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Why don't half of us have situs inversus?
I don't see any possible evolutionary disadvantage in situs inversus(the condition where major organs are mirrored from their normal positions) when people with situs inversus can have a normal healthy life.

Can you expand this question by adding a definition of situs inversus and maybe some material that backs up your claim of no adverse effects?

if there is no evolutionary advantage or disadvantage then its frequency is only the result of genetic drift, given that it is a recessive trait (according to wiki) then it is not surprising it presents rarely.

downvoting because you give no reasonable justification for you assumption that a neutral trait should be present in half of the population. Also, some health issues appear to be tentatively (accroding to wiki) linked to situs inversus.

I'm voting to close this question as off-topic because it is based on a faulty presuppositions (that situs inversus is completely benign, and that even neutral phenotypes should be evenly distributed throughout a population.)

During development, cilia in the node are responsible for defining the left-right axis and subsequent asymmetry. Situs invertus is often caused by ciliary defects, which disrupts this process. These defects can also cause lung defects and male infertility. It would also be reasonable to expect that whatever other molecular defects cause situs invertus would also effect other developmenal programs.

@canadianer - while situs inversus is found in diseases caused by ciliary defects (e.g. in patients with PCD, 50% aslo have situs inversus), not all ciliary defects cause situs inversus. Do you have a particular reason for saying "situs invertus is often caused by ciliary defects"? Just curious. I read a ton about this and never saw this statement.

@anongoodnurse Perhaps often was the wrong word. Situs invertus can be caused by ciliary defects. I was trying to make the point that, while situs invertus itself may or may not be detrimental, what ever is causing it can affect other processes and decrease individual fitness.

@canadianer - that, I agree with completely.

The condition is autosomal recessive so not only is there only a 1 in 4 chance that offspring to two carriers will be affected, it also requires two people with the genotype (heterozygous, unaffected carriers or homozygous, affected) to mate, and that makes the chances less likely. Also there may be many more carriers in the population, so the allele(s) responsible may be in the population at a much higher level that we are aware of... As even then 75% of the Heterozygous/Heterozygous offspring will have the phenotypically-dominant trait.

The homozygous genotype is not always benign. Your assertion that because the phenotype isn't in the population that the allele isn't in the gene pool isn't necessarily the case as carriers are phenotypically dominant, so the alleles could very well be prevalent. It is also a mutation that isn't always identified if the person does not have health issues, so its prevalence could be underreported. Finally, body plan genes are very powerful and as heterozygotes are phenotypically dominant it shows that there is no dosage dependence when there are functional copies of the gene present during dev.

Theoretically, a perfect mirrored body should be indistinguishable from the normal state and therefore there should be no effects whatsoever. And if there was no preference for left--right during development, half of us should indeed be "mirrored", as the title suggests. But this theoretical model is getting confused with the real condition situs invertus, which I guess is debilitating because the mirroring is in fact not perfect, so "conflicts" arise somehow. So it comes down to how the developing embryo can distinguish left from right, and how this goes wrong in the situs invertus.

In the Wikipedia article linked to in the question, one will note that there are several medical conditions associated with situs inversus, including congenital heart disease, primary ciliary dyskinesia, and Kartagener Syndrome. These can easily lead to reduced fitness for reproduction, especially PCD/Kartagener Syndrome, as one effect is male infertility due to lack of functional cilia on sperm.
Therefore, there likely is a negative pressure on the alleles responsible for this condition, explaining why it is so rare.

When I was a post-doc my mentor used experimental manipulation to create the equivalent of situs inversus in C. elegans embryos. The embryos hatched and grew into "left-handed" or "anti-worms." He published that as a single-author letter to Nature in 1990, and had a series of grad students working on isolating mutations in handedness. It turns out that the main way humans with situs inversus are identified is at fertility clinics. Sperm motility is cilia-based, and functional Fallopian tubes have cilia that move the just-released ovum down to the uterus.

If a polymorphism is neutral and has no effect on reproduction, it will not necessarily present itself to the population in a 1:1 ratio. For instance, for a single-gene polymorphism with two alleles in the absence of evolutionary forces like selection and gene flow, the trait will be at Hardy-Weinberg equilibrium, meaning the two different alleles will be present in some ratio (not necessarily 1:1) and will stay in that ratio from generation to generation. Of course, I'm not an expert on animal physiology and I don't know the genetic basis for situs inversus, but either way two equally fit traits may still be present in the population at very different ratios as there is no force pushing them to be present at equal ratios.
Traits undergoing density-dependent selection, on the other hand, such as sex, are under selective pressure to exist in a 1:1 ratio. There are unlikely to be any such forces acting on situs inversus vs situs solitus

I am an eighty year old woman with Kartageners Syndrome.  This means, I have bronchiectasis which was diagnosed in 1948. The disease was isolated in my left bottom lobe. I also have chronic sinusitis. I think cilia is lacking or if not lacking at least too short to be effective.  For most of my childhood I was unwell but after age eighteen I seemed to be quite a bit better and I have lived a healthy life.  It is only recently that I have had health problems relating to Kartageners and I tend to think my age is now contributing to lung infections and therefore the quality of my life is deteriorating.

@AliceD Sorry, but this answer is on topic. Kartageners Syndrome is a disease associated with situs inversus, and I believe that the purpose of the post was to refute the claim made by the OP that situs inversus is benign.

@AMR - you are right. Thanks. I flagged this answer to alert the mods that they should be dismissing my previous flag. Thanks again.

@AliceD No worries. While I was familiar with situs inversus, I was not familiar Kartageners, but after looking it up, I got a clearer picture of the posters intention, and how often do we actually get to hear from someone who actually has complications from a 1 in 10,000 disorder (that is aware of it). It seems that the unfortunate thing for this poster is that it was partial and not total, as it seems that total reversal has the same phenotypic behavior as the majority of the population, except in rare occasions. It is only those partially affected that tend to have health related issues.


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Can Leptospirosis be spread through human urine
I am wondering if Leptospirosis can be spread via the urine of an infected human individual. All of the sources I have been able to find on the web have stated that the disease is primarily spread through infected animal urine, however, none of them mention human urine.
However, Wikipedia states:

After 7 to 10 days the microorganism can be found in fresh urine

Which would imply that it could be spread via the urine of an infected individual?

It can be spread from human to human through urine but it is very rare seeing as we are relatively clean creatures (most of the time) and our excrement hardly ever comes into contact with other individuals without first being purified.
Sources:

Leptospirosis
CDC: Leptospirosis infection

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Is it possible for humans to digest and live on food that isn't based on DNA or RNA?
Our bodies digest food using enzymes that have evolved to convert food here on Earth. Could we even possibly get nutrients from something we haven't evolved alongside? - Is it possible for humans to digest and live on food that isn't based on DNA or RNA?

Welcome to biology.SE! I vote for not closing this question. Yes it is going to be speculative and probably breaks half of the "how to ask" rules (that you can find here) but an answer along the lines of non-carbon based life (e.g. sulfur-based organisms) might be interesting.

@cagliari2005 How do you want to answer this in a scientific way?

@Chris. Was reading the question as "Is there digestive enzymes for non-carbon based nutrients?". Someone might know something about that.

I was thinking of both carbon and non carbon based life - could we even possibly get nutrients from something we haven't evolved 'with'.

Then you should edit your question and add these information.

I've tried to make it less opinion based

Our food is not based on DNA or RNA. It is based on carbohydrates, fats etc. All of these can be made artificially if you want.

@Chris Thank you! - In that case, this is a rubbish question. If I edit it again to ask more about carbohydrates etc, I agree it'd be extremely opinion based.

this is still broad (after the edit)

This might be flagged for being somewhat of a subjective question, but to survey human diet:
Mnemonic SPONCH can be used to sum up the necessary building blocks of life, in the elements Sulfur, Phosphorus, Oxygen, Nitrogen, Carbon, Hydrogen. There are others, trace elements, which are necessary and come from diet (selenium, for example). These elements are used in building our biological macromolecules: Carbohydrates, lipids, nucleic acids, and proteins. The molecular interactions between these macromolecules, their cofactors, etc. are essential for life. Some of these compounds, however, can't be made in the human body from scratch; hence essential amino acids, and the necessity to consume foods which provide metals, carbohydrates, fats/triglycerides, etc.
So, at this point our body is optimized to incorporate terrestrial foods. Sometimes, though, we can see that the body will sometimes accept analogs to normal compounds, although this is often to disastrous effect (like chemotherapy in cancer). The real question, then, would be: does said extraterrestrial food compose of necessary biological elements or analogs in a way our body can actually use this food for sustenance? That, however, is 100% speculation as we have no reference in even a single case to base our assumptions.

Thanks for your reply! I've altered the question to try to make it less opinion based. Any extra thoughts based on the change?

@jenga So, here's my thoughts, in part: We can only extract energy from sources we can break apart, absorb, and transport efficiently. We have specific proteins that get this job done. If we have an enzyme to do the job, the job gets done, and if we don't.. well, vice versa. How can we make sources of nutrients we wouldn't otherwise be able to process usable? Perhaps a system of ingesting exogenous enzyme.. but it's again mostly speculation.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Do nucleosomes ever completely unwrap during transcription?
In eukaryotic transcription will the nucleosomes ever completely unwind the DNA and the histone complex disassemble? If an operon is more 160 base pairs it seems it must.

Nucleotide is the wrong term here. I guess you are talking about nucleosomes, right?

Histones can be ejected from the nucleosome, leaving free DNA. DNA can also translocate relative to histones. Both of these processes are catalysed by by chromatin remodelling proteins. It has also been shown that a protein complex called FACT greatly increases the transcription efficiency of chromatinised DNA. It does this by transiently removing an H2A/H2B dimer from the nucleosome. I'm not sure if the exact mechanism behind why this increases efficiency is known, but it does.

