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Do men and women have the same number of genes?
As far as I know, humans have 23 pairs of chromosomes, each one which contains a particular amount of genes. But in the "last" pair, men have a XY pair chromosome, and women have a XX pair chromosome. Does the missing "leg" of the XY pair make men to have fewer genes than women, and if so, how many genes do each sex have?

No a larger size human will have more genes:)

Men do have more genes than woman. As I said in this comment, there is a consensus among geneticists/molecular biologists regarding the proper definition of gene and allele, which are not synonyms. Therefore, men have more genes than women (since men have all the genes women have plus the genes in the non-homologous region of Y chromosome), while women have more alleles than men.

Also, regarding JM97 comment above: one human somatic cell, 10 human somatic cells or 500 human somatic cells have the same number of genes.

Genetic issues, just as dichromatism, which is more common in men because a gene for trichromatism is found on the 23rd chromosome, is a good example of a sex chromosome dependent gene, so my assumption is that these differences mean a difference in number of genes.

It is true that the Y chromosome is shorter than the X chromosome and that there are more genes on the X chromosome.

Do men have fewer genes?

One could (mis)understand three things in the expression "number of genes".

Number of gene copies (see Copy Number Variation)
Number of genes
Number of alleles

Thanks to @GerardoFurtado for correcting my semantic in the comments.
1. Number of gene copies
From the statement that there are fewer genes on the Y chromosome, one can conclude that men have fewer genes copies than woman.
This is the intuition the OP seemed to have.
2. Number of genes
Men also have an X chromosome. So men have the standard genes present on the X chromosome (but they only have a single copy of it while women have two copies; btw you might be interested in dosage compensation).
Because women do not have a Y chromosome and because there are a number of genes on the Y chromosome that are not present on the X chromosome, men have genes that female don't have at all. Therefore women have fewer genes than men.
3. Number of alleles
There is not much reason to expect that one gender would be more heterozygote than the other at autosomes (=non sexual chromosomes). Some may hypothesize that women may have more heterozygosity than men if there is stronger selection among sperm than among ovules or things like that but let's not get down this complicated path.
One one hand women have more gene copies and therefore might experience more heterozygosity, one the other hand, men have more genes and would therefore eventually carry more alleles. I don't know which side wins!
Did you mean number of genes per cell or per individual?
So far I assumed you were interested about the number of genes (or gene copies) per cells but if you want to compare whole individuals than it is a different story!
Men are on average taller and therefore have more cells. Therefore if you compare the body-wide number of gene copies, women will have fewer gene copy on average (Thanks to @JM97 comment).

For what I've read online, it isnt very clear how many genes the human have? According to this , counting the case of a human with XY chromosome, a human would have 31185 genes. But is it reliable or an aproximation? And how many it would be for a human with XX? https://es.wikipedia.org/wiki/Genoma_humano

This is an entirely different question. You might want to post it on a separate post. But I can give you some hints here. I don't know a whole lot about the details of the human genome project but a big issue in counting the number of genes has to do with agreeing on what we call a gene. Estimates of protein-coding genes I am used to tend to be around 20k genes rather than 30k (See for example Church et al 2009 or Clamp et al. 2007).

Your wikipedia article does not cite any reference so I can't tell much about the meaning and validity of these results. The number they cite by the way is 32185 (not 31185). As a side note, I find the english wikipedia often more complete and more proof read than wikipedia in other languages (but I don't speak spanish and never go on the spanish wikipedia).

yes, it's true, english wikipedia is more reliable, but I just found that article there.

@Pablo I don't see where you got that number. The page you quoted mentions estimates of ~20500. It then shows 32185 as the sum in the table, so I suppose that's what you meant. However, there's no citation for that and it's considerably more than the currently accepted estimates so I wouldn't rely on it.

@yes, I was talking about the 32185 genes sum . And my question was meant for an individual cell, but it's interesting the data about men having more cells and therefore having more genes in the total count of copies of the body. Anyway, I'm still wondering how the number of genes in an individual cell compare if you take any definition of gene for the comparision. I suppose that data might be known and might be online somewhere

I disagree with this answer, @Remi.b. Of course definitions depend on several factors, but it seems to me that there is a general consensus among geneticists/molecular biologists regarding the difference between a gene and a allele (thus, "number of genes" has a clear meaning and doesn't depend on what one meant). That being the case, the answer is unambiguous: men have more genes than women, while women have more alleles than men.

As @GerardoFurtado noted in his comment, males have more genes since there are genes unique to the Y chromosome, like SRY. Of course, the fact that males only have a single X chromosome means that males will only have a single allele of each gene encoded by the X chromosome, while females have two alleles for each gene they have.

Note : the number of genes evolves.
For who is interested and can understand french, heres a link speaking, in a short way, about that, and about the eventual disappearence of the y chromosom in human genom:
http://planet-vie.ens.fr/content/chromosome-y-humain
And a link about the inactivation of one of the X chromosom in women genom (corpuscle of Barr) :  http://www.snv.jussieu.fr/vie/dossiers/kx/kx.htm

@blacksun Shall we use the edit function and add this text to your other answer? I also requested the merge of both accounts into one - so you will can edit your own answer as well as having all your reputation in one account.

To Chris : in a certain way, this answer "number of genes evolves", is self sufficient, I think. But of course, the links I posted may disappear, and they are in french, sorry for that. If I find time for, I'll try to find english references, and sum up those references

To Tyto alba :I'm in fact the author of both answers ... I didn t participate for a while, because I lost the link to this subject, which I fall on working on very different things - and answering at first like on the very generalist forum I came from, thinking it was of same kind..

It might take a few hours until this happens, depending on when the community manager team has time for that.

To Chris - ok, thank you one more time ,no problem

If you are trying to call someone writing @username will ping them. Otherwise the person isn't notified.

@Tyto alba Thanks Tyto alba, I'll try to remember that in the future ^^

Note - this is a very simple way to present things, and don't have the ambition to be a biology thesis.
Men do not have fewer genes than women, but fewer allels (variations of a gene); the allels on the x-y chromosome pair are not necessarily the same on the x and on the y (for men) or second x (for women), but they are for a part of same kind - same gene. It's like if, for a part, the y chromosome was broken, missing a bar to be an x.
One example of this is daltonism, linked to the xy chromosome pair.
Let's say that the daltonism allel is a corrupted existing allel (a variation of a gene).
To be a daltonist, a woman must have the daltonism allel on both of his x chromosomes - the daltonism allel is not a dominant allel, and if there is one corrupted allel on one x chromosome, but a normal one on the other x, the woman won't be a daltonist.
But a man is a daltonist only if his X chromosome do have the "corrupted" allel, because of the missing part of the y chromosome (compared to an x one).
If a woman has both allels, one "good" and one "corrupted", she will transmit it or not to his child, depending on which X chromosome she will give to this child.
If the father is a daltonist, he won't transmit it to his child if this child is a boy (he gives him his y chromosome genes and allels, not the x ones, and the boy takes an x from the mother, so he is xy).
But if his child is a girl, the father will transmit it to her (the girl take an x from the two of his mother and the only x from the father, so she is xx)
So, a child, to be a daltonist, must have at least a daltonist allel from his mother, no matter if the woman was daltonist or not (one x allel only corrupted or both).
Then, if this child is a girl, and is daltonist, it implies his father was daltonist too.
If it's a boy, no matter if the father is daltonist or not, he will be a daltonist as soon as his mother transmitted him a corrupted allel.
If the father is a daltonist, and if the mother has no daltonism allel at all, he will although transmit the allel to his daughters, who, while not being daltonists, will be able to transmit it to their own child.
 In the same case (father daltonist, mother with no daltonism allel at all), if the child is a boy, he won't be a daltonist and won't be able to transmit it to his own child, etc, etc.
Remember, this is a simple way to present things, and do not pretend to be at the top of today's science vision, and even more not  the truth - above the fact I'm not a biology specialist, every scientific that deserves this name won't ever be claimed to say the truth, something reserved for religions - and that's why science and knowledge,  in general as well as for each people in the same spirit state, progresses ...
Last word, concerning the numbers of genes, according to Wikipedia - but you know that Wikipedia is not always the best source ;) - a human male has an estimated amount of 21 000 genes, and a woman, something between 0 and 50 fewer genes (800 genes on the x chromosome, 50 on the y one, but some of these are commons to both. How many, I don't know ...).
Sorry for the multiple edits, I try to give my 2 cents on this question after 2 days and a night without sleeping

can you add some references to your answer?

I'm a french guy, the references I took to check my knwoledge are in french ... Maybe, you can take a look at wikipedia with the words "color blindness", 'genetics' passage, and with the word "chromosome", 'human chromosome' passage, for a first approach

Note - I edited my answer, first speaking about eyes color, to explain the principles, bu t eyes colors genes are not on the 23rd pair of chromosome. I took so the daltonism, color blindness, but this exemple is still not perfect, just a simplifaction, as it seems that daltonism may comes from a gene mutation too, and his not only inherited ...
But the principle for the inherited part is the good one, and illustrate enough, I think, the  xy and number of genes discussion. Even if in fact, there is more complexity ...

As @GerardoFurtado noted in his comment, dominance applies to alleles, not genes. There's no such thing as "daltonism gene".

To Chris : I will edit it
To Dimitry: right, that's what i called "kind of gene" and "genes" to simplify, the "kind" being in fact a gene, and the "gene" being an allel .
I did proceed this way because number of people make the confusion.
And I dont want to make here a biology thesis - and I m not able to ;)
I dont want to make a biology thesis, and am not able to. But I can modify my comment i

As Remi.b said, there are different definitions of what a gene is. I found some more sources, if I understand correctly, according to the table in this wikipedia article with Data source of Ensembl genome browser release 87 https://en.wikipedia.org/wiki/Human_genome, a male human would have 14600 "pseudogenes" and a female human would have 14800 "pseudogenes" in each cell, and according this another table https://en.wikipedia.org/wiki/Chromosome#cite_note-26 , a male human would have 21000 genes and a female woman would have 21750 genes in each cell

Pablo, in fact there is no contradiction, first link speaks about 20 000 genes.
But in those genes, there are some which are not activated, called pseudogenes...

