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Influence of temperature on transcription, protein binding and decay rates
I am the kind of biologist who doesn't know much about molecular genetics and about the dynamic of biochemical reactions.
Question
My question concerns the influence of temperature on the dynamic of molecular genetic processes. Typically, I'd like to know how (quantitatively speaking, looking for the $Q_{10}$ for example) the following parameters get modified with temperature.

rate of transcription

UPDATE See How is the rate of transcription influenced by temperature?

protein binding to a DNA-binding-motif

UPDATE see influence of temperature on protein binding and decay rates

rate of protein decay

UPDATE see influence of temperature on protein binding and decay rates

rate of mRNA decay

UPDATE answered by @Chris below

Why do I ask this question?
In order to know what kind of default parameters values I should enter for modeling purposes in evolutionary biology. While our scope is large we decided we would consider parameters values that are observed in yeast.

This sounds straightforward when thinking about it but finding hard evidence is not really easy. As this is too long for a comment, I have to put it in as an answer. Just a few thoughts: All enzymatic reactions are of course temperature dependent and usually have a temperature optimum at the specific living temperatures. For yeast this is around 27°C, for thermophiles this is much higher. For transcription an number of other factors including accessibility of the chromatin and the availability of cofactors play an important role besides the higher activity of one enzyme. This paper might be interesting for you: "Direct measurement of transcription rates reveals multiple mechanisms for configuration of the Arabidopsis ambient temperature response".
DNA binding should be a statistical process between association and dissociation at a given binding site. At higher temperatures the turn-over at the binding site should be higher (because there is more energy available to promote dissociation). T

The thermodynamics of DNA structural motifs
Thermodynamics of specific and nonspecific DNA binding by two
DNA-binding domains conjugated to fluorescent probes.

Thanks a lot Chris. You articles answered my questions for both the rate of transcription and the RNA decay rate. I asked a new question here for the two protein-related questions.

Great, I wasn't completely sure about it.


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Integration of several environmental signals
I am looking for examples of different functions that are good fit to how signals are computed in order to respond to the environment. Let's make my question more copmrehensible with an example...
One example
I have been told (I haven't found an article yet) that in plants, in order to know if it is overshadowed by a big tree, the plant computes that ratio of two signals (UV intensity over Infrared intensity or something similar) so that it can decide whether or not it should grow bigger leaves or other attributes.
This plant radiation example would be an example of a species that computes the function $\frac{S_1}{S_2}$ (where $S_1$ and $S_2$ are two types of signals) in order to take decisions about their response to the environment.
Question
Can you please give me examples (examples with a diversity different functions, with different numbers of different signals) of organism using environmental signals to adaptively respond to their environment?
For example, can you give me examples of the adaptive response to the environment is giving by the following functions of 2 signals:
Continuous traits:

$f(S_1, S_2)= S_1 + S_2$

Produce a trait value at $K_1 + K_2\cdot \left(S_1 + S_2\right)$

$f(S_1, S_2)= \frac{S_1}{S_2}$

Produce a trait value at $K_1 + K_2\cdot \frac{S_1}{S_2}$

$f(S_1, S_2)= S_1^2 \cdot S_2$

Produce a trait value at $K_1 + K_2\cdot \left(S_1^2 \cdot S_2\right)$

$f(S_1, S_2)= funA(S_1, S_2)$

Produce a trait value at $K_1 + K_2\cdot S_1$ iff $S_1$ is detected.

$f(S_1, S_2)= funB(S_1, S_2)$

Produce a trait value at $K_1 + K_2\cdot S_1$ iff $S_1 < S_2$.

Boolean traits:

$f(S_1, S_2)= OR(S_1, S_2)$

Iff signal 1 or signal 2 is detected, produce the trait

$f(S_1, S_2)= AND(S_1, S_2)$

Iff signal 1 and signal 2 are detected, produce the trait

$f(S_1, S_2)= FunA(S_1, S_2)$

Iff $S_1$ < $S_2$, produce the trait

, where iff means if and only if and $K_1$ and $K_2$ are constant values.
What I am NOT asking
I am NOT interested in the accurate description of the signal transduction (Description of the kinase cascade and names of the genes and transcriptions factors). I am interested in having examples of mathematical functions that are computed by the cell in order to take decision about which phenotype to produce (plasticity).

To me, it is unclear if you are asking for cases where we have mechanistic reason/understanding for assuming a particular function (i.e. basic understanding of how the information is integrated and weighted), or just cases where a particular function shows a good phenomenological fit to data (or both). In the example you give (leaf growth), without knowing anything about this particular case, both could seem plausible to me. My point is that any statistical model that relates environmental drivers to a response can be seen as an example of an integrating function...[cnd]

[cnd:] ..., but in those cases we don't necessarily know how the integration is executed, or even if it takes place in the focal organism. Some factors could just as well be mediated through interacting species.

@fileunderwater You make a good point indeed. I haven't thought about that. I'll go for the statistical fit to the data. I rewrote my question to make this point clear. Thanks. Let me know if anything is still unclear. I welcome you to edit my question if you think can improve it according to my needs.

In that case I find the Q extremely broad, since basically any statistically fitted model relating a response (physiological, reproductive etc) to one or many environmental factors will do as an answer. Sifting through the litterature you will find supported examples of almost anything, from single regressions, multiple regressions, quadratic relationships, non-linear responses, custom functions and a mixture of all of the above. It is certainly possible to answer the Q with examples, but I dont know what would constitute a good answer, except maybe giving a taxonomy of functions incl examples

I think I understand what you mean and see what the depressant side of my question. I don't think it is easy to find an example where the function is complicated (something like $\frac{S_1+S_2}{S_3^2}$ or even something like $\frac{S_1}{S_2}$). The perfect answer would contain many referenced examples where different functions fit the way the environmental signals predict the environment.

What you are looking for sounds like the mechanism for a fold-change detector. I would recommend looking at these two papers:
The incoherent feedforward loop can provide fold-change detection in gene regulation
As an example of this working in a real system, I recommend looking at the NFkB pathway, as recently detailed by Suzanne Gaudet:
Fold Change of Nuclear NF-κB Determines TNF-Induced Transcription in Single Cells
Here are a few others that I found just by searching for "Fold change detection"
Comparing Apples and Oranges: Fold-Change Detection of Multiple Simultaneous Inputs
http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0057455
Efficient fold-change detection based on protein-protein interactions
I'm sure by looking at the referenced papers in the above you can find more examples as well.

Thank you! Seems very interesting, I wasn't aware of this kind of signal. I think your answer partially answers my question. Fold-change detector might be considered as one type of function I am interested in. As fileunderwater complained about my question, it is possible that indeed this post is hard to answer because it is poorly defined. I welcome questions and comments to help me improving my question.

I don't think that any other kind of function, which was not classified as a fold change detector would satisfy your requirements. In fact, the example you gave (of plant radiation) is exactly this.

oh really? Ok, I probably misunderstood the concept of fold-change detector then. I thought that a fold-change detector is the kind of detector that does not only sense the absolute value of a signal but sense a change in the signal intensity. So that the concept of fold-change detection would have no relationship with how several signals are computed to determine the phenotype to adopt as in the examples in my post. So, did I missunderstood the concept of fold-change detector?

I see - I am not sure if the question is clear to me, but with your recent addition, it is.
Given what you now have, I would recommend looking at Uri Alon's book - he certainly has examples of the logical operations (OR, AND, etc.) that you discuss. I doubt the more complicated mathematical functions you give exist.

Sorry about that. If you feel you can clarify things in my question, please feel free to edit it or to give suggestions on how to improve it.

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Effect of 260/230 values on PCR
To what extent does the 260/230 value affect the efficiency of PCR reactions ? Do the constituents leading to a low 260/230 value (EDTA, guanidine salts and oligosaccharides) inhibit PCR ? I have been getting pretty low values of 260/230 (0.5-1.0) for DNA extracted using Charge Switch Protocol using Magnetic beads and the PCR has been failing. Also, is there any reason why I might be getting low 260/230 values in Charge Switch method ? (I was getting good values using Phenol-Chloroform extraction method)

I've never heard of the charge switch method, I've only ever used phenol chloroform extraction and isopropanol precipitation. If phenol chloroform worked for you before, why not go back to it?

EDTA would certainly inhibit PCR.

@user137 charge switch  is adjusting the ph to change the charge of the magnetic binding bead, change in charge allows washing and elution

I doubt it would matter. 1 ul template in a 50 ul reaction - you've diluted it 1:50. There's nothing left - and you could easily go down to 0.2 ul for 1:250. Also, your enzyme makes a big difference. I would email the enzyme manufacturer and ask them.

I use a 10ul or 20 ul reaction actually, still I get your point.

EDTA carbohydrates, phenol all have absorbance near 230 nm.  TRIzol reagent is a phenolic solution which absorbs in the UV both at 230 nm and ~270 nm
Guanidine HCL used for most DNA isolations will absorb at ~230 nm also
All these things will seriously inhibit your pcr, (and lower your ratio) especially the denaturing agents like guanadine.
All these DNA kits are different spins of a pretty similar process.
If you have a good steady centrifuge stick to the phenol & ethanol. Be certain you are drying your pellet well, but don't over dry it. I'll hear my pellet at 37 for 3-4 min to get rid of ethanol. Ethanol no good in pcr. If you hate doing ethanol precipitation (which I do) cause of invisible pellets, add a high grade bit of glycogen to your aqueous phase before the precipitation. This will make your pellet visible and is completely inert.
If your cleanup isn't the problem do an annealing  and Mg gradient and up your primer quantity.
May want to give me more info like the individual absorbance, pcr conditions, template size etc
Traditionally bead purifications gives really good purity, reason I use it for microarrays. But it's expensive and not necessary for pcr.
Charge switch is just changing the charge of the bead by changing the ph.

My PCR thermocycler conditions are as follows -
Initial Denaturation - 95/30s
[ Denaturation - 94/10s, Annealing - 57/60s, Extension - 65/9m30s ] x 35 cycles
Final Extension - 65/9m30s
I am trying to amplify a 10kb fragment from the mitochondrial genome, using NEB LongAmp Taq Polymerase.
I use 10ul reactions - 5ul LongAmp MasterMix , 0.4 + 0.4 Forward and Reverse Primers (final 0.5mM in reaction), 1ul BSA (5mg/ml BSA), 1ul Mg2+ (final 1mM in reaction) (optional), 1ul template (amount 40-80ng) and make up volume with RNAase free water.

