text:
Natural enemies boost deep evolutionary fitness?

"Two species that reduce one another's fitness on microevolutionary
  (short-term) timescales can increase each other's macroevolutionary
  (long-term) fitness"

Opinions?
Intuitive Examples:

Body Size - Predator-prey relationships or interference relationships
(fighting, e.g. for territory) are often documented to put seletion
pressures to grow in body size, often a positive feedback loop. In
the short term the presence of the natural enemy in this case often
leads to decreased population fitness (probability of being
eaten/probability of fatal conflict over territory). But in the long
term such large body sizes acts as an advantage over potential future
enemies of the same kind. This is particularly relevant to marine
ecosystems - where the size of fish often determine where in the food
chain that fish is.
Speed/agility - Predators and prey that rely on speed/agility to
capture (predator) or escape (prey) undergo an evolutionary arms race
leading to positive feedback of speed/agility boosting morphologies.
In the short-term the natural enemy of the prey acts as a burden to
population fitness (probability of being eaten) but in deep time the
prey has acquired morphological advantages over potential future
natural enemies such as competitors for resources.
Venomousness -Why do venomous animals live in warm climates?

The question is interesting.
I am afraid about the use of the word "fitness" in you question. The fitness is usually defined as the number of offsprings an individual can sire in its lifetime. Most often we talk about relative fitness which is the relative number of offspring in an individual can sire in its lifetime compare to the individual in the population that sire the greatest number of offsprings.
How would you compare fitness of individuals between different species? Just by counting the number of offspring they left behind? Or did you mean that most fit species are actually those species that can outcompete others? If yes, then I would say that saying

Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) fitness

can be restated

Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) species competition ability

and it is actually just a special case of

One species that evolve under many strong selection pressure ends up being a very competing species.

The explanation is the following:
One species that undergoes one selective pressure, will see its genetic variance decreases. The weak individuals will disappear letting places to the strong individuals. Then newly arisen variance (mutation) will come up only in the strong individuals (as the other ones disapeared). This is what J.Gould meant by saying "Natural selection creates the fit". As a consequence a species that undergo many successive selection pressure will end up with purified and very strong genotypes while, in a species that were free to evolve without selection they would have evolved many different genomes with some good mutations nested in very poor genetic background.
You could as well use the concept of lineage selection and states that lineage that succeeds to outcompete others will thrive while species that suffer from competition with other species will get extinct. As a result, if you compare all species that were in competition with another species in the past with all species that were not in competition, you will find out that those that were in competition are more resistant to competition. But I guess this is not exactly what you meant when saying: "Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) fitness"
Finally you might think of the ability of species to evolve better. This ability is called "evolvability" (see this book for example). You might say that species that undergo many selection pressures were selected to resist to newly arisen selection pressure. As a result, species that are under competition might end up with a greater evolvability than those that were not under selection. Resulting that species that were under competition will tend to increase to always increase their fitness in the long term.

I believe I was not just addressing "competition". E.g. Having larger body size does not simply increase competitive ability, and may sometimes reduce it (increased resource requirements). The ramifications of having certain positive feedback loops in morphology change has a more general effect. Indeed fitness was a word I chose since I could not choose another - perhaps I mean "fitness relative to future potential phenotypes". Fitness is not just restricted to #offpspring, that is only the "life histories" definition isn't it? http://en.wikipedia.org/wiki/Fitness_(biology)

The wikipedia link you provide says: "Fitness is a central idea in evolutionary theory. It can be defined either with respect to a genotype or to a phenotype in a given environment. In either case, it describes the ability to both survive and reproduce, and is equal to the average contribution to the gene pool of the next generation that is made by an average individual of the specified genotype or phenotype." and this wiki article does not use the word life-history.

Fitness is usually considered to be the (relative or not) number of offsprings one can produce in its lifetime (or per year). It is also often considered to be number of fertile offsprings or even the number of grand-children. This concept even if it is very central. Here is a discussion concerning the concept of fitness but the discussion is still open I think.

But anyway. What is the definition of the words you're using in "Two species that reduce one another's fitness on microevolutionary (short-term) timescales can increase each other's macroevolutionary (long-term) fitness"?

Ah thank you @Remi.b. To make the "life histories" clearer, I should have asked: "Arn't you talking about reproductive success?" (the life histories definition of fitness): http://en.wikipedia.org/wiki/Reproductive_success. As opposed to the population geneticists definition (my area of research) that considers relative changes in allele frequency.

Microevolution and Macroevolution are two fields of evolutionary study. One deals with short-term dynamics such as changes in allele frequency, the latter deals with processes that span multiple speciation events.

Yes, I agree with you definitions of micro- and macro-evolution. I don't think there are any different between fitness and reproductive success except the one that a particular person wants to make. Sometimes reproductive success is considered non-relative while fitness is relative. I still don't really understand what you call "life history definition of fitness"

let us continue this discussion in chat

authors: เน็ตฟรี buy อาทิตย์


text:
Organisms as potential Bio-Weapons?
Question:
Given that with genetic engineering we can customize organisms as bio-weapons. Which species have the most worrying potential to be weaponized for mass destruction?
Background:

Biological warfare — is the use of biological toxins or infectious agents such as bacteria, viruses, and
  fungi with intent to kill or incapacitate humans, animals or plants as
  an act of war.

Examples:

E.G. bio-weapon species: Anthrax fungus -  was first tested as a biological warfare agent by Unit 731 of
  the Japanese Kwantung Army in Manchuria during the 1930s; some of this
  testing involved intentional infection of prisoners of war, thousands
  of whom died. Anthrax, designated at the time as Agent N, was also
  investigated by the Allies in the 1940s.
E.G. bio-weapon vector: Anopheles labranchiae (malarial mosquito) - According to Prof Frank Snowden, a history professor at Yale
  University whose book The Conquest of Malaria in Italy draws on
  American archives and the diaries of Italian soldiers, the scheme was
  orchestrated in the autumn of 1943 by Erich Martini, a medical
  entomologist, Nazi Party member and friend of the SS commander
  Heinrich Himmler.

When was anthrax used to assassinate US politicians?

You remember these mysterious letters in the US following 9/11 containing a white powder? This were actually weapon grade anthrax spores.

@AlanBoyd, here's the wiki all about it: http://en.wikipedia.org/wiki/2001_anthrax_attacks, i've updated the question to include some details on this

Which confirms that no politicians were assassinated.

oh my mistake! I meant attempted*

I would say by far the most worrying potential is that of H.sapiens sapiens.

