are still breathing molecules of Caesar’s dying breath, they will be quite diluted.

I wasn't expecting us to "run out" of nitrogen, since any nitrogen fixed by bacteria will eventually be released back. Aside from that, thanks for the answer.

@Pete — Seemed a bit bald without a comment. Perhaps I’ll try a different tack. The actual turnover time is a more difficult question. It may have been 50 years or for the average Roman emperor to return to the earth, but much less for the rats in the streets.

+1 Nice article (second link). I did not know that, like, no clue whatsoever. So Thanks for that.

Suggestion: The best practice is to write numbers in scientific notation in terms of the base unit kg, not the unprefixed unit g. This helps when doing calculations, e.g. kg × m/s^2 = N (newton). So, 4×10^21 g = 4×10^18 kg.

@Nayuki — You may well be right, but I am unaware of that practice. Can you provide a link documenting it? If you are correct I will change it.

The dying breath part needs fleshing.  Tidal volume = 500 mL /(15 mol/L at 37C) = 1/30 mol air = 38 mmol N2 = 2.9E+22 molecules with negligible fixation in 2000 years (0.01%).  Atmosphere has (4E21g/28 g/mol)*6E23/mol = 8.6E43.  New breath gets (2.9E+22/8.6E+43)*2.9E+22 = 10 molecules.  (Unless the old tyrant was poked so full of holes that the last breath was more like a faint gurgle, that is...  more pleasant to run this math for the Sermon on the Mount, no?)

@David I looked through the SI Brochure and it has surprisingly little to say about style. As far as I can tell, all examples in the document use kg, such as on page 150, "m_n = 1.674 927 471 (21) × 10^−27 kg".

@David Using g instead of kg is factually and numerically correct, but it makes advanced usages harder. Look at the Wikipedia page for Earth or proton, and you'll see their masses stated in scientific notation kilograms. Secondly, other units are "coherently derived" from base units, meaning that you multiply base units together with a trivial scale factor of 1. For example, 1 newton = 1 kilogram × metre / second^2 = 1000 g × m/s^2. When doing calculations, it's tremendously helpful when all quantities are stated in base units - and that means using the kilogram.

@David It's true that the other 6 base units have no prefix (metre, second, etc.) and behave nicely. But for historical reasons, the community reneged on the gram and then decided to base everything else on the kilogram - the newton, pascal, joule, volt, etc. So now we're stuck with a coherent system having a base unit that has a prefix, but does not take double prefixes (e.g. μkg → mg) and thus also behaves as though gram is the base unit for the purpose of prefixing.

@Nayuki — OK. Thanks. We biochemists tend to think small, so that the question seldom arises. Will fix when I have a mo.

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Why does adding calcium chloride aid in bacteriophage infection?
We are attempting to isolate bacteriophages from environmental soil samples and most protocols recommend adding CaCl2 to the media to aid bacteriophage infection, even though they all recommend different concentrations.
This paper claims:

Addition of divalent ions (CaCl2 and MgCl2) may also facilitate plaque formation through aiding phage adsorption to the bacterial receptor

But how does CaCl2 aid phage adsorption exactly? And by extension, is there an ideal concentration of CaCl2 that maximizes the adsorption when growing bacteria in liquid media?

Not knowing anything about phage infection itself in this context, I would guess that the ideal concentration varies depending on phage, host, and environment. There may not be a universal ("You should always use 10 mM") ideal concentration. If the papers you're reading are all dealing with the same context you are, and the recommended concentrations aren't too far away from each other, i.e., over an order of magnitude or so, then averaging them might not be a bad idea. Or, pick one paper and use its conditions as your guide so you can replicate their results.

@MattDMo we are  going to test with two concentrations since the concentration varied so much in the various papers. 1 mM/liter and 50 mM/liter. We did read one paper that seems to use 3 M/liter which seems high. None of the papers detail what mechanism makes CaCl work however.

@JohanWikström doing a range of concentrations would be a good idea - you'll likely select different populations of phage. 3M may have been a typo as I don't think there are any bacteria beyond extreme halophiles that will tolerate that sort of salt concentration. I would guess cofactor - divalent cations are commonly cofactors for proteins.

The relationship between calcium ion concentration and efficiency of phage infection has been observed since Delbrück's work classifying phage mutants.1 A short letter in Nature authored by H. Williams Smith in 1948 is the first source I can find recommending CaCl2 supplementation of media for bacteriophage propagation.2

Stassano and de Beaufort, Asheshov, Bordet, Burnet, and others have reported on the inhibitory effect of sodium citrate when added to media used for the demonstration of phage action. This suggested that a deficiency of calcium in the medium might be responsible for the inhibition of phage action referred to above. On the suggestion of Dr. G. P. Gladstone of the Lister Institute, calcium chloride in concentrations of $M$/100 were added to two of the batches of inhibitory media; the third was unfortunately discarded. The effect was striking. The media were now found to be completely satisfactory for the demonstration of bacteriophage activity.
As a result of this experience, it is considered advisable to add calcium chloride to solid culture media that are to be used for the typing of staphylococci by the bacteriophage method.

To answer your first question ...

But how does CaCl2 aid phage adsorption exactly?

... structural and biochemical studies have shown that calcium ions are important cofactors for many adhesion-related phage proteins. Some examples:

p2, a phage infecting Lactococcus lactis, requires Ca2+ to induce the "open" conformation of the receptor binding component of its baseplate.3
Bacillus phage SPP1 requires Ca2+ to stabilize the infective conformation of its tail tip.4
Escherichia phage Mu needs Ca2+ for efficient binding of its central spike to the host membrane.5

Beyond adsorption, Ca2+ has a role as a counterion during phage DNA injection 6-8 and as a stabilizing factor during capsid assembly.9,10

To address your second question ...

is there an ideal concentration of CaCl2 that maximizes the adsorption when growing bacteria in liquid media?

... that will depend on the phage-bacteria system and other details of your culture environment.

References

Delbrück M. Biochemical Mutants of Bacterial Viruses. J Bacteriol. 1948 Jul; 56(1):1-16.
Smith HW. Calcium-deficient media; their effect on phage action. Nature. 1948 Mar 13; 161(4089):397.
Sciara G, Bebeacua C, Bron P, Tremblay D, Ortiz-Lombardia M, Lichière J, van Heel M, Campanacci V, Moineau S, Cambillau C. Structure of lactococcal phage p2 baseplate and its mechanism of activation. Proc Natl Acad Sci USA. 2010 Apr 13;107(15):6852-7.
Goulet A, Lai-Kee-Him J, Veesler D, Auzat I, Robin G, Shepherd DA, Ashcroft AE, Richard E, Lichière J, Tavares P, Cambillau C, Bron P. The opening of the SPP1 bacteriophage tail, a prevalent mechanism in Gram-positive-infecting siphophages. J Biol Chem. 2011 Jul 15;286(28):25397-405.
Harada K, Yamashita E, Nakagawa A, Miyafusa T, Tsumoto K, Ueno T, Toyama Y, Takeda S. Crystal structure of the C-terminal domain of Mu phage central spike and functions of bound calcium ion. Biochim Biophys Acta. 2013 Jan;1834(1):284-91.
Fernandes S, Labarde A, Baptista C, Jakutytè L, Tavares P, São-José C. A non-invasive method for studying viral DNA delivery to bacteria reveals key requirements for phage SPP1 DNA entry in Bacillus subtilis cells. Virology. 2016 Aug;495:79-91.
Alatossava T, Jütte H, Seiler H. Transmembrane cation movements during infection of Lactobacillus lactis by bacteriophage LL-H. J Gen Virol. 1987 Jun;68 (Pt 6):1525-32.
Cvirkaite-Krupovic V, Krupovic M, Daugelavicius R, Bamford DH. Calcium ion-dependent entry of the membrane-containing bacteriophage PM2 into its Pseudoalteromonas host. Virology. 2010 Sep 15;405(1):120-8.
McKenna R, Bowman BR, Ilag LL, Rossmann MG, Fane BA. Atomic structure of the degraded procapsid particle of the bacteriophage G4: induced structural changes in the presence of calcium ions and functional implications. J Mol Biol. 1996 Mar 8;256(4):736-50.
Plevka P, Kazaks A, Voronkova T, Kotelovica S, Dishlers A, Liljas L, Tars K. The structure of bacteriophage phiCb5 reveals a role of the RNA genome and metal ions in particle stability and assembly. J Mol Biol. 2009 Aug 21;391(3):635-47.


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how do phagocytes receptors work now and in the past?
As we know, phagocytes have receptors on their cell that are used to detect pathogens which they bind to and engulf them. That seems easy.
Though, I'm trying to wrap my head around the fact how the receptors on phagocytes can detect pathogens ? I get it that they bind to molecules found on the pathogen and if binded successfuly, engulfing begins.
Question: the phagocytes' receptors that are shown in today's human body, were the same receptors present even 2000years ago ? If the answer is yes, how human body was created 2000years ago with those same receptors(as today) that can detect today's world's flue pathogens/bacterias ? If the answer is no, then do these receptors get added in the phagocytes by the vaccine that we create depending on the current virus and we know exact receptor that this virus can be detected by ?

