text:
How is pain induced by blunt and sharp objects?
Normally, when something touch you, you won't feel pain. With a great force "touching" you, you will feel pain. However, if something that is spiky makes contact with you, you will feel pain. So, how much force should be exerted by a smooth/blunt object to make you feel pain? When and how does a spiky object make you feel pain?

It is a simple matter of biology and physics actually:
Firstly, pain is caused by the simulation of cutaneous nociceptors in the body, beneath the skin and are activated when the sensation crosses a threshold.

Nociception (also nocioception or nociperception) is the encoding and processing of harmful stimuli in the nervous system,[1] and, therefore, the ability of a body to sense potential harm. It is the afferent activity in the peripheral and central nervous systems produced by stimulation of specialized free nerve endings called nociceptors or "pain receptors" that only respond to tissue damage caused by intense chemical (e.g., chilli powder in the eyes), mechanical (e.g., pinching, crushing) or thermal (heat and cold) stimulation.[2][3] Once stimulated, a nociceptor sends a signal along a chain of nerve fibers via the spinal cord to the brain. Nociception triggers a variety of autonomic responses and may also result in a subjective experience of pain in sentient beings.[3] Nociceptive neurons generate trains of action potentials in response to intense stimuli, and the frequency of firing determines the intensity of the pain.[4]

From the wiki: https://en.wikipedia.org/wiki/Nociception
Now when you consider a knife, the surface area of the knife is small enough that it can cause damage. It's akin to holding a plastic sheet stretched tight and then piercing the sheet with the point of a knife. That is because the force is being transferred on a small point and hence easily extends the pain threshold.
However, when you consider a hammer, when the hammer touches you (lightly) you don't feel the pain because the force is spread over the larger surface area of the hammer and hence doesn't meet the threshold. However, if you hammer your finger in with force, the force being transferred is enough to shatter your bones, and in that case not only the cutaneous pain receptors activate, but the somatic receptors also activate, causing the feeling of pain.
TLDR: Knife has short surface area, and hence force transfer is over a small area, subsequently causing hurt. A hammer has a larger surface area, and hence unless more force is applied, the pain receptor threshold is not met and hence no pain.


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Is it possible to amplify every single piece of DNA through PCR?
Is there a way to perform non-specific PCR amplification for the purpose of amplifying every piece of DNA present?

what is the source of DNA? If minor variation is not a problem, then you can just grind more tissue/culture volume to extract more DNA. All cells in your body and most cells in cultures have (almost) the same DNA

actually, that is how RNAseq works. A lot of DNA is produced from RNA, then fragments of DNA have adapters (know short sequences) added to its' ends, and then those DNA fragments are amplified with PCR

Are you asking about whole genome amplification?

Ah, thank you, that was what I was looking for.

In short; Theoretically yes.
In practicallity no.

I agree with this opinion.
But, there are some methods to do so.
Ligating both ends with specific tags to amplify DNA fragments with the tag specific primer set. If you have different length of DNA fragments in original sample, PCR products could be biased.

In short; Theoretically yes.
In practicallity no.
Non-specific PCR require random primers to anneal to a target sequence to initiate replication during PCR. Theoretically this should anneal to every combination of bases and therefore allow the amplification of all DNA (or at least in a fragmented form).
Practically, all the primer combinations will have different primer annealling temperatures due to the differential base composition, making the amplification of fragmentation inconsistent, and in others down-right impossible.

source: Stack Exchange

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How do we know Denisovans had 46 Chromosomes
What allows sequencers to conclude that Denisovans had 46 chromosomes rather than merely knowing Denisovans had the crossover material arranged in 48 or say 44 chromosomes?
See http://genetics.thetech.org/ask-a-geneticist/denisovan-chromosome-2
What I am asking its what allows sequencers in this case to make an inference to an actual number of chromosomes (packaging) rather than the mere presents of corresponding DNA?
In the article above, interbreeding was rejected as a sufficient condition for inferring equality to humans in chromosome number and the author points to a man in China known to have the same cross over (fusion) known in humans and only 44 chromosomes indicating having the cross over that reduced 48 to 46 is also not a sufficient condition for concluding 46.

We know Denisovans interbred with other members of the genus Homo, therefore they must have had the same number of chromosomes. Individuals with different numbers of chromosomes cannot interbreed.

The referenced link says "As of now we don’t know have any hard DNA evidence for how many chromosomes Neanderthals had.   We are guessing that since humans and Neanderthals probably had babies together that they shared the same number of chromosomes.  But this doesn’t necessarily have to be the case." so this is not the reason for the inference of 46 for Denisovans.

@MattDMo People with Trisomy 21 are fertile, although at a much lower rate than in humans with the standard set of 46 chromosomes.

John, I think the answer is that without having a living cell that we can perform a karyotype on, we cannot know for sure. That being said, telomeres and centromeres are highly conserved, so if you're sequencing a female specimen, and it gives you 23 sets of centromeres and 46 sets of telomeres, then I would say that it would be safe to make the educated guess that the individual had 2n = 46.

Also, Svante Pääbo's group at the Max Planck Institute were the ones to publish the Neanderthal Genome, so you may want to take a look at their peer-reviewed publications to see if they address this issue.

@AMR I would agree that 46 would be a very good educated guess especially if the other choice is only 48.

File under tl;dr... but this may be a good starting point. http://rstb.royalsocietypublishing.org/content/royptb/370/1660/20130387.full.pdf . This article may get more into the technical aspects http://www.genomebiology.com/2010/11/5/R47

@AMR I don't have a reference at the moment, but I would imagine that people with trisomy 21 are only fertile if the fertilizing gametes have 23 chromosomes, so it all depends on how the extra #21 segregates during meiosis.

@MattDMo Actually no. Without reproductive aid, IVF and screening, there is a 50% chance that the offspring will be afflicted. Afflicted males tend to have very low fertility rates, but it is unclear if that has to do with problems with sperm production or just a lack of sexual activity, though there are cases in record of afflicted males fathering offspring. Afflicted females have fertility rates 30-50% that of unafflicted females. So while fertility is much lower than the general population, it is there.

@MattDMo Now if you wanted to make the case that Denisovins and modern humans couldn't produce offspring because the cell surface receptors that mediate gamete fusion were incompatible, that I would go along with. I think that the lethality with additional chromosomes comes from "dosage" problems and whether or not enhancer/promoter regions were preserved and TFs responded to the same chemical signaling and could bind to the DNA to drive transcription.

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What is the distribution of the number of heterozygotes in finite populations?
Consider a bi-allelic locus with alleles A and a. We denote the frequency of the A allele by $p$. Assuming absence of selection and panmixia, the expected number of heterozygotes is $2p(1-p)N$, where $N$ is the population size. We can also calculate the expected number of AA and aa individuals.
What is the joint probability distribution of the number of AA, Aa and aa individuals?

The distribution would be binomial.

Thank you. I developed my question a little bit to improve it. I am looking for the joint distribution for each possible genotype. Probably some joint binomial distribution. If you know the answer, please make it an answer.

It is a multinomial (trinomial) distribution with $N$ trials, $p_{AA}=p^2$, $p_{Aa}=2p(1-p)$, and $p_{aa}=(1-p)^2$. The probability to get exactly $n_{AA}$ AA genotypes, $n_{Aa}$ Aa genotypes and $n_{aa}=N-n_{AA}-n_{Aa}$ aa genotypes is
$$P\left(N_{AA} = n_{AA}, N_{Aa} = n_{Aa}\right) = \frac{N!}{n_{AA}!n_{Aa}!n_{aa}!}p^{2n_{AA}}\left(2p(1-p)\right)^{n_{Aa}}(1-p)^{2n_{aa}}.$$

Thank you! I edited your answer to write out the actual distribution (let me know if I made a mistake). +1


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PAGE gel in EtBr
I have been using TBE-PAGE gel to see small fragments of DNA by post-staining that means gel is stained with EtBr after electrophoresis.
Someone told me that you can add EtBr before polymerizing acrylamide, but I have never seen protocols like that.
Have you added EtBr before polymerization? Have you compare these staining methods? Let me know your experiences and knowledge.

TBE-PAGE gels generally take a while to run (especially the big Urea-PAGE gels for RNA) and the EtBr can quickly migrate out of the gel. Since PAGE gels are relatively thinner than agarose gels, staining post-run is not a problem. However, I have not really tried adding EtBr before polymerization.

You can also add some EtBr to the running buffer in the anode chamber. The EtBr is positively charged and will migrate through the gel towards the cathode while the nucleic acids in your sample will migrate towards the anode.

Thank you for the comments, all. I seems you can add EtBr in gel before polymerization. And I could see the problem when doing so, and the solution.


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Hardy-Weinberg Equilibrium Question
I have four questions concerning H-W Equilibrium:
(i) In a population of mice, the presence of black spots is the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.15, what is the approximate percentage of heterozygous genotypes in this mouse population? (Assume that the population is in Hardy-Weinberg equilibrium.)
I thought this implies that $q=.15$, $p=.85$ and thus the percentage of heterozygous genotypes is $2pq = .255$. Online answers seem to yield a ubiquitous $.72$.
(ii) In a population of giraffes, dark brown spots are the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.10, what percentage of the individuals in the next generation would be expected to be homozygous dominant?
Is this simply $(1-q)^2 = .81$?
(iii)   In a population of monkeys, the allele that causes long hair at the tip of the tail (H) is dominant, while the allele that causes short hair at the tip of the tail (h) is recessive. If 67% of the monkeys have long hair at the tip of their tails, what is the frequency of the dominant allele?
I worked this as $p^2 + 2pq = .67$, so $q^2 = .33$, so $p = 1-\sqrt{q} = .4255$. Again, this seems to come up on the internet as incorrect.
Moreover, in the below picture:

It seems to me that the answer should be $(1-G)^2 = (1-.45)^2$, but this does not appear as an answer.
Any help appreciated.

In a population of mice, the presence of black spots is the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.15, what is the approximate percentage of heterozygous genotypes in this mouse population? (Assume that the population is in Hardy-Weinberg equilibrium.)