Danny Reinberg's group have done a lot of detailed biochemistry to show why FACT aids transcription efficiency. Part of the answer has to do with topological constraints imposed by nucleosomes.

Yes, nucleosomes are completely unwound. Histone chaperones such as FACT (for H2A/H2B) and ASF1, CAF-1, HIRA, Nucleophosmin etc (for H3/H4), associate with RNA Pol II and handle the displaced nucleosomes. As you surmised, the histone octamer complex is disassembled, into the H3/H4 tetramer and two H2A/H2B dimers. Right behind the elongating Pol II, the chaperones reassemble nucleosomes. During the process of reassembly, it has been shown that "new" H2A/H2B dimers (and possibly H3/H4 tetramers too) can get incorporated into an "old" histone octamer. Finally, nucleosome remodelling complexes such as SWI/SNF re-space the nucleosomes.
This is a decent review of the process (by one of the discoverers of the FACT complex, incidentally): "New chaps in the histone chaperone arena". Campos & Reinberg. Genes & Development (2010): 24: 1334-1338
This is a comprehensive review of histone chaperones and nucleosome dynamics during various DNA-dependent processes (such as transcription, replication and repair). There is an entire section on their role in gene transcription, which is the main thrust of this question: "Histone Chaperones: Assisting Histone Traffic and Nucleosome Dynamics". Gurard-Levin, Z.A., Quivy, J., and Almouzni, G. Annual Review of Biochemistry (2014): 83: 487-517
And finally, a good overview on histone dynamics and chromatin structure during transcription: "Histone exchange, chromatin structure and the regulation of transcription". Venkatesh & Workman. Nature Reviews Mol. Cell. Biol. (2015): 16:178–189

I should add that an inability to disassemble nucleosomes (or displace any other factor bound very tightly to DNA) can actually pause an elongating Pol II complex.

It would be nice if you could add some references to this answer.

I've added a couple more references, as requested.

Just to add very recent new information to the first answer: the initial steps of RNA Pol II transcription through a nucleosome have now been revealed at the structural level by cryoEM. See these two articles: - https://doi.org/10.1126/science.aau9904 - https://doi.org/10.1101/437574


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Epistasis Across Chromosomes and Individuals 'Homozygous for Interactions'
Apologies for any failures in nomenclature. I'm a mathematician who is making a foray into genetics for a masters thesis. Specifically, I'm generating artificial diploid genetic sequence data and phenotype data based on known epistatic interactions.
Primary Question
I am familiar with the concept that having multiple copies of a single allele (e.g. one from each parent) can actually increase expression and thereby change the quantitative phenotype (at least in some cases?). Can this also happen with epistatic effects? For example, consider the case that locus 1 ($L_1$) and locus 2 ($L_2$) exhibit some positive interaction ($\beta$) on the trait ($Y$).
$$E[Y]=\mu+\beta(L_1L_2)$$
If both chromosomes contain the allele in question at both loci, then does this individual exhibit more of a trait increase than if he only had one chromosome with the epistatic alleles?
Secondary question
Can alleles interact epistatically even when they are present on different chromosomes? e.g. assume allele A at locus 1 interacts with allele B at locus 2. Individual has A at locus 1 and b at locus 2 on chromosome 1. He also has a at locus 1 and B at locus 2 on chromosome 2. Do A and B from the different chromosomes interact? My intuition is yes but I want verification.
Many thanks!!!

Question 1: The phenomena you describe in which it matters whether you have one or two copies of an allele (e.g., the AA phenotype being different than the Aa phenotype) are known as dominance effects. Dominance effects can interact with epistatic effects (in which the phenotypic effect of one locus depends on the genotype at the another locus).
One good example is the interaction between the Agouti locus and the Mc1R locus in the oldfield mouse (Peromyscus polionotus) in determining coat color. Dark-color homozygotes for the Agouti locus have dark coats irrespective of the allele at the Mc1R locus, whereas color in Agouti heterozygotes or light color homozygotes depends on genotype at the Mc1R locus. The figure below, from Steiner et al (2007), illustrates:

Question 2: Epistatically interacting loci need not be on the same chromosome. The loci discussed above provide a perfectly good example. Mc1R is on chromosome 1, where as Agouti is on chromosome 7, yet they interact epistatically.

Ah! I can't believe I completely forgot that there were different types of dominance. Specifically in Question 1, this would be either codominance or intermediate dominance, is that correct?

I'm not sure I understand what you are asking. If we have alleles A and a, we can have dominance (Aa and AA have the same phenotype), codominance (Aa has both the aa and AA phenotypes), or incomplete dominance (Aa has a phenotype intermediate between aa and AA).


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Selection Pressure on Orca Whale Coloration
What is the proposed selection pressure that leads to the distinctive coloration of Orca whales? I can find nothing in the literature.

Hello. I want to remind you that natural selection is not the only process important to evolutionary processes. There are probably several posts that discuss that. You will find a paragraph in the first answer on this post for example.

Adding to Remi.b's comment, not every trait is adaptive. We've most recently discussed this here in this answer to a question about rose thorns.

Assuming the pattern of color would be adaptive (to a certain degree), here are few guesses. It sounds likely to me that such coloration would have evolved in reaction to recognition and signalling. Eventually due to sexual selection or to kin recognition. It may also be under selection for camouflage. Indeed orcas are black on the back and white on the belly and preys seeing from above would see a black background and those seeing from below would see a lighter background.

Clarification: I am familiar with concepts such as genetic drift and non-adaptive mutations. Given that the Orca is an apex predator, I could certainly believe that coloration doesn't confer much interspecies competitive advantage. If I were pressed to guess, I would actually guess sexual selection. I was just hoping someone actually had a theory (i.e. with some evidence) on which evolutionary process governs it.

Also, @Remi.b, I totally agree, countershading makes perfect sense. I guess was referring more to the black and white eye spots and the other well-known splotchy patterns.

Not every trait has to mean something. Orcas could have been red for no good reason. By "no good reason" I mean genetic drift, population bottleneck or something.

You can find a discussion of this topic in the literature:
Mitchell, Edward. 1970. Pigmentation pattern evolution in delphinid cetaceans: an essay in adaptive coloration. Canadian journal of Zoology 48(4): 717-740.
Perrin, W.F., 1972. Color patterns of spinner porpoises (Stenella cf. S. longirostris) of the eastern Pacific and Hawaii, with comments on delphinid pigmentation. Fish. Bull, 70(3), 983-1003
Caro, T., Beeman, K., Stankowich, T. and Whitehead, H., 2011. The functional significance of colouration in cetaceans. Evolutionary Ecology, 25(6), pp.1231-1245. http://web.csulb.edu/~tstankow/Caroetal2011.pdf
And related helpful article:
Evans, W.E., Yablokov, A.V. and Bowles, A.E., 1982. Geographic variation in the color pattern of killer whales (Orcinus orca). Report of the International Whaling Commission, 32, pp.687-694. http://www.kasatka.com/kirsten/ColorVariation.pdf
I'll let you explore these and their citations.
Remember, Google Scholar is your friend.

It would actually be better if you summarized the main points of the articles.

@kmm I was simply addressing the second part of the question: demonstrating sources in the literature. We don't have to handhold through the entire learning process...


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What is the statistical relationship between radioactivity and mutation rate?
This question tries to narrow down the scope of that question.
What is the statistical relationship between radioactivity and mutation rate? By how much would the mutation rate be lowered in a idealized world were radioactivity is absent?

According to this wiki page , the average background radiation is 3.01 milli-Sievert per year (including natural and artificial sources). This equals 0.301 rad.
I found a short letter to nature that says the average forward mutation rate in human is 2.6 * 10^-7 per locus per rad = 2.6 mutations per ten million bases. Also it say that this mutation rate is quite uniform among species. The size of the human genome is approximately 3.2 gigabases.
So doing a quick maths: (2.6*3.2*100)*0.301 = 250.432 mutations per year per human. This is an approximation because I rounded the size of the human genome to 3.2 gigabases. Also this doesn't mean that we actually acquire this amount of mutations because we have repair mechanisms.

Interesting stuff + 1 Do you really mean "250 mutation per year per human" or do you mean "250 mutation per reproduction event"? This estimate is huge! A nucleotide typically has a mutation rate of about [$10−7;10−9$]. So random variation of 1 rad (that doesn't seem that huge given the wiki page that you linked) may easily yield to a 10 or even 100 fold higher mutation rate.

You said "this doesn't mean that we actually acquire this amount of mutations because we have repair mechanisms". So they did not take into account repair mechanisms in their study? The letter is 41 years old. I would intuitively think that today's estimate would be lower.

@Remi.b - If you calculate with the mean mutation rate of the interval that you have given (10^-8), that would still give  approx 32 mutation events for the entire genome. If we take the upper limit that is 10^-7, we get approximately 320. Maybe using the term mutation event would be better in my answer but I think based on the letter and wiki info that my calculations are correct. But as you say the letter is quite old, I'll check if there's anything new. BTW this would still result in approx (250/(3.2*10^9))*100 = 0.000007826% of the whole genome.


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The selective pressure of contraceptives
Is it possible that the use of contraceptives will produce evolution humans? Contraceptives can reduce reproductive success, so shouldn't selection favour resistance to them?
In this case it might be useful to think of evolution as a "black box", an information processing mechanism  where only input and output is relevant. From this point of view, we would expect the box to produce an output comparable to the resistance that evolution will produce in a population experiencing a poisoning effect which seriously damages its reproduction mechanism.
The evolutionary "output" from such poisoning  has been studied in great detail. Are there any lessons relevant to future human evolution in these studies?

Well, it seems the subject of contraceptives as an evolutionary factor is not welcome on this website , even if common sense can determine it to be one of the most powerful evolutionary factors determining the future of the human species .  Each person can reach his own  conclution regarding this dissonans...

