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What generates variation in a species?
What is the biological mechanism behind the variation within sexually reproducing species? Obviously, the children are combinations, to differing degrees, of their parents. But how does the variation originate in the parents to begin with?
I'm not referring to evolution or mutations rather I have in mind things like facial structure and personality in humans, or fur coloring in dogs. I just thought I vaguely remembered there was some kind of driver of variation... For example, does the parent produce a variety of germ cells that purposely differ from the parent's geneome?
I just think I'm missing something here.
(I'm familiar with DNA and genetics having taken a biology class in college and remembering much of it, I just can't seem to put my finger on this point...)

After mutations, which probably is the source of most variation.  The classic biological model of variation comes from accidents of history and environment.
Many mutations disappear over time because they aren't helpful (advantageous).  The reasons variations persist for more than a few generations is that our differences have helped us to live successful lives and (in biological terms of success) have offspring.  In europe the lactate dehydrogenase gene and others like it that help people digest milk is active through adult life as the result of domestication of milk producing animals,  in asia, this trait is rarer or non existent as agriculture does not produce milk there (in most cases).
This is a broad difference, but its true in smaller ways for all of our individual traits, or so the theory goes.  Individual family traits are helpful to create stronger family bonds, so even something like distinctive dimples or foreheads have claim to being an advantageous trait.  Its possible that blonde hair is the product of such an advantage - its a strong signal to paternity if the father is blonde for instance.
Another answer to your question I think, is that there are probably mechanisms in the cell or in mate selection that increase or decrease variation in the community at given times of stress.  For instance, snakes are among the animals who have a particular ability to select gender depending upon the conditions the female is experiencing.  more males may increase variation in the community - fewer males and more females will decrease it.  (not by a lot mind you, but a bit).
Additional response added as requested:
I see what you are getting at - why do children seem like such individual and unique things sometimes?
In sexual reproduction, the offspring are the product of the shuffling of the parent's genomes through meiosis, where the pairs of chromosomes we have are combined to make a single chromosome that will be half of the children genome.
This process can result in completely novel combinations of genes while conveying many likenesses from the parent.  I would guesstimate that this is the major cause of the uniqueness of offspring/children.
Also in mammals there are some cell lines which splice families of genes which will cause offspring to be potentially quite different from either parent.  Immune genes for instance are created from scratch from a bunch of genes that the parents give.  Making each offspring unique but also the product of the parent's genetic repertoire.  This can be significant as it affects health and also to some extent attraction - studies have shown that people who smell attractive to us are immunologically distinct from us.
@David mentions epigenetic variation, which is a more recent significant development.  During our life, the germline (sperm/egg) DNA may be chemically labelled depending upon environmental conditions we experience.  A famous example is experiencing famine conditions, which caused the children to be born on the small side amongst other effects.   More recent studies have shown that this is a widespread mechanism to control cells in our body during our lifetime as well as communicate to our offspring how life is.  It is expected that this labeling does not affect us forever - the epigenetic labels change over the course of a generation quite often (we believe).

Yeah, but from where does the variety originate in the first place? Given pair of dogs, each pup is different. Is this just due to Mendelian shuffling of the parents' genomes or do the parents have the ability to produce additional variation without mutations? (I just thought I had remembered something like this in the back of my mind). I'm not referring to mutation.

@John yes, there is also epigenetics

Edited to answer more specifically

It wasn't specifically mentioned in your update on meiosis, but just to be clear for John: kids just don't get one of mom's chromosome and one of dad's chromosome for each, but the chromosomes the parents pass on go through homologous recombination. This "single" chromosome (say chr1) the parent gives is built from a "random combination" of the two chr1's the parent has.

@Steve - thanks for clarifying - indeed that's the main effect that causes offspring diversity.


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Number of beneficial mutations cataloged?
I can see from Wikipedia that there are possibly thousands of harmful mutations that have been cataloged and linked to disease. There are also unnumbered neutral mutations. But, does anyone know how many "beneficial" mutations have been cataloged in scientific literature?

A "beneficial mutation" is often hard to point out: it would likely be very slight and context-dependent. For example, a "superhero" gene is obviously out of the question, and a very small phenotypic difference would probably either be insignificant or beneficial in one particular environment but not in another.

@LanceLafontaine: you mean this (and related article)?

The problem is that "beneficial" is entirely dependent on the environment and how it changes. E.g. for fish living in dark caves, mutations that lead to loss of the eyes are beneficial.

That would be hard to say because really beneficial mutations become well distributed through the genome.  Basically the differences between us and chimpanzees are a catalog of all the beneficial (or completely neutral) mutations since the ~4.7 M years since we diverged from each other.
Separating them from changes which have no special effect would be difficult too, but more to the spirit of your question, its difficult to explain what many mutations do, unless they cause significant changes in something we can observe in the individual (like height, weight, big nasty claws, etc).
For some more specific examples you can look at Online Mendelian Inheritance in Man.  Some mutations which are useful sometimes might be related to skin color for instance (really helps when there is a lot of sun about) or lactose tolerance (a variation which is popular amongst europeans who have been drinking dairy milk for thousands of years).

I was specifically asking about the number of beneficial mutations cataloged, not necessarily examples. Thank you though.

I guess i'm saying that you will never get a number for that, or if you do it will be nearly meaningless.  Wasn't expecting to get a checkmark for this one.

Just continue scrolling down wikipedia: there are also listed two examples of beneficial mutations: the one conferring HIV resistance, and the one conferring malaria resistance.
Note that 'beneficial' is relative. The mutation associated to malaria resistance is actually causing sickle cell disease.

I was specifically asking about the number of beneficial mutations cataloged.

Others have posted that the term beneficial in genetics is contextual - single mutations may be harmless, unless another mutation is co-inherited; this is called epistasis (where more than a single mutation/genotype/allele is required for the phenotype).
I have not studied the list comprehensively, but there is a 'catalog' of all robust genome-wide association study results here. Depending on your outlook, all mutations associated with a disease are therefore also 'beneficial' if you have the protective allele and not the risk allele. Using this logic there have been many SNPs identified that are protective, rather than beneficial per se, and these are listed in the GWAS-catalog I linked to. As of 05/11/12, the catalog includes 1258 publications and 6400 SNPs.

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How does translational coupling work in prokaryotes?
Today I heard about a phenomenon called "translational coupling", where the translation of one protein influences the translation of another protein. The messenger RNA levels don't seem influenced. How does this work? Do they need to be in the same operon?

Here is a relevant reference: Tian & Salis, A predictive biophysical model of translational coupling to coordinate and control protein expression in bacterial operons. Nucleic Acids Research. 2015
https://www.ncbi.nlm.nih.gov/pubmed/26117546/ HTH

Translational coupling describes in how some cases an mRNA will code from more than one protein (i.e. will be polycistronic).  Translational coupling is thought to be mostly used as a way to make a set of genes are translated at roughly the same amount in the cell.
Translational coupling is very common in prokaryotes and nearly half of e coli genes are found in a polycistronic operon.  What we know about them is revealing.  There are some fancy mechanisms to adjust the ratios of these adjacent genes, which are still coupled, but with ratios that are not just 1:1.  Its shown that the later genes are often translated at somewhat lower frequency because the first genes are available more quickly before the mRNA degrades.
Eric Alm @ MIT wrote this great paper on how operons evolve.
I've only been able to find this reference to a eukaryotic case of "translational coupling" which is very rare, but does exist.  The most common cases of translationally coupled genes in eukaryotes are RNA viruses which usually contain only a single full length mRNA which codes for all the genes in the virus.  The selective pressures to keep the viral genome small and constrain the ratios of these genes, will cause these genes to even overlap, starting the next one before the current gene finishes.

The above answer isn't entirely accurate. It's true that polycistronic mRNAs (i.e. operons) are very common in bacteria. But this isn't what is meant by translationally coupled.
Translational coupling happens when the second gene of two adjacent genes in an operon, doesn't have it's own ribosome binding site. Instead, the ribosome ends translation at a stop codon at the first gene, and then steps back slighly, and starts translating the from the start codon of the second gene. This happens when the coding regions of the two genes overlap:
E.g.
XXXXXXXXXATGAXXXXXXXXX
-the first series of Xs is the end of gene 1
- the TGA is the stop codon for gene 1
- the ribosome slides back one nucleotide and translates form ATG
- the second series of XXXX is the second genes coding region
The two genes are said to be translationally coupled because distrupting translation of the first gene would abolish translation of the second.

Can you please add some references?

I think this is right to be an answer, and furthermore Matt is correct. Translational coupling isn't the same as polycistronic transcription - but I agree a reference or two wouldn't hurt.

Vance, it's not a comment. The original answer is 100% incorrect.

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Is it purely the nervous system causing vaginal lubrication (arousal)?
My girlfriend was watching some documentary on TLC about a paralyzed woman getting pregnant. I believe that woman still has some feeling, as she spoke about feeling the effects of a bladder inflamation. So supposedly, her brain could fire up her vagina to get ready for sex (in the sense that it gets lubricated and the labia get swollen).
But suppose a woman is paralyzed so they have no nervous connection from the brain to the vagina (or vice versa). Could she still be aroused in the sense of swollen labia, etc? (Presumably via some hormonal system?)