There is both a set "list" of agents, but more importantly, a set of properties that an organism needs to be in order to be truly worrisome.
First, the list:
The CDC classifies agents into one of three categories, Class A, B, or C.
Class A: These are organisms that are hard to control, highly transmissible, and lethal:
Anthrax (Bacillus anthracis)
Botulism (Clostridium botulinum toxin)
Plague (Yersinia pestis)
Smallpox (variola major)
Tularemia (Francisella tularensis)
Viral hemorrhagic fevers (filoviruses [e.g., Ebola, Marburg] and arenaviruses [e.g., Lassa, Machupo])

Class B: These are organisms that are fairly easy to disseminate, make people sick but don't necessarily have high mortality rates, and may be difficult to detect.
Brucellosis (Brucella species)
Epsilon toxin of Clostridium perfringens
Food safety threats (e.g., Salmonella species, Escherichia coli O157:H7, Shigella)
Glanders (Burkholderia mallei)
Melioidosis (Burkholderia pseudomallei)
Psittacosis (Chlamydia psittaci)
Q fever (Coxiella burnetii)
Ricin toxin from Ricinus communis (castor beans)
Staphylococcal enterotoxin B
Typhus fever (Rickettsia prowazekii)
Viral encephalitis (alphaviruses [e.g., Venezuelan equine encephalitis, eastern equine encephalitis, western equine encephalitis])
Water safety threats (e.g., Vibrio cholerae, Cryptosporidium parvum)

And finally, Class C, which are emerging threats that may be dangerous if engineered largely due to their novelty and their potential lethality/transmissability. The CDC uses examples like Nipah virus and hantavirus.
So that's the list of what the CDC thinks is a big deal. You'll note influenza isn't even on there. I'd argue that any given novel influenza strain belongs in Class C, and likely not Class A because, while potentially both transmissible and virulent, a known vaccine exists and simply needs to be formulated.
In terms of properties for an organism, I'd suggest the following, in no particular order (it likely depends on what said organism is meant to do):

Highly virulent: The disease needs to be able to cause human disease, with high rates of both morbidity and mortality.
Highly transmissible: Unless the goal is to cause a "one off" incident, the disease needs to be able to establish a productive chain of human-to-human infections. Humans can't be a dead-end host. Ideally, this needs to be direct human to human transmission, rather than a vector born disease like West Nile.
Stable and amenable to engineering. It needs to be something that's easy to culture and grow in large numbers. This one often gets overlooked somewhat, but despite the fact that its now somewhat commonplace, bioengineering isn't exactly easy.
Not amenable to treatment. The organism needs to not be easily treatable - broad spectrum antibiotics, existing vaccine stock, etc. mean that the normal public health infrastructure can address, or at least mitigate, an attack. For an attack to be truly effective, it needs to swamp existing infrastructure, and one way to do that is to necessitate intensive, unusual care in hospitals and out of the ordinary action on the part of public health officials.

I would put all zoonotic viruses into this. They passed a species barrier, are new to our immune system and there are no vaccines against them. The flu is one example, corona viruses are another (SARS or even newer MERS). With SARS we had a lot of luck that this didn't end in a bigger epidemic.
A good book about these viruses is the book "Outbreak" (hence the title) by David Quammen.

No doubt influenza. The horizontal shift makes it very virulent and only a few mutations allow it to transfer from birds to mammals (as little as two). See here. There was a big push not to publish these as it would be so easy to make recombinantly. However, thanks to quick work, we have determined that our seasonal flu vaccine protects against this variant.

A more abstract idea for a Bioweapon species could be one that targets key organisms required for completing the nitrogen or carbon cycle. This would likely cause the entire biosphere to collapse though.

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text:
The number of nipples (breasts) a species has?
Only mammals have mammaries and mammary glands.
What evolutionary factors determines the number of mammaries (nipples/teats/breasts) a species has?
Is it always an even number?

Heh, never thought of that. I would guess the size of the brood is the determining factor.

A bit of terminology - a mammary gland is not necessarily the same as a breast. One breast contains many mammary glands - the tissues which produce milk. These are connected via milk ducts to the nipple.

cheers @MattDMo! i've changed wording now, how does it sound?

@hello_there_andy I think the concept of homeotic genes / Hox genes will fascinate you as much as learning about Symmetry in EvoDevo.

That's the reason that Penguins can't evolve into seal and whale type animals, the child bearing.

The number of mammary glands a species has is related to litter size. The relationship generally follows the "one-half rule," which states that the average litter size is equal to half the number of mammaries. The number of mammaries also tends to put an upper limit on litter size. It's not necessarily a hard limit, but survival tends to drop noticeably when number of offspring being nursed exceeds number of mammaries.
The number of mammaries is almost always even, but a notable exception is the Virginia possum, which has thirteen.
Gilbert, A.N. 1986. Mammary number and litter size in Rodentia: The "one-half rule". Proc. Natl. Acad. Sci. USA. Vol. 83, pp. 4828-4830.

As an addition to the excellent post by Erin.
As a name-giving key feature,mammals have mammary glands.
"Animals that are bilaterally symmetric have mirror symmetry in the sagittal plane", which includes Chordates such as mammals.
Some have seen this iconic picture, showing the bilateral symmetry in chordates:

It is easy to see why most commonly even number of mammary glands are found in mammals, given that they form in pairs, distal from the notochord.
Evolutionary, an uneven number of mammaries may be explained through a subjectively-mild mutation which may be retained as a vestigial-like feature, somewhat-functional or not.
On a molecular level, unilateral mammary glands likely involve key developmental pathways such as hedgehog and likely has underlying polygeneic root causes, - for the termination of gland formation on one side.
See this intersting paper:

Kohei Amakasu, Katsushi Suzuki, Hiroetsu Suzuki* "The Unilateral
  Urogenital Anomalies (UUA) Rat", Comp Med. 2009 June; 59(3): 249–256.
We established an inbred rat strain with unilateral urogenital
  anomalies from an incidentally identified male rat with unilateral
  renal agenesis and an undescended left testis. These rats were
  characterized by unilateral renal agenesis in both sexes, undescended
  testes with agenesis and hypoplasia of the accessory sex organs in
  male rats, and complete and partial agenesis of the uterine horn in
  female rats. All of these urogenital anomalies were unilateral and
  restricted to the left side; we named this phenotype unilateral
  urogenital anomalies (UUA). Breeding tests showed that these
  abnormalities were inherited as polygenic traits