Please finish reading the [Tour] to find out how this site works. You will discover that we expect posters to have done some research on their question.

There are several different kinds of phagocytes in the immune system including macrophages, dendritic cells, neutrophils, and others. All are capable of ingesting viruses, bacteria, some parasites, cell debris, and even intact whole cells. They differ in how those materials are then processed and displayed on the cell's surface, and how the cell responds to the phagocytic event, but that is beyond the scope of this question.
Phagocytes recognize pathogens via pattern recognition receptors (PRRs) for pathogen-associated molecular patterns (PAMPs). These PAMPs are patterns or motifs that are conserved within particular types of microbes. Examples include lipopolysaccharide (LPS) in Gram-negative bacteria such as E. coli, lipoteichoic acid from Gram-positive bacteria, double-stranded RNA (dsRNA) from certain types of viruses, etc.
PRRs exist in many different organisms in different kingdoms, including the fruit fly Drosophila melanogaster and plants like Arabidopsis thaliana, also known as thale cress. They have existed in humans (and many of our ancestors) since we evolved. The exact same PRRs that you and I have in our bodies were in the bodies of humans that lived 2,000, 20,000, and 200,000 years ago. Their genetic sequences may have changed very slightly over that time, but from a functional perspective they are the same. The reason for this is that (pathogenic) microbes have had the same PAMPs for millions and millions of years. PRRs are also not sequence-specific, instead recognizing molecular patterns - the chemical "shape" of a molecule. These patterns are evolutionarily conserved, meaning they are the same in species after species and remain essentially the same over long periods of evolutionary time.
Orthomyxoviruses are a viral family from which originate the viruses that cause influenza in humans and animals. These viruses have several different PAMPs in their structure and genome that allow phagocytes to recognize and destroy free virus particles as well as infected cells. These PAMPs are conserved between the different Influenza A viruses that can cause human pandemics. However, while these PAMPs are recognized by phagocytes (part of the innate immune system), which then go on to activate the rest of the immune system to fight the infection, this activation period can sometimes take up to two weeks or more. Therefore, flu vaccines focus on teaching a different part of the immune system (called the adaptive immune system) to recognize influenza infection via antibodies and patrolling memory cells, which can respond much more quickly than the innate immune system can. The reason you need a flu shot every year is because the exact molecular components of the influenza virus can change quite quickly, meaning you need to develop new antibodies and memory cells to recognize it quickly. The PAMPs do not change from year to year.
In response to comments:
As I mentioned, one of the main viral PAMPs is double-stranded RNA, which is produced (or released) inside the infected cell by most (but not all) viruses. PAMPs are typically vital parts of the organism - LPS in Gram(-) and lipoteichoic acid in Gram(+) bacteria are integral parts of their cell walls, dsRNA is part of the viral replication cycle - and can't just be evolved away. That is likely a reason why PRRs evolved in the first place - PAMPs generally don't change much over time.
I should also clarify: 20,000 years is a very short period in evolutionary time. As an example, the last common ancestor to chimps and humans lived between 4 and 13 million years ago. While new viruses have emerged as human pathogens in the past 20,000 years (heck, the last 3 years), the families they belong to and even some of those viruses themselves are not new, and possess similar PAMPs that have existed for millions of years, which has allowed specific PRRs to evolve and remain relevant today..
Another part of the story, which perhaps isn't clear from my original text, is that phagocytosis doesn't just involve PAMPs. Sometimes the target cell recognizes that it is infected and produces various "kill me!" signals that are expressed at the surface of the cell, targeting the immune system to destroy it. Additionally, if the body has seen that type of pathogen before either from previous infection or immunization (or both), memory cells that produce antibodies will likely be present. These antibodies will bind to their targets and can induce phagocytic cells to engulf them, whether they be free virus particles, other microorganisms, or infected cells. So, in some cases, phagocytosis can occur completely independently of PRRs and PAMPs.
On the subject of malicious bioengineering to remove PAMPs to create "super pathogens" - hopefully you'll see from above that most if not all PAMPs can't just be casually removed from an existing species the way we can cut and paste individual genes from plasmids. So, any potential super-virus will likely still have dsRNA that can be recognized by PRRs. But, because the innate immune system (of which PRRs are a part) takes some time to get the adaptive immune system geared up in the absence of strong pre-existing immunity, viruses can often infect, replicate, and begin spreading before the body can completely eliminate them.

Note: I included Wikipedia links as they are generally accessible to people who are not scientists or area specialists. They contain links to relevant reviews and primary literature.

Thanks so much for this detailed answer  ! Highly appreciated.  Somehow I ended up learning immunology due to the fact that I need to learn immunotherapy. I wonder one thing: You say that PRR's don't change (the same receptors were 20,000years ago in humans as now), but if that's so, how can they still today bind to viruses and cause the special effect(engulfing), I mean, viruses have changed, evolved and how can the same old PRR(from 20,000years ago) still can detect the modern, viruses(PAMPs) ?

If you say microbes/viruses/bacterias have the same parent of PAMP, then, it should be fairly easy to create a artificial virus that don't have the PAMP thing and that's it, would be super easy to be malicious doctor and spread bad virus that wouldn't be detectable by PRR.

@GiorgiLagidze please see my edit that addresses your questions.

Thanks so much.. quick last question. In terms of covid, if it also had double stranded RNA, why couldnt our phagocytes kill it ? What happened in that case ? Also, approving the answer, but would appreciate this last bit of question to close the gap

I think phagocytes would recognize covid virus and kill it(1 cell) but since it would take more than 2 weeks for the adaptive system to kick in. Hence the damage is already done.  This makes me to believe that phagocytes are killing things very slowly and they dont seem to be many, otherwise B cell would not be necessary(if we dont count memory cells and remembering the virus).


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Haldane effect plays more important role in promoting carbon dioxide transport than that of the Bohr's effect in promoting oxygen transport why?
This is the actual question
And the correct option is "A"
But I can't figure out why
Haldane effect plays more important role in promoting carbon dioxide transport than that of the Bohr's effect in promoting oxygen transport because
(a) oxyhaemoglobin is a stronger acid which donates hydrogen ion (H) which in turn displace carbon dioxide from blood
(b) carbaminohaemoglobin is a stronger acid which splits into hydrogen ion (H+) and bicarbonate (HCO) (c) carbon dioxide reacts with to form acid
that lowers the pH in tissue (d) carbon dioxide is less soluble in venous blood than in arterial blood.

Please finish the [Tour] and the help on asking questions, particularly homework question. As with all homework questions you need to show your own attempt to solve the problem. It will help the more general biologist if you state what you think the Bohr Effect and the Haldane Effect are, and it will also be a starting point for you to weigh the merits of the different statements. Also please edit the question so that the four alternatives start on a new line.

I have sympathy for you.  "More important role" is a hard thing to quantify, and the semantics of both honorifics blur out into their inevitable chemical consequences which inevitably overlap.  This one seems better addressed by a process of eliminating the wrong answers than in trying to prove the premise true in an absolute sense.  Nonetheless, (a) is clearly true as written and it does explain why some CO2 is affected that wasn't even stuck to hemoglobin in the first place.


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Can human spinal reflexes make use of a proprioceptive input?
I was out in the car when I wondered why manufacturers place pedal controls crucial for reaction time so very far from the motor cortex.  Is there anything a spinal reflex could work with, which would not be available to the brain in the same time frame?  So I looked this up and found two recent papers:

Picton, 2021, describing sensation of lateral motion by Piezo2-expressing mechanosensative neurons.
Stanchak, 2022, describing mechanosensation in the lumbosacrol organ of birds by neurons expressing myo7a and espin.

The second paper goes so far as to suggest "spinal cords across vertebrates are capable of mechanosensation and that spinal mechanosensory networks have evolved to allow unique functions"
Speaking of function:  is there any functional evidence that proprioception could directly inform a (learned) spinal reflex in humans?  Such as a human changing the pressure on a gas or brake pedal in response to acceleration or deceleration, without needing to consult the cerebrum first.  (Any other mammal would also be relevant, but it ought to be easiest to do this sort of experiment with humans)

There's been quite a bit of sidetracking about whether reflexes could be involved in driving, so I feel like I should illustrate with a common scenario.  You're coming toward stopped cars at a traffic light, braking fairly heavily, while you've turned your head to one side to look at traffic.  At one point a piece of gravel shifts under the car wheel and you momentarily stop decelerating, so you respond by braking more heavily.  This might be the result of processing a lateral motion at the inner ear, using the cerebellum to compensate for head position and directing a new program of action at the motor cortex; but perhaps it might also involve a direct spinal response to proprioceptive input originating near the sacrum to maintain the intended degree of sensation of deceleration.

What is "functional evidence"? Also, out of curiosity, did you do a Google Scholar search on, say, "Can spinal reflexes be learned?" It seems to me that the paper you quoted does suggest(?)/state(?) that.

@anongoodnurse I'm not quite sure what you're getting at.  As you suggest, such a search does readily find articles about learning in spinal reflexes. In this case an unlearned reflex would also be satisfactory, but I doubt we can name one involving proprioception since its role is (at best) not well established.