If 260/230 is a problem, it should inhibit all PCR, but I am not getting results for long fragment amplification specifically. For around 1200 bp using Qiagen Hot Start Kit, I am getting results.

Your amplifying a pretty big fragment, your going to need close to perfect conditions. 1200bp and 10kb are pretty different in terms of pcr. Also I would check your protocol of how you are getting the mtDNA, you may need to enrich your template by doing a mito purification. Let me know if this makes sense

Also your extension times seem too long that pcr reaction must be taking half the day. What does NEB recommend for the extension?

@anurag mishra what's the melt temp of your primers?

Melting temperatures are around 60C-62C and NEB recommends 1min/kb of amplicon, hence the extension temperature. Yeah, it does take 7 hours!

So with that reaction time, your reaction really has to be crystal clean. Even trace amounts of contam would cause probs if exposed for that long. be sure your using the highest grade water, dntp's and desalted primers, That your template is fresh and without knowing the number of reactions you are running I would scale up the overall volume to increase your precision (even if that means a little waste).

Should be running multiple to compensate for fidelity and sequencing issues I would think anyways. Hard to say in this case the template gets so diluted it's rarely an issue in shorter reactions.  Check your dntp concentration it may need to be a lot higher for such a big frag. And as always double check your primer seq's good luck man

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Is the mutation rate in organisms in general consistent over the genome?
Coming from computer science with an interest in genetic programming (a process emulating evolution) I'm curious about whether the rate of mutation is homogeneous across the whole genome, or if some parts of the genome differ in the rate of mutation.
For example we could imagine, without going to into details that could invalidate the example, that parts of the genome associated with the immune system could have a relatively higher mutation rate, because this would allow for a quicker adaptation to quickly evolving pathogens.
Is there any empirical support for that different part of a genome of some species have different mutation rates, that would give us empirical support for the possibility that some species under evolution have the ability to adjust (by NS itself or even epigenetics) the mutation rate of specific parts of the genome?
Clarification
I'm only interested in the mutations happening in the scope of the lifetime of a individual organism, I'm not interested in whether the mutations persisted under NS are equally distributed over the genome.

Well, for start, there are "mutational hot spots", regions that are more prone to mutation than others.
As for immune system genes, first of all, lung cells and heart cells and retina cells don't need to mutate those genes, because they don't use them.
But you are right that in immune cells there is a lot of DNA futzing in the sequences for the heavy and light chains, in order to generate diversity in T and B-cell receptors.  Those receptor sequences are built in a mix-and match fashion, like building an outfit from a closet with a few pairs of pants and a few shirts.  Add in some messiness in cutting out the specific sequences, and you have a fair bit of diversity in receptor sequences possible from a single genome.
Later, once a B-cell or T-cell meets a matching antigen, the cell multiplies, and each descendant cell is subject to somatic hypermutation, in the hopes that one of the tweaked sequences will better match the antigen.
But none of that is going to be very evolutionary relevant, since only mutations in gametes or gamete stem cells are passed on to the next generation.

Ah, interesting. However, the immune system was only as an hypothetical example, are there any "mutational hot spots" that are evolutionary relevant?

If by "consistent" you mean homogenous, the answer is no. Regions conserved among individuals (and/or species) tend to accumulate less mutations (specially avoiding deleterious mutations). Even within a gene sequence, there are conserved regions which accumulate low number of changes, whereas non-conserved regions accumulate many mutations.

It would be great if you could provide references for your response!

I'm a little confused, what do you mean by "conserved regions"? Are you referring to the survival of the mutations in coming generations due to NS? In that case, this is not what I'm searching for in my question, where I do not care about survival of the mutations happening.

@Alex, yes, by "conserved regions" I mean a fragment of the DNA or protein sequence that is conserved. That is, if you compare the same fragment among different individuals in the same species (or among different species) you will see that most of the nucleotides/aminoacids are either identical, or very similar (i.e. similar chemical or physical properties, e.g. same charge or size). These regions frequently are functional (e.g. a conserved protein region is involved in the catalytic activity) and mutations tend to be deleterious, hence they are eliminated by natural selection.

@Bez, thanks, I will try to include some references, I am trying to find which ones are more appropriate so it may take some time.

@Alex, if I understand correctly then, you want to know the mutation rate during the lifespan of an individual, and whether this is homogenous thorough the genome? That is challenging since there is no studies (AFAIK) on the evolution of an individual's genome over time. However, swbarnes2's comment about mutation hot spots may be indeed relevant to this. For example, this paper PMID:8832894 describes the existence of nonrandom patterns (mutation hot spots) in the gene TP53 (P53) associated with lung cancer.

Another paper that might be relevant: PMID:9926936


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where to find the relative frequency distribution of synonymous codons
Most amino acids can be encoded by more than one codon. For example, Serine can be encoded by any one of {UCU, UCC, UCA, UCG, AGU, AGC}.
My question is in two parts:
1) what are the relative frequencies of those codons? This question can be equivalently phrased in probabilistic terms: What is the probability that a given amino acid was encoded by particular codon?
2) Is this probability dependent on the context (the neighboring codons/amino acids)?

The phenomenon of using different codons with different probabilities is called codon usage bias. How the different codons are used is sometimes pretty different between species and requires some care. This is especially true when you want to overexpress sequences in bacteria to produce protein, which may need codon optimization to ensure an optimal codon usage (otherwise rare tRNAs can slow down the translation process). There is a database (based on the NCBI Genbank) which gives you the codon probabilities for different species:

Codon Usage Database

Additionally, these papers might be interesting:

Synonymous codon usage in bacteria.
An evaluation of measures of synonymous codon usage bias.

Regarding your second question, I don't think (and I haven't found any evidence either) that the codon usage is dependent on the neighbours.

The codon usage biases are species-dependant, so you may have to measure it for the genome or set of genes you are interested in.
This bias is at least in some cases correlated to the genome composition in terms of A, T, G and C (see figure 3 of this paper about cyanobacteria). So in a sense, it is indeed dependent on the context if you include nucleotide composition in what you call "context".


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Does human eye lens have a magnification of its own?
I have always wondered if the lens in our eyes have any sort of magnification by default. And if yes, if we're actually seeing everything around us bigger/smaller than what they actually are!
Has any research been done on this?

What do you mean, "bigger/smaller than what they actually are"? What is your definition for seeing a thing in an absolute size, because I can think of none that makes sense? (And no, the human eye does not work like a camera, so saying that when the image of a 2 mm worm hits a 2 mm stretch of neurons in the retina you have "actual size" doesn't make sense, because it doesn't matter for your visual perception).

The magnification by the lens of the eye is well understood.  This document, written by Dr. Glenn Chapman at Simon Frasier University in British Columbia, Canada, lays out some of the technical details.  The image below is taken from that document. I modified it slightly by enlarging the $s$ and $s'$ variables because they are important for this answer.

For a simple lens like that in our eyes, magnification, $m$, is calculated as
$$m= \frac{s'}{s}$$
where $s'$ is the distance between the lens and the retina at the back of the eye, and $s$ is the distance between the object and the lens. For the human eye, the distance $s'$ is about 24 mm, or just a bit under 1 inch.  For an object to have exactly 1:1 size ratio (no magnification or reduction), it would have to be exactly that same distance from the lens. That is, the object would have to be about 24 mm in front of our eye. The problem is that, unless you are myopic (nearsighted), you cannot focus on objects closer than about 25 cm (about 10 inches)
Most objects are much farther away from the lens than 24 mm. That means $s$ is a much larger value than $s'$, making $m$ a fraction less than 1. A value less than 1 means that our lens is not magnifying the object but instead is reducing or demagnifying the object.
As a simple experiment, hold your finger upright in front of your eyes at arms length.  Bring your finger closer and closer until you feel your eye lashes. Your finger looks smallest when it is farthest away from your eye. As you bring it closer ($s$ is getting smaller) your finger appears larger and larger. When your finger gets to about 24 mm, then $m=1$. When your finger touches your eye lashes, the distance is less than 24 mm, and the finger is magnified to larger than actual size ($s > s'$ and $m > 1$).
This also explains why distant objects appear smaller than closer objects. If you see a stop sign at 500 m and a stop sign at 100 m, the closer sign looks larger than the more distant sign.  But which is the actual size? Neither, because the lens changes the apparent size. The way to see the actual size is to stand with your eye about 24 mm away from the sign. Then, magnification will be exactly 1:1 and you'll know the true size of the sign. You just won't be able to focus on it.


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Chest muscle and female breast size
Do female chest size have anything to do with muscle?
I know many female athlete and their average breast size is much bigger than normal female that does not tend to play sports. Do this have any relation to chest muscle?? If so can you explain how it does.
Thanks in advance

The female breast is composed primarily of fat and connective tissue plus lobules and ducts for milk production and delivery.  The pectoralis muscles form a thin layer beneath the breast, as seen in the figure in the link. An athletic female can enlarge the size of the pectoralis muscle and the laterals muscles, just as male athletes can enlarge their "pecs" and "lats".
Exercise burns fat so athletic women often experience reduction in breast size. Of course, other factors such as diet and genetics also influence the effects of exercise on fat burning.
So, athletic females with enlarged lateralis muscles and pectoralis muscles may have a larger overall bust size but the cup size of their breasts might actually be reduced.


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Do ants or other insects sleep, and if so why?
I was thinking yesterday about insects (as there was a spider in the house, and I couldn't help but think of anything else, even though they aren't insects), and I started to wonder if ants sleep?
After thinking about it for a while I decided that they might sleep, but then what would be the purpose of sleeping for them? My limited understanding of the need of sleep is that it is used for the brain to compartmentalise the events of the day and allow memories to be formed. But ants don't really have to think about much during the day, given that they act more as a collective than an individual. Or in the case of other insects, they have simpler more instinctive brains which rely on taxis, reflexes and kineses.
So, do ants and other insects sleep (or do they have a different type of sleep to us) and what would the purpose of it be for them?

related: http://biology.stackexchange.com/questions/19176/where-do-butterflies-sleep

What happened to the purpose of sleep as a mechanism of physical relaxation? After a hard day's work, they would need to relax.