We know the frequency of the allele (0.15) and we're looking for the frequency of the heterozygotes. $2\cdot 0.15(1-0.15) = 0.255$.

(ii) In a population of giraffes, dark brown spots are the result of a homozygous recessive condition. If the frequency of the allele for this condition is 0.10, what percentage of the individuals in the next generation would be expected to be homozygous dominant?

Yes, you are right it is 0.81

(iii) In a population of monkeys, the allele that causes long hair at the tip of the tail (H) is dominant, while the allele that causes short hair at the tip of the tail (h) is recessive. If 67% of the monkeys have long hair at the tip of their tails, what is the frequency of the dominant allele?

Although the notation is wrong ($p=1-\sqrt{q}$), the result is correct.

[last question]

As both genotypes GG and Gg are grey, we know that $p^2 + 2pq ≈ 0.45$ (Rather looks 0.48 from the figure though), where $p$ is the frequency of the G allele. From that you can calculate $p$ and $q$ and therefore calculate the frequency of the double homozygous gg

For the first one, .385 was not an answer choice.

Ha ha I somehow misread the question. Sorry about that, it is fixed now.


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Evolution of a Population
Scientists observe a newly established population of sexually reproducing plants growing on the shore of a small island. An observable trait of the plant has two possible phenotypes. It is determined by a single gene, with the dominant allele having complete dominance over the recessive allele. The first generation had 26 plants with the dominant trait and 25 with the recessive trait. The data below is from the first six generations of this population:

Use the data to explain the changes in phenotypic frequency from generation 1 to 3.  I'm not sure how to explain the increase in the recessive trait for generation $2$ to $3$. How would a population go from $p^2+2pq=1$ to $q^2 \simeq .2$?
Do you think this population is in Hardy-Weinberg equilibrium? Support your answer.  No, I don't believe so, since the population seems to change constantly in both the total number in the population, as well as the number of individuals with each trait.
Propose a possible explanation for the change in phenotype frequency from generation 5 to generation 6. Perhaps a climate change or the introduction of some new factor such as a  drought or new preadator?

You should probably take a step back and review Mendelian genetics first. It has to do with the fact that the dominant trait has complete dominance over the recessive trait. This means that while the offspring of a homozygous dominant and homozygous recessive plant will all be genotypically heterozygous, their phenotype will still be of the Dominant trait. So if Red flowers are the dominant trait and White flowers are recessive, then the heterozygous genotype will have Red flowers, and you will not be able to tell genotype from phenotype of thing individual offspring until the next generation.

So let's say that all of Gen 1 is genotypical homozygous. WW for red flowers and and ww for white flowers. To get generation two all of the ww plants will have had to be pollenated by WW plants. This will lead to 100% Ww offspring for those pollinations. There could be WW offspring as well in the mix, but you cannot be certain. The only thing that you know for sure is that no ww pollenated another ww in Gen 1 because you would have seen a phenotypically recessive trait. When Gen 2 breeds, if a WW pollenates a Ww, then the 50% WW and 50% Ww, but still phenotypically red.

If however, two Ww's breed, then the distribution is 25% WW, 50% Ww, 25% ww. As the 75% Red 25% White distribution in the Gen 3, then you can go back and say that all of the offspring from Gen 2 were Ww, so no WW pollenated another WW in Gen 1, besides the fact that no ww in Gen 1 pollenated a ww. I am going to leave you to think about the other questions on your own.


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Why does Nature use a 4-level system to encode information in DNA?
First, I am not a biologist, so this question might be naive:
Computer information processing and storage is based on 2-digit system of bits with values 0 and 1. Now, DNA stores the information in a 4-digit system: A, C, G, T. Three base pairs form a codon and can encode 43 amino acids.
Is there a good reason why a 4-level system (which can store 2 bits per encoding entity) evolved rather than a 2-level or a system with a larger number of symbols in the alphabet?
Put differently: Why was a binary system not preferred for storage and processing of data? In computing, binary is much easier, and the very few tests of exotic higher-level data processing have not really been successful.

At an abstract level, both systems perform information storage and processing. My question was not whether living organisms are computers, but why - on the abstract level of information, why a 4-level encoding system has been favoured. Your comment seems to be not constructive - but maybe I misunderstood something?

Why not? There is no inherent drawback in a base 4 system instead of a base 2. In the absence of selection pressure, the precise system evolution ended up with may just be a coincidence.

It's an interesting question but I doubt that it has an answer, only hypotheses. This paper may interest you.

@Roland how do you know there was no selection pressure; i can't imagine that this was the first and only system that was developed - Looking at the complexity, I can't believe that there were no prior steps of more primitive information encoding systems, and not more than one of such systems competing.

@canadianer thanks for this paper, that looks pretty cool! as far as i see, they start already with 4-nary logic. but the structure of the info-encoding, using two nb per codon is great!

Well, we really have no way of knowing, but I for one can't imagine what the selection pressure in favor of a binary system would be. Can you give an example? If anything, since a base 4 system carried more information per base, it seems more economical. But my guess is the chemistry was much more important than any of this.

The basic question perhaps is, "why DNA has 4 bases at all".  Next comes "why use three for a codon".. In any case the answers can only be speculations.

@Roland as a physicist I can only speculate, so that might be naive; but of course i can see reasons favoring binary systems (involved logic is much easier thus error correction might be much easier; maybe with binary only, there is a simpler chemical system to encode information, which might be significantly smaller/more robust than DNA); or higher-level systems (more information in less carriers, so the code might be much smaller). I'm sure there were real biological scientists who asked that questions, and came up with different interesting hypothesis. That's what I'm searching for :-)

My understanding of the information content, and coding capacity is that a single nucleotide site can contain a maximum of 2 bits of information, and therefore a codon triplet can contain a maximum of 6 bits of information. Where did base 4 come in? You may find reading Tom D Schneider's treatment of the ~ 70% efficiency of the genetic code both interesting and germane.

@mdperry If one nb carries 2 bit of information, it is (at least) a 4-level system. the 4 levels in DNA are A,C,G,T. Did you read my question?

When you say 'one nb' is that an abbreviation for 'nucleotide base'? The common abbreviation is 'nt' for 'nucleotide'. Reading back through this thread I see some people are using 'base' as in nb or nt, but some posts use 'base' for a counting system so base 2 is binary, base 10 is decimal. I am ignorant of the term you use '4-level' or '2-level' for that matter. I was probably confused.

"All of our information processing and storing is based on 2-level logic, bits with 0 and 1." You take it as a given that this an organic, long-standing construct, but it is intimately related to the mechanisms by which computers work. Transmission of data and calculations using computers rely on circuits which output either high or low voltage signals based on the voltages of their inputs. Because the exact voltage can vary significantly system to system and circuit to circuit, fidelity is maintained by differentiating only between  high voltage and low voltages (on and off or 1 and 0).

I would argue that in the modern computers the system is not actually just binary. Given that words are 32/64-bit long, the base can be seen as 2^32 or 2^64 (if we draw the parallel with DNA encoding). But at the very least the base is 256 (byte).

The current hypothesis is that RNA came first, DNA and proteins came later. So the reason that four bases are used might be related to the initial RNA world, and then DNA just reused the already existing RNA bases in a slightly modified form. In the RNA world, all functions had to be performed by RNA. Having more bases available than two would likely be important to be able to adopt various structures and create binding pockets or active sites for ribozymes.
You can't really think of the genetic code as an abstract data storage device. There are physical and chemical consequences to the choice of encoding. For example, proteins have to be able to bind to DNA and recognize particular patterns. With your binary code, the recognition sequence would have to be longer, because each basepair contains less information. The tRNA anticodons would have to be larger for protein biosynthesis to work with the binary code. Another issue that plays a role in some processes is that GC base pairs are more stable than AU/AT base pairs.
These are all just hypotheses. Evolution doesn't necessarily choose the best option, sometimes it is just the most convenient one that still works well.
I also found a review titled "Why are there four letters in the genetic alphabet?" that makes a similar point as my first one.

All present models to explain the fact that we have four base types in
  our genetic alphabet hinge, in covert or overt form, on the assumption
  that the genetic alphabet evolved in an RNA world

Another factor I didn't think of that is mentioned there is that while more bases make better ribozymes, more bases also decrease the accuracy of  replication.

In summary, two-dimensional RNA-like structures (and, presumably also
  the three-dimensional structures) become better defined as alphabet
  size increases, whereas the accuracy of replication decreases.

that is a wonderful answere, thank you! there are some insights I haven't thought of - especially the RNA world hypothesis. great! And thanks for the link to the paper!

"You can't really think of the genetic code as an abstract data storage device. There are physical and chemical consequences to the choice of encoding." This is a really good succinct sum-up.

Why does nature use a 4-level system (DNA) to encode information?

Short answer: Ease of manufacture, simplicity of matching, sufficiency for requirements. Fewer simple bases take less effort to create, provide fewer possible matches, yet is complex enough to code what is required while retaining sufficient degeneracy for success. Also it was the coincidence of replicase–alphabet co-evolution, both occurring in the same place at the same time.
Longer answer:

First, I am not a biologist, so this question might be naive:

Beginners and experts are welcome at SE.

All of our information processing and storing is based on 2-level logic, bits with 0 and 1.

Euler's number ($e$) is defined as the sum of an infinite series $\sum_{n=0}^\infty \frac{1}{n!}$ and has the lowest radix economy, but it's not convenient to implement in logic circuits. With the radix economy of $e$ set at 1.000, ternary is 1.0046 and binary is 1.0615.
Ternary computers have been constructed using ternary logic and while they are uncommon ternary logic is used in SQL; even in binary based computers.
Most, but not all of our information processing and storing is based on 2-level logic.

Now, DNA stores the information in a 4-level system: A, C, G, T. Three basepairs form a codon and can encode 4^3 amino acids.

