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Does every mitochondrion in a cell contain the same DNA?
I know that mitochondria of eukaryotes have their own DNA, more similar to that of bacteria than to the rest of the cell's DNA. I also know that a cell can have plenty of mitochondria, and I understand each of them has it's own DNA. Is it the same DNA?
I know that when a human is conceived, the mitochondria of the sperm are destroyed and don't contribute to the new cell. If there were no mutations and the process started with a cell with homogenous mDNA, that would mean that the mDNA not only within one cell but among all of the descendants was the same. But there are mutations because we have different mDNAs. Then shouldn't the mutations cause variety within single cells? It's hard for me to believe that there can even be a single human cell in the world that has homogenous mDNA because, if I understand correctly, an ovum retains many mitochondria during conception, not just one, so at least some of the variety within the ovum should be passed over to the conceived human. But perhaps it's extremely difficult for a cell with variously DNAed mitochondria to survive? Can it be estimated what the percentage of human cells with homogenous or nearly homogenous mDNA is across the world?
I'm asking this because I've heard that the mDNA can be considered another chromosome. I wonder if then every single piece of mitochondrial DNA should be considered another chromosome.
Please note that all I know about biology is what I learned in high school several years ago and the bits I know from Wikipedia and other internet sources. I would like to ask for possibly accessible answers.
EDIT: Reading up on this, I came across the term heteroplasmy. So it does happen that mitochondria of an organism can store different genetic information. But the article seems to suggest that it is an anomaly rather than the normal course of things. That seems strange to me. I understand of course that some mutations have to be harmful, but shouldn't some mutations and some kinds of in-cell variety turn out to be neutral or even advantageous?
I've also just read that a mitochondrion stores more than one copy of its DNA. That seems to allow for variation even within a single mitochondrion.
EDIT 2: I think it's possible that my question is unclear. There seem to be four levels on which mDNA variety can be considered: a species, an organism, a cell, a mitochondrion. I ask the answerers to focus on the third one. I will be happy to learn about the other levels too and I will consider such information on-topic, but my main question is about what happens in a cell.

Why would be mtDNA any different from nuclear DNA in that sense? They are both sensible to mutations.

@nico Yes, of course there are mutations in mitochondrial DNA. Otherwise there would be no mDNA variety across the human population. But nuclear DNA is different from mDNA in that the latter occurs in very many (possibly thousands as I understand) copies within a single cell so there is room for variety within that single cell. That's impossible with nuclear DNA.

sure, but what I wanted to say is that by the same principle you may as well ask "does every nucleus contain the same DNA"? Surely, having thousand of copies increases by 3 orders of magnitude the probability of having mutations, no doubt about that. I am wondering, however, if there are repair mechanisms for mtDNA... I would assume so but I am not sure

@nico That wouldn't be exactly the same kind of question, although certainly related. I'm asking about what happens in a single cell. There is only one nucleus in a single cell so your question has to be about a larger structure like an organism. I will edit the question to make it clear.

oh, OK, I am sorry I read the question too quickly and I misunderstood what you were asking :)

This link seems to have good information that answers most of your questions.
In my mind, there are two types of mitochondria: ones that work and ones that don't. Mitochondria do have DNA but that mDNA is there to encode proteins for their specific functions (e.g. to create ATP). So, although the mDNA may not be uniform for every mitochondrion in your body, it is most likely functional unless you have a mitochondrial disease. If you do have a mitochondrial disease then it suggests that some of your mitochondria are functional and some are not (otherwise you would be inviable).
As discussed in the comments, all DNA undergoes mutations so that even identical mDNA genomes may vary after undergoing some mutations. It's possible that only one genetic line of mitochondria was passed to you from your mom. In this case all the mitochondria in your body would be identical (except for minor mutations). It's also possible that your mom inherited and passed on to you more than one genetic line (as is the case in viable mitochondrial disease).
Mitochondrial repair mechanisms do exist but they differ in various ways from nuclear DNA repair and may be more prone to damage.

Thank you. The first document seems to be concerned only with the mutations that make genes faulty. But surely there must be mutations that are not harmful to the cell or the organism? Is it more difficult for an mDNA mutation to be neutral or advantageous than for nuclear DNA mutations? Is it common for a cell to have several different but (nearly) all perfectly good sets of mDNA in its mitochondria?

You're correct, there are mutations that are not harmful to the mitochondria or cell. 2) Mitochondrial mutation is probably more likely to be harmful than nuclear DNA mutation since it is much less vast. Nuclear DNA is much larger and thus there is less change to mutate something important. 3) I don't know how common it is, but it is possible.


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Does every gland type have stem cells for regeneration?
Is there any gland in which there are no stem cells?
I know that:

sebaceous gland is maintained by unipotent stem cells
thyroid gland - some stem cells, apparently unipotent

Glands about which potency I am not sure

pancreas gland - contains probably many types stem cells, at least unipotent
pituitary gland - not sure if any exist

I cannot find any such gland that does not have stem cells.

Interesting question! You can add pituitary and pancreas to the mix.

Stem cells are not all 'unipotent' - they cannot necessarily differentiate into any type of cell. For instance, resident stem cells in tissues such as muscle - myo-satellite cells - are partially differentiated and during cell division one daughter differentiates further to become a myocyte (for example), and the other daughter the replacement myosatellite cell. As far as I'm aware, the majority of tissues have resident stem cells in varying degrees of differentiation (exceptions might include neurons and cardiac muscle, where cells are not replaced over the lifespan of the organism).
Here is some evidence for resident stem cells in glands;

The adult pituitary gland shows stem/progenitor cell activation in response to injury and is capable of regeneration (Fu et al, 2012),
The pancreas has been heavily studied from the perspective of diabetes research, with many studies looking to implant stem cells from elsewhere (Rezania et al, 2012). However there is some evidence for resident stem cells of the pancreas that may turn out to be more promising as treatment strategies in the future (Xu et al, 2004, Venkatesan et al, 2011),
Sebaceous glands are found throughout the skin, and secrete 'sebum' which keeps the skin waxy and waterproof. There is plenty of evidence for epidermal stem cells (Eckert et al, 2012),
There is also recent evidence for the existence of thyroid stem cells too (Fierabracci, 2012, Malaguarnera et al, 2012),
Saliva is mainly produced by the submandibular glands also contain resident stem cells, with this paper stating that stem cells have been isolted from salivary glands in humans (Okumura et al, 2012),

Given the limited (and very recent) evidence for the above (relatively well characterizd) glands, it seems likely that other glands will also have resident stem cells that remain to be identified.
Ageing: The so-called stem-cell pool gets depleted over a lifetime, so tissues lose the regenerative potential. However rejuvenation medicine is becoming a heavily invested in area of research (see www.SENS.org).

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Why is selfishness the 'obvious' strategy?
Thinking of behaviours an organism can adapt, at the very base an action can always be either selfish or altruistic (cooperative).
Usually, selfish behaviour is assumed to be the preferred choice and the question is how altruistic behaviour comes about.
But if reciprocal altruism can give both participants a higher benefit than their respective costs (which it usually does), why would selfish behaviour (in the sense of behaviour which reaps benefit at another entity's expense) be what we assume to happen? If evolution tends to optimise things, why does it not optimise this?

What about Symbiosis? In the end you can see every kind of cooperative behaviour as a selfish one if you want to...

Thanks for the comment. You made me realise that the question needs more clarification and at the same time you helped me find the answer to it myself :) I will update the question and add my own answer.

It basically comes down to a question of the unit of selection.
From the common viewpoint, in which natural selection is seen as acting on individual organisms, it's almost a tautology that the organisms favored by selection are those that maximize their own reproductive fitness.  Thus, the possibility that some organisms might engage in acts that help another organism at their own expense may seem like a paradox, or at least a puzzle in need of explanation.
One solution to this puzzle is offered by the gene-centered view of evolution, where selection is viewed as acting on genes, with organisms being merely convenient (and usually, but not always, cooperative) collections of genes that (usually) reproduce together.  From this viewpoint, it is not at all surprising that evolution might favor genes that cause an organism to help other organisms, provided that there's a statistical tendency for those other organisms to also be carrying the same gene.
Other mechanisms for the evolution of cooperation do also exist.  For example, organisms with sufficiently advanced cognitive capabilities may indeed engage in reciprocal altruism, where they help others only if those others have shown themselves willing to help them in exchange.  Such exchanges, being mutually beneficial, do indeed help both participating organisms, and are thus selected for even at the organism level.  However, to persist (in the absence of gene or group level selection effects), they generally need some form of enforcement and/or learning mechanism — if cheaters can keep receiving help without ever helping anyone else, they'll do better than the cooperators and eventually displace them.
Also, in some situations, an organism acting simply to help itself (e.g. by modifying its environment to be more suitable for itself) may also end up helping other organisms that just happen to be nearby.  In such a situation, selection indeed favors cooperative behavior in isolated organisms by default, with the evolution and persistence of "freeloaders" (who spend less effort on improving their surrounding, relying instead on others to do the work) being only possible as long as there are sufficiently many cooperators around.
Of course, none of these mechanisms are mutually exclusive.  Indeed, the presence of some gene-level selection effects tends to be unavoidable in any realistic situation involving cooperative interactions; it's hard to come up with a setting in which no two interacting organisms ever share genes, and obviously the fact that two organisms share a common genetic predisposition to cooperate makes them more likely to do so when they meet.
(However, one not-so-realistic theoretical limit case where that does happen is that of an infinitesimally rare cooperative mutant invading an infinitely large and well mixed population.  The popular use of this simplifying limit assumption in classical models of evolution may be one reasons why cooperative behavior is so often seen as something remarkable and hard to explain by evolutionary theorists.)

This is essentially what I was going to write myself: because there is such a thing as individuals which differ, and individuals who do better (variation and competition due to finite resources), individuals who do themselves best are successful. The biggest exception is probably kin selection since altruism towards relatives can benefit the own genes more than selfishness.

