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Why don't bacterial cell walls prevent bursting when attacked by the complement?
The complement system creates pores in cell membrane which leads to influx of lots of water thereby causing lysis of bacterial cell.
But what I fail to understand is that if bacteria have cell walls around them, why will they burst ? Shouldn't they simply become turgid just like plant cells do ?

Cell wall is porous enough to allow water and other small molecules to pass. Influx of water will still destabilize the cellular environment and in essence rupture of the cell. Bursting, IMO is quite a dramatic term for this.

Although this seems to be a simple question on the exterior, the answer is going to be confusing and unclear because we still don't know the answer exactly.
Short answer - MACs are bactericidal not because of water gushing in. It is due to other mechanisms effected by damage to membrane integrity.
Long answer
First of all, I am assuming you already know the complement cascade, the pathways and the like, and I won't get into it. But to mention in passing, MAC is not the only way the complement can help the immune system. It can also opsonise antigens and release anaphylotoxins to modify the immune response.
Most studies concerning the assembly of the MAC and the resulting membrane lesions have been conducted in model systems, e.g. erythrocytes and artificial lipid bilayers. The advantage of these systems is the ease of characterizing the membrane lesions compared to bacterial membranes. Also, complement fixation tests (which use erythrocytes and complement) have been widely used even diagnostically until not very long ago. The osmotic damage, ion effluxes that you talk of happen here and leads to the lysis of erythrocytes. Even in their case, there are 2 models of how MACs work - one is by making a pore (in the pic) and the other is by forming leaky patches in the membrane. However, the way bactericidal MACs work is thought to be different and a little more complex than this -

This picture may have been used for just didactic purposes but cannot be applied in a bacterial system simply because bacterial cell envelopes are different. The two major groups - Gram positive and Gram negative cell walls are important to differentiate while discussing the mechanism of MAC bactericidality. It is important to note that MAC mediated bactericidal action has been reported predominantly only in Gram negative organisms. This resistance in Gram positives is thought to be not because of the osmotic turgor or turgidity but because of the thick peptidoglycan in Gram positive bacteria, preventing access to the inner cell membrane where the MAC assembles. There are MAC resistant Gram negative bacteria too, but let's not discuss that here. It is not off-track to mention here that species like Neisseria where the capsule is thin and the peptidoglycan is too, are more susceptible to complement damage.
So, assuring that the MAC mediated bacterial lysis is not just water gushing in, how is it thought to happen??
For this, we need to revisit the structure of the Gram negative cell wall. The cell wall structure is quite intriguing since there happen to be two lipid membranes enclosing a periplasmic space which contains little peptidoglycan that Gram positives have much more.

Since there are two lipid membranes, technically, there's a possibility that the MAC can be formed on both these layers (MAC's assemble on hydrophobic membranes). MACs assembling on the OML (outer membrane layer) are not sufficient to cause lysis. It is confirmed that the damage has to occur to the IML (inner membrane layer). Inner membrane damage is thought to be bactericidal since it is more restrictive in its permeability than the OML. Also, the IML is linked to several important cellular, metabolic functions that require proper ionic gradients. One example is the oxidative phosphorylation that takes place around the IML.
This should answer your question in that the mechanisms of cell lysis seem to be slightly different in bacteria than the model systems (erythrocytes), but let us delve a little deeper into this.
One persistent question is "how can something as huge as the MAC, penetrate the OML and the peptidoglycan layer, to reach the IML to cause damage?" The hypotheses that MAC just forms a hole in the OML and other serum factors seep in and cause damage to the IML has been ruled out since complement alone can be bactericidal in nature. To explain this, two models have been proposed -
One, where the complement attaches at special sites in the membrane where both OML and IML approximate (at special sites where large proteins span both membranes) and another where, the complement creates a pore to allow C9 monomers to leak in, in turn polymerizing to damage the IML.
I assume this explains it all. Still, I implore you to refer to the link below and correct me if I've been wrong anywhere.

Reference : The bactericidal mechanism of the complement membrane attack complex, Lars Ootes, (PDF)


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Determination of genes to be modified in epigenetics
It seems that during reproduction particular genes are targeted for modification (mutation, deletion, insertion, etc.) given environmental inputs of either or both of the parents.
If a creature was fit given its environment, its seems there is little mutation. However, if the creature becomes less fit (i.e, due to increasingly becoming prey to a predator) it will undergo increased rate of mutation to find a successful adaption to the new environment. But it seems that the mutation is also targeted to particular genes that maybe most beneficial to mutate (i.e, to develop camouflage).
This begs the question - given environmental inputs, is there something that controls gene modification during reproduction? More specifically, is there a process that targets a specific gene or trait?

Before the rants are coming in from the evolutionists and geneticists shooting this question to pieces because evolution is not a teleological thing - isn't it indeed so that certain loci are hot spots for mutations while others are conserved thereby allowing evolution in certain directions? +1

@Christiaan Doesn't it has some connection with Epigenetics?

@Christiaan Then that should be the question and not the question as is.

@Christiaan I think you're right; there is a good question and premise here. But it needs an edit to make that clearer. It's not clear as it stands.

@TalhaIrfan I came across Epigenetics again for a quick refresher. It seems I wasn't completely off-base with my premise.

Mutations are not performed targeting a specific new phenotype. There is no way an organism can "know" the impact of a specific future mutation anyway. A mutation is just a mistake in the replication process. As a consequence the majority of mutations are deleterious and only a handful of mutations are beneficial.
It is true though that the mutation rate can be affected by the environment or the stress induced by an individual (Agrawal 2002). It seems more intuitive that these are just a consequences of the cost of the DNA replication machinery and DNA repair machinery but it is not impossible that such changes in mutation rate could eventually evolve as a bet-hedging strategy. In the extreme case where the same types of environmental change happen over and over again, it is not impossible that a lineage could evolve the ability to modify the mutation rate at a particular locus. However, to my knowledge this has never been found.
You might want to follow an introductory course to evolutionary biology. You might also want to read this post too that gives a mixture of related information

It turns out there is some level of targeted mutation, but not direct mutation of genes. Without mutating any of the underlying DNA, environmental inputs can affect the repressors of a gene, resulting in altered gene expression in reproduction.

Predicting the protein interactions based on a DNA change, let alone overall organism traits and impacts, is far beyond the processing power of any system except reality itself. You can think of evolution as brute forcing problems with a vulnerability to partial solving. Obligatory: https://xkcd.com/1605/

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Photosynthetic Absorption Spectrum - Pigment vs. Absorption Spectrum
This is a very confusing question to me that came up while I was studying photosynthesis.
Halobacterium has a photosynthetic membrane that is colored purple. Its photosynthetic action spectrum is exactly complementary (opposite to) the action spectrum for green plants. What wavelengths of light do the Halobacterium photosynthetic pigments absorb?
A) red and yellow
B) blue, green, and red
C) green and yellow
D) red and green
E) blue and red
I don't understand how the answer to this is possibly "blue and red," since the pigment is purple (eliminates violet end of spectrum since purple is transmitted) and the question says the action spectrum (synonymous with the absorption spectrum) is complementary to that of green plants. Green plants absorb best in the blue and red ranges, so naturally I would think the answer is C, green and yellow. What am I missing? Am I confusing the color of the photosynthetic pigment with the absorption spectrum?
Thanks!

Halobacteria use bacteriorhodopsin in a photophosphorylation to synthesize ATP. Their bacteriorhodopsin pigment absorbs and uses the yellow green middle of the visible spectrum and reflects both ends, which would then be visible as purple, so you are correct, the answer to your question is C)

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How do mosquitoes orientate in the darkness?
An annoying mosquito (Culicidae) which kept me awake nearly the whole night lead me to this question.
I have heard that mosquitoes can smell CO2 which could help them to orientate in the darkness, but how do they avoid obstacles and know where to land? I was browsing the wikipedia article but did not see an explanation for this, can somebody explain this to me?
I also wonder about the purpose of their loud, annoying sound (afaik only females produce it), which i would think as an evolutinary disadvantage, but this would be another question...

What is the purpose of their loud, annoying sound?

Both males and females produce a sound when flying but not at the same frequency. I would think of the male sound as mainly an artefact of flying and don't really know if it has any usefulness. I would note though that before mating both gender tend to synchronize their sound (Gibson and Russel 2006). On the other hand males are very attracted toward the sound of females.
In nature, mosquitoes make swarms. Male's job in the swarm is find find female, courtship and mate. This means that males need a cue to detect them from far away and this cue is their sound. Males evolved large and fluffy antennas (with which they hear) while females only have small antennas Charlwood and Jones 2008.

How do they avoid obstacles?

They have eyes! It is never complete darkness and they just move around, see things and sometime bump into something and keep flying until they reach their goal.
I can't offer you a citation for that but as I worked with mosquitoes in the past, I think it is a good description.

Thank you for the answer. Do mosquitos have a very high light sensititvity? Because I can see barely nothing add night in my room, but they seem to navigate quite good. And when i turned on the light, they stop flying and hide till i turned it off again.

You might get the info in Gabriella 2008 (I can't access the paper for the moment). I know that mosquito have a range of vision that is narrower than ours (they can't see red).

Some researchers found that they may sense obstacle in the dark from the sound of their wing beating against the obstacle and modifying the air flow around them:
"Nocturnal mosquitoes exhibit a behavioral response to divert away from surfaces when vision is unavailable, indicating a short-range, mechanosensory collision-avoidance mechanism. We suggest that this behavior is mediated by perceiving modulations of their self-induced airflow patterns as they enter a ground or wall effect"
About the purpose of their their loud sound, indeed it is a disavantage for the female when flying close to their blood host, but it is believed to be a way to be heard by the male in the mating swarm. In addition, there is an auditory mechanism in mosquitoes which allow to use its own flight sound to amplify the sound of the nearby mate (ref1, ref2). The "harmonic convergence" theory (ref3; saying that mosquitoes actively changes their wingbeat frequency to harmonize between each other) starts being out of date (ref4).

