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How does the brain alter/inhibit muscle reflexes?
I can find lots of information on how stretch-reflexes/reciprocal-inhibition/autogenic-inhibition work but from them all it's unclear how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?
Can it alter the weighting of inhibition in antagonistic muscles?  As well as 'set the length' for a stretch reflex to target?  Or does it somehow control both 'with one value'.  Where and how exactly does it interject into the feedback loops?
I am trying to understand it more from a programmers pseudocode or equation point of view rather then get lost in meandering biological terms I have seen everywhere that gloss over this point.

how exactly the brain interfaces/controls/disables such automatic muscle reflexes when it needs to?

A: At multiple places within a hierarchical system:
In a  simplified way, the Motor cortex is the executor of movement via projections to the brain stem and spinal cord, this is accomplished via excitatory signals to a muscle, the agonist, and inhibitory signals to the antagonist, so in one sense, spinal interneurons would be the answer, since they interface with the motor cortex and alpha motor neurons at the muscle site.
There are also feedback loops all over the motor hierarchy, premotor and supplementary motor cortex regions for instance help plan the movement direction, we don't seem to code a target in the strict sense, but rather a movement direction and then correct via sensory feedback.
The cerebellum projects to premotor, motor cortex and the brainstem, and receives projections from premotor areas, it is involved in stopping and timing movement,the brakes for action if you will.
The circuitry of the Basal Ganglia  which loops with premotor and projects to the motor provides the go, no go and graded modulation via inhibition to the motor cortex, which in turn affect less spinal interneurons, so in another sense this circuitry would be responsible.

Can it alter the weighting of inhibition in antagonistic muscles?

Yes, via spinal interneurons (Henshaw cells, Ia inhibitory interneurons and Ib inhibitory interneurons)

As well as 'set the length' for a stretch reflex to target?

Yes, via a the motor,basal ganglia,cerebellum motor hierarchy, although as mentioned, there is no target but rather a direction vector and feedback that tells you when to stop the movement, i.e. you reached your target. ( Higher cognitive areas do seem to have a representation of the target though).

Or does it somehow control both 'with one value'.

Depends on the interneuron, but basically they serve as information relays ( they also convey sensory information )

Where and how exactly does it interject into the feedback loops?

As mentioned there are multiple feedback loops, the brain is not a unit, but a system and as such I would rephrase the question as which subsystems, brain regions, neuronal tracts and neurons create feedback loops in the motor system.

I am trying to understand it more from a programmers pseudocode

I am a software developer myself, so let me try switching hats, this is one scheme:
If all you want is to control agonist/antagonists, tie up 2 or more variables together such that when one goes up, the other goes down, and presumably change 2 effectors ( virtual or real ) and their position relative to each other,
If you want specific control, you would then need to send 2 channels of information and modulate both variables, if you just send one to either one, the other will respond based on the above configuration.

Thank you so much for your helpful insight.  So I think a basic simulation model might best have a ‘brain’ supplying 3 parameters per muscle: a target length (or angle), an error correction rate, and a reciprocal inhibition weight - assuming every muscle is antagonistically paired.  All error corrections could be computed first, then brain weighted reciprocal inhibition could happen between antagonistic pairs using something probably a little more complex then a straight inverse linear modulation - I guess partially due to muscle strength varying depending on length.


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DRAQ5 and PI incompatible?
I'm interested to analyse hemolymph cells from a marine mollusc. I wanna count only "alive" cells so my strategy was the following: DRAQ5+ (nucleated cells) and PI- (alive cells) and identify population in FSC vs SSC.
Staining independently with DRAQ5 and PI I found positive and negative populations for each one but, in the fully staining I lost DRAQ5+/PI+ population... (https://ibb.co/VpgcCTN)
Does anyone know if DRAQ5 and PI are incompatible?
Note:

DRAQ5: excitation with 640nm and emission filter 675/25.
PI: excitation with 488nm and emission filter 585/40

Rieger et al. 2010 seems to be relevant. -- "Gating on the population of PI+/DRAQ5+ cells, we used the similarity feature to determine the degree of similarity between PI and DRAQ5 stains in goldfish primary kidney macrophages (Fig. 3A). We found that there was a sizable proportion of falsely stained PI positive in these cells, as well as in all unfixed primary cells and cell lines tested (Fig. 3B)."

For my proposal, I prefer to have more false-positive than false-negative cases. The problem here is that I don't have double staining as you can see here. Independently, I have DRAQ5+ and DRAQ5- populations, the same happens with PI, I saw PI+ and PI- populations. But, adding both stains together I lost DRAQ5+/PI+ population...

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DNA genetic testing from dried sweat crystals?
My sons' dad died and I wanted to do any sort of genetic testing possible, as a gift to my sons.  The only item available is dried, crystallized sweat from the bridge of his Oakleys, sadly.  Would there be any significance found in such results?  And, who does this sort of testing?  Thank you.   JK

He wore these sunglasses while bicycling, intensively, 14 miles or so in one trip, mixed terrain, so I'm thinking the sweat residue may have a high concentration of his cells.

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Is there a biological urge to have children in women?
Searching information about this subject often leads to personal stories from women making the choice to live childfree and women stating they either always wanted to have children or experienced a sudden 'baby fever'. Often this baby fever is understood to be a biological urge.
In this article a link between hormones and the need for own offspring is made a couple of times, but also contradicted.

In  the  context  of  evolutionary adaptedness, all women were exposed
  to babies and infants, and the ‘default’ setting for the female  body
  is  to  have  experienced  both nurturing  and  pregnancies  by  the
  early  twenties. Rotkirch therefore suggests that longing for a baby
  develops out of hormonal changes evolved to prepare women for
  motherhood. These might be triggered by falling in love; the ‘nesting’
  behaviour associated with settling down; exposure to infants or the
  aging process. Conversely, however, Kravdal has found evidence in
  Norway of a demographically significant cohort for whom reproduction
  and finding a long-term partner and ‘settling’ down’ are quite
  exclusive (Kravdal 1997).

In the same article, the effects of hormones on human intercourse and attractiveness between men and women is briefly explained. However, to me it seems that the urge to have sex is something different from the urge to have babies or to become a parent. I would like to know if there are hormones or other biological changes in women that cause something like 'baby fever' or if it is rather more of a more psychological or social environment phenomenon.
Other relevant articles are often not accessible to me or prove too difficult to understand with basic biology knowledge.

Interesting though this question is, do you really think you will obtain a definitive answer? What would that be? That it has been shown by experiments on a large statistical sample of human subjects that injecting a cocktail of defined compounds leads their having more children than a control group injected with a placebo? I think you are left with individual anecdote or subjective opinion.

I was not thinking along the lines of a individual anecdote, those are easy to find anywhere. I was hoping there perhaps might be a study that shows something along the lines of increased hormones when women are subjected to children, other women having children or simply aging. Or a test that shows brain activity when testsubjects are exposed to images relevant to nurturing a child. Testing whether that happens seems doable to me.

Also, a definite 'No, this has not been proven and/or is impossible to research on a large scale because A and B' would be an answer that would clarify things.

The biological urge to find a mate means that an innate desire for children is unnecessary. Having sex with a partner pretty much guaranteed children before contraception was available.
It's hard to imagine why an urge to have children would exist, but that's not the same as saying it doesn't -- but I also can't imagine how you'd be able to pull apart biological vs social pressures in such a complex and core part of being human.

This is an argument but not an answer backed by facts in terms of SE Biology. "is unnecessary", "It's hard to imagine". The simple reason is that it is not really a question that it is suitable for SE Biology and therefore one that one is advised not to answer in the help.

Fair enough, would this have been appropriate as a comment?

— yes I think so.

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Did the first cell self-replicate or was it multiple first cells?
We're almost sure by now that the first cell was born in a some kind of underwater vents environment which harvested all the necessary conditions for it to exist.
However, did the first cell self-replicate to have other cells or did the same process lead to the birth of others as well? If the latter is true, doesn't this make the evolution of cells more common once the primitive conditions exist?

Your question implies that the first life form (however you want to define that) had a cellular shape, but this is not necessarily the case: you can have i.e. self-replicating RNAs that don't need any form of 'cell' and could represent some sort of precursor stadium to cellular lifeforms in general

Welcome to Biology.SE! This is an interesting area to speculate about, but due to the paucity of evidence there is no consensus about the origins of life. As a result your question is probably beyond the scope of this site. ——— To learn more you may wish to check out the help pages starting with [Ask] questions effectively on this site. Thanks!

Good question. Simple answer here: we have absolutely no idea.
I would hazard a guess to say that the first proto-cell probably did not have the ability to replicate, so there must have been many proto-cells prior to the occurrence of the first true cell with the property to replicate itself with some degree of fidelity. Whether or not at some point cells existed that could be traced to two or more independent abiotic generations, that is unknown. The likelihood of this event is all we can talk about. I defer to biochemists working on this (still very open) problem, but I think it is honest to mention that they too have no idea, really. This is because, as we can surely appreciate, likelihood and outcome are two entirely different things. And unlikely events happen all the time. Each life form and individual is astonishingly unlikely, but historical contingency so happens to have brought us all here despite the odds.

"The likelihood of life occurring by chance is fantastically improbable". Everything indicates that life shouldn't exist and yet here we are. Plus, everything is connected too; if a single link was missing, we wouldn't be here. It will always blow my mind. I'll give time for other answers to be fair. Thank you!!