Selfish behaviour is not necessarily preferred. It depends on the game (game theory). For example, in absence of relatedness and reciprocity, we would expect:

All the population defect in the Prisoner's dilemna
Some defect and some cooperate in the snow-drift game
Either all inds defect or all inds cooperate (depending on initial condition because it is an unstable equilibrium) in the stag hunt game.

When there is relatedness (genetic correlation) between individuals, Hamilton's theory of inclusive fitness says that:
$$R\cdot\frac{dw(x,y,z)}{dx}>\frac{dw(x,y,z)}{dy}$$
where the letter d means partial derivative, the function w() is the fitness function and the parameters of the fitness function represent the trait of the focla individual (x), the mean trait in the subpopulation (y) and the mean trait in the populaiton (z). For more information This fitness function depends one the ratio of the fecundity function of cooperating over defecting.
These fecundity functions in the prisoner's dilemna equals the baseline fecundity (usually we write down 1) plus the payoff when the other cooperate times the probability that the interacting individual cooperate plus the payoff when the interacting individual defect times the probability that it defects. It gives:
$$f(cooperate) = 1 + (B-C)x + C(1-x)$$ if the individuals get the payoff B-C when the interacting individual also cooperates and Cwhen the interactzing individual defects. xis the probability that the other individual cooperates.
Usually, the first equation above is written under the form:
$RB>C$
Instead of R, you might as well consider another correlation, a correlation of behaviour due to reciprocity. The equation becomes:
$kB>C$
You might as well consider both, reciporcity and relatedness which give:
$$BR-C+k\cdot(B-RC)$$

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Why is 'Grudger' an evolutionary stable strategy?
I am currently reading 'The Selfish Gene' by Richard Dawkins, which I am sure many here have read. The topic are evolutionary stable strategies (ESS) regarding cooperation.
I apologise for the long question. If you are already familiar with the topic and Dawkins' model of Cheat, Sucker and Grudger: my question is, how can Grudger be an ESS if it could be invaded both by Suckers (because they have no disadvantage against Grudger) and Cheats (because a Cheat minority is unlikely to meet the same Grudger twice, turning Grudger into Sucker effectively)?
More detailed:
The model
Near the end of chapter 10 (p 185 in my version), Dawkins uses a model of birds who clean each other of parasites, therefore helping in survival (as cleaning themselves they cannot reach every spot of their body). He defines three different behaviours for the model:

Sucker - birds who indiscriminately help and clean other birds
Cheat - birds who let others help them but never do so themselves
Grudger - birds who help others and remember who they helped. If the same bird does not help them later (reciprocate), they will not help that bird again.

Claim: Cheat and Grudger are ESS
He claims that both Cheat and Grudger in themselves are ESS - that is, if all birds behave this way, none of the other behaviours can develop because they will be immediately penalised by lower chances of reproducing.
The part that makes sense: Suckers is not an ESS, Cheat is
Sucker is of course not an ESS. If all birds were Suckers, any Cheat that developed would have a huge reproductive advantage and Cheat genes would overtake the population.
Being an ESS makes sense for Cheat. If all birds cheat, nobody will ever be helping each other. A minority of Suckers would be spending all their time helping and not getting anything in return, Cheats have the advantage and Suckers die out again. Grudger would be unlikely to meet a Cheat who they helped before again, so they too will spend all their time helping and die out again.
The part that confuses: Grudger is an ESS?
But Dawkins also claims that Grudger is an ESS, and he seems very confident in that. Now I don't consider myself enough of a smartypants to claim that he's wrong, but I don't understand how Grudger can be an ESS. If all birds behave in this way, and for any reason some Sucker developed - the Sucker would have no disadvantage. All birds would still always be helping each other, so nothing would stop the Suckers from propagating equally well as the Grudgers, invading the gene pool. That's already the ESS broken, but even further, the presence of Suckers would mean that if Cheats came up, they would have a realistic chance of surviving - Grudgers would shun them after having helped once, but if the number of Suckers is large enough, Cheats will have an advantage.
Moreover, back to the initial setting of Grudgers only - if a Cheat developed, he would be unlikely to meet the same Grudger twice, receiving the benefit all the time but never paying the cost. He would have an advantage and spread Cheat genes.
The problem
I'm not familiar enough with how these kinds of models are calculated in order to state chances that Cheats will take over completely, but however I think of it Grudger does not seem to be an ESS to me.
Does anyone have an explanation why Dawkins is so sure that it is? Seeing as in nature we do see patterns like Sucker and Grudger all the time, I must be missing something important here.

great question. I hope one or all answers address group selection. Which I don't think was widely accepted at the time that the selfish gene was published.

@David It still isn’t widely accepted. There are some attempts to put it on a new footing but they certainly don’t represent the majority view of the evolutionary biology crowd.

It's not an evolutionary stable strategy from selection alone. For any positive integer n no matter how large, always defect is an evolutionary stable strategy because no mutants with any strategy in a population with the pure strategy of always defect will be selected for. However, in real life, if the prisonners dilemma is iterated 4,000,000 times, genetic drift will kick in leading to a mixed evolutionary stable strategy of complex strategies all of which are a type of grudger.

Unfortunately it is not necessary to invoke group selection to answer this question.  This is one of the reasons that Dawkins likes this discussion so much - he does not believe in group selection and so the discussion in SG does not invoke group selection.  ESSs are described in the book as the product of direct competition or interaction between genes.
ESSs in this case, can be described in terms of game theory.  In the famous Prisoner's Dilemma experiment, Grudger is similar to tit for tat, which 'won' the competition in the original Axelrod contest.
To see how this works you make a simple win/loss game matrix:
     G        NG
G    win 1    win 3
NG   lose 3   lose 1

if you are groomed you win 1, if you are groomed, but you don't have to groom - even better win 3 (say)
If you groom but are not groomed, lose 3
If neither of you are groomed, you both lose 1
one might argue the exact proportions, but the point is that getting some thing for nothing is better than reciprocating, and getting nothing for your efforts and time are a loss, because you could have been getting groomed by someone else. As you can see cheaters end up in the top row all the time.  grudgers end up along the diagonal, and once in a while in the lower left, Suckers get stuck in the lower left a lot whenever there is a cheater around.
now run this encounter over and over.  A behavior which scores negative the more times you run is not stable - they are going to disappear from the population, at least if this disadvantage is real
It has more than one stable outcomes in populations, a population that is full of Grudgers will all groom each other as before you know everyone, you assume they will reciprocate.  Everyone wins!
Any invading Cheaters will quickly be at a disadvantage, in that they will not be groomed more than N times where N is the number of grudgers in the community.  Note that there is an equilibrium here - the Cheaters may exist in a small number - when N is large enough for a cheater to get enough grooming to make a 'living'.
Suckers can also exist within a population of grudgers, but a population of Suckers where Cheaters show up are quickly sucked dry by the cheaters over several generations where you tally up 'points' and give more, healthier offspring to high scorers.  They are not ESS stable.
Cheaters are also stable - nobody ever wins, but they don't lose big either and any invading grudgers can't get groomed.

Thanks for the detailed answer :) After reading on, I found an explanation two chapters later, essentially what you said - Cheaters may exist in a small number and so may Suckers, but they would be decimated by the Cheaters again once both became significant. Dawkins admits this is not truly an ESS and instead offers what Axelrod called it, a 'collectively stable strategy'.

“… as the product of” is missing a few crucial words at the end. As an aside, your gibe at Dawkins’ opposition to group selection is really mis-placed. Last I looked his is still the majority position among evolutionary biologists, and this isn’t the right place for a detailed discussion of the subject, and your current formulation is putting Dawkins’ intelligence in question (“does not believe in”) and accuses him of using a sleazy argument (“[which is why] he likes this discussion so much”) which is quite inacceptable in polite conversation.

@Konrad Rudolph  yes, but EO Wilson et al's arguments (to cite one example) are serious ones.  Fortunately Science is not a democracy and alternative investigation is still allowed; There is still substantial reason for question and the best journal editorial boards still see this as a reasonable question to raise.

@Armatus this is an important point- it is essentially the reason one might find selfish genes.  Selfish Genes are the small proportion of 'cheaters' in the community of otherwise 'grudger' genes. It is the prediction of the existence of Selfish Genes, that proves that Genes are the medium of Genetic Selection that motivates Dawkins to write the book.  I personally think Dawkins is a man of great insight, but don't feel that means we must totally agree with the axiomatic assumption that DNA must be the only medium of selection in biology.

@shigeta I can’t personally comment on the validity of his arguments (but I will note that others who can have described them as “[revealing] a rather disturbing lack of familiarity with a huge body of scientific literature from the past few decades”, implying that their arguments are rather vacuous). But that’s not the point here. You didn’t raise a reasonable question, you used a questionable opportunity to accuse another scientist of intellectual dishonesty without a shred of evidence.

@shigeta You are using 'Selfish Gene' in a different sense than Dawkins explains, which has nothing to do with selfish (Cheat) behaviour. He also doesn't state DNA is the only medium of selection. But my question is answered and this is not the place for discussions like this. Thank you :)

@Armatus see http://en.wikipedia.org/wiki/The_Selfish_Gene#Genes_can_reproduce_at_the_expense_of_the_organism  Selfish genes are genes that reproduce at the expense of other genes in the same organism.  They are I think very much like Grudger - who takes reproductive advantage from other community members, the analogy I believe is made in the book because Dawkins wants to support his main point - why the prediction of the Selfish Gene and its subsequent discovery is so important to biology.  Maybe I should ask -why you think he discussed it in this book?

@shigeta It is very clear in his book that 'Selfish genes' are not a kind of genes. He explains how all genes are 'selfish' - please read the correct section of the Wikipedia article (http://en.wikipedia.org/wiki/The_Selfish_Gene#.22Selfish.22_genes). I personally find his choice of word an unlucky one because it asks for misunderstandings like this.