There is a good open access review about the effects of different hormones on sexual arousal. In most instances, the hormone is acting on the brain, which signals the information to gonads and genitals via nerves (i.e., the hypothalamic-pituitary-gonadal axis). However, in a study in which I have participated, we found a more direct and probably ancient signaling pathway where the mouse liver, in response to protein intake, was sending a permissive signal to the uterus for reproduction. Whether this holds true for vagina lubrication was not investigated, but I would be optimistic that mechanisms other than nerve communication could play some roles.


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Finding and Comparing Homologous Genes
I have a gene of of interest that I would like to compare between homologues. How does one go about finding a gene from known coding sequences across phyla? Afterwards I imagine I could do a Clustal sequence alignment to see how the sequences match.

There are various databases of homologs, for example:

eggNOG
Ensembl Compara (accessible via BioMart, I think)
Homologene
OMA
TreeFam

The advantage of using an existing database is that more sophisticated methods for detecting orthologs than simple BLAST searches have been used (see "Computational methods for Gene Orthology inference" for a review), and everything is already precomputed, so it's much faster. The downside is that all precomputed methods need to use a snapshot of the genomes from the past, so not all currently available genomes will be there.

If I understand your question adequately, the Genome Browser at UCSC is a great place to start. If you know the name of the gene, you can search for it. For example, here is the page for human insulin receptor 1. From there you can compare 46 genomes, with alignments.

Wow that is an ugly interface. How do I use that thing? I think that's what I'm looking for. Looking at the INS-R1 gene as an example, I see chicken, zebrafish, a cluster of 46 vertebrates. Can I use this tool to create a consensus sequence of the conserved regions?

If you don't have any idea where your gene will have a match with other genes, try something like Blast at the NCBI website.
This will give you a list of hits that you can then use to align with a multiple sequence aligner (MSA). The same NCBI page can give you a tree reconstructed from the results of the searching process, although there is a variety of methods that can be used if you just download the sequences and attempt to build the gene family alignment yourself using "[x] Select All -- Get selected sequences" in the NCBI blast results page, then downloading them in FASTA or other format with "Send to -- File -- Format FASTA -- Create File".
If what you want instead is to include your gene sequence into the best aligning place in an existing gene family alignment, you can try PAGAN.

maybe you'd like NCBI/Homologene instead.  http://www.ncbi.nlm.nih.gov/homologene
or just using psiblast against NR if you have a nucleotide or protein sequence.
http://blast.ncbi.nlm.nih.gov/Blast.cgi

Just adding my 5 cents, there is a recent database called metaphors:

MetaPhOrs is a public repository of phylogeny-based orthology and
  paralogy predictions that were computed using resources available in
  seven popular homology prediction services (PhylomeDB, EnsemblCompara,
  EggNOG, OrthoMCL, COG, Fungal Orthogroups, and TreeFam). Currently
  above 306 millions of unique homologous protein pairs are deposited in
  MetaPhOrs database. These predictions were retrieved from 705 123
  phylogenetic trees for 829 genomes. For each prediction, MetaPhOrs
  provides a Consistency Score and Evidence Level describing its
  goodness, together with number of trees and links to their source
  databases.

It is particularly good because:

It is the only homology database I know of that gives information on paralogy vs orthology.
It is linked to UniProt names
It provides a pretty good python API for batch queries


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Death because of distilled water consumption
One of my friends said that I would die if I drank distilled water (we were using it in a chemistry experiment) I gave it a go and surprisingly did not die.
I did a bit of Googling and found this
It said that drinking only this kind of water could definitely cause death, as distilled water was highly hypotonic and it would make the blood cells expand and finally explode and ultimately cause death.
I wanted to know exactly how much of this water on an average was needed to be consumed to cause death.

He said it would kill me, so I drank it.  Love it!

@RoryM that is precisely what happens when kids are told about dangerous stuff.....

An empirical if not wise approach

For the opposite scenario, see: http://biology.stackexchange.com/questions/3909/why-cant-humans-drink-sea-water

"experimental" tag added - he did test the hypothesis of his friend!

On a related note, what if you stick your hand in distilled water, will it disintegrate slowly? Or will your hand quickly alter the water, rendering it harmless. What if you jump into a pool of distilled water, would you slowly explode cell by cell? If not, what if you had a machine very quickly replacing all the water with previously distilled water, would you then explode cell by cell? I guess I should make this into it's own question, but it just seems related to heart of the issue here.

P.S. From now on, I will be adding a tiny bit of high quality, full spectrum salt to my distilled water before drinking it so as to avoid self asplosion.

I think I just invented the shower of the future! You just feed previously distilled water to your shower head! The water takes off the outer layer of your skin and hair along with the dirt, germs, viruses, and other things living in your hair. No shampoo or soap required! You can be super lazy! Just stand in the water for a few minutes! In a hurry? No problem, just increase the rate of flow to have it spray lots of water at you at high speeds, and you can be clean in a matter of seconds!

Don't Inuit drink nothing but distilled water?

I'm extremely skeptical of @leonardo's answer.  I suspect that what would happen if you drank only distilled water is nothing perceptible.  The only place where concentrations of distilled water would ever be high enough to conceivably matter is in the tissues of the mouth and throat, and even there, the effect would be temporary.
Compare drinking 8 glasses of either distilled or tap water every day.  With tap water, you're looking at less than 200 ppm of Mg, Na, K, and Ca combined.  That's less than 400mg of total mineral content per day.  Given that the combined RDA of all of those minerals is on the order of 7g for an adult male, this is not nothing, but it's certainly small.  Your dietary intake of these minerals probably varies by more than this daily, and your intestines, kidneys, sweat glands and mineral storage organs (like your bones and muscles) are constantly maintaining the mineral blood levels within a very narrow range, despite handling a throughput of several pounds of water and food daily.  They might have to work slightly harder to manage this range if you drank nothing but distilled water, but in a healthy adult, normal intakes already vary by more than this amount without major problems.  For example, the average American consumes more than 3.4 grams of sodium daily, while a low-sodium diet is on the order of 2g.  Low-sodium diets have been widely studied in the medical literature, and are considered safe.
As for pH, the lowered pH is caused by increased carbon-dioxide absorption to form carbonic acid.  Just as carbon dioxide is more soluble in distilled water, it is less soluble in stomach acid, and may be burped out.  Would you die of acidosis from drinking seltzer water all the time?  If that were the case, I'm sure there would be big health warnings about drinking soda, while it seems relatively benign. Furthermore, your body produces and excretes (through the lungs) around 1kg of CO2 daily, dwarfing any extra CO2 you might get by drinking distilled water.  If the small amounts of CO2 found in distilled water were dangerous, jogging would be invariably fatal.
If you were to drink nothing but distilled water, and eat no food, you probably would die of hyponatremia within a few weeks.  But you would also die of hyponatremia if you were to drink nothing but tap water, though perhaps slightly more slowly.

+1. I'm with Recursivelyironic. Most of the ions in our diet come from the foods we eat, not the water we drink. Unless you're sucking down softened water in the shower, your salt and calcium should be coming from your big dietary sources - fruit, veggies, meat, seasonings, etc.

+1  Unless you drink to hyperhydration, which is not what the original question was about at all, distilled water will not cause problems at all, literally zero problems.  You can buy distilled water by the gallon at the grocery store for goodness sake, and people commonly have reverse osmosis filters for their drinking water in their sinks, producing almost exactly the same effect.

Well, there are big health warnings about drinking excessive amounts of soda. But not because of its acidity.

Drinking a little bit of distilled water is not fatal. Drinking only this kind of water and ingesting nothing else will eventually be fatal because it is highly hypotonic as you've found out.
Salt balance in the body is largely maintained by passive diffusion. Salts diffuse from areas of relatively high concentration (eg, stomach) down to areas of low concentration. For example, if you have just eaten a meal, the stomach contents are relatively higher in salt concentration compared to the surrounding tissue and the blood. Salt diffuses out of the stomach and into the stomach lining, intestines and blood. Tissues have to make sure they don't get too much salt or they will take in too much water and burst, so they have active transport mechanisms to remove excess salts and they go into the blood as well. Now that the excess salts are carried in the blood, they ultimately get filtered at the kidneys and excreted in urine. The kidneys are able to filter the salt by taking advantage of this gradient moving salt once again from high to low concentrations. The exact details are not important for this discussion, other than to know the kidneys need a highly concentrated store of salt to function.
Distilled water on the other hand, has no salt. It is pure water. Distilled water will pull salt out of the tissues because now it is the absolute lowest concentration of salt. Tissues will also take in a lot of this water because it too passively diffuses and it is hypotonic. When this happens in the blood, red blood cells tend to burst because they can't tolerate a terribly large change in tonicity, and so some red blood cells die. The other problem is also that the salt control mechanisms in the kidneys malfunction because too much salt gets leeched out of them and passed in your urine.
After drinking too much distilled water, electrolytes and important minerals get leeched out of your body and this creates electrical abnormalities in your body leading to irregular and weak heart beats (from hyponatremia and hypokalemia), poor muscle strength, high blood pressure and fatigue. Distilled water as mentioned, is fairly acidity (can be as low as pH 3 when freshly distilled) and leads to acidification of the blood (acidosis).
There is no exact amount of water that one needs to drink to die. This mode of death is related to hyperhydration/water intoxication. This can happen from over-hydrating with regular tap water, but will take longer than distilled water because of the salt content in tap water.

How much distilled water do you have to drink to get acidosis? Coke has a pH of ~2.5...

BTW How will one generally feel when he or she starts to drink the second bottle of distilled water?....anemic?(but isn't the blood still there in the body?)