"act more as a collective than an individual" That's just perspective, same can be said for humans.

@Jonathan Yeah I completely agree, I meant more of a collective intelligence. Badly worded :p

Sleep can have many uses, and may have different uses for different species. NIH claims that sleep may be used also to help remove toxins from the brain, which would be beneficial for ants, too.

Do amoebas and other single cellular organisms sleep?

Wow, this is a really interesting topic. I had no idea arthropods required sleep. Perhaps the purpose of sleep is more than just the consolidation of memories - and some insects do, in fact, have memories - including neural repair and rejuvenation. Maybe the neural systems have to be turned off for maintenance to be effective.

A quick search on Web of Science yields "Polyphasic Wake/Sleep Episodes in the Fire Ant, Solenopsis Invicta" (Cassill et al., 2009, @Mike Taylor found an accessable copy here) as one of the first hits.
The main points from the abstract:

Yes, ants sleep.
indicators of deep sleep:

ants are non-responsive to contact by other ants and antennae are folded
rapid antennal movement (RAM sleep)

Queens have about 92 sleep episodes per day, each 6 minutes long.
Queens synchronize their wake/sleep cycles.
Workers have about 253 sleep episodes per day, each 1.1 minutes long.
"Activity episodes were unaffected by light/dark periods."

If you study the paper you might find more information in its introduction or in the references regarding why ants sleep, although there doesn't seem to be scientific consens. The abstract only says that the shorter total sleeping time of the workers is likely related to them being disposable.

Interesting, a queen gets 9 hours of sleep, a worker only 4.5 hours...

@tohecz: also queens sleeps are much longer & less interrupted -> more quality sleep time.

Are there animals that don't need sleep?

The short answer is apparently yes.  Studies on sleep in insects date back to papers published by Phil and Nellie Rau in 1916 and 1938. Hussaini et al. (2003) showed that sleep does affect memory formation in honey bees. They showed that retention of extinction learning is significantly reduced in bees that were sleep-deprived.  More about sleep in honeybees can be found in this paper by Eban-Rothschild and Block (2012).
I did not find anything on sleeping in ants after a brief Google Scholar search but ants and bees are both hymenopterans, so it's reasonable to hypothesize that many of the effects of sleep (and sleep deprivation) found in bees could also apply to ants. The Eban-Rothschild and Block paper linked above has some comparisons of circadian rhythms between ants and bees before discussing sleep as a function of circadian rhythms.


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XXY (Klinefelter's) & Trisomy 21 & X-inactivation
I read that X-inactivation doesn't tend to happen in males, but then when someone is XXY, they are a male because of the Y. However these individuals tend to live. So does that mean that X-inactivation happens in males or else these individuals would die?

Trisomy 21 (of the 21st chromosome) and being an XXY individual are two quite different things. Isn't your question about the XXY sexual chromosome pattern (which is BTW not trisomy, but Klinefelter's syndrome)? Or is it about a special case of Klinefelter AND trisomic 21 individual (I don't even know if that exists...)?

Do you confound the Down syndrome (Trisomy 21) and the Klinefelter Syndrome (XXY)?

So basically, the question is: "Do XXY (Klinefelter Syndrome) individuals inactivate (dosage compensation) one of their X-chromsome?". Why is it written Trisomy 21 in the title?

X-inactivation does occur in XXY individuals.
In phenotypically normal XX females, one X chromosome is inactivated.  Which one of the two X chromosomes is inactivated in any given cell is random. Therefore, about one half of the cells should have the maternal X active and the other half should have the paternal X active.
XXY individuals show a wide range of clinical symptoms and intellectual ability.  Iitsuka et al. (2000) suggested that this variation may be explained by a bias in X-inactivation.   They found that about 31% (5 of 16) individuals (either XXY or XXYY) shows a very strong bias of X inactivation, which they defined as at least 80% of the cells inactivating one particular X chromosome. Two individuals has biased inactivation of the paternal X and the other three had biased inactivation of one of the maternal X chromosomes. The sample size is rather small (not surprising) but X inactivation is occuring.  Samango-Sprouse (2001) argues that incomplete inactivation of one X chromosome may also explain some of the more severe clinical mental disorders.
For Trisomy 21 (Down's Syndrome), the individual as three copies of chromosome 21, so X inactivation is not an issue. However, scientists are studying whether Xist can shut down the third copy of chromosome 21.  The Xist gene is transcribed to produce a large molecule of RNA. That RNA is what usually causes X inactivation.  Jiang et al. (2013) were able to show that Xist can coat one of the chromosome 21 copies, performing essentially the same inactivation function that it does for the X chromosome. So far, though, this work has been entirely in the lab (in vitro).


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Difference between thylakoids and lamellae in a chloroplast?
I'm slightly confused as to the difference between thylakoids and lamellae. My understanding was that thylakoids are 'discs' that are stacked into grana and there is a membrane between the grana called the integranal lamellae. However in my text book it says that 'the inner membrane is folded into lamellae, which are stacked up like piles of pennies. Each stack of lamallae is called a granum.' This sounds to me like the description of thylakoids.
It later says 'grana are stacks of flattened membrane compartments, called thylakoids'...
Could someone clarify this?
Thank you in advance :)

thylakoid is the individual disc, and the granum is the stack. That's the basics of it

The answer above goes in depth so I will try go off that.
Firstly, lamella is the word used to describe plate-like structures. A thylakoid therefore, being a flattened vesicle, would fit this description, so a thylakoid is a type of lamella.
As mentioned earlier, a lamellar system consists of uniform thylakoids, the thylakoids being the individual lamella.
I have the same textbook as you, OCR A2 Biology, and I must admit I had the same confusion. What this textbook fails to mention is the fact that thylakoids are just one type of lamellae.
The textbook also states that the inner membrane of the chloroplast is "folded into lamellae (thin plates)". There are two types of lamellae in the chloroplast, thylakoids and intergranal lamellae, both are stacked, however only thylakoids appear as "piles of pennies" as it states. Intergranal lamellae look nothing like pennies, which is why the textbook is strongly misleading, they are big flattened bits of membrane that connect together different grana (stacks of thylakoids).
Note: my answer comes in 3 years late (I'm currently doing my A2), and the textbook in question will see its last use this year as the current A2 level syllabus is updated, I hope my answer still helps to clear up any confusion should OCR mess up again on this one

can you give some references for additional information and/or to back up your answer? It's something that we always appreciate in this community.


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Nucleotide sequence for STRING protein sequence
I have protein sequences from STRING database:
The amino acid sequence files are like this:

4932.Q0010 (Saccharomyces cerevisiae)
  MYYIMFLYNMLLIIILIFYSIVGVPIIIFNNNYYWDPDIFLFIIYYFIKFIIIFNLYLYYMINYIVYTPSGSPPGRGTYI
  LLYNMLYSYNMFIDYVMKFITCVTYMYLMFWLLSPTPSPYYVSEVPVS

I want the corresponding nucleotide sequence for the same protein ID.

4932.Q0010

I tried emboss http://www.ebi.ac.uk/Tools/st/emboss_backtranseq/
But emboss is based on codon usage and backtranslate and it doesn't give me the original nucleotide sequence.
Then I tried DDBJ http://getentry.ddbj.nig.ac.jp/top-e.html
But DDBJ gives only amino acid sequences for corresponding Uniprot ID.
How do i get the original nucleotide sequence for the STRING protein sequences using STRING id or UniProt ID?
Any help in this regard is highly appreciated.

This should effectively clear your question http://www.uniprot.org/help/canonical_nucleotide

What is meant by canonical UniProtKB sequence?

@Raghavakrishna As it says, although most proteins derive from DNA translation, there isn't only a single way in which you can back translate the protein into nucleotide sequences.

@VivekRai But emboss can be used to backtranslate? http://www.ebi.ac.uk/Tools/st/emboss_backtranseq/

Google is not a bad resource for such a question.
In this case I find that the Yeast Genome site has a button which returns the nucleotide sequence. You can select the genomic sequence for the locus or the coding (CDS) sequence.
http://www.yeastgenome.org/cgi-bin/locus.fpl?locus=Q0010
They also give a link to NCBI at the bottom of the page.  I think the reason you were having such a hard time is that UniProt extracted the protein sequence from the mitochondrial genome record.  Like many genome ORF predictions, Q0010 does not seem to have a distinct nucleotide record assigned yet.
Summary:
In general  you can do a web search for the uniprot id to start.  In many cases, like this one you will find that the nucleotide seq is only a chromosomal sequence record.   Biodatabases are a bit of a maze - there are scores of them out there, you may find that someone has clipped the nucleotide sequence of the gene out, which is helpful if there are introns!

OK for yeast,This is good.But for other organisms what is the way out?

i added a note to the post...


text:
Why sleep? No, actually, why wake?
I was just reading the sleep threads, and I wondered, why is the body so constructed so that sleep is necessary? (Is it just a design error?) But then, how do things come to be awake at all? How did this happen? Yes, I can see the advantages, but how did it happen? What is "awake"? Are single-cell animals awake?
The question I want to ask is, how did things progress from just sitting around ingesting and growing, like plants, to being something more? Is it more? What do "wakers" have that the rest don't?
Sorry, I'm not a biologist, this may be a foolish question, or in the wrong place.

Hi and welcome to the Biology part of SE! I think you're tying in a few different concepts here, and they're really more philosophical than biological. I don't think it makes for a good SE question, but feel free to join me in Chat and I can talk you through some of the basics that I'm aware of.

We should be fine using this: http://chat.stackexchange.com/rooms/1997/biology

That chat room won't let me in. Never mind. But if you want to copy my question I could follow other people chatting about it...

these are fundamental questions in sleep research done by neuro/sleep biologists... probably a field which is poorly represented in the stackexchange community. Its a common question about sleep, but also regarded well enough for it to be funded by the NIH for research...