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Recessive is Dominant to Dominant?
If a gene has for instance three alleles, p, q, and r, then could p be dominant to q, q be dominant to r, but r be dominant to p? Can a gene that is recessive to one allele not be dominant to another allele that is dominant to the second? If it can, what are some examples of traits that do this?

I'm not sure, if it's possible. See what "dominance" really means here (first answer). https://biology.stackexchange.com/questions/44475/can-difference-in-the-expression-potential-of-alleles-lead-to-dominance

To some extent, it depends on what you mean by "dominance". If you take a phenotypic definition of dominance, then the answer is (technically) yes, you could imagine such a gene system.
That is, imagining alleles p, q, and r, and three phenotypes P, Q, and R, with the following homozygous behavior:

pp ➞ P
qq ➞ Q
rr ➞ R

Then you could theoretically imagine the following heterozygous behavior:

pq ➞ P
qr ➞ Q
pr ➞ R

In that sense, p is dominant to q, q is dominant to r, and r is dominant to p.

The problem arises in trying to figure out the underlying biochemical rationale for such a system.
In the typical cases where we talk about dominant and recessive alleles, we're talking about a single axis of functionality, particularly an all-or-nothing case: The dominant gene has activity, and the recessive gene doesn't. If you have one or two dominant alleles, you have activity and thus the dominant phenotype, and if you have no dominant alleles you have no activity and thus the recessive phenotype.
It doesn't have to be all or nothing. That's where incomplete dominance comes in. If you have two dominant alleles you have a lot of activity. If you have one dominant allele you have less activity If you have no dominant alleles, you have no activity.
In some cases, dominance is not gain of activity, but rather loss. This is termed a "dominant negative". The normal, recessive allele has a certain activity, and the dominant negative allele can come in and shut off that activity. A frequent mechanism of action for a dominant negative is to non-productively out-compete the recessive allele for binding sites.
Such a single-axis explanation of dominance can't contain your proposed system. However, there are systems where there are multiple axes of activity. The ABO blood group system is a good example. Here you have three alleles, a, b and o. a codes for A activity. b codes for B activity, and o is inactive for both. Thus you have both a and b being dominant to o, but neither is dominant to each other, resulting in an AB blood group when both are present.
However, as long as we're just adding activity, we still can't realize your cyclical dominance system - we'll be stuck with co-dominance.
Totally hypothetical system:
To support your cyclical dominance system, we can possibly combine multiple activity a dominant negative. Here's one possible system that I came up with.
The allele p induces activity A, but is a dominant negative (that is, actively suppresses) toward activity B. The allele q induces B, but is inactive toward A. The allele r is inactive toward B, but is a dominant negative toward activity A So we have the following:

pp ➞ A ➞ P
qq ➞ B ➞ Q
rr ➞ O ➞ R
pq ➞ A ➞ P (q tries to have activity B, but is suppressed by p)
qr ➞ B ➞ Q
pr ➞ O ➞ R (p tries to have activity A, but is suppressed by r)

Is there a set of genes which has such a system? I'm not aware of any. Notice that to get such a cyclical dominance, you need to not only have multiple activities but also dominant negatives - and in the correct correspondences. If such a system exists, it would be very unlikely.

Dominance by silencing the other allele
The mechanisms by which dominance work are still very much unknown. One type of mechanism that will be of particular interest to this question is the modifier of dominance where the protein product of an allele silence the expression of the other allele in order to cause dominance relationship.
Is the pattern you describe possible?
In such system, I can imagine a case where allele A1 would silence A2 which would silence A3 which would silence A1. I can't think of any reason such a pattern should not exist. However, I am not aware of evidence of such pattern.
The interesting case of SI in Arabidopsis thaliana
This type of dominance (dominance through silencing the other allele) has been reported in the self-incomtability locus of Arabidospsis theliana (Durand et al. 2014). At this specific locus there are 6 alleles but they have a very hierchical relationship where A1 silences all other alleles, A2 silences all alleles but A1, A3 silences all other alleles but A1 and A2 etc..
Related posts

Evolution of dominance of alleles
What determines if a gene is dominant or recessive?


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Species Identification - small insect
I found a few of these walking in the middle of the night (about 3 AM) on a wall in my room near the floor. They are at most a few millimetres long (no more than 2 I would say). I am living in Poland, in a block of flats.
EDIT:  Since I first wrote, I have seen few more - very small - less then 1 millimetre long. They seemed to be coming from behind the baseboard. This time I've seen them during daytime.

Looks kind of like a termite. It's generally helpful to include an approximate location in species ID questions to help us narrow down the possible species.

This would be helped with some better quality images - currently its hard to distinguish key features

@rg255 they are very small so I doubt I can get a better picture with my compact photo camera

I think @fileunderwater is definitely right, these are psocids (of the family Psocoptera, AKA booklice).
Specifically, the body shape looks very similar to that of Dorypteryx domestica or some closely related species.

See here for an additional photo.
According to this site, the species is present in many countries including Poland.
The source cited at this site (Kučerová 1998) mentions that this species can be brachypterous (i.e., having very reduced wings. I can't tell from the quality of the photo whether your specimens has tiny wings or not. Your top picture looks like it might.
Citations:
Kučerová, Z. (1998). Wing polymorphism in Dorypteryx domestica (Smithers) (Psocoptera: syllipsocidae). Insect Systematics & Evolution, 29(4): 451-57.

It could be booklice (Psocoptera), but the picture is a bit unclear. Booklice are harmless, but could indicate moist conditions and/or mold in the building (see first link for more on their biology). Termites are generally at least twice as large as booklice (>4mm), and the size you indice rather points to booklice.
Here is an example of what booklice look like:

(picture from Penn State University: Dept. of Entomology)

Thank you for your response. I was wondering if they are booklices myself, but on the photos their legs seems thicker near the body and I do not see that on the photos I've made. Since I first wrote, I have seen few more - very small - less then 1 millimeter long. They seemed to be coming from behind the baseboard. I also have added one more photo to my original post (I am not sure if that's helpful). Is there a way to verify if they are in fact booklices?

@man There are many species and the thickness of femur can probably differ between species (and is in either case difficult to evaluate in your pictures). Considering their shape, size, light colour (almost translucent) and long slender antenna they are probably booklice. Does the wall or wallpaper appear moist close to the baseboard?

I'm not convinced, the head, body and legs are all very different to the booklice in the image here

@rg255 This is a single example picture. There are e.g. >60 species in Sweden only (probably about the same in Poland)

wow, didn't realise there are so many species!

@fileunderwater The wall appears normal, but on the other side of the wall is a shower, there are probably water pipes inside the wall and I do not know how the situation look behind baseboard. Additional info: the room is a bedroom.

To be clear, the point of this answer is to indicate the taxonomic order to the OP, not a species identification. I though that would be useful, but apparently certain voters find it "not useful".

My initial guess was psocid, too, but the OP's picture really doesn't look like the typical psocid body shape I've come to expect. The OP's specimen does look A LOT like the one here, which is identified as a psocid but not from a trustworthy site.


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What are the characteristics of a living organism?
It seemed fairly basic at first, and yet I have to ask because even a quick Google search reveals that it doesn't seem to be quite so straight-forward anymore. After more research, I found multiple lists, some with six points, others seven or eight. Some lists shared six points and only differed on one, but others had five different points and divided and named the points differently such as Respiration vs Metabolism, Adapt vs Evolve, Homeostasis vs simply consisting of cells, etc.
Maybe it never really was simple, but when I learned basic middle school life science in the 1990s I seem to remember a clear and concise list of 7-8 distinct terms. I know they were just the summary given by the author of whatever textbook we used, but I remember several sources having similar lists (cannot say for sure if they were exactly the same), including a textbook, an educational video game, and a poster.
I'm also told that this has become a bit of a debate in the biology community, whether such a black and white distinction of "living" or "not living" is prudent. Questions such as this one on viruses are an example of how it is difficult to categorize life. However, I noted in my research that there was still clearly overlap in meaning of definitions, it was just in description and division of points that they differed. This suggests to me there is still a generally agreed upon core definition that is simply described by different people, specifically authors, with a few areas of possible debate.

What are the current generally agreed upon characteristics, the common denominators? (They all reproduce?)
What characteristics are commonly debated and therefore would unwarranted to claim? (Specifying cell structure?)

With the understanding that an answer will require an objective synthesis of a range of content and opinions, debate on what should or should not be characteristics is discouraged. Rather, an impassioned summary of the current  scientific consensus on this question is what I am looking for.
It seems to me that even if this is a topic of opinionated debate, it is certainly at the core of Biology and would be worthwhile to be addressed in an academic manner, be accessible, and available to reference on this site.
(PS - Not in any way a homework question, never was, just a curious 30-year father. Unless you are counting questions I have to answer from a curious little boy.)

I asked a related question. "Does it have it's own ribosomes?" is a good objective classification, but why should anyone care? Ultimately any answer is subjective.

The definition of any subject is open to subjectivity. Asking "What is maths?", "What is programming?", "What is beginners English?" or "What is religion?" in the respective SEs would all be equally be off topic. Additionally, I think the attitude of approaching a new community expecting their answers and then insulting the community is particularly unpleasant.

@James I agree...if that is what I had asked. But I am asking "What are agreed upon characteristics?" This can be done objectively by simply reviewing  all the subjective definitions and summarizing what they agree upon. As you say, everything is subjective at some point, so that is why scientists have peer reviews and such, so by the use of consensus of experts we can arrive at a conclusion that can be labeled objectively correct. And I still believe that voting to close a question with no comment as to why, when it is not obvious, is far more insulting than anything you think I've said.

@James if I am simply not communicating it well I will try to make an edit this evening. But it is a bit difficult to know what to correct with no constructive feedback (besides your own recent comment which did help) so if you or anyone else thinks they can see where I'm going wrong here I'm still just not sure, even after an edit, that it won't be closed again for some unknown reason. Maybe I've expressed my frustration poorly, but can you see that the attitude of approaching a new member of a community and expecting them to know what's wrong without telling them is equally unpleasant?