The topic is certainly welcome. Your question was closed for being unclear rather than off topic. It would have been nice if any of those who voted to close would have explained why. I've editing the grammar a bit and given it some structure.

I think it need works on clarifying a) what you expect to happen if a population of humans has access to contraception b) why you expect that outcome c) why you think it has consequences for human evolution @user3407

@kmm Do you understand the question?

@canadianer Is there any work on novel selective pressures resulting from widespread use of contraceptives and can these selective pressures be modeled on the selective response in the same way as antibiotic resistance or strong truncating selection?

question is very vague and what @kmm rephrases, seems to me, is far from the OP statement, which appears to be looking for opinions

Once you bring choice and selective breeding into the equation, you are pretty much circumventing natural selection. You only need to look at domestication to see how an understanding of cause and effect in breeding can introduce significant phenotypic differences into the population. You could also implicate all of Modern Medicine as circumventing evolution. Children who would have died 1000 years ago prior to reproduction now survive to reproduce. Young adults are kept alive and can go on produce more offspring that would never been a part of the population if NS was not bypassed.

Your choice of words such as "poisoning" and "seriously" reflect that you have a clear bias against contraceptives.

@kmm The question is loaded and isn't really looking for a real answer, it is asked to pose a particular bias against altering human reproduction and introducing choice into the equation. The OP is making a statement in the form of a question. A neutral question, looking for a productive and informative answer would have simply been to ask how does the use of contraception effect evolution and is there evidence that shows that it has introduced new forms of selection. I have a doubt that even a well researched answer would sway the OP. I agree with the original vote to close this question.

There is another point that this question misses, and that is that selection acts on the species. As long as enough of the sapiens species is reproducing, it really doesn't matter evolutionarily what a given individual choses to do. Homo sapiens genes will live on, as Neanderthal genes do in sapiens of European and Asian descent and even if the next species of hominid evolves from sapiens and takes over the Earth and sapiens go extinct.

Relevant, although not a serious answer: http://www.smbc-comics.com/index.php?db=comics&id=2632#comic

Contraceptives are not like most other toxin . Contraceptives are hormone analogs that disrupt natural signaling process.

Interesting question, but the answer is simpler than you might think.
Antibiotics put selective pressure on bacteria. Bacteria resistant to that antibiotic evolve as only the resistant ones survive. But this is the key, there has to be at least some already resistant bacteria from which the new (resistant) population will emerge.
With contraception, this is not the case. There are no spermatozoids capable of penetrating condoms, for example, and you should also bear in mind that in most cases mild hormonal disbalance is enough to prevent conception. It's a very delicate process, and contraception is basically an overkill.
Even if some spermatozoids could penetrate condoms, that trait would have to be hereditary in order for evolution to occur.
If you'd want to prove that contraception constitutes selective pressure on humans you'd first have to prove that there are spermatozoids and egg cells that can beat contraception, and that it's hereditary.
Evolution doesn't work the way you think it does. If you kill a random person, even if you kill a million people, it's not necessarily selective pressure. There are rules to evolution, and one of them is that it has to be hereditary.
This is not.
It wouldn't even come close to being artificial selection, let alone natural selection.
Besides, there's 7.3 billion of us. More than ever. We can hardly say contraception is reducing the world's population.
You also fail to see one thing, that a person who uses contraception in teenage years still has kids as a young adult. Contraception just delays pregnancy until you're ready. In evolution, there's a concept of "surviving long enough to reproduce". You can both use contraception and be an organism with 10 kids - though not at the same time.

Interesting question. I did not fully understand the entirety of your post so I will answer the question posed in the first sentence, namely:

Does it seem probable that the existence of contraceptives (which has reduced human reproduction to below survival-level in many populations) will be a completely new selective pressure on human evolution?

Yes, the use of contraceptives is a selective pressure. The couples that don't reproduce simply don't pass on their genes so evolution "is favouring" those couples that don't use contraception. This is a bit tricky because if a couple uses contraception for life and doesn't reproduce at all, they are evolutionary dead ends and selective pressure can't act on them because there isn't anything passed to the next generation.
For the couples that use contraception for longer or more often, leading to delayed childbirth or less children born, then the parents would have contributed less genes to the next-generation's gene pool so they may be wiped out more easily. Thus contraception reduces the fitness of humans using it if used often enough to keep the populations using it below replacement levels.

Choice implies that selection is artificial as opposed to natural. Natural selection relies on random changes to the organism and the environment that organism inhabits and favors the organisms fitness to survive in that environment. There are some that would argue that in a society with finite resources, that those who limit their offspring increase the advantage that they give their offspring to thrive, survive, and succeed in passing on the genetic inheritance.

If you keep a population below replacement levels, all genes will be lost regardless of how well you train your offspring. Yes, there is a balance between number and quality of offspring but only if you have enough to propagate the genes forward to the next generation. I.e. there is a lower bound which is around 1.2 or so and some countries are close to this already.

I placed the comment on the original post, but when looking at selection, you have to look at the species as a whole. And as a whole Homo sapiens birth rates far exceed replacement levels.

If contraception helps us to achieve the proximal rewards of sex without reaching one of the ultimate goals (reproductive success), you could say that the availability of contraceptives inhibits reproductive output. But, I don't think that it's as simple as that. The availability of contraception merely means that the desire to have sex no longer automatically leads to the conception of children. Instead, a wish to have children often first needs to get into play. Thus, you would expect a strong fitness reward for individuals who are capable of effectively planning for children and not postponing it indefinitely into the future until they are no longer fertile.
As mentioned in previous answers, you won't get too see condom-tearing supersperm any time soon, but I dare predict that we should expect to see an increase in condom-tearing behavior over the next century or so. Currently, I think there's definitely a shift in selective pressures on behavioral genes related to reproduction.
A caveat is of course that changing behavioral output could also be induces by cultural evolution. Cultures may instill taboos on contraceptives (think of the Catholic Church's attitude towards condoms), or cultures may facilitate child care to stimulate child-bearing at a reproductively healthy age.
An altogether other possibility is that the average age at which the decline of fertility sets in will significantly increase.

Can you provide links that support the selective pressures toward behavioural genes? Also, unless most babies are born thanks to condom-tearing-sperm I don't see how it would be selected for genetically.

Sorry, I should have mentioned that my answer is entirely speculative. Also, I don't mean condom-tearing behavior of sperm. I'm talking of behavior on an whole-organism level.

In principle, contraceptives are a barrier to reproduction, and selection will approximately operate by maximising reproductive. Therefore, one would expect that selection would favour "resistance" to contraceptive methods. However, there is a big difference between selection and adaptation (evolution by selection).
An adaptive response can only evolve if there is heritable variation for the trait, in this case, resistance to contraceptives. For example, imagine we had a pill taken by men which disrupts sperm production as our only contraceptive method. This pill is not 100% successful, as some men still produce viable sperm because they have a gene/allele which prevents the pill from damaging sperm. Given enough time (and assuming no other contraceptive/abortive measures can be taken), then this gene should spread through the population, because carriers will produce more offspring (who in turn are likely to carry the gene).
This hypothetical scenario is similar to that of the evolution of antibiotic resistance in bacteria. We use antibiotics to kill populations of bacteria, but some members of the population have genes that protect them from the effects. The carriers of the resistance genes will then produce the next generation, all of whom carry the resistance gene.
Similarly, you can think of populations where toxic chemicals are more present. In some populations, arsenic is present at high levels. Arsenic is toxic and will decrease reproductive success (because there is a higher tendency die before proper opportunity to reproduce), so consider the environmental arsenic as our "contraceptive" in this scenario. Genetic variance in the ability to metabolise arsenic arose (e.g. by mutation) and spread through a population because of the advantages it gave.
In reality, there is little-to-no genetic resistance to plethora of contraceptive methods we can deploy - the failure of contraceptives is random not genetic. Therefore, we are not going to evolve resistance to contraceptives any time soon.
Furthermore, contraceptives may reduce the rate at which sex leads to reproduction, but it may allow parents to choose when to produce offspring and how many to produce more easily. As such, the children might be provided with better developmental environments or have a lower rate of infant mortality etc. so fitness could be higher in this group compared to those who are resistant to contraception. If so, this could select against contraceptive resistance. It's not reproductive success that matters, but the tricky concept of fitness.

Do you mean that (A) the choice of using contraception is part of the human phenotype and we can study the selection pressures that apply to it or that (B) you consider the absorption of a contraceptive as an external selection pressure and are wondering what evolutionary answer this selection pressure will cause?
If (A):
One can only study the evolutionary pressures applying on the use of contraception under the following conditions:

The choice of using contraceptive is inheritable
People who do use contraceptive have significantly less (or more) kids over their entire life than people who do not

I am not sure any of these conditions is fullfilled.
If (B):
If it was as simple as a "poisoning effect which seriously damages its reproduction mechanism", you could expect the emergence of a resistance allele (for example that would make females insensitive to oestrogens in oral contraceptives).
However I guess that persons who use contraception are likely to choose abortion if pregnant, decreasing the fitness effect of such a potential resistance allele.

I want to upvote the rest of this answer, but can't whilst you generalise people who use contraceptives as people who will readily have an abortion. That statement has no grounding whatsoever.

@GoodGravy As that portion of the answer is speculative, and likely not supported by references, you can edit it to improve the answer.