@Odin You are mistaken by saying "Everything indicates that life shouldn't exist and yet here we are." . The probability of life forming is unfathomably low but the sample space is unfathomably large. With sufficient time and sufficient chemical reactions, it becomes a statistical inevitability for a molecule like RNA to form. The period of almost a billion years between the formation of the earth (4.5 Ga) and the emergence of life (ca. 3.7 Ga), along with the inordinate number of molecules in the primordial soup outweighed the miniscule probability of life emerging

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Properties of berries that are not shared by strawberries
What are examples of properties that (all) berries (from a botanical point of view) have and that strawberries do not have? This does not need to be the exact reason, why strawberries are not counted as berries. I'm more looking for properties that emphasize the difference.
Since I'm not a biologist, I'd be happy about simple examples. Thanks a lot!

Did you check out wikipedia on berry?

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!

Botanically a berry is something quite different from what is commonly termed a berry in English.
From that Wikipedia page:

a berry is a fleshy fruit without a stone produced from a single flower containing one ovary

...

Berries so defined include grapes, currants, and tomatoes, as well as cucumbers, eggplants (aubergines) and bananas

On the other hand, many things called "berries" (including strawberries) are actually aggregate fruits, which are

a fruit that develops from the merger of several ovaries that were separate in a single flower

Therefore, the botanical difference is the originating tissue of the fruit: a single flower/one ovary, versus a collection of ovaries grouped together.
These botanical groupings don't have much relevance to practical use (i.e., cooking/nutrition) and there aren't other properties that are definitive for what a berry is and is not. For that reason, there is nothing wrong with referring to strawberries, raspberries, etc, as "berries" in cooking: berry simply has different meaning in botany and culinary fields, just like the many culinary "vegetables" that are botanically "fruits."


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Age until physical growth ceases, mammals
Fairly basic, but I am seeking a table showing how many years from birth it takes for the best-known mammals to stop growing.  (Including the latest on humans - ie. 0-17..?).

Welcome to Biology.SE!  This is a very broad question and it isn't clear what you mean by "best-known" mammals. The answer is also going to depend on environmental factors (e.g. nutrition) and what parts of the body you consider — consequently even an answer limited to humans is going to be difficult and probably not definitive. ——— Please take the time to go through the [tour] and then the help pages starting with [ask] questions effectively on this site. Thanks!

You might need to construct the table to match the conditions & assumptions you need.

I only meant what you could call gross height in humans, say.  Ie, total height!  The same for other mammals, ie, top of head from the ground.  Other hominids, apes, chimps...  Elephants ..?  Nothing too esoteric, perhaps 30 or so examples, preferably closest to humans, whether taking longer or shorter periods to fully grow than we do.


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Why do some texts say that noncompetitive antagonist dose no change in ED50 of agonist in Dose-respond curve?
Competitive antagonists increase the ED50 while the Emax remains the same. Non-competitive antagonists do not change the ED50 while decreases the Emax.
I wonder how does this happen as Non-competitive has no effect on ED50.


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Is variation a result of Evolution?
We know that the DNA copying mechanism that replicates DNA during cellular division is not 100% accurate and the resultant errors are the source of variation in the members of a population.
At the same time, we are also aware of the benefits of variation - how it is useful in ensuring the survival of a species over time and leading to evolution.

I would however like to know if 100% accurate DNA replication is possible (even if hypothetically) - because in my opinion, organisms can surely survive (atleast individually) without variation or evolution.
If it is so, is it possible that organisms with 100% accurate DNA replication did exist, but eventually their populations died out (due to natural selection) and we were left only with organisms that showed variation?

Putting in simpler terms, it is possible that evolution itself is the cause of variation that now causes further evolution?

Related: https://biology.stackexchange.com/questions/378/has-there-been-any-observation-of-species-adapting-the-evolution-process

For your question about whether 100% accurate replication is possible, think carefully about multicellular organisms. Any evolutionary benefit to mutation would have to be in the germ cells. For non-germ cells, you (in most cases) want as little variation as possible since that variation will never been heritable.

There are many kinds of DNA replication errors that lead to mutations some of them could be 100% error free some are inherently not possible.

Hypothetical questions of this sort — in this case flying a kite rather than posing a question that can be answered objectively — are off topic here.

@David I would like you to elaborate.

@Cell Thanks for the response. I am interested in knowing more about the same.

@BryanKrause I totally agree. How does that but explain my doubt.

@MrigankPawagi I'm trying to steer you towards a more answerable, non-hypothetical question. If 100% error free replication is possible, we'd have something like it in somatic cells. If allowing errors in germ cells is beneficial, we'd expect higher error rates in germ cells.

If you go to the Tour, you will read: "Focus on questions about an actual problem you have faced. Include details about what you have tried and exactly what you are trying to do. Ask about... general questions about biological concepts, questions about the biological mechanisms behind medical conditions, questions about techniques in a biological or biochemical laboratory". And "Not all questions work well in our format. Avoid questions that are primarily opinion-based, or that are likely to generate discussion rather than answers."

Another piece of advice in regard to posting questions is to do some research on the topic first. I suggest you read about Errors in Replication in this Scitable article. Here you will read "Fortunately, cells have evolved highly sophisticated means of fixing most, but not all, of those mistakes." Think about it.

error free replication would only be helpful if a species was perfectly adapted for its environment AND its environment never changed. because environments change constantly it would never be an advantage.

You're asking if cells arose with 100% replication accuracy and if lower accuracy was selected for under a feedback loop. Maybe there was a sweet spot for DNA replication accuracy in terms of efficiency, but it's highly unlikely that our ancestor cells had 100% fidelity in DNA replication because if we look at yeast for example, there are many genes dedicated to different types of post-replication repair including mismatch repair, base excision repair, and translesion synthesis. All of these can lead to mutations if they aren't working properly and some (translesion synthesis) inherently generate mutations. It doesn't seem consistent for a cell to develop all of these sophisticated post-replication repair systems to protect itself from DNA damage and then to give some more leeway to DNA replication because it was just too accurate.
Also there are papers like this that talk about how E. coli have increase mutation rates under stress. But if your hypothesis was true, then E. coli would ideally have 100% replication fidelity under normal conditions and lower it when stressed, or they would just have a higher baseline mutation frequency all the time. But, neither of these is observed. What makes the most sense when all this information is put together is that cells try to have as high DNA replication fidelity as possible under ideal conditions.
As per your other question, maybe it's possible to have a 100% accurate DNA polymerase  NEB engineers high fidelity polymerases for lab use maybe someday it can reach 0 errors. But there are other sources of mutations like the spontaneous deamination of cytosine that can generate mutations during replication, but that depends on the chemical properties of cytosine so it's not really fixable unless you use different nucleobases.
Reference:
Mutation as a Stress Response and the Regulation of Evolvability. (2012)
By: Rodrigo S. Galhardo, P. J. Hastings, and Susan M. Rosenberg

Great answer. I have read about E. Coli and I am totally convinced with your point about the post-replication repair in yeast.

There is previous research for that field of macroevolution.... Horse shoe crabs change slowly and tropical fish change fast.
You are right, it's not just random variation, it's fine tuned by DNA transcription processes which are too developed to be random, so the complexity of the processes leads scientists to think "WTF" regarding epigenetics, transgenerational phenotypic plasticity, paramutation, genetic drift, DNA mutation types, Specifically: "no systematic cross species studies of variation have been conducted (most focus on model organisms)", because the topic is so intense.
You don't have to change the DNA code of alleles to go from a chimpanzee to a human, most of the changes come from pre-existing genes that are varied to produce different results.
The texts for macroevolution fine-tuning of variability talk about: variability, gene flow, constriction, epigenetics, of traits of adaptive significance, of DNA mutations, their mathematical measurement... it can be summarized by this statement:
" variability has been a dilemma of evolutionary biology. Considering the pattern of increased genetic variation associated with environmental clines and heterogeneous environments, selection in heterogeneous environments has been proposed to facilitate the maintenance of genetic variation. No comprehensive models have been developed, likely due to the genetic and environmental complexity of this issue. " ref
Many books are devoted to the subject, so there is lots to read through, and there are mutation-control systems that fine tune variability, so it gets complex:
"... Epigenetic modifications, such as; DNA methylation, together with covalent modification of histones, are thought to alter chromatin density and accessibility of the DNA to cellular machinery, thereby modulating the transcriptional potential of the underlying DNA sequence" ref
There are genetic switches, which vary which DNA sequences are expressed by different species... Humans and chimps are 98% the same, and genetic switches can change the species selectively without having to change the DNA itself... "regulates when and where genes are turned on and off and how much protein they produce. The regulatory machinery works when proteins called transcription factors bind to specific short sequences of DNA that flank the gene, called transcription factor binding sites, and by doing so, switch genes on and off." ref
sharks ahve less less variability than humans and 1.5 times bigger genome...
"The researchers found that the white shark genome contained a lot of genes responsible for maintaining genetic stability — things like DNA-repair genes and tumor-suppressing genes. And when the researchers compared the white shark's stability genes with analogous genes in other vertebrates, they found small changes in the gene sequence that suggest a specific pattern of evolutionary adaptation for these genes in white sharks."
Only a few epigenetic processes for transgenerational epigenetic inheritance have been discovered, which vary species traits independently of the DNA sequence, so we don't even know how they compare between animal families.