@anongoodnurse  For "functional evidence" I was imagining some clever experiment might prove quite a bit simply with reaction time.  Maybe if you jerk a person's seat backward in the lab unexpectedly, and they respond by increasing pressure to a simulated gas pedal?  But I can't say how you would prove this isn't the result of a stretch reflex, crossed extensor reflex etc.  The same problems apply even more so in the case of tripping, which all the reflexes are designed to prevent.  Still, just because I don't have an idea right off doesn't mean no one has ever come up with one!

Did you know that pedals on cars used to be purely mechanical? If you're rolling down a hill in a wagon, would you rather brake yourself with your foot or your pinky finger?

And I am confused here too; the reason driving involves cerebral actions is much because reflexes can be as dangerous as long reaction times (due to alcohol for instance). If I'm on the highway with a lot of cars around me and suddenly I see an animal on my lane, my reflex would be to smash the breakes and save the critters a$$, at a second thought, I think of the fact I'm cruising at 100 km/h with a fender bender on my tail -- now would a reflex have helped you, or resulted in a pile-up instead?...

...I understand the question, but I think you should frame it in a different way, because in its current state the driving scenario distracts folks from your real question.

@AliceD For analogy, consider the role of the quadriceps stretch reflex.  Striking your patella with a rubber mallet seems like a poor contribution to driving, yet you use the same reflex moment-to-moment to help make sure your leg is in the position you think it is on the pedal.  Higher level processing modifies the reflexes, so you can bend your leg to different positions without being defeated by a reflex action and without losing its benefit in the new position.

@MikeSerfas - I'm more confused now. You can't "override" a spinal reflex, but it is possible over time to modify it some. (Also, nit-picking, but you don't elicit a reflex by hitting the patella, except for maybe the "WTF?" reflex with a grimace of pain. You strike (gently) the patellar tendon.) An example of setting off a spinal reflex is touching a hot iron. You can with repeated effort put your hand on the iron and leave it there, but it isn't activated by other activities. Not every stretched muscle twitches, or we wouldn't be able to walk. It's not a matter of cortical overriding. ...

... IOW, your cortex isn't modifying how your leg responds to proprioception; you're simply using your leg muscles differently, and appropriately so, to achieve the same effect. You can learn (cortical) to fall flat on your face without protecting it, overriding a reflex, but that takes time and effort. Also, it's not very helpful to health or longevity. I'm not a neurologist or neuroscientist, so I don't understand the question as @AliceD seems to. The paper in the link you provided (as well as others) answers in the affirmative. What else are you asking?

@BryanKrause - I agree you would use one of your strongest muscles to stop a car. With hydraulic brakes on 4 wheels, a pinky would work as well if not as instinctively initially. (Instinctively as in, resisting a forward force, you'd use your legs instinctively.)

@anongoodnurse My point is that OP's question is based on a false premise; they're thinking that someone designed a car thinking a leg muscle would be a fast way to respond to things. In reality, cars are designed that way because once upon a time someone needed to actually transmit force through the pedals.

@BryanKrause - Understood. The whole question/premise is questionable imo. The reaction time difference between arms and legs based on their distance from the cerebral cortex is questionable when discussing a spinal reflex. What fraction of a second difference does arm length vs leg length make? I never noticed any lag in reaction time between the biceps and knee reflexes.

The intercept of 182 ms is an estimate of the time needed for internal processing and response generation; the slope of 45 ms/m for distance; (22 m/s)... So it's 45ms difference between hand/foot. Unlikely is that the number of muscles involved in coordinating the leg and foot to apply brakes, is too complex for mechanosensory response vs a learned reflex which is integrated with learnig logic and the motor cortex. A non-cortex reflex has to also know which of 250 muscles to apply when sensing 100ds of stimuli, i.e. a stone hitting the foot zone under the car.


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Do secretomotor neurons activate for secretory cells due to the absence or presence of water and electrolytes? Why?
I read this passage in a book called Integrative Action of the Autonomic Nervous System by Wilfrid Jänig. In this book, he states

Reflex pathways involved in the regulation of secretory cells and/or local blood vessels (arterioles) have been much less explored than enteric reflex pathways that are involved in regulation of motility. This applies to the organization of the reflex pathways connected to the mucosa and mucosal blood vessels as well as to their coordination with the reflex pathways that are integrated into the regulation of motility. Activation of secretomotor neurons stimulates epithelial cells to secrete chloride ions into the intestinal lumen, taking with them sodium ions and water. The physiological stimuli that induce a reflex activation of the secretomotor neurons are mechanical stimulation of the mucosa (shearing stimuli) and chemical stimuli (e.g., glucose or proton ions). The most important activator of the reflexes is the absorption of water and electrolytes by nutrient transporters. For example, glucose transport involves the Na+-transporter and each molecule of glucose is accompanied by Na+, counterions and water. Absorption of 100 grams of glucose is accompanied by 1.8 liters of water (Furness 2006). The purpose of the secretomotor reflexes in vivo is therefore to preserve whole-body fluid balance. The intraluminal stimuli triggering secretion appear to be the same as those causing enteric motility reflexes in the intestine. The stimuli activate the IPANs via enterochromaffin cells (EC) in the mucosa, which release 5-HT and excite the IPANs, or possibly by other cells releasing CCK or motilin (Figure 5.13). The IPANs excite enteric neurons synaptically by release of acetylcholine and substance P. Intraluminal toxins, such as cholera toxin, lead to pathological activation of secretomotor neurons. This overwhelms the fluid-balance role of the reflexes, causes copious fluid loss and, if unchecked, death, because the fluid ultimately comes from the circulation. Secretomotor reflexes elicited by intraluminal physiological stimuli are always paralleled by enteric vasodilator reflexes mediated via the enteric neurons.

I am specifically confused by the sentence

The most important activator of the reflexes is the absorption of water and electrolytes by nutrient transporters.

Is he saying that the secretomotor neurons are triggered by the absorption of water and electrolytes? Or is he saying the absence of absorption triggers the reflex?

I read the text without having looked at your specific question, and I was confused in much the same way. I'm looking forward to the answers.


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immune system - how does adaptive work without innate?
The way I understood immune system is that:

phagocytes detect viruses and present it on their surface and become antigen presenting cells.
Then, T-helper cells try to bind to these phagocytes that have antigen on their surface and found, T-helper cells become effector T-helper cells which then cause the activation of B-cell.

Question 1: If phagocytes can't detect virus, that means T-helper cells wouldn't be activated(there would be no process of cytokines) and if no cytokines, B-cell activation wouldn't happen. and if no B-cell activation, no antibodies releasing. So This means unless phagocytes detect the virus, B-cell activation doesn't happen, but this would be too bad, because if B-cell activation depend on the phagocytes finding the virus, this means if innate immune response fails, adaptive also fails. I'm wondering when would still B-cell be activated even without phagocytes finding the virus in the first place ?
otherwise, B-cell always depending on phagocytes would be too bad...
Question 2: Am I right that B-cells can detect/identify the virus that couldn't have been identified by the phagocytes ? I think so, because phagocytes have general PRR which sometimes might be unable to detect, but B-cells have more combinations of variable portion proteins that could detect more stuff ?

B cells can be phagocytic, and can present antigen to T cells both via MHC-I and MHC-II pathways. Different PRRs can be found in many cell types so they can detect infection and signal that to the immune system. You might be interested in the topic of immune evasion.

Thanks for the answer. But am I right about my 2nd question ?


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cancer cell - antigen presenting cell
We all know that if normal cell contains virus inside it, normal cell has mechanism inside it that can detect that it has abnormality inside(virus) and what it will do is present the virus's protein(antigen) with MHC I on its surface, so T-cytoxic cells can kill it.
But cancer cells don't have virus inside. They still look healthy. I mean the cell itself has different proteins(derived from mutation), but cell itself thinks that it's healthy. So would it put anything on its surface with the MHC I ?

If the answer is no, then we got a problem, as it would never, ever be recognized by T-cell to kill it.

If the answer is yes, I guess, it would just put its modified protein, though, in that case, that means that every cell(in our body, even normal ones), they all put their protein representations on their surface. Because if cancer cell(which thinks it's healthy put it, then every cell which is also healthy should put it, seems logical)

Maybe my question should be: What is MHC I exactly ?
In case of normal cells(healthy ones), only MHC I is put on the surface and MHC I is proteins taken from within the cell.
In case of the cell that contains the virus, MHC I is the proteins from within the cell that aren't part of the virus protein. So here on the surface, it puts MHC I and virus protein(antigen) separately(MHC I + antigen).
In case of cancer cell, what is put on the surface ? just MHC I (which are modified proteins within the cell) or we also have somehow MHC I + antigen, but I don't understand how we would have MHC I + antigen combination as the cell doesn't know that it has antigen(thinks it's normal).
What do you think ? I'd appreciate the clear explanation.

This is a really big field. I think that there is a lot of complexity in how the immune system recognizes cancer cells. Yeah there are specific epitopes that get displayed, but I'd suggest just googling "how does the immune system recognize cancer cells", and you will get lots of helpful results like this.

I'm voting to close this as "Needs more focus." @MaximilianPress is correct, this is a huge field, and even a simplified answer would need to be textbook chapter-length in order to be complete.