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What are the typical values of probabilities for nonspecific binding to an antibody?
I'm physicist by training, so please excuse me if I don't use the proper terminology.
I think there is a way to make a sensor that detects if a single antibody has caught something from the flow. So I'm trying to figure out if this would be a useful sensor, but this depends on how specific the antibodies really are.
When I ask biologists "How specific are antibodies?", they reply: "Very-very specific", but provide no values that I understand on microscopic level. But I am trying to make a quantitative estimation, e.g. for the following thought experiment:
Suppose I have attached an antibody to inorganic surface. It's an antibody for catching object X. And I flow blood over the surface, slowly. Suppose there's no X in this blood at all. But there are lots (maybe 1017, or some crazy number like that) of other stray particles flowing by this antibody every second, right? So, when one of these particles bumps into this one antibody, what is the probability that it would stick to this antibody? Is it really 10-17 ? Is it really so small?
And, in any case, how do I estimate this probability at least to 1-2 orders of magnitude?
Also, how do I estimate the "collision cross section area" through which an object has to fly to make an attempt to bind to an antibody? In other words, does it only have to touch it slightly, or bump into antibody in a hard and messy collision?
Does the probability of successful bind depend on the flow speed?
How would the values change if I take serum instead of blood?
Could you please point to some relevant papers, books or just keywords? I would very much appreciate any help.

You have to keep in mind antibody structures are complex as well as the antigens they bind to.  I think it really depends on an antibody with a specific structure (the binding site of the antibody, the sequences in its hypervariable site) that's being measured.  This is an older paper that touches on anitbody binding specificity.  http://pellegrini.mcdb.ucla.edu/Lab/publication_pdfs/M4Xl99-fulltext.pdf

The specificity of antibodies can vary. Also, the binding/unbinding rates can be different. You can look at 1977 Gillespie's paper on how to convert deterministic rate constants to reaction probabilities. For incorporating flows you need to formulate partial differential equations or corresponding stochastic models.

TL;DR Specificity of antibody can be not superb. It can give false-positive results in up to 90% of experiments. However, some essay are 90% specific.
That is an interesting question and there sure a lot of research done to understand specificity and strength of binding of antibody to its target.
First of all, let me say that antibody-epitope interaction is, as many biological processes, probabilistic process, which means it can go either way, however, after binding antibody need a lot more energy or time to "fall off". Direct contact is always required for establishment of non-covalent bond between antibody and epitope, because characteristic length of that interaction is very low (order or angstroms, 0.1nm and less). Point here is that you don't need to run antibody in stream, rather let is sit in solution with your sample or mix gently, random thermal motion will take care of them finding each other. In flow you will waste a lot of antibody, which is expensive.
I think that you can estimate probability of given antibody binding given molecule from their 3D structures, but this is extremely burdensome calculation. What you can do experimentally, I suppose, is label "right" epitope with red fluorescent tag, and every other molecule in your solution with green tag. Then run solution through column with antibody sitting on beads (as in chromatography), elute everything and compare green to red signal. Measuring accurately, this will tell you how much "junk" antibody picked out of solution.
Now, to numbers. Here Abcam talks about its antibody for progesterone. Molecules, closely related to progesterone, are recognized with 40-90% efficiency, compared to true-positive target (progesterone). But this is absolute-worst case scenario, because those molecules are so closely related.
On other note, antibody specificity is very important when essay is used, e.g. for HIV diagnosis. Here is nice page from U Penn, that discusses issues with specificity:

For example, in one study of 290,000 asymptomatic Minnesota blood donors donating 630,000 blood units, the false positive rate when both the screening and confirmatory assays were positive was was 0% per donation (95% confidence interval 0% to 0.0006%).
...
For example, in one study of asymptomatic Italian blood donors, only about 13% of donors with repeatedly-reactive EIA tests were confirmed to be HIV-infected on the basis of positive immunoblot. However, in a high risk population the false-positive rate can be much lower, as low as 1-3%.

I couldn't find any more precise data or studies. In biological imaging (my field) antibodies are split into "works" and "don't work, drop it" (aka high background) groups.

Your first statement is not always true: the specificity of antibodies can vary; some can be extremely specific. Also, in antibody based chromatography there is flow, however, the antibody is immobilized and it is the antigen that is flowing.

Specificity of antibody can be not superb 2) I could not find data :-( My antibodies are working nice for imaging. 3) In chromatography flow is pretty slow, I think. But yes, if you fish antigen out of solution, you don't waste precious antibodies

Clarify, when you say "antibody" do you mean a monoclonal antibody (where every antibody is identical, and therefore a pure population), or do you mean a polyclonal antibody (which is a mixture of antibodies that all recognize the same antigen, but may each be recognizing different epitopes on the antigen)? A monoclonal Ab (mAb) recognizes a single epitope.
Textbooks and supplier catalogs often act like Ab binding is absolute, as if you could not measure the three quantities: molar concentration of free antigen, molar concentration of free mAb, and molar concentration of bound antibody antigen complex. In other words, as if every antibody is fully occupied all the time, once the Ab encounters a molecule of free antigen.  But I think you can discern from the discussions and answers above that not all Ab are created equally.

In cases where people have measured this Kd (the dissociation constant) for a "tight" binding antibody the value is in the order of 10EE-14 or smaller (as I recall).  When we say tight binding we usually mean that the so-called off-rate is very slow, with a t1/2 on the order of hours. In a typical reaction the on-rate is usually limited by the rate of diffusion, and cannot be faster (but search for discussions of lac Repressor DNA binding protein finding its targets with kinetics that are faster than the rate of diffusion!)

The device you are describing (that detects binding events using fixed proteins on a surface and target proteins in solution) measures surface plasmon resonance, and at one point was available for purchase under then brand name BIAcore. It was developed by Mel Simon, at CalTech.
Finally, if your goal is an automated way to use antibody reagents to detect vanishingly small quantities of antigen in a complex mixture of fluid, you would do well to familiarize yourself with the radioimmunoassay (RIA), it can be exquisitely sensitive.  Keep in mind that all of these different techniques will have a lower limit of detection such that a negative result ("We could not measure any of protein X in the sample from this patient") always has to be considered with the proviso of "using this particular detection assay". So it is a type of confidence level.

I understand that you talk about false-negative binding. $K_d$ is about probability of false-negative binding — antigen is present, but antibody doesn't bind it despite being specific to it. What I'm asking is the probability of a false-positive binding — a probability that non-target particle will bind to this antibody. That is, a particle that is not the antigen this antibody is specific for.

Thanks for the links about BIAcore, but their methods don't count individual single particles. They measure the average signal over entire sensor surface, in an ensemble-averaging way. I'm talking about seeing a single bound particle - as in the detection scheme by Zybin et al.


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Circadian Clock During a Flight
I am interested in knowing how our Circadian Clock responds (and if there are resultant changes) when we travel across Time Zones?
UPDATE 24th April
I am reopening this question as the statement in the answer "When you travel to different time zones, your circadian clock will be off" has further confused me. If it's the case, then I am looking to get a better explanation than that (with solid references). Thanks

Welcome to Biology S.E.! From what I understand, the actual time zone shouldn't cause too much of an issue. However, flying from light into darkness or the other way around seems it could confuse your internal clock. And if you crossed several time zones and then tried to sleep at your normal time and it was still light out... That could be confusing as well.

Just removed some irrelevant tags.

When you travel to different time zones, your circadian clock will be off (incorrect). The reason your circadian clock will be off is because your body has adapted to the time zone you are from. When you enter a new time zone, your circadian clock will still be functioning on the old the time zone. If the time zone difference is $\pm 12$ hours, this is a huge adjustment.
However, your body takes inputs from the environment. That is, you may see it is day light when your body is under the impression it is evening. Your circadian clock is controlled by your master clock located in the hypothalamus. As you take in these external inputs that counter your circadian clock, a group of nerve cells called the suprachiasmagic nucleus will slowly make the master clock adjustment [1]. This resetting can take a few days.

NIH Jet Lag Prevention Guideline

Additionally, there has been a bit of research on exercise reducing jet lag. In a study, researchers test outdoor exercise with flight crew members and found that the group that exercised outdoors had a hastened re synchronization of their circadian clock [2].
Another interesting article is Jet Lag in Athletes.

Thank you! May I have reference for "When you travel to different time zones, your circadian clock will be off."

@dustin - that sentence confused me too; as it stands, it reads like "when you travel to different time zones your circadian clock will be [switched] off". I had a raised eye brow and had to re-read it too.

@AliceD you can edit if you want. It makes sense to me, so I don't see the issue.

@dustin - up to you, it may just be a language barrier making me to mis-read your sentence. It's not critique, just an attempt at analyzing POs question on the reference :)


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Why does a "cascade" of events happen during signal transduction?
I've been watching some videos on signal transduction and it says that because there are enzymes being activated by the signal, then there is a "cascade" which happens afterwards...I don't understand why?
Thanks.

Is your question "Why a long cascade instead of more simple, shorter cascade?"

There is one main reason: Amplification of the signal. You can start a signal downwards the cascade with relatively few receptors which need to be activated which allows even for weak signals to be translated into the nucleus.
This figure shows this for G protein coupled receptors (from here):

For example one molecule of cAMP can activate many molecules of pKA until it's hydrolysed which in turn can phosphorylate many other protein molecules.
For more information you can read the references articles (at least the introduction) and follow the references in them.
References:

Ultrasensitivity in the mitogen-activated protein kinase cascade
Noisy signal amplification in ultrasensitive signal transduction

Ok I think I get it now. It starts with ONE ligand, the epinepherine.
However it says that after the ligand binds and thus activates the G protein, it has 100 molecules activated? I thought that 1 ligand activates 1 G protein?
I think I'm a bit unsure on what exactly the G protein is and what the G protein RECEPTOR is?

No, 1 ligand activates one receptor. The receptor in turn binds inactive G-proteins and activates these (as long it is active himself). The activated G proteins are released from the receptor and activate downstream targets of the cascade. This is the first step of amplification.

So the G proteins are not on the membrane already? Does the ligand bind the receptor, which in turn recruits G proteins in the cytosol up to the membrane or? The information is very blurry on this. It seems to assume the G proteins and the receptor as one unit.