I would add your comment to my post, but since I'm not very familiar with all of this, I might slightly or moderately missunderstand you, so may be you want to add this comment to your post, and make a reference to mine stating that there isnt a contradiction in both lists. If some of them are pseudogenes because they arent activated, why in the table they only have an entry for "pseudogenes" (and not for those which are activated and which would be called simply genes?)


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How Dark skin protects humans in sunnier climates?
According to Physics, Black Body absorb all incoming light reflect nothing when compared to White body. This phenomenon is called Black-body radiation. So Melanin should turn your skin into white for protect the body from harmful rays in sunnier regions, that is not happening in Biology of Human Beings.
This is why Most of School Uniforms are specifically white on Saturdays (Because of intensity of sunlight is more on that day)
Then How Dark skin protects humans in sunnier climates?
My Question is different from this question because I mentioned physics subject also in my question.

"This phenomenon is called Black-body radiation". No, Black-body radiation has nothing to do with this. Black-body radiation is the electromagnetic radiation emitted by a black body when heated to a certain temperature, which depends only on the temperature itself and not on the molecular composition of the black body. Planck's explanation of the black-body radiation, proposing the "quanta" of energy, initiated what is now called quantum physics.

Also, Saturdays are in no way any different from any other day of the week in terms of average sun intensity. Where did you even hear this???

I suggest that you do some more of your own research on the topic to learn more about the issues/errors in your arguments that led you to ask this question in the first place. Then, you can try to edit this question to improve it's quality to avoid having it closed.

Your question is based in a wrong assumption: that the epidermis should be white or that a white epidermis would reflect electromagnetic radiation and, therefore, protect the DNA against the ionizing portion of that radiation.
Before anything else: human epidermis without pigments (like melanin) has no color, that is, it's transparent. The white color we see in people with low melanin concentration is mostly due to the collagen in the underlying connective tissue1.
So, we have two possibilities:

A transparent epidermis, which allows ionizing radiation reaching the living layers of epidermis (stratum granulosum and below, see the image) and dermis;
An epidermis with a pigment that somehow "blocks" (absorbing or reflecting) the ionizing radiation.

Of course, it's not a good idea allowing all that ionizing radiation getting to the DNA, and because of that possibility #2 was the selected one. Therefore, there is production/accumulation of a pigment in the epidermis.
But which one, a white one or a black one?
Two important pieces of information may help you to understand this point.
First, the white pigment assumption doesn't mean the pigment need to be white: the pigment only have to reflect the ionizing (UV) section of the spectrum. It could be of any color, even almost black. Actually, melanin does reflects some UV radiation2.
Second, and the most important: if a given pigment just reflects the radiation, this radiation can still go to other nuclei and reach DNA, just like the scattered blue light in the sky goes everywhere, up and down. It's way more logical (I'm not implying that evolution operates logically, I'm just addressing your question) having an pigment that absorbs the ionizing radiation, which is the case of melanin.
By absorbing ionizing radiation, melanin (partially) avoids this ionizing radiation reaching the DNA.
References:

Skin: A Natural History; Nina G. Jablonski, ISBN: 9780520275898, February 2013
Brenner M, Hearing VJ. The Protective Role of Melanin Against UV Damage in Human Skin. Photochemistry and photobiology. 2008;84(3):539-549. doi:10.1111/j.1751-1097.2007.00226.x.

Nice answer, +1! I've added a references section so that readers know which articles you're citing, without opening them. Feel free to roll back :)

It's way better now, thanks!. I'm still editing just to improve the grammar/wording.

Melanin is an antioxidant and absorbs free radicals associated with UV rays, iron, metals etc. This explains why anemia correlates with melanin.
Wetter climates have more diseases and free radicals, which is why moister climates are melanizing as well.
Melanin can potentially crowd in the body's own oxidants, such as testosterone, because it removes external oxidants.

Thanks for your contribution...can you add some references to your answer? We always appreciate cited references for everything on the site - it helps individuals who are less familiar with the subject area read more about the question/answer.

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Why heart beats increase when we are in a state of tension even though it is a disadvantage?
Suppose a poisonous snake bites you; this will likely cause hypertension, and it will result in your heart rate increasing dramatically.
Because of the high rate of heart beats, your body will make the snake poison circulate throughout the whole body even faster. This will likely bring about death even faster. (definitely 100% disadvantage)
Why do heart beats increase when we are in a state of tension even though it is to our disadvantage?

Do autonomic nervous system differentiates a snake bite and a dog bite?

What research have you done before asking it here?

Hypertension and increased heart rate are not necessarily the immediate effect of ANY snake venom. In fact, Captopril is a drug for treatment of high blood pressure, which was derived from the venom of a Brazilian pit viper (see here and here for more information). So it really depends on the snake.
Also consider the fact that snake's and potential prey's evolution may not have each other's best interest in mind...

The heart rate increases due to any acute stress, it is part of the flight or fight response. This is part of the responses that readies the body for rapid extreme effort.
The body is not selective about it, any acute stress causes it. One idea why is that a hormone response is slower than a direct nervous response so the preparing the body needs to happen as fast as possible since it takes longer to complete, compared to an actual identification, decision and movement.
Also remember that only for a small number of snake bites is this counter-productive, for others it does no additional harm but helps get you away from the snake. Snake venoms vary greatly in their effects.

Because it's a poison so it has to do it's work which is making as much harm as it's possible.
Also, I'm not sure if heart beats faster because of poison or because of how you react for being in danger.
If it's because of the danger then it works with all dangers. Of course some situations could be better handled without this adrenaline rush but evolution shaped us to increase adrenaline so in most cases it helps - and the same reactions is visible in other animals.

Welcome to Biology.SE! Please add some references to your answer.

It has to do with the fact that blood needs to circulate faster when your body is in stress. Blood pressure tends to rise, and blood tends to pump faster to the brain, to compensate with the stress factor.
Even so, If you are bitten by a poisonous snake, your body has no choice. It is basically programmed to do what it does.

Welcome to Biology.SE and thanks for your contribution. Biology.SE is a scientific stack and we therefore ask users to mention their sources, and preferably references to articles in credible journals in their answers to allow other users to background read on the topics covered.

I disagree that your body has no choice.  If you panic as the result of a snake bite (or even just seeing a snake), your body will release adrenaline (& perhaps other hormones?) that causes increased heart rate &c.  If you don't panic, it won't - or at least not nearly as much.  If you've ever had allergy tests, where adrenaline is injected to counter the allergens, you've experienced the reverse of this: you get the increased heart rate & other physical fight/flight responses, without experiencing the mental state.

Your heart rate elevation is part of the body's fight or flight response, to essentially prepare your body to either fight the danger or to flee from it. Now, it doesn't matter if a snake is threatening you or you are in a stressful situation, the body reacts to it the same way. This is a basic response in almost all animals. So yes, the increased heart rate does help in getting more blood to your muscles which basically need all the energy they can get in tense situations. It's actually the same mechanism for any sort of stress, including fear (you might have noticed during a horror movie!). So while it is a disadvantage if you get bitten, most of the times it is serving to get you away from the snake ASAP.
https://en.wikipedia.org/wiki/Fight-or-flight_response

Please add some more details to your answer.

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Why do sharks continually regrow their teeth?
Other animals don't do this. What is unique about sharks that requires them to regrow their teeth over and over, or what benefit does it provide them (that wouldn't also be evolutionarily advantageous to other animals)?

They routinely lose them in struggles with prey. I suppose a backup is useful. See this question on why traits with an advantage don't evolve. That should explain why perhaps other species don't have this ability:

Actually, most animals with teeth are polyphyodonts - they regenerate teeth throughout their lifespan. This includes sharks, crocodiles, fish and some mammals (kangaroos, elephants and manatees). Diphyodonty (only replacing teeth once) is the exception. I have a vague memory from undergrad that the evolution of specialised teeth in mammal-like reptiles, and specialised jaw musculature (which happened at the same time) is/was believed to be the reason behind this - for a reason I can sadly no longer remember, tooth specialisation and tooth regeneration are incompatible. When I can find more details and a source for the latter I'll edit them in.


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Meaning of "primers IL-2" in a scientific article
From an article ("Amelioration of Experimental Autoimmune Encephalomyelitis in Lewis Rats by FTY720 Treatment", 2003):

We performed PCR amplification in a 100-μl reaction mixture containing 200 μM of each of the regular dNTPs, 10 pmol of each primer, and 2.5 U of TaqDNA polymerase (TaKaRa) using primers IL-2 (300 base pairs; bp), 5′-CAGCTGTTGCT GGACTTACAGG-3′ and 5′-CACAGTTGATGGCTCATCATCG-3′; IL-6 (294 bp), 5′-GACTTCACAGAGGATACCC-3′ and 5′-TAAGTTGTTCTTCACAAACTCC-3′; INF-γ (310 bp), 5′-GGATATCTGGAGGAACTGGCAAAAG-3′ and 5′-GCTAGATT CTGGTGACAGCTGGTG-3′; β-actin (461 bp) 5′-CATCGTGGGCCGCTCTAGGCA-3′ and 5′-CCGGCCAGCCAAGTCCAGACGC-3′.