Not sure this is the case.  The Selfish Gene he gives as an example is a gene which does nothing for the organism or other genes.  See Triver's work on Selfish Genes. Triver's predicted their existence.  Some selfish genes literally freeload off of other genes.  Most other genes are cooperative.  I'll leave it at that for this question.

on Selfish Genes: "As Austin Burt and Robert Trivers show, these selfish genes are a universal feature of life with pervasive effects, including numerous counter-adaptations. Their spread has created a whole world of socio-genetic interactions within individuals, usually completely hidden from sight."  http://www.hup.harvard.edu/catalog.php?isbn=9780674027220

Yes, they may use the term "Selfish Gene" this way, but the conversation here was about Dawkins and as it seems, he uses the term differently (which is his good right). His theme is not that "selfish genes" exist, but that all genes are selfish, and nothing else - since all altruism/cooperation is merely a product of lower-level selfishness. I think I remember the "selfish gene" example you mentioned, but he used it only to illustrate that genes' interest does not have to be the organism's and he most definitely did not say that only this specifically was a selfish gene.

In an infinite, well mixed population with single pairwise encounters, Grudger is indeed not an ESS.  In fact, as you correctly note, in such a model the Grudger and Sucker strategies are indistiguishable, as the probability of anyone encountering the same individual twice is zero.
To make it possible for the Grudger strategy to survive against invasion by Cheaters, we must somehow extend the model to allow pairs of individuals to meet more than once.  Some ways to achieve this include:

Finite population size: if there are n individuals and they each participate on average in m encounters during their lifetime (or during the average time for which their memory persists), then each of them will encounter every other individual m / (n−1) times on average.
Viscous population: this is a general term for populations that are not well mixed.  For example, if individuals live on a spatially extensive landscape, have limited movement rates and interact only with nearby individuals, then two individuals that meet once have a higher probability of meeting again due to spatial proximity.
Iterated encounters: in these types of models, pairs of individuals are assumed to interact with each others some (fixed or random) number of times before parting and finding new partners to interact with.  In this way, repeat encounters can be included even in infinite, well mixed population models.  While this may be a reasonable approximation in some cases (e.g. for models of spousal cooperation in serially monogamous species), frankly the main reason for studying such models seems to be that they're mathematically simpler than finite or viscous populations.

Not entirely coincidentally, many of these mechanisms can also permit the survival of pure Sucker or altruist strategies against invasion by Cheaters through group and/or kin selection (or more general forms of assortment).
Ps. Even with these mechanisms, Grudger will never be a strict ESS anyway, since in any population consisting of only Grudgers and Suckers both have the same payoff.

BTW, if you have even a single cheater (which due to random mutations you usually will end up with), "Grudgers and Suckers both have the same payoff" becomes false.


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What value type would a chromosome position be in a database or form?
I wanted to create a tool for some fields like SIFT, Phenotype, etc..so for example I know Phenotype will have "Text" values or SIFT will have some determined values from a drop down list...but what about Chrom Positions? what are some valid sample values for that? so I can know what type I can use for it.

(1) Since this is a purely bioinformatical question, it should be closed and re-asked on http://biostars.org. (2) Are you concerned with the position on a chromosome (i.e. a one-based offset like 123456) or a genomic position including the chromosome (e.g. X:123456) or? Then there’s leonardo’s answer which uses a different format to store the same information.


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Do trees really get a large share of their mass from the carbon in the air?
I remember hearing that trees and other plants actually obtain a large amount of their mass from the carbon floating in the air, not the ground beneath them. Does the makeup of air actually contain enough carbon to support this theory, and is a tree's surface area actually large enough to obtain the amount of carbon it needs directly from the air?

Sure! Trees get most of their carbon from CO2 via photosynthesis, which is converted to glucose and then to other organic compounds.

Related video on YT: Where Do Trees Get Their Mass From?

The vast majority of a tree's carbon comes from the air, which averages 0.03-0.04% by volume (300-400 ppmv) CO2.  This is fixed through photosynthesis and eventually stored as glucose which the plant can then use for its metabolism.
Doing some quick math, this means that in order to produce 1 kilogram of carbohydrates (e.g. cellulose) a plant needs to process on the order of 2000-3000 cubic meters of air (and ≈550 g or mL of H2O), which would fill a cube measuring 13-14 meters on a side.  Note this is an ideal figure; a plant's fixing efficiency will likely fall as it depletes the air of CO2.
Plants do take a great deal from the ground, namely water, fixed nitrogen (for proteins),  phosphorous (for nucleic acids), and several ions (sodium, potassium, calcium, among others)

I'm surprised nobody has mentioned Jan van Helmont. To summarise Blankenship's account, in the 17th century, he (Helmont, not Blankenship) grew a tree in a known dry weight of soil and weighed the fallen leaves of the tree, and then eventually the whole tree including the root system. He found that the mass of the soil had barely diminished and concluded that the tree's mass was overwhelmingly due to watering (CO2 had not been discovered.)1
With the benefit of knowledge of CO2 we can conclude that the mass of trees comes from the fixation of CO2 and H2O as well as the presence of H2O as a biological solvent.

(1) Blankenship, R. E., Molecular Mechanisms of Photosynthesis, Blackwell Science, 2002, p. 26

Yes. In fact the organic compounds' mass comes mostly from the air, since Photosynthesis essentially builds up glucose by only adding hydrogen to CO₂. The 2 H₂O → 2H₂ + O₂ reaction can be treated seperately, as was determined by Sam Ruben and Michael Kamen with ¹⁸O isotope tracing, i.e. in fact only the hydrogen in the carbohydrates comes from the soil, and this has of course a much smaller mass.
As said by Nick T, the more complex compounds also incorporate other elements that the plants get from the soil, but most of them still consist mainly of C and O. The total mass of a tree of course also has a lot of water and some minerals in it, but it's still safe to say that a tree "consists mainly of air".
To your question about surface area and air CO₂ content, neither is usually the limiting factor: in nature, light exposure, water and mineral supply are (although in enclosed spaces like greenhouses CO2 fertilization is sometimes necessary).

If increasing CO2 increases plant growth, then CO2 by definition limits plant growth. Your answer is good and but the limitation of plant growth is more complex than implied.


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Is there a relationship between Melatonin, Norepinephrine and depression in humans?
I'm reading a booklet on melatonin published in 1996, titled "Melatonin and the Biological Clock". This particular paragraph caught my attention and I would like to better understand what it means:

The requirement of intact beta-receptor function for melatonin
  synthesis, and the stimulatory effect of norepinephrine on melatonin
  synthesis and release, point up a theoretic relationship of melatonin
  to depression.

I've been looking at the biosynthesis of norepinephrine  and tryptophan metabolism and do not see how the two cycles are connected. Is there a connection between the norepinephrine system and the melatonin synthesis in humans?

This answer addresses your question about a link between norepinephrine and melatonin, but I have nothing to say about depression.
In vertebrates, the link between norepinephrine (NE) and melatonin lies in the regulation of the melatonin biosynthetic pathway.
Arylalkamine N-acetyltransferase (AANAT) is an enzyme in the biosynthetic pathway for melatonin, and controls the diurnal rhythm of melatonin production in the pineal gland. NE is released as a neurotransmitter by neurons innervating the pineal gland, and which themselves are regulated by the circadian pacemaker of the hypothalamus. One of the effects of NE on the pineal gland is to elevate the transcription of the AANAT gene via adrenoreceptors and cAMP levels.
The paper cited below describes this, and other relevant diurnal rhythms in the viscacha, a rodent of the chinchilla family. This animal was chosen because it has an interesting diurnal behaviour pattern with two apparent peaks in melatonin biosynthesis. It's a good starting point for further research into the literature on this topic.

Calderon,C et al. (2008) Daily rhythms of norepinephrine, β1-adrenoceptor mRNA, serotonin, arylalkylamine N-acetyltransferase mRNA, arylalkylamine N-acetyltransferase and hydroxyindol-O-methyltransferase activities, and melatonin in the pineal gland of viscacha. Biological Rhythm Research 39: 93-107

Thank you Alan! As far as I understand, there are two transferases, first AANAT and then HIOMT that are involved in Melatonin production from Serotonin. NE elevates the AANAT levels, influencing transormation of Serotonin to N-Acetyl-5-HT


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Epilepsy explained by computational neuroscience
A few years ago, on my maths masters, I did a module in theoretical neuroscience. I was shown that the mathematical framework the course developed for neurons, with a small adjustment in the parameters, would produce spike trains similar to those observed during epileptic kindling. These parametric tweaks could be attributed to mutations in ion channel/receptor structures. This was one of the highlights of the course, and when I came to apply for a math/bio interdisciplinary doctoral program, I cited it as such in my personal statement.
Now the interview is fast approaching, and I'm pretty sure it's going to come up, but for the life of me I can't track down a reference. After four years out of the game, my memory is hazy at best.
As I recall, this had something to do with short term plasticity. Normal neurons' response to unrelentingly high frequency spike trains decayes over time, while pathological neurons' does not. This may however be entirely wrong.
What is a reference for the model I describe above? An introductory/educational treatement is prefered, but the original paper is fine.

To meet the standards of SE please consider concentrating on asking a well-pointed question (not on personal story, urgency, ...).

I echo Piotr's sentiment, but is this the article?  Lopes Da Silva is a leader in the field.

@PiotrMigdal I don't think there is an inherent problem with adding a person flavour to a question, as long as the question is still clear. In this case it is a reference-request for a very specific result.

@ArtemKaznatcheev Yes, as long as one does not need to read one's life story before the actual question. Personally I am irritated by 'questions' in which I need to search for the actual question.

Unfortunately, epileptic spiking can occur very easily in many neural modeling studies, and therefore one should be very careful in asserting the possibility of certain aspects of model as a cause for epileptic activity. One possibility, as you mentioned, is the lack of short-term depression which prevents long sustained firing. But again, a simple increase in the global excitatory coupling can also exhibit similar dynamics.
Good luck on your interview.


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Why does replication require primers while transcription does not?
In transcription, there is no need for any primer. I guess the basic mechanism of DNA polymerase & RNA polymerase is the same. So why does replication have the need for a primer?