@The-Ever-Kid, the point to which you develop acidosis is just as subjective as how much distilled water kills you. It depends on current blood pH, buffering capcity in your blood, nutritional status, etc. I would speculate that you would feel fatigued (anemia is a chronic condition with fatigue really being the only symptom one can "feel"). This would happen over an acute period of tens of minutes to hours. You still have blood, but some of it gets destroyed.

But if you drink distilled water and eat salt, there should be no effect?

As long as you have the right salts and the right quantities, then yes. There is the possibility of still drinking acidic distilled water to worry about, but it should not be too dangerous (similar pH to sodas).

This answer was borderline wrong. Specifically I take issue with Drinking only this kind of water will be fatal because it is highly hypotonic as you've found out -- I drank only distilled water for over 5 years with no ill affects whatsoever. As you explain later in the answer, it's about salt balance, and there's more than enough salt in food (at least in America where I am) to compensate for drinking distilled water. So, maybe you'd die from drinking only distilled water and not eating, but I can confirm that drinking distilled water is not a sure path to death.

Does this mean that the whole "when stranded on a deserted island, distill your own pee/ocean water for drinking water" will eventually kill you anyway?

"drinking a little bit is not generally fatal" ? when was it fatal?  no references here... clearly we'd like some for this part.

Sorry, I took the question to mean drinking distilled water only, and ingesting nothing else. I entirely agree that my previous answer was misleading, and @recurivelyironic and TonyH give much better answers for acute effects or drinking distilled water while still eating normally.

+1 for adding "and ingesting nothing else", but I am afraid the bounty goes to RecursivelyIronic as I promised it to his answer was when I offered it :-)

Drinking distilled water is perfectly fine, you just won't get all your trace minerals that's normally in tap water, etc. Consider, rivers like the Rio Tinto in Brazil have "black" water which is devoid of minerals and almost like distilled water, just with tannins in it. Lots of fish live in these waters and breed. Humans can drink water from these rivers. Also, rain water is almost like distilled water. If no air pollution, it is perfectly fine to drink it.

Leaf cells observed under a microscope will burst when you put distilled water on them. But after you add some salt to the water this does not happen. Cheek cells also burst from distilled water. So the real question is, at what point does the saltless distilled water, combine with salt already in your system to render the water harmless? What parts of the body are exposed to the unsalty water and start exploding cell by cell? Or would pre-existing salt in these cells prevent them from exploding? I have no idea really...

@leonardo, You stated that "distilled water will pull salt out of the tissues", then after that happens, where does the now non-distilled (salty) water go?

-1. I am pretty sure distilled water is neutral, not acidic. Can you provide a source for your claim?

pH of pure water (true distilled water) is by definition 7 - but when exposed to air, it absorbs carbon dioxide and becomes very slightly acidic.  That said, even tap water is hypotonic compared with biological tissues, there are multiple misunderstandings...

I'm not sure why no one mentions this, but any food you eat would negate this effect entirely.
Assuming then, that you had no food, the lack of minerals in this pure water would simply be another deprivation for your body. The intestinal track actively reabsorbs ions, countering this. However, in this water-only deprivation, those mechanisms might fail as some are glucose dependent.

In general, if you want to know "exactly how much of X on an average is needed to be consumed to cause death", then the magic search term for Google is "LD50", that is the dose that kills 50% of victims.
I've seen the LD50 for water quoted as 90ml/kg for rats (that is, 90 ml per kg of body mass), for example on this safety data sheet. I presume that figure comes not from theorising about salt intake, but from giving measured quantities of distilled water to rats and counting how many die.
It's likely of the same order of magnitude for humans. Unlike many "poisons" it's not about subtleties of liver chemistry that will vary by species. What killed the rats was the swelling by osmosis of cells and tissues that they didn't want swelled.
For a largeish human that dose is 7 litres, approx 14 pints, drunk at a sitting. Which is fairly unlikely in a school chemistry lesson. Besides, with effort you could drown in less than that!
The distilled water in your chemistry lab has a relatively much larger chance of killing you for some reason other than its inherent toxicity (although it's still fairly unlikely in absolute terms). For example if it's stored for a while there could be legionella in the tanks. Probably best not to drink it, just as it's best not to drink any water that may have been sitting around for weeks in an unsealed container.
Definitely don't drink other stuff from the labs that your friend tells you is poisonous, because some of it really is. In particular the one everybody thinks of (because, like the water, it's similar to something they know about): lab ethanol can have methanol as an impurity, and may well have had benzene intentionally added because that's an easy way to get the last 4.5% water out that otherwise cannot be removed by distillation. A mouthful of ethanol isn't normally lethal (although it might be illegal), whereas methanol and benzene are both "properly" toxic in the sense that a few grams will kill you.
By the way, I can confirm that in my school days I obtained the same experimental result you did.

Drinking 7 liters of water in one sitting (30 minutes?) is unlikely physically possible and if it is it will quite likely kill you. People have died from drinking as "small" amounts of water as 6 liters in few hours. You can't establish LD50 for water without knowing the time in which the water is drunk (you can safely drink 12+ liters of water per day when needed), the hydration status, sodium consumption, etc.


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How to store vegetables in the refrigerator: In plastic bags or not?
My wife and I are having a debate similar to this one:
I claim that it's better to take the fresh veggies out of the bags and put them in the crisper with humidity control because:

That's what the crisper with humidity control is for.
If they are in the (plastic) bag, the humidity control is pointless.
It's easier to notice vegetables in their early stage of rotting (it doesn't feel right to throw out an entire bag of rotten cucumbers or zucchinis before we got a chance to enjoy them).
It's more pleasing to the eye. It's more convenient.

She claims that it's better to leave the fresh veggies in their supermarket bags when putting them in the fridge because she could swear she noticed that they rot more slowly when left in their bags.
As you can see from the few links in this question, I tried to conduct my own search on the subject, but all answers seem to be opinions or "experiences", not an authoritative answer based on scientific research or knowledge.
So I am hoping that with the help of biology professionals (or students) I can finally find an authoritative answer to the question: Do vegetables really last longer if they are kept in their (supermarket) plastic bags when put in the crisper?
Update: I found this formal excerpt from the refrigerator's manual:

Low (open) lets moist air out of the crisper for best storage of fruits and vegetables with skins.

Fruit: Wash, let dry and store in refrigerator in plastic bag or    crisper. Do not wash or hull berries until they are ready to
  use.    Sort and keep berries in original container in crisper, or
  store in a    loosely closed paper bag on a refrigerator shelf.
Vegetables with skins: Place in plastic bag or plastic container and store in crisper.

High (closed) keeps moist air in the crisper for best storage of fresh, leafy vegetables.

Leafy vegetables: Wash in cold water, drain and trim or tear off bruised and discolored areas. Place in plastic bag or plastic container and store in crisper.

While this seems a bit more authoritative (because it comes from the manufacturer of the refrigerator), it still leaves quite a few questions open:
If leafy vegetables should be "placed in plastic bag or plastic container and stored in crisper", why set the humidity on "High"? How does humidity get the lettuce inside the plastic bag or plastic container? (is it sealed?)
Assuming that some humidity does get into the bag, why is the bag needed? Why not let humidity flow freely?

Apples and other kinds of fruit use ethene as a hormone which promotes ripening. They give it off themselves and they also utilise it themselves - but it can affect fruit around them once it's in the air. I don't know whether vegetables use the same mechanism but maybe that will lead you to find some things.

@Armatus That's a great tip. I wish I had enough points to vote your comment up. To simplify my question I am trying to stay focused on vegetables only, but the truth is that we use the refrigerator's crisper for both fruits and vegetables. Your answer may hint that if we keep each fruit/vegetable in its own bag, perhaps that will slow down ripening/rotting? If so, by how long? This is truly intriguing.

If you only store one kind of fruit, it wouldn't do much - they wouldn't "pool" their ethene anymore but they would still accumulate their own in their bag. But if you separate different kinds of fruits with bags, it can keep apples from making bananas go bad quickly. I haven't actually read this in a scientific context though, I'm not sure where I got it from :)

You may want to make a scientific experiment with your own fridge. That would be the most authoritative source for your own conditions. Just split the same veggies in two groups (with or without bag) and consume them after few days. Replicate the experiment at least three times. If you find differences, you have the evidence. If you don't find differences, forget the conundrum and make peace with your wife.

If you put ripen fruits together with fruits that use the same hormones for maturation in the same bag, they will all mature quicker than they would if you keep the unripe ones in a separate bag. There are roughly 4-5 classes fruits by their hormones, although new subclasses and mechanisms are still being discovered.

Related on Seasoned Advice: http://cooking.stackexchange.com/questions/23691/how-can-i-let-fruit-ripen-faster/ and http://cooking.stackexchange.com/questions/12014/is-it-scientifically-verified-that-bananas-will-ripen-faster-when-kept-in-a-bowl and http://cooking.stackexchange.com/questions/23237/what-to-do-with-under-ripe-figs and possibly others

One more important thing would be rotting. If one veg or fruit rots, all other vegetables are liable to rot as well

Based on what I've been able to locate on the USDA website:
Refrigeration & Food Safety
It would be better to take the foods out of the bags and put them in the crisper if you're using the crisper solely for vegetables:

Some refrigerators have special features such as adjustable shelves, door bins, crispers, and meat/cheese drawers. These features are designed to make storage of foods more convenient and to provide an optimal storage environment for fruits, vegetables, meats, poultry, and cheese.