I didn't mean to say everything is subjective. There are empirical evidences. The issue comes when trying to devise a test to answer "what is living?" Many philosophers have moved away from the living/non-living divide & prefer something a little more nuanced. You've unwittingly stumbled into an age-old, unoriginal, unanswerable question. Here, we like questions that are answerable & want to avoid questions that induce debates. Because of this I'm not sure if any amount of edits will help. Recently in the chat we even considered closing that virus question for the same reasons.

@James I hope with my edit you can see that an answer to this can be even more objective and less contentious than your own on viruses. I'm simply looking for summary and synthesis of material. Not conjecture. Trust me, from my time at Christianity.SE I've learned the fine line between a "truth" question and a verifiable summary.

In meta we're struggling with hwk questions and how to deal with poorly researched/trivial questions & there is some over-zealous closing in the meanwhile. Personally I closed the question because it is too subjective to be answered with empirical biology. A similar question was closed on Philosophy.SE. They said there was no line & the division came down to semantics. It's very unsatisfying.

If you want a practical answer, you can just ask: Is this thing in the tree of life?

@joshua if you read the help pages and meta regarding homework closure you will understand that it was closed not because we literally thought it was your homework

@rg255 Yes, I realize this. I did read it. (Which is why I make light of it mentioning my boy...) And its why I detailed my prior research better in this edit. I considered giving a few sample lists, but...well research it with "characteristics of living organism" Google search and you'll see what I'm talking about. Me quoting multiple lists in the question isn't going to benefit anyone who is actually attempting to answer the question.

I don't think bio.se is the place for this question. However, I'd thoroughly recommend Koshland's 2002 Science article "The Seven Pillars of Life". It has excellent detail & justification for what "life" is. P(rogram), I(mprovisation), C(ompartmentalization), E(nergy), R(egeneration), A(daptability), S(eclusion), PICERAS, for short—are the fundamental principles on which a living system is based.

First of all, you have to note that there is no such thing as a scientific, objective definition of life, and that many scientists disagree on a given definition, and that every definition has it's limits.
However, the one from wikipedia

Since there is no unequivocal definition of life, most current definitions in biology are descriptive. Life is considered a characteristic of something that exhibits all or most of the following traits:[10][12][13][14][15][16][17]
Homeostasis: regulation of the internal environment to maintain a constant state; for example, sweating to reduce temperature
Organization: being structurally composed of one or more cells — the basic units of life
Metabolism: transformation of energy by converting chemicals and energy into cellular components (anabolism) and decomposing organic matter (catabolism). Living things require energy to maintain internal organization (homeostasis) and to produce the other phenomena associated with life.
Growth: maintenance of a higher rate of anabolism than catabolism. A growing organism increases in size in all of its parts, rather than simply accumulating matter.
Adaptation: the ability to change over time in response to the environment. This ability is fundamental to the process of evolution and is determined by the organism's heredity, diet, and external factors.
Response to stimuli: a response can take many forms, from the contraction of a unicellular organism to external chemicals, to complex reactions involving all the senses of multicellular organisms. A response is often expressed by motion; for example, the leaves of a plant turning toward the sun (phototropism), and chemotaxis.
Reproduction: the ability to produce new individual organisms, either asexually from a single parent organism, or sexually from two parent organisms.

Encyclopedia Britannica

Metabolism
Respiration
Sensitivity (responding to stimuli like gravity and sunlight)
Nutrition
Excretion (getting rid of CO2)
Growth
Reproduction
Homeostasis

"you have to note that there is no such thing"... Part of this question is about dealing with just that. Generally agreed upon. Consensus. But you dismissed it and just gave me the results of a Google search (which I've already done). Was hoping for more. The latter encyclopedia version is what seems to me to have been a pretty standardized answer in the 90s. It was in textbooks, educational video games, etc. So if there was consensus then, why not anymore?

@Joshua "textbooks" are not consensus. They are the opinions of the publisher. Anybody can write one, and if it's cheap enough schools will buy them. Textbook authors generally take the viewpoint that younger readers can't handle ambiguity, and so create facts where none actually exist. I'm willing to bet if you traveled back to your childhood, all the media you mentioned didn't completely agree.

@MattDMo if you combined that with a summary of what various definitions do agree on and what they don't, you'd have a winning answer.

Just wanted to alert you that the question has been edited considerably. I believe its still the core question I intended, but hopefully I'm more clear this time. Thanks.


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Isolating the gene of interest for protein production
For protein production, the gene of interest is inserted in an expression vector and introduced into a suitable host for expression. But how is the gene of interest for the desired protein isolated from the organism which possesses it?
One way could be to synthetically make the DNA sequence coding for that protein. Another could be to identify the gene of interest from a pre-existing genomic library or cDNA library of that organism. Are they the only methods?
The organism's entire genome could be taken and cleaved with restriction endonucleases, and a Southern blotting technique (i.e. electrophoresis followed by probe hybridisation and autoradiography) could be used to screen the gene of interest from the fragments produced. Of course, for this the gene sequence must be known beforehand, in order to synthesise the probe. Is this method also adopted? It seems inefficient - given that the fragments are assumed to have the intact gene of interest, and the gene should have been sequenced beforehand.

As you already wrote there are two basic ideas: Synthesis of the desired gene sequence and use of existing DNA.
DNA Synthesis is getting cheaper so it is becoming the method of choice for generating DNA-samples up to about 5000 bp (for example see the IDT-page for commercial gene synthesis). If this is too short for your desired sequence there is the possibility to split the gene to different of those synthetic sequences and to fuse them using Gibson-Cloning (Gibson et al. 2009) - after adjusting the synthetic sequences so that there is an overlapping sequence. Alternatively you could use classical cloning - provided there are suitable cleaving sites in your sequence.
If you don't want to synthesize the DNA and have a template available you could design suitable primers and amplify the gene from the template using PCR and purify it by gel-electrophoresis. Inserting the sequence into a vector then requires that you find suitable cleaving sites within the sequence and the vector.

Using existing DNA as in using it from a genomic library or by isolating gene of interest from the organism's genome by the method described in the question?

You could either use a genomic library or you could isolate genomic DNA from the organism. In both cases you wouldn't have to digest it as described in the question, but you could amplify the gene of interest directly from a low amount of DNA (NEB state 10000 copies of DNA are necessary for sufficient amplification in 25-30 cycles).


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How do harsh conditions cause an increase in the male birth ratio?
I've heard that in harsh conditions more human baby boys are born than girls because a bigger ratio of them will die before reproductive age. But in which aspects of the random gene combination while conception can harsh conditions (and which of their characteristics) actually can make a difference?

edited - gender is a social construct

@Christiaan Yeah but now it looks like I'm talking about sexual selection.

Your last sentence doesn't make sense. Maybe improve the question somewhat.

Don't understand the question and video at all. In this video host doesn't give us any proofs that's difference (where is the source) is significant assuming we have $p_{xy} = \frac{1}{2}$.

"Why is there a male-biased sex-ratio at birth in harsh conditions?" would be a better way to express this... As someone studying the effects of environmental conditions on the evolution of lifespan in humans, I'm going to say the video wasn't great.

Nature vs Nurture. Good example is a David Reimer story. So, gender is not a social construct, is biological construct.

@chupvl I don't understand the question but I really don't see how it could relate to the very popularized nature vs nurture discussion. Also, gender is a social construct. It is not a question open to debate as gender is defined as a social construct (just have a look at its definition on wiki > gender). The fact that gender correlate quite well with sex does not change anything to the fact that gender is defined as a social construct.

an individuals gender is not defined by their sex @chupvl

Issues with the post
Sexual selection is a mode of natural selection where members of one biological sex choose mates of the other sex to mate with (intersexual selection), and compete with members of the same sex for access to members of the opposite sex (intrasexual selection). This question has nothing to do with sexual selection.
What do you mean by random gene combination? More globally I don't understand the last sentence.
As a consequence, I don't understand the question. IMO, the post should be closed as unclear. However, I can imagine a question that I would consider interesting. I am answering to the question Is it possible that selection yield to a sex-ratio that deviates from 1:1 at equilibrium? How does it relate to environmental conditions?.
Fisherian scenario
Evolution of sex-ratio under a standard Fisherian scneario is often refered to as Fisher's Principle.
Basics
In the vast majority of strictly sexual species, every individual has exactly one mother and one father. It means that at equal sex-ratio the average relatedness of all offspring and all males in the previous generation is equal to the average relatedness of all offsprings and all females int he previous generation. When the sex-ratio is biased toward more females (for example), males have on average a higher reproductive success than females. As a consequence individuals that produce more males will increase their fitness and will increase in fecundity. As a consequence, the adult sex-ratio will always go back to 1:1 (fifty-fifty).
Adult vs baby sex-ratio
Now, it is important to understand that the adult sex-ratio is not necessarily the same as the babies sex-ratio. If typically, there is higher mortality in males than in females (could happen depending on the species and the environment), then selection would favour a bias sex-ratio toward males in babies. The adult sex-ratio will in any case be 1:1
Kin/group selection (non-fisherian scenario)
See for example the case of social spider Aviles (1993).
What is good for the population?
Thinking about the same problem but thinking about what is good for the population (rather than for the individual). For the population, the limiting factor in the number of babies produced are often the females. As a consequence, it would be good for the population if the sex-ratio were biased toward females.
When can alleles that are beneficial for the population overweight what is beneficial for the individuals
Under a standard fisherian scenario this cannot happen though selection will increase the frequency of alleles that spread the best and not the ones that are good for the population. However, typically when the relatedness within the population is high enough (you should read about group selection and kin selection) such trait that are good for the population may evolve.
Recommendation
I recommend that you take some time an introductory class to evolutionary biology such as Understanding Evolution for example. It is fast and you will learn more and faster than what you can learn here with your question. I think I already gave you this suggestion a number of times.

Oh, sorry, I let myself the second part on later and now I can see there's not much of an example of an actual non-fisherian scenario. Is there any actually found in nature? From the video I got that there is because otherwise it wouldn't be about the ratio of born males - which is the same for the fisherian scenario.