Interesting Answer indeed. I would suggest reading Cell's argument about yeast as well (on his answer)

In short, no evolution is not a result of variation. Evolution is a process in which each population in a system compete for a limited number of resources and each population has a fitness score (how well suited for the environment they are, this score is a man made concept to help illustrate the point), the populations with a higher fitness score tend to outcompete other species and so they are more likely to survive. This process occurs on a more individualistic level too, individuals in a population can be given a fitness score and individuals with a higher fitness score are more likely to survive and reproduce. Fitness scores are altered by mutations in individuals which may enhance/reduce the function of a certain behaviour/reaction that is required for survival. More advantageous mutations are inherited more often and so accrue within a population and thus over time the fitness score of a population increases too. Mutations are fairly random (they have a higher frequency at certain locations, but it is generally random) and they often occur due to the inherent instability of the bases present in nucleotides. These mutations thus result in the gradual changing of genomes throughout a population, leading to subsequent changes in phenotype - evolution.
With regards to whether an organism ever had 100% accurate copying mechanism, the answer is no again. It is not possible for an organism to achieve this level of fidelity to the nature of the bases used in organism. The DNA bases are inherently unstable due to tautomerisms, deaminations... they can also be altered by natural external factors such as UV radiation which base dimerisation as the electrons in the rings are excited and form new bonds. Although cells have repair mechanisms, these are not 100% efficient as tuatomersiation can occur when the base is in the active site of the polymerase, alternatively, the mutation may occur in a very crowded region in the nucleus, limiting the ability of repair machinery to encounter the DNA by diffusion. Finally, cells are often unable to recognise foreign DNA that has been integrated into their genomes, which will also cause mutations.
Although polymerases have and will continue to undergo extensive rounds of directed evolution it will be almost impossible to produce a polymerase with 100% fidelity unless the bases themselves are changed to being pretty much inert with a ridiculously high stability (remember there are millions/billions of bases in a cell so even if the mutation rate is low there will likely still be some mutations).
In response to Mrigank in the comments (my answer was too long for a comment :/) yeah pretty much  Now it may be possible that we can develop polymerases through directed evolution to have even higher fidelity (although this may be difficult as it could slow down the catalytic rate and then implementstion is alsonhard) and to improve the DNA repair pathways through directed evolution but the bases are inately unstable and there is always some chance of them converting through processes such as tautomerism. Additionally, b cells use a process called somatic hypermutation to actively mutate the DNA of b cell receptors/antibodies for affinity maturation in the dark zone so if we had a system that did not allow for variation there we may have a weakened immune system. Additionally, some repair pathways such as non homoogous end joining don't faithfully repair the DNA they just quickly repair double stranded breaks which can be lethal and this process can result in insertions and deletions. Then at the level of meiosis, since nobody has exactly the same genome and the child gets a chromosome from each parent variation is generated there. Things like viral integration, damage from external mutagens and free radical attack also occur which all lead to mutations. So I don't think it's possible for DNA polymerase to replicate DNA with 100% fidelity and I don't think it's possible in a looser sense for the DNA sequence to not change, hence variation is inevitable.

Thanks fo the direct Answer. So that means DNA can naturally never be replicated 100% accurately and hence variation is inevitable.

Please see the edited answer

Is variation a result of Evolution?

No, you're putting the cart before the horse & mistaking cause for effect.
Variation is the result of mutation (whether caused by copying errors, radiation or whatever).
Evolution is the result of variation.
Mutation > Variation > Evolution
Evolution is merely the winnowing process by which more beneficial variations (as in terms of fittest to survive in the existing environment, which includes competition from other variations) 'succeed' & less beneficial ones don't, it doesn't cause the variations.
Variation can happen without evolution but evolution can't happen without variation.


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what is the difference between osciloscope and electrocardiograph?
I am completely confused about these two devices! as far as I know, oscilloscope and electrocardiograph, both, show the heat waves(P, QRS, T) so what is the difference between their job?

I would say that electrocardiograph is a specific case of oscilloscope. The main difference, perhaps is that "oscilloscope" is a device for visualization on a display ("scope" from greek "look out"), whereas "electrocardiograph" is primarily used to record ("-graph" from greek "to write").
Oscilloscope is design to visualize an electrical signal, that changes in time (generally speaking). Nature of that signal is not important, it can be radio signal, electrical signal from some device (Arduino), or sensor (thermometer). You can detect earthquakes if you have particular sensor for vibration.
It is just that these devices should output signals of particular frequency, usually general laboratory oscilloscopes are designed to work with signals up to few MHz. If you attach sensor that "feels" muscle contraction, you will have a tool for electromyography.
Electrocardiograph, by definition, is a device that visualizes electrical signals acquired via electrocardiography. It is just that usually when people and doctors perform electrocardiography, they use specialized devices, not general-purpose oscilloscope. For example, cardiac signals are usually well below 0.5-1KHz, you can save a lot of money and complexity by not having to worry about higher frequencies in your device.


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what is the exact definition of entdothelial cell fenestrae?
In fact, I want to know that are fenestrae 1.holes which exist between cells or 2.they are holes in a cell( for example, a cell is like a paper we have punched it and the holes are called fenestrae). which one is true?

Fenestrae are basically holes within the cytoplasm of the squamous cell, that allow the transmission of macromolecules, therefore, according to the two options you've provided, your second example is the correct one.


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Are mutations a source of genetic variation?
Here is a question from the book SAT II Success Biology E/M (where the SAT is the exam taken by the American high school students):

Which of the following statements is true about mutations?
  (A) Rates
  tend to be very high in most populations.
  (B) generally lethal
  (C)
  irreversible
  (D) Only certain gene locations are affected.
  (E) source
  of genetic variation

In my opinion, we can definitely eliminate A, B, and D.
Then, I struggle between C and E since I think mutations are definitely a source of genetic variation but are as well generally irreversible (I've found evidence on different websites, including this http://hawaiireedlab.com/wpress/?p=154 where the author writes that only some mutations are reversible).
In the end, I think I should have probably gone with E because C can be seen as having some exceptions.
Then, here is the book explanation for this question:

The correct answer is (C). These recent conclusions about
  mutations—recall that Darwin did not know of mutations—are all the
  reverse of those listed in the choices, with the exception of choice
  (C), the correct answer. Rates, in fact, tend to be below in
  populations, mutations are generally not lethal, any gene location can
  be affected, and they are felt to be the source of genetic variation.
  Darwin felt over-production of offspring was the source of potential
  variation.

The answer is C here. However, I didn't particularly understand why E wasn't considered a correct answer.
Could you please explain why C, and not E, is correct?

The answer is clearly and unequivocally (E). Mutations introduce genetic variation. Period. As for (C), mutations are certainly reversible. If you can mutate a base to another base, you can mutate that base back to its original base. This is a simple fact of chemistry. Mutation is not an irreversible event. The answer should certainly be (E). The book is wrong!

Is the author of the book supporting so called inteligent design theory ("there is no evolution - only devolution")?

I think you need to take this book back to the bookstore and demand a refund. It's got two clear errors in it already.

@SPr They're almost irreversible in practice. It's just about the probabilities and concrete mechanisms involved. The observations we have suggest that mutations are strongly preserved throughout lineages. But that only highlights how ridiculous exams like the SAT are - you can't reduce such questions to choice answers. If you do that, the best you can do on the test is learn exactly what answers are expected on the test - not exactly something that makes you more educated :)

Going through the possible answers

(A) Rates tend to be very high in most populations.

This is a very unclear statement. What does "high" mean? In humans, the average mutation rate per reproduction per nucleotide is of the order of $10^{-8}$ (Rahbari et al., 2016) (hence of the order of 10 - 100 mutations for the whole genome). Whether someone wants to call that high or low is up to this person original intuition.

(B) generally lethal

No, that's wrong (Robert et al., 2018)

(C) irreversible

It is a little unclear. By "irreversible", do they mean that the function of the gene (or of any other functional element in the genome) cannot be restored or do they mean that a specific mutation cannot be exactly undone by a future mutation. In both cases, however, it would be wrong!
Mutations that restore the function of a gene (or any other genomic functional element) are called reverse mutations (aka. suppressor mutations; I personally don't know of any difference between the concepts of reverse mutation and suppressor mutation). Most reverse mutations are likely to act via a second mutation that restores the function of the gene rather than undoing the previous mutation. It does not mean however that it is impossible a mutation that perfectly undoes a previous mutation. Consider a substitution inverting A into T. A reverse mutation could do just the opposite.

(D) Only certain gene locations are affected.

Mutation rate varies throughout the genome but all of the genome is subject to some non-zero mutation rate.

(E) source of genetic variation

Yes, mutations are the ultimate source of genetic variation in populations, while genetic drift and directional selection removes variation.
As other users have highlighted in their answers, many mutations (incl. synonymous mutations but not only and soma mutations) do not bring up any the underlying genetic variance of phenotypic traits. These details are however mainly irrelevant; what matters is that it still remain true that (some) mutations increase genetic variance.
We could also add the complication as to wonder whether by "genetic variance", they meant "genetic variance underlying phenotypic variance" (which is its standard usage) or "genetic variance where one allele is given an arbitrary value and another (problem arising for loci with more than 2 alleles segregating). More information about the terminology and the math when it comes to quantifying genetic variance in the post Why is a heritability coefficient not an index of how “genetic” something is?
What I would have answered

The correct answer is (C). These recent conclusions about mutations—recall that Darwin did not know of mutations—are all the reverse of those listed in the choices, with the exception of choice (C), the correct answer. Rates, in fact, tend to be below in populations, mutations are generally not lethal, any gene location can be affected, and they are felt to be the source of genetic variation. Darwin felt over-production of offspring was the source of potential variation.

I disagree. To me, B and D are wrong, A is unclear, C is slightly unclear but wrong in both interpretations I can think of and E is correct. I would have answered E.
About the justification given

Rates, in fact, tend to be below in populations [..]

This piece of the sentence is not even grammatically correct. Below what? It highlights that A is unclear.

they are felt to be the source of genetic variation

The term "felt" is poorly chosen here IMO, but this piece of the sentence seems to rather give credit to answer E. I think, whoever wrote this answer mistakenly wrote C instead of E

Darwin felt over-production of offspring was the source of potential variation.