And:

Sealed crisper drawers provide an optimal storage environment for fruits and vegetables. Vegetables require higher humidity conditions while fruits require lower humidity conditions. Some crispers are equipped with controls to allow the consumer to customize each drawer’s humidity level.

Therefore, keeping your stuff in the bag would negate the purpose of these specialized compartments. Too bad the USDA doesn't specifically address the issue of bags...


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Restriction Mapping of Plasmid Assignment

pUWL22 is a circular, double stranded, 10.5 kb plasmid. It contains a
  gene encoding an enzyme that confers ampicillin resistance in the host
  bacterium. Cloning into the kpn I and Sst I sites abolishes ampicillin
  resistance, whereas cloning into other sites on the plasmid does not.
  Digestion with the following restriction enzymes singly and
  combination results in the following data:

Enzyme Digest     ()()()()()()   Fragments Produced (kb)

Hind III  ___________________________10.5

Kpn I  _______________________________10.5

Not I  _______________________________10.5

Pvu II  ______________________________10.5

Sst I  _______________________________10.5

Stu I  _______________________________10.5

Hind III + Kpn II  ___________________8.5  _______________2.0

Hind III + Not I _________________8.0  __________________2.5

Hind III + Pvu II ________________6.0  __________________4.5

Hind III + Sst I _________________7.5  __________________3.0

Hind III + Stu I _________________7.5  __________________3.0

Stu I + Not I  ____________________10.0  __________________0.5

Stu I + Pvu II  ____________________7.5  __________________3.0

Now the actual questions:

A) Create a circular map of pUWL22, designating the Hind III site as
  the position 0 on the map. Once you have completed the map, indicate
  the relative position of the ampicillin gene.

My plasmid mapping:
What I need help with in indicating the relative position of the ampicillin gene. In the statement above it said "Cloning into the Kpn I and Sst I sites abolishes ampicillin resistance." Does that mean its inbetween Sst 7.5 and Kpn 8.5? Please tell me where it is and why its there.
P.S. I made a mistake on the on the Sst I enzyme, it's suppose to be @ 7.5 not 7.8.
The question after that is:

B) Propose 2 other double digests that could be done to confirm your
  analysis. Predict the sizes of the fragments that would be generated
  from these digests.

Please answer this and explain why.

Please note that you will get much better responses to your question if you explain what you have tried far or give your solution and ask if it is correct.  Also, it never hurts to include at least some formatting in your question rather than just a block of text.  Welcome to the site regardless xD

i drew out the diagram, that wasnt a given, im stuck on the part indicating the relative position of the ampicillin gene and question B.

I tried laying it out the best i could, thanks for making it nicer btw

A) Here is the correct map:

You made a mistake on your map at the PvuII site (it is not on 6.5kB from the start of the plasmid, but on 6kB).

Can the Kpn I not go on the 8.5 site, it still creates the 2 and 8.5, so isn't there more than 1 correct option for plasmid map?

Yes. What you need to do in order to make the correct map is try all possible positions of the restriction sites:

You start with HindIII and place it at position 0 of your vector.
The KpnII site can be either at 2kb (left of HindIII) or at 8.5kb (right of HindIII). Draw both versions of the plasmid.
You place the NotI site that can either be at 2.5kb or at 8kb. Now you have four different possibilities for the plasmid:

HindIII[0], KpnII2, NotI[2.5]
HindIII[0], KpnII[8.5], NotI[2.5]
HindIII[0], KpnII2, NotI[8]
HindII[0], KpnII[8.5], NotI[8]

Then you do the same for the rest of the restriction sites. When you get to the last two digests, there is only one option for the correct plasmid left in the following order, depicted on the plasmid map below.

I have to point out though that StuI and SstI can both be at 3kb (they can be next to each other). Then the 2 fragments from the digest will be ~3kB and ~7.5kB. So technically, there are two possible versions:
correct
a) HindIII[0], KpnII2, NotI[2.5], StuI[3], PvuII[6], SstI[7.5]
b) HindIII[0], KpnII2, NotI[2.5], StuI[3], SstI[3] PvuII[6]

If u can, can u please elaborate on question b as to why there is one correct option for the plasmid map? Also, what do they mean by double digest to confirm ur analysis?

A double digest means that you cut your plasmid with two different restriction enzymes at the same time. As you already have a putative map of the plasmid, you can predict which would be the expected bands. If you observe the expected sizes, then your design is correct and your analysis are confirmed.
To check which one is correct I would do a double digest with:
1) SstI and PvuII, generating a 1.5kb and a 9kb bands if design a) is correct or                              3kb and a 7.5kb bands if design b) is correct
2) StuI and SstI, generating a 4.5kb and a 6kb bands if design a) is correct or                             a 10.5kB band if design b) is correct

To confirm the "ampicillin gene" starts at kpn I 2.0 and end at the 3.0 stu I site right?? So the amp gene is 1 kB long?? So the relative position of the amp gene starts at 2.0 and ends at 3.0.
  Why is it that in the question it says cloning into the kpn I and sst I sites abolishes ampicillin resistance whereas cloning on other sites does not?
  What do they mean by this? Is the ampicillin resistance gene diff from the ampicillin gene??

The ampicillin resistance gene and the ampicillin gene are the same. It refers to an enzyme (beta lactamase) which degrades ampicillin, and thus the cells that harbour the ampicillin-containing plasmid can survive when plated on ampicillin.
Are you sure that the resistance is disrupted if cloning into SstI site and not StuI? If this is really the case, then the StuI site and SstI sites are next to each other, as first you have the SstI site, followed by StuI. The amp gene
The gene is a little above 1kb, so it starts upstream of KpnII and ends right after SstI, but it doesn't disrupt StuI. If something is cloned into KpnII or SstI sites, then the open reading frame of amp is disrupted, and the protein cannot be functional.

Heres the solution

i got 1 mark off for the position of Not I


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Genetic networks vs genetic architectures?
What is the difference between the terms genetic network and genetic architecture? I've heard both in a variety of contexts used by different people, so I am interested in what people think they mean, other than what is described in Wikipedia:
Genetic architecture refers to the underlying genetic basis of a phenotypic trait
Genetic regulatory network (GRN) is a collection of DNA segments in a cell which interact with each other indirectly and with other substances in the cell, thereby governing the rates at which genes in the network are transcribed into mRNA.
EDIT: so what I take from the answers so far is that a genetic network is the molecular wiring of all the interacting loci, whereas genetic architecture describes the phenotypic consequence(s) one would be able to see from that network. Then, trying to bring the two definitions together, if we would assume we knew all the molecular details of a genetic network, we would only need to add the other factors in the model, such as environmental perturbations, to end up with the description of the genetic architecture, right?

You can think of a genetic network as a network of interacting genes, turning each other on and off based on complex relationships and external stimuli. A genetic network is typically characterized in terms of graph theory--connectivity, density, etc.
The term genetic architecture, on the other hand, typically refers to a trait or phenotype and the characteristics of the gene(s) that contribute to that phenotype (this is what the Wikipedia article means by genotype-phenotype mapping). Characterization of a phenotype's genetic architecture involves describing how the phenotype(s) is/are related to the genotype(s). For example, for a particular trait or set of traits, is there a one-to-one relationship between gene and trait? Or do multiple genes contribute to a single trait? Or are multiple traits affected by changes in a single gene? The relevant terminology is discussed briefly in the Wikipedia article: polygeny, pleiotropy, etc.

Ok so what I take from your answers is that a genetic network is the molecular wiring of all the interacting loci, whereas genetic architecture is the phenotypic consequence(s) one would be able to see from that network. Then, trying to bring the two definitions together, if we would assume we knew all the molecular details of a genetic network, we would only need to add the other factors in the model, such as environmental perturbations, to end up with the description of the genetic architecture, right?

@130490868091234 You can characterize the genetic architecture without knowing much about the details of the molecular wiring. But yes, understanding how the molecular details of genetic networks influence important observable traits is one of the grand challenges of integrative systems biology.

As I understand it "gene network" refers to functional 'pathways' that a gene is involved in. For instance there is an extensive gene network around the p53 tumour suppressor - many different gene-products regulate and are regulated by p53, which make up this particular network. These interactions are often visualized using flow-chart-like diagrams, with the stimuli at the top, and the 'outcome' of the network of interactions at the bottom.
Genetic architecture refers to the actual structure of the gene itself. For instance, the coding sequence length, the intron:exon ratio, the 5' and 3' UTR lengths, are all traits relating to genetic architecture.
You have presumably already read the Wiki pages so I've given you my take on the meanings, as I understand them in a general manner - this may well differ from others.

I think you may have confused the term genetic architecture with gene structure.

Determining gene structure is one of the primary goals of genome annotation. See http://en.wikipedia.org/wiki/Genome_project#Genome_annotation. This description of gene annotation is a bit narrow, but it gets the basic idea across.


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Decreasing the alcohol proof and faster in hangover, why?
My russian friend says that the USSR agents used/use the trick that they offered the victim first vodka and then last wine.
I have noted that this puts you faster to hangover: decreasing the alcohol proof.
Some people lose their motor function immediately and some their memory only.
Why does a decrease in the alcohol proof cause you a) faster intoxication and b) faster hangover?
Probably the change in the concentration of alcohol inside cells of brain tissue affects some parts of your brain like the cerebellum. I would like to have an explanation in Biochemistry.
Is there any truth in my friend's argument?