Yes, some social spider for example have a biased sex-ratio toward females Aviles (1993).

I'm grateful for that the answer contains the reason why these traits should evolve, but I didn't catch mutch about the true mechanism an organism can affect which sex will the fetus be when the gamets fuse.

@Probably The mechanism is totally different discussion and is out-of-the-scope of this post. The above answer assumes that mutations can change the offspring sex-ratio of an individual to any value between [0-1]. Before understanding this mechanism you will need to understand the sex-determination systems.

Typically for an ESD (Env. Sex Setermination), the mother can affect the sex ratio of the, say eggs by modifying the temperature of incubation (which can be modified by the characteristic of the nest or how deep they are burrowed). But manipulation of sex-ratio in pure GSD (Genetic Sex Determination) exist too such as killing the offpring very early depending on the sex or by making the sex determination under control of several loci you can reach all kind of sex-ratio in offspring.


text:
What actually happens to the human body during fasting/starvation?
I recently came across a UN study which advocated that controlled fasting can be beneficial for the the human body and I am fascinated by stories of wilderness survival against the odds.
It piqued my interest to ask; what exactly happens to a human body during fasting and ultimately starvation?
I understand that there is a period of glycogen use/exhaustion and functioning becomes impaired but what medically happens to the human body (organs, muscles, protein, body fat, cognitive processes etc) and over what timeline (24 hours to death).  I read that halitosis is an interesting side-effect etc.
Assume the human body has ample access to water and can avoid dehydration.

Have you read this?

I have now - it raises a few more questions though;  how long after running out of glycogen does the body wait before using adipose tissue?  Does it burn adipose as long as it exists or does it dual-use muscular fuel as well?

Please [edit] your post and update it with your current question.

This is a very broad question, there are tons of literature on how the human body adapts to fasting in various ways. Please be more specific.

Actually, the body goes into the fasting state about eight hours or so after the last meal, usually when the guy finishes absorbing nutrients from the food.
Normally, body glucose, which is stored in your liver and muscles, is your main source of energy. When in a fasting state, your body uses up the glucose that you have stored to provide energy. If you are still fasting after this store is used up, your body will start to burn fat to create energy, therefore leading to weight loss.
After fasting for a few days, there will be a higher level of endorphin in your blood which will cause you to be more alert and, weirdly, giving you a feeling of mental well being.
Eventually, if you are starved for too long, your body will start to break down muscle protein in order to create energy (that is why, during WWII, most POW's held by the Japanese were very thin - they were starved and in order to survive, their bodies had to 'eat' their own muscle)
Technically, starvation is when your body starts to eat your protein, i.e. Muscle.During starvation, your body will thin out, because your fat has been burned and your muscle is being 'eaten'. This obviously leads to weakness.
When your fat is being burned, you go through a detoxification process which is caused because any toxins stored in your body's fat are dissolved and removed from the body.
Your kidneys are very efficient in being able to maintain the body's water and salts, like potassium and sodium. But these can be lost through perspiration.
This eventually leads to dehydration which does many things to your body, like: not allowing for your body to regulate body temperature; your heart works harder (most of your water is in your blood (about %$60$) and when you lose the water, your heart has to 'catch' up and pump more to keep the blood flowing and cooling you down - now, your heart is working harder which could give you a greater risk of heat exhaustion); you can feel cranky, drowsy, confused, forgetful.
These are a lot of things that happen when your body is deprived of what it needs in terms of food and liquid.
This is what happens, and this is very general, when your body is in its starvation mode. I am sure that there are many more things, but I could only give a brief answer.

Please edit your answer, you have been misled about the detoxification. There is no scientific evidence that what you describe happens during a fast. See https://en.wikipedia.org/wiki/Detoxification_%28alternative_medicine%29 or http://skepdic.com/detox.html . Thank you.

Some people believe that muscle loss happen early when fasting. But like you rightly pointed out, it doesn't happen until the body fat is gone. This web page supports this: https://www.dietdoctor.com/does-fasting-burn-muscle. A comparison between day 42 and day 70, in Table 2, shows this clearly..

The only reason for muscle-loss during a long fast, or during many consecutive fasts, would be that weakness due to lack of energy, or at least willpower, prevents too much muscle exertion, leading to  loss of muscle strength and mass.


text:
How do I tell if the mosquitos in my New York City apartment can carry Zika?
The species that carries Zika, A. aegypti, is unlikely to be found in New York. However, the related species A. albopictus is prevalent and quite concerning. So this question is focusing on A. albopictus (if I may editorialize I would suggest leaving the title closer to the real question of interest, and disambiguating the species as the first step in resolving it).
According to the CDC

Zika virus is transmitted to people primarily through the bite of an infected Aedes species mosquito (A. aegypti and A. albopictus).

I understand New York has IIRC the aegypti species and Zika has appeared.
My apartment gets mosquitos rather randomly every couple months. Understandably I want to figure out how much effort I should put into preventing or getting rid of them. I can describe their behavior here and maybe that's enough information. If not, do I need to get out a magnifying glass or sequence DNA? (Which I did once in college but I wasn't very good at it).
Their behavior:

I get "bursts" of them at random times in the year - more in the warm months but also in November. We had a warm winter but this still surprised me.
They seem to bite me at night but I've never had a mosquito bite on me. I've had mosquito bites from being bitten by mosquitos before, so unless I've developed a resistance to that in the last few years, that's strange.
I haven't found any evidence of standing water nearby. They don't hover around my sinks or toilets. I read once the Zika carrying strain is on the hardy side and can live off of moisture in walls so this is troubling.

If you're curious my preferred life hack is keeping my living room slightly warmer than my bedroom. And also, you know, killing all of them.
So, are these behavior traits useful? Can I identify them as opposed to other New York inhabiting mosquitos? Is a DNA test necessary?

This is a reasonable question, and I was surprised to find that official information on whether Aedes aegypti is present in NYC isn't very clear. I personally would have thought that NYC was quite far beyond the range of Aedes aegypti (the 'yellow fever mosquito', believed to be the main vector of Zika virus in the ongoing emergence event in South America), and the New York City Department of Health apparently agrees with me:

Aedes aegypti has not been found in New York City.

...(emphasis theirs) which seems pretty clear cut. However, the CDC recently published a map claiming that NYC is within the potential range of Aedes aegypti.

It's not really clear exactly what they mean by this. From the webpage:

The new estimated range maps have been updated from a variety of published and unpublished sources.
These maps show CDC’s best estimate of the potential range of Aedes aegypti and Aedes albopictus in the United States.
These maps include areas where mosquitoes are or have been previously found.

A related species, Aedes albopictus, is sometimes found in NYC during the summer and is probably capable of transmitting the strain of zika virus currently circulating in the Americas (see for example this recently-published experimental infection study). Aedes albopictus has been the major vector in some previous zika outbreaks in other parts of the world.
(Edit (14th June): A group of mostly-CDC entomologists just published a map of locations where Aedes aegypti and Aedes albopictus have actually been collected between 1995 and 2016 here, and there's an NPR article explaining why the maps are different here).
Whether the density of this species or the temperatures are sufficient to sustain transmission for any length of time in a climate like that of NYC is a more complicated story. The CDC even adds:

Maps are not meant to represent risk for spread of disease.

But you've asked whether the mosquitoes in question can carry zika, not whether they're likely to be good at it, so I'll leave it there. The short answer is that if they're Aedes mosquitoes, then they might be able to.
So how do you know if they're Aedes mosquitoes? Aedes are visually quite distinctive; they have black bodies with white stripy abdomen and legs:

(Image taken by Muhammad Mahdi Karim; details and license here).
Aedes are also generally day-biters, so if you're getting bitten at night that makes me suspect you've got something like Culex mosquitoes instead (which might be able to spread West Nile virus, although that's a different story). These are dull brown.
If you do find you have Aedes and you'd like to try to identify them to species level, you could collect some dead ones and look at their thorax. If you take some photos and post them here as a species-id question you'll probably get an answer pretty quickly, but this figure illustrates the difference between aegypti and albopictus:

(Image from WHO (1995) Guidelines for Dengue Surveillance and Mosquito Control, Second Edition)
There are better images here but I think these are under copyright.

You're very much out of range of Aedes Aegypti, which is the primary carrier of Zika. Albocitus is a much more theoretical carrier, whose potential for spreading disease is much less. There have been no locally acquired cases in the mainland US this year. The odds of a New Yorker being the first to catch it are ridiculously long.

Well, there are 78 reported cases of Zika in New York so far. Apparently the concern is Aedes albopictus.

Edited question to note that the CDC is concerned of A. albopictus. I don't know the state of the research on A. albopictus + Zika but I can only hope the city has looked into it given they're about to spend millions of dollars fighting it.

This does not provide an answer to the question

New York is an international hub, just because there are reported cases doesn't mean that it came from the native mosquito population.

From the link: "All cases contracted Zika while visiting other countries"


text:
How does a higher channel density increase speed of propagation of an Action Potential?
If there is a higher density of sodium channels then there will more Na$^+$ flux in the cell. So it's like trying to pass more material through a pipe and therefore the speed of action potential (AP) propagation will be more. This is what comes to me intuitively, but I am not sure about my answer.
Can anyone explain in better words, how the speed of an AP increases with increasing channel density?

Its actually quite opposite: action potential speed is inversely proportional to channel density. That's why myelinated neurons conduct impulse way faster than non-myelinated ones.

Can you give a reference from where you concluded these lines (first paragraph)?

I have edited your post to replace AP by action potential. Such abbreviations will not be familiar to many people and should not be used in titles.

As @another'Homosapien' mentioned in the comments, the reality is actually the opposite:  action potential speed is inversely proportional to channel density.

In other words: lower channel density increases speed of propagation of an Action Potential.

If you decrease the density of ion channels, you increase membrane resistance. This results in less "leakage" of cations, which allows voltages to spread farther and thus reduces the number of action potentials that need to be generated. This results in increased conduction velocity.

 Long Answer
It's important to note two things about action potential propagation:

Each action potential takes time to occur.
The charge (i.e., voltage) that is created dissipates with $ \uparrow $ distance.