Most, but not all.
The five canonical, or primary, nucleobases are: adenine (A), cytosine (C), guanine (G), thymine (T), and uracil (U). DNA uses A, G, C, and T while RNA uses A, G, C, and U.
In the laboratory DNA has been created with 6 and 8 bases, it is functional.
See the (paywall) report: "Hachimoji DNA and RNA: A genetic system with eight building blocks", Feb 22 2019, by Shuichi Hoshika, Nicole A. Leal, Myong-Jung Kim, Myong-Sang Kim, Nilesh B. Karalkar, Hyo-Joong Kim, Alison M. Bates, Norman E. Watkins Jr., Holly A. SantaLucia, Adam J. Meyer, Saurja DasGupta, Joseph A. Piccirilli, Andrew D. Ellington, John SantaLucia Jr., Millie M. Georgiadis, and Steven A. Benner. (Google Cache version).

"Fig. 4 Structure and fluorescent properties of hachimoji RNA molecules.
  (A) Schematic showing the full hachimoji spinach variant aptamer; additional nucleotide components of the hachimoji system are shown as black letters at positions 8, 10, 76, and 78 (B, Z, P, and S, respectively). The fluor binds in loop L12 (25). (B to E) Fluorescence of various species in equal amounts as determined by UV. Fluorescence was visualized under a blue light (470 nm) with an amber (580 nm) filter.
  (B) Control with fluor only, lacking RNA.
  (C) Hachimoji spinach with the sequence shown in (A).
  (D) Native spinach aptamer with fluor.
  (E) Fluor and spinach aptamer containing Z at position 50, replacing the A:U pair at positions 53:29 with G:C to restore the triple observed in the crystal structure. This places the quenching Z chromophore near the fluor; CD spectra suggest that this variant had the same fold as native spinach (fig. S8).".

Centrifuge tube C contains the spinach with the DNA containing eight bases.

Is there a good reason for why during early evolution, a 4-level system (which can store 2 bits per encoding entity) is favoured over a 2-level system or over larger systems?

Yes.

Copying fidelity decreases roughly exponentially with increasing size (N pairs) of the alphabet (keeping the length of the genome fixed). The reason for this is that as one adds more letters to the alphabet, they will resemble each other more and more, and hence the chance of mispairing and mutagenesis increases.
Overall metabolic efficiency and fitness are determined by the size, we have 20 amino acids to code for (smaller makes 16 or less) and 3 stop codons. So we have a space for 64, and rely on degeneracy to provide a degree of 'error correction' (synonymization) where errors are converted, usually to produce non-fatal errors. While seldom fatal translation errors can still cause rare diseases.

We are already running inefficiently, going to a larger number of pairs introduces unnecessary complexity and going smaller isn't available for the number of amino acids that must be coded for. Increasing the codon length makes DNA larger, as it is it must already be coiled to stuff it into the cells; one third larger DNA would better fit cells that are also one third larger.
In the opinion piece "Why are there four letters in the genetic alphabet?", Nature Reviews Genetics volume 4, pages 995–1001 (2003), by Eörs Szathmáry there are the following observations:
Page 995:

"There are four main constraints on the successful incorporation of a new base pair$^{[6–8]}$:

chemical stability (the base should not readily decompose);
thermodynamic stability (new base pairs should not destabilize nucleic-acid structures);
enzymatic processability (polymerases should accept the base pairs as substrates, catalyse addition to the primer and be able to carry on the process); and
kinetic selectivity (orthogonality to other base pairs).

All four criteria are important but the combination of the last two, which we might call replicability, has received particular attention
  because it is the main obstacle to adding to the genetic alphabet.".

Page 997:

"Theoretical arguments
  The feasibility of alternative base pairs raises the question: why are there four bases in the natural genetic alphabet? As Orgel pointed out, there are two types of answer: either evolution has never experimented with alternative base pairs or four bases ‘were enough’$^{[20]}$. The first option might hold for the hydrophobic base pairs discussed above (an adequate early synthesis might be lacking), but it is unlikely to be true for all of the hydrogen-bonding bases in a prebiotic ‘chemical mayhem’. At any rate, it does not explain why we do not have only two bases$^{[21–24]}$. It therefore seems worthwhile to pursue the second option: why might four bases be enough? If ‘enough’ is understood in terms of evolutionary stability, it means optimality within the frame of the structural constraints that are afforded by natural selection. Here, I describe attempts to show that four bases are optimal under STABILIZING SELECTION, especially when we consider MUTATION–SELECTION EQUILIBRIUM. I then discuss evidence for the optimal size of the genetic code obtained from in silico DIRECTIONAL SELECTION and finally analyse a more abstract contribution from so-called ERROR-CODING THEORY.".

Page 1000:

"Theoretical investigations based on structural, energetic and information-theoretic studies confirm the view that increased alphabet size
  decreases copying fidelity while increasing information density. This indicates that there must be an optimum alphabet size in terms of fitness, whether we assume that the genetic.alphabet was fixed in an RNA world or not.
...
According to the RNA-world-based view, the genetic alphabet became fixed more than 3 billion years ago$^{[31]}$, and the origin of the genetic code and translation happened subsequently$^{[42]}$. This line of reasoning indicates that the informational/operational division of labour between nucleic acids and proteins$^{[43}]$ has uncoupled the genetic alphabet from
  enzymatic functionality constraints. As the genetic code evolved in the context of a certain genetic alphabet, any further change of the alphabet would have been unnecessary and/or extremely unlikely.
If, however, the genetic code originated by the simultaneous co-evolution of nucleic acids and proteins (a much more complicated model), then the fixation of the genetic alphabet must be considered in this complex context. Here, the general insight of Mac Dónaill$^{[38]}$ helps: the information density of the alphabet is a useful concept, whether the exercised function is ribozymic or a messenger function in protein synthesis. In this case, the problem of the size of the ‘catalytic alphabet’ (the number of encoded amino acids) readily arises: why do we have 20 rather than, for example, 16 or 25
  different amino acids? It has been pointed out that some of the considerations discussed in this article (effects on catalytic efficiency and translation fidelity) apply to this related problem$^{[32}]$. However, another crucial factor is likely to be involved: the metabolic cost of producing amino acids. An amino acid that belongs to the same biosynthetic family$^{[43]}$ is expected to increase catalytic efficiency only modestly and its metabolic cost is likely to be small. By contrast, an amino acid from a new biosynthetic family is likely to confer a high enzymatic advantage, but is expected to incur high metabolic costs (for instance, many new ATP-requiring steps).".

References:
$[6.]$ Mathis, G. & Hunziker, J. Towards a DNA-like duplex without hydrogen-bonded base pairs. Angew. Chem. Int. Ed. 41, 3203–3205 (2002).
$[7.]$ Ogawa, A. K., Wu, Y., Berger, M., Schultz, P. G. & Romesberg, F. E. Rational design of an unnatural base pair with increased kinetic selectivity. J. Am. Chem. Soc. 122, 8803–8804 (2000).
$[8.]$ Kool, E. T. Synthetically modified DNAs as substrates for polymerases. Curr. Opin. Chem. Biol. 4, 602–608 (2000).
$[20.]$ Orgel, L. E. Nucleic acids — adding to the genetic alphabet. Nature 343, 18–20 (1990).
$[21.]$ Orgel, L. E. Evolution of the genetic apparatus. J. Mol.
Bio . 38, 381–393 (1968).
$[22.]$ Crick, F. H. C. The origin of the genetic code. J. Mol. Biol. 38, 367–379 (1968).
$[23.]$ Wächtershäuser, G. An all-purine precursor of nucleic acids. Proc. Natl Acad. Sci. USA 85, 1134–1135 (1988).
$[24.]$ Zubay, G. An all-purine precursor of nucleic acids. Chemtracts 2, 439–442 (1991).
$[31.]$ Szathmáry, E. Four letters in the genetic alphabet: a frozen evolutionary optimum? Proc. R. Soc. Lond. B 245, 91–99 (1991).
$[32.]$ Szathmáry, E. What is the optimum size for the genetic alphabet? Proc. Natl Acad. Sci. USA 89, 2614–2618 (1992).
$[38.]$ Mac Dónaill, D. A. Why nature chose A, C, G and U/T: an error-coding perspective of nucleotide alphabet composition. Orig. Life Evol. Biosphere 33, 433–455 (2003).
$[42.]$ Szathmáry, E. The origin of the genetic code: amino acids as cofactors in an RNA world. Trends Genet. 15, 223–229 (1999).
$[43.]$ Wong, J. T. A coevolution theory of the genetic code. Proc. Natl Acad. Sci. USA 72, 1909–1912 (1975).
Further Information:
Eörs Szathmáry’s Wikipedia web page
http://www.colbud.hu/fellows/szathmary.shtml - The Collegium Budapest is closed.
Scripps Research Institute
Steven Benner’s web page
http://www.chem.ufl.edu/benner.html - Dr. Benner left UoF in 2005.

Asked differently: Why did evolution not prefer to have a binary system to store and process data? For us, binary is much easier, and the very few tests of exotic higher-level data processing were not really successful.

Binary has nothing to do with evolution. Few of us can count to 255 in binary, we prefer decimal. Both ternary computers and SQL are "really successful", people prefer the alternatives.
This is intended to be an answer suitable for a layperson. Eörs Szathmáry’s article and it's associated references can be consulted for more details.

Thank you for this very interesting answer, after 3.5years. it gives a quite broader perspective.

@NicoDean You are most welcome. I referred to the newest information available and used it for my answer but ultimately an old opinion article offered a simpler explanation. There exists many theories, not all of them are disproved.

Just came across this post. Nice answer, @Rob. Really great effort. Your answer serves as a superb example of the high quality, well-cited answers we're looking for here. Thanks

General answer
The use of binary in computers arose primarily from practical considerations of how to represent digits using electric current or voltage (i.e. either ‘on’ or ‘off’ is the least equivocal). Such representation was not only — or even primarily — for storing information of different numerical types, but for programming logic using Boolean algebra. Physical storage of data can be in various different formats (magnetic, optical, electrical) but these are functionally equivalent and the retrieval and conversion of binary data into integers real numbers, text or images is predominantly a mathematical rather than a physical concern.
DNA has various functions, but these do not include a concern with programming logic. In  storage of data of different types, there is no problem representing different bases or radixes — sufficient different nucleic acid bases are available to represent base-4 digits. The most pertinent question in storage is one that does not arise in computer memory, that is the physical transformation of the information into other molecules. This can take the form of inverse copying of a genomic nucleic acid (DNA or, perhaps originally, RNA) in replication, the copying of one strand of information in a DNA duplex into a single strand of a related but not identical nucleic acid in the transcription to mRNA (messenger RNA), and ‘reading’ (translation) of the information in the chemical bases of the mRNA to produce a protein composed of amino acids — quite different chemical molecules.