Really, who cares about Darwin thoughts on the subject here?! But in any case, this sounds like a misrepresentation of Darwin's ideas. More info can be found in Charlesworth and Charlesworth (2009) and also maybe this post

FYI, I think below is a typo for "be low". Also, I completely agree with this answer. Mutations are definitely reversible, and a source of genetic variation.

Agree about the clarity of these questions and answers, they are worded very poorly. And these are from standard US exam questions? Very concerning.

@ESR. The question is from SAT Bio exam prep book, not from exam itself.

unfortunately even the best prep books (and they do vary wildly in quality) are often written by people unfamiliar with the actual field of study, they often suffer  from being bulked out by copy pasted Q&A from other sources. Which ironically enough often suffer from distortion as they are edited over and over again.  Your prep books is just wrong.

IMO, E feels like an absolute statement, as if mutations were the only source of genetic variation.  I probably would have gone with C, arguing that E rules out homologous recombination

@Punintended The idea that recombination create genetic diversity is a common misconception (see for example this speech from Sally Otto or many of her early papers). Some people may mention migration as a source of genetic diversity but ultimately, it is still mutations who created this genetic diversity and migration just mix them up together (a bit like recombination do among different haplotypes). So, yes, it is a pretty absolute statement! Of course, by mutation, I mean any type of mutations (incl. large chromosome duplication for example).

@Remi.b That's fair.  I was also thinking about viral transposition, which results in a mutation if it chooses a site in the middle of a gene

It is true that recombination (viral transposition and some other concepts) are often causing agents of mutations.

I suspect that the question printed in the SAT Prep book contains a typo (or a deletion mutation).  If the answer to choice E. were to read “NOT a source of genetic variation” it clearly becomes the opposite of recent conclusions. Since some single nucleotide variants are clearly reversible under certain conditions (cf. Crick et al paper on the Nature of the genetic code published in the journal Nature ~ 1962) then the person who composed this question is not sufficiently familiar with the scientific literature.

Mutations are one of multiple reasons for genetic variation, hence phenotypic variation. By definition, mutations are alterations of genetic code and unpredictable changes in nucleotide sequences {in nucleic acids(level)}.
So yes, mutations are responsible for variation, but not all the time, and not all mutations actually result in variation. Silent mutations are neither harmful nor beneficial. They do not improve organisms by any means. On the other hand, nonsense mutations are readily harmful and can result in death.
Other sources of variation include:

Independent assortment of chromosomes (meiotic division), as per Mendel's first law of independent assortment.
crossing over of bivalents
environmental changes, which subsequently lead to beneficial mutations.

It depends. A mutation in somatic cells is not a source of genetic variation because they are not inherited by offspring. But mutations in the sex cells are a source of variation. Your answer key does not appear to be sure of the correct answer because it says the reverse of every answer but C is true of mutations but then agrees with answer E. Also unless part of the question is missing, what Darwin thought is not really relevant. Also, more offspring means more chances of offspring carrying a mutation.

Yes, the part about Darwin was confusing to me as well. The question or answer choices did not include any parts about his work, so I didn't particularly understand why his name appeared in the explanation...

That question was graded incorrectly.
(A) Rates tend to be very high in most populations.
That's a badly designed answer. What populations are they discussing? In lower-order life forms (viruses and bacteria for instance), mutations are the main source of genetic variation and occur often, which they thrive on (often to our detriment). Complex life forms, especially those with long life-cycles, tend to have much lower rates of mutations.
(B) generally lethal
No debate here, obviously wrong.
(C) irreversible
Wrong wrong wrong. No idea what the grader was thinking when this was picked as the "correct" answer. There's always the possibility that a base could change in a species, and later be flipped back to the wild-type in a distant descendant - by random chance alone.
(D) Only certain gene locations are affected.
No debate here, obviously wrong. Mutations can happen anywhere in the genome.
(E) source of genetic variation
This should be the correct answer. If you start with a bunch of bacteria (same species, no plasmid transfer or other shenanigans allowed), obviously they can only gain new alleles and functionality via mutations.
Now if you consider the recombination and meiosis approach: you still need mutations to produce varying alleles that can be mixed and matched. If every human had the exact same* genome (for purposes of simplicity assume there's only 1 possible X chromosome and 1 possible Y chromosome across the species, females get 2 copies of the exact same X chromosome while males get 1 each of X and Y), you can recombine all you like at each generation and everyone ends up being a genetic carbon copy of each other (all differences at adulthood would be purely chalked up to nurture as opposed to nature).


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Is it possible to intentionally limit bacteria's lifespan?
Say I have a species of bacteria. I want this species to only persist for a set number of generations, after which it simply stops reproducing. Is it possible to do this at all (with known genetic engineering techniques), and if so, how do you prevent bacteria from evolving against it?


text:
Cellular Respiration in Boiling Conditions
Here's the question:

Imagine that you are given 25 germinating pea seeds that have been placed in boiling water for 5 minutes. You place these seeds in a respirometer and collect data. Predict the rate of oxygen consumption (i.e. cellular respiration) for these seeds and explain your reasons.

I'm thinking that there will be no cellular respiration and thus no oxygen consumption because the boiling probably messes it up, but I'm not sure why that is...

What does boiling do to proteins? Why would that impact cellular respiration?

Does it denature the proteins in the Electron Transport Chain such as ATP synthase?

It would denature a lot of proteins, not only respiratory proteins. Denaturation means unfolding followed by incorrect refolding so the protein can't do it's job. Until recently, this was seen as permanent damage, however research published in ChemBioChem 2015 shows that the denaturation can in theory be reversed.

Extending on @ANONGOODNURSE, @SAPPHIRA and @JAMES.
Something you should know about proteins, they have primary, secondary, tertiary and quaternary structures all due to specific folding of the proteins. These foldings are mainly connected via hydrogen bonds to each other along with other bonds (Alberts et al., 2002). On the action of heat, the molecules composing the bonds are vibrated due to higher kinetic energy resulting in the breaking of the bonds which causes unfolding of proteins (Wikipedia denaturation of proteins). This phenomenon is called Denaturation of Proteins which causes the loss of protein function due to loss of shape.
Read this QandA in Reference.com for more information about denaturation of proteins.
Read this for more information about proteins: Molecular Biology of the Cell. 4th edition.
Link this idea to cellular respiration and how Electron Transport Chain and the Krebs Cycle (Citric acid cycle) involve proteins for the completion of the respective processes.


text:
Can the calcification response of a marine organisms, at different pH conditions, be assessed by the calcium magnesium ratio?
Can the calcification response of a marine organisms, at different pH conditions, be assessed by the calcium magnesium ratio?
the calcium magnesium ratio is a proxy  of calcification?


text:
Actively Harmful mutations
Usually harmful mutations are those which disrupt a vital function, what you might call "passively" harmful. What about a mutation that makes a protein, which is not just useless, but actually toxic to its host?  Are there any known examples?

There are definitely examples! For one, you might consider sickle-cell anemia to fall into this category.
The mutation that causes this disease leads to abnormal strands of hemoglobin that distort the shape of red blood cells, to the point that those cells can directly disrupt blood flow.
Interestingly, carriers of the sickle-cell trait actually have some protection against malaria, which explains the high incidence of the allele despite the dangerous consequences of the disease.
You can find many other examples in the category of autosomal dominant disorders (though note that sickle-cell is considered recessive, though carriers can still have some negative effects). Because these disorders only require one copy of a gene to cause illness, there is often some toxicity of the mutated protein, whereas in what you refer to as "passively" harmful mutations, one healthy copy can often compensate, fully or partially. Of course these are general statements and there will always be exceptions, but I hope thinking about it this way can guide your curiousity!


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Research from the early molecular genetics era that supported protein as the primary carrier of genetic information?
I can't seem to find anything on my own. Surely there were experiments performed (possibly using bacteriophages) that managed to come to this conclusion?
Specifically I'm interested in anything pre-Hershey/Chase.

do you want primary literature or just something that talks about the historical aspects? have you tried google?

@VanceLAlbaugh I have tried google, I have also searched my schools' library/journal database (and looked at the genomics shelves in person). I would appreciate primary literature or a historical piece that references primary literatures/goes into more detail than "...molecular geneticists felt that proteins had to be the primary carriers of genetic information because they could be much more differentiated than the 4-base DNA molecule" and the "1 enzyme 1 gene" hypothesis.

This is a wild guess, but have you looked at Schrödinger's What is Life? It's not a primary report on experimental results, but might have useful refs.

It’s difficult to be convincing with a negative answer, but I venture that the answer to your question is that the idea that protein was the genetic material was not supported by any experiments, but was a supposition based on the conventional wisdom that proteins were more complex and therefore more suited to the job.
I suggest that you should be thinking earlier than bacteriophage and Hershey and Chase. Bacteriophages only came into genetic research after the war, and the Hershey/Chase experiment (1952) was only a rigorous confirmation of the conclusion of Avery et al. in 1944 (mentioned in this Scitable article). The system that Avery et al. used (bacterial transformation) went back to Griffiths in 1928 and must have been the first that allowed any sort of experimentation in this area. And I think it was more a question of working out what was happening than devising an experiment to distinguish between protein and DNA as the genetic material.
To my mind this illustrates something about how science progresses. It is often dependent on advances in technology and changes in the conceptual framework in which scientists work. (Sometimes — e.g. Mitchell’s Hypothesis — it needs the experimental results to change that conceptual framework.) Coming back to the Hershey/Chase experiment, this was performed when the balance of scientific thought had already changed to DNA as the genetic material.
Footnote: It’s earlier than you think
I generated the Google ngram below to put the term you use, ‘molecular genetics’ into historical perspective.