It is noteworthy that the mammary glands in the male human population didn't decrease fitness to such a degree where evolutionary pressure would have lead to cease gland formation altogether, by adding extra information to the sex-chromosome(s). As such human males retain mammary glands, albeit typically never reaching a functional state.
The factors weighting against such additional genes are, that the default formation in most mammals is the female body plan, which conserves functional mammary glands to potentially feed their offspring, chipping away at the chance of genes involved in the cessation of mammary gland formation.
Secondly, selection pressure for information retained on the sex-chromosomes is higher, as opposed to autosomal (non-sex) genes. (See this nice concise post by Danielle Venton,  The Degenerating Y Chromosome,Genome Biol Evol (2011)  3  1338-1339. )
Concluding, naturally, it would be easy for an asymmetric sponge to have an uneven number of protrusions or orifices, less so for humans, unless the orifice is located along an axis of symmetry.
See also:

http://en.wikipedia.org/wiki/Hedgehog

Ad biological symmetry:

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text:
Body size, what are the evolutionary trade-offs?
Background
Considering just the "Kingdom Animalia" branch of organisms. It is clear that bigger does not necessarily mean better - there is large variation in body size...
From the 94 µm long Tantulocarid arthropod (Stygotantulus stocki)

To the 25.5 m long Blue Whale (Balaenoptera musculus)

Questions

What trade-offs exist between having a particular body size (very large, very small) to other traits and factors?
Alternatively, what evolutionary/ecological advantages/disadvantages are there to having a large or small body size?

Thank you!

I saw something recently that claimed that, in general, lineages evolved to become larger more often / more consistently then to become smaller. It seems like it might be relevant to this question, but I can't seem to find the citation - maybe someone else can?

Ah, apparently it's Cope's Rule, and it's still a pretty hot topic of debate for and against.

You should quote or summarize this rule as an answer!

Have you read the book WHY SIZE MATTERS by Bonner? It's an excellent book covering every aspect of size in an easy to read manner.

There is the classic essay "On Being the Right Size", J. B. S. Haldane

I don't think one can fully answer to such a broad question. It depends on the population, the environment (presence of predators for example), the genetic background (having a big stomach is good but only if the intestin is big too), the population's social relations, .. Many traits are correlated and one might want to say that a given trait is beneficial but it is not because this trait is correlated (because of genetic, physical or social constraints).
Trade-offs
Here is a list of possible advantages/disadvantages.

visibility to predators
ability to hunt bigger preys or to manipulate smaller preys
running faster
be more impressive
fighting ability
energy consumption for maintaining a body
Quantity/quality of food to be found
homothermy (heat loss)
sustaining its own weight
Rooms for the organs
Attractiveness to the other sex
being more able to move freely (in viscous environment (water))
mechansisms for bringing nutrients and air to the tissues
density of the body (water)
excretion of wastes
moving in small habitats
Hiding in small areas
bearing big and complex structures
Parental care
flying better
acceleration in each movement
etc...

Allometric relations
You might be interested in life-history traits, and in allometric relations. You might be interested by this article as well. The reason for allometric relations can be found here:

If an animal were isometrically scaled up by a considerable amount, its relative muscular strength would be severely reduced, since the cross section of its muscles would increase by the square of the scaling factor while its mass would increase by the cube of the scaling factor. As a result of this, cardiovascular and respiratory functions would be severely burdened.
In the case of flying animals, the wing loading would be increased if they were isometrically scaled up, and they would therefore have to fly faster to gain the same amount of lift. Air resistance per unit mass is also higher for smaller animals, which is why a small animal like an ant cannot be seriously injured from impact with the ground after being dropped from any height.
As was elucidated by J. B. S. Haldane, large animals do not look like small animals: an elephant cannot be mistaken for a mouse scaled up in size. This is due to allometric scaling: the bones of an elephant are necessarily proportionately much larger than the bones of a mouse, because they must carry proportionately higher weight. To quote from Haldane's seminal essay On Being the Right Size, "...consider a man 60 feet high...Giant Pope and Giant Pagan in the illustrated Pilgrim's Progress.... These monsters...weighed 1000 times as much as Christian. Every square inch of a giant bone had to support 10 times the weight borne by a square inch of human bone. As the human thigh-bone breaks under about 10 times the human weight, Pope and Pagan would have broken their thighs every time they took a step." Consequently, most animals show allometric scaling with increased size, both among species and within a species.
The giant monsters seen in horror movies (e.g., Godzilla or King Kong) are also unrealistic, as their sheer size would force them to collapse. However, the buoyancy of water negates to some extent the effects of gravity. Therefore, sea creatures can grow to very large sizes without the same musculoskeletal structures that would be required of similarly sized land creatures, and it is no coincidence that the largest animals to ever exist on earth are aquatic animals.

This post talks about the reasons for the allometric relations between animal size and speed of movements.
Concerning the relation between heat loss and size, you might be willing to have a look to the Kleiber's law. This law has been extensively debated and is today thought (or known) to be wrong.

Just a philosophical note
You might also be interested in the philosophical discussion of adaptation, optimality, cost and benefit like this book (which I haven't read!) for example.

cheers for this, I now realize the issues you've raised. What do you think of me re-wording it so that I ask for "general and commonly observed" advantages/disadvantages? E.g. there may be some evolutionary reasons that hold true to all clades? E.g. the surface area to volume ratio effect for heat retention.


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Chills down the spine with certain music?
I am sure many of us know the feeling of that tingling chill down our spines when listening to certain music.
I experienced this most when my younger brother played an emotional piano piece for a talent show (brought me to tears).

What causes that?
Is music the only stimulus to elicit that spine-tingling?
And in terms of evolution, why?