I'm not completely sure: do they mean that the primers are "specific to the IL-2 gene"?
Do they mean "5′-CAGCTGTTGCT GGACTTACAGG-3′ and 5′-CACAGTTGATGGCTCATCATCG-3′ are primers that are specific to the IL-2 gene"?

Looks like they're missing a semi-colon so yes, primers; IL-2...

From the description, yes, those primers are supposed to be specific for the IL-2 gene. The way they would be used would be on mRNA, not DNA, so you could use them to quantify the level of IL-2 transcription. However, there seems to be some glitch in there, because while the first sequence (5′-CAGCTGTTGCT GGACTTACAGG-3′) matches rat IL-2 mRNA starting at 120 in the sequence,  the second one (CACAGTTGATGGCTCATCATCG) does not match any IL-2; a BLAST search only turns up random and irrelevant matches.
This may be an error in the paper (copying and pasting the wrong primer, which is extremely common, unfortunately); it may have been an error in design (someone used the wrong primer and got lucky results that seemed to match what they expect); or I may be doing something wrong, which I'm not going to try to troubleshoot any more than this.
(Edit, as @VonBeche points out in comments the reverse primer is almost a match at 398, with a one-nucleotide mismatch that screwed up my search -- possibly allelic variant, but equally possibly a mistake)

The reverse primer starts at 398. Nice trick for blasting specific sequences like this: set the species to rat (or whatever you need). Especially with short you'll find too much uselessness otherwise.

Annoyingly it's not a perfect match (A/C at 9) so my grep on the sequence didn't find it.

@iayork, That's why we have BLAT ; )


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Cortical projections from layers 2/3 back to 4?
As all excititory neurons in layer 4 are stellate - they have no apical dendrites that could project to layers 2/3. However, I have seen some diagrams showing axonal projections from layers 2/3 back to 4, but then I see other diagrams that don't show it.
Is there enough evidence to show axon projections from 2/3 to 4? If so why do so many diagrams leave them out?

I've upvoted both Q&A but referencing your question would greatly improve both Q&A

Excitatory neurons in layer 4 are not all stellate in all cortical areas, for example see Smith and Populin, 2001 who show clearly that in auditory cortex most excitatory cells in layer 4 are pyramidal. There are also many cortical areas that have no clear "layer 4" and also do not contain spiny stellate cells.
In general, intracortical circuitry is not fully understood. Although your question shows understanding of this next point, let me highlight it anyways because it is a point that is often forgotten: neither axons nor dendrites are constrained to the layers containing soma. Therefore, it is possible for a cell of "layer A" to contact a cell of "layer B" even if the "layer A" cell has no axons in "layer B" and the cell of "layer B" has no dendrites in "layer A": they could have axons and dendrites in "layer C", for example.
One approach has been taken by some such as Binzegger et al., 2004 is to estimate intralaminar cortical connectivity based on co-occurrence within a given layer of axons and dendrites. This approach is an approximation, of course, because there is no guarantee that axons contact dendrites randomly within a given layer. For example, axons could preferentially contact the dendrites of inhibitory rather than excitatory cells, and this would fundamentally influence the circuit dynamics.
The result from Binzegger et al (their Figure 1 is a fairly clear summary figure, if you want to start there) is that, although there are some predominant patterns of connectivity, there is no pure feed-forward circuit: all of the connections are at least partially reciprocal. For the example you gave, layer 2/3 to layer 4, the number of connections from layer 2/3 to layer 4 is estimated to be about half as many as the number of connections from layer 4 to layer 2/3.

Figure from Binzegger et al, 2004; Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License
However, it is also possible that these connections preferentially target inhibitory cells rather than excitatory cells in layer 4: see Thomson et al., 2002.
It is likely that the variety in sources/diagrams you are familiar with is simply because people take different approaches to complex systems (and different approaches may be warranted in different situations). Some people choose to highlight the most salient features, perhaps the strongest layer-to-layer connections, in the hope that this produces an understandable, though simplified, model. Other people choose to highlight the vast complexity, emphasizing all of the smaller details that may actually be important.
For an analogy, a chef is likely to just deal with olive oil. They don't care that olive oil is actually a collection of several fatty acids: it's just olive oil to them, and the importance to them is that olive oil is distinct from another vegetable oil. A biochemist, however, might be interested in the specific fatty acids and might point out that those specific fatty acids are found in all sorts of other oils. Neither one is likely to convince the other that they have the better answer for all purposes.
Neither approach is strictly incorrect or better than the other, until better understanding makes one of the approaches obsolete.

References:
Binzegger, T., Douglas, R. J., & Martin, K. A. (2004). A quantitative map of the circuit of cat primary visual cortex. Journal of Neuroscience, 24(39), 8441-8453.
Smith, P. H., & Populin, L. C. (2001). Fundamental differences between the thalamocortical recipient layers of the cat auditory and visual cortices. Journal of Comparative Neurology, 436(4), 508-519.
Thomson, A. M., West, D. C., Wang, Y., & Bannister, A. P. (2002). Synaptic connections and small circuits involving excitatory and inhibitory neurons in layers 2–5 of adult rat and cat neocortex: triple intracellular recordings and biocytin labelling in vitro. Cerebral cortex, 12(9), 936-953.

I really would like to see more diligent users as you here. +1. I hope my bounty has helped in your sustained release of awesome posts :-)


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How would you identify the independent variable in an experiment where it isn't specified?
I know that the above question is broad, but I specifically want an answer in terms of the following investigation - all of question 3 (ONLY) of this paper.
The independent variable, according to this mark scheme is the presence of hidden food in the cage to which the rats are released. How am I to identify this if it's not stated that the investigation investigates the ability to learn with the presence of hidden food.

Please include the question from the external site. There are good reasons to do this. The main one is: once the link breaks, your question is worthless. I'm voting to close this question as unclear because even though I have read the exam question and helped to edit the previous version of this question, you still do not have a specific question. Are you asking "what is an independent variable"? I sympathise with your question. It's a poor exam question in my opinion.

@James, it does indeed indicate that. The exam question claims that the difference in the percentage of mice in group P and Q who found food in the second experiment was due to the fact that the group P mice had to look for food when they were released the into the cage the first time around. In the first version of the question, I had completely missed the fact that there IS indeed an independent variable in this question. I deleted the other question. I am absolutely baffledas to how one can note the independent variable in this investigation when the question does not state it at all.

Yet, we seem to be required to notice such an independent variable. How? That's my new question, and it's completely different from the previous one. Does that make the question more specific? :)


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When analyzing whether selection favors an allele that allocates indiscriminately, should the initial frequency of the allele be considered?
For example, Refardt, Bergmiller & Kummerli (Proceedings Royal Society-B, 2013; http://rspb.royalsocietypublishing.org/content/royprsb/280/1759/20123035.full.pdf)
model bacteria that have been infected and that commit suicide  in order to prevent the spreading infection to the rest of the population.  They do so even though relatedness is low, approaching zero.
Two questions:

In section 3c, they write

(A)ltruistic host suicide cannot evolve with $r=0$ because populations
  go extinct before invasion of the Abi trait is possible.  Thus, we
  predict marginal relatedness ($r < 0$) to be required for successful
  invasion.

I am assuming this is a typo and they mean $r>0$?
In a situation in which altruism is not directed toward any particular individual(s) but is rather allocated to the whole population, doesn't $r$ depend upon the frequency of the allele that is engaging in the altruism?  If it is a new mutation and there is no other allele in the population to receive the benefit, then r=0.  If the allele has gained fixation, $r=1$ and selection is much more likely to favor the altruism.

What is a way of modeling whether selection will favor fixation of a new mutation that allocates benefits to the population but not any particular individual (e.g., by committing suicide), given that the new mutation is not shared by (m)any other individuals and consequently, $r$ is initially very low?  I would think there is a way of determining the odds that genetic drift would lead the new mutation to develop a substantial enough frequency to increase the odds that the resources would benefit holders of the allele.  But I am unfamiliar.

I have not read the paper but here is my guess and a hint

Is it a typo?

Yes, I think so

In a situation in which altruism is not directed toward any particular individual(s) but is rather allocated to the whole population, doesn't r depend upon the frequency of the allele that is engaging in the altruism?

Yes

f it is a new mutation and there is no other allele in the population to receive the benefit, then r=0. If the allele has gained fixation, r=1 and selection is much more likely to favor the altruism.

If the allele that is causing altruism has reached fixation, then there is no more selection as there is no genetic variance in the population.

"If the allele that is causing altruism has reached fixation, then there is no more selection as there is no genetic variance in the population."
You're right.  I apologize.  That was a mistake.  But the question still stands:  If it's a new mutation, r=0.  If the allele has substantial frequency, r is closer to 1, and it is more likely to be selected.
The ways of modeling drift and selection that I have seen involve stable fitness.  Is there a way of modeling the effects of drift and selection when fitness is frequency dependent?


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Do Asian koel males communicate through calls?
Male Asian koels are heard making long koo-Ooo s  which are returned by similar koo-Ooo s1 from some far away place. While the female makes short shrills.
I never had the opportunity to see the other bird and find out its sex. But it sounds just like the first one.
Is it actually communicating with a male bird? What is the known reason if so?
1 The reply calls (to be found around 0:29) in the video are really low.
Note:

A singing male bird also gives desperate accelerated calls when  mimicked.
Its breeding season has just begun in India and this communication can be heard.

I'm not sure about this particular species of bird, but males of numerous species call throughout their territory to inform other males of their territory. This is especially true of migratory birds that move in and out of areas (with recently sexually mature males now trying to find their own territories and fighting for limited space) "Responses" could very well be males in nearby territories doing the same thing. Just a thought...

Also, I don't hear any response in the video you link to -- it just sounds like echoes of the male in front of the camera. Are you referring to that sound, or is there another call I missed?