Based on various comments, I've expanded this answer. Though long, I cannot cover the depth of the topic of sleep but I tried to address the issues asked in the original question while broadly highlighting various aspects about sleep research. I welcome any suggestions for improvement.
What is sleep?
To know what it means to be awake, you must know what it means to be in a state of sleep. These are two alternative states for animals that sleep.
Finding a concise scientific definition of sleep is difficult, probably because sleep is a very complex process. For example, Diekelmann and Born (2010) state that,

Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory...

and later

Sleep is characterized by the cyclic occurrence of rapid eye movement (REM) sleep and non-REM sleep, which includes slow wave sleep (SWS, stages 3 and 4) and lighter sleep stages 1 and 2....

Most attempts to explain what sleep is include the four stages of sleep along with REM (rapid eye movement sleep). The stages are nicely explained by this National Institutes of Heath website on Brain Basics: Understanding Sleep. Each stage of sleep can be identified by specific types of brain waves, shown below (image from here).

Notice that the first wave pattern is characteristic of being awake.  The wave patterns change as an individual becomes drowsy and then falls asleep. While asleep, the brain cycles through the different stages, each with its characteristic brain waves.  Associated with these stages are changes in metabolic activity and physical capabilities. For example, the Brain Basics site notes that we become less responsive to external stimuli and metabolic activity slows. During REM, breathing becomes rapid and we can't move the muscles in our arms or legs. Similar states are found in other invertebrate and vertebrate organisms, which suggests that these are common indicators of sleep or a sleep-like state. Some examples of these states are given in the citations and links below.
Defining "awake" seems just as difficult as defining "asleep" but once again neural activity seems to be key indicator. As shown in the figure above, being awake has characteristic wave patterns in the brain that are distinct from the wave patterns associated with sleep. In addition, none of the physiological/physical states associated with sleep stages are present when you are awake.
In both cases, asleep and awake, the indicators seem to be based on characteristic neurological activities in the brain or, in the case of some invertebrtes, the organized nervous system.  This interpretation is important when considering whether organisms without any type of nervous system is capable of sleep or the alternate state: awake.  More on this at the end.
Why sleep?
Science magazine, in the 125th anniversary issue, made a list of 125 big questions that remain to be answered by scientists. One of those questions was "Why do we sleep?" The role of sleep remains elusive but many ideas have been put forth about the role of and the evolution of sleep. The leading idea seems to be memory consolidation. This article by Kavanau (1997) reviews ideas about the function of sleep and why it evolved.  He suggests that sleep and memory evolved as as ways to improve or maintain effective connections among the nerve cells in the brain. Some circuits are used frequently, such as those used to process sensory information like vision. Other circuits are used less frequency, such as circuits that can be used to store memories. Sleep may allow those infrequently used circuits to be activated and used without causing conflict with the circuits used during "restful waking." In other words, sleep may allow the lesser used circuits to be exercised, which can help to consolidate memories. So, at least one function of sleep may be to help maintain efficiency in how information is moved around the brain by maintaining the brain circuitry.  See also this review by Siegel (2005) and the previously mentioned article by Diekelmann and Born (2010).
This Scitable article has a nice overview of the importance of sleep for humans, as does the Brain Basics site.
What organisms sleep or have sleep-like activity?
Sleep has been well-studied in vertebrates, from fishes (Marshall 1972) to mammals (Pace-Schott and Hobson 2002). However, not all vertebrates necessarily sleep (Kavanau 1998). For example, continuously swimming fishes like some sharks and blind cave fishes may not sleep. These are just three references of many about sleep in vertebrates.
Sleep and sleep-like activity has not been as well studied in inertebrates. As noted in this thread, there is evidence for sleep in at least some insects. Cephalopods like octopuses show signs of sleep (Mather 2008). Caenorhabditis elegans, a nematode worm and model biological system, shows sleep-like states tht are similar to mammals and fruit flies (Raizen et al. 2008). The most basal organism that shows evidence of sleep-like patterns is a jellyfish called Chironex fleckeri (Kavanau 2006). Cnidarians like jellyfishes are the basal (most "simple") group of organisms with an organized nervous system. Interestingly, C. fleckeri process a lot of visual information obtained through their 24 eyes. Twelve of the eyes are simple, light-receiving structures but 8 of the eyes are camera-like, meaning they have a lens.  Kavanau (2006) argued that sleep (up to 15 hours) in this jellyfish allows time for its simple nervous system to process the visual information obtained while it is awake. The presence of sleep-like activity in jellyfish and nematode worms suggest that sleep is an evolutionarily ancient phenomenon.
This Wikipedia page on sleep in non-humans overviews evidence for sleep in vertebrates and invertebrates. It's not clear whether androids sleep or what they dream about if they do sleep.$^1$
Do single-celled organisms sleep?
This is (to me) a tricky question. Sleep is associated with specific types of neural activity in the brain or nervous system. In addition, sleep-like neural activity has been found in diversity of organisms with some type of nervous system, and seems evolutionarily old. I therefore think that any organism that has some form of organized neural center (brain, brain-like organ or centralized nervous system) has the potential to show some type of sleep-like patterns.
In contrast, organisms lacking any type organized nervous system would not be capable of sleep, at least as currently defined. If they do not sleep, then they also cannot be awake because being "awake" seems to be recognized as neural activity not typical of sleep.  Therefore, it seems to me that single celled organisms like bacteria and paramecium are neither sleeping nor awake.  Plants are neither sleeping nor awake. They are metabolically active but they are neither asleep nor awake because they do not have any type of neural activity.
I'm not a sleep researcher (but sometimes I am a sleepy one) nor am I a neurophysiologist. I just walked through my train of thought. I welcome contrary views along with the supporting science.
Literature Cited
Diekelmann, S. and J. Born. 2006. The memory function of sleep. Nature Reviews Neuroscience 11: 114-126.
Kavanau, J.L. 1997. Origin and evolution of sleep: Roles of vision and endothermy. Brain Research Bulletin 42: 245-264.
Kavanau, J.L. 1998. Vertebrates that never sleep: Implications for sleep's basic function.
Kavanau, J.L. 2006. Is sleep's 'supreme mystery' unraveling? An evolutionary analysis of sleep encounters no mystery; nr does life's earliest sleep, recently discovered in jellyfish. Medical Hypotheses 66: 3-9.
Marshall, N.B. 1972. Sleep in fishes. Proceedings of the Royal Society of Medicine (abstract).
Mather, J.A. 2008. Cephalopod consciousness: Behavioral evidence. Consciousness and cognition 17: 37-48.
Pace-Schott, E.F. and J.A. Hobson. 2002. The neurobiology of sleep: Genetics, cellular physiology and subcortical networks. Nature Reviews Neuroscience 3: 591-605.
Raizen, D.M. et al. 2008. Lethargus is a Caenorhabditis elegans sleep-like state. Nature 451: 561-572.
Siegel, J.M. 2005. Clues to the functions of mammalian sleep. Nature 437: 1264-1271.
Footnote

I could not resist.

I think your answer can be considered totally complete to this broad question if you could add a bit more about the standard definitions of "sleep" and "awake" in science and precise for which species the concept of sleep applies.

@Remi.b Thanks for the suggestion. I'll try to carve out time later today after my classes.

That article is really interesting. I think you have answered my question, and in doing so, have made it seem more reasonable than it was. I look forward to the changes Remi.b suggests.

So sleep is the brain defragmenting itself. OK. If you don't have any software running you don't need to sleep. OK. And the reason we do it is that evolution threw it at us and it seemed a good idea. OK. I would give you +10 if I could.

@RedSonja Yes, sleeps helps to consolidate memories. Having memories, even very simple ones, may provide an evolutionary advantage (remembering where food resources are, what food is safe to eat, which organisms are dangerous, etc.). You accepted the answer (thanks!) but you can also click on the upward arrow to say "Good answer" if you wish.

All organisms (except viruses?) need some kind of nutrition to survive and reproductive activities for the species to survive. As humans don't do these while asleep in a first approximation I would consider those life phases as sleep when these do not happen. In this sense clostridium bacteria could be considered asleep when in their endospore states, a sunflower seed could also be considered asleep as it is inactive.

So we could say sunflower seeds wake up at some point?

@RedSonja Yes, along the above I would consider the seed awake as soon as it starts using up its stored food.

I don't think I can see any phase of a plant's life as being awake. No. But then I don't really know what "awake" means.

Sleep is associated with neural activity. Bacteria and sunflowers do not have a nervous system so could not have any form of sleep. Endospores and seeds can be dormant but not asleep.

@MikeTaylor Is the “neural activity” criterion widely accepted in the definition of sleep?

If “neural activity” is a necessary condition to call a state of an organism “sleep”, then the original question “Are single-cell animals awake?” makes little sense to me.

Sleep includes changes in neural activity patterns of the brain see here. These changes in neural activity do cause changes in metabolic activity, such as rapid eye movement and suspension of voluntary muscle activity. I agree than awake doesn't make sense for organisms that don't have sleep-like patterns but I did not address the philosophical implications of that part of the question.

btw, it always sounds a bit weird to say "for the species to survive". It seems like you suggest an evolutionary goal to allow the species to survive.

@MikeTaylor It's not a philosophical implication introduced by the answer, rather one of the original questions you have ignored: “Are single-cell animals awake?”. If you think that question does not make sense then please criticise the question, not the reply that takes it seriously and attempts to give a logical answer.

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


text:
What would happen if one eats silica gel?
What happens if one actually does go about eating the beads in those "do-not-eat" packets?

did.... did you ask this question after ingesting a packet of silica gel?

@jamesmassey uhm...just asking for a friend-

Usually, nothing happens if you eat silica gel. In fact, you eat it all the time. Silica is added to improve flow in powdered foods. It occurs naturally in water, where it may help confer resistance against developing senility. Silica is just another name for silicon dioxide, the main component of sand.
Mayby you think if silica is harmless to eat, why do the packets carry the warning? The answer is that some silica contains toxic additives. For example, silica gel beads may contain toxic and potentially carcinogenic cobalt(II) chloride, which is added as a moisture indicator. You can recognize silica containing cobalt chloride because it will be colored blue (dry) or pink (hydrated). Another common moisture indicator is methyl violet, which is orange (dry) or green (hydrated). Methyl violet is a mutagen and mitotic poison. While you can expect most silica you encounter will be non-toxic, ingestion of a colored product warrants a call to Poison Control.

Also, even if no additives were added deliberately, the silica may contain traces of harmful substances left over from the production process. It's a legal/regulatory issue that silica meant for consumption is strictly controlled and of high purity, just like other food additives, while silica for technical uses is regulated differently. So the warning tells you that this particular silica is not licensed as food additive, but it's not necessarily poisonous.