It will be pretty hard to explain this in detail here in the comments (and is not well liked as well). I suggest you open a new question on this with detailed things you want to know about it.

@Chris Does this multi-step process allow for finer regulation of the event?

@jerepierre There are more potential points to terminate a signal. But it also allows crosstalk between different pathways and more noise. See here for some more information.


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Richard Goldschmidt's “systemic mutations”?
[TLDR] I dont understand the fault people had/have with Richard Goldscmidt's concept of systemic mutations [/TLDR]
As a preface, I am a undergrad biology student, so sorry if this is a "Stupid question".
How does Richard Goldschmidt's concept of systemic mutations, reject the classical gene concept, why were biologists so against it?
From what I  understand he used the concept of systemic mutations and developmental macromutations in his lectures to explain how macromutations could cause speciation(macroevolution?). The results of the developmental macromutations, if I understand him correctly would be then the Hopeful Monsters?
And from what I have read on a timeline of his work, systemic mutations describe the "large rearrangments of the chromosome", with a new arrangement meaning a new phenotype?
How is that wrong though? Do chromosomes not have rearrangements via cross over events during meiosis or via transposable elements? Or is he referring to something else, since I understand at the time, meiosis and TE's were not understood well.
The source i was reading from was:
(Richard Goldschmidt: hopeful monsters and other 'heresies' by Michael R. Dietrich) Available from http://www.dartmouth.edu/~dietrich/NRG2003.pdf

His notion of systemic mutations involved the postulation of massive chromosomal rearrangements (not mere recombination/crossing-over) as mediators of speciation in one-step. While whole genome duplications have been shown to induce speciation (see, for example, cryptic speciation in Hyla versicolor) they are not large scale rearrangements as he suggested. Additionally, while there is evidence for multiple large scale chromosomal arrangements at once in cancers (Chromothripsis) , there is no evidence of a similar process resulting in immediate reproductive isolation.


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Water soluble molecules
I believe I may have misunderstood water solubility this entire time.
I assumed that water soluble meant that it would literally dissolve in water. It would break down into atoms. A sugar molecule would break its bonds and become something else...
However I must be mistaken because I'm reading about why DNA is spiral shaped and it says that it is to keep the hydrophobic bases inside the spiral to protect them from the water, but keeping the hydrophilic phosphate and sugar molecules on the outside.
I would assume that because these molecules are hydrophilic they would disassociate from each other but this has to be incorrect. What am I misunderstanding about water solubility and what would happen if the bases were exposed to water?

Water solubility only means that a substance is soluble in water. Usually it will not decompose (break into single atoms) in this step, as dissolving is a purely physical process.

So why is phosphate a "water soluble" molecule but yet it stays as "phosphate" in water? It doesn't dissolve in water it stays phosphate?

@BjarniJóhannsson see my answer below for an accessible explanation. If you are having trouble with the English words, you may want to look them up in your native language. You are confusing dissolve with hydrolyze.

You might be thinking of simple ionic compounds like sodium chloride, which when dissolved do separate into their constituent ions (e.g. sodium cation and chloride anion).

This question would be more on-topic at Chemistry.SE, but I'll give you a quick answer. A substance is soluble in water when its solid form (such as a sugar cube) completely dissolves in water to become a sugar solution. The sugar molecules themselves are unaffected, essentially - instead of all being bound to one another in a crystal, they are now floating around in the water, hydrogen-bonded to the water molecules. The proof is in the taste - solid sugar and sugar solutions taste pretty much the same. If the sugar had been broken down into component hydrogen, oxygen, and carbon, it would taste much different!
On the other hand, hydrolysis is what happens when water actually participates in a chemical reaction to break one or more molecular bonds within a certain molecule, breaking it down to two new molecules (or one molecule and an atom, or whatever). While sugar can be hydrolyzed, it requires either very high heat, or the presence of a catalyst such as an enzyme.

And it's more: If you remove the water, the substance will be the same as before. Dissolving is a purely physical process which will not change the molecule. This is only done during chemical reactions.

Except for ionic compounds which do dissociate when dissolved

It's about sugar and DNA. It is fine here at Bio.SE. Well answered too. +1

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


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Core Biological concepts explained to a Computer Scientist?
I am a computer scientist delving into Bioinformatics and I need to gain insight in biological phenomena. How would you explain three core concepts as:
Evolution, Selection and Variation, to a Computer Scientist? I am looking for something in the middle. I read Futuyma's book and was very useful, but I would like an explanation I can relate with my background, something to start building "bridges"...
Bibliography suggestions are welcome.

You might be interested in mathematical formulations of evolutionary processes. Here are some book recommendations. As you are a computer scientist, I suppose that you are aware of what a genetic algorithm (artificial intelligence) is. Genetic algorithm also provide good analogies.

@Remi.b +1 for the genetic algorithms

how about just open a molecular bio textbook?

Read on fishers fundamental theorem, the price equation, the breeders equation, and evolvability

Evolution

Evolution is the accumulation of genetic mutations that results in phenotypic variation (physical characteristics) where surviving variations are more suited to the environment the organism lives in, thus allowing it to survive better and -- critically -- reproduce as-good-as or better-than its competing organisms.
In terms of computer science this would be like a starting with basic CPU design with all the absolute necessities. Now, let's pretend every generation of CPU after your first is going to be randomly designed by something called "Pressure OS". Pressure OS doesn't care if the CPUs it designs match the needs of the consumer. PrOS is unfeeling. An OS of pure logic. ALL it will do is make a bunch of random ones, note which ones sell the best, and make the best-selling ones to be the template for its next round of random designs.

Selection and Variation

Selection is the process by which environmental pressures (low moisture, high heat, high altitude, available food, extreme pressures at the bottom of oceanic trenches, etc.) dictate how well each successive generation of organisms survive.
In our analogy, the Pressure OS is the cause of Selection. Some CPU designs aren't going to meet the needs of consumers (first-gen Atoms which could barely operate a toaster). Those ones won't be produced again. Others will be very successful (like the Pentium-4 Series which lasted for years) and will quickly outnumber the inferior ones.
Some designs, as odd as they are, will find success in areas outside enthusiast desktops or workstations. Like ARM designs which were never part of the desktop market, but found lots of success in phones and business devices.
Market requirements/environments, as met by the random variations produced by Pressure OS, created Variation in the types of CPUs available.
ARM Snapdragons could never, ever compete in the desktop enthusiast market. That's the realm of Sandy Bridges, Haswells, Semprons, and Phenoms. Then again, they're dramatically different designs -- which stem from common designs decades ago that have been heavily modified over the years -- that don't need to compete. Snapdragons and Semprons can co-exist because they fill different niches.
Now, when consumer needs change again -- if everybody gets tired of mobile phones, tablets, and desktops in favor of cone-shaped personal assistants which go in your ear -- then designs will change again under that new pressure. Eventually CPU one design will become the standard for that particular piece of hardware, and you could say that CPU variation had evolved to get there via selective pressure from consumers.
Biology operates in the exact same way, except the selection process is instigated by environmental pressures to produce organism variations that can successfully reproduce. It's also been going on for >3 Billion Years.

I'm happy to see that someone came from the hardware point of view :) I really like your examples.

Please note that these are just analogies not exact definitions.
Okay so let's imagine DNA as string of 4 letters that is the program code of an organism. Also the running environment is a good analogue to the biological environment (RAM, CPU time, disk space - as resources like food, water etc.) Genes of organism could be imagined as methods of an object like in object oriented programing. Let's define some functions:
Reproduction: copies the string and creates a new instance of the organism (like a new instance of the program) - cell or an offspring - this stands for asexual reproduction. Sexual reproduction takes two instances of the program and randomly exchange their functions and create a new instance with this shuffled code (recombination).
Mutation: induces random changes to the string at random times. This ensures that different "versions" are present of the code. You need mutation for evolution to work.
Also you need Selection - or rather selective pressure -  that is like changing the environment - more efficient codes will survive, the rest die of (aka crash, run out of memory (food)) etc.) Selection drives evolution forward. Also programs can interact with each other and function as a selective pressure - think of anti-virus programs and trojans or viruses - you need better and better AV programs because new viruses come out, and bad guys need new viruses because AV virus programs keep getting better and better - they both put selective pressure on the other and drive each other's evolution.
(Genetic) Variation: think of a group of softwares with similar function: like text editing. These are like different individuals of a species because they can do the same thing but they are all a bit different. These "species" evolve by gaining new functions by mutations (the programmer adds new code sections - mutation), and after they gain enough new function they turn into a new software - new species. Evolution takes a lot of time to produce new species - as does coding a new software :).
I hope this helps.

It might be good to remind your readers that analogies are just analogies. One must not make the mistake of bringing such analogy to far away and complain about incompatibilities. Selection that is like changing the environment. A changing environment would rather be a change in selection pressure. For example the concept of variation is limited to genetic variation in the analogy you presented.

@Remi.b - Thanks for pointing things out, I'll edit and refine my answer.

Why the downvote?

I want to make a declaration of innocence for this downvote :) Unexplained downvotes are always bothering me too.

@Remi.b - I've not accoused anyone, I'd not assume that you or anyone would down vote a competing answer (if it has no obvious incorrectness etc.) - that's just low... But i see down votes as tool to indicate more serious problems with a post.

@Remi.b - Oh and by competing I mean friendly sharing of different opinions / viewpoints not some "who's the big boss around" type race.


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Why do naked mole rats live in colonies with a queen?
What was the evolutionary advantage in having queens? Is it because the ones that had queen like tendencies in the new environment had kids that cooperated better giving higher chance of survival of the colony? Do the worker naked mole rats have an evolutionary advantage in not reproducing because it allows them to devote more energy to the long journey to make one of their siblings the new queen?

Hello! Do you already have a good understanding in social evolution? If not, you will probably want to read this post first. The above post only talks about how genetic correlation between individuals can lead to social traits. It doesn't talk about behavioural correlation due to reciprocity for example. Make sure to read all that.