Are we speaking of faster hangover or faster intoxication? In the second case the answer is trivial I would say... in the former I wouldn't see the utility for a secret agent to do that

@nico I am interested in the both cases. I do not know why decreasing the alcohol proof causes faster intoxication. Can you please explain.

well, it's not the decrease, but the fact that if you start with vodka rather than wine you'll get intoxicated faster, as there is more alcohol in it.

@nico I am not sure whether your point is the case here. Like taking "shot, wine, shot, beer, shot" will get you faster down than "beer, wine, shot, shot, shot". I do not know why, but the changing alcohol proof seems to affect some structures in the brain or tissues that affect your motor functions or memory. So in the first, there are two decreases, while in the latter zero.

I would argue that your central point is intrinsically flawed. Your claim is that starting at a high alcohol percentage, then gradually decreasing alcohol content, gets you intoxicated faster. @nico is correct that you will get drunk faster this way (more alcohol sooner rather than later, so this is trivial). If we allow only one variable to change, the alcohol content (and therefore the water content), then the first drink is the most potent, and each drink afterwards is getting progressively more dilute, then this implies you are able to rehydrate better the more you drink. This argues exactly opposite to your claim.
Since you offered up the example of vodka to wine, this introduces two new important aspects: fermentation impurities and sugar content. Vodka is distilled and relatively pure, so it offers little in addition to alcohol and therefore easy to process by the liver. Scotchs and whiskeys are low sugar, higher impurities, and so would be a bit more troubling to filter and process. As you move down to wine, impurities rise and sugar content is much higher. This added sugar load dehydrates faster as well as causes a cascade of hormonal changes that are more immediately troubling than the alcohol. Beer would generally be the extreme end of the impurity and sugar continuum.
Since you bring up the USSR and the KGB, I imagine that if they did stick to this regimen of interrogation, it could be more effective by power of suggestion. The victim believes they are more intoxicated than they are, and perhaps more likely to offer up their secrets.

Lol, the thing is simpler than I first thought. Thank you for your answer!

This has more to do with the person's tolerance to alcohol than the trick itself. People will be affected by different amount of alcohol differently. From personal experience in college, I have seen many people take several shots of vodka and still carry on a conversation. In the same night, I have seen others take a glass of wine and be out for the night.

Without supporting references only an expert in this area could evaluate your answer. Consequently, answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). ——— You may also wish to take the [tour] and then consult the help pages on the standards for additional advice on [Answer] effectively. Thanks!

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


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What makes E. coli yellowish?
LB, TB media, and yeast extract are also yellow but at the heart of the question. What chemical(s) make E. coli yellow?

If I had to guess, I would say FMN/FAD.

It's likely the proteins (general, nebulous answer). Yeast extract of course tints the LB and TB media. There is obviously a range of compounds involved because we are seeing the result of non-yellow wavelengths being absorbed.

I think of E. coli being more white than yellow.  When you compare E. coli and S. aureus on an agar plate, the Staph colonies have a much more distinctive yellow tint.  The yellow tint in Staph colonies is due to staphyloxanthin, a carotenoid pigment.

You will be surprised that when describing the colonial morphology of E. coli on a Blood agar plate, the word choice for colour is "grey". I believe that user leonardo up there had a very good explanation about this "yellowish colour" question.

Bobthejoe's comment is the best answer so far.  Despite many other types of bacterial colonies being "more" yellow than E. coli, E. coli is definitely not white.
Flavins, especially riboflavins, are the predominant compound responsible for this coloration.


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

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

Haha, looks like you already posted it there!

@Daniel Standage Lol ^_^

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

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

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

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


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Human Body "Fat" Equilibrium
Here's my theory:

If you consume x calories each day with y amount of caloric expenditure each day you gain zero weight, regardless of x and y being out of balance.
If you then mechanically remove a large percentage of body fat (surgically), the fat should not come back.

Is this a true theory or not? It seems to me that if the body is stable at the current consumption of x and expenditure of y then the removal of excess weight/fat should not affect anything.
Anyone have thoughts on this? Is my thinking flawed? Why? Even if x and y were equal why might the fat come back if there is no net gain when the fat exists?

The fat that you removed has some non-zero metabolic cost that you need to account for. Your x-y=0 balance will be off.

What makes you think your theory is true? Definitely your first premise is false, otherwise nobody would ever gain weight...

Kevin- so if you consume less calories after the removal with all things being the same the removed fat should not return right?

Nico- true- but generally, very very generally, most people stay the same regardless of x and y. Within a range of course.  this is what I would consider the equilibrium point. If the fat is removed, why would it come back if it wasn't increasing before?

@nico Some people have very different metabolisms: i.e., gaining weight although they are eating healthy or staying skinny although they eat garbage. This definitely isn't the case for everyone, but I'm okay entertaining the premise that some people can maintain weight equilibrium even though x and y are somewhat out of balance.

@helicopterjeff I would, however, recommend clarifying your wording. Currently, it sounds like your assumption is that x and y can be completely off balance and yet you always maintain weight equilibrium. I don't think this is what you're trying to say. If I understand, you're suggesting that for some, weight equilibrium is possible even if x and y aren't balanced. Is this correct?

@DanielStandage: that is exactly my point. As it stands it looks like with any combination of x and y you will never gain weight. I am not doubting that SOME people may not gain weight for y<<x but that would definitely not be the norm.

I guess my ultimate question is why do people who have had liposuction or some other kind of fat removal surgery gain the weight back if their diets remain the same?  Usually, from what I can tell the body before the surgery was not gaining/losing weight. it was just there. After the surgery it eventually comes back. That doesn't make sense to me.

I'm not quite sure what you mean by

regardless of x and y being out of balance.

Surely it would make more sense to assume you gain 0 weight if x and y are balanced? The prime reason why people get obese is probably because x and y are not balanced for them (there are other reasons though, as well as reasons why people can have it imbalanced and still not gain weight).

Even if you consume exactly as many calories as you expend in a day, you may gain weight depending on how (ratio of protein/fats/carbohydrates) and especially when you consume the calories. The body may for example store consumed amounts as fat after eating and then use carbohydrate storage from liver and muscle when starving, so long term you would still gain weight.
Adipose (fatty) tissue requires energy too. If you consume in the same manner after as before cutting a large amount of it away, you may just regain it until x=y again.
Also consider: if people ate just half an apple a day more than the exact amount of energy they need, they should gain more than a kilo on average every year. But they don't, and you can hardly assume that people manage on average to consume the exact amount their body needs.

The reason for that is probably leptin. It is a hormone produced by adipocytes (fat cells) and essentially indirectly reduces food uptake and increases expenditure, among others by decreasing your appetite. This has been regarded as a sort of "adipostat"; your leptin system creates a genetically determined level of body fat that you will tend to obtain. Dieting or cutting away fat will cause a drift to return to the previous weight because of a lower level of leptin (due to reduced fat cells). Of course it's not as simple as that though, so it's also possible that you will actually long-term reduce weight through those methods. E.g. exercise seems likely to be an exception somehow.

x and y being out of balance meaning that most of us, in the USA anyway consume WAY more calories that we expend. Yet in many cases no weight gain is seen. I am personally in that boat. Despite diet, I'm not gaining or losing.
So I am wondering why then if the fatty tissue is removed why does it come back?
The leptin system is probably what is at work. The body wants to be at a certain weight. If you starve it you're at a lower weight.

There are many reasons why that can happen. Regarding leptin, something could be wrong with its production or its reception at the target sites. The same is the case for me though even though my leptin is probably ok. It's most likely due to a kidney malfunction which my dad and brother have as well (we're all slim the same way). There's probably other different causes as well.


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Are quaternary protein monomers unique to a particular protein complex?
I know that quaternary protein structures are formed exclusively via non-covalent bonds. My biochemistry professor discussed a viral capsid that is essentially one quaternary structure with 240 individual monomers of 4 kinds. I suspect that for this protein coat to be stable, the non-covalent bonds holding it together must be rather stable. He also mentioned that different monomers can join to form the functional protein complex from relatively far distances, like across an entire cell, which once again leads me to believe that both monomers must be interacting with each other very strongly.
My question is: Since a strong non-covalent interaction is required between (at least) two protein monomers to form the functional quaternary structure, can one particular protein be a monomer to an array of different quaternary complexes? Are there any examples of this?

I realize that this question isn't exactly "precise", and I might be using the wrong terminology. Feel free to edit or let me know how I can improve the question.

Are you limiting this to protein complexes which assemble irreversibly? Otherwise anything where two proteins attach temporarily to form an active enzyme would be an example. E.g. cyclin-dependent kinase (CDK) and the different cyclins.

I had originally asked this question with irreversability in mind, but just activation would make a great addition to the answer.

I would say that there are quite a few quaternary protein structures that are connected by intermolecular cystine bonds.

If I understand the question correctly, you're thinking something along the lines of modular tertiary domains, but in a quaternary sense?
For a reversible interaction, heterotrimeric G proteins spring to mind. Once activated by a G protein coupled receptor (GPCR), the alpha subunit and the beta-gamma complex dissociate from the receptor and from each other. They can both go on to affect signaling by binding to various effector proteins, depending on the particular pathway in which they are involved, and their activities can be mediated by other proteins (e.g. the alpha subunit GTPase regulated by GAP proteins).
I spoke to my Protein Engineering professor, and she also directed me to a few examples, although I'm not sure they're quite what you're looking for in the strictest sense.