I read somewhere that the difference in catalytic activties of DNA ploymerase and RNA polymerase lies in the structure and geometry of theirbactive sites.But, i have studied in ' Lehninger principles of biochemistry' by Nelson and Cox that the active sites of both the enzymes contain highly conserved asp residues and they require magnesium ions for catalysis. Then why is a primer not required for RNA polymerase? waiting for a good,logical answer.

There are always two kind of answers to this sort of "why" question. One is mechanistic and simple — once you know the mechanism of action — they are built differently to work differently. The more fundamental question (and to me more interesting question) is why they got that way — why didn't DNA polymerase evolve the capacity to do what RNA polymerase does? I imagine nobody knows, but my conjecture is that it must be something to do with the replication evolved  from an RNA to a DNA world. Someone else must have thought about this before me, though.

I'm no expert at transcription but from what I can figure out here and here transcription requires a promoter region acting as a template-directed mechanism for allowing transcription, which presumably bear a certain sequence recognised by the RNA polymerase and associated complexes. However DNA polymerase requires primers to guide it to the correct location on DNA.
EDIT: In light of comments below, according to here and here, RNA polymerase is capable of de novo synthesis meaning it is capable of initiating synthesis of RNA without primers and this is done by RNA polymerase binding to two nucleotides rather than nascent RNA polymer and a single nucleotide. Initiating nucleotide hold RNA polymerase rigidly in place, facilitating chemical attack on the incoming nucleotide. For bacteriophage T7 RNA polymerase, transcription begins with a marked preference for GTP at the + 1 and + 2 positions. DNA polymerase cannot add primers, and therefore, needs primase to add the primer de novo.

The point of primers is that the DNA polymerase cannot make new chains de novo meaning it has to connect them to an existing strand. For RNA Polymerase II this is obviously different and the other general transcription factors present at the transcription initiation site seem to play an important role, too. I think it is also possible that RNA Pol II has primase activity itself and can make strands de novo. But I haven't found any details on this yet.

yes RNA polymerase has a primase activity itself. I don't know the structural basis of it; so I did not comment or answer.

@Chris I made an edit to the answer, which highlights the de novo aspect of RNA polymerase. Many thanks for the pointer!

thanks all of u....but i'm not fully satisfied.please give me more information

which subunit of RNA polymerase has primase activity? ..@WYSIWYH

@anamitraruj.. Primase is a type of RNA polymerase.. but as I said I haven't compared the structures.. I'll let you know in a while

Just thought if add that I was taught that the linker between regions 3 and 4 of the sigma factor helps orient the template strand so it's in the correct position for the first polymerization reaction.

The primer is an universal recruiter, for all DNA polymerases, bringing them to the DNA template. You must have both strands in place for a DNA polymerase to stop by. Moreover, the catalytic activity of all the polymerases requires a preexistent 3' end on the growing strand. You must have a 3' free end near a template, for a DNA polymerase to act. (A far longer description of the chemistry is at http://www.ncbi.nlm.nih.gov/books/NBK22374/ .) In contrast, RNA polymerases, including primase, are recruited to the template by DNA-binding proteins, such as ori-binding proteins, transcription factors etc., meaning there is no need for primers.
It may make some functional sense too. Once a cell decides to replicates, its ori-binding proteins are synthesized and/or activated. They bind the DNA template, and bring in the primase. Only after the primase does its job, DNA polymerase can take over. The cell needs stringent regulation only at the level of the ori-binding protein, because DNA polymerases are so strongly dependent on the preceding steps.
If we think in evolutionary terms, and we accept the RNA world hypothesis, the RNA polymerases (or at least their ancestors) should have evolved earlier than the DNA polymerases. In these conditions, the earliest DNA polymerase came in a world where double stranded RNA already existed, meaning it had access to a primed template. There was no immediate need for a primer-independent DNA polymerase, and no urgent need afterwards.
All these are speculations. There seems to be a primer-independent DNA polymerase in a thermophile bacterium (DOI: 10.1021/bi0489614). Its existence may be interpreted in two opposite ways: ancient mechanism, or recent evolution, forced by the special conditions where these bacteria live. The former will deny almost everything I wrote. "Why?" questions in biology are always tricky.

" You must have a 3' free end near a template," should not read "...of the template"? - That may have been it: RNA polymerase doesn't start at "ends", it's in the middle. Isn't promoter and primer basically i.e. funtially synonomous?

In replication you have 2 strands made.
In transcription you have 1 strand made.
Transcription uses ONLY the 3' → 5' DNA strand.
This eliminates the need for the Okazaki fragments seen in DNA replication (on the lagging strand).
And it removes the need for a RNA primer to initiate RNA synthesis, as is the case in DNA replication.
Edit; instead RNA Polymerase binds to Promoter region to initiate transcription, in replication (leading strand) DNA uses 1 Primer to initiate. And as AMR comment, RNA Polymerase dont need to add nucleotides to existing part.

Hi, welcome to Biology SE, thanks for answering - could you possibly add some supporting material (references to books, peer reviewed papers, reputable websites etc.)? This helps to maintain standards and helps users find good reading material on the subject which may help them further.

Actually that is not the reason. In order to polymerize a DNA daughter strand, the DNA-dependent DNA polymerase requires a free 3' hydroxyl group with which to catalyze the reaction. DNA-dependent RNA polymerase has no such requirement and therefore can catalyze the reaction without the need for a starting 3'-OH group.

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


text:
Parsimony (cladistics)
I don't understand how to sum the changes in a phylogenetic tree.
Here for example: http://www.med.nyu.edu/rcr/rcr/course/phylo-cladistic.html
How do you end up with 8 for the first and 9 for the second ?

It seems to me that they are not summing the changes correctly in this page.
They are summing the lengths of the paths to the root (and for the fig 2, they assume that the terminal branches, from left to right are of lengths 3, 2, 1 and 1). This doesn't make sense to me.
The correct way to count changes using parsimony is to consider each site in the alignment, and try to put the minimum number of mutations on the tree to explain the states observed at the terminal branches. Then, sum the number of mutations across alignment sites.
Here, for figure 1, I get:
site 1: 1 mutation, either on the left (T->A) or on the right (A->T) internal branch.
site 2: 1 mutation on the 4th terminal branch (T->C)
site 3: 0 mutations (all terminals have C)
site 4: 1 mutation on the 2nd terminal branch (G->C)
Total: 3
for figure 2:
site 1: 1 mutation on the branch leading to the most recent common ancestor of the two right-most terminals (A->T)
site 2: 1 mutation on the right-most terminal branch (T->C)
site 3: 0 mutations (same reason as for figure 1)
site 4: 1 mutation, either on the left-most branch (G->C) or on the branch leading to the most recent common ancestor of the 3 right-most terminals (C->G)
Total: 3
The trees are equi-parsimonious.
I hope I did not make any mistakes.
There exist algorithms to do this. For instance, Wagner parsimony.
Don't trust a course on phylogeny that resides on a medical center web page.


text:
Membrane potential after exposure to glutamate

Neurons were kept in a physiological solution. During the resting
  phase, the membrane potential in the axoplasm of neurons was negative
  compared to the extracellular space and a potential difference of -70
  mV was observed in this phase. Neurons were then treated in two
  different experiments with either gamma-amino butyric acid (GABA; an
  inhibitory neurotransmitter) or glutamate (an excitatory
  neurotransmitter) and the membrane potentials were recorded. Choose
  the correct statement/s:
(A) The resting membrane potential of -70 mV would not change with
  either GABA or glutamate treatments.
(B) The membrane potential would be even more negative than resting
  phase with GABA treatment.
(C) The membrane potential would be positive when the neuron was
  exposed to glutamate.
(D) The membrane potential would be more negative than resting
  potential after glutamate treatment.

I feel, since, glutamate is excitatory, so resting potential should decrease when exposed to glutamate and increase when exposed to GABA. So (A)&(D) automatically gets eliminated and (B) is correct answer. I am confused at (C)

This is a homework question, right? If so, please provide what you think about it, otherwise this will be marked off-topic.

@Chris Yes, this is a homework question. However, I am not being able approach the question. What do I do then?

No thoughts about it?

I feel, since, glutamate is excitatory, so resting potential should decrease when exposed to glutamate and increase when exposed to GABA. So (A)&(D) automatically gets eliminated and (B) is correct answer. I am confused at (C)

positive membrane potential cannot be maintained...

It is more correct to call it "resting potential difference" (like your question), because electrical potential is relative, not absolute.
That phrasing exposes a crucial point: The difference of what? Cell cytoplasms are negatively charged (to remember this, it helps to remember that protons are usually pumped out of the cytosol either into the periplasm, vesicles, mitochondrial intermemberane space, or outside of the cell). If you subtract the potential of the outside from the inside, you'll get +70. If you do it the other way around, you'll get -70. By convention, the (+) probe of the voltmeter is stuck inside the cell, and the (-) is stuck outside, so we end up with the "official" figure of -70 mV.
Nature obviously does not like this potential difference, and wants to neutralize it by pushing current across the membrane. Luckily the membrane is not very conductive, and the cell can expend energy to undo the effects of any leaking and prevent the potential [difference] from drifting toward 0 (it would actually drift toward a number above 0 because potential difference isn't the only factor, there is also the concentration difference).
So the cell is like a battery that keeps itself charged. It also has a threshold, and it will only empty itself if it has discharged at least to a certain point. That point depends on the cell, but a typical value is -55 mV (so closer to equilibrium point than the resting -70 mV).
What will an inhibitory chemical like GABA do? It will pull the cell further away from the threshold, so it's harder to overcome it. Bringing -70 mV to -90 mV would be lowering it (because the number goes down).
What will an excitatory chemical like glutamate do? It will bring the cell closer to the threshold, so it's easier to overcome it. Bringing -70 mV to -55 mV would be raising it (because the number goes up).
The question, unfortunately, does not specify whether the action potential fires. Typically, the peak of the AP is +40 mV. In theory, you could have a threshold say, at +20 mV, and then perhaps the potential could go positive (eg. +10 mv) and stay there. But I really, really doubt you could find a cell with a threshold above 0. If the threshold is below zero, then the cell will reach a positive potential difference (if you use enough glutamate to elicit the AP), but it will only stay there momentarily before collapsing back to -80 mV (the refractory state).