Then, well... I don't know what's causing social (or apparently social) behaviour in naked mole rats. Here is an article that will likely bring some light to the discussion


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Myopia as a microscopic superpower?
A few years back my Physics professor made a joke that his myopia (i.e., nearsightedness) gave him a "superpower" that allowed him to see close objects much more clearly than someone with typical eyesight. For example, reading small fine print or tiny details on a surface. The physics made sense, as a person with myopia should have a closer near focus point.
Recently, this belief was challenged by a normal-sighted friend. I did some Google-ing and couldn't find any evidence or articles confirming or refuting this belief. All I found was a lot of anecdotal evidence.
My question is: Is this belief correct? Are there any scholarly articles or similarly trustworthy sources confirming this?

I have never seen such an article, but I agree with your professor. I used to have 7 degrees of myopia, and it allowed me to see insects very close, in great detail. Now I have operated, and don't have this "superpower" anymore.

I would love to find more details about this, only found this old thread from 2015. I have myopia and can say that this is true, I called a superpower myself a couple times too, hahaha. It’s actually helpful for some ordinary tasks during your day. It would be nice to find some tests about this subject.

Short answer
Myopes may have some benefit in terms of identifying small objects due to their ability to focus objects nearer to their retina than emmetropes, but only marginally so.
Background
The more myopic you are, the more blurred your distance vision, but the closer up you can see clearly. Hence, myopes have a range of clear vision that is closer to their eyes than emmetropes (normally sighted people) (Triad Publishing).
A young emmetropic adult can focus at an object some 10 cm away, which is defined as an amplitude of accommodation (lens adjustment) of 10 diopters.
A severely myopic eye can be up to minus 6 diopters, bringing the tally from 10 to 16 diopters, meaning you can view something up to 6 cm instead of 10 cm.
Bringing objects closer increases retinal image size and hence increases spatial detail. Going from 10 to 6 cm increases the retinal angle by 10/6 = ~1.7 x, so not even a doubling of the angle.
A random search for a magnifying glass for the visually impaired that aids in reading small print (newspapers etc.) yielded one that magnified 4x (16 diopters):

Clip on reading aid. Source: Eschenbach
Microscopes typically have lenses with magnification factors from 4x to 100x.
So in all, myopes do not have microscopic superpowers. A standard magnifying glass for the visually impaired magnifies several times more than a severely myopic eye.

The changes in image size in myopic eyes are not as large as one would imagine. In fact, they are pretty close and the myops are probably not aware of them until the proper correction is placed which affect the image size in a much greater degree.
You can see on the image that the sizes of retinal images are very similar - the uncorrected image size is shown in Y' row:
(Y'' is an image size with a proper corrective lense)

It is true the near point of accommodation of myopic eye is closer that of emmetropic eye, but it is war away from "superpower" mentioned by the professor.
In addition, the discrimination ability in myopic subjects are greater than of emmetropes, because they able to see smaller points, but at the same time the image quality is affected as well, thus overall image quality is more compromised compared to emmetropic eye.


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Why reference genome is a reference?
I have heard that a reference genome such as humans is generated by randomly choosing samples from a group of donors. But why do we call the DNA sequence generated as a reference? Why should we believe those few samples can represent all humans, from which we need to align with?

Good question. It is a quirk of history - the initial genome sequencing work was WAY too expensive and WAY too laborious to even contemplate sequencing multiple genomes. Thus, an initial genome (later extended to a couple of genomes) was used as a "reference".
However, technological advances mean we can sequence genomes for under $1000 in a day now. Thus, the advent of things such as the 1000 genomes project (http://en.wikipedia.org/wiki/1000_Genomes_Project).

Having said that, as the answer below points out, the variation between humans is tiny compared to the overall similarities. Thus, a "reference" can be generated from a sample of one or few.

The main reason is because the genetic differences between individuals of the same species are tiny. For the vast majority of studies, they can simply be ignored.
Differences between individuals are usually (not always, but mostly) differences in SNP genotypes. These are single nucleotide differences which, while they can have phenotypic effect, don't really affect the ability of sequences to align. Sequence alignment software is designed to be able to deal with such small differences. For example, consider these two random sequences:
>seq1
ACCTTGCATCGGATCGAATTCGCGTTAGCGATCG
>seq2
GCCTAGCATCGGACCGAATTCCCGTTAGCAATCG

If we align them, we will get:
seq1            ACCTTGCATCGGATCGAATTCGCGTTAGCGATCG
seq2            GCCTAGCATCGGACCGAATTCCCGTTAGCAATCG
                 *** ******** ******* ******* ****

As you can see, despite the small differences in sequence, the two can be aligned very well. The same is true when you look at real data. My haemoglobin gene, for example, will align perfectly well against both yours and the one in the reference genome. In fact, they will almost certainly be identical or, at best, have a couple of different residues.
So, when doing work that is not about studying specific polymorphisms, we need a representative genome. Anyone's will do, unless they have a particularly serious mutation such as a chromosomal translocation.

To put some number, the average homology between human genomes is approx. 99.5%. As @terdon described, this relatively high homology (i.e. ~2,850,000,000 base pairs out of the total 3,000,000,000bp of the human genome will be identical) allows to align any human sequence to this so-called reference. This is of course in the scenario of no major chromosomal translocation, which usually leads to diseases.

@vajra78 it probably never will actually. These differences are irrelevant for most studies. You almost never care about individual genotypes, not unless this is a medical issue involving a specific individual. The point here is alignment and that is not affected by such small changes. Studies at the species level (looking at evolution or genetic regulation etc) rarely, if ever, need to take into account the intra-species variation.

Reference genomes do not accurately represent the set of genes of any single person.it is created by fragments of various donors, which when built,is used as a template for creating the real genome. Though we will find All humans are 99.9 per cent identical and, of that tiny 0.1 per cent difference the reference genome might not be 100% identical to the real genome.Every reference genome con be sequenced again and the gaps can be reduced each time. We can reach a point where we can say that the accuracy is high enough to be used as a reference platform for constructing the real genome

The same question sticked in my mind a month ago. Even @terdon gave an explanatory answer, I want to make a small contribution.
When I asked similar question on seqanswers *, one of users gave the link of the study Ashley Lab in Stanford. They generated the "Synthetic major allele human reference genomes".  (1)
They combined the current reference sequence (in that time it was hg19), with the 1000Genomes data of variants with high allele frequencies. This combination creates three different reference genome of three human population (YRI, CEU and CHBJPT).
This synthetic reference sequences represents the variants that are highly seen in these population. It is possible to download these genomes from their page.

Dewey FE, et. al. (2011) Phased whole-genome genetic risk in a family
  quartet using a major allele reference sequence. PLoS Genetics 7(9):
  e1002280. http://dx.doi.org/10.1371/journal.pgen.1002280


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What's the frequency resolution of the human ear?
I was thinking about audio compression (namely mp3), that "filters" out sound that we would not likely hear.

The MP3 lossy audio data compression algorithm takes advantage of a perceptual limitation of human hearing called auditory masking.
  from: http://en.wikipedia.org/wiki/MP3

I've also checked the wiki entry for auditory masking, and found this:

If two sounds of two different frequencies are played at the same time, two separate sounds can often be heard rather than a combination tone. The ability to hear frequencies separately is known as frequency resolution or frequency selectivity. When signals are perceived as a combination tone, they are said to reside in the same critical bandwidth.

My question is how much is this critical bandwidth or what's the smallest frequency difference we can perceive as two different tones, if you wish. Let's assume that both tones are equally loud, are coming from the same direction and distance and we are in a quiet room - so basically we eliminate as much noise and affecting phenomenons as possible.
As @ sanchises pointed out (thank you again!) in the comment section the frequency resolution is 3.6Hz between 1 and 2kHz. But since perception threshold is a function of the pitch of the sound I'd assume that the ability to resolve two tones would change with pitch too. Does anybody have any data on that? For example resolution X pitch graph.

possible duplicate of What are the lower and upper hearing limits of the human ear?

Just googling 'frequency resolution human ear' yields the wikipedia page on Psychoacoustics: Frequency resolution of the ear is 3.6 Hz within the octave of 1000 – 2000 Hz.

@Dane Not a duplicate; this question is about resolution, not range.

@Dane - I"m aware of the lower and upper bounds of human hearing, my question is not about that. I've specifically linked that my question is linked is related to auditory masking and the critical bandwidth.

@sanchises - I've googled many things, yet not the most obvious :S I got stuck around audio compression, and forgot to take a step back....

@poka.nandor - don't hold back on shooting at my answer - no worries :) Good question, and hard to answer! Feel free to criticize.

I would also ask - especially given the context of the question - whether there's any sort of training effect.  Certainly I can perceive a difference between classical music compressed with MP3, and the same piece at full CD resolution.  Which itself involves some downsampling compression: I recall that when CDs first came out, some audiophiles claimed to hear a quality difference between them and an analog recording, though I never could.

The frequency limen, or frequency resolution can be determined in various ways using psychophysical measures. You refer to a simultaneous method, in which two (or more) frequencies are presented at the same time. This has consequences for the test as different frequencies are perceived with different perceived loudness under constant sound pressure levels, meaning that additional cues are present besides pitch cues.
One carefully controlled study Zwicker et al (1957) in this regard defined the critical band basically as "those frequencies where no intensity summation occurs", meaning that adding those frequencies (below or above the center frequency) do not result in differences in loudness perception (as expressed in acoustic threshold of the center frequency). This method nicely prevents loudness summation cues by deploying them in the criterion. This article shows the following picture (after Zwicker et al. (1957)):

The critical band (upper graph) is dependent on frequency, and ranges from 0.1 kHz to >2 kHz.
The markedly lower difference limen of 3.6 Hz as touched upon in the comments may have been obtained using an alternative psychophysical test where the test frequency is modulated by another frequency (bottom graph). This procedure is based on adding a frequency to a certain sinusoidal stimulus, basically resulting in a single stimulus instead of two (or more). This procedure is technically not defined as a critical band and indeed results in a difference limen of ~3.5 hz and up. The other graph plotted in the figure is a masking procedure (middle plot), which basically determines the physiological overlap between frequencies in the cochlea in the intensity domain by determining the amount of masking from one frequency by another.
NB: The authors worked with headphones so no effects of direction.
Reference
Zwicker et al. JASA 1957; 29: 548-57

I guess you had to dig really deep to find this paper.... thank you!