Thus, the electronic or mathematical considerations that lead to the statement “In computing,
  binary is much easier” have no relevance for DNA and the genetic
  code, where chemical and structural molecular considerations are
  paramount. The supposition that there is a need to explain why information
  in DNA is not specifically binary is therefore false.

Speculation on the structural chemistry of the evolution of genetic information
The question of why 4-digit system (rather than 2- or 6- etc.) is still valid, but cannot be answered definitively. However, it is worth discussing to illustrate to numerical scientists the ways in which structural considerations might have determined the choice of information system. I shall consider two early stages in biochemical evolution at which the 4-digit system may have been selected for, after which — one should recognize — there might have been severe barriers to further change. Giving up Java and moving to Python (or even just changing from Java I to Java II) was probably not an option.
THE CHEMISTRY OF THE SELF-REPLICATING GENOME
I shall assume one of the main tenets of the RNA World Hypothesis — that RNA preceded DNA as the cellular genome. Even if the original genome were DNA, the question is the same — why four nucleic acid bases rather than two or six etc. — and the requirements of its chemical constitution are similar: to allow self-replication (hence the need to consider even numbers).
One might consider that an RNA with two bases arose first — let us assume adenine (A) and uracil (U) for the sake of argument. Later the cell acquired the catalytic ability to synthesize guanine (G) and cytosine (C), so that development from a self-replicating AU genome to an AUGC genome became possible. Assuming that this occurred before the amino acid-coding potential of the RNA had arisen, what might have favoured the more complex genome? It might have been something to do with the fact that there are three, rather than two, hydrogen bonds in a GC base-pair, perhaps producing a different RNA:RNA structure which was either more stable or easier to replicate for some reason. Alternatively it may have had nothing to do with the structure of the RNA:RNA helix, but was a side-effect of the acquisition of additional bases the greater chemical versatility of which enhanced the enzymic functions (ribozyme activity) of primaeval RNA.
If more meant better, why not six bases, rather than four? There might be specific chemical reasons like the slower development of the enzyme activities to produce other nucleic acid bases, or that with more bases the possibility of mispairing of bases was higher. (The ‘Goldilocks principle’ takes one a long way.) Or it may have been that the system worked well enough, was followed by the development of a triplet code, at which stage the system was frozen.
THE STRUCTURAL CHEMISTRY OF TRANSLATION
The die may have already been cast in the genome, above, but it would be a shame not to look at the chemistry of the decoding of the genetic information, as it is hardly a consideration for computer systems. So let us consider a competition between closely related organisms, one with a two-base genome and another with a four-base genome (and even a six-base genome). The requirement is to encode the information for a number of amino acids that can give proteins functional versatility — somewhere about the 20 (plus termination signals) we have today. The  size of the codon  (the word size), is 3 in a 4-bit system, accommodating 64 (43) possible codons in a (the standard) genetic code. If a 2-bit system of data storage were used then a word-size of 5 would be required to generate 32 (25) possible codons, whereas a 6-bit system could reduce the word-size to 2 with 36 (62) possible codons.
The physical consequences of such different systems would be seen in the decoding process where an adaptor molecule — transfer RNA (tRNA) — delivers amino acids to the peptidyl transferase centre of the ribosome (at one end) while interacting with the messenger RNA (mRNA) at the other end through codon–anticodon base-pairing. One might argue that the tRNA anticodon of three bases fits into the loop at the end of the helical anticodon stem in a manner that allows it adopt a relatively precise position (yes, I know about wobble) where it can make appropriate contact with the mRNA codon bases (see diagram below).

A quintuplet anticodon and five-base interaction (although not impossible) would appear less naturally adapted to the structural chemistry of RNA. Similar objections would not apply to a  two-base interaction, although one might argue that total energy of interaction between two base-pairs was insufficient to prevent errors. The error consideration also applies to a binary system where the difference in energy between a five-base interaction and a four-base interaction (i.e. a simple mismatch) would be low. Indeed, if the hypothetical competition between 2-bit and 4-bit organisms had occurred, the 2-bit system would also have been more prone to error frequency through slippage during replication.
The Last Word…
…goes to Steven Benner, whose group has constructed 8-base DNA in the laboratory:

“The ability to store information is not very interesting for
  evolution. You have to be able to transfer that information into a
  molecule that does something.”

Just came across this post. Nice answer, @David. Really great effort. I certainly appreciated reading your succinct but detailed response. Always nice to see multiple excellently-written answers to a single question. +1. Thanks

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


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Rattlesnakes developing stronger venom
I have heard that rattlesnakes are developing stronger venoms causing more people each year to die from rattlesnake bites.
But why would a snake that is already very venomous need to develop stronger venoms? I mean for the venom resistant ground squirrels couldn't the snake just wait longer or maybe strike more than once before it eats?
And I could see this going to venom overload in the next few centuries. If rattlesnakes keep developing stronger venoms at the pace that they are then rattlesnakes could become as venomous as a cobra or worse. Along with that it might rattle less and less until it just stops using the rattle.
Is is because of the fact that we are developing stronger pit viper antivenoms(mainly by injecting rattlesnake venom, copperhead venom, and cottonmouth venom into an animal with a stronger immune system like a horse and after a while, getting the antibodies needed for the antivenom) that rattlesnakes are developing stronger venoms?

Can you add the source which says that the venom is getting stronger?

https://www.youtube.com/watch?v=CRf4u8qE4Vs This video mentions rattlesnake venom getting stronger and ground squirrels becoming more resistant to rattlesnake venom.

@Caters Youtube is not generally considered a valid source of reference. There must be some kind of report that says so, unless they wouldn't have made the documentary. Even though the documentary is from a credible source, the first exercise should be to verify it. Because the rest of the question is based on the assumption that the initial statement is correct. Also, one cannot watch the entire documentary for a specific fact.

Also have a look at this

I did find an article which mentions the venom strengthening:
http://www.sciencedaily.com/releases/2012/06/120605102638.htm
It may be an evolutionary bonus. Snakes with the most potent venom may leave fewer survivors, particularly with something like humans who would hunt down a snake if they could find it. A snake which leaves fewer survivors may be better able to escape. It may also have more successful hunts which may have been what lead them to become poisonous to begin with.
Unlike the antibiotics arms race against bacteria, it's unlikely that antivenoms are the cause of more dangerous snakes.
As far as "centuries from now" we really can't hypothesize whether more potent venom will continue to be a more helpful evolutionary trait. More potent venom doesn't have an infinitely continuing effectiveness. After a certain point, whatever bitten isn't any more dead with a stronger poison.

Please vote for my answer and marked it as "answer" (the check mark) if you found it at all helpful. Your questions are conjecture and you are not understanding how ecological systems work. The changes in venom are small and not infinite. Other systems tend to balance changes appropriately. The only big changes happening more rapidly than nature is able to cope with are those made by man. It is highly unlikely that a small increase in poison effectiveness will throw the entire system off course.


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Nature of Dengue Fever Genetic Material
Once the genetic material for Dengue Fever is inserted into the human DNA, would the Dengue Fever molecular material be in the form of its own isolated DNA fragment or will it be inserted directly into some existing piece of our DNA?

I'm looking at the life cycle for dengue virus, it looks like a positive-sense ssRNA virus. The viral genetic material doesn't integrate into the host genome. Someone correct me if I'm wrong!

@Kendall you are correct. ss(+)RNA viral genomes behave like mRNA in the host, and are directly translated by ribosomes. The viral proteins thus produced then direct production of more genomes and the assembly of virus particles to infect more cells and other hosts. Viruses that integrate into the host's genome are called retroviruses.

Ah, thank you for the clarification. If you wouldn't mind posting that as an answer I could accept it.

In a 2011 Nature review they provide a figure for the life cycle of the Dengue virus,

Source: Immunity to dengue virus: a tale of original antigenic sin and tropical cytokine storms
The Dengue virus is a positive-sense ssRNA virus. This means the ssRNA that enters the host may immediately be translated. The viral ssRNA does not integrate with the host genome!


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Are gizzard muscles voluntary or involuntary?
I started raising chickens this year. They have amazing appetites, and I often wonder what eating is like for them. They have no teeth, so they don't chew their food as they eat it. They do seem to have some sense of taste, because they often bite off a bit of something and then spit it right back out. But the only equivalent of chewing for them occurs in their gizzard. Because the gizzard is pretty far down the digestive tract, I would assume that it's an involuntary muscle. But all chewing being unconscious for them also sounds kind of crazy.
I'm trying to discover the answer to this question on the internet and I'm surprised that the answer hasn't been easier to find. Does anyone here know? Do birds masticate unconsciously?

As a guess, I think it would be controled by smooth muscle tissue since wikipedia states that it is a "modified stomach". Therefore, since smooth muslce tissue is controled by the Automatic Nervous System, I would say they do not have conscious control. Although I have read that some birds swallow stones to aid in digestion. https://en.wikipedia.org/wiki/Gizzard  , https://en.wikipedia.org/wiki/Peristalsis , https://en.wikipedia.org/wiki/Enteric_nervous_system

I found the same in this book, published just over 100 years ago. The book appears to be the result of some pretty rigorous study, so I expect it is a reliable source.
On page 294, it refers to the gizzard as an involuntary sphincter, and again on page 302 it refers to the grinding of food in poultry as involuntary. In fact it says that because poultry grind all of their food, whether it needs it or not, they found that chickens digest whole grain corn more completely than if the grain is first cracked or ground. That is in contrast to other farm animals studied. I also find that odd, because I have noticed that my hens strongly prefer cracked corn. I've often seen them pick up and cast aside whole or mostly whole kernels. I guess digestive efficiency is not their top priority.