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immunotherapy - how would the inhibitor detect
It's a known fact that if PD-L1 happens to be on cancer cells, it will signall off to the T-cell's receptor(PD-1) to turn off its activation, resulting in a fact that cancer cell won't be destroyed.
Question 1: Even if with immunotherapy, we stop the blockage (PD-1 vs PD-L1), (Let's say PD-L1 was expressed high with NGS), why does this mean that T-cell now will kill the cancer cell ? Yes, we removed the blockage, but it could still happen that binding between the proteins of T-cell and proteins of cancer cells might still result in NO T-activation, hence no cancer cells being killed. So If I'm right, having PD-L1 expression high on NGS still doesn't give you anything and you gotta risk it and see !
Question 2: It turns out some healthy cells also have PD-L1 expression on them, but much less amount than on cancer cells. For simplicity and example, let's take our body's own cell (cell-Y - I just named it up). This cell-Y has PD-L1 as well. If we give the Atezolizumab(tecentrik) to the body, which will stop the blockage between PD-1 vs PD-L1, would the T-cell now destroy this cell-Y ? I'm asking this because it's said that using PD-L1 inhibitors also cause good cells to destroy. But I don't get why. Even after stopping the blockage, T-cell shouldn't kill cell-Y, because this cell-Y is body's own cell, the other proteins it has on the surface, binding it to the T-cell, still shouldn't cause destruction. What do you think ? or this is random and nobody knows ! the only protection our immune system had for cell-Y was PD-L1 on it, but if we block it, then we get to the random scenario and got no idea whether T-cell now can destroy it or not(depending on their receptors binding). Question is, do we actually get to the random scenario or we know for sure that without PD-L1 on cell-Y, T-cell will always kill it ?
Question 3: How is it possible that with tecentrik immunotherapy, T-cells don't kill good cells, but kill cancer cells ? I've read somewhere that it's about the dosage and frequency, but how would that work ? how does the process differ between giving high dose of tecentrik and low dose in a sense that it's possible that T-cell won't kill good cell even after blocking PD-1 vs PD-L1 ?

These are technically complex questions. Can you please restrict yourself to one question per question?

Can you link or cite sources for your statements? It would be nice to look at the basis for your question to evaluate how best to answer it. (Also, Chris is right)


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How does labelled N from tyrosine appear in phenylalanine if the latter is an essential amino acid?
A certain question (not my course or instructor or even university) goes:

Exposed to regular metabolic activity in a rat liver, a 13C label in tyrosine will not appear as a 13C label in phenylalanine. However, a 15N label from tyrosine will appear in phenylalanine (among other amino acids) under the same conditions.
Explain and show why this is so using appropriate structures and reactions.

Tyrosine metabolism is well-discussed in any undergraduate biochemistry text and takes the following route (courtesy Voet, 5e):
Since phenylalanine hydroxylase catalyzes an irreversible reaction,1 radiolabels ought not to distribute back from tyrosine to phenylalanine. Where am I going wrong?
Footnotes
1: Remember that phenylalanine is an essential amino acid and cannot be synthesized in animals.

What does "Exposed to regular metabolic activity in a rat liver" mean? This phrase seems to apply to radioactive labelled atoms, which is linguistic nonsense. Does the question really say this, or have you garbled it? It smells a little of a trick. And are the rats growing or adult, and did the question say that Phe is an essential amino acid in rats? I cannot find a definitive source for that.

I suspect that the answer might be that there is some phenylpyruvate in rat liver, and that this can be transaminated to phenylalanine using glutamate, the N of which would have become labelled from the Tyr to OH-Pyruvate reaction, but glutamate C would not. This would require that rat liver had enough phenylalanine deaminase to generate phenylpyruvate from dietary amino acids, and that some sort of cycling occurs. I have not provided this as an answer because I don't know if it is true. I can find some papers that suggest these enzymes are present, but the whole things seems rather obscure.

OK, I checked the original paper. The question is just badly phrased.

I simplified the title. A label is a label. We don't need to know what isotope it is, which solves the problem of the superscript.

This isn’t really a question that most people would be able to answer without reading a lot of literature. I suspect the professor of this course taught a case study about phenylalanine metabolism, which would make it an appropriate question for an exam. My guess is the same as @David ‘s: cycling by a transaminase. It’s of note that this enzyme is related to the metabolic disorder phenylketonuria, which make’s it use in a case study more likely.

@canadianer — Agreed. Doesn't look as if there is a suitable deaminase in mammals, but there are reports of a phenylalinine/glutamine transaminase. Of course the reaction would have to be in an equilibrium that allowed the generation of some hydroxy-pyruvate and its reversal, which is perhaps what the "regular metabolic activity" is intended to imply. I don't think data on that are easy to come by. Most of the papers I can find are from the 70s.


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Can color-blind people see the effect of combining red, green, and blue light beams?
When combined, red, green, and blue light beams result in white light. This effect is observed by most of us, but can color-blind people also see this effect?

There are many kinds of colour blindless, and most kinds aren't black/white.

Remember the comments on your previous version of this question? Please include your research when posting.


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Why Fertilisation occurs only in Fallopian tube?
The Ova is released and stops in the fallopian tube for the sperm..The Fertilisation occurs at the Fallopian tube, but as the zygote divides and forms an embryo, it attaches to the lining of uterus.But why doesn’t the egg come to the uterus and the fertilisation occur in Uterus?? Simply,Why cannot the site of fertilisation be the Uterus?

Welcome to the site. What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Hello Respected Sir! I’m a 14yr old Student..These subjects are out of my syllabus.But Still, I Would like to learn each topic, but to learn i have to ask questions. I Have gathered only this information regarding this.I Know you are helping me in a way to learn something myself.But I Would like to ask these questions so that i can self learn. I Don’t simply come to SE community and asks questions, i search the questions or info in google or youtube, when there is no help, i just ask here.
I’m Sorry, If I’m Hurting you! But I’m just a beginner and there are many other students in SE Like me!!

good for you for being curious! By previous research, I mean what did you learn when you took the title of your question and asked it on Google? What resources there helped? What are you still confused about? Essentially, the answer is that Fallopian tubes evolved to be the place where fertilization occurs in humans, and the uterus did not evolve to be very conducive to fertilization; rather, it is good for implantation and growth.


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Naming the Rings of Flagellar Structure
I will apologise ahead of my very basic question.
I just read about Flagella Structure and learned that there are 4 rings, namely "L Ring", "P Ring", "MS Ring", "C Ring".
I tried looking online for why the rings are named as such, but i could not find anything related to their naming.
I am guessing
L Ring = lipid ring?
P Ring = Periplasm ring?
MS Ring?
C Ring = Cytoplasm ring?
Thank you in advance for enlightening me.

Your guesses are correct. More detailed, assuming you are referring to Gram-negative bacterial flagella and flagellar motor structure:

L ring associates with the Lipopolysaccharides (more general S-layer for archaea and Gram-positive bacteria)
P ring associates with the Peptidoglycan layer
MS ring is embedded in the plasma Membrane (not sure why S maybe tranSmembrane?)
C ring is a Cytoplasmic protein attached to the MS ring acting together as the rotor of the flagellar motor

As a structural biologist here is some recommended literature on high-resolution (cryo-EM) structures of flagellar proteins:

3D cryo-EM imaging of bacterial flagella: Novel structural and mechanistic insights into cell motility
Structure of the molecular bushing of the bacterial flagellar motor


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Glycemic Index and AUC Curve: why do two different foods have differing numbers?
The AUC Glucose/Blood Level curve Integral (area under curve) is used to calculate the Glycemic Index of certain foods. I have a question on why two sample foods with the same mass of carbohydrates can have different AUC Integrals or Glycemic Indices. I have some possible theories and would appreciate guidance.
Are these numbers different between the same sample size of 50 g of carbohydrates due to differing blood glucose levels, yet the same energy delivered to the body (perhaps in another form other then rising glucose)? Are the levels different due to differences in the body's digestion of the food? Or, is part of the glucose/blood integral of some lower Glycemic Index foods passing beyond the 2-hour window of measurement, which would cause a smaller integral and lower Glycemic Index?
BACKGROUND:
To be clear on definitions, the Glycemic Index is calculated using the relative rise of a blood glucose level two hours after consuming a food and it is the integral of (area under) a 2 hours glucose/blood response curve, following a 12 hour fast and ingestion of a sample food with 50 g of carbohydrates. The Index is calculated specifically using the ratio of a blood glucose AUC integral, ignoring the area below the fasting baseline (start of curve rise), for some carbohydrate source and a reference source. The reference source is usually either glucose or white bread. The trapezoidal rule is typically used to calculate the integral, although any method can be used. The Glycemic scale places pure Glucose at 100. The index is calculated using a ratio of two integrals using this formula: (SAMPLE_FOOD mmol/L * time)/(REFERENCE_FOOD mmol/L * time) * 100.
Where I'm confused is that two sample foods with 50 g of carbohydrates should have the same energy in calories, typically 200 kcal (4 kcal/g carb). I see the integral of the AUC curves for different foods can be different, indicating different glucose/blood level changes for each food over the two hour window. This makes me think, the foods have the same energy content, but are changing the body's blood glucose levels differently, resulting in different curves and Glycemic Indices. I first questioned whether the reason for this was that part of a food's curve lied outside the 2-hour window, raising the Glycemic Index slower than another food. I also read that the glucose levels will change differently depending on the type of carbohydrate, and some form of carbohydrates are even impossible for the body to digest and are either digested by bacteria in the gut or simply excreted in the feces, which would resulting in a lower glucose/blood level rise.
For example here is a 2-hour AUC curve of some fruits against glucose reference:

Your question points to the entire point of glycemic index: two foods with the same carbohydrate content (by mass) do not necessarily enter the bloodstream at equivalent rates.
Picture a gram of glucose; we know it's energy content (about 5 kcal) but how quickly will it get into the bloodstream? Whatever that answer is, now picture the same gram of glucose packaged as a time-release capsule. The time-release glucose will get absorbed into the bloodstream much slower so the peak glucose concentration will be much lower.
This fact -- that the peak blood glucose is lower for the time-release 'food' -- is what's quantified by the glycemic index. Since foods vary in the rapidness in which sugars are absorbed (and metabolized into insulin-eliciting sugars) the total carbohydrate content isn't a direct predictor for the peak blood glucose (or insulin); that's why glycemic index is a (theoretically) useful concept to assess the endocrinologist effects of different foods.
And yes, the slower peak means a) more of the curve lies outside a 2h window and b) more of the sugar is metabolized as its absorbed. Both factors decrease the total area of the integral. But it's the peak concentration that's thought to have the largest effect as the endocrine signal to release insulin.

Asparagus has a Glycemic Index of 15, does that imply that metabolism of glucose into the bloodstream occurs over about 6 hours, vs 2 hours for pure glucose (100 GI)?

I don't think I follow your math...the GI is only based on the 2h post-ingestion part of the blood glucose. The whole treatment doesn't address how long it takes for all th glucose to be absorbed into the bloodstream. 50g of asparagus only has about 0.94g of glucose in it! So the peak blood sugar could be as much as (50/0.94) 53 times higher for pure glucose compared to asparagus.


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Converting microequivalents per liter to mg for sodium?
I read that a normal blood sodium level is between 135 and 145 milliequivalents per liter (mEq/L). Hyponatremia occurs when the sodium in your blood falls below 135 mEq/L.
How do I convert mEq/L to a value in milligrams (mg) so I can understand how many mg of sodium should be normally be ingested into the body?
I understand the values is between 250-500 mg/day, but would like to see this correlated with the mEq/L units.

This is not a good way to determine "how many mg of sodium should be normally be ingested".

Is there no conversion of the units?  What is the preferred way?

It just has nothing to do with the goal you are wanting to achieve. If you borrow a car and want to replace the gas you used, it doesn't help you to know how much fits in the tank.

@BryanKrause I don't understand your reasoning and analogy.  Can you explain in terms of units, metric and science what you are trying to say?  mEq/L is a concentration of sodium per liter of blood.  1 mEq/L = 1 mmol/L, 1 mmol/L = 46 mg/L.  I'm confused because this suggests 135 mmol/L * 46 (mg/L)/(mmol/L) = 6,210 mg/L concentration of sodium.  If the body has 5L of blood, then 6,210 mg/L * 5L = 31,050 mg of sodium is well above the RDV of 2,300 mg.  Ideas?

You don't need to eat as much salt as you have in your body (e.g., size of gas tank). You need to eat as much salt as you lose: through urine/feces, sweat, etc.

Does this suggest, based on above math in comment, that the body keeps 31,050 mg of salt in it's system and perhaps loses 250-500 mg of salt per day (through sweat and urine)?  Therefore we need to ingest 250-500 mg of salt per day to keep up with the loss?


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What motivates an organism to reproduce?
What is the biological factor (gene or something else in case of humans) which motivates an organism to reproduce?
By reproducing the evolutionary success of an organism increases. But why would an individual organism care about evolutionary success? Is there something inherent in the body of an organism that motivates the organism to take part in reproduction? From an organisms point of view, it can very well live happily without reproducing, in fact, the act of reproduction might lead to eventually more difficulties (raising the offspring, protecting the offspring etc.).

"But why would an individual organism care about evolutionary success?" - Every organism that didn't died without reproducing; you only see the ones that reproduced.

"you only see the ones that reproduce" - so the evolutionary success is the driving force of reproduction? I don't think a simple life form (let's say a bacteria) can understand evolutionary success, but still it none the less optimises for evolutionary success? What forces it to optimize for it?

Nothing forces anything; organisms with a genetic tendency to reproduce will reproduce and you'll see their offspring in a future generation. Any organism with genes that prevent it from reproducing will not reproduce, and you won't see their offspring in a future generation.

As a new user of this site we expect you to do us the courtesy of finishing reading the [Tour] to find out how this site works and read the Help on asking questions. We expect posters to demonstrate that they have done some research themselves. This topic must be covered amply on the Internet. If you find the answers there unsatisfactory, please tell us why.

You are confusing proximate and ultimate causes.
What causes an organism to keep eating, most are not smart enough to know they will die if they don't eat. The ultimate reason may be to keep from starving but that is not the proximate reason.
The proximate reason they eat is because their brains are built to want to eat when their senses detect food. to get hungry and feel pleasure when that hunger is sated.
eating, drinking, scratching, pain, disgust avoidance, vomiting, reproduction, they all come with basic urges, proximate motivations. the brain is built to want to do these things under the proper conditions. Why do songbirds sing, because they want to, they have a desire to and acting on that desire in the correct circumstances gives them pleasure or not acting on it causes discomfort.
Animals have sex because they want to, that is the proximate cause. The ultimate reason they want to is brains with that desire are the brains most likely to pass on their genes to the next generation. Thus genes that make brains that get the animal to reproduce are the genes most likely to make it into the next generation.
To look it another way you are the product of an unbroken line of genes that built brains that reproduced, because genomes that did not don't leave descendants.

+1 for introducing a new idea.

I reached to this independently and I had no idea before just randomly.

Life processes are ways of long term survival of genetic information, being carried by individuals with momentary lives inside their cells.
Since each individual life is momentary, only that genetic information survives for a long time which has developed efficient ways to ensure individuals continue to bud off new ones before they die.
In other words, individuals are only tools in the control of the super-organism of genetic information. And thus, it is not surprising to find only those variations of genetic information continuing to survive around us which have been able to drive their individual buds to continue to replicate. This includes driving the individual to resist death, driving it to seek and gather resources, and driving it to reproduce.
The tree of genetic information continues to find these ways of driving individual buds primarily through chance, enabled by the huge number of tiny variations that it introduces in each individual, and the humongous numbers of individuals; when a branch (or twig) of the genetic tree can no longer ensure it, it dies out.

I always thought sexual urges had something to do with it.

"Individuals are only tools in the control of the super-organism of genetic information." I'll use that line next time someone takes themself too serious if you don't mind.. ;)

-1. Humans aren't forced to reproduce. More and more humans don't reproduce now that 1. children are no longer necessary for labor/elder care and 2. contraception is widely available. Many humans who accidentally may or do conceive prevent or end their pregnancies. If we were forced genetically to reproduce, these choices would not exist.

@anongoodnurse I agree that "driving" could be a better verb than "forcing" here. Thank you so much for pointing it out. I have replaced it. I am sure you know that my usage of "force" wasn't meant to be irresistible; quite difficult to resist but not irresistible.

@iLuvLogix Thank you so much for valuing it, and thank you even more for telling me that you value it. I also find the idea philosophically humbling. I have now emboldened it for cursory readers.

@David Thank you so much for your comment. Sexual urges in individual buds are only a tiny part of how the super-organism of genetic information ensures its survival. If you think about it, all of our living processes are primarily designed around its survival. That is why, I have mentioned "This includes driving the individual to resist death, driving it to seek and gather resources, and driving it to reproduce."


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Can dogs see infrared radiation, i.e., heat?
I, like most of my fellows, prefer my meals served piping hot. As all know, humans sometimes feed their dogs table scraps. If I put down a small piece of chicken from within a piping hot chicken pot pie and alert my small pet dog that it's for her, she'll stand back 2 or 3 feet away from it for a while before eventually consuming it. I am starting to believe that she only does this behavior when the food I put down is too hot for her. So it begs the question I here pose: are dogs able to see heat radiation from afar?

Welcome to the site. Please visit the [help] and take a [tour] to find out more about what this Stack Exchange site does. In particular note the homework page. Questions on here generally require some evidence of prior attempts by the asker to answer it themselves. So - what does a simple google search for "dogs infrared" bring up. I can see a Nature paper...

Why "see" infrared radiation?  You can feel the heat of a fireplace even if the fireplace is covered by some glass that prevents the outflow of hot gasses. Or, one can sense that the sun is shining intensely even with one's eyes closed.