Still working on this question and the following are the findings:

The male bird when mimicked possibility mistakes the mimic as an intruder in its territory and so it gives louder & accelerated calls.

The male while defending its territory gradually approaches its adversary, hopping from twig to twig calling loudly and displaying its threatening posture. ( B S Lamba (1969) )


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CRISPR/Cas9: What are the main differences between sgRNA and the Cr:TracrRNA ?
So from what I understand, in gene editing, the CRISPR vector expresses a small RNA sequence comprised of a small guide-RNA that is complementary to your target sequence. The sgRNA comprises a 20 Bp CrRNA and a truncated (cut down) TracrRNA right ?
My main question is how does this truncation enable gene editing ? After all, the bacteria have a full TracrRNA and not a truncated one.

You are correct about the components of the sgRNA.
However the truncation of the tracrRNA does not enable gene editing. Rather it is all that is required.
In bacteria the crRNA and tracrRNA are distinct molecules which must pair through the complementary palindromic repeat sequences. This is not the case in gene-editing as the crRNA and tracrRNA have been fused with a synthetic stem loop. Thus the palindromic repeat sequence is not required and the tracrRNA is shorter.
Check out Cong et al. (2013) in Science.

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


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How does translation invariance in vision happen?
Convolutional neural networks are very popular these days in computer vision.  One of the things they do quite well is recognize objects with translation invariance.  The way they do this is by "tying together" the strengths of certain synapses, so that they all change in the same way during learning.  This is apparently not biologically plausible.
My question is this: what is known about how biological visual systems achieve translation invariance.  For example, how is it that if we learn to recognize a new object with our left eye, we are automatically also able to recognize it with our right eye.  What is the neuro-biological basis for this invariance?  My field is mathematics/machine learning, not biology, so I would appreciate responses that are not overly technical (although I understand that might not be possible).
Thanks!

Great question - unfortunately I think what you are asking is actually quite broad. I'm hopeful someone might come along with a reasonable answer, but in fact this is a very open field in biology right now. We know a bit about what areas of visual cortex show some translation invariance in their tuning, but my understanding is that's about it, beyond computational modeling that shows feasible approaches.

From the perspective of machine learning, consider that the visual cortex has many more layers than a typical artificial neural network, and the layers are interconnected in a much more complex and less strict hierarchy. This organization allows for incredibly complex computational abilities. Importantly, biological neural networks have simultaneous bottom-up and top-down processing, allowing brain areas with very abstract representations to make predictions about less abstract features. Additionally, attention and related processes allow for online reorganization of networks.

@BryanKrause you gave a very good general insight to seemingly broad question. I would like to know if you pulled this insight from a paper? I would like to read it. Especially about "simultaneous bottom-up and top-down processing".

@gfdsal I didn't have a single paper in mind, but Felleman, D. J., & Van Essen, D. C. (1991). Distributed hierarchical processing in the primate cerebral cortex. In Cereb cortex. is a good place to start. You could also look for recent reviews about "predictive coding", though this is only one of the schemes/frameworks used to think about hierarchical processing and it remains to be seen if it's the best description. I also think you'd find at least some discussion in an undergraduate neuroscience textbook like Purves or Kandel.

+1 for providing credible references and direction to take.


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Are there any fruits that rely on dispersal of their seeds using excrement?
Are there any fruits that have seeds which can survive the digestive entirety of an animal's digestive system and remain germinable once passed on in animal excrement?
Perhaps this is the primary function of all seeded fruits and I'm just fundamentally unaware of the intended biological processes. If so, then why do poisonous seeded fruits exist?

Yes, many. A common example is the fruits containing capsaicin (e.g., hot peppers): this compound is an irritant to mammals but does not affect birds. This adaptation seems to have evolved to discourage consumption of the fruit by mammals, whose digestive systems damage the seeds, and to encourage consumption instead by birds, which distribute the seeds effectively.

Seeing as the main premise of your question is completely wrong (meaning that loads if not all fruit can survive the digestive system of an animal), I am voting to close as unclear. Please do some research (just glance through a wikipedia page or something) and ask something a bit more specific.

@terdon https://biology.meta.stackexchange.com/questions/2961/voting-to-close-a-question-as-off-topic-because-it-is-based-on-a-faulty-presuppo

@canadianer yes, but my vote wasn't because the premise was wrong but because, given that the premise was wrong, the question is unclear. I mean, the question in the title can be answered by "Yes, most of them" but I don't think that's very interesting to the OP.

That's really kind of the point of having fruit in the first place. Why would the plant waste valuable nutrients just to feed animals? That doesn't mean that all fruit seeds survive the digestion of all different kinds of animals, of course, but the whole purpose of a fruit is to be eaten or carried (a lot rarer) by animals for dispersion.


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Good resource for penguin behavior for non-specialists
I just returned from Antarctica where we made many shore excursions and spent a great deal of time among penguins -  mainly Gentoo, and some Chinstrap species.
They were fascinating and there were several distinct behavioral patterns that I observed but did not understand.   I'm not really asking for explanations here, but just a good introductory source of penguin behaviours.  When I've searched online everything I've seen is either too general and basic to be helpful, or too technical and specialised for me. I have a strong general science background and I'm an AAAS member and I have one ethology course from decades ago, but reading peer-reviewed research papers on this would be over my head.   We were there in March (late summer) so the juveniles were adult-sized but still had juvenile plumage.
Examples:
(Gentoo) being on beach or snowfield where there was a dense, mainly uniform distribution of adult and juveniles standing or laying around, when in the midst of this a line (typically 4-8) of adults would walk briskly, single file, through the groups of standing individuals, and even through the groups of standing humans, all looking straight ahead and apparently with a sense of purpose.  They would walk out of sight.   Why, and are they connected or related somehow?
(Gentoo) coming up to us and grabbing anything loose like backpack straps, number tags on lifevests, or pantlegs flapping in the wind and pulling.  This was not pecking like they would trying to get an adult to feed them, but I mostly saw this with juveniles.  We were under instructions to not make any noise or motion that would alter their behavior but when one started tugging on my lifevest inflation tab I had to yell to stop him.  (IAATO guidelines are to stay 5m away from wildlife but the penguins didn't attend our orientation seminar and anytime we stood still they came up to us)  Juveniles frequently nestled between our legs if we stood still (all of us were wearing thick, insulated, multi-layers of pants), but this is easy to explain regarding chicks nestling in the adult's brood pouch, since we frequently saw adult-sized juveniles exhibiting other chick behaviours, eg, food-seeking from adults.
(Chinstrap) large groups (30-50) of individuals standing tightly together when many (but not all) would suddenly point their heads up and start to vocalise, sometimes flapping their wings.  This would go on for a minute or so and then stop suddenly. I made videos of this.  I never saw any sign of a threat, say from a skua or seal, nor did they seem to be looking at anything, and nothing obviously changed that made them stop.

Not an answer, but Michelle LaRue (@drmichellelarue on twitter)  is a penguin biologist and is always very generous about answering questions-- she encourages people to ask her questions all the time.


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ID a shell from Puerto Rico
I recently found this in Rincon Puerto Rico on the beach.
I assumed it was a baby sea turtle shell or some kind of turtle. Someone that frequents Puerto Rico said it was not. Does anybody know what this is?

Welcome to Biology.SE. Nice pictures fo ID. Would be good to see the other side though.

Well it doesn't appear to be any of the marine species or native freshwater species of turtle that frequent Puerto Rico.

This is the shell of a marine mollusk called a chiton.

They are also sometimes known as sea cradles or "coat-of-mail shells", or more formally as loricates, polyplacophorans, and occasionally as polyplacophores.

In Puerto Rico, they call these animals "Quitones."

All chitons bear a protective dorsal shell that is divided into eight articulating aragonite valves embedded in the tough muscular girdle that surrounds the chiton's body.

My initial guess as to the species is: Chiton tuberculatus.
 (Disclaimer: I know almost nothing about these animals, so this is at best a guess).

 Source: NATURAL HISTORY MUSEUM ROTTERDAM

 Source: NATURAL HISTORY MUSEUM ROTTERDAM
You can find additional images that look even more like your specimen here and here
According to Wikipedia:

This species can be found under rocks and in spray zones of rocky shores, in the intertidal, shallow subtidal zone of Western Central Atlantic (USA, Colombia, Bermuda, Mexico, Venezuela and the West Indies)

This includes Puerto Rico

Based on Fig 1 of Crozier (1918) showing typical sizes of various ages of C. tuberculatus, you have a fairly young specimen (likely only a few years old).
The Quitones of Puerto Rico by Cedar García Ríos (ISBN: 1-932271-16-3) is probably a good tool for definitively IDing your specimen to species.


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Why is thymine not incorporated into mRNA?
I am aware that in transcription uracil bonds to adenine and not thymine. But what is it that actually prevents thymine from bonding to adenine in transcription, that is not present in replication?