It is called a frisson, and actually, there has been a study about it, available here.
The frisson is kind of the same you get from cold weather, fear, or... well, other things not suitable to discuss if not knowing how old people reading this might be.
Actually, they found that this works best if you include familiarity. In their case, asking study participants to bring their favourite emotional music, in you case hearing it played by your brother.
How this evolutionary came by is unclear. But as it resembles the shivers you would call "a tingling sense of danger" it might stem from a reaction to uncertainty or at least unclear danger. In this case, it is meant to enable you to concentrate on whatever is coming, and maybe (but that's one of my own theories) this is how it came to connect to pleasant emotions as well: You want to be able to concentrate, delve into the emotion. This could explain, why it works best with familiar pieces: you already know that you want to listen closely.

frisson! - will be saying that more often now, cheers for the insights @skymninge

Music and Emotions
The most difficult  problem in answering the question of how music creates emotions is likely to be the fact that assignments of musical elements and emotions can never be defined clearly. The solution of this problem is the Theory of Musical Equilibration. It says that music can't convey any emotion at all, but merely volitional processes, the music listener identifies with. Then in the process of identifying the volitional processes are colored with emotions. The same happens when we watch an exciting film and identify with the volitional processes of our favourite figures. Here, too, just the process of identification generates emotions.
An example: If you perceive a major chord, you normally identify with the will "Yes, I want to...". The experience of listening to a minor chord can be compared to the message conveyed when someone says, "No more." If someone were to say these words slowly and quietly, they would create the impression of being sad, whereas if they were to scream it quickly and loudly, they would be come across as furious. This distinction also applies for the emotional character of a minor chord: if a minor harmony is repeated faster and at greater volume, its sad nature appears to have suddenly turned into fury.
Because this detour of emotions via volitional processes was not detected, also all music psychological and neurological experiments, to answer the question of the origin of the emotions in the music, failed.
But how music can convey volitional processes? These volitional processes have something to do with the phenomena which early music theorists called "lead", "leading tone" or "striving effects". If we reverse this musical phenomena in imagination into its opposite (not the sound wants to change - but the listener identifies with a will not to change the sound) we have found the contents of will, the music listener identifies with. In practice, everything becomes a bit more complicated, so that even more sophisticated volitional processes can be represented musically.
Further information is available via the free download of my e-book "Music and Emotion - Research on the Theory of Musical Equilibration"
or on the online journal EUNOMIOS.


text:
Can pets catch the cold?
Last night I was drying my cat with a towel after shenanigans in the rain and she sneezed!
Questions

Can cats/dogs/hamsters or other pets catch the cold?
How quickly do they recover?

I know from my own practice that lab mice can catch a cold. The get infected, are less active and sneeze. It takes them a few days to clear this. That was the reason we where usually not going into our mouse facility when having a cold.

@Chris I guess that is quite revealing! Quite interesting actually, I suppose we can then catch it off them too?

I am not sure. Our immune systems share similarities, but they are not completely indentical - something very important to keep in mind when you want to to immunological experiments on model animals. Especially when it comes down to surface receptors of cells (important when a virus wants to enter a cell) there are slight modifications possible which can inhibit an infection.

Yes they can. The viruses that cause a cold include rhinoviruses (up to 80%), coronaviruses and influenza (together accounting for much of the remaining 20%) and a small percentage of adenoviruses. When discussing cross species transfer, influenza is the most important to discuss as it is a fairly common cause of the "common cold".
Influenza A has humans, pigs, bird and horses as its host. Different influenza strains have different hosts. Influenza can recombine if two strains infect the same host (antigenic shift) and also mutate (antigenic drift). With a combination of these influenza can and has numerous times crossed the species barrier which has caused the major flu pandemics as well as swine and avian flu. It's this reservoir that makes these viruses so hard to eradicate. When we are the only host such as in polio virus, it is a lot easier. Pigs don't adhere to national flu guidelines.
Comparing recovery times, all mammals are roughly similar although due to our slightly more evolved immune system as well as social factors of knowing what to do when we are ill we recovery very slightly earlier.

The influenza virus doesn't cause a cold. It causes influenza. Colds are cause by completely different virus families (Rhino-, Entero-, Corona-, Mastadenoviridae to name only a few). The influenza belongs to the orthomyxoviruses. The other thing: Viruses do not cross necessarily species borders again, when they did this once. This ist mostly a matter of chances and contact and doesn't happen too often (luckily for us), since zoonotic viruses are usually pretty dangerous.

@Chris Influenza causes around/up to 20% of "common colds". I have updated my answer to reflect this. Also Rhinoviruses are part of the Enteroviridae family. Also the question was whether it is possible which it is, but I agree that it is fairly rare. Whether it is dangerous is another question, initially they often are as they are maladapted. As time goes on they are less dangerous which is something that is hypothesised may occur with HIV.


text:
How does the telomere repeat sequence vary in Eukaryotes?
Question:
How does the telomeric repeating sequence vary in non-vertebrate Eukaryotes? If you know the repeating sequence of a given species I would appreciate hearing it.
Background:
Telomerase is a ribonucleoprotein enzyme that adds DNA sequence repeats to the 3' end of DNA strands in the telomere regions, which are found at the ends of eukaryotic chromosomes.
In vertebrates the conserved telomeric repeating sequence is "TTAGGG".

A database that answers the question, charting telomere repeat sequences for all known species, is: http://telomerase.asu.edu/sequences_telomere.html
For example in Yeast:

TTAGG telomeric repeats have been found in several insects. From Sahara, Marek & Traut (1):

(TTAGG)n-containing telomeres were found in three Lepidoptera species,
  the silkworm Bombyx mori (in which the telomeric sequence was recently
  discovered), the flour moth Ephestia kuehniella, and the wax moth
  Galleria mellonella, in one species of Hymenoptera, the honey bee Apis
  mellifera, in one species of Coleoptera, the bark beetle Ips
  typographus, in one species of Orthoptera, the locust Locusta
  migratoria, and in a crustacean, the amphipod Gammarus pulex

C. elegans have TTAGGC repeats.(2)
The TTAGGG motif is also common in filamentous fungi, while Saccharomyces cerevisiae telomeres have TG(TG)(TG) repeats. Many plants have TTTAGGG repeats.(3)

For additional references, see the introduction in Wu et al.(4)

Cheers jarlemag, +1. I wont tick yet till more answers come through :)


text:
Organisms with the most extreme sensory capabilities? (sight, smell, sound)
Background
It is quite mind boggling to imagine what it would be like to be missing sight, sound, touch, smell, taste etc.
Question

Which organism holds the record for most extreme sensory limits for: sight, smell and sound? (one for each)

This would help give an idea of the "biological limits" of sense.

I believe this is too broad. There is a plethora of various kinds of neural sensors in animals, ranging from electric impulses to ultraviolet vision. Listing them all down might not be feasible.

hmm well this in itself was insightful thank you, I suppose if people list some nice sources to learn this kind of information would still be so helpful... in any case who says there is a limit to how many answers there can be...

@hello_there_andy Please read through this section of the Help Center - particularly "Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much."