A dog's nose can even sense weak thermal radiation, as found out recently by researches at at Lund University and Eötvös Loránd University. So strong thermal radiation can be detected from a couple of meters away which would explain your observations.
Citation from this article:

To test the idea, researchers trained three pet dogs to choose between a warm (31°C) and an ambient-temperature object, each placed 1.6 meters away. The dogs weren't able to see or smell the difference between these objects. (Scientists could only detect the difference by touching the surfaces.)
After training, the dogs were tested on their skill in double-blind experiments; all three successfully detected the objects emitting weak thermal radiation, the scientists reveal today in Scientific Reports.
Next, the researchers scanned the brains of 13 pet dogs of various breeds in a functional magnetic resonance imaging scanner while presenting the pooches with objects emitting neutral or weak thermal radiation. The left somatosensory cortex in dogs' brains, which delivers inputs from the nose, was more responsive to the warm thermal stimulus than to the neutral one. The scientists identified a cluster of 14 voxels (3D pixels) in this region of the dogs' left hemispheres, but didn't find any such clusters in the right, and none in any part of the dogs' brains in response to the neutral stimulus.
Together, the two experiments show that dogs, like vampire bats, can sense weak hot spots and that a specific region of their brains is activated by this infrared radiation, the scientists say. They suspect dogs inherited the ability from their ancestor, the gray wolf, who may use it to sniff out warm bodies during a hunt.

Here's the scientific article if you want to dig your nose in a bit further (pun intended)..


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Can arthropods rotate their joints?
I've been recently researching arthropod exoskeletons, and one thing I've seen more than once is that exoskeletons, due to how they work, only really allow for hinge joints. However, from seeing flies and mantises, I've more than once seen tilting or even rotation of the head. I've tried searching more, but all I found was how mantises are the only arthropods capable of rotating their heads, a process that I couldn't find an explanation for.
Essentially my question is: can arthropods in general rotate their joints or are mantises truly alone in their ability to have rotation with an exoskeleton as far as we know? While it's not the main goal of the question, I'd really appreciate an explanation on how exactly mantises achieve this rotation


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Texas butterfly with dull underwings, but blue/purple on overwings
I was walking in the grass near the Trinity Trail in Fort Worth, Texas about two weeks ago, and saw these tiny purple streaks flitting about at mid-calf level that turned out to be butterflies.  I followed and tried to get lots of pictures, but the butterflies were quite fast and tiny, and I only got one decent close-up.

Its wings were a dull brown/gray colour when closed, but I couldn't get any better pictures than this grainy one.

Because of how fast it was moving, I couldn't really estimate size reliably, but it was probably slightly wider than the width of my thumbnail when its wings were open.  With its wings closed, the height of the butterfly was about the longest height of my thumbnail.  These are very rough estimates.
It looked quite a bit like the linked picture of a purple moonbeam—one of Google Lens's suggestions—but those seem to be Australian butterflies.

No, not much size variation. Try LYCAENIDAE (gray wings belong to this family as well.) There are smaller ones (called "blues") very similar to gray hairstreaks, e.g.the Echo Blue. Hard to find the distribution, though, but definitely Southern N.A.

@anongoodnurse, thanks!  Google Lens also turned up Echo Blue as a suggestion, but, as you say, I couldn't find information about their geographic distribution, or even a picture like you offer.  The size seems right, so it could be!  Searching also turned up the Melissa Blue, whose overwings look just right, but not the underwings.

@anongoodnurse, re, I think enough time has passed to regard that as the most definitive answer I'll get. If you would be willing to post it as an answer, then I will accept it.

What an odd coincidence: I thought of you today when I saw this video, wondering if it was your Melissa Blue. Thanks for the offer, but I'm disinclined to post a guess as an answer. I hope you understand. :)

@anongoodnurse, re, I do.  Would you mind if I posted it, with credit to you, just so that I can mark this question answered?  Incidentally, I saw a few Melissa Blues this year, and one literally just today! I can't remember perfectly, but this one seems about the same size and overwing colours, just different underwing, so Echo Blue seems likely—and I've almost certainly forgotten any more details than that that some future sleuth might rely on anyway.

Whatever you want to do is fine with me. I agree the underwing is much like a grey hairstreak. I've never seen a Melissa Blue; lucky you!

@anongoodnurse said:

Try LYCAENIDAE (gray wings belong to this family as well). There are smaller ones (called "blues") very similar to gray hairstreaks, e.g.the Echo Blue. Hard to find the distribution, though, but definitely Southern N.A.

Since this was a guess, they said that they preferred not to post it as an answer, but also that it was OK for me to do so, with attribution.  To avoid reputation, I am making this answer CW.
Though I no longer have a perfect recollection of the fine details of this sighting, and only the grainy photograph to jar my memory, I believe, based on later definite sightings, that the butterfly in the pictures above is indeed an echo blue.


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Receptor tyrosine kinases: What is meant by basal phosphorylation of the receptor?
I am reading a journal paper about the insulin receptor. The insulin receptor is a receptor tyrosine kinase, and upon ligand binding, undergoes autophosphorylation of intracellular tyrosine residues.
Regarding this paper, the terms "basal phosphorylation" or "phosphorylation in the basal state" of the insulin receptor is frequently used. However, I am unsure what the exact definition of basal phosphorylation is.
Is it the phosphorylation the receptor undergoes under physiological/normal conditions in vivo without the addition of exogenous insulin?
For example in the paper, they treat brain slices from wild-type mice with exogenous insulin, and they report that the phosphorylation of the insulin receptor exceeds the basal state.
Any insights are appreciated.

I think these excerpts are helpful in understanding the authors' use of basal, both in reference to insulin levels and insulin receptor phosphorylation --

As expected, insulin receptors from untreated WT slices are not detectably phosphorylated in the presence of low basal levels of insulin, but become rapidly phosphorylated upon exposure to exogenous insulin. In contrast, insulin receptors from MHCI-deficient $β2m^{-/-}$ $TAP^{-/-}$ hippocampi show significant basal phosphorylation, which is comparable in magnitude to insulin-stimulated phosphorylation in WT slices (Fig. 1A).

By increasing the threshold for insulin
receptor activation, MHCI ensures that dynamic insulin sensitivity is preserved, even on a background of basal circulating insulin.

In this context, I would interpret basal phosphorylation to mean the extent of receptor phosphorylation in tissue in the presence of a stable concentration of circulating insulin concomitant with fasting levels of blood glucose.

Your final definition is circular.  How does “baseline” clarify “basal”? You need to reword that.

@David good point. I've attempted to clarify -- I'm open to suggestions if still unclear.

That fits. “Basal” is not a precise term anyway. It is used to acknowledge that even without experimental manipulation, the molecule or process you are stimulating is not completely absent.


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Why do humans see exactly one octave of light?
The visible spectrum of light is often defined as 350nm to 700nm. On Wikipedia, it says 380nm to 750nm. Either way, the upper bound is very close to double the lower bound. This means humans can see exactly one octave of the EM-Spectrum. (By octave, I mean the interval on a logarithmic scale corresponding to 2:1)
Is this a coincidence? Is there an evolutionary advantage to it?
As far as I know, our cone cells work on the principle of resonance. But they do not seem to respond to harmonic frequencies. Why?
To be clear. I am not asking why our vision is in the range it is. I am asking why the bounds are so close to 2:1.
There has been a similar question on Physics StackExchange, but the answer does not address the octave part.

Why do you think there should be a reason?

Maybe related: https://biology.stackexchange.com/q/57708/27148

trivial answer: it is the most intense portion of the spectrum that we experience.

It isn't really true that the human eye sees "exactly one octave of light".
The visible spectrum does not have precise boundaries, so the choice of "350-700 nm" is a bit arbitrary and might even just reflect a human bias towards integer ratios.  Wikipedia gives "380-750 nm" as the typical range for the human eye, and if you look around online you'll see lower limits that range from 350 to 400 nm, and upper limits from 700 to 830 nm.
For sufficiently bright sources, human perception may actually extend down to 310 nm and up to 1100 nm.
Humans can see the spectrum they do because of a combination of eyes being optimized for seeing in sunlight and avoiding the biochemical and biophysical challenges of detecting longer and shorter wavelengths.
Visible and near-visible light is the "sweet spot" for biological vision on Earth. The human eye could probably not operate over a much larger wavelength range, and a range much less would inefficiently waste available light. There is no reason for the visible range to be precisely a factor of 2, but it would be surprising if the range was very much larger.
As noted in the comments, the range of human vision almost exactly matches the wavelength region of peak solar irradiance on the Earth's surface. The full width at half maximum range for sunlight is about 300-900 nm.
As noted in the answers to "What is the biological potential for vision of wavelengths outside the human visual range?", shorter wavelengths tend to destroy biological structures and longer wavelength photons don't have enough energy to be easily detected individually.
The human eye doesn't "respond to harmonic frequencies" because it it detects light via quantum processes, which are not the same as the classical resonances such as a vibrating string. Just because a molecule absorbs photons of a given frequency, doesn't mean it will absorb photons of twice that frequency.
Another issue is that if you double the frequency of light, you double its photon energy, which for visible light takes into dangerous wavelengths.
Even for creatures whose eyes work into the ultraviolet, their range doesn't go much below 300 nm, which is not surprising since 300 nm (4 eV) photons can break carbon bonds and 250 nm (4.5 eV) photons can break C-H bonds.
Interestingly, however, the eye has been observed to respond to sub-harmonic frequencies. Intense infra-red light can be seen as green, because two infra-red photons can activate the rhodopsin receptor that normally is activated by a single green photon.  This requires very bright infra-red light since such two-photon processes happen rarely.