I don't think it would harm you: apparently silica gel is a widely-used food additive. According to Wikipedia:

Silica gel, also referred to as silica aerogel or hydrated silica, has FDA GRAS (generally recognized as safe) status, meaning it can be added to food products without needing approval. Silica is allowed to be added to food in the US at up to 2% as permitted under 21 CFR 172.480. In the EU it can be in up to 5% concentrations.
Listed uses include: anticaking agent, defoaming agent, stabilizer, adsorbent, carrier, conditioning agent, chillproofing agent, filter aid, emulsifying agent, viscosity control agent, and anti-settling agent.

However, obviously, you shouldn't plan on eating lots of it.

it is the same as eating sand right?

The main problem is that small kids get hand on this and get it into the airways.


text:
DNA extraction from oil-containing seeds
Which protocol of DNA extraction from plant oil-containing seeds take fast and good result in purity that can use in RT-PCR(Real Time polymerase chain reaction)?

I guess you mean realtime with RT, right?

@Chris yes that's right

Maybe this is interesting for you.

@Chris you should post that as answer. You can copy paste the protocol

The paper "Modified method for combined DNA and RNA isolation from peanut and other oil seeds." has a nice protocol for isolating DNA and RNA (which later can either be differentially digested or precipitated) from oil seeds for PCR. You can find the complete paper in the link above, the materials and methods sections says the following for the extraction method:

RNA and DNA isolation
Approximately 1–1.2 g of dried seed of each genotype was utilized in
  extraction. Seeds were frozen with liquid nitrogen and pulverized by
  grinding with mortar and pestle until a fine powder. Tissue was placed
  into 10 mL solution I (100 mM Tris, 150 mM LiCl, 50 mM EDTA, 1.5 %
  SDS, 2 % PVP-40, 1.5 % b-mercaptoethanol) buffer, pH 7.5, and mixed
  thoroughly by vortexing or inversion.
To the homogenized tissue, a 5
  mL acid phenol, pH 4.3 (Fisher Scientific, Pittsburg, PA) was added
  and tissue was mixed thorough for 5 min, followed by the addition of 5
  mL chloroform:isoamyl alcohol (24:1) and mixed for an additional 5
  min. The homogenate was centrifuged for 10 min and the upper aqueous
  layer (around 9 mL) was transferred to a fresh 40 mL tube containing 9
  mL of solution II (2 M guanidinium thiocyanate, 0.5 M sodium citrate,
  1.5 M ammonium acetate, 1 % N-lauroylsarcosine) buffer, pH 5.2, mixed by gentle inversion, and allowed to incubate for 10 min at room
  temperature.
After incubation, a 4.5 mL phenol:chloroform:isoamyl
  alcohol (25:24:1), pH 6.7 was added, mixed thoroughly for 5 min,
  centrifuged for 10 min at 13,000g, and the aqueous layer (around 16
  mL) was transferred to a new 40 mL tube.
To the transferred solution,
  9 mL 1.2 M NaCl and 9 mL isopropanol were added, mixed, placed on ice
  for at least 1 h, and centrifuged for 15 min at 13,000g. The liquid
  was discarded and the resulting pellet was washed with 2 mL cold 70 %
  ethanol, dried, and resuspended in 4 mL RNase-free water.
4 mL 4 M
  LiCl was added, mixed, placed on ice in the refrigerator for at least
  1 h, and centrifuged for 15 min at 4°C at 13,000g. The supernatant
  (around 8 mL) was transferred to a new 40 mL tube for DNA isolation
  and the pellet was retained for RNA isolation. For RNA isolation, the
  pellet was washed with 2 mL ice-cold 70 % ethanol, dried, and
  resuspended in 750 lL RNase-free water.
For DNA isolation, 8 mL
  isopropanol was added to the transferred supernatant tube, mixed well,
  centrifuged for 5 min, discarded the liquid, washed pellet with 2 mL
  ice-cold 70 % ethanol, dried, and resulting pellet was resuspended in
  500 lL 10 mMTris, pH7.5. The amount of DNA or RNA was determined using
  Nanodrop 2000c spectrophotometer (Thermo Scientific, Wilmington, DE).


text:
Are there known downsides to removing UV mutation hotspots to prevent some skin cancers (Genetic sunblock)?
Khavari et al. recently demonstrated that a significant fraction of  one of the major forms of skin cancer (cutaneous squamous cell carcinomas) are associated with a mutated KNSTRN gene (a protein associated with the kinetochore). They identify a specific region of the gene as being a hotspot for UV induced mutation and suggest that these mutations may be an early event in the development of this type of skin cancer.(1)
Abstract from their nature paper (paywalled):

Here we report the discovery of recurrent mutations concentrated at an ultraviolet signature hotspot in KNSTRN, which encodes a kinetochore protein, in 19% of cutaneous squamous cell carcinomas (SCCs). Cancer-associated KNSTRN mutations, most notably those encoding p.Ser24Phe, disrupt chromatid cohesion in normal cells, occur in SCC precursors, correlate with increased aneuploidy in primary tumors and enhance tumorigenesis in vivo. These findings suggest a role for KNSTRN mutagenesis in SCC development.(2)

My question:
Scientists could theoretically alter the nucleotide sequence of the KNSTRN gene to remove the mutation hotspot, potentially lowering the incidence of this type of skin cancer. But are there any downsides to doing so? Are there any cases where a UV mutatable hotspot has shown to have some useful function in a cell or organism?
Thanks!

http://www.sciencedaily.com/releases/2014/09/140907181722.htm
http://www.nature.com/ng/journal/vaop/ncurrent/full/ng.3091.html

Short-wave UV light (UVB and UVC) causes transition mutations at dipyrmidine sequences (ref.). In the work presented on KNSTRN quoted by the OP the authors report that 19 from a panel of 100 squamous cell carcinomas (SCC) contained a mutation in KNSTRN (and furthermore three of these contained no other mutation across the six genes that were analysed (Fig. 1b)). Normalising for ORF length this makes it the 3rd most recurrent mutated gene. It would seem therefore that it a fairly important mutagenic target. In a broadened set of SCCs they found a total of 29 KSTRN mutations, and of these 13 were Ser24Phe (TCC>TTC) mutations, which they refer to as a 'hotspot'.
Accepting the arguments in the answer from @Chris it is still interesting to consider how one might remove such a hotspot. The normal amino acid at this position is a serine. Here is the human codon useage for ser, obtained from here:

TCT 14.6%
TCC 22.0%
TCA 15.0%
TCG  6.0%
AGT 11.9%
AGC 19.4%

It would seem therefore that it would be theoretically possible to edit the Ser24 codon from the UV-sensitive TCC to AGC, essentially eliminating this 'hotspot'.
This, of course, doesn't answer the question - are there downsides to this? I already selected a synonymous codon with a similar frequency of useage so that shouldn't be a problem. However here is an example of a synonymous codon substitution which has an effect upon splicing of the LMNA gene resulting in muscular dystrophy, and the paper cites several other examples of this. (I haven't actually checked to see where the Ser24 codon lies in relation the exon-intron boundaries in the KNSTRN gene.) No doubt there are other mechanisms by which my proposed edit could have unwanted effects. It would have to be tested carefully, and so we come back around to a cost-benefit analysis - would it be worth developing this editing idea (even if it were feasible as a therapy) given that there are clearly many paths to SCC not involving this specific mutation.

This is a good point. In addition to maintaining the same amino acid and taking care to avoid splice site junctions, you'd have to consider if there were any protein, DNA or RNA interacting sequences encoded in the region of interest. If the region were in a non-coding transcript it could also be problematic. Anything else?

The region can also contain regulatory regions (also when this inside a gene) which you probably mess up with.

This is actually a bad idea for severeal reasons: First it is not a good idea to tamper with genes, especially not with ones which are involved in the regulation of mitosis and the correct segregation of sister chromatids. Remember that a one amino acid exchange because of a C to T transition causes the problems with SCC? Into what do you want to change the sequence anyway?
Then this is not the only mutation linked to SCC - mutations in TP53 and CDKN2A are more important here. And even if you manage to change the sequences here which are the causative reason for SCC there are other mutations that will then occur. Simply by chance. It is probably a good idea to target the mutant KNSTRN protein with a treatment as this is already done for other proteins (although these are usually enzymes), but changing it will most likely not only not work but cause other problems as well.
Another problem (even when you use a synonymous codon which does not lead to an amino acid exchange) is that you can disrupt genetic regulatory regions. Not all of these regions are located in the promoters of genes, quite a number of them are found inside of genes. Here even a single nucleotide exchange can prevent a transcription factor from binding to its recognition site. A prominent example for the is the HERC2/OCA2 polymorphism where a single nucleotide polymorphism in HERC2 alters a transcription factor binding site and thus alters the expression of OCA2.
The solution here is pretty easy: Avoid prolonged exposure to UV light whenever possible.

This is generally true, but for the specific regions in question, transgenic mice could be used to test these hypotheses, assuming the same effect held in mice.

The problem with mice is that they usually don't develop skin cancers. You need to use mice with other defects as well and this makes the model much weaker.

sure, though I think its far from saying that this is not a testable hypothesis, and that they will try to do so.

The problem with mutations is that this will cause severe problems when we change the code like this. So you have to think about cell type specific knock-ins (probably inducable) and then see what the outcome is. This is surely interesting in terms of basic research, but I don't see any practic use for it (which is no reason to not analyze this).

fair enough, @Chris!

@Chris I can see you're point but my question assumes a bit of technical knowledge - obviously one would want to avoid amino-acid changes. I realize other mutation will continue to occur elsewhere and that the engineered site may itself ocasionaly mutate - the point is to lower the mutation rate at this specific site. I think preventative genetic intervention could be vastly superior to antibodies, small molecules or other protein targeting methods but the technologies aren't quite there yet.


text:
Transcription rate expressed in microarray per hour
This article gives measurement of transcription rate  and the unit they're using is microarray per hour.
For example, at 27°C the average expression of their genes is 236.1 microarray per hour (page 4). What does this unit mean? Given that each DNA spot in a microarray contain 1 picomole of DNA (wiki), does it mean that the gene is transcribed into 1 picomole of RNA (or of nucleotides?) per hour? Or does it mean that 236.1 RNA are created every hours?