I think you have already gotten ur question answered. The human auditory system has the resolution of 640 different frequencies, so dividing the hearing frequency range by this you could see the smallest frequency. although the bandwidth is not constant in the whole range (100 for frequencies below 500 Hz and 0.2f for frequencies above 500 Hz). Also, the auditory system of ours has a dynamic resolution of less than 1 dB.
hope I got it right :)

It is important to add references to improve the quality of the answer.


text:
How to do Sliding 80mer Window search against a database with fasta
I know how to do a 80-mer window search against a single protein
fasta35 -k 0 -w 80 -a -m 9 -C 20 -Q -3 -E10 -d20 -B tempQuery:0-80

FASTAbyGI15/378405189
fasta35 -k 0 -w 80 -a -m 9 -C 20 -Q -3 -E10 -d20 -B tempQuery:1-81 FASTAbyGI15/378405189
fasta35 -k 0 -w 80 -a -m 9 -C 20 -Q -3 -E10 -d20 -B tempQuery:2-82 FASTAbyGI15/378405189

....

This will give me the detailed results but I want to do the search against a database in Fasta like this website:
http://www.allermatch.org/allermatch.py/form
Can anyone help me?

Fasta utilizes a k-tuple method to fasten up the search. You could try and set the default ktup parameter to 80 ( you might have to recompile from source to do that). Or you could try brute force and manually chop your input to 80 amino acid windows and call fasta search for each, and then collect all the results and filter out those that are above the threshold.

I don't think fasta is the tool you want use, because the speed of a fasta search against a database involves a step where each record in the database is chopped up into shorter substrings, e.g. 3-mers or 4-mers, and that pre-compute step takes awhile. Then, for each search your query sequence is similarly chopped up into a list/table when you submit the job. Your query runs quite fast (yes that is how they named it) compared to the classical hamming distance calculation, because the best hits are targets with the largest number of k-mer matches (that is a slight simplification).

Yeah, what @poka.nandor said. I was going to add that classical textbook dynamic programming would be another approach to explore


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What is the maximum number of babies a human woman can have?
I know you could divide the female fertility period (~40 years, right?) by 9 months which would give something like ~50 kids (with no multiple kids per pregnancy). The limiting factor in this calculation is time but is there a biological upper limit as well?

How do you define the biological limit?
It very much depends on how you define a biological limit. If you prefer, it very much depends on how you define a human! Some women are completely sterile while others are highly fertile and there is genetic predisposition to that.  How much "perfect" should the genotype of an individual be so that it is still considered as a human? There is genetic variance underlying fecundity that is important to consider. For example, in your calculation you took lifespan as a constant but it obviously is not a constant. Fecundity is reduced by all these small mutations segregating in the human populations that reduce the fecundity of any single human. There exist no human that is free from all deleterious alleles. Imagine a giant woman with 10 independent reproductive system! Would she still be a human? That was probably kind of a too extreme thought experiment. Imagine a woman that can have a reproductive lifespan of 100 years. Would it still be a human? The issue behind this question reminds me an old post (now closed, I can't find it anymore) that asked whether a leopard would run faster if it had more legs. Well... one can imagine something running faster than a leopard, but it would not be a leopard anymore. So how many changes from a leopard are we allowed to make to answer the question. So I had to chose a definition of what a "perfect woman" is. Or a definition of a woman that would set this so called biological limit.
The definition I am using to answer this question
In the below answer, I will assume that by biological limit you mean the expected fitness of a female that would live in the same environment than we live in today but would not carry any single of the deleterious locus that are segregating in the human population. In other words I assume that you accept that the "perfect woman", that is a woman that would not carry any single of the deleterious mutations that segregate in the populations will set this biological limit to woman maximal fecundity.
Mutation load Theory
The decrease in the mean fitness of an idealized population where no deleterious mutations would exist compared to the realized mean fitness of a population is called the mutation load. The mutation (in an infinite population) is a function of the genome-wide mutation rate only. Let the genome-wide mutation rate in human be $U=2.2$, the mutation load $L$ in the human population is equal to $L=1-e^{-2.2}=0.89$. The estimates are taken from this video. You may want to have a look to the video in order to have a better understanding of why $L=1-e^{-U}$ and what are the assumptions of these calculations. The main assumptions are 1) infinite population size, 2) multiplicity of fitness effects at different loci and 3) additivity of fitness effect between alleles at the same locus.
So what does mutation load theory predicts?
The above calculation means that segregating deleterious allele reduce the fitness of the average woman by 89%! If we assume that an average woman can have 10 babies (this number is just a random guess) if she wants to, then the maximum biological limit of a "perfect woman" (in a world where there is no more competition than the one in which we are living) is $\frac{10}{1-0.89}≈91$  babies!
According to wikipedia, the world record is 69 and is owned by Mrs. Vassilyev. It is reasuring to see that the observed world record (69) is lower than the the biological limit we just calculated (91). If we were to know the distribution of maximal number of babies per woman (not to be confused with the realized number of babies), we could calculate the probability to have 69 or more babies and compare this probability to the total number of females that has ever lived (or the total number of females that would have never had the idea to have so many babies). Always according to wikipedia, the world record for men would be 867 and is owned by Ismail Ibn Sharif. However, sounds possible to me (but I really have no idea) that some sperm donor may have overshoot this number today.

Did you mean reassuring 69 ?

With many typos and english mistakes I meant It is reasuring to see that the observed world record (69) is lower than the the biological limit we just calculated (91) I edited the answer. Does it make sense? Thanks

Thanks! This is a very interesting approach to the question. Would be interesting to get an estimate of the number of babies for the average woman which would set a more accurate theoretical maximum. Btw isn't the perfect woman a Puerto Rican? Too bad she does not belong to the human genera :) (see PC3). This goes exactly along your thoughts.


text:
How can I use this data to make a function?
I'm currently in high school biology (final year) and am currently working on an assignment. I need to create some sort of interactive model, so I've decided to make a simulation-type program.
I've looked a bunch at lots of papers and journals and I was wondering how I could take the data and make a function out of it.
Here is one example (Pleasants & Oberhauser, 2012):

In particular, I want to know how to make sense of the values F_1,11; r^2; and P. I am finding a lot of these values in the papers I'm looking at so it would be awesome if one of you guys could point me in the right direction.
Thanks!

This is not really related to biology more like mathematics. The values you're interested in come from statistical tests, in your case linear regression that is indicated in the last line under the image. You should check math and statistical books for these.

Thanks for the advice. I thought posting under biology would be better than math because the function could be specific to biology? Clearly, my knowledge in this is pretty thin so thanks for pointing me in the right direction.

@poka.nandor yes this question is about statistics but those measures are so often used in biology that I consider them "part of the job".

Clearly, this question is about statistics and is off-topic here. cagliari2005 answered the question though. The answer might be a bit complicated though. You may want to follow an introductory course in statistics. You can find here an excellent introductory class of statistics. Good luck.

I'm voting to close this question as off-topic because it is about statistics. CrossValidated.SE would be a better fit.

@Remi.b. Agree might be a bit complicated. On the other hand I couldn't really explain it more simply as some fundamental bases in statistics are needed to understand p and r-squared.

I think it will likely get shut down on cross validated because it's about basics - open an introductory statistics book/ Web page/ Youtube video and you'll be able to get an answer, then if you're stuck ask about specifics on cross validated

I will not go too deep into the details but here some information to facilitate your understanding of these ubiquitous statistics in biology.
The F, $r^2$ and p-value are all equivalent statistics to measures the goodness-of-fit of a model against the data.
The F is the ratio of the $unexplained~variance~/~explained~variance$. I let you look out what the variance is. The F (originating from a F-test) allows, using the proper F-distribution cumulative density function (cdf) for the number of observation you have, to compute a p-value.
The p-value gives you the probability of obtaining the observed fit with your model (here a linear one) by random chance only. For example in your case a p-value=0.01 means that you have a 1% chance to observe this correlation just by chance. Usually the p-value threshold used to claim statistical significance is 0.05 (i.e. 5% chances to observe that fitting by random chance). In linear regression, the lowest the p-value the closest the distance (called variance) of the observed data point to the line.
The $r^2$ is the coefficient of determination (or the square of the correlation coefficient). This measure is very interesting as it give you an estimate of the "proportion of the data" explained by your model. For example a $r^2$=1 means that 100% of the variance of the data is explained by your model, in other terms your model perfectly fits the data. A $r^2$=0 in the other hand means that your model does not at all explain the data (no fits between your model and the data).
The $r^2$ and the p-value can be computed for any type of fitting, like trying to fit an exponential curve instead of a linear one. What you usually look for when modeling data is the highest $r^2$ possible. As all of this statistics are linked a higher $r^2$ means a lower p-value for an identical number of observations.

p.values are by themselves not probabilities, and nor do they refer to the probability of observing the fit by random chance only. P.values are the frequencies at which you would expect to see an effect size (be it difference in means, or a goodness of fit) as large as your observed one if the null hypothesis were true. Eg, a null hypothesis for a two sample t.test is that the means of the samples are equal).
probabilities are degrees of belief, p.values don't give you the probability of the null hypothesis being true.