Nice question! But sadly, it comes under the category of questions about which we don't know everything yet. We don't yet know how RNA Polymerase differentiates between uracil and thymine while adding nucleotides to growing mRNA chain (at least, I was unable to find research papers online), most probably because it has proved difficult to know the exact mechanism of RNA synthesis which RNA polymerase undergoes. But we do know what factors it could use to do so. For general introduction, these factors are:

mRNA chains contain NTPs instead of dNTPs. Now, TTP is very (very) rarely found in cells. So, RNA Polymerase can look for 2'-OH in nucleotide for adding base (pay attention that RNA polymerase is not known to have proofreading mechanisms, but there is growing evidence that RNA polymerase can correct a faulty base pair matching, see Thomas et al). RNA polymerases are known to be able to distinguish between NTPs and dNTPs (Svetlov et al), although the precise mechanisms in multi-subunit RNA polymerase remain elusive. Yet, this property certainly plays a role (refer to EDIT 1 for details about this).
UTP and dTTP have another basic structural difference: of a methyl group. This difference is crucial for differentiating the two, especially for DNA repair machinery. It is so because cytosine can spontaneously convert to uracil (by deamination). So, there has to be something for repair enzymes to look for while repairing mutated cytosine, and a methyl group saves thymine from repair. See the following image for comparison:
source

Just for information, we know the flip side i.e. how DNA polymerases prevent dUTP from adding in DNA chains, because dUTP is much more common than TTP. Simply saying, they don't. Mutations can (and do) occur, leading to faulty addition of dUTP in DNA. But, this is where repair machinery helps. Cells contain an enzyme, uracil DNA glycosylase, which replaces uracil by thymine in DNA (Longo et al). So, until we find the exact mechanism for RNA polymerase, you can assume that it uses much similar mechanism for proofreading (along with the first one of course).
EDIT 1: I will add some details about the mechanism of base pair matching by RNA polymerase as just leaving the point at yet, this property certainly plays a role makes the answer misleading to some people. But, because putting the whole mechanism here would make the answer too long and also out-of-scope (keeping in mind you asked 'why', not 'how'), I'll try to keep this part as small as possible. Giving a diagram for better understanding:

Pay attention at the Tyr639 and His784 (sugar discriminators), this is how the RNA polymerase distinguishes NTP from dNTP. It has also been shown that removing Tyr639 will convert the RNA polymerase to DNA polymerase(!), though removing His784 would just decrease its activity, suggesting its role to be minor w.r.t. Tyr639. For more information, have a look at this page from Brooklyn college website.
EDIT 2: In another answer, the answerer says RNA synthesis requires rNTPs instead of dNTPS as precursors, but does not explain why it is so (which is indeed an important part). So I'll add that part in my answer. It can be explained by following points:

The sugar discriminators of RNA polymerase (describe above) do not allow dNTPs to add to the growing chain. Thus dNTPs cannot act as substrates for RNA synthesis.
The enzyme for synthesis of thymine (dTTP) is thymidylate synthase, which requires dUMP as substrate. Thus, it is not possible to create rTTP instead of dTTP.
Conversion of uracil to thymine requires energy, meaning uracil is energetically less expensive than thymine. This also directly explains (partly) why mRNA doesn't incorporate thymine into the chain.
Degradation of mRNA requires an enzyme ribonuclease which cannot degrade dNTPs. Also, in the mechanism of degradation of mRNA, 2' -OH plays a role. This can be explained by diagram below:

As is visible, 2' -OH is an important part for RNA degradation. Thus, it wouldn't be possible to degrade mRNA in this way if it contained dNTPs.

References:

Matthew J Thomas, Angelina A Platas, Diane K Hawley, Transcriptional Fidelity and Proofreading by RNA Polymerase II, Cell, Volume 93, Issue 4, 15 May 1998, Pages 627-637, ISSN 0092-8674, http://dx.doi.org/10.1016/S0092-8674(00)81191-5.
Svetlov V. Vassylyev D.G. Artsimovitch I. Discrimination against deoxyribonucleotide substrates by bacterial RNA polymerase J. Biol. Chem.  2004 279 3808738090
Mary C. Longo, Mark S. Berninger, James L. Hartley, Use of uracil DNA glycosylase to control carry-over contamination in polymerase chain reactions, Gene, Volume 93, Issue 1, 1 September 1990, Pages 125-128, ISSN 0378-1119, http://dx.doi.org/10.1016/0378-1119(90)90145-H.
Dziuda, D.M. (2010). Data Mining for Genomics and Proteomics: Analysis of Gene and Protein Expression Data. Wiley
Roberts, Gordon C. K. et al. “THE MECHANISM OF ACTION OF RIBONUCLEASE.” Proceedings of the National Academy of Sciences of the United States of America 62.4 (1969): 1151–1158.

Not trying to be too critical, but I think that's a bad assumption to make. Also, the structural difference between thymine and uracil doesn't seem particularly relevant since RNAP could not possibly use it to distinguish them. The mechanism of sugar selection by nucleotide polymerases seems to be pretty well understood. See this article, for example. Combine that with your assertion that TTP is rare in cells and a plausible answer seems apparent.

@canadianer dude thats jackpot! Where did you find that paper? Also, the point with base selection is that its precise mechanism in RNAPs is not known (thats why you also said possibly). And as long as something is quite not known, I don't think any assumption could be bad. Yet, its about opinions, who knows even the assumption might get true? :)

One main feature of polymerases is that they have multiple substrates and don't disntiguish them by the nucleobase. Given that they have to accommodate larger purine moieties, I don't see how the methyl group of thymine could be used to distinguish it from uracil.

@david any doubt that arises from my answer is a demand for me clear it out. Anyways, your opinion has only made my answer better, and thanks for that :)

The answer to this question is quite straightforward:

Thymine is not incorporated into mRNA because the precursors of RNA
  synthesis are ribonucleoside triphosphates (not the free bases) and
  there is no pathway for the synthesis ribothymidine triphosphate
  (rTTP) in cells — only for the synthesis of deoxthymidine triphosphate
  (dTTP).

I suspect that this rather naïve question arises from the misconception, common among those exposed only to brief popular accounts of the topic, that free bases are the precursors of nucleic acids. In fact it is the nucleoside triphosphates, that are the precursors, and the key difference between RNA and DNA is between the sugars ribose and 2-dexoyribose. It is obvious that RNA polymerases are specific for ribonucleoside triphosphates, otherwise deoxyribose would be found in RNA.
Rider: Why is there dTTP but not rTTP?
Although not strictly part of the answer, I think that it may provide a perspective on the topic to explain why there is no rTTP in cells, even though there is dTTP. This is because of the way dTTP is synthesized — not the trendiest of topics — but one involving enzymes that are so crucial to DNA synthesis that certain large DNA viruses encode their own copies.* The diagrams below are my own. A more extensive account can be found in Chapter 25 of Berg et al. online — Nucleotide Biosynthesis.
There are synthesis pathways for rAMP, rGMP, rUTP and rCTP. (The first three of these need to be converted to the triphosphates for RNA synthesis.) For DNA synthesis the ribose ring of the rNDPs is reduced to deoxyribose. Note that this produces dUDP which is subsequently converted to dUTP:

To produce dTTP, dUTP is converted to dUMP, which is methylated to dTMP by the enzyme thymidylate synthase. (dTMP is then converted to dTTP.)

The free bases do not occur in cells as a result of synthetic reactions, but as nucleoside monophosphates. However free thymine is generated during the degradation of DNA. This can be ‘salvaged’ by the pathway including thymidine kinase:

*These are the herpes viruses. Although not found in every case, the following enzymes occur in various herpes virus genomes: ribonucleotide reductase, thymidylate synthase, dUTPase, dihydrofolate reductase and thymidine kinase.

Although an answer has already been accepted, I have posted this because I think the accepted answer confuses the issue. It may seem strange that I have added a long rider regarding DNA metabolism when the question is about RNA, but I think it important to understand the metabolism of thymine in cells in order to appreciate why there is no rTTP. It also helps to illustrate the metabolic interconversions (and their energetic costs) that were required to allow DNA genomes to supplant the presumed earlier RNA genomes.

Although the accepted answer is a beautiful one, full of information, this is the one that actually answers the question. Good on you. On a side note, it would be very interesting explaining why, evolutionaryly speaking, there is no U in DNA (the answer is, of course, deamination).

I only found first two paragraphs of your answer relevant to the question. Also, just writing "RNA contains uracil because uracil is precursor of RNA synthesis" doesn't really answer the question. The question just changes to "why is uracil a precursor of RNA synthesis?" in this case. See my answer, I've that part in it too.

@another'Homosapien' — I have edited my answer slightly to make it clear that the section on lack of rTTP is a rider rather than an essential part of the answer. By presenting the answer as a single sentence in highlighted quotes, I allow the reader to see my point immediately. He may chose whether or not he wishes to read further about the metabolism of thymine, which the heading makes clear is a rider to the answer. I think it is illuminating, you do not. We are each entitled to our opinons.

@GerardoFurtado — Thank you. Your answer to the question of why T not U is used in DNA is already on SE Biology at: http://biology.stackexchange.com/questions/171/why-is-thymine-rather-than-uracil-used-in-dna/24785#24785.

@another'Homosapien' I will (civilly) disagree. The answer to the question ("what prevents thymine from bonding to adenine in transcription?") is just "there is no TTP, only UTP". Of course, this brings up another question: "Why there is UTP but no TTP?". However, as I said, that's another question, do you agree?

@gerardofurtado actually both yes and no. When I read the question, I still get it as "why does mRNA not contain thymine in place of uracil?" because thats what (IMO) OP wants to know (as they selected my answer when I answered that part). So, from my side, this answer does seem insufficient, but it would be sufficient for the ones who take the question in its literal meaning.

The question is clearly mechanistic/practical with its focus on the hydrogen bonding of the bases. There is no way the poster is concerned with the philosophical/evolutionary question of why if thymine is "good" didn't it replace uracil in RNA. I have posted that as a quite separate question: http://biology.stackexchange.com/questions/57990/why-is-uracil-rather-than-thymine-used-in-rna


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What could be the reason for the large difference between sodium and potassium blood concentrations?
Reference values for sodium and potassium concentrations in blood tests are usually in the range of 135-145 mEq/L and 3.5-5.1 mEq/L, respectively.
My question is what could be the reason for this (relatively) large difference in the blood concentrations of these two ions which are together responsible for cells function and communication? What other roles does sodium play outside of cells that require it to be a lot more abundant in the blood than potassium?
Also, a follow-up question: is this proportion more-or-less maintained in other animal species?