@MattDMo I see, cheers for that clarification I will edit it right away then


text:
Empirical evidence for Group Selection?
A controversial concept in Biology "Group Selection", has caused confusion and conflict amongst scientists since the since the mid 1990s. The more general realm of study is termed the "unit of selection" discussion.
Definition
A simple working definition for "group selection" (edit/discuss this!) is:

"Selection for traits that would be beneficial to a population of units at the
  expense of an individual unit possessing the trait" (here)

Question

"What examples of group-selection are there?"

To add more structure, perhaps answers would consider the following details:

Organism/Species in question
Unit that experiences cost in fitness
Group that experiences benefit in fitness
Group-selected trait
Explanation

Forward Example (trait whose presence benefits the group)

Organism: Homo sapiens, Humans
Unit: Cells and their genes
Group: Collection of all cells in one individual Human body
Group-selected trait: anti-cancer traits, e.g. apoptosis (programmed cell death) via p53 ("guardian angel" gene that "kills" cancerous cells)
Explanation: Apoptosis is costly to the perspective of a cell, since it kills the cell and its genes. This enables the individual as a whole to live for long enough to mate and yeild offspring. Fitness of cells relative to other cells in the body is reduced, but fitness of the genome as a whole of that individual is increased relative to other individuals of that population -as a result of cancer-directed apoptosis.

Reverse Example (trait whose absence benefits the group)

Organism: Cervus elaphus, Red Deer
Unit: Individual red deer and their genomes
Group: Isolated population of red deer and the population gene pool
Group-selected trait: Lethal potential of antlers (e.g. sharp single antler instead of two blunt antlers).
Explanation: Consider a one-antlered stag, whose single antler is imbued with a jagged edge and is the product of a point mutation in his genome. During a rut he is able to win against other males as his antler inflicts potentially fatal injuries. This allows him to mate many females and have many offspring - however this leaves the population at risk of becoming extinct since the mating season would either have too few males to form a rut, or due to deleterious inbreeding defects in the next generation.

Links

Wiki: http://en.wikipedia.org/wiki/Group_selection
History: http://ib.berkeley.edu/courses/ib160/past_papers/beroukhim.html
Published Review: http://arxiv.org/abs/1204.6491

Of course do not feel restrained in your answers by the above suggestions - the point is to discuss the topic and learn!

possible duplicate: http://biology.stackexchange.com/questions/10970/empirical-evidence-for-species-selection

no.. species selection is entirely different. See: http://en.wikipedia.org/wiki/Unit_of_selection

I might had better not to write "possible duplicate". Sorry about that. I am not quite sure of how these processes differ. So I asked this question before trying to answer yours.

For your question, would you accept examples where the group is the organism and the lower unit is the gene? You might be interested by the book genes in conflict by R. Triver and Burt. You might be interested by this post as well.

ah no problem, species selection I hear is even more controversial than group-selection. Which is confusing since the more higher taxonomic form "clade selection" is deemed less controversial! Clade seletion is where multiple different species have traits selected that help each other - which occurs in symbiosis, e.g. Mycorrhiza. I truely cannot think of a species selecting example.

@Remi.b I do accept that as an example. In fact the other author of that book, Prof. Burt is my research supervisor!!

And do you accept as suggest in this article that kin selection and group selection are the same process? If yes, ants would be an example of group selection. Note: I deleted my question on the difference of meaning between species and group selection!

Considering that you are working in this field I think it's silly of me to ask but....Have u read the selfish gene ?

@user4058 not a silly question. I have to say I have only read 1/5th of it. To tie that book into the discussion, I propose a conjecture: "All genes are selfish, some genes depend a group's survival to be more selfish". I hope we both have similar definitions of the word selfish.

@hello_there_andy How do you define clade selection in relation to species selection, since you seem to imply that they deal with different things? After all, a species is a clade. I see the concepts as largely interchangeable terms (often along with lineage selection), and they are often used this way. All terms deal with selection for emergent traits at levels above the individual level. Also see Jablonky 2008 which use the terms broad-sense and narrow-sense species selection.

Could you define what you mean by "forward" and "reverse"? Do you mean that these examples support or reject the model? FWIW, I think your example of multicellular organisms is kin selection, which should be viewed as being separate from group selection (otherwise, group selection is just a confusing way to say kin selection). Do you mean to include kin selection in your group definition? For group selection, I would look to symbionts.

Yes sorry about using jargon like that, 'Forward' means it is an observed example whose presence implies that trait is positively selected (i.e. natural selection acts to preserve and encourage the emergence of that trait), 'Reverse' means the absence of such a trait (lethal horns in Red Deer) implies there is a "negative selection pressure" for that trait (i.e. natural selection seems to repel the persistence of such traits)