This shows that the term ‘molecular genetics’ was hardly in use at the time of the Hershey–Chase experiment and Watson and Crick’s postulate of the structure of DNA in the early 1950s. I think that this reflects the fact that the concept was not current. The more popular term, ‘molecular biology’ gained currency on the basis of the structural work on DNA and proteins, and the name of the journal in which much of the work was published (Journal of Molecular Biology). The question is assuming a state of science that did not actually exist before the 1950s.

If it helps here's the Avery et al. bibliography.

I am relying heavily on Morange's book (quoted below) for what follows.
As pointed out by David, the definitive experiment showing that nucleic acid, rather than protein, is the carrier of genetic information is that of Avery, MacLeod and McCarthy (1944). Their conclusion that DNA is the 'transforming principle' was, however, very reluctantly accepted by the scientific community, in particular by the biochemists (see Cobb, 2014), and it was not until the famous 'Waring blender' experiment of Hershey and Chase (1953), and beyond, that it was accepted that DNA is the hereditary material.
So, to attempt to answer your question, what was the evidence for proteins (in particular enzymes) being the hereditary material?

It was known that proteins are one of the two components of chromosomes (Morange, p 35)
The tetranucleotide hypothesis of Levene, published about 1910, held that DNA was made of a monotonic, tetranucleotide repeating unit, and this gave rise to the idea that DNA had only a non-specific structural rule in the chromosome (Morange, p 34).
By the 1930's, several enzymes (including urease) had been crystallized by
Northrop and Sumner and it was unequivocally established that enzymes are proteins and are macromolecular, thus ushering in the great era of enzymology. Compared to the dynamic world of enzymology, DNA was considered boring.
In 1935, Wendell M. Stanley had isolated TMV virus as "a crystalline protein possessing the properties of Tobacco Mosaic Virus" and had published the results in Science. Crystallization (wrongly) implied purity and it probably understandable that such a high profile result lent weight to hypothesis that genes and proteins are intimately connected. This result was criticized, however.  Bawden & Pirie (1938) in the UK repeated the experiment but (unlike Stanley) found  6% RNA in the final product (Morange, p 65).
Beedle and Tatum (1941) had published the 'one gene one enzyme' hypothesis and (to again quote Morange) [p 35] this "had reinforced the more or less conscious identification of genes with enzymes and proteins". The idea that enzymes must be important in hereditary was further reinforced by the work of Garrod on inborn errors of metabolism, which also associated enzymes (specifically, the lack of them) with hereditary factors (Fruton, p431)
Avery's work was sharply criticized in some quarters, most notably by Alfred E. Mirsky, who pointed out that trace contamination by proteins could not be ruled out as an explanation.  A great account of the controversy with Mirsky and of the reasons why Avery's work was only slowly accepted is given by Cobb, 2014 [pdf]. One interesting stat from this paper: Hershley and Chase did not quote any of Avery's papers and Hershey is quoted  as saying that “I wasn’t too impressed by the results myself”  (Cobb,2014). This despite the fact that the DNA preparation of  Hershey and Chase contained maybe 20% protein, but that of Avery and colleagues contained less than 0.2% (Cobb,2014). A key paper in the controversy (by Mirksy) may be found here [pdf]

J.B.S Haldane stated (in 1942) that "the size of a gene is roughly that of a protein molecule and it is very probable that genes are proteins" (quoted by Fruton, p 430).
So the biochemists, it would seem, felt that proteins were the 'holy grail' of hereditary, and this attitude prevailed in some quarters long after Watson and Crick.  Morange (p 232) points out that Arthur Kornberg discovered DNA polymerase in 1958 and was (jointly) awarded the Nobel prize in 1959.  Watson and Crick, whose seminal paper on DNA was published in 1953, were not so honored until 1962.  That is an interesting, and perhaps very revealing, point.
And speaking of Nobel prizes, Avery did not get one (he died in 1955), perhaps in part due to the controversy with Mirsky (see Cobb).  Erwin Chargaff - he of the A/T and G/C ratios - (who accepted Avery's work as of fundamental at a very early stage) is quoted as saying that Avery's work deserved two Nobel prizes. And, of course, Chargaff himself did not get one, which he surely deserved. As well as the famous ratios, Chargaff was one of the first to suggest that "Differences in the proportions or the sequence of the several nucleotides forming the nucleic acid chain also could be responsible for specific effects" (see Cobb).
Fruton (pp 416-417) quotes Francis Crick as saying about the reception of the double helix. "The reaction of many biochemists, including Joseph Fruton, ranged from coolness to muted hostility. They had long considered the biology of the gene to be based on proteins, not nucleic acids, and thought the problem far too difficult to tackle in the immediate future. It did not help that the structure had been put forward by two people who were not obviously card-carrying biochemists".  Fruton (p 417) rejects this view and points out that in their classic text book (with Sofia Simmonds) the Watson and Crick structure for DNA was readily accepted, and concludes (p 417) that "I can only surmise that Francis, who showed me much kindness during my stay in Cambridge during 1962 - 1963, may have accepted too readily some idle gossip".
All this and more may be found not only in Fruton and Morange, but also in Judson's great book The Eight Day of Creation (which I don't have to hand at the moment).
Edit
After replying to David's comment, I dug out some further quotes by Sydney Brenner from  Biochemistry Strikes Back which are also (somewhat) relevant.
"In years gone by, biochemists viewed most of the rest of biology as a
descriptive science and from the even loftier standpoint of physics,
Rutherford dismissed it as stamp collecting.
The early days of molecular biology were marked by what seemed to
many to be an arrogant cleavage of the new science from biochemistry.
People like myself, whose application for admission to the Cambridge
Department of Biochemistry was ignored and who did not even receive the
attention of a rejection letter, often expressed exaggerated
views of our relationship to biochemistry. However, out argument
was not concerned with the methods of biochemistry but only with
their blindness in ignoring the new field of the chemistry
of information". (Brenner, 2000)
(He goes on to say: "I once made the remark that
two things disappeared in 1990: one was communism and the other
biochemistry and that only one should be allowed back.  Of course
biochemistry never really went away but continued to flourish in
the thousands of unread pages of biochemical journals") (Brenner, 2000) .
Some great references:
Cobb, M (2014) Oswald Avery, DNA, and the transformation of biology
Current Biology, Volume 24, pR55–R60 free pdf
Fruton, J. S. (1999) Proteins, Enzymes, Genes. The Interplay of Chemistry and Biology. Yale University Press.
Judson, H. F. (1996) The Eight Day of Creation. Makers of the Revolution in Biology (25th anniversary edn). Cold Spring Harbor Press.
Morange, Michel (1998) A History of Molecular Biology (translated by Matthew Cobb).  Harvard University Press

A much more complete answer than my tentative contribution.


text:
How do you identify this particular snake shedding?
Aloha,
Snakes are illegal in the State of Hawaii, with the exception of the Hawaiian Blind Snake (Brahminy Blind Snake (Ramphotyhlops braminus)). I've read through a plethora of articles to no avail. It also doesn't help that snakes are virtually non-existent in the Hawaiian Islands.
I would like to identify this particular shedding, however, it has proven to be just as difficult as I predicted. Could anyone identify the species of this shedding?
Mahalo


text:
How do leafcutter ants choose what plants to cut?
I know that leafcutter ants don't actually eat plants and only use them to harvest fungi. How do they choose what plants to cut?
They won't touch anything in my garden, but if I plant roses, they'll completely wipe all the leaves and petals in a single day.
If some plants are better suited than others for their "farming", how do they know them?


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What is the evolutionary purpose of shingles afflicting only one side of the body?
A question here asks for the name of the category of viruses that affect only one side of the body. My question is about the  evolutionary purpose of that 'affects only one side' behavior.
Chicken pox is not usually fatal, and it's not clear to me why evolution would set such a low bar for eliminating the weaklings in the herd. On the opposite end, small pox was excessively fatal; I guess that's the price of evolution biohacking its way by trial and error.
On the other hand, I can see how shingles, afflicting people only in later life, can be debilitating enough to keep one from going hunting and gathering and moaning one's way to death by starvation. But for that to happen isn't it more efficient for the virus to resurface across the entire nervous system instead of parts of just one side? If shingles happened, say, in the late teens, I could understand that 'affects-only-one-side' eliminates only the weaker part of the herd. But it's mostly older people, well past their reproductive prime, who get shingles, and get it only on one side. I see no benefit to the individual or the group of contracting an 'expire by date' virus early in life and then the virus goes about its expiration-dance in a half-hearted, tentative way. Makes no sense.

You seem to assume that the virus does not evolve or maybe you mean that it is selected for hurting its host (which is wrong). It is quite unclear what you mean by "evolutionary purpose" as well. You might take advantage of following a short intro to evolutionary biology such as Understanding Evolution for example. You might also want to have a look at Why do parasites sometimes kill their hosts?.

This is a bit like asking what the evolutionary value is of developing cancer in only one lung. There is none. Cancer is cancer; it has to start somewhere. Shingles is a physiological process involving viral reactivation in one dorsal root ganglion. Why should it be bilateral? You're looking at this from a teleological standpoint, which is very often a mistake in science.

Well since the chicken pox virus (hhv 3) that also causes shingles, practically spares no one, is it not already successful?

@Polisetty Good point and similar to one in the accepted as answer below. @ anongoodnurse Cancer is the cell division system gone haywire (even if triggered possibly by a virus such as HPV?), whereas a virus is not intrinsic to its host?