Cyclin-dependent kinases, as @Armatus mentioned, bind to all sorts of different cyclins. (I get the sense that subunits found in multiple protein complexes will probably be more common in signal cascades. I don't have any real data on that, but it makes sense that a signal protein could interact with two or more protein complexes and even have slightly different functions in each.)
Alcohol dehydrogenase (ADH) is an example of a protein with different quaternary structures between species. According to my professor, it occurs as a homodimer in mammals, but as a tetramer with some slightly different residues in budding yeast. I can't say whether the sequence changes are what affect the oligomerization, although my prof also mentioned "oligomerization domains" that could mediate protein-protein interactions.
She also directed me toward a slightly more interesting example (in my opinion), though, again, it's also more along the lines of oligomerization. Small heat shock proteins (sHSPs) undergo something called "dynamic subunit exchange" and can take on a wide variety of oligomeric architectures. Binding is transient, but it's still kind of neat. There's a review here: http://www.sciencedirect.com/science/article/pii/S0968000411001903. Figure 3 shows different oligomeric architectures from the one monomer.

It seems that pretty much any protein that interacts with two or more separate protein complexes could be considered an answer. Neither I nor my professor have managed to come up with an example of an irreversible assembly of common subunits, but she is of the opinion that, in all the different possible protein structures, there is probably at least one example of everything, no matter how outlandish it seems.


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

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

Since it sounds like you are the one designing the database, you can make this a number of ways. The simplest is probably to reduce it to two variables, likely two decimals.
See this hemoglobin example for a chromosomal locus example.

There are N chromosomes (23 for humans, if you like, sex chromosomes can be treated as a pair).
There are 2 chromatids per chromosome.
The part of the chromatid is either p or q (short or long arm).
Then there is the location on the portion of the chromatid (eg, 15.5).

Chromatid can be easily represented as a decimal, where the integer portion is the chromosome number, and the decimal portion corresponds to the chromatid and arm.
The chromosomal locus can be another decimal, such as 15.5 for the example above.
This is of course one way, and there are many other ways you could do this.

This sounds a bit convoluted, to be honest. Why not use a compound type to store the separate bits of information in their respective fields? For instance, putting chromatid and arm into a decimal point number isn’t only “dirty”, it’s also unnecessarily complicated. Even if the database doesn’t support enumerations (wot?!), this could still be represented by separate bit fields.

Yes it absolutely could, and should be done this way. This was one (crude) way to do it as the OP did not post any details as to the kind of DB or format he expected to use.


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What are the positive and negative effects of insulin on cognitive function?
A UCLA study seems to imply that insulin interferes with cognitive function.

The DHA-deprived rats also developed signs of resistance to insulin, a
  hormone that controls blood sugar and regulates synaptic function in
  the brain. A closer look at the rats' brain tissue suggested that
  insulin had lost much of its power to influence the brain cells.
"Because insulin can penetrate the blood–brain barrier, the hormone
  may signal neurons to trigger reactions that disrupt learning and
  cause memory loss," Gomez-Pinilla said.
He suspects that fructose is the culprit behind the DHA-deficient
  rats' brain dysfunction. Eating too much fructose could block
  insulin's ability to regulate how cells use and store sugar for the
  energy required for processing thoughts and emotions.
"Insulin is important in the body for controlling blood sugar, but it
  may play a different role in the brain, where insulin appears to
  disturb memory and learning," he said. "Our study shows that a
  high-fructose diet harms the brain as well as the body. This is
  something new."

At the same time, increased levels of IGF-1 seems to be implicated in higher level of intelligence. IGF-1 is not the same thing as insulin, but it does seem to have many similar effects.

And the question is?

Don't take it personally, but this is a ridiculous question. You have in hand a study that "seems to imply" it has an effect, but you ask anonymous users of an internet website to tell you whether the authors are right or not - something which only further experiments can clarify. The only answer to such a question is "Do your own study, and then draw your own conclusions".

Diabetes
I've not read about any conclusive evidence for a link between insulin and differential cognitive function, but I have read studies that link type-2 diabetes and impaired cognition (1). I will point out now that this is cross-sectional, so the study only reports associations (i.e. diabetes may not necessarily cause the cognitive impairment).
The study I have mentioned does not conclude that this is caused by raised insulin, but rather the effects on the vascular system (specifically microvascular). They also find a significant interaction between diabetes and smoking status, in the context of cognitive impairment. Again, this seems likely to be the vascular system, rather than insulin levels.
A recent review paper also refers to the links between diabetes and executive function (2), but again makes no reference to insulin as the cause, but rather microvascular changes, hypertension, and other associated traits (again, the causes are not known, these are speculative based on the evidence).
Diabetes may not be the best model for studying this though, as it can be characterized by either high insulin (tolerance), or low insulin (impairment) - therefore the association may not be found this way.
Insulin
In a separate review (this may be the best one for you if you only read one of the papers I've referenced) the author posits that whilst insulin may have a neuroprotective role, it also increases amyloid-Beta metabolism and tau phosphorylation, possibly contributing to Alzheimer's-like pathologies (3). Studies have found that insulin directly improves cognitive performance (4) after infusion of insulin, but the long term effects are less certain - it is unlikely to improve overall health having constantly raised insulin serum levels!
However the link between IGF-1 and improved cognition is less disputed, so you may well be right in thinking that the 'overall' effect of insulin on cognition may be protective, but this may just be a marker of good health overall, which is certainly protective!


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Modern Whales with Vestigial legs Myth?
Is it a myth that modern whales have been found with hind legs sticking out of their sides and full formed tibias, fibias, and toe bones? I keep finding assertions, but no citations. For example, the wikipedia page has no citation for it.
http://en.wikipedia.org/wiki/Whales#Appendages

This might be better suited on Skeptics. @Rory, what do you think?

I posted this here because I was looking for a statement of fact. A simple "do we observe this" or not, whole vestigial limbs "legs" on modern whales that is. Whether the small bones in the pelvic area of modern / fossil whales are part of their skeletal anatomy or vestigial is another question.

@KonradRudolph I'm never 100% on what's suited to skeptics, I've only really lurked and read some of the higher voted questions.  Sure Mad Sci. will come across this later anyway xD

The link you give doesn't mention limbs sticking out of the body wall, but only vestigial hind limb elements. Many whales do retain pelves and femora, as this page at the Bergen Museum shows. Given the variation in limb development across vertebrates, it would not be surprising to find more distal elements (but I would be very surprised if they extended past the body wall).

So the stories I've heard of fishermen pulling whales out of the sea with legs sticking out their sides are myths/exaggerations? I just want to make sure I have my facts straight, that's all.

probably... lol.  Natural science was historically more of a circus business than institutional science as we know it.  People would garner fame, attention and wealth by bringing in animal stories and artifacts that confirmed ancient myths or fantastic ideas.  Examples are the market for narwhal horns which were sold as unicorn horns and mermaid exhibitions (http://en.wikipedia.org/wiki/Mermaid#Hoaxes).

Whales? I think not. However a dolphin has been seen with four flippers. (https://www.google.com/search?q=dolphin+with+hind+flippers&source=lnms&tbm=isch&sa=X&ved=0ahUKEwjbmK3N287TAhXF4iYKHb6LA4AQ_AUICigB&biw=1138&bih=515)

@JayCkat Dolphins basically are whales. Or rather the informal term "whales" randomly seems to exclude in its everyday use those dolphins who aren't already well-established whales (e.g. Orcas). So your evidence seems pretty rock solid in relation to OP's question!

Yes there are several published sources (with photos) of whales born with protruding vestigial legs.
http://digitallibrary.amnh.org/dspace/bitstream/handle/2246/4849/N0009.pdf;jsessionid=55D6453968F5461B1B6BFF8D53C81F16?sequence=1
Modern Right Whales have rudimentary legs--completely inside their bodies.
"approaching the inquiry with the most skeptical determination, one cannot help being convinced, as the dissection goes on, that these rudiments [in the Right Whale] really are femur and tibia. The synovial capsule representing the knee-joint was too evident to be overlooked. An acetabular cartilage, synovial cavity, and head of femur, together represent the hip-joint. Attached to this femur is an apparatus of constant and strong ligaments, permitting and restraining movements in certain directions; and muscles are present, some passing to the femur from distant parts, some proceeding immediately from the pelvic bone to the femur, by which movements of the thigh-bone are performed; and these ligaments and muscles present abundant instances of exact and interesting adaptation. "
http://etb-whales.blogspot.com/2012/03/hind-limb-rudiments-on-modern-whales_1221.html


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What risk to DNA does long-term exposure to low-dose radiation pose?
A new study from MIT scientists suggests that long-term exposure to low-radiation poses no risk of DNA damage for mice (it is also important to note that mice are unusually susceptible to cancer). So apparently there may be a threshold for radiation damage to DNA.
But is this study conclusive? What are some other studies that show the biological effects of long-term low-dose radiation on DNA?
There are some studies that do show increased rates of cancer in frequent flyers. So are are we going to reconcile this finding with the finding above?

Can you say that anything in science is conclusive?

@Kevin Yes of course. Why not? “conclusive” doesn’t mean 100% sure – otherwise nothing would be conclusive, thanks to Gödel’s incompleteness theorem. It just means “reasonably sure” given some fitting threshold.