This is much too broad. Some reading on your part about homeostasis is in order. If you still have a question then, and can explain why it is unclear from your reading, that would be a narrower question. The short answer is because it's necessary for life. When we die, equilibration occurs (more or less).

Although this is a fairly broad question, I think it could still be given an appropriately-scoped answer. One bit of information missing from the question that would make it more interesting is the imbalance between extra- and intra-cellular concentrations: not just that Na+ concentrations are greater than K+ in the blood but that the opposite is true in a typical cell.

@anongoodnurse, I have studied some basic physiology, including nervous system physiology, and I am aware of electrical activity in the cell, membrane potential, ion pumps etc. This question focuses on a very narrow (in my opinion) aspect of this very broad subject, which is merely the quantities. Actually, it came up when I was reviewing a patient's blood tests - I looked at the normal ranges and asked myself: "how come sodium blood concentration is 30-40 times greater than potassium?", or in other words, why did evolution settle on this proportion? Perhaps no one knows, but worth a try.

@Don_S - Sorry, the question read like a beginner's. In that case, God only knows, but it is still too broad. (I was a Molecular Biologist before I became a physician.)

Wait, here's an idea: nothing else lived long enough to reproduce. That answer is probably as accurate as any.

Well, thanks for sharing your thoughts. For me, this is the place to come before giving up... I hope the question won't be closed, at least 3 people liked it...

Sorry that this is an extremely simplified answer, but basically, cells make use of the concentration gradients (and some cells the electrical gradients) produced by pumping sodium out of cells and pumping potassium in. A lot of that functionality would be achieved by simply pumping sodium out, but something has to go in its place or else you would have osmotic effects. The "choice" of sodium/potassium is reasonable because those ions are freely available where life evolved, but are probably still used because a shift would be an enormous challenge to overcome.

I hope someone will come along with an actual full answer but in the meantime I just hope the question isn't closed, I think it's a good one for people at many levels of understanding. As far as other animal species, to my knowledge yes the general pattern is maintained. It likely originates from "extracellular" ion concentrations being seawater, so it is very old.


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What are some good examples of phonotaxis in plants and other inanimate beings?
Reaction to the sound waves by plants is commonly unobserved. A physical movement or chemical release examples due to phonotaxis would be good to know about.


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Prehistoric fossils
I have found very old seashell fossils (clamps) on a hill. They may be as old as a million years. Who can tell me how old they may be looking the pictures shown.

Hi @gio ! Welcome to Biology S.E. Could you please attach the pictures you mention in your question.

Fossils are dated in several ways. Radiometric dating, which we cannot do over the internet and if you're asking on the internet then you can't do it either. Identifying the fossil's species, which allows you to have a range of when the fossil could have been from insofar as other, better-dated discoveries of fossils in that species tell us when that species existed, and finally identifying the geological layer the fossil was found in. In other words, you should give a picture of the fossil so people can find the species and say exactly where you found it and what the surrounding area was like

Also the location where you found it.  If it comes from an undisturbed rock layer, that would help pin down a date.  Though perhaps not: the area I grew up in (upstate New York) had a good many rocks with fossil shells that were glacial erratics from the last Ice Age.


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How are sequential patterns grouped into meaningful objects in the brain?
The background how I came up with this question derives from information theory so I am not sure that it will formulate it well.
What I am looking for it is the process how our brain forms patterns.
Lets say I have word “Hello” (It is a complex example, but lets say that our brain is blank and sees it for the first time and somehow it can form only this pattern).
How our brain (neurons, synapse connections) “knows” that certain signals should be grouped and after “H” waits for “e” and “l” and so on.
Why it makes certain connection or just “cuts” and waits for new one.
As our brain is so complex, I am not looking for all scenarios how in could be influenced in terms of chemical neurotransmission, but I am looking for a basic principle of how it is done, i.e., how our brain manages to translate patterns into certain connections inside the brain.

I don't have time to write a full answer, but I'd suggest you look superficially into how artificial neural networks learn new patterns: although the structure of many such networks is not biologically plausible, some of the more general concepts are both motivated by the biology and support our understanding of the biology. The short, simplistic answer is that patterns themselves are associated with more abstract concepts. It isn't likely that the brain processes "hello" as h-e-l-l-o, but as a full word: hello, whether heard or read.

3/1 Well, I want to bridge from the information theory perspective to the biological perspective, but still want to keep biological background. I know that “Hello” it is not that great example as it is already complex structure and looking for very basic principle or lets say very beginning how those patterns are created.

3/2 Scenario:
If we receive different sound frequency or combinations of different light lengths,  somehow our body should differentiate inputs and “assigns” it to neurons (guessing). Based on this assumption I looking for an explanation that could explain how those differentiated and “assigned” signals to neurons, creates a connections between each other.
How those neurons that represents different signal spectrum end up connecting and form certain mirror of that signal complexity.

3/3 Brainstorming:
Is it almost the same timing and chemical released that allows neurons connect together.
Is it near the same location where signals are sent and neurons forms connections there with help of chemicals.

I'm a little confused by what type of answer you are looking for, because you talk about information theory but you aren't using any of the terminology of information theory (except "information" which is pretty broad and colloquial). I think you are also asking for answers at too many levels of analysis: you are asking about information and systems level organization and at the same time asking about neurotransmitter release and spike timing dependent plasticity. Can you try to clarify a bit what you are looking for?

At this case I think I am looking for spike timing dependent plasticity as the first step even though my question asking is complex, as I see now. Your question gave better insight in to mine own question.

The key here is the Gestalt principle formulated in the early 1900's consists of a set of 'laws' describing how perception elements are grouped into recognized objects. The Gestalt laws "prescribe for us what we are to recognize 'as one thing'". Recent data support this view (Pelli et al., 2009).
On a more fundamental level working memory is essential in this process. It is a form of short term memory. An example where short-term memory comes into play is when information is cut up in pieces, like in your example - 'Chunking' is the organization of material into shorter meaningful groups to make them more manageable.
Short-term memory is supported by transient patterns of neuronal communication in the regions of the frontal, prefrontal and parietal lobes of the brain. Long-term memories are maintained by more stable and permanent changes in neural connections widely spread throughout the brain.
The hippocampus temporarily stores information and gates it to the long-term memory. Typically, information is transferred from the short-term working memory to the long-term memory within just a few seconds,
Reference
- Pelli et al., Cogn Neuropsychol (2009); 26(1): 36-49


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What inactivates pepsin in infants?
In infants, rennin helps in digestion of milk. Pepsin is also present in their stomach.
Why do infants need rennin for milk digestion, at the first place? Why does pepsin not act on the milk proteins in infants? Does the production quantity of rennin play a role in inhibiting the action of pepsin?

EDIT: Thanks a lot to @abukaj for pointing out the mistake in my answer (and to @paracetamol for asking such a beautiful question). I am rewriting my answer to incorporate the (hopefully) correct background knowledge this time.
NEW ANSWER: As @paracetamol and @AlanBoyd (in their answer) pointed out the lack of credible support for the claim that infants produce rennin/chymosin, the previous answer attributing the digestion of casein in infants to chymosin had to be corrected. So, lets now look at the other possible candidates for casein (or, more specifically, $\kappa$-casein) digestion in infants.
As Martin et. al. (2016) claim, milk casein has some bioactive roles, such as forming masses with calcium and phosphorus1. Also, infant milk formulas mostly have higher casein content than human breast milk, making the former harder to digest than the latter. Back to the digestion point, human breast milk is known to contain many proteases in itself, including anionic trypsin, elastase, plasmin, cathepsin and kallikrein, while prothrombin has also been identified in human colostrums2. In fact, Ferranti et. al. (2004) also identified fragments of casein created by plasmin cleavage3. However, Chatterton et. al. (2004) were able to detect $\beta$-casein after 1 hour of in vivo gastric digestion in 8 day old infants, but not in 28 day old infants, suggesting the increase of digestive capacity of the infants4. This increase can be attributed to the development of gastric acid production system in the infants. For the case of newborns, Nakai and Li-Chan (1987) suggested that Pepsin C, also called gastricsin, can hydrolyze casein at the pH range of 4-5 (the lowest pH newborns can reach)5. However, the buffering effect of human and bovine milk proteins does not allow the gastric pH to reach the optimum pH required for activity of pepsin A and pepsin C.
How, then, is casein digested by infants at all? This is summarized (to some extent) by Chatterton et. al. (2013), according to which, although gastric pH is unable to reach the optimum pH for pepsin activity, it is sufficient for minor initial digestion of human milk proteins. This causes the release of glycomacropeptide, the C-terminal portion of casein. The combination of this initial digestion and the gastric pH, close to the pI of caseins (~ pH 4.6) causes precipitation of caseins and slowing down of their digestion. The casein peptides, on the other hand, are absorbed into plasma where they show a number of biological activities, including inflammation modulation and blood pressure regulation6.
Thus, even though infants lack chymosin and a fully mature digestive system, this is compensated by a combination of proteases in breast milk and the slower digestion process until the digestive system of the infants develops completely.
source
References:

Martin CR, Ling PR, Blackburn GL. Review of Infant Feeding: Key Features of Breast Milk and Infant Formula. Nutrients. 2016;8(5):279. Published 2016 May 11. doi:10.3390/nu8050279
Dallas DC, Underwood MA, Zivkovic AM, German JB. Digestion of Protein in Premature and Term Infants. J Nutr Disord Ther. 2012;2(3):112. doi:10.4172/2161-0509.1000112
Ferranti, Pasquale & Vittoria Traisci, Maria & Picariello, Gianluca & Nasi, Antonella & Boschi, Velia & Siervo, Mario & Falconi, Claudio & Chianese, Lina & Addeo, Francesco. (2004). Casein proteolysis in human milk: Tracing the pattern of casein breakdown and the formation of potential bioactive peptides. The Journal of dairy research. 71. 74-87.
Chatterton DEW, Rasmussen JT, Heegaard CW, Sørensen ES, Petersen TE. In vitro digestion of novel milk protein ingredients for use in infant formulas: research on biological functions. Trends in Food Science & Technology. 2004;15:373–383
Nakai, S. and Li-Chan, E. (1987) "Effect of Clotting in Stomachs of Infants on Protein Digestibility of Milk," Food Structure: Vol. 6: No.
2, Article 8.
Chatterton, D. E. W., Nguyen, D. N., Bering, S. B., & Sangild, P. T. (2013). Anti-inflammatory mechanisms of bioactive milk proteins in the intestine of newborns. The International Journal of Biochemistry & Cell Biology, 45(8), 1730–1747

@mesentery Pepsin can too digest casein, but at lower pH, and yes, chymosin is just another name of rennin...I'll add that part. Quite clever BTW :D

Are you sure infants produce chymosine? Please see: https://biology.stackexchange.com/a/65017/33294

@abukaj oh boy, thanks for pointing this out. I've edited the answer, feel free to let me know if you find another error(s) :D

Milk contains a protein called caesin which gets digested in an adult body with the sole help of pepsin.But pepsin requires lower pH for digesting caesin. Since infants are basically fed on milk and they have a higher pH which makes pepsin incapable of digesting caesin in their body.Therefore infants need an enzyme named renin for this purpose.