In fact, we have equations to calculate both the time a voltage change takes to occur and how current flow decreases with distance.

You can read more about the mathematics behind this and passive membrane properties in general here and here.

Importantly, these equations rely on two constants: length and time.
The time constant, $\tau$, characterizes how rapidly current flow changes the membrane potential. $\tau$ is calculated as:
$$\tau = r_mc_m$$
where r$_m$ and c$_m$ are the resistance and capacitance, respectively, of the plasma membrane. (See this previous answer for an explanation of resistance and capacitance. )
Importantly, these variables partially rely on membrane structure.

c$_m$ (the capacitance of the membrane) decreases as you separate the positive and negative charges.
r$_m$ (the resistance of the membrane potential) is the inverse of the permeability of the membrane.

The higher the permeability, the lower the resistance.
Lower membrane resistance means you lose ions quicker and therefore signals travel less far

But why? This is where that length constant becomes important. The length constant, $\lambda$, can be simplified to:
$$ \lambda = \sqrt {\frac {r_m}{r_e + r_i} } $$
where, again r$_m$ represents the resistance of the membrane and r$_e$ and r$_i$ are the extracellular and intracellular resistances, respectively. (Note: r$_e$ and r$_i$ are typically very small).
Basically, if the membrane resistance r$_m$ is increased (perhaps due to lower  average "leakage" of current across the membrane) $\lambda$ becomes larger (i.e., the distance ions travel before "leaking" out of the cell increases), and the distance a voltage travels gets longer.
 Why am I telling you all of this??
How are the time constant and the space constant related to propagation velocity of action potentials?
The propagation velocity is directly proportional to the space constant and inversely proportional to the time constant. In summary:

The smaller the time constant, the more rapidly a depolarization will affect the adjacent region. If a depolarization more rapidly affects an adjacent region, it will bring the adjacent region to threshold sooner.

Therefore, the smaller the time constant, the more rapid will be the propagation velocity.

If the space constant is large, a potential change at one point would spread a greater distance along the axon and bring distance regions to threshold sooner.

Therefore, the greater the space constant, the more rapidly distant regions will be brought to threshold and the more rapid will be the propagation velocity.

Sooo....
If you decrease the permeability of the membrane (i.e., if you prevent ion pumps from moving ions in/out of the axon), you increase the resistance of the axon membrane, which allows for the voltage created in the action potential to travel farther before dissipating.

By allowing the voltage to spread farther before necessitating the generation of another action potential, you reduce the time it takes for signal propagation.

In other words, if you decrease the number of ion pumps, you increase  membrane resistance (r$_m$). This causes voltage to spread farther and thus reduces the number of action potentials that need to be generated. The result? increased conduction velocity.

Interesting answer, I'll think about it...certainly higher resistance means better propagation of electrical signals, but I am not as convinced that this is necessarily the correct answer to the OP's question. Also, note that ion pumps and channels aren't the same thing.


text:
Can you identify this animal?

It was in the bathroom, 2cm in lenght (or so). It has two small antenas on the head. I live on Balkan peninsula, inland.

Looks like a millipede, maybe a centipede. I can't count the legs.

That is a European Millipede.

I found this picture by searching European Millipede. Obviously there are different types - and this is the one you have.
Here is a wiki link I found: https://en.wikipedia.org/wiki/Cylindroiulus
I think your specifically is a Cylindroiulus britannicus
.

do you have any reference to add; what made you think that this is a european millipede?

Sure. I will edit the post.

Why would C. britannicus be in the Balkans? I couldn't find a habitat range for the species, but its name would suggests otherwise.

@MarchHo- I think they were imported somehow. I am not sure, but I can look that up.

It is certainly a millipede, but I doubt it is C. britannicus. They live in natural habitat, like forest floors. In the balkan, greece and cyprus, there is a millipede that commonly lives near and in houses, I have encountered it often. Unfortunately, I haven't been able to find the name (yet).

@RHA, same - but it looked very, very similar so I assumed that that was it...


text:
why selecting cells after gene editing with CRISPR Cas9?
I am new to the CRISPR Cas9 genome editing system and I have the above basic question.
Another way to think about this: what would happen if after cells are transfected, the cultures are left to grow without any selection. Thus, if a mutation disrupts a cell cycle gene (e.g. p53), such cells will proliferate more and the culutre will be populated by those cells rather than healthy cells.
Is this a valid reasoning?

Your suggestion of using CRISPR to disrupt P53 and hope for selecting cells that grow out of control isn't what most CRISPR experiments aim to do. CRISPR is used to get precise mutations, but doesn't always work. Only a small percent of cells will be successfully edited, so you have to screen for them and find a good one. This is what makes CRISPR so hard to use in vivo, where you can't just kill off 99.99% of cells and let the good ones grow back.

user137 is correct. Screening for successful CRISPR/CAS9 mutation is a headache. You typically need to either titrate your cells down to 1 cell/well of a 96-well plate, let them expand and genotype, or something more rigorous like this:  http://bmcgenomics.biomedcentral.com/articles/10.1186/1471-2164-15-1002


text:
Why do people cut back on kilo-calories?
I am learning about specific heat in science and I learned about how the specific heat for water is called a calorie, but that is different to what is on the food label.
On the food label, that calorie is actually a kilo-calorie. My teacher went on to explain that if somebody handed you a bowl of ice-cream that contained 500 Calories (i.e. Kilo-Calories) then, that was enough to raise 500kg of water 1°C.
If a kilo-calorie is just raising your body temperature, why do we cut back on calories?? What effect does a kilo-calorie have on your body other than raising your temperature?

P.S. How can we burn calories?? This seems, at least to me, like an abstract thing... burning heat....

Yeah. Burning calories is a misleading term. Actually pretty unscientific. What it basically means is that you are converting X calories of your reserve chemical energy (in the form of fat) to some other form such as mechanical energy, thereby getting rid of it. We don't really burn the fat and heat that is produced is much less than what you would get by combustion (even though both are oxidation). The combustion engines in automobiles actually convert chemical energy to heat (by burning the fuel) and subsequently heat to mechanical energy. Our body works differently.

The calorie is a unit of energy. Our body uses the energy found in food to create ATP (a molecule that is handy to deal with energy) with the help of oxygen (that we breath in). ATP can then be used for plenty of tasks such as importing ions through a cellular membrane or more ultimately walking, talking, warming up your body, etc...
Saying that some food contain 100 calories (not kilo-calories) does not mean that it will heat up 100 grammes of our body water by one degree (Celsius). It only means that we are ingested the same amount of energy than the one that is needed for warming up 100 grammes of water by 1 degree (Celsius).
You might to have a look at CrashCourse video on ATP and respiration.


text:
What is the difference between the neural tube and the dorsal ventral cord?
I was wondering what the difference is between the neural tube and the dorsal ventral cord.
I know that the neural tube forms during embryonic development from the ectoderm layer that folds inwards.
I thought that the neural tube gave rise to the central nervous system, however sometimes I see the following:

"the central nervous system develops from the hollow dorsal nerve
  cord"
   for example: https://en.wikipedia.org/wiki/Dorsal_nerve_cord

question
What is the difference between the neural tube and the dorsal ventral cord or are they both the same?
(talking about humans)

The terminology can be confusing, and I suspect the question you meant to ask was: what is the difference between the neural tube and dorsal nerve cord?
In vertebrates, the neural tube and the dorsal nerve cord are two names for the same structure. It develops into the brain and spinal cord.

Neurulation occurs during the early embryogenesis of chordates, and
  it results in the formation of the neural tube, a dorsal hollow nerve
  cord that constitutes the rudiment of the entire adult central nervous
  system.

Source: Colas J-F and Schoenwolf GC. Towards a cellular and molecular understanding of neurulation. Developmental Dynamics. 2001. vol 221(2): 117–145.
This differs from invertebrates, some of which have a ventral nerve cord that does not invaginate and form a neural tube. As the name suggests, in contrast to vertebrates the nerve cord in these species is located ventrally.
In summary:
Dorsal nerve cord = neural tube
Ventral nerve cord ≠ neural tube

The neural tube (Fig. 1) is the embryo's precursor to the central nervous system, which comprises the brain and spinal cord. Its structure can be described in standard anatomical terms of location and their respective axes.
The dorsal - ventral axis (back to abdominal side) can be visualized by dissecting the neural tube transversely (Fig. 2). This axis is important for development. In the spinal cord, for instance, the dorsal region is the place where the spinal neurons receive input from sensory neurons, while the ventral region is where the motor neurons reside. In the middle are numerous interneurons that relay information between them. The polarity of the neural tube is induced by signals coming from its immediate environment. The dorsal pattern is imposed by the epidermis, while the ventral pattern is induced by the notochord (Gilbert, 2000).
Conversely, the anterior - posterior axis (head to tail) can be seen by a longitudinal transection (Fig. 1). Here, the important regions of the brain can be identified; the neural tube balloons into three primary vesicles, namely the forebrain (prosencephalon), midbrain (mesencephalon), and hindbrain (rhombencephalon). The prosencephalon becomes subdivided into the anterior telencephalon and the more caudal diencephalon (Gilbert, 2000).
Hence, regarding your question - there exists no such thing as a dorsal ventral cord.

Fig. 1. Anterior-to-posterior axis of the neural tube. Early primary structures (left) and adult structures (right). source: Gilbert (2000).

Fig. 2. Dorsal-ventral axis of the neural tube. source: Gilbert (2000).
Reference
- Gilbert, Developmental Biology. 6th ed. Sunderland (MA): Sinauer Associates (2000)


text:
Why would worker bias sex-ratio toward workers?
This question prompts for explanation on a topic, an interpretation of this topic is given. A simplified question statement is also given at the end for those who do not wish to read.
Topic
In the Self Gene by Richard Dawkins, it was suggested that genes are the fundamental units of evolution.
In one of the chapters of this book, animals such as the ants are discussed. These animals are specified to have the following properties:

They live in colonies consisting of sterile workers and reproductive queens.
Worker ants possess half of the genes from its queen and half its genes from the king, which is not living in the colony because it died after fertilizing the queen.
The queen produces male "drones"--potential kings for future colonies. Drones are genetically identical to the queen.