I agree with @Kevin - there are no ultimate statements in science. The answer is 'its all relative'.
With radiation and risk, more radiation means more risk of cancer or any number of other types of damage that can result.  The question is is this significant?  And this is a somewhat subjective question.
When someone says:
'there is no health risk from XYZ'
what they mean is..
"to the extent that we can determine, we can't see any more chance of adverse health if you are exposed to XYZ conditions than if you weren't"
DNA damage happens all the time.  The frequent flier study you cite is trying to see if the additional exposure to cosmic radiation while flying, which is largely blocked by the atmosphere, causes a change in the rate of some cancers.
Radiation and cancer is like a lottery.  If you buy just one ticket you might win.  If you step outside, the thousands of extra gamma rays you get outside might start a cancer that will eventually take your life.  If you buy 20 million tickets you will very likely win.  If you hang out next to high levels of radiation, even for a short while, you will get so much damage you will not live long.
Its difficult to study the effect of low levels of radiation. The lower the levels of radiation we are asking about, the longer you will have to wait to see if there is an effect.  If 10% more people get cancer, you have a very real concern that some of these folks might have done something else, like sunbathe or live in a poorly ventilated basement for too long.
The real question is, what is significant?  I once saw a 60 minutes segment where a dermatologist said that she simply never directly exposes her skin to direct sunlight.  I'm betting she never got a melanoma.  She carried a parasol and wore light gloves outdoors.  (sorry I can't find the link)  She was at least in her 50s and she had the skin of a teenager.  I still go out in the sun.  I assume my risk of melanoma is 5-10 times more than hers was (this was a pretty old broadcast).  (mine is 0.03% in the next 5 years btw).  Its just not worth it to me.

See my answer to Kevin’s comment. This is a red herring, “conclusive” isn’t the same as “ultimate statement”.

In the astrobiology community, radiation is a ubiquitous factor in the survival of life in space. It's the current understanding that, while high doses of radiation over a short period of time are lethal, an equivalent dose over a much longer time period (maybe 1000x longer) is much less harmful.
The basis for radiation lethality lies in the ability of high-energy particles (that's what radiation is) to damage DNA. When DNA gets damaged, there are some issues:

The normal, regular structure of the molecule gets disturbed. The genome is a very delicate structure. It is linearly sequence-dependent, and it is only singly redundant (there are two strands of DNA, so if one strand becomes damaged, it can be recopied from the other one).
Our cells are under unrelenting barrage of oxidative stress, EM radiation, radioactive radiation and physiological stress--this is no exhaustive listing of the constant fight our bodies' cells put up all the time. There are repair mechanisms in place to automatically fix the damage done by high-energy radiation, and if it turns out that a particular cell has sustained too much damage--well, it commits suicide. This process is called apoptosis and its importance ranges from proper embryonic development to prevention of cancers.
In short, there are two ways that excess radiation can cause an organism to die: a) DNA and cellular damage to an irreparable extent, and b) mutagenesis to cause cancers and other cell-cycle diseases.

We don't quite know the full extent to which we can expose our bodies to long-term high-energy radiation, but the answer is sure very complex. Different tissues, cell lines, and regions of the body receive and cope with radiation in very different ways.


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How to find ion/water channel related genes
We now have a collection of transcripts at hand. We would like to investigate some particular ones, which are ion/water channel related. How to perform this? Could anybody point out how to find the annotated genes those are ion/water channel related? If there are some places particularly for fish, that would be perfect. Thanks.

In case you don't know it, this should be of help: http://www.geneontology.org/

i'm afraid a literature crawl is the only reliable way to get domain knowledge like this.

I think your best bet is to blast your transcripts against the TCDB which has all ion channel templates you can get in the literature. Second best would be to blast against a general protein database like UniProt.


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Why do we grow so much hair on our heads compared to our bodies?
I've been wondering about head hair, facial hair in particular. Human males can grow very extensive beards should they choose to not shave - however you do not really see this in our chimpanzee cousins! Yes, they have little pseudo-beards, but the difference being that they do not shave, that is just the length they reach. Whereas in humans we can grow to our hearts content (*this may not be the case, see this question).
I can't really see why this would have been selected, unless it's simply that (evolutionarily speaking) women like men with long beards?
So my question is: why can humans perpetually grow head hair, yet we have lost the majority of our body hair, in comparison to chimpanzees and other ape family members?

This is closely related to this question - perhaps not an exact duplicate though?

@RoryM thanks for pointing out that question - it certainly goes some way to helping answer this one. I have differentiated my question a bit further so that it's definitely not a duplicate.

Wheeler (1992; and previous) discusses the evolutionary loss of "non-functional" hair in hominids from the perspective of water balance.
Wheeler's hypothesis is that naked, bipedal hominids could have tolerated higher ambient temperatures as well as elevated metabolic heat production. Naked skin would confer higher levels of evaporative cooling, but would have entailed more water loss.
Wheeler argues that bipedalism necessarily would have preceded loss of hair, which seems to agree with Carrier's (1984) hypothesis that early hominids were distinguished not by large brains but by upright, bipedal postures with striding gaits. Humans are unique among similarly sized mammals in their capacity for endurance running.

Interesting! May we have kept hair on our heads to keep the sun from directly heating our brains? Bit off topic, but do you suppose the increased endurance running is simply that running on 2 legs is more efficient than using all 4?

Hair on the head is an excellent built-in sun protection at minimal resource cost. If we didn't have hair on our heads then we would have to apply sunscreen on the scalp or take cover more often (often impossible for hunter-gatherers).
No sun protection = sunburns and risk of skin cancer.


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The evolution of dogs through domestication and artificial selection
I am currently reading Richard Dawkins's book 'The Greatest Show On Earth: The proof for evolution' and in the second chapter he talks very much about the evolution of dogs.
He says centuries ago there was only such dog-like creature as the wolf, but in a matter centuries the wolf has evolved into the many breeds of dog we have through artificial selection conducted by man.
This to me seemed very peculiar and quite frankly untrue, and I may be getting the wrong end of the stick and he is in fact being analogous, although I'm pretty sure he's not.
So, did wolves evolve into the many breeds of dog we have through artificial selection conducted by man?
If so, how many centuries did this take?
(Dawkins's point was that if the wolf can evolve into the vast amount of breeds of dog we have at the moment from artificial selection over a matter of centuries, then surely over many millions of years, the evolution we claim to know of through natural selection could definitely have happened).

What makes you think it is untrue? Domestication is the process of artificially selecting a wild species in order to benefit humans.

@nico The reason it would seem quite untrue is because (to me) even through artificial selection, evolving from a wolf to the vast amount of breeds of dog we have now in centuries seems like a very short amount of time. But I do accept it's true and don't doubt him. Do you know roughly how long ago it was when only wolves were present?

Would you say my reason seems unreasonable?

@Olly Your reasons are in fact spot-on but if I remember correctly (but it might have been another of his books), Dakwins explicitly mentions that in order for changes to occur so fast, the variability in the genome has to be already present.

That would make perfect sense, I couldn't imagine it happening in such short time if there wasn't variability in the genome, thank you.

I just wanted to add that although we are pretty confident that domestication of wolves created domestic dogs in pretty short order.  In addition to the fact that they can still interbreed and the taxonomical resemblence of dogs to wolves and finally the genome sequence, probably the most awesome evidence is the domestication of the silver fox.
Russian biologists at the Institute of Cytology and Genetics (ICG) in Novosibirsk, Russia in 1959 started with 130 foxes.  Even though they can be bred in captivity and they are close to dogs, they had never been domesticated.  By selecting the animals with the least aversion to human contact over 10 generations, they were able to breed foxes that were very much like domestic dogs.  They follow humans around, enjoy contact with humans, and generally act friendly.  In addition they also bred the most averse animals to human each generation as a control (sure enough these animals would rather nip your fingers off before letting you rub their belly!) there are videos of these animals floating around.
Ten generations of animals ended up being less than 20 years.

Yeah I read about this, their appearance even changed dramatically!

@OllyPrice like dogs, their appearance change is an unexpected effect of such strong selective pressure.  The fact that the coat changes color, the ears get softer and floppier.  Its strange how they sort of get cuter when they are domesticated.  This should be a coincidence, aggression and physical competition might be associated traits, but its a little odd when you think about it.

+1 for the fox example! This shows how few genetic polymorphisms and how fast domestication (ie, taming) can occur. Other studies have shown that a few genetic polymorphisms can lengthen snout, shorten legs, alter other characteristics which are used to distinguish a breed of dog.

You say strange, but then surely (and this is where natural selection would no doubt come in), the genes of those dogs that were 'cuter' AND friendlier would have passed on more often than the others.

In the case of dogs, yes.  In the case of the foxes the scientists were trying to be pretty clinical about it. They had a test where someone would approach the animal and they would try to rate the reaction alone.  ugly but friendly foxes were a distinct possibility here.  The fact we think they may be cute might come from some other interesting possibilities, including that friendlier genes may come from some arrested development in the animals which may maintain juvenile traits for instance, which are usually cuter. just a thought.

According to Serpell, 1995 (http://books.google.co.uk/books?id=I8HU_3ycrrEC, page 8), wolf bones in association with human bones have been found from as early as the middle pleistocene (126,000–781,000 years ago). I think we're talking about more than a few centuries here :) It's still relatively little in comparison to naturally selected evolution, but that's probably the point he is trying to emphasize.

If I remember correctly his argument was that the transformation (if I may use such a word) from wolf to dog did indeed occur over a much shorter time span. I’m pretty sure Dawkins was making a factual claim, and since he’s well-versed in dog-breeding and researches all his books with great care, I’d be surprised at such a blunder.

Later on in the book he does mention that it's 1million years ago that the wolves started becoming village-scavengers (which of course kicked off the domestication of them), I had asked this question before I read that part.