@AnkurChakravarthy Frequencies are the exact equivalent of probabilities in this case. Having a frequency of FDR of 0.01 is exactly the same as saying you have 1% chance to observe this fit by random chance (or more precisely to reject the null hypothesis by random chance). I used probabilities as it makes p-values much more understandable (and useful) in my opinion.


text:
How does a microelectrode work?
On Wikipedia, the entire microelectrode page states only the following:

A microelectrode is an electrode of very small size, used in electrophysiology for either recording of neural signals or electrical stimulation of nervous tissue. Initially, pulled glass pipette microelectrode was used with later introduction of insulated metal wires. These microelectrodes are made from inert metals with high Young modulus such as tungsten, stainless steel, platinum and iridium oxide and coated with glass or polymer insulator with exposed conductive tips. More recent advances in lithography yielded to silicon based microelectrodes.

Can someone provide a more elaborate explanation of how it works?
Like ideally, I would like something as specific as the usual descriptions you see in introductory chemistry books for how emf works in a battery. In other words, I know how electric potential works, but I am not understanding the exact mechanism of the microelectrode works.
If there are many types of microelectrodes, just give me the properties of one involving small shafts of hollow glass filled with a conductive salt solution.
Pictures would be great.

A microelectrode is quite literally a small electrode and they come in a variety of shapes.
The glass pipette electrode you are specifically referring to is mostly used for patch clamp experiments. Patch clamp experiments are performed using various configurations:

Source: Leica
So basically there is the cell-attached configuration, where a patch of cell membrane is sucked slightly into the pipette. Upon stronger suction the membrane is ruptured and the whole-cell patch clamp configuration is obtained. Here, access is gained to the cell, but a high-impedance seal is maintained between pipette and cell membrane. Lastly, there is a configuration where the patch is broken off the cell to exclude effects of the entire cell. This patch configuration is often used to obtain single-channel recordings. Dependent on the exact technique an inside-out or outside-out patch configuration is reached (see the picture above).
Hence, the glass pipette is basically only there to obtain a proper seal (cell-attached), to gain access to the cell (whole-cell), or to break off a piece of membrane. Notably, in whole-cell mode the pipette provides a means to administer compounds into the cell (think ions or drugs).
The recording electrode is situated inside the pipette and is a simple metal wire (platinum or platinum/iridium) and nothing different from any microelectrode as you rightfully state in your question. The electrode wire simply picks up a voltage difference (or current flow) between the interior of the cell (in whole-cell mode) and the exterior. The exterior is measured using a reference electrode outside the cell.
Furthermore, current can be injected to stimulate the cell, or to current-clamp the cell at a specific current. Likewise, voltage can be applied to voltage-clamp the cell. Therefore, an inert material is often chosen such as platinum or platinum/iridium to maintain integrity and prevent electrolytic breakdown. Electrodes are made out of metal to provide a low-resistance means to pick up currents or voltage-differences.
Voltage differences or currents can be amplified with an amplifier, registered and analyzed. See the following picture for the basic recording setup:

Source: Robinson et al. (2013)
Reference
 - Robinson et al. Front Neur Circuits 2013; 7: 1-7


text:
Are all action potentials the same shape and amplitude when graphed with respect to time?
The most common visualization of an action potential is a graph of the difference in membrane potential (y axis) at a particular time (x axis).
According to my textbook Cognitive Psychology by E. Bruce Goldstein, an action potential sent from neuron down the axon remains the same. That is, if we plot the action potential as described above, then at each as it is propagated down it will have the same shape on the graph (within some range of error obviously, but he is saying the error is trivial).
But he then says on page 34

One way to answer the question of how action potentials determine different qualities [(e.g. taste of something sweet)] is to propose that the action potentials for each quality might look different. However, [Edgar] Adrian rules out that possibility by determining that all action potentials have basically the same height and shape.

My Question
Can someone confirm these two facts:

Once an action potential is sent from a given neuron down the axon, does the shape and amplitude remain constant as it is propagated?
Do all action potentials have the same amplitude and shape?

Generally speaking, yes. For reference see this paper in Nature
This is Fig. 7 from it with comment:

Reason is that most axons are not passive tubes of electrolyte with leakage (in which case AP would be attenuated along it) but rather active media with membrane potential across that have ion channels that reproduce initial action potential along the axon. However, in more passive tubes, like in dendrites, action potentials might be attenuated.

Generally, no. Amplitude of action potential depends on properties of ion channels, at what potential, for example, $K^+$ channels will open to start repolarization (peak of AP). Duration also depends on properties of ion channels. But since there are not a lot of variability in ion channels and extracellular ion composition is mainly same in animals, most of APs will have same shape/duration/amplitude.

Short answer
Action potentials differ in shape between neuronal cell types, and action potentials may even change shapes during action potential propagation within one and the same axon.
Background

Once an action potential is sent from a given neuron down the axon, does the shape and amplitude remain constant as it is propagated?

Although the textbooks will typically say action potentials are transmitted without their amplitude being changed this claim is theoretically virtually impossible due to the many variables encountered in and around the axon. For example, axons in the sciatic nerve may extend to a meter and it is virtually impossible to keep the exact conditions along that length exactly identical. The amplitude of the action potential is mainly dependent on the influx of Na+. Slight variations in membrane potential, concentration of sodium, or channel (subtype) densities may therefore change the amplitude. In addition, temperature affects action potential amplitude (Hodgkin & Katz, 1949) and slight temperature differences along long axons may therefore be expected to alter amplitude. Likewise, shape may alter as well. For example, glutamate released alongside axons of hippocampal pyramidal neurons results in widening of action potentials (Sasaki et al., 2011).

Do all action potentials have the same amplitude and shape?

Therefore, given the answer under question 1 no, they do not have to. Even a propagated action potential in a given axon may change amplitude and shape, as said. Most notably, different neuronal types may in fact be classified according to their action potential morphology, such as the various neuronal types in the dorsal root ganglia of the spine that can be differentiated based on their duration (Villiere & McLachlan, 1996).
References
 - Hodgkin & Katz, J Physiol; 109: 240–9
 - Sasaki et al., Science 2011; 331: 599-601
 - Villiere & McLachlan, J Physiol 1996; 76: 1924-41


text:
How does a change in the potential across a neuron's membrane get turned into a signal that is sent down the axon?
I understand

How a signal is propagated down the axon.
How the membrane potential of a neuron changes during the course of it's "firing".

But I don't understand how physically the change in the membrane potential actual starts the signal down the axon.
A stimulus causes the voltage gated sodium channels to open and sodium ions rush in. This creates a positive charge density inside the cell and negative charge density outside. This difference is by definition a potential difference.  Potassium gates sensitive to this difference then open, the potassium ions to rush out, which again flips the polarity of the inside and outside such that positive charge density outside the cell and negative charge density inside.
But how does that actually lead to the signal that is propagated down the axon? Can someone explain?

As you pointed out sodium as sodium enters the cell depolarizes (becomes more positive). Recall the sodium gates open the more positive the voltage is, which in turn opens more sodium gates. If a patch of neural membrane is depolarized, the charge  diffuses into the nearby patches of neural membrane. This will open the sodium channels of the nearby membrane patch. Now once enough sodium channels open, the neuron will fire a action potential, at this point potassium channels open and potassium rushes out of the cell repolarizing it(making it more negative). Furthermore the sodium gates close at positive voltages which further repolarizes the neuron and prevents back propagation.
So the key is the influx of the sodium ions diffusing down the axon and causing a downstream depolarization of the axon.
I find this website instructive, as well as this picture:

Update:
As the voltage builds up in the soma the charge spills over into the Axon Hillock (an area of high concentration of sodium and potassium gates) If enough sodium ions diffuse into the axon hillock and passes a (somewhat ill defined) voltage threshold then the sodium gates will open and start the action potential. Then the action potential proceeds down the axon as described above
A useful metaphor is the soma, and by extension the Axon Hillock, sums up the synaptic input from the dendrites, and again, if its over the threshold then the sodium gates open, if not, they slowly return to rest.
The synaptic input can be excitatory (cause depolarization) or inhibitory(hyper polarization) depending on the type of receptors and channels in the dendrites, but in general these voltage changes in the dendrite diffuse down into the soma and are eventually reach the axon hillock.


text:
Solid mouse (C57BL/6) WT primers
I am trying to get a good pair (or better yet, library of pairs) of primers that give me one band in WT mice (C57BL/6). Do you know where I could find such a thing?
Alternatively, I thought of just designing a few sets of primers myself for highly-conserved regions. But that's quite a bit of guessing work (what regions, what pairs from what eprimer3 will calculate for me etc.).
So:

Do you know where such a database could be found?
If not, could you help me get started with creating it myself? What specific regions would in your opinion be particularly good for this purpose?

One band of what? Just a random genome segment, or are you looking to amplify something more specific?

Something I can rely on is there in all WT and most if not all transgenes.

This is impossible to be done. You can make primers to distinguish between mice which are mutated and wildtype mice (at least for one gene or locus), but you cannot do this for the whole genome. Here you could sequence your mouse and compare it to the reference sequence. What is your gene of interest?

I just want a pair (or library of pairs) of primers that will ~always work. As a positive control.

then use actin, or tubulin, or GAPDH, or one of a thousand other genes.

As @MattDMo mentioned use one of the so called housekeeping genes.

I have settled for two GAPDH primers with a short amplicon (~50bp):
>gapdh_rv3 <unknown description>
GAGACCTGAATGCTGCTTCC

>gapdh_fw3 <unknown description>
CTCCATTTCCCCTGTTCTCC

They provide consistent and good controls, as seen here (lower bands):

how do you know those aren't primer-dimers?  you should aim to amplify >= 100bp

Because my primers aren't complementary, and the band only appears if there is sufficient mouse DNA in the sample