Let's start with your definition.
"Selection for traits that would be beneficial to a population of units at the expense of an individual unit possessing the trait"
This is not a good definition of group selection. In reality, selection can act on groups regardless of the direction of selection at the individual level. This definition sounds to me (your link is directing me to somewhere unpleasant) like one that has been set up in order to study whether group selection can act as an explanatory principle for the evolution of individual-level altruism, which is an altogether different question than the title of your post (the two questions are often conflated for historical reasons).
To expand the debate, I will introduce two formal definitions of group selection both of which are defined by alternative forms of Price's equation (See Okasha's book Evolution and the levels of selection for a thorough analysis).
Interdemic group selection
Interdemic selection occurs when selection acts on both groups and individuals within groups separately. That is, both groups and individuals within those groups must be units of selection in their own right. We must be able to assign fitness to both levels of selection some way, and track the offspring produced at each level. In this form of group selection, group fitness corresponds to the ability of a group to survive and produce more groups of a similar kind, and individual fitness corresponds to the ability of an individual within a group to survive and produce more individuals of a similar kind within that group. A good example  is selection on multicelullar organisms and selection on cells within those organisms. If there are greater than two levels of selection, interdemic selection is commonly referred to as multi-level selection 2 (MLS2) (see Okasha).
'The extinction of some groups and the ``reproduction'' of others are essential features of evolution by group selection. If groups are the units of selection, then they must have the properties of variation, multiplication, and heredity required if natural selection is to operate on them.' Maynard Smith
Intrademic group selection
Intrademic selection occurs strictly among individuals within a meta-population. That is, individuals are the only units of selection we study. The groups in which individuals reside are seen as part of the structure of the environment in which individuals live. In this form of group selection, individual fitness corresponds to the ability of an individual to survive and produce more individuals of a similar kind, given that they reside in a particular group. A good example of this perspective on group selection is selection cells of the quasi-multicellular organism Dictyostelium. Cells of this species are units of selection in their own right that occasionally group together into bodies that may also act as units of selection. If there are greater than two levels of selection, intrademic selection is commonly referred to as multi-level selection 1 (MLS1) (see Okasha).
'A way of looking at this is that the [intrademic] group selection approach looks at the evolution of individual characters in a group structured population, whereas the [interademic] group selection approach looks at the evolution of group characters.' West et al
Equivalence
It is worth pointing out that there is currently equivocation in the field about whether these two selective processes are different perspectives on the same underlying biology or distinct causal processes.
Another important point to note is that it is the intrademic form of group selection that leads to the conclusion that kin selection and group selection are really just different perspectives on the same selective process. This has been shown mathematically by Queller.
There is not yet a conclusive proof either way showing that interdemic group selection and kin selection are equivalent or not. Some evolutionary theorists feel that they are, while many feel that they are not.
Group selection versus group adaptation
It is also important to point out the distinction between the process of selection acting on groups (which most evolutionary theorists accept - I mean, it definitely does happen!), and whether or not this selection gives rise to group adaptations (which evolutionary theorists are equivocal about). Some argue that all adaptation can be explained from selection acting on lower-level units (right down to the gene, remember Dawkins?), whereas others think there may be nested levels of causality that cannot be reduced in this way.
Empirical research
There are many examples of laboratory and field based studies of group selection. Too many to list here. In a response to a theoretical paper by Gardner, a history of empirical research on group selection was given by Goodnight. The original paper, its response, and its counter response are worth a read to understand some of the different perspectives on the debates. In particular, two different perspectives on the evolutionary dynamics of cancer are presented that nicely illustrate the differences between MLS1 and MLS2 thinking.

This article claims to be a new level of evidence for group selection.  Its a little early to tell at this point whether the critics will be moved.  They have not been in the past!
sorry if this is a bit short - its late, but i'll try to come back and do more later..

This does not contribute enough to be answer. You should have posted this as a comment and come back later and written a comprehensive answer if you have one.

Shigeta, we are still eagerly waiting :)


text:
DNA mutations in CHO-KI mammalian cells
The mammalian cell line CHO-K1 has 24,383 genes. After 70 doublings (from a starting number of cells, 1) a
total of ~4,000 mutations have occurred in the overall population of cells (i.e. not all in one cell), due to incorrect DNA breakage repairs (non-homologous end joining), with the mutations randomly distributed throughout the genome. Assuming that 2% of CHO genome consists of crucial genetic information (1.5% coding and 0.5% regulatory). What number of genes will be affected by these mutations?
My attempt:
I was thinking that the mutations should be spread randomly and so 24383*70/4000 genes may be affected but doesn't that assume the mutations are one per gene and the affected areas are actually important to protein expression?

70 doublings from starting number of cells = ?

starting number of cells = 1

I suspect this question is a lot easier than it makes itself out to be, though I may not be thinking straight. It doesn't matter how many cells you start with or how many doublings there are. Nor, for that matter, does it matter how many genes each cell has. There's a 2% chance that a random mutation will affect "crucial genetic information"; I must assume that that refers to genes. So $0.02*4000=80$ mutations would be expected to affect genes.

Just to be picky: the concept of gene is always a bit fuzzy and many regulatory regions being so far from the coding regions that many would not consider most regulatory sequences as being part of genes. However, introns which are in the other 98% category would quite definitely be considered part of a gene.

@Remi.b Agreed, though in that case there doesn't seem to be enough information to answer the question. Or perhaps they are expected to just use the 1.5% value for CDS.

Some definitions of a gene: https://en.wikipedia.org/wiki/Gene, but it would be better to follow convention: http://www.ensembl.org/info/website/glossary.html, or if that does not engage sufficiently then perhaps some video tutorials? https://www.vectorbase.org/tutorials/other-bioinformatic-resources-tutorials/galaxy


text:
Binucleate cells of transitional epithelium (bladder)?
Working through Histology slides of the transitional epithelium (urothelium) of the urinary bladder, I noticed that the dome-shaped cells at the top of the transitional epithelium are frequently binucleate.
In doing research, I found that the top cells of the transitional epithelium are 'often binucleate and usually polyploid'

Why is this?
  What purpose does this serve?
  Is the binucleate feature consistent enough across slides to be used as a common identifying feature to recognise transitional epithelium from the urinary tract? Is the absence/over-abundance of binucleate cells characteristic of certain diseases?

I also see prominent granules (of glycogen, I presume?) in these cells.

Is this glycogen? & What purpose does this serve?

Also, I'm having difficulties recognising transitional epithelium in slides. Does anyone have any tips to share on how to easily recognise transitional epithelium as such (common features to look out for, etc.), especially in distinction to pseudo-stratified epithelium, which often looks similar?

At what magnification you are seeing slides?

Magnification of x540 @JM97

please don't ask more questions in a single post, its against the site's guidelines.

Upvoting because these easy-to-see features of dome-shaped cells go seemingly unexplained in all major histology textbooks. My PubMed searches have not been helpful so far. Specifically, are the dual nuclei the result of an incomplete mitosis, or do cells fuse together into a syncytium?

This might help: https://www.nature.com/articles/s41598-018-19690-7  They had occasional multinucleated cells, but couldn't find a good literature reference for how many to expect (in mouse).  General discussion - https://en.wikipedia.org/wiki/Binucleated_cells

In other stratified epithelium, it is the basal cells that replicate to replace the cells lost in the top layers.  In transitional epithelium, which is also a stratified epithelium, the most superficial layer of cells are replaced or  turnover occurs because of mitosis of the superficial facet cells themselves.  In this case it is not unusual to see dividing cells in its last stage of division as a large cell containing two nuclei, which soon that cell will be 2 cells.

Welcome and thanks for your contribution. Can you add sources to your answer? I have to banner it for now. Ping me once you referenced your answer and I'll remove that banner.