Hello Pooja. Can you please add some references to support your answer? Good references include peer-reviewed articles, books and websites of scientific organizations. I should also point out that you have not added anything more than what is already mentioned in the existing answer. Moreover, the picture you have put is irrelevant. You should remove it.


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When does histone synthesis occur in relation to DNA replication?
Do histones have to be synthesized before DNA is replicated to allow the DNA to coil around histones?

Only nucleic acids are replicated — proteins are synthesized from mRNA. If you didn't know this you shouldn't have posted but done some preliminary work instead. However your basic question on the coordination of DNA and histone synthesis is worth asking, so I have edited your question appropriately.

I love this question the way it is.

Yes, they have to. But that is just half of the story.
The (canonical) histones which are used in DNA replication are synthesized at the beginning of the S phase, and subsequently transported into the nucleus. Studies have shown that newly synthesized DNA is immediately packed into nucleosomes. Thus, it is necessary that these structures are available prior to (or at least just in time with) the replication.
However, there are different models on how the histones are inserted into new DNA. One model assumes that old and new nucleosomes are both incorporated into newly synthesized DNA after the replication fork. Others assume a semi-conservative approach where the old histones are disassembled into their subunits and then mixed together with the newly synthesized ones. For example, there is a model that proposes that the parental H2A/H2B and the H3/H4 dimers disassociate, while another assumes a disassociation of the H3/H4 dimers as well.
Figure: Nucleosome synthesis models for DNA replication

References
a Angélique Galvani and Christophe Thiriet (2013). Replicating – DNA in the Refractory Chromatin Environment, The Mechanisms of DNA Replication, Dr. David Stuart (Ed.), InTech, DOI: 10.5772/52656. Available from: https://www.intechopen.com/books/the-mechanisms-of-dna-replication/replicating-dna-in-the-refractory-chromatin-environment

In Molecular Biology of the Cell (Chapter 4), it is written that

The major histones are synthesized primarily during the S phase of the cell cycle and assembled into nucleosomes on the daughter DNA helices just behind the replication fork (see Figure 5–32). In contrast, most histone variants are synthesized throughout interphase. They are often inserted into already-formed chromatin, which requires a histone-exchange process catalyzed by the ATP-dependent chromatin remodeling complexes discussed previously

This is too much simplified. Old histones are reused, and probably mixed together with new ones.

@adjan You are right. If necessary I will put my answer as a community wiki in order to improve it with your explanation. Otherwise, we can leave them side by side.


text:
Do presynaptic neurons and postsynaptic neurons have different compositions of neurotransmitter receptors and transporters?
For example if certain neurotransmitter is released, will there be neurons that won’t be even potentially affected, because it doesn’t have such type receptors?

Typical bouton-spine synapses are formed as an active process between the pre- and post-synaptic cells, there is communication between them through structural proteins, etc. Therefore, as part of the normal developmental process, usually postsynaptic cells will have receptors for the major neurotransmitter released by the presynaptic cells. However, some neurotransmitters are released more broadly into the extracellular space rather than at highly specialized synapses: in this case, the neurotransmitter is not likely to have an effect (or the same effect) on all nearby dendrites.

@BryanKrause - that would be an excellent answer.

@AliceD Took me some time to get back to this and compose a properly-cited answer.

Typical bouton-spine synapses are formed as an interactive process between the pre- and post-synaptic cells (Scheiffele, 2003). There is communication between pre- and post-synaptic cell through guidance cues, growth factors, and structural proteins, as well as neurotransmitter release itself. Therefore, as part of the normal developmental process, postsynaptic cells will usually have receptors for the major neurotransmitter released by the presynaptic cells: they find each other rather than connecting at random.
Synapses that become inactive or have lower activity than their neighbors can also degrade and disappear entirely (Purves and Lichtman, 1980) by a competitive process (Balice-Gordon and Lichtman, 1994). Because of this process, I would expect that even if some developmental fluke led to a formation of a synapse between mismatched pre/post neurotransmitter release/receptors, the result would be that the synapse would get no stimulation and would be pruned according to the normal process.
However, some neurotransmitters can be released more broadly into the extracellular space rather than at highly specialized synapses (including serotonin, dopamine, and acetylcholine - note: these neurotransmitters can also be released at synapses) (De-Miguel and Trueta, 2005; Trueta and De-Miguel, 2012) and call also 'leak' from synapses into the extrasynaptic space: in these cases, the neurotransmitter is not likely to have an effect (or the same effect) on all nearby dendrites, only those that express fairly high-affinity receptors that can detect the neurotransmitter at an extrasynaptic concentration.
References:
Balice-Gordon, R. J., & Lichtman, J. W. (1994). Long-term synapse loss induced by focal blockade of postsynaptlc receptors. Nature, 372(6506), 519.
De-Miguel, F. F., & Trueta, C. (2005). Synaptic and extrasynaptic secretion of serotonin. Cellular and molecular neurobiology, 25(2), 297-312.
Purves, D., & Lichtman, J. W. (1980). Elimination of synapses in the developing nervous system. Science, 210(4466), 153-157.
Scheiffele, P. (2003). Cell-cell signaling during synapse formation in the CNS. Annual review of neuroscience, 26(1), 485-508.
Trueta, C., & De-Miguel, F. F. (2012). Extrasynaptic exocytosis and its mechanisms: a source of molecules mediating volume transmission in the nervous system. Frontiers in physiology, 3, 319.

Nice one +1! I tried to find an answer for this to no avail. Intuitively I expected something in the line of your answer, but I couldn't back it up constructively.  Awesomeness.


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Which requirements are needed for 2 different species to be able to have offsprings?
Sometimes different species mate and they are able to have offsprings, usually with anomalies. Are there known requirements for 2 different species to produce offsprings? Why species like the lion and the tiger, which seems to have many differences are able to produce offsprings, when others which supposedly share 99% of the DNA can't?

Lets break this down like a logical problem. In reality, it involves the correct gene expressions at the correct time, place, etc. But that would be a book.
Prezygotic reproductive isolating mechanisms
Environment
A bull and a whale can't mate; they don't live in the same environment. Lions and tigers similarly do not mate in the wild due to lack of overlap in the environment. In captivity, yes.
Delivery of gametes
Sperm must be able to be delivered to the ovum for fertilization to occur. Some species just can't get this part right. Your house cat would not be a suitable donor for an elephant.* In closer species, say a chicken and a peacock, the rooster's courtship display (which is nowhere near as spectacular at the peacock's) will not be accepted by the female; no opportunity for delivery of gametes.
Some gametes can be delivered but not ova (the female isn't "in season".) Zero there as well.
Unity of gametes
If the gametes are both delivered at the correct time, can the sperm bind to the egg? Successful binding requires a receptor-ligand interaction which actually has a high degree of species specificity. So binding requires that the sperm and the egg can, say, "communicate" successfully. Dog sperm doesn't "speak" cat ovum.
If they do "speak the same language", can the sperm penetrate the ovum's protective coating (the zona pellucida)? Assuming sperm capacitation (a big hurdle right there), the sperm may not have the correct enzymes in it's 'head' to penetrate zona pellucida. Not all enzymes carry out the same function on all molecules, and if the correct enzymes are present to digest/break through the zona pellucida, is there enough? Is the sperm active enough? I'll liken this kind of communication to 'pillow talk'. We're getting much closer. Let's say the sperm has his pillow talk down, and can penetrate the layer.
Postzygotic isolating mechanisms
Viability
The hybrid embryo must be able to develop into a zygote. Hybrid inviability means there wasn't enough similarity to proceed to a blastocyst and the hybrid dies.
Say viability is achievable. The blastocyst/blastomere must "communicate" with the mother so that attachment is not only possible but can be sustained. In effect, it must "shout" to the mom, "I'm here! Pay attention to me!" (In humans, this involves secretion of large quantities of a hormone called chorionic gonadotropin, which stimulates continued secretion of progesterone, thus no shedding of the uterine lining. Not all mammalian blastocysts communicate the same way. If what we have here is a failure to communicate... as with Cool Hand Luke, the result is not good.
Hybrid sterility
The species were close enough for the conceptus to be heard by the mom. The right chromosomes with the right gene expression results in a live birth.
Success!
If the hybrid is fertile, it is by one definition not a different species. (There is much debate as to what exactly defines a species. See the references.)
If you are still left saying, "But why?", then it must be explained on a genetic/molecular level, with sentences like,

The zona pellucida of mammalian eggs is composed mainly of three glycoproteins, all of which are produced exclusively by the growing oocyte. Two of them, ZP2 and ZP3, assemble into long filaments, while the other, ZP1, cross-links the filaments into a three-dimensional network. The protein ZP3 is crucial: female mice with an inactivated ZP3 gene produce eggs lacking a zona and are infertile.