The units here are relative units of intensity.  There may be about a picomole of probes on a microarray spot, but the units of intensity are not scaled to the precise concentration of DNA on the spot.
There are many variables which make exact measurements of intensity difficult to translate into the number of RNA bound to a spot.  The main one is nonspecific or non-target binding.  The oligomer on the array surface is typically between 25 and 50 bases long - it isn't the entire length of the RNA being tested by a given spot.  Another RNA may have some or most of the same sequence as a probe, or some labelled RNA will tend to get associated with some spots.  Usually factors such as the position of the spot on the array surface, the GC composition of the probe and variations in the batch of RNA preparation will also cause the intensity to vary.
Still, even with all this, with the same prep conditions and with an identical set of arrays, its valid to look at the intensity over time.  In this paper, the investigators took array measurements at different time points and at two different temperatures after 4-Thiouracil  is added to the cells, which allows one to follow RNA produced by transcription at a given time.
Since the units are arbitrary but still proportional to the mRNA found in the cells, a difference experiment like this is valid, even if the absolute concentration of any given RNA is still a bit of a mystery.


text:
Influence of temperature on protein binding and decay rates
For computer modeling purposes, I am looking for some referenced quantitative measurements of the effect(s) of temperature on the dynamic of biochemical reactions.
Question
In particular, my question is:
How does temperature influences rate of protein binding to a DNA-binding motif?

I am NOT looking for..
I am not looking for a theoretical explanation of how temperature influences this process (I have basic understanding of the importance of the activation energy as displayed on a Maxwell-Boltzman distribution and of the michaelis-menten equation).
I am looking for..
I am looking for a function (eventually expressing the michaelis-menten constant as a function of the temperature) that I can plug in my algorithms to incorporate the influence of various temperatures on the process I want to simulate. I want to simulate the average gene network from an average standard eukaryote. For other purpose, I chose parameter values coming from the yeast. A index such as the $Q_{10}$ would be very useful as well.
Similar already-answered question
A similar question (influence of temperature on transcription rate) has been asked and answered (by @rhill45) here.

Let's do your second one first, you want to find the rate of binding:
Yes you are right you need to calculate for km
I think I found the paper that ties temp into the reaction rate:
statistical approach called response surface methodology (RSM) is used for the prediction of the kinetic constants of glucose oxidase (GOx) as a function of reaction temperature and pH. Lineweaver–Burk transformation of the Michaelis–Menten equation was utilized as the integral part of the RSM algorithm. The effects of variables, namely reciprocal of substrate concentration (0.033–0.5 mM−1), reaction temperature (14.9–40.1 °C) and reaction pH (pH 4.4–8.5) on the reciprocal of initial reaction rate were evaluated and a second order polynomial model was fitted by a central composite circumscribed design (CCCD).
Biochemical Engineering Journal
August 2005, Vol.25(1):55–62, doi:10.1016/j.bej.2005.04.001
A new approach for determination of enzyme kinetic constants using response surface methodology
İsmail Hakkı Boyacı
For the decay
I'm still working on the first I'm suggesting to check this out but need sleep I can read it tomorrow
http://www.eastcoastbio.com/productcart/pc/stability_testing.asp

Nice. Your article answers my second question (although the article is about enzymatic reaction and not specifically about protein binding). I made the mistake to ask several questions in one post. I restricted this post to one question and checked your answer. Here is the other question. Thanks a lot


text:
Can mosquitos bite in self-defense?
When chasing away wasps or bees there is a danger of them stinging us in self-defense.
Can a similar danger arise when chasing away a mosquito which is otherwise not hungry? I understand that mosquitoes bite to feed (by sucking blood), but do they use their bites in self-defense against large targets, like humans? Mosquito bites can be somewhat painful or at least uncomfortable, and can carry dangerous diseases, making them theoretically viable as a self-defense weapon.

Probably not. An immediate defense against predators requires an immediate response. The sting of Hymenoptera like the wasps and bees has an immediately painful reaction.  In addition, in the eusocial (colony-forming) species, multiple individuals typically contribute to defense of their nest. One sting may not deter a predator or invader but dozens or hundreds of stings would create an immediate deterrent.  See for example this paper by [Breed et al. (2004)] on the defense behavior of honey bees.  Animal bites that are immediately painful, such as an ant bite or dog bite create an immediate response in the organism being bitten. Spines and thorns on plants deter organisms from biting the plant. Odors released by skunks and some insect provide an immediate response.
The bite of blood-sucking mosquitoes does not provide an immediate deterrent. (Not all mosquitoes suck blood.) This paper by Ramasubramanian et al. (2008) provides a detailed explanation of how a mosquito penetrates the skin.  The paper is related to microneedle design but they are using the mosquito as a comparison for painless needle design. Go to page 3 to get a description of the mosquito anatomy and piercing behavior. Comparison of painless microneedle design to the mosquito's proboscis is instructive.
The proboscis is the set of modified mouth parts the mosquito uses to penetrate the skin and suck the blood.  The study states that microneedles that penetrate human skin less than 1.5mm is usually painless or effectively so. These needles have a very small diameter, only about 40-100 micrometers in diameter, similar to the width of a human hair. The mosquito's proboscis is about 1.5-2.0 mm long. The diameter of the various structures used to cut through the skin and suck the blood are all less than 40 micrometers in diameter. Thus, the size of the mosquito's proboscis is so small that it does not cause immediate pain, or the pain is so little that it is an annoyance at best. In addition, the proboscis is weak enough that the moquito may have to probe the skin several times before a spot suitable for penetration can be found.
Finally, only the females of blood-sucking mosquitoes feed on blood and have the penetrating mouth parts. Males do not. They feed entirely on nectar and water. Males would thus not be capable of such defense.

Don't they also inject a painkilling substance into the skin, which allows them to be done sucking blood, before their victim even realises, that they where bitten?


text:
Fire Ant Behavior
I've noticed for the past few weeks that near a small fire ant nest near my house there will be a new concentrated "large" pile of dead fire ants every few days. I went and checked out the pile and noticed that one ant in the pile was very slowly moving so I moved it in front of a nearby ant to see if it would take it back to the pile. The ant immediately picked up the slowly moving ant and took it back to the nest, passing right through the dead pile I might add. I'm curious what would invoke this type of behavior among the ants. I'm also curious if fire ants dispose of all of their dead this way.

This might be a duplicate of Do insects respond to the detection of dead insects?

Although similar, this question asks about returning the live ant back to the nest rather than back to the "dead pile." The behavior might still be related to necromones.

I'm sure there is a more detailed answer out there, but ants identify the dead ones by smell.

@fileunderwater The question does help and I find the answers quite interesting but it still doesn't quite explain the the second part of the question. Thank you though.

They do! It's called necrophoresis, and it's a way of keeping infections from spreading. A paper published in 2009 suggest that ants constantly produce "I'm alive" chemicals while they're alive; once they die, the chemical is no longer produced and the ants are carted off.


text:
How is the rate of transcription influenced by temperature?
How is the rate of transcription influenced by temperature? More precisely, I am looking for an article who quantitatively measured the rate of transcription of an "average gene" and show how this rate is influenced by temperature.
On this question @Chris found this article where such measurement were performed but they were using some arbitrary unit (as it as been pointed out by @shigeta here) that cannot be related to any comprehensive unit such as "mole of amino acid per hours" or something like that.

Also see this answer

If your looking at transcription then your talking about RNA POLYMERASE.
And there are many variants. Here's a good Nature paper that discusses temperature and RNA Pol
http://www.nature.com/ncomms/journal/v1/n6/full/ncomms1076.html
And another:
http://www.ncbi.nlm.nih.gov/m/pubmed/12729734/
I couldn't get full access to this JBC paper but I think the answer would be clearly in here, prob worth a look
M. Chamberlin and J. Ring. Characterization of T7-specific ribonucleic acid polymerase. 1. General properties of the enzymatic reaction and the template specificity of the enzyme. J Biol Chem. 248: 2235-44 (1973)

Very nice. Thanks a lot. I found the answers I needed in the Chamberlin and Ring article. There's a similar question here if you feel you can answer it $\ddot \smile$


text:
Why do birds move their heads abruptly?
When we humans look around, we pan smoothly from one side to the other. Birds on the other hand seem to point their head in one direction for a while, then abruptly point their head in another direction and stay in the new position for a while. Then they continue with the abrupt movement. Why is that?

Was exactly my question.

Most species of birds have 2 foveas, the temporal fovea and the central fovea.

temporal fovea, which is like ours in the sense that it looks straight
  ahead and offers binocular vision (i.e. the temporal foveas of both
  eyes point in the same direction). But birds also have a central
  fovea, which points sideways and is, obviously, monocular (i.e., the
  central foveas of both eyes look in opposite directions).

So the bird has a choice of which fovea it wants to look through.

It can look straight ahead with its temporal foveas, to the left with
  the central fovea of its left eye, or to the right with the central
  fovea of its right eye. And this is not a hypothetical possibility:
  Birds actually do switch between foveas all the time! This is why they
  tend to swing their heads erratically in turns of about 90° (reference).

Do you have any more references to back this up? An unreferenced answer from another Q/A site (Quora) can hardly be seen as a reliable source.

@fileunderwater changed the whole answer and added a proper reference. Hope that helps.

If the bird can look sideways,why move it's head at all?

Many birds, especially birds of prey and owls, have eyes that are proportionally much larger than that of similar-size mammals. Most birds are only capable of limited orbital movement, typically 10—20°, as with larger eyes there is little or no room for the required musculature.
This, in addition to having two foveae as @The Last Word mentioned, necessitates that a bird move its head to change viewing angle. The relatively rapid movement of a bird's head is analogous to that of the more subtle, but still rapid movement of your eye as you view different subjects within a frame of vision without moving your head.
Birds have more vertebrae (13-25) in their neck to provide additional flexibility, which provides for their quick head movements. Some birds, such as owls, can turn their head 270 degrees. Other birds have a wide field of vision because their eyes are located on the sides of their head. This degree of flexibility or field of vision provides birds with good compensation for being unable to move their eyes.
These characteristics, combined with the physiology of two fovea, make the abrupt, seemingly unusual movements of birds' heads more easily understood.
For additional insight, consider the book Bird Sense: What It's Like To Be a Bird by Tim Birkhead or Manual of Ornithology: Avian Structure and Function by Noble S. Proctor and Patrick J. Lynch; both of which I own and can recommend.