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text:
Superhuman eyesight
My ten year old son was reading car number plates that were too fast, too far away and at the wrong angle for any of us to read or even believe that it was possible for him to read. We thought he was lying as he reeled off the whole number plate and not just some. My husband went across the road to prove him wrong and get him to admit he was making it up but he wasn't. We even asked people in the restaurant and waiting staff for their opinion and everyone was blown away. I'm totally astonished and slightly freaked out by his sight and I'm hoping someone can explain for me.
Specifics

I believe it was approx 20-25 metres away and I am under guessing.
He had only 1 or 2 seconds as the cars drove left to right.
Cars would be travelling 30/40 kmph along that road.
We were sitting in the restaurant at night time so not in a car
ourselves

Why is this off-topic or unclear? Please comment and we can work on the question. Aging is a hot topic in Bio.

You should provide additional details about approximate distance and speed of your car relative to other cars and size of the letters. Otherwise it would be difficult of anyone to ascertain if that was really an above-average perception.

He could perhaps be far-sighted.  How does he do with close-vision tasks like reading?

Thank you for all your responses! I believe it was approx 20-25 metres away and I am under guessing. He had only 1 or 2 seconds as the cars drove left to right. Cars would be travelling 30/40 kmph along that road. We were sitting in the restaurant at night time so not in a car ourselves

@Claire the distance may have helped with the speed - something further away has a lower angular speed and so is easier for the eyes to track (think of an airplane in the sky that is moving hundreds of mph but is very far away)

If memory has anything to do with it, I'll call - with high statistical sensitivity over specificity- Aspergers!

@jamesqf he is not as fluent with his reading as his 8 yr old sister although he can read and doesn't have trouble with pronunciation. I put it down to a girl/boy development thing....I have just booked an eye test because everyone's valuable comments are making me think about all possibilities....

@hello_there_andy memory?? Not in the case of the other night as it was there and then however he has an absolutely amazing memory too? He remembers things that he has seen that most people would not even bother to notice, ie that car (recollecting colour, model and plate) is always parked there, or, that lorry was the one that we saw driving down the highway when we were on our way to 'xyz' and it was raining really hard and u had a blue top on mum.....two yrs ago! Are you suggesting that eyesight and memory are an indication of aspergers?? I know little a out aspergers, maybe I should read

@Claire it really is a long-shot and I fear of making a hassle and run into a common cognitive bias related to self-diagnosis (see wiki: labeling theory). I'm a strong believer that society and expectations of people with disorders hinders them (see wiki: Daniel Kish for inspiration on what Humans can do w/o social expectations).

@hello_there_andy just briefly read symptoms for aspergers and there is not one symptom that I could say is possibly apparent. He's advanced beyond his years socially and has been from an early age, motor skills- fine, rides quads and bikes and horses from a young age...above average academically and extension in lots of subjects too. The only thing with social or behavioural interaction is his frustration at others and often not handling situations calmly enough?

I know what you mean, it appears that there are so many labels on lots of people compared to maybe the odd person years ago who was categorised as dyslexic if they couldn't spell and sometimes wonder what new labels will be born over the years ahead. I haven't ever felt alerted by anything enough to look into labelling for him however sometimes amazing traits such as this baffling eyesight and prob memory too, could also fall under such umbrellas as you've suggested. Maybe not aspergers but there may be another label for him!?

@Claire: I didn't mean reading ability, but reading (especially small print) as one example of a task that would require good close-up vision.  Other examples might be threading a needle, or assembling electronic parts on a circuit board.

Short answer
Visual acuity decreases with age. Your son's age is within the age range that visual acuities are best. Acuity starts to decrease from about age 45.

Background
Visual acuity (visual resolution) first increases from birth up until around 4-6 years. Note that in the following graph better acuities are represented by lower numbers (logMAR scale):

Source: Pan et al, 2009
Visual acuity starts to decrease after 45 years. The acuity of a 6-year old is about 1 on the scale in the next figure, showing the decline in acuity in older folks. Note that the graph starts at 30 years and acuities are already less than that in the former study's end point (look at the lower set of lines, i.e., the uncorrected ones). Also note that better acuities are higher up in the scale as this graph expresses acuities in decimal Snellen equivalents

Source: Gittings & Lozard, 1986
Hence, very likely, your 10-year old's vision is not superhuman (sorry!), it's just a lot better than yours. However, if you are younger than 45, we might conclude your acuity should be comparable and your son may be a visual rock-star - statistical outliers do exist and a simple visit to the optometrist will tell you! However, if you are near-sighted and are not using corrective vision aids (glasses or the likes) then this may be the cause of your lesser visual acuity.

References
Pan et al., Optom Vis Sci 2009;86:607–12
Gittings & Lozard, exp gerontol 1986;21:423-33

Thank you. Yes I am 40 which is why we asked others in the restaurant and one guy was 18 and he laughed but I hadn't thought that he perhaps had terrible vision for his age! My 8 yr old daughter also couldn't decipher even one letter either so may be more important to check hers! It was approx 25 metres away, was dark and there was prob 1 or 2 seconds for him to capture it as it drove left to right and at a speed of 30/40kmph

@AliceD, Why did you protect this thread for? It's only 2700 views.

@Pacerier - not so much because of #views, but it has received multiple good quality answers and it was drawing in low-quality answers (since deleted and hidden from your view).

He may have extreme acuity, or he may even have an extra cone type that allows him to see extra colors (and more color attunement may allow easier reading of those particular plates). But, you won't know anything for sure by asking on here. Take him to an ophthalmologist and let us know what the doc says! If you aren't 40+ and have 20/20 vision and he's seeing things better than you, then yeah, he probably is special!

Thank you for your reply! My daughter is 8 and she could just see a blur and the 18 guy sitting next to us just laughed and said no chance he could see either but yes as per other responses above, I hadn't thought that everyone else compared may have particularly poor eye sight! I think I shall pop to have his eyes tested and will post on here the results

@Claire you should get in the habit of upvoting answers that have helped, some of us crave unicorn points

@hello_there_andy......how do I do that apart from singing praises in comment box!?

@Claire Just click the up arrow at the top left of the answer - but you need to collect some amount of points yourself first - so maybe it does not work yet - there would be a message explaining it when you try. You have 36 points "rep" ("reputation") currently. Three upvotes on your question would get you to 51, for example.

A functional male tetrachromat has yet to be found.  Finding one might count as "superhuman" vision, as much as any trait possessed by a human could be called such.

Hi everyone that kindly commented on my question a month ago. I have been to the optometrist this afternoon as suggested with my son and she has confirmed that he has 20/10 vision.


text:
what does sequences overlap indicate
what does it mean if different protein sequences overlap upon multiple alignment, are they the same, do they have a common ancestor, are they recombinants of each other
and how does one go on to prove this
many thanks

At first it only means that these sequences share a similarity (sorry, but its not more). This can mean that they are smaller parts of a bigger protein which has been broken up, it can mean that you aligned different proteins which are only partly similiar and so on. To go over this, you have to provide some more information. And/or show an image of the alignment if possible.