Involuntary. The gizzard, like our stomachs, works unconciously. However, chickens do choose to peck up stones to help along the process, whether that is by instinct or otherwise. (I raised chickens a long time but a proper reference is below)
This book on commercial poultry raising says involuntary


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Is T7 promotor leaky in DH5 alpha?
In my experiment I found that a GFP gene under T7 promotor in high copy number pTAC-2 vector is showing green fluorescence producing colonies of DH5 alpha under UV light. what could be the possible reason?

Shouldn't pTAC have the tac promoter and not T7?

You got a T7 phage contamination?

Did you eliminate autofluorescent activities?

Confirm your strain has DE3 or other mutated lacp? Best practice to include selection antibiotic for the lac cassette as well. Also @243 answer above. Finally Check agar for any supplements and run map on plasmid to confirm it is ptac

Consider the phenomenon of zygotic induction, as originally observed by Art Pardee, Francois Jacob, and Jacques Monod (sometimes called the "PaJaMo", or "PaJaMa" experiment): regulation of a repressed promoter can be affected by the copy number of the promoter in the cell. Put another way, if the copy number of the lac operator in the cell is high enough to bind or titrate all of the available lac repressor protein in the cell, then some of the lac promoters in the cell will be expressed.


text:
Seeing through the rain
This question leads me to wonder about seeing in and through rain.
From visual point of view, rain is light-bending droplets moving downwards, unformly in steady rain, less uniformly if there's variable strong wind. At least human brain is pretty good at filtering out the rain and seeing the stationary background.
Is this ability just physics, and no special adaptation needed? Or is it a biological ability, our eyes and brain doing some "heavy lifting" to be able to see as far as possible in rain?
If it is biological, evolved ability, then is there difference between different animals on how well they see in rain, compared to how well they see in clear weather? Has the ability evolved rarely, or does it arise naturally and easily if it gives advantage to a species? I suppose the only interesting animals here are those, which see far in clear weather to begin with.
I'm obviously looking for some real research done on the subject, not just speculation.


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Trial pre-registration service that accepts non-clinical trials, or specifically ecology?
I'm in the early stages of designing a trial in ecology. I'm interested in pre-registering the trial, as suggested here.
My concern is that all of the registries (that I can find) deal specifically with clinical trials, not ecological or general natural-sciences research. Does anyone know of a service that would accept pre-registration of non-clinical biological trials?

Did you try OSF.io?
They offer a free service where you can preregister trials and give them a timestamp with a DOI number etc.
I do not know if this is exactly what you are looking for, but it's the easiest solution for preregistering and I am quite sure that it would be enough to get the "preregistration" badge when you are finally ready to publish.
Here is more info on how to do it and what is essential for preregistration.

It looks like the 'Registrations' feature of OSF should satisfy a reasonable journal-editor that a study has been pre-registered. Answer accepted.

An addition to that - it seems that OSF plans to offer a "financial reward" for pre-registration, see https://osf.io/x5w7h/


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How to know the gestation time of pregnant mice?
In lab mice I wish to establish how many weeks my animals are into their pregnancy. Is there some way?

This is generally done by checking for the vaginal plug in the female after you have set up the breeding. If the plug is visible then it means that copulation has happened. However, this is not a foolproof test because the vaginal plug just indicates copulation and not pregnancy. This, nonetheless works in most cases and helps you in timing the pregnancy (Reference: JAX notes).

For most strains, the rate of pregnancy is highest among
  estrus-suppressed females with vaginal plugs found the third day after
  being placed with a male. As examples, whereas the rate of pregnancy
  is ~100% and 44% respectively for C3H/HeJ and BALB/cJ females with
  plugs found on the third day, it is only 62% and 31% respectively for
  those with plugs found on the fifth day. In contrast, whereas the rate
  of pregnancy for C57BL/6J females is only 39% for those with plugs
  found on the third day, it is 69% for those with plugs found on the
  fourth day.
If the plugged female is pregnant, the first day of gestation is
  considered to be the day after the plug is found.

You can also monitor for an increase in weight of the mouse. This is not a foolproof technique but serves as a secondary evaluation method.
If you have not timed your breeding and checked for these markers, then you may have to rely on ultrasound.

Checking for plugs is regulary done and the results are ok. The only drawback is that you need to check your mice at least twice daily (hence the 0.5 in most embryonic dates) which can be a lot of work.


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What is the effect of temperature and carbon dioxide on the opening and closing of stomata?
I am teaching biology in an academy. The question which I had asked above had been raised by on of my students. I tried my level best to search out the answer to this question but I could not find the answer. I had read a number of answers to different questions from this website. So that's why I thought to Post my question on your website

I like the reference book Plant Physiological Ecology for stuff like this. I know one of the authors is Thijs Pons.
When temperatures become high, plants may close the stomata to conserve moisture. When the stomata are open, usually in daylight hours, the open stomata allow $CO_2$ to enter the leaf. This carbon is needed to form glucose and many other products a plant makes from photosynthesis. Most plants will not open the stomata in the absence of light.
(I use the above text as the reference. I can't give you pages right now, but I was reading this a couple of days ago.)


text:
Is galvinoxyl antioxidant assay possible using NMR spectroscopy?
I would like to perform an antioxidant assay using the galvinoxyl protocol. The protocol states that we need EPR spectroscopy, but only NMR spectroscopy is available at my institution. Is there an alternate way where I perform a galvinoxyl assay using NMR spectroscopy.

Galvinoxyl is a free radical, which means it has an unpaired electron that can be detected with EPR. Antioxidants reduce the radical, which is then not detectable in the EPR anymore as it doesn't have an unpaired electron. What you need the EPR for in the assay is to determine how much of the galvinoxyl is still a radical.
Paramagnetic molecules like galvinoxyl are problematic for NMR, they bleach signals in close proximity to the radical and cause line-broadening. You still might be able to quantify the amount of oxidized and reduced galvinoxyl, but I'm not sure how reliable this would be. The oxidized galvinoxyl would probably be not visible in the NMR, while the reduced version would give a signal. You'd have to measure a few spectra to see if you can determine the percentage of reduced galvinoxyl from the NMR spectra.
EPR is the far easier method here, while I don't think doing this with NMR is impossible, there are quite a few ways it could be inaccurate. I'd strongly recommend to either use an EPR machine somewhere else, or use an entirely different assay that doesn't require such specialized equipment. I have no experience with antioxidation assays, but I'd guess that some exist that don't require EPR.


text:
How does the embryo inside a shelled egg get oxygen?
If I'm not mistaken a typical animal in the womb will get oxygen via the umbilical cord from the mother. Thus allowing it to "breathe" in a liquid environment. I thought maybe shells are permeable and allow air to come in through the shell, but then I thought of eggs laid in the ground like turtles do.

How do animals in soft/hard shells get their oxygen?

Both forms are ultimately by diffusion.

The key point in both cases is that the eggshell and membrane are permeable to oxygen, as you thought. There are subtleties - for instance, the oxygen-permeability of avian (hard-shelled) eggshells changes during development.
In the case of eggs laid underground, as in sea turtle eggs, the leathery shell is still permeable to oxygen. The sand restricts oxygen flow, but turtles seem to take care to not bury their eggs too deep for oxygen to diffuse to their developing nest.


text:
Did I just watch a spider die?
So I'm sitting in my office and all of a sudden a small spider is gliding down on a web string from the ceiling, right in front of my eyes, and down onto my desk. It proceeds to make a few awkward movements which looked like it was having problems correctly coordinating its legs. Then it flipped on the back and had its legs curled up (like it was dying).
A few seconds later it suddenly started moving with the awkward movements (like it was trying to walk) for a few seconds before collapsing again. It's been doing this on and off about 3 to 4 times. As far as I can tell, the unconscious periods are becoming longer and the waking periods shorter.
What's happening here? Is it dying (of stress / bitten by a female spider / old age) ?
Edit: The whole process has now been going on for over 30 minutes. During the times it moves, it looks like it cannot use the foremost pair of legs. Here are two pictures of the (really tiny) spider with a shopping cart token coin for scale:

Images of the spider and your location will be helpful.

I'm voting to close this question as off-topic because this is anecdotal.

Well thanks @AliceD, maybe you'd also like to point me into the right direction on how to ask this question without being anecdotal?

March Ho made an excellent suggestion. That would help and make it evidence based. Feel free to edit and I'm happy to retract. As of now all we can do is guess. Pointless.

Taking somewhat good pictures took a while, and I'm afraid they won't do you much good as it's really hard to get a good shot of something so small. I hope it helps!

So--did it die?

Appearently, yes. However, it went on for over 16 hours, because when I came in the next day, the spider had moved again. Ever since then, it hasn't been moving again and I'm starting to think that it is really - finally - dead.

However, what kind of agony goes on for 16 hours for this little guy? I would have really liked to know some possible reasons, but it looks like nobody with enough knowledge about spiders is around :)

@AliceD why is this off topic? The underlying question seems to be "what happens when a spider dies"? It seems on topic as far as I can tell.

The mortality rate of spiderlings is very high and their death is a natural process. Since there was no source on energy available on the desk death occurred after stored energy was depleted.

I have just witnessed the same thing occur! The spider (which was in my bathroom) looks to be the same species judging from size and coloration. This seems to me like a natural body process of sorts. At first I was skeptical it could be a sort of infection or parasite, as it was odd that a spider would, by itself, walk into a well-lit area and then roll over to die. However it seems incredibly unlikely that is the case, due to the similarities our spiders share. What are the chances of the same thing happening twice, even if it IS a parasite? Must've died or old age, or venom from another spid

Spiders do curl up their legs when they die. Since they do not have muscles for extending the legs at their joints, they control the haemolymph pressure in the legs by using the blood pressure spike from their heartbeat to extend their legs out or walk. And with no heartbeat (when the spiders cease to exist), they curl up upon death.

Source: http://www.informationsociety.co.uk/why-do-spiders-curl-up-when-they-die/

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


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transitional mutation, repair mechanism
I have read an answer to a question about dna repair during and after replication.
But how is dna repaired if a deamination of of 5-methylcytosine happens? How does a repair mechanism identify which base was mutated (on '3 or on '5 strand, a C to T, or on the complementary strand an A to G)?