As i understand it:
Birds can't move their eyes around the way we can (excepting cormorants and maybe some others), and the result is that they don't have stereoscopic vision when they don't move their heads. More than that, their field of focus is very small if their heads are kept still. That last is also true for us.
The chickens we raised have their eyes even more on the sides than pigeons. They would look at us with one eye ---- then the other eye, then the first eye again, etcetera. This gave them a wider field of view and a stereoscopic view of us and their environment.
Try: Look at a letter somewhere near the center of your screen. Without moving your eyes or head, how many words can you make out up, down, left, right of your point of focus. If you can't move your eyeballs (as birds can't) you can only get the wider view by moving your head.
Plus, pigeons are prey animals and therefore have eyes on the sides of their heads which lets them see movement a lot further behind than we can. (https://en.wikipedia.org/wiki/Field_of_view) We have a horizontal field of view of about 210 degrees and "Pigeon FOV is around 340-degrees horizontal and about the same 135-vertical degrees as humans, but their vertical field is even more asymmetrically oriented toward the ground."(https://www.quora.com › What-does-a-pigeons-field-of-view-look-like)

"We" don't, always.  In addition to the factors in other answers, there's a simple matter of size and inertia at work.  If you look at small mammals like squirrels or mice (and presumably small monkeys, though I've never observed one for any length of time), you'll notice that ALL their movements seem to be quick and "jerky", because their heads and other limbs are small, and so have little inertia.  (It's a matter of scale that's not limited to animals.  Consider how small engines or fans can spin much faster than large ones - motorcycle vs diesel truck, computer cooling fan vs wind turbine, &c.)
Larger animals like humans (and dogs, horses, &c) CAN move their heads quite quickly, as when they're startled by something, but it takes effort and is rather uncomfortable.  (Try it!)  But virtually all familiar birds have small heads, though it'd be interesting to look at something like a pelican or toucan that has a large beak.


text:
Why doesn't water enter my body through my anus or genitals when swimming?
So when we swim, we can make water not enter through our nose and mouth, simply by holding our breath. However, the mouth and the nose aren't the only cavities. What about the anus and the genitals? They obviously can't "hold breath", so how do they stop water from entering?
I thought the reason is gravity, but then, people would be killed when diving because your butt is facing up, against the gravity.
Another explanation might be that the internal pressure is higher than the external one, but I fail to recall any organ that creates the pressure..

It is worth noting that some small amount of water can get in through these openings as there are a few parasites that rely on this as their transmission vector.

"We can make water not enter through our nose . . ." this is not as simple as you make it sound. I rely on a noseclip. Conversely, the other orifices you mention at least have a sphincter.

@RBarryYoung the Candiru is a good read. For the nose, Naegleria fowleri

@RBarryYoung and then we could discuss the iris sphincter muscle admitting nightmares!

For the same reason that when you urinate or use the toilet, you have to exert pressure and urine or faeces just does not simply leak out when you stand up. The urethra seals shut when the urethral sphincter muscles relax. Similarly Sphincter ani externus muscle seals shut in the anal canal when there is no antagonistic force. So water can't just simply enter our body in such huge quantities that we die. It is possible to get more water through your anus with some pressure which is what happens when you get an enema.


text:
How much time is required between repeated exposures to sun to prevent sunburn
After being in the sun, how much 'rest' is required before you can expose yourself again?
e.g. from Wikipedia:

Sunburn can occur in less than 15 minutes

So if you were in a place where sunburn would occur after 15 minutes and you stayed in the sun for 10 minutes you shouldn't get sunburn.
How long would you then have to stay out of the sun before you could go into the sun again for 10 minutes without getting sunburn?
I'm pretty sure that 1 minute wouldn't be enough, but 24 hours would be fine, is there any logic as to where between those two figures it actually is?

This could depend on a number of factors such as light intensity, skin color, and more. This may be a better question for a medical expert.

It seemed more scientific than a doctor would go into. I've tried searching repeatedly for it, but all you get is medical sites that never consider how the sunburn builds up, just how long in the first instance you can stay in the sun. I figured though that everything would be relative - so if you burned after 15 minutes that would indicate how long it takes to recover?


text:
Why is defibrillation in asystole ("flat line") useless?
In most popular medical dramas, when a patient has a cardiac arrest and "flatlines" the doctors many times use a defibrillator to "shock the heart back into rhythm'. I know that actually, the proper protocol is CPR and epinephrine (if possible), and that you should shock rhythms such as ventricular fibrillation. But why doesn't shocking the heart in asystole help?
If anyone could please explain, that'd be great.

In layman's terms: an Asystole is not affected by the electric shocks of a defibrillator. A defibrillator is used when the heart goes in fibrillations because it actually CAUSES an asystole. The idea is that you basically reset the heart to a blank state so you can start normal CPR procedure to help the heart go back to a normal rythm. That's why you see them applying CPR between shocks.
sources:
http://emedicine.medscape.com/article/757257-treatment
http://en.wikipedia.org/wiki/Defibrillation#In_popular_culture (citation needed)
http://calsprogram.org/manual/volume3/section12/CV/08-CV7AsystoleTreatment13.html

Would you please provide a reference or two to support your answer?

@MikeTaylor I added a few references. While I cannot find an obvious reference for the "causes asystole" bit, I think that the calsprogram link might have it in a linked page.

@GeorgeDaccache Please note: I have ZERO medical experience or knowledge about defibrillators. All this info was found in 5 minutes of googling. I really suggest you try doing this research yourself next time. It'll be faster that way.

CPR doesn't put the heart back in normal rhythm. That's an electrical phenomenon initiated by pacemaker cells in the SA node (which I agree can be allowed to function normally by means of defibrillating VT/VF but not asystole). CPR merely provides a semblance of circulation mechanically while the heart is not doing so intrinsically due to whatever arrhythmia.

The heart has nerve cells which are supposed to fire synchronously. This is what allows the heart to pump effectively. Fibrillation is when nerve cells (or the cardiac cells themselves, which have some "pacemaker" activity) are firing asynchronously, which means blood isn't getting pumped.
The shock causes all of the units to fire at once (which isn't exactly asystole), in the hopes that when electrical activity resumes (after giving a shock, we wait and look at the monitor to see if there is a regular heart beat, we do not start CPR unless there is not), it will do so in an orderly, synchronous manner.
In asystole (flat line), there is no longer any effective electrical activity of the heart. There is basically no disorganized electrical activity to try to reset with a shock.
That is why it makes no sense to shock someone in asystole. On television, people in flatline are shocked into a stable sinus rhythm. That just doesn't happen in real life. Neither does a deep breath and fluttering open of eyelids, as often shown on television when someone arrests and resuscitation is successful.
Asystole @ Medscape.com
Treatment of Asystole @ Medscape.com

Defibrillators are used to correct certain cardiac arrhythmias (heart is beating out of rhythm) like fibrillation - hence the name defibrillator.
It basically shocks the heart to make it stop beating completely, and hoping that when it starts beating again the arrhythmia will be corrected. It is kind of like "turning it off and turning it on again" to solve a computer problem.
When you're asystole, shocking it will do nothing because the problem lies elsewhere. It would be like trying to reset a computer when you have no power.

@VanceLAlbaugh - The request for references if fine. If you think the answer is too simplified, write your own. The answer - though it's an analogy - is basically correct. In fact, the more I think about it, the more I would like to see your answer.

When the heart is in "ASYSTOLE" mode and you visualize a straight horizontal line on the screen it means there is no electrical signal passing through the ventricle which is the discharging chamber contracting to pump blood from the left side to systemic circulation. "SYSTOLE" means contracting. "ASYSTOLE" means not contracting. There is no activity in the ventricle to fix so no point shocking the heart when there is no power on that is in "ASYSTOLIC" mode but when you visualize an so abnormal rythm such as seen in VF or in V-Fib then you shock the heart to jumpstart it back to a normal rythm.

Hi Welcome to Bio.SE! We ask that answers provide sources to back up their claims. Anecdotal info or info "based on experience" alone is great, but without further sources (preferably reputable sources) they belong as a comment. Please see here for a guide to writing good answers in this community. Thanks!


text:
How does one determine intracellular concentration?
The TL;DR version
Is there a fast way to determine what the cell environment of a particular cell (E.g RBC) is? (in terms of solute/ionic concentration)

I'm not sure if the question belongs here, but hear me out. I was doing revision and I kept coming across the line "put the cell in a solution which has the same solute/ionic concentration to prevent the cell from bursting or shrinking"
I get that concept, basically it's sort of replicating the internal environment of the cell with the buffer/solution so that the cell feels "at home."
Then my question is, how does one go about finding out how much exactly for each cell? I would think different cells have different internal environments and I don't believe that scientists actually just have stock solutions of buffers ranging from 0.00001M to 100M and trying every single solution until they find the perfect concentration.

patch clamping is how it's done.also enriching the fraction you want to study, losing the cells and measuring conductivity would work

@rhill45 how does one "enrich" a fraction?

In this case you would want a cytosolic fraction: 1. Was cells well in pbs, pellet at low speed, sonicate at lowest setting to break membrane only, add wAter to dilute. Spin at 80,000 x g 4c fixed angle. The top fraction should be your cytosol. All measurements times 2 since you diluted in water once

In fact the line that you quote doesn't mean that the solution is formulated to be identical to the cytosol. All that it means is that the solution should be buffered to physiological pH (typically slightly alkaline); should contain a relatively high concentration of sodium ions and a low concentration of potassium ions; and should be isotonic (i.e have the same osmolarity as the cytosol) to avoid osmotic effects such as plasmolysis (shrinkage due to loss of water) or osmotic lysis (bursting due to uptake of water).
There are many such solutions, but a commonly used simple one is phosphate buffered saline. Another is Ringer's solution. If the aim is to keep the cells metabolically active these are often supplemented with glucose or lactate, depending upon the cell type.
Addendum in response to comment from OP
According to the WP entry for Ringer's solution, Sydney Ringer determined the requirement for Na, K and Ca salts in a specific proportion when carrying out experiments with perfused frog hearts. This was in the late 19th century. A  Google search measurement of intracellular ion concentrations reveals current methods.
This review starts off with a discussion of early measurements of intracellular pH (see page 298). Basically these all consisted of making cell lysates, with various attempts to prevent post-lytic changes. If you do a Google search determination of intracellular pH you will find lots of current methods.

as in how did scientists derive that- what sort of tests did they do?