If this is the level of explanation you seek, there's a book for you: Molecular Biology of the Cell. Alberts B, Johnson A, Lewis J, et al.
Fertilization
The Process of Speciation
Fertilization
*Note here I'm referring to morphological differences, one way used to define species.

@BryanKrause - I realize that this is in a bit of flux. Also, I know that there are different definitions of "species", but there aren't any definitive answers, so I simplified a bit, relying on Ol' Faithful... One can say, because of fertile hybrids that they are subspecies like Drosophila ssp. that can have fertile offspring that becone infertile after a couple of generations.... And so on.


text:
is there any theory about why life evolved to have DNA with 4 different bases and not 6 or other number like in organisms created with artificial DNA?
If organisms can carry DNA with 6 bases which supposedly stores increased genetic information, why living organisms evolved to have DNA made of 4 bases and not 6 or other number? is there any theory about this, were the chemical process to reach those 2 additional bases much more complex or something?

There isn't a theory about that particular question as far I know of, but a possible answer is in the issue of complexity optimization in evolution. See, life is like a well-oiled machine-it always chooses the simplest and most reliable solutions to any problem it can face. What is simple in this case-a code of 4, 6, 8 or even more bases? Since it's double pair code the number must be even and 4 is the second even number-e.g. complex enough to provide redundancy but as simple as possible at the same time. The best optimization point possible. I hope this might serve as your answer.


text:
Why do mosquitoes hover over our heads?
So I play soccer in evening at a nearby park. I noticed many times that after the game and even during it many mosquitoes hover over some of us. They sort of form a structure like a tornado.
The more the one is sweaty, the more the mosquitoes.
What can  be the possible reason?

Maybe they swarm all around our bodies, but we only notice them near our heads because that's where our eyes and ears are.

mosquitoes are attracted to CO2, lactic acid, and the bacteria that live in sweat (old sweat) physically active human emit all three. It makes sense that blood seeking parasite would be attracted to smells indicating blood containing organisms.

In many mosquito species (and other diptera) males make swarm to attract the females. The vast majority of individuals in swarms are therefore males (but there are always a number of females in them as well).
These swarms are a type of lek mating which is also very common in midges (thanks to @arboviral for this info). Are you sure those you see are mosquitoes and not midges?
In order to produce these swarms, they typically hover a recognizable element in nature to swarm around, such as a small tree, a bush, a big stone, etc... On a soccer field, players are a distinct element to swarm over!
Of course, females are attracted to $CO_2$, warm bodies and odour of sweat but this is IMHO likely not an important factor causing the swarms you see. See @Kiny's answer on the subject.
References:

Takken et al. 2006
Yuval et al. 1994

Also, why is this in the evening?

Mosquitoes typically start mating at the beginning of the evening and then forage during the night. However, this varies quite a bit from species to species. Aedes egypti for example, forage day and night while species of the genus Culex forage only for a few hours after the sun has set.
Such variation in the timing of mating behaviour can lead to (pre-zygotic) reproductive isolation between lineages. Potential reasons for being active at specific times and not others include temperature management, easier to parasite for females during the night (only females bite), timing with flowers (as both males and females feed on nectar). I would not be able to argue for why a specific species shifted its circadian rhythm in a specific way though.

Also, why is this in the evening? Not in the morning or afternoon

@ASuckerinMaths Please see edit

Gah - beaten to it! For reference this is called lek mating. You most commonly see it with midges, rather than mosquitoes, though.

@arboviral Thank you! I edited the post to add the term lek mating.

I found an interesting paper about the subject that could contribute to answering your question.
There are volatile substances that we produce that help attracts and repels mosquitoes such a geranylaceton, octanal, nonanal, and decanal (Logan et al.)
The tests showed that those substances can both be used to attract and repel depending on their concentration with geranylaceton having a constant decrease in attraction.
Curious for more I have decided to look further into the subject and found another paper studying these components which states:

A blend formulated from the four aldehydes and combined with CO2-baited CDC trap without a light bulb doubled to tripled trap captures compared to control traps baited with CO2 alone. David P. et al.

Those four aldehydes referring to heptanal, octanal, nonanal, and decanal. which suggests that their attractive effect is stronger joined than separated.
Therefore, besides the "CO2, lactic acid, and the bacteria that live in sweat" stated by John, the reproductive behaviour stated by Remi.b there is also other volatile substances that make our attraction to mosquitoes stronger(or weaker).
References:
1. James G. Logan, Michael A. Birkett, Suzanne J. Clark, Stephen Powers, Nicola J. Seal, Lester J. Wadhams, A. Jennifer Mordue (Luntz), John A. Pickett. Identification of Human-Derived Volatile Chemicals that Interfere with Attraction of Aedes aegypti Mosquitoes.
2. Tchouassi DP1, Sang R, Sole CL, Bastos AD, Teal PE, Borgemeister C, Torto B. Common host-derived chemicals increase catches of disease-transmitting mosquitoes and can improve early warning systems for Rift Valley fever virus

Oh! Your right! thanks for pointing it out. Indeed after rereading it and without the acess to the paper my post makes little sense. I'll correct this right away.

Again, welcome to Bio and +1 for a well-sourced answer

Kiny, when you write to another user, make sure to add the '@', so to reach Mesentery write ' @Mesentery bladibla ' [I don't recommend adding the bladibla though ;-)

@AliceD Oh! sorry! This is the first time I am partecipating in this sort of websites and as such I have no knowledge of how to properly go about doing things.

@Kiny stop saying sorry! We're here to help

@AliceD Understood xD I'll try to stop. I apreciate the help. It is a pleasure to meet you.

@kiny Thx for the info. By the way, are these substances excreted out of skin?

@ASuckerinMaths Yes, all of those substances where identedied by studying the air around humans (in the first paper, specifically the hands).

"James G" is actually James Logan; it looks like something's happened to the formatting of the author list.

@arboviral did that fix it? Thanks for pointing out a issue. If you see another please let me know.

Partly - I've done the rest and added links to the papers. Thanks!


text:
Can methylisothiazolinone/methylchloroisothiazolinone (MI/MCI) behave as bacteriostatic in low concentrations?
Wikipedia mentions this as a biocide. It also mentions that low concentrations of certain bacteriocides is bacteriostatic. (I am assuming that biocide and bacteriocide play the same role, here.)
Hence, the question. (The only information I can find about MI is with regards to allergies.)

Yes, MI/MCI can behave as a bacteriostatic at low concentrations.
Check out table 1 in this paper: The Mechanism of Action of Isothiazolone Biocides. For a bunch of different isothiazolones (including the two you're interested in, though they call them MIT/CMIT instead of MI/MCI) it gives the Minimum Inhibitory Concentration (the concentration at which the isothiazolone acts as a microbiostatic) and the Minimum Biocidal Concentration (the concentration at which the isothiazolone acts as a biocide)*.
It's my understanding that basically everything that can act as a bacteriocide can also act as a bacteriostatic at a lower concentration. At low concentrations bacteriocides will kill some cells while leaving others alive in a stochastic (ie random) fashion. At some concentration this stochastic killing will balance out with the natural growth rate of the bacteria, and so thus act as a bacteriostatic.
*It should be noted that the paper lists these values for isothiazolone activity against yeasts, but the results would likely follow the same trends for isothiazolone activity against bacteria, since "CMIT/MIT has broad spectrum efficacy versus bacteria, algae, and fungi" (from the above cited paper).

Is my understanding right that "this sort of bacteriostaticity is different from the one caused due to bacteriostatic drugs such as tetracarbon/tetracycline"? And should we be worried about MI/MCI, present in Dettol Liquid handwash and some cosmetics, going down in water drains, where bacteria may develop resistance for it, due to its low concentration present there? Also, can we discard the risk that MI/MCI can lead to bacterial-resistance against other bactericides? (This risk was present with tetracycline & other bacteriostats, which FDA banned.) [Sorry for the late reply; not-my-field.]

There are plenty of antibiotics that can only be administered to human patients at bacteriostatic concentrations, but any bacteriostatic will become a bacteriocide at some concentration.

@Shubham1999 The answer to your question about resistance is that yes, of course it can develop, and low concentrations are usually where it occurs. There's been a lot of good research work recently about how populations of bacteria will "pioneer" niches with successively higher concentrations of some antibiotic.

@Shubham1999 While multidrug resistance is a real thing (which probably hasn't received enough study to date), it's not necessarily something you have to worry about. In fact, there's good evidence that in many cases a bacteria that becomes resistant to one drug will become more vulnerable to one or more others. Essentially, a bacterium will always pay a price (in terms of its overall fitness) for any given resistance.

This paper is something - tetracycline as a bactericide! So, all-in-all, would it be right to avoid using bactericide/bacteriostat (antibiotic) in places where soap-water does the job to the required quality, and get done away with antibiotic containing products if their efficacy is to be maintained as long as possible? (Is this question more suitable for Sustainable-Living-Stackexchange?)

@Shubham1999 What you say about biocidal soap makes sense, and I think overall it's correct (here's another question with a a lot of really interesting details: Is there an advantage to antibacterial soap?). In reality though, there's still a lot we don't understand about how resistance occurs, how it spreads though a population, and how different resistances interact. Also, as it mentions in that question I linked to, some biocides just don't cause resistance at all.