I don't have time for an answer right now, but you can look up very short patch repair for bacteria. For higher organisms where methyl-C occurs in CpG sites, repair enzymes can recognize the mutated strand by the presence of methylated CpG on the complementary strand.

DNA Glycosylases, like UDG, and hSMUG1 contribute to specifically sniffing out instances of Uracil that occur in the DNA. Havent time for a full answer myself, but these are just a few resources.

Deamination of 5mC gives T, not U.

Yikes, that's embarrassing! Disregard my above comment unless you're curious!


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Identifying flying insect from northern Poland / Baltic Sea area
Found during this year vacations at Baltic Sea (northern parts of Poland):

I don't have a picture containing other object, for size verification, but I'd say, that it was 3-4 cm long.
There were two interesting characteristics of this insect, that I haven't found in case of any other:

it was not flying / running away, when when being chased / waived by a hand; you actually had to snap it with a finger and sent it airborn, to make it fly away,
once touched by finger or upon falling from certain height it was pretending dead, but when you tried to remove "dead body" it turned out in most cases that it is alive and it was flying over.

This is all I can tell about this insect. Can someone help me with identifying, what species is it?

A weevil perhaps? Somewhere to start!

It is possibly a vine weevil (Otiorhynchus sulcatus)

Others of the family:

Looks like a good guess, however this part: "The adult weevil is matte black with fused wing covers, and is unable to fly" is making me a little bit susspicious, because I'm pretty sure, that insects observed by me were able to fly. Or maybe they were just jumping quite high? I'm not sure.

Also, notice the absence of the stripe on the pronoto in your guess that is very clear in the OP's specimen. I think you're right that it is likely a weevil of some sort, but you do not have the correct species.


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What does NaOH do for the plating of Bacillus subtilis?
A book called Molecular Biological Methods for Bacillus called for plating Bacillus subtilis cells on LB-agar plates with the following components:

A general-purpose medium containing per litre:
Bacto-tryptone 10 g
Bacto-yeast extract 5 g
NaCl 10 g
1 M NaOH 1.0 ml
Autoclave (151b/in^2, 30 min). For LB agar plates solidify with 1.5% (w/v)
  agar; for LB overlay use 0.7% agar.

The first three components and their corresponding amounts are the same as what I normally work with, but I usually add distilled water for plating E. coli instead of NaOH. According to Wikipedia's entry on lysogeny broth, NaOH can be added to adjust LB's pH. But the protocol here mentions nothing of that sort. In other protocols of the book, at least it would say "adjust to pH -- with 10 M NaOH" or 1 M NaOH, etc. So if it is not to adjust the pH for the growth of Bacillus subtilis, what other purpose does NaOH do for the bacteria?
Also, I usually autoclave my LB or LB-agar for 2 hours instead of 30 minutes. Would autoclaving at 2 hours instead of 30 minutes affect NaOH?

The NaOH is to adjust pH. They must have determined that that much NaOH with those ingredients makes a suitable pH, but I think your much safer to titrate.

Why 2 hrs? Why change the recipe? @canadianer is quite correct, per usual, the only reason to add a small amount of extremely strong base to your media is to adjust the pH. And yes, if the pH of the broth and the plates is crucial for your experiment it would be much wiser to titrate the solution. The distilled water pH will vary, as will the agar and the other ingredients (slightly, from batch to batch). also, I would be concerned that autoclaving for extended periods of time could also affect pH by breaking down the ingredients in the complex mixtures

http://www.ncbi.nlm.nih.gov/pubmed/11700343

I think NaOH is added to bring up pH not to get too acidic. I feel autoclaving LB or LB-agar for 2 hours is too long. During autoclaving, some components are gradually degraded.


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Can the regeneration mechanism of lizards be used in humans?
Is there any mechanism or specific protein which helps lizards to regrow their tail? Can the mechanism of regeneration be used in humans to regenerate our limbs? Is there any other animal which has this kind of ability?

Here is a list of animals that can from wikipedia: https://en.wikipedia.org/wiki/Regeneration_(biology)#In_animals . I think the regeneration mechanism is due to stem cells and how cells differentiate. https://en.wikipedia.org/wiki/Regeneration_(biology)#Tissues

Actually there are some studies to find out your answer. Some of the studies claim that they have found a special enzyme and some say micro RNAs give salamanders the capacity of regeneration. But until now, humans couldn't use salamander's regenerative ability. Maybe you would like to know there is a mammal (african spiny mouse) with special regenerative capacities which include regeneration of its skin and cartilage without scarring.
References:

'Skin shedding and tissue regeneration in African spiny mice (Acomys)' Ashley W. Seifert,   Stephen G. Kiama,   Megan G. Seifert, Jacob R. Goheen, Todd M. Palmer & Malcolm Maden
Microarray analysis of microRNA expression during axolotl limb regeneration.
For further studies I recommend searching "salamander and regeneration", "african spiny mouse and regeneration" in pubmed ;)

Since you weren't able to get them on, I suggest you provide the name of the website(s), so that we know which ones to look at :)


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Why Do we close our eyes while sneezing?
Google says germs  may fall on eyes from our sneeze but it happens all the time . Also it says it a part of contraction. What may happen if we sneezing wirh our eyes open ?

When I sneeze i keep my eyes open esp when driving.

Mythbusters did this one!
The simplest response is that your eyes close as a reflex, because the nose and eyes are linked by cranial nerves which brings the sneeze signal to the brain and then to the eyes, making them blink. Would you eyes pop out if you managed to sneeze with them open? (a common urban myth) No! Your eyes are attached by strong muscles and it would take a lot more force than a simple sneeze to lose them.
Mythbusters article on the subject
I would love to give you a more scholarly article but this is the same one referenced on wikipedia on the subject, plus it's hard to find academia in the fluffiness of this question.


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Nature vs Nurture in Rooster mating dance: Are roosters lame dancers because they never learned any better?
I've seen, read about, or heard several avian courtship dances, flights, songs, and other rituals. They are general very impressive, fancy, and beautiful. Roosters, by comparison, are quite lame. The link is a pretty good example of the sort of best effort I've seen or read about from a rooster. A lot of them seem to do quite a bit less than that.
Some time ago, I remember hearing about the various distinct finch calls, and the fact that these songs seem to be largely a learned behavior. In a modern factory style farm, chicks are usually hatched in an incubator and raised by humans in a brood of similar aged chicks. Some chicks, on more traditional farms perhaps, are raised in more natural settings with a mother hen present, and perhaps a rooster too, but even when a rooster grows up observing his father's behavior frequently, I wonder how often such a parent child example extends beyond just a few generations. In other words, I doubt that any chicken benefits from a long lineage of fine courtiers like their wild finch cousins.
My question then is primarily whether there is potentially a learned component of roosters' dancing, and secondarily whether a lack of sustained parental lineage stunts the development of proper dancing in a rooster. They certainly have some sort of instinct driving them, and they're beautiful birds, but their mojo falls flat compared with more wild relatives, like this pheasant. To avoid soliciting opinion-based answers, I want to focus this question on specific verifiable knowledge. For example:

Are there any actual studies on this topic with roosters or close relatives? Or is there any husbandry knowledge on the subject? For example are specific steps recommended to preserve the beautiful mating behavior of pheasants or pea fowl in captivity?
Is there any evidence of learned avian  mating behavior other than song?
Are there any notable recorded differences between the mating dance of an orphan rooster compared with roosters that have grow up with fathers?

Don't feel like you need to address every point for a good answer. I'm just trying to provide a framework for avoiding opinion-based answers.

Maybe the hens think differently and do not see their roosters behaviour as lame? I mean, how is a human supposed to judge? Also, the hens have nothing better to compare to. So why the effort to improve?

@skymningen While I can certainly agree that chicken thought is very foreign territory, I do think there is a reasonable case that appreciation of beauty, music, and dance is somewhat shared between our species, the primary evidence being the fact that we do in fact appreciate most of these things in birds. Many have theorized that music and dance are features of bipedal existence. The other evidence is the seriously cool dance of close relatives to chickens.

@skymningen I think your point about having no need to improve is probably very accurate as most coops are limited to one rooster. But this goes right along with the point of my inquiry. That limit is part of the artificial bounds we set, and goes hand in hand with the lack of good example from older roosters.

I totally agree with you that the appreciation of beauty is shared, my idea is only that the perception of beauty might be completely different. Think of some animals that are attracted to smells or sights which for humans are disgusting.


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Methylation Data for Erythrocytes (Red Blood Cells)?
Why is it that white blood cells (leukocytes) are highly characterized in DNA methylation pure cell line profiling, but I can't find any profiles of red blood cells (erythrocytes)? Is blood considered a pure tissue type?
I'm following the deconvolution of DNA methylation data by cell type (white and red), but I can't do this without pure cell line methylation data. Can anyone help me understand either:

Why red blood cell DNA methylation data has not been purified and collected yet.

OR if it has...

Where can I access the methylation data for red blood cells (erythrocytes)?

Thanks so much for any help!!!

The answer is relatively simple: Mature erythrocytes do not have a nucleus and thus you cannot study methylation patterns there. You can do this in young, developing erythrocytes which still have their nucleus.


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Why would a venus fly traps mouth that's still "chewing" die?
A venus fly trap produces leaves that act like traps for insects. A trapped insect is digested over several days. The trap then opens again to catch another insect.
These traps regularly die off. They turn black. They are replaced with new ones. I'm not sure why that happens. As far as I know this is a swamp plant, which makes it unlikely that the traps die off due to being in contact with water. I read that a trap can only be reused 7 times. So I guess the traps are replaced by the plant in some interval.
As the dead traps start to rot in the pot, I pick them up from time to time and throw them away. Recently, during that process, I found this:

and it made me wonder why this mouth would die off. It looks like it caught something. As the mouth is still closed, I think the digestion process is not finished yet. But why would the plant give up this valuable resource?
Is it because the trap could not close entirely? There are signs of rot on the insect, but I don't know if that happened after or during the digestion process. Would rotten prey be a problem chemically? A human can dissolve quite a few things in its stomach, so I guess this could work similarly.
What are the reasons for the traps to die off in general?