The following interaction is suggested: worker ants, being less related to the drones than they are to each other, will manipulate the colony to increase the number of workers and reduce the number of drones present. They may do this by eating some drones before they hatch.
The reason why the workers do this is explained and interpreted as such:
The workers wish to produce more individuals that are more closely related to themselves; other workers are more closely related to a worker than a drone is to that worker; therefore, the worker prefers another worker over a drone.
Question
The Selfish Gene suggest that genes are the fundamental units of evolution, therefore a successful gene must be able to displace its alleles by being better at propagating itself.
Suppose gene-A incentivizes workers' drone-eating behavior, this gene in the short term and within one colony can produce a larger number of its own copy, but all of these copies are inside sterile workers, none of which can propagate gene-A.
When the colony containing gene-A spawns drones and potential queens, there are two cases to consider:

Gene-A is present in drones: If this is true, then by incentivizing the occasional drone-killing by the workers, gene-A has reduced the number of gene-A carrying drones, this is deleterious to gene-A. When workers of the new colony is born, gene-A reduces the number of possibly non-gene-A-carrier drones and decreases the fertility of the new colony in general.
Gene-A is present in female offspring: gene-A decreases the fertility of new queen, making her produce less gene-A carrying drones, this is again deleterious.

So far, gene-A has proven to be often deleterious to itself by restricting the number of reproductive individuals that may carry it. In terms of competition, gene-A may harm its alleles when the queen carries the allele and the king carries gene-A, but this will stop being beneficial when the number of gene-A and the number of its Alleles reach a 1:1 ratio, since after that point, the probability of harm is equal for both.
So, why is the drone-killing behavior still exhibited in animals such as ants?
Simplified question
Worker ants sometimes kill male ants in its colony because they are less related to the worker ants than the latter is to each other. Since worker ants can't reproduce, why do they bother about the number of close relatives who also cannot reproduce?

+1. The question is a little long though :) This question has bugged me already in the past. I don't fully remember how I ended up accepting it. There are good evidence for the existence of different sex-ratio depending on the number of fathers though.

Note btw, that there are a few sentences that make no sense in the post such as gene-A has proven to be often deleterious to itself. A gene cannot be deleterious, only an allele can. Also, "deleterious to itself" is either senseless or terribly redundant. Similar issue with gene-A may harm its alleles.

Is there any rephrasing that you suggest?

I'd suggest rephrasing the title - it's currently quite uninformative / nonsensical.. also is this purely hypothetical or has this behaviour been demonstrated? Could you point me to where in the book it talks about it?

@rg255 ha ha the title is the only thing that I edited.

@user289661 I have to confess that I am too lazy to read the whole post entirely so I upvoted hoping somebody else would make the corrections. If it is unclear to you why sentences like gene-A may harm its alleles make no sense, then you might want to follow a quick introductory course to evolutionary biology such as Understanding Evolution for example


text:
Any idea what this red plant is?
I live in South central Indiana, US, and these have just started appearing in the grass in my yard. I just bought this house last fall so I've never seen them. Anyone know what they are? Are they harmful to dogs?

It is indeed Mock strawberry and they are not toxic, from personal expirience and http://www.accessdata.fda.gov/scripts/plantox/detail.cfm?id=13794

Likely you are telling about red ball-like thing. Which are this-plant's leaves?

We called those "Indian strawberries". They are also known as Mock Strawberry (Duchesnea indica). Survivalists are pretty familiar with this plant.

They are a lot like strawberries in appearance, but the berry is rounder, not pointed, and held upright (they point up) on the stem, not pending. Though the berries are edible, they don't have much flavor at all. The leaves are also similar, and the flower is yellow, not white. The fruit's seeds are the same color as the fruit. They flower late spring and throughout summer. Your specimen looks like it was nibbled on at some point. The inside of this berry is white and kind of spongy and dry (especially compared to the real thing, i.e. wild strawberries.) The stalk it's on is hairy (as it should be) but damaged, and only one part of the leaflet is visible in your photograph.

They're in the Rose family, but there's some discussion about what genus they really belong to; may be more similar to Potentilla.
See also http://www.sierrapotomac.org/W_Needham/IndianStrawberry_080617.htm


text:
Can ncRNA convert to coding RNA/mRNA by mutations?
DNA has transcribed into RNA (Non-coding). Can this RNA mutate and become a Protein-Coding one/mRNA? Have there been any such instances reported by scientists?

The ncRNA will be transcribed from nuclear genomic DNA.  Therefore the mutagenic events would take place in the DNA that codes for that ncRNA gene.  It has nothing to do with the relative chemical stability of the different types of nucleic acids.  There are viruses with RNA genomes, that do not require a DNA intermediate for replication, like Q-Beta, which codes for its own RNA-based RNA polymerase (as I recall).  Are you familiar with the so-called "Central Dogma" of molecular biology? DNA makes RNA. RNA makes Protein (or in this case, the RNA does not code for a protein).

@mdperry Let me rephrase it: Can a ncRNA (transcribed product from DNA) convert into a mRNA? By mutation, I mean mutation in RNA, not in the DNA which makes that RNA (as it has already transcribed now)

If you had a gene that mutated its start codon or something, so that it was still transcribed, but the RNA could not be translated, that could be considered ncRNA. If that mutant gene had another mutation that fixed the original error, it might be translated again and become a coding RNA. But mRNAs typically need a start codon, kozak sequence, etc. These features would be hard to find on a ncRNA that didn't originate from a mutated gene.

@user137 Thanks! I got you! Yeah it seems highly unlikely to have that much modifications/mutations to ncRNA. You made an interesting statement in start of your comment. Can you please explain it further (start codon or something)?

Answers

Possibly, but with such a low frequency as to be unimportant and undetectable. (Monkeys with typewriters producing Shakespeare’s Hamlet comes to mind.)
No. Because it would be extremely difficult to detect, it would seem to be of no importance if it did occur at a very low frequency (you make no suggestion of why it would be of interest) and therefore there would be no reason for anyone to try.

Why would it be difficult to detect?
The difference between mutations that occur in DNA and any that might occur in RNA, is that a mutation in DNA can give rise to a population (e.g. of bacteria, or offspring) all of which carry the mutation. Thus, even though the chance of the particular mutation may be very low (say 1 in a million or less), a situation can arise in which the whole population is producing the RNA transcribed from the mutated gene and the protein encoded by the RNA. If RNA mutation occurs with the same frequency and managed to change a non-coding RNA (perhaps a pseudogene with a frameshift) to a coding RNA, only 1 in a million transcripts would be changed. Therefore if one sequenced the RNA the incidence of such changed RNA would be too low to detect, or if detected would be below the error margin in such experimental work.
Why has nobody looked for it?
Experimental science costs time and money. Scientists explore theories that have an importance and probability of success that attracts competitive funding. If there is no particular reason to look for something and the chances of seeing it are minute, nobody will waste their time on it, and they would certainly not get funded to do so.


text:
What is a "monomeric polypeptide"?
In the sentence: "Bacteriophage (viral) polymerases are typically monomeric polypeptides".
I know that polypeptides are chains of amino acids monomers. But what is a "monomeric polypeptide" and what other kinds of polypeptides are there?

You're right to highlight this confusing statement. As David's answer points out, this is a case of tautology. The term "monomer" or "single polypeptide chain" would be more appropriate I believe. It's a very minor point though and the sentence does technically make sense.

Monomer in this context means the protein has only one polypeptide chain. In some  proteins, after the individual chains have folded into their 3D or tertiary structure, they associate (generally non-covalently) into a higher order or quaternary structure. A protein with a quaternary structure containing  two copies of the same chain would be called a homo-dimer. One with one copy of each of two different chains is a hetero-dimer.
Haemoglobin is a well-known example of a protein with quaternary structure — it has two copies of the alpha- and two of the beta- chain. Further elementary treatment can be found in Berg et al. and explanation of the nomenclature in this Wikipedia page.
Monomeric polypeptide is somewhat misleading in the sentence quoted. Monomeric protein would have probably been better as you wouldn't be likely to say ‘dimeric polypeptide’, given that polypeptide implies a single chain.

A small doubt: What would you call mature insulin? It has two polypeptide chains covalently linked via disulphide bonds. It is a monomeric protein, however.

@WYSIWYG I wouldn't use my first sentence as a definition of monomer, just as an explanation of what the writer meant. In talking about insulin I personally would say that although it has two polypeptide chains it consists of a single globular subunit and therefore cannot be said to have quaternary structure (as I would define it). This is easy to justify since we now know that the general tertiary structure of insulin is formed by the folding of a single polypeptide chain, proinsulin, which is cleaved to activate it (with a small but significant change in tertiary structure).


text:
How can you develop a bacterial infection when taking antibiotics for another area of the body with a bacterial infection?
How can you develop a bacterial infection when taking antibiotics for another area?
For example, "if someone was prescribed an antibiotic for a bacterial infection of the throat and while taking the antibiotic tablets they developed a bacterial infection in their toe.  Explain why the antibiotics taken for the throat did not prevent the growth of the bacteria in the toe".
Is it because the bacteria in the toe is a different type and didn't respond to the bacteria developing the toe (don't think so, but not sure), or
was It because antibiotics don't prevent the development of bacteria they only inhibit it once grown and kill it, or
something else?

More information would be needed to answer this properly, but it sounds like you've got it. The antibiotics for the throat infection would be present in the toe, so one should conclude that those antibiotics are ineffective against  the bacteria causing the new toe infection. If this is homework, please add the homework tag, whereas if this is a personal medical question, I'm afraid it's off-topic.