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Should I scare the swan to help him survive?
There's a young swan in my local park. He is young and I don't see his parents around. The young swan isn't affraid of humans and one can easily feed him from one's hand, and even pet on his head.
But I think that the swan has too much faith in humanity, and someone evil (or an excited toddler) can easily hurt the swan.
Should I try to spook the swan without hitting him? This way he will learn to avoid humans.
Am I wrong, and this would be bad for the swan? Or maybe this is a non-issue, and I'm just overthinking?
I googled relevant questions, but I only get answers "how to train bird to trust you" etc.

The way I see it, if you were to try to "spook" the swan (which, for the record, I don't recommend), you would be one person trying to teach it one lesson ("Don't mess with humans, we're dangerous!") while the vast majority of the humans it interacts with would be implicitly teaching it the exact opposite. Which do you think would be the lesson that sticks? Scaring it also has the potential of stimulating it to act defensively or aggressively towards the next human it encounters, which could end badly. I suggest engaging your local wildlife protection authority and getting them involved.

+1 for your care and concern.
No
It is likely to hurt both the swan and the humans interacting with the swan. From The role of animals in education:

Animals are increasingly being incorporated into the American school
setting to help teach students important behavioral and academic
lessons (Chung 1994; Dalton 1999; Mallon 1992; Pavia 1997). In a 1998
study, Beck and Rud surveyed 1,999 elementary school teachers
throughout the State of Indiana about the presence of animals in their
classrooms. The results indicated that 20 to 25 percent of the
teachers surveyed incorporate some type of animal in their classrooms.
Researchers have found that interacting with animals can help people
in numerous ways. Levinson (1962) was the first to formally theorize
that a dog could serve as a transitional object or "bridge" with which
an individual could form a nonthreatening relationship, which could
later expand to include other humans. Beck and Katcher (1983) found
that interacting with animals almost always has positive influences on
children. Mallon (1992) suggested that animals play a role in
socializing and humanizing children. Many researchers and writers have
noted the value of utilizing animals as mediators to help people who
are not being reached by other methods (Corson, Corson, and Gwynne
1975; Johnson 1983; McCullough 1982).
Some reasons that interventions involving animals produce results when
other methods fail include issues of trust, nurturance, social
perception bias, physiological response, resistance to treatment,
nonverbal communication, identity, control, and touch.
Trust. Many researchers, including Levinson (1965) and Ruth (1992),
have observed that children who are not comfortable interacting with
other humans often do not feel the same inhibition with animals. As
Levinson (1969) stated, when interacting with an animal, a child can
assume the role of teacher, parent, or anything else without fear of
rejection. Gonski (1985) postulated that animals provide a safe means
for children to begin to trust nonjudgmental beings, before trusting
humans. Whatever the reason, some children find interactions with
animals less stressful than those with humans (Brickel 1982: Levinson
1965; Robin et al. 1984; Ruth 1992). Many claim the reason is that
animals provide unconditional acceptance and love, without the
criticism that so often accompanies human interactions (Beck and
Katcher 1983; Levinson 1969; Siegel 1962).

Further reading:

Treating Human Trauma with the Help of Animals: Trauma Informed Intervention for Child Maltreatment and Adult Post-Traumatic Stress
Research in the use of animals as a treatment for humans

There is also the ethical question of betraying an animal that trusts you.

This answer is about the utility to humans of interacting with animals, which isn't the question being asked. OP is asking about somehow trying to teach the swan to "act wild" again, to not be trusting of humans and keep its distance.

Fascinating, well researched and sadly, not what the question asked. Unless you're suggesting that the local school should be contacted as potential candidates to adopt the bird.... Maybe, but swans are not small nor quiet (and they seldom do their homework).


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Fibrosis vs stenosis vs sclerosis
I can't figure out the key distinguishing factors between these three and I keep seeing them being used almost interchangeably.
For example aortic valve fibrosis and aortic valve stenosis.
As much as I have understood:

Fibrosis is related to muscle tissue and myofibrils
Stenosis is the result of fibrosis, because muscle tissue loses the ability to expand
Sclerosis is the thickening of the tissue

What are the distinguishing notes between them?
update
One example is this YouTube video from Ninja Nerds.

As you may know, on this site, prior research is required by the OP. It would be more helpful if you actually cited sources for the definitions of fibrosis, stenosis and sclerosis, e.g. "this site defines fibrosis as...", etc. By those means, you're much more likely to get an answer. Thanks.

@anongoodnurse thank you so much. The question is updated.

To begin, look up the three terms in Wiktionary, which actually has a decent set of etymological connections for the words.  You'll see fibrosis is about [typically collagen] fibers, stenosis is about narrowing, and sclerosis is about hardening.  Of course, in any specific context these meanings don't get you that far by themselves - multiple sclerosis is about a lot more than hardening per se.

You already answered yourself the question: these three words are here to designate different phases of a general process. This general process is triggered by the appearance of fibrosis, which is an alteration of a "normal" cicatrization process.
What happened -simplified way- is:
When a part of the body is attacked, a repair process is triggered. Stem cells activated and duplicate to replace the destroyed part of the body. But the process is not entirely "one for one":

For genetic gene alteration reasons, some stem cells will not function
Because the signal that triggers reparation could use various paths, some paths will push stem cells into differenciation, thus the end organ will have less stem cells that at the beginning
For some reasons I don't understand to explain them, some tissues of the organ will expand faster than others. If parenchymal tissue is less expanded than connective tissue during the reparation phase, the overall new "material" (=a mix of the different types of tissues) in the destroyed part of the organ will be "dead tissue"

These three causes and their immediate consequence are called fibrosis.
Because of the third point, there is stenosis in the dead tissue: it cannot expand anymore.
Because the dead tissue is attacked again and again, it will be reduced and could not be replaced: this is sclerosis.


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Chloroquinaldol and fresh peppers tasters and non-tasters?
Chloroquinaldol is an over-the-counter antiseptic drug sold under many names, often in the form of lozenges for mouth infections.
I absolutely hate its taste. The unpleasant sensation is unlike any other bad taste - it feels metallic, "chemical" (like the smell of the storeroom behind the chemistry lab at school) and sends shivers down my spine like bitter taste does - but it is not bitter taste.
To most people Chloroqinaldin is just a sweet lozenge, but I have met a few people who describe the same reaction to the drug.
Interestingly, the same people (me included) also describe a similar reaction to fresh bell peppers, equally puzzling to "non-tasters". Thermal processing as well as pickling removes the awful taste, so this specific aversion is distinct from simply not liking bell peppers in any form. In fact I love grilled stuffed peppers my dad makes, and I would probably be emptying jars of pickled peppers while sleepwalking if I sleepwalked ;)
Is this a known phenomenon? Could it be similar to how PTC can be tasted by most but not all people, except here the tasters seem to be a minority?


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Do monoecious plants have bisexual flowers?
I used to think that monoecious plants have male (unisexual) flowers and female (unisexual) flowers on the same plant but on different locations. But recently I learnt that monoecious plants also have bisexual flowers,  which means the male part and the female part in the same flower.
Thus, I am confused. Can someone clarify?

Welcome to Biology StackExchange. Please, read some basics about the terminology (for example Wikipedia page on plant reproductive morhpology), then let us know if you still have any misunderstandings by editing your question.

You are correct that monoecious describes plants where the male and female structures (cones or flowers) are on the same plant but in separate locations. Plants that produce hermaphrodite flowers together with either female or male flowers, are termed gynomonoecious or andromonoecious, respectively. A plant with separate male, female, and hermaphrodite flowers is trimonoecious.
Monoecy is not to be confused with monoicy. In monoicy, both gametes, sperm and egg, are produced by the gametophyte (e.g., some plants with gametophyte-dominant life cycles [bryophytes]).

Monoecious plants have both female and male flowers in the same plant. They can be male flowers, female flowers or a mixture of the two in the same plant.

You repeated what the questioner wrote and even left out some detail they established. You should provide better detail, maybe break down what word monoecious means or provide explanation of the other types of reproduction in plant to make the point of a monecious plant more clear.


text:
model organism for maize
Since I am trying to find the functions of some transcription factors of the maize,  I would like to try a search on the model organism transcription factor databases.  Which model organism would anybody suggest?
Edit:
Sorry for the incomplete information provided.  Since a transcription factor database could provide the experimentally verified information about the model organism, some transcription factors of the maize have one defined function, e.g. matters about flowering and I would like to know the transcription binding in the model organism in order to clarify the function of these transcription factors.  As a result, I could connect these functions dot to dot instead of carrying out the actual experiments.
The model organism provided in the ans. helps me limit the further searches and helps me use the right algorithm to relate the transcription binding of different plants, e.g.  I could relate the transcription factor of flowering in maize to the similar motif in model plant (organism).