Contrary to your answer, GABA does not necessarily move a cell further from threshold for an action potential or even necessarily change the resting membrane potential at all.  GABAa receptors, e.g. have a reversal potential around -70 mV.  See my answer.

@Chelonian To be honest I'm not an expert on neuroscience and I was not aware of this. My undergraduate neuroscience classes have always said GABA is inhibitory and hyperpolarizing, without emphasizing whether it is GABA-A or GABA-B. I assume that in such simplified discussions about ways of manipulating the membrane potential, when one says "GABA" without specifying subtype, it is to be understood that the more interesting GABA-B is meant.

@Chelonian Furthermore, even with GABA-A the potential would still go down if the cell's resting potential was above -70 to begin with, am I wrong?

I wouldn't say GABAb is necessarily "more interesting" (though I could see why one might feel that way). Given how important GABAa are, I would want to include both in any discussion. In fact, most initial undergrad treatments of GABA receptors start by making it seem like it is only GABAa (because GABAb is a metabotropic receptor and that's a more complex story to explain). And yes, if the neuron were sitting more negative than -70 mV, then even GABAa receptors would bring the membrane potential down to closer to -70 mV.

I believe C is also correct. The excitatory neurotransmitters open $\ce{Na}$ channels which makes the cell membrane more permeable to sodium as compared to potasium and therefore the equilibrium membrane potential would be much closer to the nernst potential for sodium. Now, since the concentration of sodium outside is much greater than inside, the nernst potential for sodium is positive with respect to the inside of the membrane. This makes the overall potential also positive.
If you want further clarifications regarding the calculation of the equilibrium and the nernst potential across the membrane, feel free to ask.
ADDENDUM
The approximate concentrations of sodium and potassium inside and outside a cell are :-
$$\ce {Na+_{in}}=10 \text{mmoll}^{-1}$$
$$\ce {K+_{in}}=105 \text{mmoll}^{-1}$$
$$\ce {Na+_{out}}=140 \text{mmoll}^{-1}$$
$$\ce {K+_{out}}=5 \text{mmoll}^{-1}$$
The Nernst potential is given by $E=-\frac{RT}{nF}\ln\frac{\text{in}}{\text{out}}$
Which for the given concentrations comes out to be $+67.7mV$ for sodium and $-78.1mV$ for potassium. During a sufficiently strong action potential, the relative permeability of sodium with respect to potassium becomes $10$. Using the GHK equation(ignoring the contribution of chlorine) gives us a net potential of $+47.5mV$.
The graph of the action potential clearly indicates that at the peak of the AP, the membrane potential is positive. Source : Graph of action potential

It would be helpful if you could add calculation of nernst potential.

@Rudstar Added in the answer.

peak is positive, but it won't be positive for a long time. the question is ambiguous in that aspect...

"excitatory neurotransmitters open Na channels":  Glutamate generally opens a mixed cation conductance of Na+, K+, and Ca++.  The equilibrium potentials for all three ions comprise the overall reversal potential, which is around 0 mV., not really near Na+'s equilibrium potential of +67.7 mV. (Also, it's chloride, not chlorine.)

I don't think any of the answers here are quite right, so I'll give a try:
(A) The resting membrane potential of -70 mV would not change with either GABA or glutamate treatments.
The answer here is:  "It depends".
For glutamate, if the neuron only had NMDA receptors that were not "open" at -70 mV, there would be no change in resting membrane potential. If there were at least some AMPA receptors, though, the membrane potential would change to more positive.
For GABA, if the cell has only GABAa receptors, then the resting membrane potential wouldn't change, because the reversal potential for GABAa is right there at -70 mV.  But if the cell had at least some GABAb receptors, their reversal potential is around -100 mV, and so would cause a change in the resting membrane potential to something more negative than -70 mV.
(B) The membrane potential would be even more negative than resting phase with GABA treatment.
Again, if GABAa receptors only, then no, it would be no more negative and would in fact stay the same at -70 mV.  If there are GABAb receptors, then yes, the resting membrane potential would be even more negative.
(C) The membrane potential would be positive when the neuron was exposed to glutamate.
Maybe--it depends on whether the neuron is allowed to have an action potential. Glutamate receptors generally reverse around 0 mV.  0 mV is neither positive nor negative. If there were no action potential in this neuron, we should therefore not say the membrane would be "positive" (though this is splitting hairs, I suppose). However it could be said to be "more positive than -70 mV". However, if the cell were allowed to have an action potential, then yes, the membrane potential would shoot up to about +20 mV, so could be said to be positive.
(D) The membrane potential would be more negative than resting potential after glutamate treatment.
No. Again, glutamate receptors' reversal potential is about 0 mV, so it would only move the membrane potential to more positive values, close to or right at 0 mV.

I suspect that you are over-thinking this likely undergraduate-level question: 3 of your answers are "maybe" and one is "none"; you are unable to execute the prompt of the question ("choose the correct one" whilst there is not a single statement that you think is correct). I'm not saying the exceptions you point out are not valid or important, but I think the question was meant to be definitely answerable, not open-ended.

@Superbest Sure I'm over-thinking it!  For fun. The point is, neuroscience is so darn complex that you can have fun with even the professor's questions which, in this case I think (and I may be wrong) actually doesn't have an air-tight only-one-correct-answer. In fact, I guarantee someone can come along and improve my answer because I left out some other corner cases (like the fact that there are some excitatory GABAa receptors in certain cases, and probably stuff I am not even remotely aware of). Along the way, I felt it was roughly still in the spirit of answering the question.


text:
Prenatal hyperkinetic dysfunction and its effect on endurace
Do people with an hyperkinetic dysfuntion have a better endurance?  Are they fitter in cause of their Dopamine-overdose or any other reason? I have a case, where someone does not do any sports, but has an endurance way better than most of others who does no sports. He even can compete with some amateur athletes.
Just for comprehension: He does not eat well, sits most of the time (during work, at home), does not do any other activities except eSports (onlinegames).
Maybe someone has an answer, at least I hope you have.

cross posted here: http://cogsci.stackexchange.com/questions/6429/do-people-with-prenatal-hyperkinetic-dysfunction-have-better-endurace

changed to not be a crosspost


text:
How do changes in temperature affect body weight in humans?
What would be effect on weight of individuals if we bring a fully adapted (to cold climate ) human individual and a fully adapted to very hot climate individual to a moderate climate region?

Can you expand your question some? Are you only interested in weight changes? Your title mentions metabolic rate, which is related to weight gain but certainly not the only factor. "What would happen" is very broad. What kind of animal(s) are you thinking of?

You would see moderate weight gain in both subjects.
Since humans thermoregulate and aren't terribly "adapted" to any extreme for either very hot or very cold climates, anything outside of short range of temperatures will cause us to either sweat or shiver.
Sweating or shivering will cost kcals ("Calories", "Joules"), and the extra energy expenditure will keep the subjects' weights lower than they would otherwise be.
Once the subjects enter an environment where they no longer need to sweat, shiver, or basically maintain a wide gap between the outside temperature and their body temperatures (which is the real driver here - the difference between the two), they will no longer expend as much energy maintaining human body temperature.
How much energy are they saving? Not much. I wish I could find the article again, but you're talking an extra 50kcal or so an hour saved - or a few pounds until the energy required to maintain the extra weight reaches equilibrium with the energy saved.
There are a few assumptions built into the above, which sees the question as more of a physics-oriented hypothetical than real-world example. In reality you have some large complications - getting anything done in cold temperatures is going to require a much larger energy expenditure, as you're usually carrying 30-50lbs of gear to not freeze to death, for example. A person used to wearing a dozen kilograms of animal furs during their weekly routine would gain a lot more weight than hypothesized above if they suddenly entered a mild climate with similar food intake, but without the constant load on their muscles.


text:
Why is epinephrine not part of the somatic nervous system?
I learned that the adrenal medulla releases epinephrine, which is a vasodilator of the vessels that lead to the skeletal muscle.
I also learned that somatic nervous system only uses Achetycholine as its hormone (not epinephrine).
I also learned that the somatic nervous system controls skeletal muscle.
So, why is epinephrine not considered a part of the somatic nervous system hormones, if it is controlling the skeletal muscle? What is wrong here?

You are confusing different functional systems. Epinephrine released by the adrenal medulla circulates in the blood and indeed dilates the blood vessels in skeletal muscle. This ensures that enough oxygen and nutrients are available for the muscles to perform in a fight/flight response.
The somatic nervous system utilises acetylcholine not as a hormone but as a neurotransmitter. It is not released into the blood but only into the tiny (about 10nm wide) gap (synapse) between the nerve cell's axon terminal and the next nerve cell or muscle cell respectively.
This release by the somatic nerve cells causes an electrical potential in the muscle which makes it contract.
In summary:
The somatic nervous system controls the muscles because it stimulates the contraction which makes e.g. your arm move. Epinephrine released into the blood by the adrenal medulla serves to ensure the muscles have the blood supply they need in a stress response (e.g. a dangerous situation).
Along with muscular blood vessel dilation, epinephrine in the blood for example also stimulates the heart to beat faster and stronger, and dampens down mechanisms involved in digestion - essentially it does everything necessary to allow a quick escape or a strong fight.

Ah, yes, thank you. Confusion between hormones and neurotransmitters. Thanks!


text:
Gametes of two different species
I always wondered why gametes from two different species dont fuse together to form an offspring. eg a donkey (sperm) and a female dog (egg)
I know this is not possible but I'm just curious.

Circular reasoning warning: because that’s how species are defined (i.e. two individuals belong to different species if they cannot produce viable, fertile offspring). Now, this definition breaks down in some cases but it’s still the common definition.