Many dog breeds went through genetic bottlenecks about 200 years ago. Many of today's breeds either did not exist a couple to few hundred years ago or looked rather different than the breed looks today. It doesn't take long to change the characteristics when selective breeding occurs.
One may need to consider the co-evolution of Homo sapiens and Canis familiaris. Our close friendship with dogs tipped the balance in favour of modern man over the Neanderthals, who had previously occupied present-day Europe for a staggering 250,000 years. More on how dogs helped human hunt and be watchful is explained here.
This other report, just out, states that modern dog breeds are genetically disconnected from ancient ancestors. Cross-breeding of dogs over thousands of years has made it extremely difficult to trace the ancient genetic roots of today's pets, according to a new study.

Pat Shipman's suggestion seems very unlikely, earliest evidence for a domestication event of the gray wolf is maybe 32,000 or 40,000 years ago, the last Neanderthals died out 42,000 years ago in Gibraltar & 44,000 years ago in the rest of Europe, the math doesn't stack for dogs to have any involvement in the Neanderthals demise.

Hmm.. on the other hand (sorry, I think I was sitting on it earlier) the common ancestor of wolves & dogs obviously predates those domestication event dates (which come from genetic evidence rather than fossil record iirc), obviously those animals may have been extant as partners used by humans for some time b4 the (probably not so deliberate) selective breeding diverged them from the wild ones that evolved into wolves, that may push the association with humans back far enough it is possible.

A couple more links to compliment your one: National Geographic / The Guardian


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Why is proteinase K digestion performed at 50 °C?
Many DNA isolation protocols use a Proteinase K digestion to remove proteins. This is often performed at 50 °C. Why is this?

Proteinase K activity is greatly increased by addition of denaturing agents like SDS or urea (Hilz et al., 2008), indicating that the denaturation of the substrates helps Proteinase K to degrade them.
Increasing the temperature to 50°C will also unfold some proteins already, making it easier for the Proteinase K to degrade them. The proteinase K seems to be a pretty stable enzyme, and  can still work at this temperature.

In your linked wiki article: "An elevation of the reaction temperature from 37 °C to 50 - 60 °C may increase the activity (of Proteinase K) several times." The enzyme works faster at 50°C.

some proteins are deactivated at that temperature... they are all different, aren't they?

@shigeta yup, they are all different.


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How is human biological clock modelled in modern science?
Im an engineer by education and i program a lot, so the question sounds weird to people from other disciplines.
Im trying to better understand the human biological clock. Yet i do not really know what it is. I read about clock genes, endogenous cycles, and other observed phenomena that is time sensitive or cyclical in nature. But is there a centralized model of what the circadian rhythm is or how itis exhibited within the human body?
For example an electrical clock can be modelled with feedback loops or electrical flip flops that control the timing. Ive seen the heart modelled as Van Der Pol oscillator.
Does modern science have some notion of how the "master" clock within the human body work? Is there a feedback or an oscillator model of the master clock?
Thank you for any articles or keywords that ican use to research this question!

Lacking references, this is only a comment instead of an answer. But the central point of any answer will be: biological clocks also use feedback loops (which form oscillators), albeit (sometimes vastly!) more complex ones than mechanical clocks. There are some fascinating studies which have identified specific gene regulatory feedback loops which control the cyclical expression of specific phenotypes.

I'm looking at this link that was posted around here earlier: http://www.ncbi.nlm.nih.gov/pubmed/21811695 The first image in this link, would that count as a model of the "master" clock?

I’m not sure. The image surely shows a feedback control due to the overall self-inhibitory function. But I cannot comment on whether it’s self-sufficient in maintaining a consistent oscillation frequency or whether it needs external input (the existence of the “clock/npas2” gene seems to imply that).

The situation is quite complex, and there are certain things that we do not fully understand, but I will try to give you an explanation.
First of all, at the cellular level, you have the genetic components of the circadian clock, the clock genes and their protein products.
You can divide clock proteins into positive and negative regulators: the positive regulators modulate transcription of clock-controlled genes and are inhibited by the negative regulators in a loop that lasts approximately 24 hours (in Latin: circa = around and dies = day).
For instance the Clock and Bmal1 nuclear proteins, when present in sufficiently large amount, will dimerize and act as transcription factors on a series of genes that contain a region in their promoter element called E-box. Amongst these are the Period (Per) genes.
Per is then synthesised, and exported to the cytoplasm. Here, if in a sufficiently large amount, it can heterodimerize with the Cryptocrome (Cry) proteins: the dimer will then enter the nucleus and inhibit the transcription actions of the Clock/Bmal couple. This will in turn, block the transcription of Per, that will therefore not be able to dimerize with Cry and stop the inhibition of Clock/Bmal and so on. All of this takes approximately 24 hours.
This basic loop (and some more) is nicely schematised in this review by Reppert and Weaver
Coordination of circadian timing in mammals. - Reppert and Weaver, Nature. 2002 Aug 29;418(6901):935-41.

I report here the legend of the figure:

The clock mechanism comprises interactive positive (green) and negative (red) feedback loops. CLOCK (C, oval) and BMAL1 (B, oval) form heterodimers and activate transcription of the Per, Cry and Rev-Erbalpha genes through E-box enhancers. As the levels of PER proteins increase (P, blue circle), they complex with CRY proteins (C, diamond) and CKIε/CKIδ (ε/δ, circle), and are phosphorylated (p). In the nucleus, the CRY–PER–CKIε/CKIδ complexes associate with CLOCK–BMAL1 heterodimers to shut down transcription while the heterodimer remains bound to DNA, forming the negative feedback loop. For the positive feedback loop, increasing REV-ERBα levels (R, circle) act through Rev-Erb/ROR response elements in the Bmal1 promoter to repress (-) Bmal1 transcription. CRY-mediated inhibition of CLOCK–BMAL1-mediated transcription de-represses (activates) Bmal1 transcription, because REV-ERBα-mediated repression is inhibited. An activator (A, circle) may positively regulate Bmal1 transcription (?) alone or by interacting with mPER2. There are probably kinases (?) other than CKIε and CKIδ that participate in phosphorylation of clock proteins.

The clock machinery, however, is even more complex than this and different tissues need to integrate different signals (e.g. light, hormonal concentrations and so on).
However, as nice as this may be, our bodies are not constituted by one single cell... if we "zoom out" a little bit and we go to the tissue or the whole body level, we see that circadian rhytms are present in all sorts of tissues and involve all sorts of different physiological processes. A very interesting question is then: how do cells from different organs coordinate each other so that the interrelation of different circadian processes is always the same? For instance, the release of cortisol peaks in the morning, our body temperature has a peak in the late afternoon and a trough in the early hours of the morning, and our heart rate is higher during the daytime.
In 1972, an article by Moore and Eichler was published, showing that lesioning the suprachiasmatic nucleus (SCN) of the hypothalamus (a region at the base of the brain) resulted in the "breakage" of the circadian rhythm of corticosterone (the stress hormone).
Loss of a circadian adrenal corticosterone rhythm following suprachiasmatic lesions in the rat. - Moore and Eichler, Brain Res. 1972 Jul 13;42(1):201-6
The fact that lesioning a bit of the brain resulted in loss of circadian rhythm in the adrenal gland was obviously a very big deal: the central circadian clock of the organism had been discovered.
I will not going too much into that but, since 1972 many advances have been made and nowadays we know that, although the role of the SCN is very important, it is not the only clock in the body. Several peripheral clock exist, in organs such as the pituitary gland, the liver or the pancreas. How all these clocks communicate between each other and what is their contribution to the generation of non-circadian rhythms (ultradian and infradian) are questions that still have to be solved.
A few interesting papers on the matter:
A riot of rhythms: neuronal and glial circadian oscillators in the mediobasal hypothalamus. - Guilding et al., Mol Brain. 2009 Aug 27;2:28.
A clockwork web: circadian timing in brain and periphery, in health and disease. - Hastings et al., Nat Rev Neurosci. 2003 Aug;4(8):649-61.
Peripheral circadian oscillators in mammals: time and food. - Schibler et al., J Biol Rhythms. 2003 Jun;18(3):250-60.

A fantastic answer! This is the second time I'm seeing a diagram of PER and CRY, and still, I cannot understand it. What I read is that DNA is involved. Does the clock involve the DNA, or is it an "external" protein structure that only touches the DNA?

@AlexStone: well, DNA is used to code for mRNA which in turn generates protein. So, for instance, you will have a Cry gene, which will generate a Cry mRNA which will give the CRY protein. The passage DNA->RNA is due to the fact that certain proteins, called transcription factors, bind to the DNA and allow the initiation of transcription (through another protein, called RNA polymerase). Transcription factors, being proteins, have also been derived from the translation of some mRNA, which was derived from the transcription of some DNA. CRY, PER and the likes are, in fact transcription factors.

@AlexStone: so, in essence you have some transcription factors that control the transcription of each other through their corresponding proteins. Because there is a delay for the cellular machinery to transcribe, translate etc. and the concentration of the proteins need to be sufficiently high, this is not immediate, but takes ~24h. Note that circadian clock proteins do not just regulate their own transcription, that would be useless. They can act as transcription factors for many other genes. Hope it is clearer now, you may have a look at http://en.wikipedia.org/wiki/Crick%27s_central_dogma

I've stumbled upon a detailed explanation of the Biological clock. This one is broken into multiple steps and helped me better understand what PER and CRY are. I cannot vouch for the scientific accuracy of the diagrams, but they make sense when combined with text.