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Why not maize itself? (And other grasses)
If for some reason you need something that is more explicitly a model organism, I suppose you could look at Arabidopsis. That link actually includes a large number of plants, but Arabidopsis is almost certainly the best described.
But the maize data itself should be quite good (as well as containing orthologs from other Graminaceae.


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Advantages of NADP+ dependent Isocitrate Dehydrogenase
I came across a question (Q-5b) that asks:

Isocitrate Dehydrogenase in the [human] TCA cycle is associated with NAD+.
Why does it make good metabolic sense that it should use NADP+? Explain and show why this is so using appropriate structures and reactions.

This interesting paper argues the evolution of NADP-dependent IDH in prokaryotes as an adaptation to the need for growth in acetate. In the case of glucose growth, NADH can be obtained from the oxidative branch of the pentose phosphate pathway; in contrast, for acetate growth, PPP cannot run efficiently and IDH provides the predominant share of NADH. However, this ought to be a really irrelevant reason concerning IDH enzyme in humans since we do not have enzymes like isocitrate lyase etc. to entertain acetate growth!
Standard textbooks in biochemistry (Voet&Voet, Lehninger, et al) do not offer anything relevant except a generic note that NAD+ and NADP+ are respectively favored for oxidative and reductive metabolism. I am unsure about reasoning using this bit of trivia since TCA is an oxidative pathway! Fwiw, a question had been asked in Biology StackE about NADH vs NADPH where the accepted answer restates this.
To conclude, what is the metabolic advantage? Does there exist a way to arrive at the advantage using the fundamentals of biochemistry?

I find the question most ambiguous. The context is presumably human, given the preamble in the exam paper. The first sentence says that ICDH "is associated with" (presumably he means "is specific for") NAD+. The second sentence talks about it making metabolic sense to use NADP+. But it doesn't — only in the cytoplasmic form mutated in tumours, which is not involved in the TCA cycle. I can give an answer to a question on the use of NAD v. NADP in mitochondrion and cytoplasm, but I can't answer a question that appears self-contradictory. How do you understand it? Seems like a typo to me.

Mitochondria also contain an NADP-specific isocitrate dehydrogenase which probably plays no role in the TCA cycle (but not everyone agrees!). See here, for example, one of several seminal papers on this enzyme from the Roberta F Colman group

And, of course, there is also a cytoplasmic NADP-linked isocitrate dehydrogenase. See here, for example

For an interesting take on why there are two pyridine nucleotide cofactors (ie NAD and NADP), see Why NADP? by BT Kaufman, who postulates that " blocking the 2'-position of NAD with a phosphate group, thus yielding NADP, shields a potential pool of pyridine nucleotide cofactor from the drastic effects of ribosylation reactions"


text:
Calvin cycle question
Why does the 6-carbon molecule produced when Rubisco attaches a Co2 onto RUBP split into 2, 3 carbon molecules? Is it because its unstable or is there another reason?

Welcome to SE Biology. It is important that new users learn how this site works. First, finish the [Tour]. We know you haven't because you don't have the badge, and it can appear discourteous when posters don't do so. Second read the Help on asking questions where you will see that you should do research before posting. This includes searching the site to see if the question has already been answered, which yours has.

Does this answer your question? Why the C6 intermediate molecule in the Calvin cycle is so unstable


text:
In this representation of the tree of life, what are the lateral connections?

I found this simple representation of the tree of life in a wikipedia article, and I was curious what these horizontal connections shown here are supposed to be, like the ones between plants and protists, or bacteria and protists going to plants. Do they represent things like lateral gene transfer or potential endosymbiotic origin relationships? (like the theory that eucaryotes came from a merging of a bacteria with an archae).

they likely represent the inclusion of mitochondria and chloroplasts into eukaryotic cells.

thanks john, that makes sense :)

Yes, pretty much! Lateral branches here indicate endosymbiotic events and major horizontal gene transfers.
I'd warn though that the diagram is not very accurate, and additions I'd make would complicate it further as a bush (rather than a tree). Each branch root itself is an instance of cladogenesis, and for this reason the diagram is not very accurate (e.g. fungi and metazoans seem to arise within the same "branch"), and also misses a few lateral branches that otherwise exist. My favorite example of atypical horizontal gene transfer is that of prokaryote-insect transfers which occur frequently. This has been known for some time; many insects contain genes of Wolbachia origin and some (not all) are definitively functional, and are understood to facilitate obligate (fully-dependent) mutualisms.

Thank you so much for your detailed answer! Very interesting stuff. You mind if I bother you for a recommendation for a book reference on this topic? I've been reading "Assembling the tree of life" which I'm really enjoying, but I was curious if there was a newer reference (the book is from the early 2000s), that is as large in scope as this one, since from what I've heard phylogenetics has grown quite a lot with computational models in the last 20 years.

Unfortunately I don't think I am familiar with the most recent literature on the most comprehensive phylogeny of all life available. Perhaps you could take a look at the Tree of Life Explorer OneZoom, maintained for years and most recently a publication with plenty of explanations was made about it in 2021. You're right, we still catalogue new species and next-gen sequencing and related tools are helping resolve a lot of phylogenenies quickly. To compile all this is a mammoth task, and is of course ever-ongoing.


text:
What are the priorities of blood group that a person with AB group can recieve?
Suppose a person has a blood group of AB. I read somewhere that it is best to transfuse blood of type AB into that person, as opposed to groups A, B, or O. If AB is not available, however, it might be better to use types A or B than O. Why is that?

Blood groups are nothing but the classification of Red Blood Cells based on what particular molecules they have on their surfaces. A person with an A blood group has an A antigen (think of it as a protein) on the surfaces of their blood cells, while a person with a B blood group has a B antigen. People with AB have both the antigens, and people with O have none. The immune system produces certain antibodies that helps protect the body against foreign invaders. An antibody is a substance that helps kill foreign antigens. An antibody in a healthy individual will not attack the body's native cells. Thus, people with an A blood group only have anti-B antibodies, and vice versa. O people have both the antibodies and AB people have none.

This means that if a type A person receives type B blood, the newly introduced blood cells will be destroyed, due to the presence of anti-B antigens. Similarly a person with O cannot receive AB blood due to the presence of both antibodies in their plasma. However, AB people can receive any blood type, since they have no antibodies in their plasma. O people can donate to anyone, since they have no antigens in their RBC, but they can only receive donations from other O people.

This is why people with an O blood group are known as universal donors and people with an AB blood group are known as universal receivers.
A similar effect occurs with the Rhesus Blood Groups (+ve and -ve), where Rh+ people can receive either type, but Rh- people can only receive Rh- blood. Thus, Rh- can donate to either type, and Rh+ can receive either type. This means that O- can donate to any blood type, and AB+ can receive any blood type.
In terms of your question, suppose that a person with blood type AB needs to receive a blood transfusion. As explained above, a person with AB can only receive blood of type AB. This is why it's the "highest priority" to use blood of type AB. Although not medically recommended, A or B type blood has a better chance of compatibility with the receiver than type O, since type O has both the antibodies while type A or B only have one. Thus, the AB has the "highest priority" with type A or B having more "priority" than type O.
Hope this answer made things clear. Cheers!

Well illustrated answer - I think what the OP meant with 'priority' can be explained in the following scenario: Let's say you have a certain amount of 500 ml blood of each of the four types, the types should be prioriticed according to the blood type distribution of that country and the donor/receiver ratio - a simple mathematical formular based on availability and the blood type distribution of possible receivers in need. But that's just my assumption..

I read the question, and I think I understand what the OP meant. Suppose a person has a blood group of AB. When transfusing blood to that individual, it is best to use blood of type AB. If AB is not available, A or B might be better to use than O. I don't think it's recommended to use anything other than AB though. Perhaps it's worth a try if the condition is critical and no AB blood is available.


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How are correlations between genes and observed traits made?
If a given organism has a certain characteristic (a chemical that's produced, a place an organ or organelle is in, a particular behavior), what's the general procedure for correlating that characteristic to a particular gene?
As I understand it, there are two main ways of doing, the first being to take a sample from two populations that do and do not have the characteristic respectively, then find the genetic correlation between the two populations. The second way I've heard of is by inserting or removing a particular gene and then observing the organism after it has grown, either inserting some marker gene (fluorescence is a popular one) or removing a gene believed to be responsible for the characteristic (something like leaf or petal pigmentation).
Are these the only effective ways of forming these correlations? What sorts of correlations could be made in silico? If two different species create the same chemical, and you know the gene responsible for that chemical's creation in the first species, would you be able to somehow infer which gene is responsible in the second species? What happens if you don't have a population without the given characteristic you want to correlate?

Have a search for the terms gene and homology; that'll get you started on most of an answer.

Ah thanks! I figure the subject is a pretty common question, but I couldn't get the right keywords for what I was looking for.

I have edited your title, despite voting to close the question, because what you are asking is the correlation is between a gene and a trait, not genetics and trait. Genetics is the overall study of this topic, and the methods of making such correlations have varied historically with the development of scientific methodology and knowledge, and differs between organisms. Your question is therefore impossibly broad for this site, and what you need to do is read a book on — yes — genetics.

Ok do you have a recommendation?

I recommend looking into genome-wide association studies, genetic mapping, etc.