As an exception to this rule, you may want to read about the amazon molly or the fire ants. You'll find more info about these species and references in this answer

Daniel's answer excellently explains the issue in an understandable fashion, though you may have been looking for a more cell biological approach.
According to Immunological aspects of sperm receptors on the zona pellucida of mammalian eggs, 1976, Dunbar & Shivers, the egg cell has a receptor construction which is necessary for the sperm to attach. If the receptor is too different from what the sperm is built for (which will be the case in different species), it will not be able to attach and fertilise the egg.

+1 Indeed, I may have overlooked the point of the question, if indeed fusion was the keyword. Excellent answer in any case.

The biological environment in every cell and tissue of your body is an extremely complex, tightly controlled system. There are tens of thousands of genes in a typical eukaryotic genome, and depending on tissue types and environmental conditions, these genes are turned on and off in a very controlled manner. There is regulation at every point in the flow of genetic information: nucleosome disruption to expose DNA; RNA transcription from the DNA; protein translation from the RNA; and in some cases, additional modifications of proteins or intermediate mRNAs. At early stages in development, regulation of RNA and protein levels is even more crucial than, say, when an organism is fully developed and healthy.
All living organisms share some basic building blocks--DNA, RNA, and proteins work pretty much the same in all of life (there are a few rare variations of the genetic code but the basic premise is identical). However, the way that specific genes, transcripts, and proteins work together to sustain life varies widely between different organisms.
For a very rough analogy, imagine you want to bake a batch of cookies. Then consider the three following scenarios.

You look at two different recipes for chocolate chip cookies. They will have some slight differences, but they will share a lot in common. If you put the ingredients for both recipes in one bowl, it's likely you can still come up with some pretty good chocolate chip cookies in the end.
You look at two different recipes: one for chocolate chip cookies, and one for chocolate muffins. There will be some big differences in these recipes, but combining all the ingredients and baking, you still might be able to come up with something edible (and maybe even tasty).
You look at two different recipes: one for chocolate chip cookies, and one for French onion soup. If you combine the ingredients from these recipes and try to cook or bake them, there is no way you will come up with something that anyone would want to eat.

The first example we can relate to two individuals of the same species mating. Of course there is natural variation in the population, but this doesn't typically lead to lethality during development. The second example we can relate to individuals of two related species (such as a horse and a donkey). Sometimes these matings can produce viable offspring, although these offspring are often sterile. The third example we can relate to individuals of two very divergent species (such as donkey and dog in your original question). The biological systems inside donkeys are just so different from those inside dogs that this mating cannot produce a viable offspring.
Admittedly this is a rough analogy, but hopefully is sheds some light on the issue.

+1 because i found it quiet informative but i found Armatus' answer better answering the question. Thanks

No worries, I spoke very generally and he spoke very specifically. He deserves it!

Often, they do fuse together but the chromosome pairing is not precise enough to guarantee faithful cell division without loss of genetic material. Consider for example a simple inversion of one large part of a chromosome. In a closely related species that does not have this inversion, either the inverted part pairs or the non-inverted ends pair, but never the whole chromosome. That leads to strand-breaks and loss of large amounts of genetic material. That's an easy event for speciation, since it does not disrupt much. Only the ends where the inverted piece joins has two disruption. So, maximally two genes might be broken, but the chromosomes modified in this way won't pair.

I can answer this for mammals.  The mammalian oocyte (egg) is surrounded by a layer called the zona pellucida. There are three well-characterized proteins in this layer, called ZP1, ZP2 and ZP3 (not very imaginative, I know).  I don't know much about ZP1 but ZP2 and ZP3 are involved in fertilization.  The sperm's outer surface has receptors for ZP2 and ZP3.  Part of the 'zona reaction') to prevent fertilization by more than one sperm) involves destruction of these sperm receptors.  The ZP proteins are species-specific, meaning that ZP receptors on, say, human sperm, would not recognize ZP2, ZP3 on the zona of hamster eggs.
There is a test that was used in fertility assessments of human sperm, checking their ability to fertilize an egg.  Human eggs are kind of difficult to come by, so they developed a test based on the ability of a human patient's sperm to fertilize a hamster egg.  For that to work, they had to first remove the zona from the hamster egg, so sperm had direct access to the egg membrane.
This might not be freely available, but here is a link to an article:
https://humrep.oxfordjournals.org/content/13/3/624.full.pdf
There is also a brief wikipedia page about this test.


text:
When to measure resting heart rate and blood pressure for following day-to-day trend?
I'd like monitor my resting heart rate and blood pressure to see how they are affected by regular cardiovascular training and other events in life.
When should I take the measurements in order to reduce day-to-day variations? In the morning or evening? Before or after eating? Right after waking up?
Of course I'll make sure to follow good routines when measuring, but the ones I've found prescribed by hospitals don't state an appropriate time of the day.

I would be very surprised if the time of day made a difference.  I've personally never heard mention of such a phenomenon in discussions with intensive care practitioners (where of course HR and BP are measured constantly).  However this is only the case during rest, this paper (on horses) suggests that there is some difference in HR and BP after exercise depending on time of day.
You are right to attempt to control it however, I suppose.  It doesn't matter when you take your measurements, as long as you take them at the same time each day.
I would say that one of your first suggestions of taking the measurements almost immediately after waking.  Of course you would have to be relaxed as you assembled your equipment then rest for a few minutes in the posture you have chosen (this will matter) before taking the measurements but otherwise I can't see you having too great a problem.

It kind of depends.  If you want to compare apples to apples, check it first thing in the morning.  However, that's going to be at the lowest point. It's also important to know what your blood pressure is during the day, when you're living your normal daily life.  I recommend checking fairly regularly in the morning so you'll know what your true baseline is and whether it's trending up or down, and to "spot-check" occasionally at different times of the day to see how your body is handling the normal daily stress

Actually in my research into circadian events, the hourly differences in blood pressure was the first thing that I found. Based on this, I'd state that there are hourly differences in blood pressure and cardiovascular efficiency.
Because these changes are circadian, measuring these values at the same time every day (ex: 1 hour after wake up time or 1 hour before bedtime) would reduce variation. Just be aware of your caffeine intake - it may skew the measurements.
I do not have access to the scholarly library that I used then, so the chances of finding the article are slim to none.


text:
Question: Annotation search in scientific literature
In a scientific paper I have been studying ("Predicting Novel Human Gene Ontology Annotations Using Semantic Analys" S.Draghici et al., 2010), I have read that authors checked the accuracy of their annotation predictions by searching on available literature the scientific evidence of their discoveries.
So, for instance, if they predicted an annotation X, they would search for scientific papers that prove that the predicted annotation is correct.
I think I could use the same method for my annotation prediction experiments, but how to do it? How to search evidence of a certain annotation by browsing literature?
Should I just visit PubMed website and use annotation id as keyword for search? And which source (EntrezGene, etc) id should I use?

Text-mining the scientific literature has become a very popular topic recently. I think this question is definitely on-topic, but you're likely to get a better response from http://www.biostars.org, where I've seen many more questions related to mining the literature.

Haha, looks like you already posted it there!

@Daniel Standage Lol ^_^

Might be more likely to get a good answer at Academia.SE?

Well here's my take.
Too bad there is no open access to this article.
I see that they only had statistics for the top 50 annotations, which implies a fairly manual process - you are going to have to read a bunch of articles or abstracts to decide directly whether the software is right.
In this case, the authors are using a weighted latent semantic indexing method, which have started with a bunch of articles for each gene.  In this case they would need to only look over the data they put into their training.
That might not answer your question though.  If you wanted to search through the literature to confirm annotations generated by a different method...you could create a semi automated process perhaps like this:
Do a rough search from NCBI in an automated fashion (I use biopython) and then read every article for validation of the Gene Ontology result.
Its possible you could search for the gene and the GO term if to get a more focused result, load them into a database or just create a set of files with the data.  I would build a little website that would let me scan through the abstracts with links to the complete articles (pubmed supplies DOI numbers) and just check 'yea' or 'nay' on whether confirmation happened.
There's other potential options on finding articles for search.  the Genbank record for the gene often has a few references in it. One might use pubmed's referencing feature, where you can start at these confirmed articles that describes the gene in question and use pubmed to show articles that have referenced that first article.  I'm not sure if this is accessible by API, but you can build an article graph by crawling the bibliographic references.
For anything that was neither directly contradicted nor confirmed you would have to go back to google and look until you found something.  Clearly there are genes for which you will find no reference at all, and you will have to avoid these for confirmation.
I'm not sure if they checked for any biases here. If something like interpro2go which generates GO mappings from protein domains was used to generate the annotations, you would want to take care that you weren't just rediscovering the references which helped generate the annotations in the first place.

I face a similar problem. I know that something is a fact but i am not able to get the exact references for them. A big problem is how to select appropriate keywords that describe the fact. Do you have an idea about this?? And Is this topic worth a new question ?

it might be worth getting a new question started, but I recommned Latent Semantic Indexing or Dirchelet decomposition, or Bayesian filtering (google plan for spam) if you are something easier.


text:
Why do rod cells not recover after bleaching upon exposure to bright light?
I'm confused as to why, when exposed to bright light, rod cells cease to function.
I understand that exposure to bright light bleaches all of the rhodopsin, but...so what?
Why doesn't the bleached product (opsonin/retinal) simply get re-synthesised back into rhodopsin as it does in dim light, and therefore continue the cycle and enable impulses?

In rods, the pigment Rhodopsin can be thought of as a receptor protein with a pre-bound chemical agonist. The receptor protein is called Opsin, and the pre-bound agonist is called retinal. The absorption of light causes a change in the conformation of retinal so that it activates the opsin, causing bleaching (changing the wavelengths absorbed by rhodopsin). The bleaching of rhodopsin stimulates a G-protein called transducin in the membrane, which activates phosphodiesterase, which in turn breaks down cGMP that is normally present in the cytoplasm of the rod and is necessary for the continued operation of the sodium channel sending the neural signal.
In the dark, the channel is open and the Rods are active. In bright light, due to the amplification from cascade effects, all of the channels will be closed, stopping the Rods from sending their normal signals until cGMP levels are able to compensate.
My guess is that the bleaching ceases fairly quickly and the proteins return to their original conforms shortly, but it's the cGMP levels (remember, cGMP is destroyed, so any new cGMP replacing the old must be synthesized first) that take a long time to recover as the signal to destroy the cGMP initiates a cascade that results in strong amplifications.