The premise of your question is wrong. Although evolution is often a good guide when looking for "purpose" in biology, sometimes there are other proximate causes.
Shingles is caused by activity in a previously dormant version of the virus that causes chickenpox. Essentially, your immune system clears out the virus from everywhere in the body except some that hides in the nerve roots.
Peripheral nerves to the skin are arranged into "dermatomes" which are essentially the group of nerves that enter the spinal cord at a particular vertebra.
Shingles happens when the virus becomes active again. Since a dermatome only covers one side of the body, shingles usually only affects that side of the body (in particular, that dermatome).
http://www.webmd.com/skin-problems-and-treatments/shingles/shingles-cause looks like a decent reference for this information.
I don't personally know of research on the evolution of varicella zoster, but if you want to think up a speculative evolutionary process, you should be thinking about the virus and spreading of the virus, which is the activity that natural selection will support. In that case, lying dormant can give the virus an opportunity to spread again at a later date, preventing it from being completely eliminated by the host's immune system. All the business about rashes on one side of the body comes about by 'accident,' as a matter of convenience since the virus hides out in peripheral nerve roots.

The virus' replication and its own spread makes sense. I was looking at a greater degree of symbiosis, if you will, between parasite and host. Unlike the common cold virus which typically has non-fatal affects on humans and hard to say surviving a makes one stronger than another. I think you can make that argument that only people with stronger immune systems survive the small pox virus. I am still puzzled by the chicken pox virus - non-fatal in kids, hibernates for 25-30 years before re-emerging - why? Why this cicada-style lagged cycle?

While symbiosis is possible between "parasite and host" it isn't necessary; many parasite/host relationships are not at all symbiotic. It isn't correct to say that a virus that kills people with weaker immune systems is symbiotic by "improving" the immune systems of the population of hosts. The hibernation is a way for the virus to avoid the host's immune system while that immune system is most prepared to hunt it down; it doesn't need to have any benefit to the host.

Understood - a consequence of a small pox epidemic be people with better immune systems but that 'gain' is not necessarily obtained via a symbiotic relationship.

Yeah, I'm not certain that treating that as a 'gain' is really appropriate - stronger immune systems might also lead to autoimmune disorders, for example. I think it is safer to think of it as an evolutionary adaptation: animals including people evolve defenses against viruses of all types because those viruses cause harm if not kept in check. But that is a result of the evolutionary process, not a "reason" or "purpose" for viruses to exist.

@Bryan Krause Symbiosis is an interaction between two organisms. May be parasitism, mutualism or commensalism. Although its just semantics, still, its a consensus. https://en.m.wikipedia.org/wiki/Symbiosis so all parasites are in a symbiotic relation with the host

@Polisetty Thank you for clarification; the wikipedia article you link actually describes the controversy on terminology a bit, where symbiosis was originally used to describe a beneficial interaction but now that has changed where mutualism has supplanted the earlier definition.


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Whole Genome Sequencing vs Whole Exome Sequencing
I am working on a project where I want to discover causative genes for a certain disease I may have. I was wondering whether to get WGS or WES to perform this experiment:-
I am looking at SNP's and CNV's of my genes and I want to compare my data with that of normal and diseased individuals. For a gene I calculate the document distance for each group (normal and diseased) using this algorithm (https://math.stackexchange.com/questions/1080377/how-close-apart-are-two-message-document-distance-algorithm) as this will allow me to determine which genes I have that are abnormal or are "close" to being classified as abnormal and which genes are normal or "close" to being called normal per the algorithm and the data obtained from the two groups.
To perform this experiment I need to sequence my genome AND identify databases that would allow me to conduct my analysis. I wanted to know which is better for my experiment WGS or WES as publicly available data might also influence the decision.
Also, I believe alternative splicing adds a layer of complexity and wanted to know why WES is performed anyways.
Thanks in advance for your replies. Please do answer whatever you can. Thanks once again!

Hard to answer without knowing more about the disease. I think in many cases exome would be fine, since whatever disease you have is probably caused by a malfunctioning protein, but the mutation could also be in a splice site or regulatory sequence. With whole genome sequencing you'd get a LOT of crap, since we're all genetically dissimilar.

Possibly excepting some CNVs, a "distance" measure of genome sequence differences is unlikely to yield anything useful.  A single base difference can have huge consequences or have no consequence whatsoever despite having the same distance measure.

Thank you both for your replies! I have a list of candidate genes that were identified by GWA studies. I was thinking of profiling only those genes and looking for clues. As @mgkrebbs pointed out rightly that a single base difference can make all the difference or no difference whatsoever makes me question my method. Can you guys suggest alternatives?

If you have the money and decent computers then go for WGS. It is definitely more informative that WES. People do exome sequencing primarily to save resources.

@WYSIWYG it is also much, much easier to extract meaningful information from WES.

WES, almost certainly. First of all, the vast majority of phenotype-causing variants are found in exons. For most analyses that are looking into disease causing mutations, WGS is pointless. It only makes your analysis harder and doesn't actually add anything useful.
If you know you're interested in CNVs, that's different. CNV detection is hard in general but is particularly hard from WES data. Detecting CNVs in WGS data is much less error prone. However, you really should bear in mind that there are currently no 'good' methods to detect CNVs. This is a non-trivial problem and still in its infancy. While there are various methods that can detect CNVs, none of them find all (or even close to all). In fact, this is such a problem in the field that the currently accepted wisdom is that you should use multiple methods and combine the results. In fact, many recent CNV detectors do exactly that. And they still don't find all of them (especially not in WES data). Basically, CNV detection is not for the fainthearted and is certainly not for the non-expert.
The good news is that if you do have a disease causing mutation, it is very unlikely to be a CNV. It is far likelier that you're just looking for SNPs. Which brings us to the next issue. I'm afraid the algorithm you linked to, from what I can tell, won't help you at all. You're not trying to compare your gene to a list of healthy and unhealthy ones and figure out which group is most similar to what you have. First of all, because there are many differences (mutations) that don't actually have any effect whatsoever. These so-called synonymous mutations would still be counted by your algorithm but should be ignored. Second, because tiny differences can be enormously important. There are specific tools for what you want to do; don't try and apply broad, general mathematical approaches. You need algorithms that are specifically designed to deal with biological data and which take the underlying biology into consideration.
So, what you're looking for are programs called "Variant Callers". Two of the most popular ones are GATK and FreeBayes. These will read an input genome and compare it to a reference genome and give you a list of "variants", sites where the input differs from the reference. You then want to use resources like ClinVar or MutationTaster to check whether those variants are considered pathogenic. This is a bit of shameless self-promotion since I work for the company which created it, but VarSome, "The Human Genomic Variant Search Engine" is a new variant search engine that combines information from many different sources in a centralized and easy to search repository. I recommend it highly (and it is free).
However, before you get to finding your variants, you will need to align your genome to the reference. Basically, modern sequencing methods work by cutting the genome into many, many small pieces, copying each piece multiple times and then sequencing each piece. So the output of a sequencing run is a text file that looks like this:
@SN956:1934:H55WMBBXX:2:1101:0:15733 1:N:0:NTTACTCG
NCCCCAAGGAGACTTGCTGAGACCTTGAACAAGTGACACAATGTGAGCAGAACTTGTCTTGACAGAAAATGCTTTG
+
#AAAFJJJJJJJJJFFJJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJAJJJJFAJJJJJFJJ7
@SN956:1934:H55WMBBXX:2:1101:0:15743 1:N:0:NTTACTCG
NCTTCCTCACTAAAGTCCCATTTAGTGCTGATTGTGCTTTGGCTACTTCTCCTCTTGCCATTTTCCTGAACCCACG
+
#AAFFJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJJJJJJJJJFJJJJJJJJJJJJJJJJJJF

This is usually several gigabytes (something like ~2-3G for WES and >80G for WGS). Therefore, the alignment of these sequences needs a powerful machine and you don't even want to try to align WGS sequences on your laptop. It will take weeks and will probably fail. Another reason why you should prefer WES over WGS for this. In my work, I routinely align WGS data to the reference genome and that can easily take >100GB of RAM.
The bottom line and what this rambling answer is trying to get across is that:

WES is better than WGS when searching for disease causing mutations. It is far easier to analyze the data and 99% of the cases you want are in exons. It is also much, much cheaper.
This isn't simple. You seem to think you can sort of waltz in and do it yourself. You can, but it is very far from trivial. It is also not cheap.

So, if you do actually have the money to pay for a WGS analysis (this costs several thousand euros/dollars, in case you didn't know), which is very surprising if you're just a private individual, instead of spending it on WGS, get a WES and spend your money on getting an expert to analyze your data for you. Seriously, this is what I do for a living, you really don't seem to have grasped quite how complicated it is. And no, I am not suggesting you hire me :). There are, however, companies that offer this sort of service. Use them, don't reinvent the wheel.
References
Useful review articles for CNV detection:

Zhao et al. BMC Bioinformatics, 2013, 14(Suppl 11):S1 (DOI: 10.1186/1471-2105-14-S11-S1, link)
Tattini L, D’Aurizio R and Magi A
Front. Bioeng. Biotechnol, 2015. 3:92. (DOI: 10.3389/fbioe.2015.00092, link)


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Looking for books on How the limbic system works and it role in non-verbal behavior
This is my first post. I just read and I'm currently studying a book called "How everybody works" as a guide to understanding nonverbal behaviors.
After I'm done studying it and while I experiment with its claims; I'm looking to understand more of how the limbic system works and its role in human emotions.
The book's premise is that the limbic system makes us react to certain situations in such ways that nonverbal behavior is expressed; therefore by understanding the limbic system and nonverbal behavior we can ascertain a person's reaction to outside stimuli and gain insight.
If anyone could provide recommendations on books about the Limbic system
that are up to date with current finds or any other books that relate to the topics above I would greatly appreciate it.

not sure if you are still looking, but I have two recommendations for you.