A friend once figured that if his trap caught big ants, the traps often would blacken and die off. We guessed this could be related to the ants acid. My own trap that I had long ago used to "choke" on too big food and also have traps die off if they caught comparatively big insects. But all of this is just based on personal experience.

I remember reading somewhere that cultivated flytraps are much weaker than venus flytraps found in the wild, and they can't digest food that is too big. so this might be why they would fall off mid meal.

There are many things that could affect the rotting of your venus fly trap while digesting including: size of the bug, age of the trap, and temperature.
Sometimes a venus fly trap will turn black and fall off while it's digesting a bug when the trap is very old. As the trap ages, the digestive juices are recycled and as a result form a weaker mixture which slows the digestion process.
The bug it was digesting was also probably very large or had a hard shell inhibiting the trap from properly closing. This allowed bacteria and mold into the trap to digest the insect also proliferating the rotting of the fly trap itself in the process.
Temperature also has an effect on the trap's digestion where higher temperatures speeds up the enzymatic process of digestion. However, this is probably not a factor in your case.
It's not so much that your venus fly trap decided to give up on the valuable resource, it was either too old to properly digest the bug or it couldn't close properly because the bug was too large that bacteria infested the bug and the trap speeding up the process of the trap falling off the plant.
For more detailed explanation see: http://science.howstuffworks.com/life/botany/venus-flytrap4.htm


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Can ' functional' stress 'forced upon' a cell actually cause cell mutations when they divide and reproduce?
If a group of cells are forced to go beyond their regular biological parameters that they should be under given ' healthy' functioning and while existing in these stressed states some of the cells divide and multiply would the added stressful states make them mutate?

On a tangent, lots of stressors abrogate division completely in healthy cells. One of the first things cells do in response to heat stress, for example, is stop pushing toward replication and begin transcribing heat shock factors. Compression can lead to cell cycle arrest, and establishment of many cells in a given area leads to contact inhibition of cell division.

Can prolonged exposure to various environmental toxins,even if in low doses, cause 'functional' stress on certain cells subject to the exposure and eventually abrogate cell division or accelerate it or cause it to operate unpredictably?

TL;DR Yes! I would take a look at how normal, healthy cells progress into neoplasia and eventually cancer. Up to a certain point cells will undergo apoptosis, in effect dying before becoming "too abnormal," but one of the hallmarks of cancer is that the cell may somehow evade death (in addition to abnormal proliferation, etc.). Certainly, stressors which cause damage to the DNA (but not so much that the cells dies) are, at least over time, are going to begin to cause abnormalities in the tissues they affect.

Asbestos exposure comes to me as a good example: http://www.atsdr.cdc.gov/csem/csem.asp?csem=29&po=10

If some type of 'functional stress' causes a cell or a group of cells to mutate and gain more and more mutations does this eventually cause the cell's apoptosis mechanisms to 'malfunction? Do some of these mutations 'interfere' with the functioning of the apoptosis 'mechanisms'?

Since it is a 'normal' cell ('before' 'functional stress' and any mutating ) that is gaining mutations does it have 'natural' abilities to avoid immune system attacks?  And if so these abilities that are within it and its 'progeny' when mutated help them to avoid immune system detection ; is this true?


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Partial Contribution By One Parent
For flowering plants, what might cause the genome size of offspring from a cross between 2 diploid parent of differing genome size to reflect only a partial contribution by the larger genome size parent?
Many hybridizers of Rhododendron attempt wide crosses between two sections of the genus. In some cases the resulting hybrids show physical characteristics of both parents. However, flow cytometry indicates that instead of the offspring being half the sum of the 2 parents genome sizes the genome size is actually twice the genome size of the smaller genome size parent.
See Evergreen azalea X deciduous azalea
Can a successful cross result in a reduction in normal contribution of one of the diploid parents after fertilization?

We have seen instances where the genome size of the offspring are significantly less than the genome size of either parent.


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Can anyone ID this ant queen species?

It was found in Hong Kong! Below are a few basic information:
Place: Hong Kong
Habitat: Forest. I live very close to a mountain with lots of forestation.
Where Collected: Found it in my window slit of my apartment.
Coloration: Major body parts are black, but legs are light brown.
Distinguishing characteristics: Appears to have one spine in the mid-body (not sure); Huge mandibles
Length: 14mm to 15mm
Width: 3mm
Anything else distinctive: It could move incredibly fast (like a cockroach). Also, it appears to be quite aggressive. When I put in an ant (male ant with wings) of a different species to its tube, it attacked the introduced ant with its mandibles immediately. During its attack, it shook its abdomen periodically.

The species in the photo is a carpenter ant (Camponotus irritans), possibly C. i. hongkongensis. More info, photos, and video here.

Also, it's a worker, not a queen.

No it is a queen (broad thorax and abdomen) hence the eggs.

The thorax and gastor (abdomen) are actually typical of Camponotus workers. Also, the presence of eggs is not solely evidence that it is a queen; worker ants frequently carry eggs to and from the nest.


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In which phenomena does one gene pair hide the effect of other unit?
This question was asken in an exam,

The answer they are saying is "Epistasis". But I think "Dominance" fits better,  because it is not mentioned whether genes of same allele are to be considered or different allele. Also it is not told whether genes in same locus are being talked of or different.
Please give some reference if you can. I know only school level biology. I do not know even in detail what allele and locus are. As far as I could understand from wikipedea and other sources I think "Dominance" is correct.

Even I thought it to be dominance, but the above explanation makes everything crystal clear. Thanks @mdperry

The definition of "gene", according to The American Heritage Science Dictionary is:
"A segment of DNA, occupying a specific place on a chromosome, that is the basic unit of heredity. Genes act by directing the production of RNA, which determines the synthesis of proteins that make up living matter and are the catalysts of all cellular processes. The proteins that are determined by genetic DNA result in specific physical traits, such as the shape of a plant leaf, the coloration of an animal's coat, or the texture of a person's hair. Different forms of genes, called alleles, determine how these traits are expressed in a given individual. Humans are thought to have about 35,000 genes, while bacteria have between 500 and 6,000. See also dominant, recessive. See Note at Mendel."
So, when the question refers to genes, it must be referring to two different genes on two different loci. If the question was referring to alleles of the same gene on the same locus, the correct answer would be dominance, but since it is referring to two different genes, the answer is epistasis.

"So, when the question refers to genes, it must be referring to two different genes on two different loci". Why is that? It is not mentioned   whether same loci are being discussed or different.

When you talk about two separate genes, you are always talking about two separate loci ("specific places on a chromosome"). Two different genes cannot occupy the same locus. Different alleles can occupy the same locus, but different alleles are just different forms of the same gene.

Consider two different genes (call them two different loci, if you like). Gene A where + is a wild-type, functional copy of the gene, and a is a mutant, loss-of-function copy of the gene. Gene B where + is a wild-type functional copy of the gene and b is a mutant, loss-of-function copy of the gene.
An individual with this genotype:
+/+; +/+
Will be wild-type. And if the a allele of Gene A is recessive, and the b allele of Gene B is recessive, then an individual with this genotype:
+/a; +/b
Will also have a wild-type phenotype. In a diploid organism, dominance is when +/a individuals have a mutant phenotype.  The same holds true for +/b individuals, if one copy of the mutant allele causes a mutant phenotype then the b allele is dominant to the + allele of the B gene.
If both mutant alleles are dominant then this individual would have two mutant phenotypes:
+/a; +/b
Most mutations, however, are recessive to the wild-type allele, so you would not see a mutant phenotype until there are two mutant copies and no wild-type alleles. Either:
a/a; +/+
or:
+/+; b/b
The double mutant would have this genotype:
a/a; b/b
You cannot interpret, or make logical sense, of an epistasis experiment unless the alleles are recessive.
If this individual does not have a double mutant phenotype, but instead only shows the 'A' gene loss-of-function phenotype:
a/a; b/b
Then we would say that the A gene is epistatic to the B gene, because homozygous A gene mutants "hide" the B gene mutant phenotype.
If, instead the double mutant only has the 'B' gene mutant phenotype then we would say that the B gene is epistatic to the A gene.
If the double mutant has both phenotypes then there is no epistasis between these two genes, or loci.  Conversely, if the double mutant has a wild-type phenotype then the mutations are suppressing each other.


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Bioinformatics - DNA binding, sequence-specific protein data
I am a computer scientist and we are working on protein function prediction algorithms. Right now, we would like to examine protein-DNA binding properties computationaly. For this, we would make use of datasets about containing DNA-binding proteins and the DNA sequences they bind to. I was looking on Gene Ontology and Protein Databank where I'd expect such informations, but I was unable to find it. Are such data presently difficult to obtain? Or are simply not collected? Or could you give me some direction where to look for such data. Thanks.

Try these searches: TRANSFAC, JASPAR, ENCODE, position weight matrices (or PWMs)

You are seeking a database of transcription factor binding specificities. Some model organism databases (which are manually curated), such as Wormbase contain some of this annotation. I suggest you search PubMed for papers by Tim Hughes at the University of Toronto. He has published extensively on this topic over the past 5 years.  Papers he cites, and papers that cite him, will let you bootstrap your way in to the topic.


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How much oil you can get from a dead animal
This is purely speculative, but is there a formula to calculate how much oil you can get from 1 Kg of biomass?
I've seen bioreactors in farms where they put dung, vegetable scraps, and all bio scraps, where bacteria transformed the biomass in methane gas which then was used in powering electric generators or cooking stoves.

Well as I checked the internet and noone has done this experiment. So, it is a bit hard to answer it.

Oil is not biogas. what do you mean?

I was interested to know (at some point) how many dinosaurs had to die to create 1 kg of oil. I am aware that the oil deposits were formed by other type of organism not dinosaurs, but I was curious to know what mass of biological organisms needs to create 1 Kg of oil.
I wanted to be able to tell "You know, you just burned 1 TRex driving here."


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Is there an organism which is "The Opposite of Hydra"?
My understanding is that if hydra is cut into pieces, each piece can evolve into a new hydra. What I'm looking for is whether there exists an organism with a this property reversed, that is, if two or more such organisms meet, they would form new organism with the same property.
UPDATE: I do not mean the mythical creature, but this one. I should also have stated that I'm (obviously) not a biologist, so my terminology and information about the Hydra genus might be wrong. Despite that, I hope the question is still valid.