A good guess but you need some kind of a reference for it


text:
Why do animal teeth get darker if exposed?
I was wondering why the teeth of cats (And dogs, as far as I know, plus possibly some other animals or even humans) get darker if they are exposed to air / light?
Example:

(See the lower end of the tooth, which sticks out if the mouth is closed. No, the cat was not resisting, just slightly annoyed.)
So, my question is:

Why does this happen?
Would it happen to human teeth, if they would stick out of the mouth like the ones of cats do?

My guess is that it has something to do with the teeth reacting to air and corroding, but all my knowledge about biology comes from two years of biology in school, so I'm asking here.

Could you provide evidence that this is frequent or invariable? I can think of an explanation, but I'm unsure if this is common.

it probably wouldn't happen if they brushed their teeth more.  Its hard to imagine human teeth are that different... :)

Yeah. I think it has something to do with REDOX.

As far as I know, oxygen and other oxidizing agents make the teeth whiter by bleaching it (Potassium permanganate and hydrogen peroxide solutions are used to bleach teeth). Anyways, your question isnt  addressable as long as you dont support this with some more evidence. [More biological replicates!!!   :P ]

The incisal and occlusal edges of teeth are more translucent since there is only enamel in this area and the dentin core is deeper inside. The dentin is more opaque and reflect the light back and it looks lighter whereas the enamel is translucent and allow more light to pass through and less light is reflected back so it looks darker. Many human teeth the incisal edge is translucent or darker for the same reason.

According to me animals use these teeth to chew meat particles etc. So because they don't brush these food particles get exposed to bacterial agents which in turn causes corrosion of teeth. As we see the structure of the animal teeth the food particles are trapped in between resulting into high bacterial corrosive activity. But in humans, regular maintenance and high use of water it decreases the acidity caused by the food in our mouth this prevents excessive corrosion and bacterial activity and growth. On the other hand canines have an initial use of tearing so the usually are not much affected by the food particles and also because of their protruding shape.
The exposure of air and light increase the bacterial activity.

Do you have a reference other than yourself?

This has the right idea, but the baffling (if refreshingly honest) "reference" needs to be corrected.


text:
Why should benzalkonium chloride (an antifungal agent) be used during your laundry machine's "rinse" cycle, not its "wash" cycle?
I'll first provide lots of background information. My actual question is at the very end.
Background
The spread of athlete's foot
Athlete's foot is a fungal infection which is mildly contagious. The infection can be spread by skin particles left on towels. (Source.)
If one person in a family has a fungal infection (e.g. athlete's foot or jock itch), their laundry may also contain fungi. I suspect that towels and laundry machines might make it easier for these fungi to spread: e.g. from the patient's feet to their groin. See, for example, here.
Water at 140 °F
You can kill fungi using water at 140 °F (60 °C). Unfortunately, your water heater probably doesn't produce such hot water, because such hot water is dangerous and can kill unsuspecting individuals. (Sources.) Still, you can make such hot water in other ways. (Source.)
Antifungal rinses
Another option is to use a suitable antifungal rinse.
The most common cause of athlete's foot is T. rubrum. (Source.)
T. rubrum is a dermatophyte-type fungus. Dermatophytes spread through spores. These spores can sometimes live for up to 20 months. (Source.)
Canesten Laundry Hygiene Rinse is 7% benzalkonium chloride. (Source.) A competing product is Bluo Laundry Sanitiser, which is also 7% benzalkonium chloride. (Source.) These products are sold in Australia but not in North America. (How safe are they? I dunno; I'm not a toxicologist.)
The Canesten rinse label makes an impressive claim: "eliminates ... fungi from your washing". Still, it looks like these rinses' fungistatic effects are stronger than their fungicidal effects. In reality, they're not perfect at killing T. rubrum, but they're still better than nothing. An Australian lab found that, in 20 minutes, these types of rinses reduced T. rubrum by between 90% and 99%. (Source.)
(Each rinse is marketed as both antifungal and antibacterial, though there's limited evidence that people can catch bacterial infections from clothing. I'm not convinced that their antibacterial effects are really necessary.)
Use during the rinse cycle, not the wash cycle
Each manufacturer says that its benzalkonium chloride rinse should be added during your washing machine's final rinse cycle, not its initial wash cycle.
You can do this using your clothes washer's fabric-softener dispenser, if present. On a top-loader, this is usually a cup-like device on top of the machine's central agitator post. (Source.) Or you can buy a softener dispenser ball, though they're not always 100% reliable. Or you can add the rinse manually at the correct moment.
A sample washer program
Washing machines can vary. Here's a description of the normal program of certain inexpensive top-loading Whirlpool agitator-type washing machines:

Fill - agitate: 16 minutes.
Drain: 2 minutes.
Spin: 2 minutes.
Rinse, fill, & agitate: 4 minutes.
Drain: 2 minutes.
Spray & spin: 2 minutes.
Spin only: 4 minutes.

Total: 32 minutes.
(Based on: wiring diagram W10118358, rev. A.)
The wash cycle is longer than the rinse cycle.
My question
To summarize the above background information: Canesten laundry rinse (7% benzalkonium chloride) has both antifungal and antibacterial effects.
And so I wonder: Why does the manufacturer recommend that it be used during your laundry machine's rinse cycle instead of its (longer) wash cycle?
Any answers or guesses are welcome.

I think your question has been answered below (with the caveat that you should stop the washer in the rinse cycle to allow more time to disinfect.) But please note that a contaminated towel usually means an unwashed one. I strongly suggest you do not use benzalkonium chloride in the wash. Tines pedis is not highly infectious in the home. It is rather much more related to your individual susceptibility to the fungus. People live together for decades without ever passing it on to members in close quarters. The potential to harm the environment far outweighs the benefits here.

I've since done some more research.  Indeed, it turns out that an expert body doesn't recommend to use benzalkonium chloride to kill fungi in the wash.  Instead, it recommends the use of a washing powder containing activated oxygen bleach, as well as various other techniques.  See this post for more details.

The label of the veterinary product Fung-A-Way, which is Benzalkonium Chloride 0.15%, states that "Efficiency is neutralized by soap or detergent residues."
The website http://www.mpbio.com has the following under its description for Benzalkonium Chloride:
"Incompatible with anionic detergents, such as soap, and with nitrates."

Benzalkonium chloride is what's known as a quaternary ammonium cation, or quat. These are disinfectants commonly used in medical settings, for example. The mechanism of action is thought to be due to the long alkyl chains, causing membrane leakage (ref1, ref2).
Like any disinfectant, however, two things are required for effective disinfection: The appropriate concentration, and the minimum required contact time. The following report goes over the importance of contact time but also makes a significant discovery: many disinfectants dry before their required contact time while failing to marginally kill anything except bleach.
The required contact time for quats happens to be 10 minutes. So on a hard non-porous surface youd spray it wet, come back in ~5 minutes and spray it wet again to ensure disinfection. The reason you would want to introduce a quat on the final rinse is because if you immediately wash it off or wash it off within minutes, your disinfectant is most likely to do nothing.
Edit: You said laundry but when I think washer in the US, I think dishes, which made no sense anyways.

My question describes a sample laundry-machine program. It looks like the "wash" cycle is about 15 minutes long. Wouldn't this be enough time for the disinfectant to kill enough fungi?

A) Find a top-loader agitator laundry machine. Use your thumb (or a scrap of cardboard) to defeat the lid switch. (Also watch the drain hose, if the machine drains into a sink.) You'll quickly learn that the wash cycle does not provide a constant clean water flow. The machine fills itself, agitates for 15 minutes, then drains itself to prepare for the rinse cycle. B) OK; good to know. On second thought, I'm thinking I'll indeed avoid the chemical.

Interesting! I redacted that last comment because I obviously know nothing about my own appliances. So some extra thoughts: I don't know how the quat reacts with your clothes over time, if it'll ruin them, or if the detergent may block the mechanism of action. The manufacturer might be able to tell you if you call them.

This is actually very informative. Maybe OP should rinse the suspect items, then leave them to soak in benzalkonium chloride and only then add them to the wash. Environmentally cleaner soaking options are soda, vinegar or boiling water.

Most disinfectants are rendered ineffective or much less effective in the presence of organic materials. Washing your clothes prior to adding Canesten in the rinse allows removal of organic matter and therefore more effective action.

Welcome to Biology.SE! Your answer is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


text:
A study found that the hepatitis C virus can live on surfaces for six weeks. Did they end the study before the seventh week began?
A study once found that the hepatitis C virus (HCV) can remain infective for six weeks on ordinary household surfaces. You can see the free full text, or a summary for busy clinicians.
What happened in the seventh week? Did the virus cease to remain viable, or did the study just end suddenly?
From part B of this figure, it looks to me like the study just ended suddenly. But I'm not a biologist, so I'd like to hear your opinion.

The place to find this information would be the Methods section of the paper.

We spotted 33 µL of plasma spiked with HCVcc on the 24-well plates. They were either immediately tested for viable virus or stored at 4°C, 22°C, and 37°C for up to 6 weeks before testing.

They tested their samples for (up to) 6 weeks. At the time of the 6th week they still found infectious virus. They did not test samples beyond 6 weeks so they can't say anything about infection past that time.

I appreciate your answer! ❧ I've now asked a follow-up question: "We know that the hepatitis C virus can live on surfaces for at least six weeks. Maybe longer. The infectivity study ended after just six weeks; why?"