"Limbic systems for emotion and for memory, but no single limbic system" is a really long, but really great article on the topic.  You can find that online here:  https://www.sciencedirect.com/science/article/pii/S0010945213003110?via%3Dihub
It's been a while since I've read this one, but the book Synaptic Self:  How Our Brains Become Who We Are is a good read on this subject.  It's about the brain as a whole, but focuses a lot on the limbic system and amygdala (it's author, Joseph LeDoux, did much of the pioneering work on the amygdala).  It is from 1996, so the science isn't super up to date, but I still think it's a good read if you're just curious about the brain and limbic system.


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Shell in garden snail
I was wondering that how does shell of garden snail "grows " with growth of snail.
Small snail possess shell as its size but as it grows shell grows. How do they enlarge cavity inside shell?

The snails enlarge the shell by adding material at the lip.  The addition of material is sometimes noncontinuous and shows up as rings, sort of like tree rings.  You can see the growth rings in this photo.

I found the photo here http://ediblesouthflorida.ediblecommunities.com/things-do/snails-slugs-millipedes-oh-my
As the shell spirals outward the diameter of the added rings gets larger and larger.  It has to get larger if it is to spiral - addition of the same sized rings would make a donut-like torus.


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T lymphocytes and HIV-AIDS
in studying maturation of lymphocytes into two different types-T LYMPHOCYTES and B LYMPHOCYTES. it is mentioned that if a lymphocyte matures in thymus gland it becomes T LYMPHOCYTE and becomes B LYMPHOCYTE if matures in bone marrow {bursa region}.
also HIV virus attacks helper t lymphocytes . I was thinking that if we could make the initial immature lymphocytes in thymus made outside in vitro  { like from stem cells or likewise from clone etc or some other alternatives} and then inject them in patient so as to overcome their deficiency .
is it possible?

The deficit here is that HIV invades and depletes arguably the most important immune cells you've got: CD4+ T lymphocytes. The concept behind your question is sort of like an expensive bandage you always have to get when your CD4 counts drop into AIDS territory. Does that make sense? It's like feeding the virus more host cells without addressing the virus.

@CMosychuk, my point was regarding replenishment of depleted t-lymphocytes. We have produced clones, we know about totipotency of cells. Also hiv virus should be given some other treatment. What do you think? Do make me aware about this. Thanks


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The title et al
I have found the extension "et al" with biologists from different nationalities like : Avery et al ; Taylor et al etc.
My question :
1. What does it mean?
2. Why only biologists?

It is just to abbreviate the names of the authors that is used in all fields of knowledge. For example, if I have to refer to this paper that has 9 authors, I will not write every name, I will just write Gilbert et al. 2017. I am not sure why you would care more about nationalities than whether they prefer chocolate over caramel. They are just authors.

I am voting to close because your question is off-topic here but would be on-topic on Academia.SE (although they will likely say "Just google it!").

I'm voting to close this question as off-topic because it is not about biology.

The Latin phrase et alia (abbreviated et al.) means and others.
It is not limited to biologists, nor those of different nationalities. If I refer to this computer graphics article, I can refer to it as "the paper written by Henrik Jensen, et al., regarding physically based modeling of fire..."
Note that the expansion of et al. can also be et alii and et aliae, which are the masculine and feminine forms, respectively; et alia is the neuter form.

@GerardoFurtado - So how do we know to which "et al." is referring? And if the genders of the authors are mixed, why isn't it, et. al. et. al.?

@GerardoFurtado - I was pilling your leg. :) I love Latin; I taught it for about six years. But there is no one - and I mean no one - I know that shares that love of Latin, so you were the victim. Please forgive me. :)


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Comparison of examples in incomplete dominance and Co dominance
When we consider examples of incomplete dominance we take that of FOUR O CLOCK plant -
We say that alleles for red and white colour of flower are not completely dominant against each other. Hence in hybrid progeny we
Say (as in standard textbooks) that pink colour appears due to "expression of single gene for pigmented flower which produces only pink colour (quantitative inheritance )"
In codominance concept we take example of SHORT HORNED CATTLE which again appears as same case white and red cattle produces roan coloured hybrid progeny but due to "juxtaposition of small patches of red and white colour hair"
The same principle can be applied to four o clock plant too. Suppose pink colour of flower is too due to juxtaposition of red and white coloured elements.
Then where is the difference between the two concepts?
Further the thing which puzzled me more was that - "initially cattle example was considered to be in complete dominance. Later it was CORRECTED to codominance "
Also incomplete dominance is also known as "mosaic dominance" but actually mosaic happens in codominance.
Kindly clarify my doubts

Mosaic dominance
I think your confusion comes from the statement

incomplete dominance is also known as "mosaic dominance"

I had never heard of mosaic dominance before and I could not find much on this concept. I found a few papers but they either referred to mosaicism (see below) or they did use this term only a few times without defining it. There is an entry for mosaic inheritence in the online medical dictionnary though (here). The definition they give is

inheritance in which the paternal influence is dominant in one group of cells and the maternal in another.

It is a little vague to me as 1) the phrasing is a little unusual and 2) it does not specify the underlying mechanism. If anything, it feels like a synonym of codominance and not of incomplete dominance.
Mosaicism is a thing in genetics but it is mainly unrelated to the concept of dominance as it refers to genetic polymorphism among cells within an organism.
Where did you read about mosaic dominance? Can you please give a direct quote?
If anything, mosaic dominance sounds like a synonym of codominance and not a synonym of incomplete dominance.
Codominance vs incomplete dominance
Outside the above issue, I think you pretty much define these two terms through your examples. You might want to have a look at the post (although it is a post who did not get much attention)

How is incomplete dominance different from codominance?

In short, codominance implies that the specific phenotypic effect of each allele is being visible in the heterozygote, while incomplete dominance implies that the heterozygote has a phenotype that is somewhat intermediate between the two homozygote phenotypes.

Well thank you very much for the answer. There is no direct quote on mosaicism but it is written like this-"incomplete (partial or mosaic) dominance is the phenomenon where none of the two contrasting alleles ir factors is dominant. "

But there is still one doubt does pink appears due to expression by single gene for pigmented flower, if yes how did that gene form? Or it is mixed effect of red and white colouring proteins as written above , if this is true then why it is not included in codominance


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Can vitamin B17 cure cancer?
I have heard that a 'vitamin B17' can cure cancer, but that the medical industry never talks about it, since making it legal would cause them loss of billions. But I have never found a reliable report on whether B17 really works or not. There is a question on 'vitamin B17' deficiency as a cause of cancer (see this post), however, not on 'vitamin B17' as a possible medication for cancer. What are the proposed mechanisms? And is there evidence that 'vitamin B17' really works in curing cancer?

The short answer is "no", but if you find a notable referenced claim saying that, you could try your luck on [skeptics.se] for confirmation.

@Mesentery: Even though related and heading towards the same direction I would not see it as a duplicate. Supplementing a deficiency or using a substance as a treatment for a disease are fundamentally different, justifying both questions independently. I will edit my answer to address that more directly.

@AlexDeLarge - duplicates are marked as such because of question similarity, not answer differences. If you could edit the question and stress the difference between this and linked question?

I'm voting to close this question as off-topic because it is better suited to SE Skeptics http://skeptics.stackexchange.com.

@AliceD: In the proposed edit, the question is rephrased and I added a query for possible mechanisms by which 'vitamin B17' could potentially cure cancer - which also makes it suitable for Biology.SE.

@David Just because a question is a "better" fit for another SE network site doesn't mean that it's off topic on this one. While SE Skeptics would be a good place to find sources which refute a particular claim, Biology SE is a perfectly fine spot to ask about the underlying biology of the topic.

@R.M.— No. But it is an excuse that can be employed to off-load stuff that is obviously undesirable but not covered by the criteria presented to one when one votes to close a question.

No such thing as B17: https://en.wikipedia.org/wiki/B_vitamins

@David I see no reason to close these sorts of questions if they can be answered with biology. This is my interpretation of the current meta as well. If you disagree, I would suggest raising the issue in meta.

@BryanKrause — I certainly did not and do not solicit a discussion here. I voted to close and had to explain why, which automatically generated a comment. This provoked other comments to which I replied. I suppose it could be raised on meta, but for various reasons I'd prefer to leave it a while.

I agree that, although this question would be well fit for posting on Skeptics.SE, this question is on-topic here.

Look here for an explanation why the "medical industry" wouldn't want any cancer cure to be kept secret, and wouldn't "loose billions" if such a cure existed and was made public: http://skeptics.stackexchange.com/questions/22770/has-the-cure-to-cancer-been-hidden-by-pharmaceutical-companies

Obligatory XKCD: https://xkcd.com/1217/

Of course a mere vitamin can cure cancer. That's why millions of scientists world wide are spending their lives looking for a cure. /s

There is no such thing as "vitamin B17". You can take TNT, call it "vitamin B52" and try to sell it to people but it doesn't make it a vitamin.

See also Is laetrile an efficient drug against cancer? on [skeptics.se].

@Agent_L I see what you did there.