Not that it really matters, but the hydra myth involves its heads, specifically.  Cut one off, and it would grow two (or three or more, depending on the myth) from where the first used to be.  The whole creature wouldn't duplicate.

@Nerrolken, sorry, should have been more clear. Updated my question.

Perhaps sea sponges might satisfy your criteria? There were some classic experiments where two distinct sponge colonies were dissociated individually into small clusters of cells, and then the two suspensions were mixed. As I recall like sorted with like.

Siphonophora (these are close relative of hydra). They are considered to be a colony of zooids. I am not sure if that is what you are asking. You an also think of Dictyostelium. They can aggregate to form fruiting bodies.

Possible duplicate of http://biology.stackexchange.com/q/37473/3340


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What do the names of Immunoglobulin subtypes mean?
What is the exact meaning and full form of  IgM, IgG, IgA, etc? What is the rationale behind the names of the isotypes, if there is one? For example, what does "M" mean in IgM?

what  M stands for in IgM?

Have you done any research on your own? Like a Google search?

Yes but I did not get the full form of M!!

The constant region of heavy chains of IgA are called α (alpha) chains so the English translation of the greek alphapet is A.

Ig stands for immunoglobulin. The isotype names have various origins. This paper provides an interesting story:
Black CA. 1997. A brief history of the discovery of the immunoglobulins and the origin of the modern immunoglobulin nomenclature. Immunol Cell Biol 75:65-68.
A brief summary, in order of characterization and naming:

IgG - named gamma globulin because it migrated in the gamma band of electrophoresed blood plasma (the bands were named in order of mobility: alpha, beta, etc)
IgM - named macroglobulin because it sedimented faster than IgG (ie was larger)
IgA - found in the beta and gamma bands of electrophoresed plasma and initially named β2A and γ1A, later renamed to alpha globulin
IgD - named by process of elimination: IgA was taken, murine immunoglobulins were expected to be named beta, the letter C has no Greek equivalent
IgE - named because it was most reactive with a fraction of pollen proteins (fraction E because it induced erythema)

What is the full form of IgM?


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What is the highest pressure at which plants can survive?
Inspired by this awesome question, I'm looking for the corresponding maximum: what is the highest air pressure at which plant life can survive?
For example, Venus's atmosphere is about 90x as dense as Earth's.  Aside from the other obvious factors, like sulphuric air and boiling temperatures and otherwise resembling hell in every possible way, can plant life survive in such a condition?
Additionally, are some types of plant life more adaptable to high pressure environments than others?  (I'm assuming an air environment, and excluding deep-sea life, etc.)

See Effect of very high pressure on life of plants and animals (2012).

Judging from the fact that all the living creatures we have examined, both animals (tardigrades and Artemia) and plants (Ptychomitrium, Venturiella and white clover) were alive after exposure to 7.5 GPa, it was suggested that most of the proteins of those creatures which unfolded at the early stage of the compression remain principally unchanged after exposure to the very high pressure of 7.5 GPa. It was also suggested that the unfolding of proteins was completely reversible up to 7.5 GPa.
The maximum hydrostatic pressure applied to all the living specimens investigated in the present experiments corresponds to that in the upper mantle, at the depth of 180 km from the surface of the earth.

So survival of plants at 75,000 times atmospheric pressure is possible. In this experiment the exposure times were 30 minutes and 1 hour for the plants and 13 hours for the animals.


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connect three coding sequences with IRES
To express two proteins at once in mammalian cells, expression vectors carrying an IRES (internal ribosomal entry site) are available. Does anyone know any attempt to express three proteins using two IRESs or more. The third gene may be expressed very low, but it may be acceptable depending on experiments if it works.

http://www.ncbi.nlm.nih.gov/pubmed/14667529 :: https://www.abmgood.com/Bicistronic-Tricistronic-Promoter-Lentivirus.html ::
Let me know if this helps!

@Kendall Thank you, the information was useful.

You might be interested in the Foot and Mouth Disease 2A Peptide, a self-cleaving peptide sequence that can be inserted in between two proteins. The proteins are translated as one sequence, but cleaved at the 2A peptide to form 2 proteins. If I'm reading the source right, they used 4 genes in a row with 2A peptides between them. The 2A peptide has the advantage of being much smaller than most IRES elements, while being more reliable than IRES or internal promoters.

Thank you. I asked this question out of curiosity. But you are right. 2A peptide could be convenient to this purpose.


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Is the ringing sound in the ears caused by dying ear cells?
I was recently watching the movie "Children of Men" (great movie) by Alfonso Cuarón. Now in a certain scene, the lead actor happens to be nearby a loud explosion. Later, when he complains about the 'ringing-sound' in his ears due to the explosion, a co-actor replies:

Julian: You know that ringing in your ears? That 'eeeeeeeeee'?    That's the sound of the ear cells dying, like their swan song. Once it's gone you'll never hear that frequency again. Enjoy it while it lasts.

How true is that statement?
Do the ear-cells really die after such an incident?Can you really never hear that frequency of the ringing-sound again?

Welcome to Biology. The statement maybe true dependent on the loudness of the explosion. In turn depending on the power of the explosion and the distance od the listener to the sound source.

Short answer:
That MAY be the sound of the damaged hairs dying. You MAY not hear that frequency again but that's unlikely.
Long answer:
Okay, so tinnitus, or ringing in the ears, can happen because of many reasons. There are three real kinds:
1) Spontaneous tinnitus can happen because of slight shifts in the acoustic systems of the ears, some of the hairs in the cochlea may amplify wrong and create a tiny feedback loop and ring for no reason. see this article about that kind of tinnitus here
However, that's not the kind of tinnitus you're referencing. That kind, post acoustic trauma, is more serious.  This kind (which can result in hearing loss) results from either 2) one really loud noise OR 3) prolonged repetitive exposure to certain frequencies (like how your mom told you to turn your headphones down or you'd go deaf. Lower frequencies move a lot of air and can indeed be dangerous to your hearing.) Just how serious the damage from a single acoustic trauma event like the explosion from Children of Man would be to you would depend on just how loud the noise was you were exposed to, the frequencies of it, and how close you were.
So now that we've gone over the different kinds of ringing-in-the-ears (tinnitus), we can talk about how it works in this situation.
This is a great article on acoustic trauma tinnitus.
So these characters didn't rupture their eardrums or they'd be in a lot of pain and unable to hear at all in one side. Instead what happened was the tiny hairs that send electrical signals to the brain were probably bent and crushed (see awesome images on the article above of before, at, and ten days after acoustic trauma.) Three possibilities from here: either the hairs recover, they partially recover, or they don't recover at all. The most likely situation is that they do recover in a matter of days, leaving the characters with undamaged hearing. Some of the hairs (usually lower frequencies) may be more damaged that others. Those may dim or cut out frequency ranges in hearing. Multiple hairs cover the same range, so some of them may be out of commission while others survive, leaving you with diminished hearing of that frequency. However, that is not likely to be related to the buzzing/ringing frequency we first hear after acoustic trama, which is the sound of all damaged hairs freaking out and sending signals at once.
Great article on how we hear frequencies
source: Sound engineer. Protect your ears, guys!


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Can an organism exist as a single cell but come together as multi-cellular during certain times?
I am trying to remember a particular segment from a BBC special, about a single celled species. However, at certain times all the individual cells came together to form a structure, not unlike a mushroom, to scatter something like spores into the wind. Afterward, the individual cells separated and continued on as individuals.
Am I remembering this incorrectly? Is this even possible?

Welcome to Biology StackExchange.

Am I remembering this incorrectly?

No, you're remembering it correctly.
I think you're talking about slime molds. You'll find more information on the wiki page
Is this the video you saw? These images are pretty cool.

Is this even possible?

Yes (given that it exists). There is no way to correctly answer this question as it really is an open-ended question. But here are a few words that may push you writing further posts.
Just a few words on the evolution of altruism
The main interest behind this life-cycle is that not all individuals reproduce. Some individuals form the stalk while others go through meiosis (see below on the life-cycle).

How unfair does it seem to those who form the stalk! Why would those individuals forming the stalk spend energy to help other individuals to reproduce?
Kin selection
Let's think about us, vertebrates, "real multicellular" organisms. The cell that is in your eye is never going to reproduce. Although it is spending all its energy into helping your ovules/spermatozoids to fuse. Why would this cell in the eye make such an effort? The genes in the spermatozoids/ovules are essentially the same as those in the "eye cell". Therefore, by helping your spermatozoids/ovules the eye cell is actually contributing to spreading copies of the genes that it is carrying. This is referred to as kin selection.
Slime molds and altruism
Now, the story is not exactly the same for the slime molds. The cells in the stalk can be quite different from those that are undergoing meiosis. Altruism can exist in a variety of different mechanisms and it would take several books to go over the literature about the evolution of altruism. Without knowing the literature specific to the slime molds reproduction, I just want to notice that the cell in the stalk will die anyway, whether or not it spend energy helping other cells reproducing. There is, therefore, no fitness cost into construction a stalk. Little population structure (causing higher relatedness within deme than among demes) could be enough to allow this behaviour to evolve.
Just a paper (that I haven't read) on the subject
Hudson et al. 2002
Genetics of the fruiting body
Interestingly, similar genes are being used in Dictyostelium discoideum (slime mold) to create this fruiting body than what is used in multicellular eukaryotes (ref.). Thanks to @Tim Cutts for this info.

The interesting thing about /dictyostelium discoidium/ and similar slime moulds is that the mechanisms they use to form their multicellular fruiting body use related genes to those used in development of true multicellular organisms. They are thus very instructive as to how multicellular development works, and show that these mechanisms evolved very early

"Kin selection" - also why the traits for being (perhaps) a celibate priest or (on more solid evidential ground) a worker bee are not ruthlessly selected against :-)

I would add two other examples: biofilms and Myxococcus xanthus fruiting bodies.

Fun fact : Slime molds have been used by artists to make some really great works ! I remember seeing a TED talk on it.