Patch clamping
Or
Ultracentrifugation to get soluble fractions. If you get enough of it and u have validated its purity you could runs conductivity probe into your fraction


text:
Why do I only breathe out of one nostril?
I was just sitting with my hand next to my nose and I realized that air was only coming out of the right nostril. Why is that? I would think I would use both, it seems much more efficient. Have I always only been breathing out of my right nostril?

Excellent question :) I've wanted to know this for along time. You will find that if you check on your nostrils for a long time that you alternate, after some time you breath mostly out of your left nostril instead, and then after some time it will switch back again.

I wonder how many people are sticking their fingers up their nose to test this out now.

This can also be caused by Nasal septum deviation

Related: https://skeptics.stackexchange.com/questions/19596/

This topic was covered on the British comedy panel show Qi: http://www.youtube.com/watch?v=E1jvRJV91co

Apparently you're not the first person to notice this; in 1895, a German nose specialist called Richard Kayser found that we have tissue called erectile tissue in our noses (yes, it is very similar to the tissue found in a penis). This tissue swells in one nostril and shrinks in the other, creating an open airway via only one nostril. What's more, he found that this is indeed a 'nasal cycle', changing every 2.5 hours or so. Of course, the other nostril isn't completely blocked, just mostly. If you try, you can feel a very light push of air out of the blocked nostril.
This is controlled by the autonomic nervous system. You can change which nostril is closed and which is open by laying on one side to open the opposite one.
Interestingly, some researchers think that this is the reason we often switch the sides we lay on during sleep rather regularly, as it is more comfortable to sleep on the side with the blocked nostril downwards.
As to why we don't breathe through both nostrils simultaneously, I couldn't find anything that explains it.
Sources:
About 85% of People Only Breathe Out of One Nostril at a Time
Nasal cycle

I just thought there was something wrong with me. I've been meaning to go to the doctor for it for about a year now.

I'd like to ad that there is some research done in the correlation with the used side of the brain, and while it has not been proven as far as I know, some researchers believe you think relatively harder with the side of the brain near the open nostril. Which may mean you have a 150-minute cycle of rational-emotional thinking.

"As to why we don't breathe through both nostrils simultaneously, I couldn't find anything which explains it." http://youtu.be/eiAx2kqmUpQ has the answer (with sources in the description): some things are easier to smell in a high-flow nostril and some things are easier to smell in a low-flow nostril. By having both at once, we can easily smell a wider range of things.

Does Viagra have any effect?

There is some evidence that this is to increase the spectrum of chemicals that we can smell. Some chemicals react immediately so the fast breathing nostril can detect them quicker. Some chemicals are slow to react so the fast breathing nostril wouldn't be able to detect them. The slow breathing nostril however can usually detect them as smells. Why not always breathe slowly? I guess the fast breathing nostril is an optimization to detect as smell as quickly as possible even if it can't detect the full spectrum of smells.

The TodayIFoundOut source is relatively unsupported by evidence and this comment debunks most of the claims about oxygenation, blood glucose, and left/right brain use.

This is a natural phenomenon called the nasal cycle. It is discussed in this paper by Telles et al. (1994), among many others. The nostrils are used on an alternating cycle of about 2-3 hours, controlled by the autonomic nervous system. If you notice alternating congestion, that also seems to be coupled to the nasal cycle (Hasegawa and Kern 1977, 1978).
Normally, the direct cause is blockage caused by alternating engorgement of erectile tissues on each side of the nose.

Below, I explain that the nasal cycle may be an artifact of the way the autonomous system works in humans (and some other organisms) or it may provide a first barrier against invasion of infective organisms via the nose. The full answer requires some background information.
Wikipedia and the nasal cycle
The Wikipedia article on the nasal cycle, nicely paraphrased in the answer by George Daccache, offers hints but not real answers.  For example, the Wiki section called Research on the effects states,

In 1994, breathing through alternate nostrils showed effects on brain hemisphere symmetry on EEG topography.

suggesting that perhaps natural nasal cycling relates somehow to communication or coordination between the two brain hemispheres. However, the cited study (Stancak and Kuna 1994) is based on forced alternate nostril breathing (FANB). The Wiki section then states,

D.S. Shannahoff-Khalsa published in 2007 on the effect of this cycle and manipulation through forced nostril breathing on one side on the endogenous ultradian rhythms of the autonomic and central nervous system.

All this sentence ultimately says is that a 2007 paper looked at the effects of FANB on ultradian rhythms. The Wiki section doesn't actually include results from the study so it provides no useful information.$^1$ I will try to explain with more depth.
What is Forced Air Nostril Breathing?
Forced Air Nostril Breathing (FANB) requires a person to close one nostril, breath in, close the second nostril and open the first nostril, and breath out. The person repeats this process several times in a 10-15 minute period. In fact, FANB is a yoga technique called Nadi Shodhan Pranayama. The Telles et al. paper mentioned above used FANB, as has nearly every study on the effects of the nasal cycle.
None of these studies actually explain the natural nasal cycle.  FANB is not natural. It changes natural breathing rhythms and requires the person to focus on the physical movements of the fingers to close the alternating nostrils. FANB occurs for a 10-15 minute period of time and is finished. This is not the same as the 2-3 hour natural nasal cycle. In my opinion, any conclusions drawn from studies using FANB apply only to FANB but not to the natural nasal cycle.
Then why does the nasal cycle occur?
The nasal cycle is a natural ultradian cycle (see here and here. Not only is it present in humans, but the nasal cycle has also been observed in rats, rabbits, domestic pigs, cats and dogs (see references in Eccles 1996]). Thus, the nasal cycle may at least be a feature of mammals but it may be a feature of other bilateral animals that use nostrils for respiration. In addition, the nasal cycle may be an artifact of the evolution of bilateral symmetry in animals, and how the autonomic nervous system operates between the two sides.
The autonomic nervous system controls the nasal cycle. The autonomic nervous system has two divisions, the sympathetic nervous system and the parasympathetic nervous system. Interestingly, these two divisions show a lateralized ultradian rhythm (Shannahoff-Khalsa 2007).  This means that the parasympathetic nervous system dominates one side of the body and the sympathetic nervous system dominates the other side of the body. The two systems later switch dominate sides. This dominance switching back and forth between the parasympathetic and sympathetic happens with a regular rhythmic cycle every few hours. As it happens, this switching between sides correlates very well with the nasal cycle (Shannahoff-Khalsa 1991).  When the parasympathetic-sympathetic systems switch sides, so do the nostrils. This is also associated with a switch in EEG activity between the two brain hemispheres (Werntz et al. 1983).
Therefore, the nasal cycle may not have a specific function, adaptive or otherwise. Instead, it could result from dominance of the parasympathetic system. Whichever side is dominated by the parasympathetic system will have the primary nostril in use for respiration. However, others have argued that the nasal cycle does provide a function. For example, Eccles (1996) argued that the nasal cycle may function as a respiratory defense mechanism. They found that the rate of cycling increases when nasal infection is present in the nose. They argue that the congestion-decongestion helps generate "plasma exudate" (nasal fluids derived from blood plasma) which may help remove bacteria and viruses.
The nasal cycle is an interesting phenomenon but whether it evolved as an adaptation (such as a mechanism proposed by Eccles et al. (1996) or is simply an artifact of the operation of the autonomic nervous system may never be known for sure.
Footnote

One of many reasons why you should always interpret Wikipedia entries very cautiously, even skeptically.

Citations
Eccles, R. 1996. A role for the nasal cycle in respiratory defense. European Respiratory Journal 9: 371-376.
Hasegawa, M. and E.B. Kern. 1977. The human nasal cycle. Mayo Clinic Proceedings 52: 28-34.
Hasegawa, M. and E.B. Kern. 1978. Variations in nasal resistance in man: a rhinomanometric study of the nasal cycle in 50 human subjects. Rhinology 16: 19-29.
Stancak, A. and M. Kuna. 1994. EEG changes during forced alternate nostril breathing. International Journal of Psychophysiology 16: 75-79.
Telles, S. et al. 1994. Breathing through a particular nostril can alter metabolism and autonomic activities.
Werntz, D.A. et al. 1983. Alternating cerebral hemispheric activity and the lateralization of autonomic nervous function. Human Neurobiology 2: 39-43.

I find it sad that this well-referenced answer is out-voted by a more recent answer, that is incomplete and only contains web/wikipedia references.

Interesting, I wonder do other mammals have a cycle of this kind?

As others have said, this phenomena is called the nasal cycle, a process controlled by the autonomic nervous system that alternants congestion between your nostrils. Mentalfloss of all places has an article about this that explains:

...it makes our sense of smell more complete. Different scent
  molecules degrade at different rates, and our scent receptors pick up
  on them accordingly. Some smells are easier to detect and process in a
  fast-moving airstream like the decongested nostril, while others are
  better detected in the slower airstream of the congested nostril.
  Nasal cycling also seems to keep the nose maintained for its function
  as an air filter and humidifier. The alternating congestion gives the
  mucous and cilia (the tiny hairs up in your nose) in each nostril a
  well-deserved break from the onslaught of air and prevents the insides
  of your nostrils from drying out, cracking and bleeding.

link: http://mentalfloss.com/article/30363/why-does-your-nose-get-stuffy-one-nostril-time

hmmmm.... I don't really buy the smell part. The nasal cycle lasts 2-3 hour, which seems to long to account for desensitization to smell...

The article doesn't mention anything about desensitization to smell, though; it only suggests that the nasal cycle keeps either nostril from drying out.  As for whether the difference in airflow allows the two nostrils to each sense certain smells better, a better source would be Stanford University, which published an article about this in Nature.  http://news.stanford.edu/pr/99/991103smell.html http://www.nature.com/nature/journal/v402/n6757/abs/402035a0.html