Your first assumption is mostly correct

Bacteria in the toe is a different type and didn't respond to the
  [antibiotic taken for the throat infection].

the reason being because it outlines some essential characteristics of "antibiotics" and antimicrobial drugs in general.
Selective Toxicity and Mode of Action
A very important characteristic of an antibiotic is its selective toxicity. An ideal antibiotic has a high level of selective toxicity meaning that it will only target the bacteria that is causing an infection while not damaging the host tissue (cells) and the person's biota (resident microorganisms). This characteristic generalizes antibiotics into two categories; broad-spectrum (low selectiveness) and narrow-spectrum (high selectiveness). For example, a broad-spectrum antibiotic will target both gram-positive and gram-negative bacteria while a narrow-spectrum antibiotic will either target gram-positive or gram-negative not both.
Another characteristic of an antibiotic is its mode of action or in other words the area of a bacterium that it targets to inhibit/kill it. Most commonly antibiotics target one or more of the following areas/processes:

Cell wall synthesis,
Cell membrane function,
Protein synthesis, and
Nucleic acid synthesis

It is important to know this because mode of action goes hand in hand with selective toxicity, for example an antibiotic that targets membrane function might prove ineffective against bacteria that form capsules another themselves.
So to answer your question

why [did] the antibiotics taken for the throat not prevent the growth of
  the bacteria in the toe?

We can reason that the selective toxicity of the antibiotic taken for the throat was narrow or that its mode of action only targets the bacteria causing the throat infection but not the bacteria causing the toe infection.

Thanks that's exactly what I needed! Thank you for that I understand now :)


text:
What is this little white creature?
Please identify this little and soft white creature. Since childhood I am seeing this things flying in my surroundings and nowadays they are seen occasionally.

it's a seed - similar to dandelion, many species use wind dispersal

It's indeed a seed. It could help if you mentioned the geographical origin of the seed, but it could help even more if you could trace it back to its source plant.

@DvPr could you tell your seed-like structure at centre of white circle on photo; whether was 1. narrow long (as looking in the photo), or 2. flat, (photographed at edge, so looking narrow rod-like)? Also, could you tell country or climate, and few more detailed photographs?

Okay I'm converting these comments into an answer. I wrote them as comment when I was new; so I wasn't used-to with the SE structure.

It is, as stated by @rg255 a seed (or actually a fruit, see below). The seed itself is the small brownish thing. The white hairs are attached to make the seed fly with the wind. Looking at the seed and the hairs, I think the seed belongs to the daisy and dandelion familie asteracae/compositae. Altough there are other possibilities, see comments.
EDIT:
@AlwaysConfused is right if he states that in case of daisy family, it should be called a fruit, that containes one single seed. To be more precise, it is an Achene/Cypsula. In many species, what is often referred to as the "seed" is actually a fruit containing the seed. The seed-like appearance is owed to the hardening of the wall of the seed-vessel, which encloses the solitary seed so closely as to seem like an outer coat. Info derived from here on fruits and seeds and more specifically on Achenes/Cypsela here

Thanks for this update; I'm converting the comments to answer. I wrote these comments when I was very new to SE so I was then not accustomed with the details of SE structure. Later I came to know that answers in form of comment is troublesome and considered as bad.

Almost certainly a fruit or seed, having wind-dispersal mechanism.
But it could be

a seed, having one-bunch of "coma" (bundle of hairs on a small spot on a seed). Seed with coma is common in members of family asclepiadaceae and apocynaceae.

Asclepias syriaca

(Wikipedia page) (Wikimedia)

Daemia extensa (Synonymous to Pergularia daemia)

( Text and Photo source )

Calotropis procera

Wikimedia

Or may be a

Fruit of Compositae (Asteraceae)  with Pappus.

Pappus looks same as coma; but from viewpoint of development it is different from coma. Most of the asteraceae member's fruits (these grain like structures are not seeds but fruits ('Cypsela', as user @RHA mentioned), containing 1 seed), contains persistent calyx; which is known as pappus, and commonly adapted for dispersal with air.

A flower of Tridax procumbens showing epigynous calyx, which will later be persisted with fruit (from inferior-ovary) as pappus. Image Source

Pappus of Vernonia cinerea (Synonymous with Cyanthillium cinereum)

(Source) ,  (image)

Pappus of Tridax procumbens

(Source) , (image)

Taraxacum sp. (Dandelion)

wikimedia
This is a Taraxacum inflorescence (matured), showing fruits with pappus, attached with the receptacle, and a single fruit is like this:

(Source) , (image).

Source:

College Botany, Vol. 1 by Gangulee, Das and Datta; New Central Book Agency.
BOTANY for Degree Students / A. C. Dutta / Oxford


text:
Are plants really oxygen neutral?
This accepted and most upvoted answer to the question Does grass alone produce enough oxygen for life? claims that plants are oxygen neutral:

Plants are oxygen neutral The question wording is a bit misleading, as
  – surprise – plants do not produce oxygen. They produce oxygen only as
  long as they are growing, binding carbon in its mass. In long term all
  plants are oxygen neutral, as all oxygen which is created by them is
  again consumed when they dissolve, burn or are eaten, as carbon stored
  in them reacts with oxygen back to CO2. The more correct view how to
  describe this is not that plants produce oxygen, but that they store
  carbon.

I realize that a huge portion of our atmosphere's oxygen was produced by Phytoplankton, but the idea that plants produce zero net oxygen seems absurd to me. Is the information provided by that answer scientifically accurate? Please explain.

Plants produce oxygen throughout their lifetime by photosynthesis. If you look in a VERY long time period (many generations), then yes plants are oxygen neutral.

Plants are oxygen generators.  Plants plus decomposition (i.e. the whole system, plants plus bacteria and fungi and fire and cows and termites) are oxygen neutral. So the statement is literally wrong, but may be functionally correct in the current environment.

@iayork  Could you turn your comment into an answer?

This question seems to hinge on the exact definition of "oxygen neutral". So when asking it, you should say which definition you are interested in.

Plants are oxygen generators. Plants plus decomposition (i.e. the whole system, plants plus bacteria and fungi and fire and cows and termites) are oxygen neutral. So the statement is literally wrong, but may be functionally correct in the current environment.

Photosynthesis basically means 6 CO2 + 6 H2O --> C6H12O6 + 6 O2
Combustion/decomposition means the reversal... C6H12O6 + 6 O2 --> 6 CO2 + 6 H2O
Sequestering carbon dioxide is only temporary. However, the trees' reduction reaction provides us animals with that sugar and oxygen to burn. Without sugar and oxygen, practically all animals on earth would die. The trick to staying ahead of the curve for us now is to sequester more carbon and oxygen than nature can provide (for less money than it costs to dig for oil)... because it just so happens that we are pretty much consuming all the carbon and oxygen that farming plus living plants can supply, plus the fossil oil sequestered over millions of years.
Will grass be enough? No... neither the rainforest nor the algae in the ocean will be enough to offset the human over-population. We are burning far too much, far too fast for plants to keep up (naturally).

But to more directly answer the question, a 650-square-foot area of grass produces enough oxygen to sustain an average human adult's needs, whereas rainforests actually consume about the same amount of oxygen as it produces. Even though the rainforest has the highest rate of photosynthesis per unit area... it is primarily consumed (in balance) with the decomposition by the animals and microorganisms that live in it.
Or if you compare grassland to a regular forest, another way of conceiveing this is to say that a field of grass will generate more mass per year than a forest of equivalent area.
What about oceans? Well, they cover 71% of the earth and the estimated O2 production is between 50% and 85% (in the atmosphere). Since the ocean is basically able to provide about the same amount of O2 as land (plus the requirement of the sea animals), then you really do have O2 production from the ocean.
So let's just compare the star players, grass and phytoplankton. Well, phytoplankton are kind of difficult to grow in a lab and corn or wheat could be considered grass. So let's actually consider other kinds of algae and grain instead.
Without going too far in depth, some companies are claiming to be able to produce over 8 million gallons (or about 60 million pounds) of oil per acre from algae. That's a total slam dunk in the face of grass... even if they are just bragging (by a factor of 1,000). Algae fuel is the reason that bioreactors are "all the rage" right now (a veritable green gold rush), and companies are cropping up everywhere. Of course, genetic engineering has something to do with the numbers... but even if you compare algae with (genetically engineered) corn or canola, you are talking about a measly 150 gallons per acre give or take 20%. And corn definitely produces more weight (5 tons of seed plus another say 5 tons of cobs and stalks) than wheat (about 1.5 tons of seed, and about 1.1 tons of straw) per acre.

This is a bunch of interesting information for sure, but I don't think it answers the question.

@Roland it completely answers the questions by the OP! I'm totally stunned by your comment!

I believe the question was "do plants produce oxygen" + how to explain the quote from Skeptics SE, and I think the answer is basically given in @iayork's comment above. CO2 emissions / sequestrations and biofuel production are different issues I would say.

@Roland CO2 emission, sequestrations, and biofuels are the answer for the question do plants produce oxygen... and the quote from the skeptics SE... that plants are net zero. The first sentence of my answer is photosynthesis = combustion in reverse. Oil is sequestered carbon ultimately from photosynthesis. The weight of the plant is the measure of captured carbon. Oil is the most reduced form of carbon. Humans are currenly burning more O2 and reduced carbon than plants are producing. When we've burned it all it will equal zero. Until then, there's still sequestered carbon/oil on earth.

@Roland Plant weight (mostly from sugar and oil) is proportional to O2 production. When it is burned or decomposed the process is reversed. As noted in the answer of the skeptic SE, "The more correct view how to describe this is not that plants produce oxygen, but that they store carbon.". Although this is a bit simplistic, storing or sequestering carbon, means a (temporary) net production, which animals use and burn, digest, or otherwise decompose to live. As long as plants produce, animals have food and air. Tree's have produced... and fossil oils exist... but we are rapidly burning out.


text:
How long could Earth's oxygen supply last if no new oxygen were produced?
I read in an article or heard in some documentary that there's so much oxygen in the atmosphere that even if all photosynthesis stopped, there's already enough to last us a long time.
Is this correct? Why or why not? If so, how long is this 'long time', roughly? I've seen estimates between 15,000 to 150,000 years.

Interesting question (although it may be off-topic as there is not a clear specific answer). Where have you seen those estimates?