Laetrile/Amygdalin has been claimed to be a suitable treatment for 'cancer' (which is a summary term for an extremely heterogeneous class of diseases). Even though laetrile/amygdalin in these claims is often called a vitamin, it in fact is not a vitamin as the molecule is not essential for the metabolism (Greenberg (1980)).
The claimed effects of laetrile/amygdalin are not only based on supplementing the molecule to balance a putative deficiency (with the false assumption that it is in fact necessary), though. Both other putative mechanisms are based on reactions that form HCN/cyanide: the enzyme $\beta$-Glucosidase breaks down laetrile/amygdalin and this reaction releases HCN. The argument now is that tumour cells have higher levels of $\beta$-Glucosidase which leads to accumulation of cyanide in tumour cells - with the effect of killing the tumour cells selectively. This would be great... if healthy and tumour cells actually had different levels of the enzyme. Unfortunately, they seem to have similarly low levels of $\beta$-Glucosidase (Greenberg (1980)). Even more problematic, Greenberg (1980) also reports elevated levels of $\beta$-Glucosidase in the liver and small intestine ... and you would not really want to release cyanide there.
There is a second mechanism, though: The enzyme $\beta$-Glucuronidase is claimed to be at higher levels in cancer tissue than in healthy tissues (leading to the same desirable effect described above). But again, there does not seem to be a difference in enzyme levels between healthy and cancer tissues (Dorr and Paxinos (1977)), and even more: $\beta$-Glucuronidase does not even break down the molecule as laetrile/amygdalin has a glucoside bond - so there is not even any cyanide release in that case (Holzbecher et al. (1984)).
Additionally, there is no clinical evidence that laetrile/amygdalin is an appropriate treatment for any form of cancer. This topic has been reviewed substantially (see Milazzo et al. (2006) for a review and this fairly recent Cochrane review by Milazzo and Horneber (2015)) and none of the studies included and analysed indicate any positive effect of laetrile/amygdalin. On the contrary, the in vivo cyanide formation after laetrile/amygdalin uptake makes the treatment very dangerous as it can lead to cyanide poisoning (and death, eventually) - especially after oral uptake due to higher $\beta$-Glucosidase concentrations in the digestive system. The authors of the Cochrane review therefore conclude that

The claims that laetrile or amygdalin have beneficial effects for cancer patients are not currently supported by sound clinical data. There is a considerable risk of serious adverse effects from cyanide poisoning after laetrile or amygdalin, especially after oral ingestion. The risk–benefit balance of laetrile or amygdalin as a treatment for cancer is therefore unambiguously negative.

"deficiency as a cause of cancer" and "the molecule is not essential for the metabolism" seem contradictory. Maybe I'm being overly simplistic in my understanding. Nevertheless, how could one have a deficiency in something that is not necessary to begin with? It either is necessary therefore causes a problem when deficient, or not essential, therefore its deficiency would not be a cause of any problem, namely cancer.

@jlaverde: Yes, you are right. The 'deficiency as a cause of cancer' builds on the false assumption that the molecule is in fact essential for the metabolism - which it is not. I clarified.

@jlaverde The whole point is that it is quackery: it is not a vitamin. There can not be a deficiency because it isn't needed at all.


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How can some animals see ultraviolet or infrared light?
I know that some animals like birds, bees, and fish can see ultraviolet and infrared light. Whether it is to detect flowers that bear nectar, or the urine trails of prey. But what I don't understand is how they see these wavelengths. What is different about their eyes or brain that allows them to see different wavelengths than humans?

Welcome to Biology.SE. UV and IR are by definition wavelength that are outside the range of wavelength that humans can see. There is nothing extraordinary about these other wavelength and therefore the question reduced to How do we see colours?. I think this post will answer your question.

@Remi.b - it doesn't. Hyperspectral vision does warrant a specific answer

@K Gargiulio's answer is correct in that distinct cone cells allow the perception of these wavelengths. You may also be interested in the descriptions of colour vision in http://biology.stackexchange.com/questions/39882/are-some-animals-like-dogs-and-cats-color-blind-and-how-do-we-know-that/39890#39890, for further details.

This is not a duplicate because this question specifically asks about UV and IR molecular-sensors.

You might be interested in the eyes of the mantis shrimp.

Somewhere we should add that a specifically small type of iris is necessary so only relatively tiny animals can see in UV, and I expect they have some kind of lens adaption too.

Yes, they have different photoreceptors as well as the circuitry to interpret the information from those photoreceptors. Humans have 3 types of cones which are tuned to respond best to red, green, or blue light, but it's not an on or off signal. A red or blue cone may still fire in greenish light, it just fires much less often. The brain takes that input and figures out the color based on the relative firing rates of the red/blue/green cones.
So for an animal that can see in UV or infrared, they need both the photoreceptors that respond to that wavelength of light, and the ability to integrate that response into the bigger picture of how all the photoreceptors are firing.

You have still not answered which photoreceptors are those that allow UV sensing. BTW, IR sensing is not similar to that of other photoreceptors even though the perception is finally similar to vision (like in pit vipers). IR does not cause electronic transition; it rather causes activation of temperature regulated channels.

In Drosophila photoreceptor R7 and R8 are UV sensitive while R1 - R6 respond to visible light.

photoreceptors don't fire

Short answer
In mammals dedicated UV cones have been found, as well as photoreceptors with secondary peak-sensitivity in the UV range. In fact, human blue cones are sensitive to near-UV.
Background
In humans, the visible spectrum is generally accepted to range from 390 to 700 nm. Figure 1 shows the spectral sensitivities of the various photoreceptors in humans.

Fig. 1. Spectral sensitivity of the four receptor classes. Source: Wikibooks; Sensory Systems
In invertebrates sensitivity to near-UV is quite common. However, some rodents (mice, gerbils and gophers) also feature a peak in sensitivity at 359 - 511 nm. In these rodents and some marsupials sensitive to UV, it is thought to be attributable to a specific dedicated type of cone sensitive to near-UV (Jacobs et al., 1991; Winter et al, 2003). Near-UV is referred to as UV-A, encompassing 315 - 380 nm.  Likewise, birds seem to feature a dedicated, fourth cone class to detect UV (Benett & Cuthill, 1994).
In the color-blind flower bat, UV sensitivity has been attributed to a photoreceptor with two peak sensitivities - one in the green range and the other around 365 nm and running down to 310 nm (Winter et al, 2003). Hence, UV sensitivity can be conferred by cones with broad sensitivities ranging into the UV range.
In fact, the aphakic human eye (eyes with the lens removed after cataract surgery are aphakic) has been shown to be sensitive to near-UV. As can be seen in Fig.1, the blue cones are actually pretty sensitive to near-UV. It appears that the lens absorbs much of the UV, rendering UV light useless to humans with healthy eyes (Griswold & Stark, 1992).
Infrared (IR) sensitivity in snakes is mediated by pit organs and not via the eyes. Basically they are heat sensors and likely don't mediate vision as such (Newman et al., 1982). I was not able to find any relevant information on IR vision, or how it should be mediated. In fact, I doubt IR is used for vision at all, i.e., to reconstruct the visual scene. IR vision is used more in the form of general heat detection.
References
- Benett & Cuthill, Vis Res (1994); 34(11): 1471–8
- Griswold & Stark, Vis Res (1992); 32(9):1739-43
- Jacobs et al., Nature (1991); 353: 655-6
- Newman et al., Sci Am (1982); 246(3): 116-27
- Winter et al, Nature (2003); 425: 612-4


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small cocooned caterpillar found on bathroom door - what is this creature?

This larvae / moth has what seems to be a smooth gray cocoon which looks like a piece of cement. It can carry this cocoon with it as it crawls, and it can come out from both ends of this cocoon.
Would really be interested of knowing what this creature is and how it ended up in my bathroom.
Cheers!
As asked my location is Israel (Mediterranean climate)

You need to provide your location for species-identification questions

Possible duplicate of Identify this smooth-cocoon worm from Southern India

I live in South Aftica and suddenly have hundreds of these in my house. They seem to be nocturnal Would love to know what they are


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Is this a flowering plant?
I just received a small plant as a gift from a friend.

Here is its leaf:

I tried looking it up on flowers of India, but their database is too much to read manually.
Physical description:
It's short, around 5 inches, probably a flowering plant as per my experience (She says it is a cactus but I don't think so). The leaf is around 1.5 cm and has a cone+cylinder like structure.
Which species is this plant, and is it a flowering one?

Any help would be great.

@GerardoFurtado Thanks, could you please write it as an answer.

Thanks again @GerardoFurtado. Could you check if this is the one Pachyphytum viride

Crassula tetragona, also known as mini pine tree (for its extreme use in bonsai technique), native to South Africa.

It is a succulent; a xerophyte (a kind of plant which needs very less water for survival), characterised with fleshy leaves developed due to evolution for storing water, this plant attains a height up to 3 meters.

Flowering in this plant usually take place in summer season, the flowers are yellowish orange and white.

Please edit your answer to add discussion of key features that led you to this conclusion and supporting references — i.e. what makes you certain this is Crassula tetragona rather than some other Crassula (or a hybrid as mentioned by @user24284). Without this a non-expert cannot evaluate whether your answer is correct. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

This seems to be of the very variable species of Cotyledon orbiculata. Probably the flanaganii variation.
If that proves to be right, your plant is very much flowering. Since it is native to south africa, I don't know if you will be able to witness its flowers in your home or garden.
In any case keep domestic animals away, since to many (including dogs) this plant proved to be toxic on ingestion.

Thank you for your answer, but I don't think this is the one.


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Role of auxin and cytokinins in vascular cambium or callus formation
Usually, auxins promote cell growth and cytokinins promote cell division. But, I got an information from my teacher that, in case of vascular cambium or callus formation, auxins promote cell division and cytokinins promote cell growth. Is this 'information' true? If true, why?