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


text:
An unexpected mushroom in my garden
My grandma is a great fan of mushrooms and knows quite a lot about them. About 10 years ago, she started throwing out mushroom remnants in one special place, in order to grow her own mushrooms. In fact, for last three years we found some parasol mushrooms (Macrolepiota procera).
Today she found something, that nobody at home can classify. From what I searched, it might be  Cortinarius privignoides, but it is marked as almost extinct here in Poland, so I doubt this classification. Maybe you have seen this or know what it really is:

The hat is light brown with faint violet shades, the leg on the outside is partly violet too, but the inside is all white.
Some more photos:
All three
The gills are lighter brown, also with a violet tone
The cut through the leg
The cut through the hat
At my parents' house I found one more mushroom atlas, and a new candidate: Cortinarius traganus, but one thing is not right - the ones that I have don't have a smell and gassy webcap should smell and taste bad.

You might be better off asking this at gardening.stackexchange.com instead of Biology, unless a Botanist happens by here. :-)

Ooo! I did't even know about gardening :) Thanks!

If you know the german language, another good page is http://de.wikipedia.org/wiki/Wikipedia:Redaktion_Biologie/Bestimmung

Thanks to MCM's advice I know for almost-certain that this is Lepista personata.


text:
How do gain-of-function alleles help with problems caused by genetic redundancy?
Genetic redundancy masks the gene functions (eg it masks diverse functions of the tumor suppressor gene). I have read on the internet that gain of function alleles can solve a such problem caused by genetic redundancy and would like to know how.

Genetic redundancy can be a problem when studying knockout or hypomorph mutations of genes, or analogues such as exogenous RNAi. The redundancy can consist either in incomplete knockout (the genome contains more than one copy of the gene but only one copy is mutated) or functional redundancy (different genes doing more or less the same thing). If you try to figure out what a gene does using a loss-of-function allele, the other copies or redundant genes may weaken or completely mask any phenotypic manifestation of the lost gene function.
Gain-of-function alleles can be useful in such a situation. A gain of function means the gene product does something different, or something additional to its normal function. Even if there are "healthy" other copies of the gene or redundant genes around, the modified function of the introduced allele will interfere with the normal behaviour of the molecular pathways it partakes in, and thus cause a phenotype.
A classic example are constitutively-active alleles. Imagine for example a tumour suppressor with a mutation that prevents it from being degraded (but imagine you don't know this gene is a tumour suppressor yet). Let's say there are other tumour suppressor genes around, so if you knock out your gene of interest, the cell behaves as normal - loss-of-function isn't useful to study what the gene does. Now, if you introduce this constitutively-active mutant variant that doesn't get degraded, it causes too much suppressive activity and drives the cell into complete cell cycle arrest, regardless of the other redundant genes being around. Based on this phenotype, you could infer that the gene is probably a tumour suppressor.


text:
Rejection of valid theories of biology on theoretical grounds
Is there a theory in biology that was initially disregarded as false (because of critical or contrasting perspectives) and only recognized as important after a considerable time, possibly only in recent years, thus significantly impeding its development?

Welcome to SE Biology. Because I assume your first language is not English and because the question relates to ideas (where language is important) I have rewritten it and made the title fit the question. Could you check that this is what you meant. There is one phrase that is unclear to me — "because of critical or contrasting perspectives". Do you mean "because it went against the prevailing ideas of the time"? If so, substitute that as it would clarify. If not, explain what you mean so we can phrase it better.

Extinction was rejected by many on religious grounds until science gained sufficient power and acceptance that the religious opinion no longer mattered. Not a theory though.

I took the liberty to modify @David 's edit and add back in part of the original phrasing that mentioned an interest in only recently accepted previously controversial theories.

I don't think this is a good question for the SE format. There are too many possible answers, and most answers will lead to a discussion of opinion over whether or not that example is an ideal example (and the meanings of words like "theory" "initially" "false" "important" "impeding") rather than anything concrete.

The idea that organisms with mitochondria derive energy from respiration through a proton motive force was considered controversial at the time.
This is the best reference I could find at the time:

His theory explained that it was the energy captured from those protons
  returning to the matrix and not energy stored in an undefined
  high-energy covalent chemical intermediate that was then used to drive
  ATP synthesis. This Nobel Prize-worthy concept (1978) was so counter
  to the leading theories of the day that the field spurned it for the
  better part of a decade.

Pagliarini, D.J., Rutter J. Hallmarks of a new era in mitochondrial biochemistry 2013  Genes Dev.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3877752/

This is a good example of a hypothesis that was not accepted initially. What took it so long to be accepted? Experimental Support! Once someone else had conducted the "acid bath" experiment (or whatever was the first piece of supporting evidence — I'm just going on Stryer) in support, the X~P intermediate that had never been found faded into obscurity. So it is arguable whether the acceptance of the hypothesis/theory without the experimental systems to study it would have made much difference.

Germs
The idea that life is not spontaneously created, but always develops from... well, something.
For decades, centuries even, the notion that invisible micro-organisms were responsible for diseases, mold etc. was controversial.
Louis Pasteur's swan necked flask experiment (in the 1860's!) is one of the last and most famous demonstrations that sterile media must be contaminated and cannot generate life from scratch. He showed that a sterile broth communicating with the outside world through a single aperture was not contaminated if the aperture was long enough to prevent accidental contact with ambient micro-organisms, whereas the broth grew turbid quickly after being directly exposed to air by removing the swan neck.
Before this theory was accepted, the notion that sterility is important notably in hospital settings was often challenged, leading to thousands of people dying of nosocomial infections.

I'm not sure Pasteur's work influenced hospital procedure. I think that the success rate of surgeons that adopted it (in Britain initially I believe) was key. And remember, Pasteur's work was extremely applied: he consulted with the brewing industry, for example. If his advice worked for the brewers it saved them lots of money, and this encouraged others to consider his approach.

I think it did, although not directly. Pasteur's work was a demonstration that there are germs everywhere - regardless of the setting. Pasteur's work was the primary source of Joseph Lister's inspiration to promote aseptic techniques. Pasteur did not make any specific point about hospital acquired infections (Lister did) but he was the starting point of a progressive realization that germs were the prinicpal cause of hospital deaths. An excellent article by Pitt & Aubin (Canadian Journal of Surgery, 2012) tells the full story in greater detail

I notice from his bio, that the poster is a mathematician, so I have chosen to answer this question as an experimental scientist (a molecular biologist with a chemical education) to a non-experimental scientist:

In my view, for biology, the acceptance or rejection of hypotheses plays only a minor role on the development of the science. This is because actions speak louder than words — it is the experimental validation or support of a hypothesis that is important. If the hypothesis is correct, but the technical or theoretical basis does not exist to test it, then that basis is also lacking to exploit the idea.

This only applies to an open society. An example of the damaging effects of false theory can be seen in the rejection of genetics by the Soviet Union in the 30s (and later) on political grounds (Lysenkoism), a rejection that did not affect science in the West, but was responsible for thousands, if not millions, of deaths by starvation because of its influence on Soviet agricultural practice.
Let us consider the two answers already given (both of which I have upvoted). First @Mowgli on Pasteur and ‘germ theory’. I would maintain that it was only when a mode of killing ‘germs’ by heat was suggested, that practical demonstrations of the effectiveness of measures to prevent spoilage of food and drink (and to prevent sepsis) was possible. And it was these practical demonstrations that overturned the prevailing theories, not the strength of the intellectual arguments against.
The case made by @Cell for the rejection of Mitchell’s hypothesis is perhaps more pertinent. Certainly Oxford biochemists were still taking about X~P (an unidentified ‘high-energy’ phosphorylated intermediate) in the mid 60s, five years after the hypothesis was published in Nature. But the key — and unusual — thing was that this was specifically a hypothesis. It was supported by a variety of arguments and equations, the latter of which would cause many to shrug their shoulders. Clearly some scientists were attracted to the idea, but it took a system with photosynthetic bacteria to provide practical evidence, as well as improved characterization of the membrane ATP-synthase (which was generally referred to as an ATPase, because that was all it could do in vitro). So the maximum of a 10-year lag in acceptance was not caused by the rejection of the idea, but the lack of a means to prove it.
Similar arguments may be made about the non-acceptances of the idea of Avery (1944) that DNA was the genetic material. Although this was based on experiments, one could argue against the experiments. It was only with the determination of the structure of DNA and the development of phage and isotopes, that the means to confirm this idea and develop the field further arose.
That’s how I see it. However I would be interested for suggestions of any other examples (template theory of antibodies?).


text:
Why do men have a greater chance of suffering from hair loss?
If we look around we'll find that men are more likely to suffer from hair loss when compared to women. Is there is any specific reason for this?

some hair loss is related to testosterone, as to why eununchs tend to preserve hair better. https://en.wikipedia.org/wiki/Pattern_hair_loss      (article about eununchs)        http://www.bbc.com/future/story/20131127-will-we-ever-banish-baldness

@RoSiv Please make an answer rather than posting an answer in the comments.

@BryanKrause      I wasnt really confidant with my answer but ok.

As per my comment above, some types of hair loss is androgenic, and therefore related to testosterone levels. This is why eunuchs can be resistant to some forms of hair loss.


text:
Number of different clones of B lymphocytes
My professor told us that there are about a million different B cells based on their surface receptor.
I have read that we have about 30000 genes in all. Since receptors are proteins how do these 30000 genes make such a large number of receptors?
I read about something called alternative splicing. Is this the mechanism behind this?

You're looking for VDJ recombination: https://en.wikipedia.org/wiki/V(D)J_recombination

Alternate spicing of mRNA is a real phenomenon, but it's not the source of immune cell receptor diversity.  The DNA of immune cells is rearranged in a slightly random manner, to make a receptor with a random sequence in the variable portion of the receptor.  As Armatus already said, the process is VDJ recombination.  Here is a link to a textbook on NCBI
https://www.ncbi.nlm.nih.gov/books/NBK27113/

Yes - in short, splicing enables one gene to be 'read' in multiple different ways. Imagine you have a set of letters; you can make one long word out of them, or cut some words out to make a shorter, different word. The same logic applies to gene expression, in that one gene could be made to code for a variety of different proteins (in this example, surface receptors).