@James this isn't Skeptic Stack Exchange, supplying sources for my claims doesnt matter, the question is simple and clear. Everyone else was able to conprehend it just fine.

This isn't skeptics SE, but I am a skeptic. I wanted that reference specifically because it might have provided some objective insight or approach (personally I think the below answers so far are very subjective to what one considers "reasonable estimates"). More generally though, you should support your claims appropriately, not only in your answers but your questions too. Else we end up in this situation.

Disclaimer:
This is going to be a very mathematical answer. Before answering it, I assume that you are only asking about humans, assuming that all other organisms don't require $O_2$ to survive (as it will complicate the answer many many times).
List of variables:
V     = total volume of air on earth (in l)
V'    = total volume of oxygen on earth (in l)
V(1)  = volume of oxygen used by 1 person in whole lifetime (in l)
V(a)  = volume of oxygen used by whole mankind (one generation) in whole lifetime (in l)
V(p)  = percentage of total oxygen used by whole mankind (one generation) in whole lifetime

Method used:
$ \%\hspace{1mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}per\hspace{1mm}generation = \underline{\hspace{3mm}Volume\hspace{5mm}of\hspace{5mm}O_2\hspace{5mm}in\hspace{5mm}air\hspace{3mm}}\times\hspace{1mm}100$
$\hspace{83mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}by\hspace{1mm}humans$
$Number\hspace{1mm}of\hspace{1mm}years = \underline{\hspace{2mm}Number\hspace{1mm}of\hspace{1mm}years\hspace{1mm}in\hspace{1mm}1\hspace{1mm}generation\hspace{2mm}}$
$\hspace{42mm}\%\hspace{1mm}Volume\hspace{1mm}of\hspace{1mm}O_2\hspace{1mm}used\hspace{1mm}per\hspace{1mm}generation$
Procedure:
Lets first find out the total amount of air on earth.
From this:

The air sphere measures 1999 kilometres across and weighs 5140 trillion tonnes.

From here:

At sea level and at 15 °C air has a density of approximately 1.225 kg/m3

Total volume of air:
$volume = mass \hspace{1mm} / \hspace{1mm} density$
$V = 5140 \times 10^{12} \hspace{1mm} tonnes \hspace{1mm} / \hspace{1mm} 1.225 \hspace{1mm} kg.m^{-3}$
$V = 4195.9 \times 10^3 \times 10^{12} \hspace{1mm} m^3$
$V = 4195.9 \times 10^3 \times 10^{12} \times 10^3 \hspace{1mm} l$
$V = 4195.9 \times 10^{18} \hspace{1mm} l$
Now, from this, 20.95% of this is $O_2$ i.e.
$V' = 4195.9 \times 10^{18} \times 20.95 / 100$
$V' = 87904.489 \times 10^{16}$
$V' = 879.04 \times 10^{18} \hspace{1mm} l$
Moving on to next part, from this:

a human being uses about 550 liters of pure oxygen per day.

From this:

71 years was the average life expectancy at birth of the global population in 2013.

$V_1 = 550 \hspace{1mm} l.day^{-1}.person^{-1} \times 25915 \hspace{1mm} days$
$V_1= 142.53 \times 10^5 \hspace{1mm} l.person^{-1}$
From this:

The world population (the total number of living humans on Earth) was 7.349 billion as of July 1, 2015.

So
$V_{a} = 142.53 \times 10^5 \hspace{1mm} l.person^{-1} \times 7.349 \times 10^9 people$
$V_{a} = 1047.452 \times 10^{14} \hspace{1mm} l$
Finally
$V_p = V_a / V' \times 100$
$V_p = (1047.452 \times 10^{14}) / (879.04 \times 10^{18}) \times 100$
$V_p = 1.191 \times 10^{-2}$
$V_p = 0.0191 \hspace{1mm} \% $
This gives the percentage of total $O_2$ in air used by one human generation. From this, we can find the number of years for which $O_2$ will last, as I have done below:
$25,915 \hspace{1mm} days = 71 \hspace{1mm} years$
$71 \hspace{1mm} years = 0.0191 \hspace{1mm} \%$
$1 \hspace{1mm} \% = 71 / 0.0191 \hspace{1mm} years$
$100 \hspace{1mm} \% = 3717.277 \times 100 \hspace{1mm} years$
$\hspace{13mm} = 371,727.748 \hspace{1mm} years$
Conclusion:
So, yes at least humans can live for a very long time without plants doing any photosynthesis (ideally). 371,727 years seems too large a period of time, but it is just based on ideal assumptions, this number would come down (maybe into your specified range) when more variables are added.
For example:
To show extent of deviation by addition of factors, I add a very general, but complex factor in the expression: air pollution.
How much $CO_2$ is released per year can be estimated from this:

In 2011, utility coal plants in the United States emitted a total of 1.7 billion tons of CO2

And with the contribution of countries like China, India, Europe, etc. that number should rise up to at least 2.5 million tonnes (its just that I couldn't find the worldwide data on it).
Now:
$1 \hspace{1mm} C + 1 \hspace{1mm} O_2 \rightarrow 1 \hspace{1mm} CO_2$
$2.5 \times 10^9 \hspace{1mm} kg \hspace{1mm} CO_2 \Rightarrow 2.5 \times 10^9 \hspace{1mm} kg \hspace{1mm} O_2$
So, 2.5 million tonnes more $O_2$ is being used each year from the environment. But, there is another twist in this. From this:

WHO reports that in 2012 around 7 million people died - one in eight of total global deaths – as a result of air pollution exposure.

It means that 7 million people less will consume $O_2$ each year i.e.
$Net \hspace{1mm} population = 7349 \times 10^6 - 7 \times 10^6$
$\hspace{32mm} = 7.342 \times 10^9$
$V_{a} = 142.53 \times 10^5 \times 7.342 \times 10^9$
$V_{a} = 1046.455 \times 10^{14} \hspace{1mm} l$
$V_p = V_a / V' \times 100$
$V_p = (1046.455 \times 10^{14}) / (879.04 \times 10^{18}) \times 100$
$V_p = 1.1904 \times 10^{-2}$
$V_p = 0.01904 \hspace{1mm} \% $
$25,915 \hspace{1mm} days = 71 \hspace{1mm} years$
$71 \hspace{1mm} years = 0.01904 \hspace{1mm} \%$
$1 \hspace{1mm} \% = 71 / 0.01904 \hspace{1mm} years$
$100 \hspace{1mm} \% = 3728.991 \times 100 \hspace{1mm} years$
$\hspace{13mm} = 372,899.159 \hspace{1mm} years$
So, overall number increases instead of decreasing. This example was just to show how adding more factors to the equation would deviate the overall answer, and how large that deviation can be.

an average of 30'000 days = 82 years, is way too high to be seen as an accurate estimation. According the the WHO it is more around 71 years/ or 25'915 days

@JordiZambrino it was just an assumption that I heard about in a TV show. Its just that I couldn't find an appropriate reference for this, but thanks for telling that :)

Average age is just a guess. We can change it and won't change answer much. Main thing is to include stochastic factors - especially pollution and I would like to know how much it will skew the answers

@TalhaIrfan as I said in the answer, adding such factors would complicate the situation to a large extent, but I don't think that polluting gases would have any effect on the amount of O2 in the environment, yeah but burning of fuels would surely do. Anyways, I'll try to add it in the answer :)

@TalhaIrfan I hope this helps. I wouldn't be shocked to see you shocked with the answer because I am already shocked by the answer, I mean just see how shocking is that ;)

My first response was: I don't want to live on this planet anymore ;) Man!! What a research and effort you put behind this answer. I am shocked this answer hasn't got the upvotes yet it deserved. One of the best answers I saw on this website in these 2 years. Awesome!

10/10 for effort. Am I right in pointing out that two critical assumptions undermine the estimate? 1.everything else stops besides humans, 2.the population stays the same.

@James yes you are correct. I am not good in calculus, so I solved it by using these assumptions and as I said in answer, such variables would deviate the answer to a large extent (I don't even know if it can be solved using calculus also). Did you give the downvote BTW?

@another'Homosapien' It was my vote :( (but you shouldn't really ask specifically as it probably isn't the person that comments). I think that whilst you do make a real effort to point out the deviation, there are too many unreasonable assumptions for the answer to be useful. The most valuable part of the answer is "Who knows?" not "372,899.159 years". Note I voted to close the question because it inevitably demands answers that make a lot of assumptions that are subjectively "reasonable".

@James thanks for pointing it out, I just wanted to give OP an idea about large or small this value can get, how hard it might get to find exact value, and how OP can calculate a much more accurate value by themselves (in vacations ;)

The answer above gives a nice calculation how much oxygen there is, and how much we use. There are some BIG other factors that warrant a second answer IMO.
Starting at 371 thousand years (above).

Animals: according to http://xkcd.com/1338/ (probably sourced somewhere reliable) humans make up only ~20% of the walking biomass, so we would burn through the oxygen supply 5 times faster.
Fuels: my guess for an average fuel consumption would be around 5 metric tons per annum (http://data.worldbank.org/indicator/EN.ATM.CO2E.PC/countries, 17 metric tons of CO2 per annum for the USA, 1,7 for India). To get 5 tons of CO2 we need 3,6 tons of O2. From the above calculation I calculate that we use 245 kg per year of O2, so for our fuel we need 15 times more oxygen than for breathing.

That leaves us with around 5000 years to live. However, from http://www.engineeringtoolbox.com/co2-comfort-level-d_1024.html I guesstimate that above something like 1-5% CO2 is not survivable on the long term, leaving us with only 250-1250 years to leave before we slowly suffocate.
Of course we would die long before that from starvation.

You can't go on burning fuels when the oxygen content of the air drops below a certain percentage. I haven't got a reference for that, but I would guess that around 15%, rather than 20%, oxygen concentration, it would be pretty hard to ignite hydrocarbons.

Didn't think of that (but it's the same with breathing of course). With methane you'd need only 12% oxygen: https://en.wikipedia.org/wiki/Limiting_oxygen_concentration