Just curious @user5182 are you currently doing a Bioinformatics MSc at ICL?

@chris yes i think that one of the sequences is the "real sequences" and the other 3 are bits of it rearranged, i am working with toxins specifically if this helps, i tried to post the sequence earlier but unfortunately as it was not in frame people complained about how it was unclear. please let me know if there is anywhere in specific i should be looking. many thanks

@hello_there_andy no im doing an MSc in pharmacy my dissertation is on toxin diversification in a coral reef

Expanding on the comment by @Chris:
Short Answer
Overlapping sequences imply evolutionarily conserved regions, i.e. preserved by evolution through time due to theirs having some important function.
Long Answer
Assuming the sequences are homologous, overlapping regions of similarity reveal "evolutionarily conserved regions".
These are regions in the protein sequence that are shared by the ancestors through ancestral history due to that shared sequence bearing some important function at the phenotypic level. Evolution acts to "preserve" the sequence through natural selection if that function was important for fitness (see Negative selection).
E.g. Perhaps the shared sequence codes for an active site for an enzyme that is shared by all the ancestors you are using in the multiple sequence alignment - natural selection will then prevent changes to that sequence from occurring.
Look at this online lecture for finer detail.

one more little piece of information: with proteins there are always short but good overlaps which in most cases indicates similarity of domains..

it means those region are conserved if you compare two sequence and find similarity one example is the hox coding region which is conserved and it shows similarity

Go on to add information on how one goes on proving this


text:
Is solving cancer required in order to avoid aging?
When the telomerase enzyme is not active the telomere shortens every time the cell duplicates leading to a reproductive limit (Hayflicks limit).
On one hand this is a believed reason for aging. On the other hand this makes a mutated cell more difficult to acquire cancer, since in order to become cancerous, it would need to mutate such that the telomere enzyme becomes active.
The telomere enzyme is not active in most human cells.
Therefore activating the telomerase enzyme in somatic (body) cells could theoretically decrease aging but would also increase the risk of cancer.
Am I right to assume that in order to avoid aging of humans one would first need to "solve cancer"?

I've put an answer explaining why aging shouldn't be avoided in first place. It got an upvote, then it was closed by moderators, saying this is not a group about ethics, but about biology. If biology can be done without ethics, than we are able to watch yet some great nightmares.

@Rodrigo I agree that avoiding aging is a highly ethical question. That said, my question targets the biology aspect and not the ethical aspect. Feel free to ask a question on the ethical/moral stackexchange

OK. I only wanted you to know what I think about this.

Interesting question. My answer is no, but it requires a rather science-fiction style answer - at least it's beyond current technology, but here goes:
My Assumptions
I make the simplifying assumption that ageing is only related to telomere length. Thus by "avoid ageing" I assume you mean "avoid telomere shortening". Also to clarify things for others, I'll clear up the role of telomeres in aging and cancer:
Telomeres in cancer - it has been hypothesised that telomeres act as "mitotic clocks" - keeping track of how many times a cell can divide before it stops. This "time limit" is supposed to put a halt to cancerous cells before becoming malignant.
Telomeres in aging - Since telomeres set a limit to the number of times a cell can divide this essentially sets a time limit for the organism as a whole - those cells that divide faster (e.g. hair and skin cells) go out first (grey hair and wrinkles) etc.
Short answer
No.
Long answer
All we need to do is come up with a way to somehow "maintain" average telomere length at some "safe" length, i.e. we keep them at a length that is long enough to prevent us from aging but short enough so that a cancerous cell will not be able to proliferate to dangerous numbers.
For example, every now and then we provide "telomere length booster jabs" (this is some abstract fictional idea of course). This is like adding more time to our lives when we are about to run out: "Oh look, I only have three months left!", "Don't you worry, with our new telomere booster jab you will have an extra 3 months!"...

Interesting answer. You give this assumption: "aging is only related to telomere length". Does is seem a reasonable assumption to you? What part of the variance in senecense in the human population has to be accounted to telomere length? (There are certainly not known answer !)

Great point you make, indeed it is murky waters for whether telomere length and aging are related to a significant degree. Here's the related discussion on stack: http://bit.ly/18tkAhp. I guess how relevant my answer here is, depends on the validity of the assumption of telomere length and aging I made.

In short, yes.
The best way to think about ageing is as an accumulation of age-related disorders. Telomere loss is one of many cellular defects that accumulate with age. Other defects include oxidative stress, accumulation of amyloid proteins and metabolic dysfunction. While these are all likely related in some way, there is no evidence that specifically preventing telomere shortening would stop ageing. In fact, while telomere length is roughly correlated with age, it is not well correlated with such age-related disorders as Alzheimer's disease.
However, it is clear that loss of telomeres is a problem. Therapies that restore telomerase function will always run the risk of causing cancer. Most cells in the human body do not express telomerase, and those that do often do so transiently during times of replication. Introducing functional telomerase into new cells could only increase the risk of developing cancer. A generalized cure for cancer would make designing anti-telomere shortening therapies much easier, because listing cancer as a side effect would not be as ridiculous as it is today.
The way I see it is that cancer is just one of those many age-related disorders that comprises the term "ageing." Especially colorectal cancers have a strong association between onset and age, hence all the colonoscopies recommended after age 50. If colorectal cancer is so well associated with age, and there is a mechanism that ties the formation of cancer to the passage of time (the build up of deleterious mutations during the many divisions that occur in colonic crypts), then I think its safe to consider it a part of ageing.
In order to stop ageing, you have to stop all of the age-related disorders, and that includes cancer.

Not exactly. However, assuming that we will eventually be able to reverse the effects of aging, cancer formation will become much more rare as a by-product. The explanation for this is a bit involved, due to the complexity of the subject.
One of the most fundamental processes that drive human aging is the irreversible accumulation of genomic (and mitochondrial) DNA mutations. The reason for this is simply because it is extremely unlikely for DNA damage to get repaired by chance; DNA is the most complex molecule in any organism, and once information in it is lost for good, there is little hope that it will be reconstructed by random chemical reactions alone.
Other important forms of aging-associated degeneration include atherosclerosis, the formation of advanced glycation end-products, the accumulation of indigestible waste products within lysosomes as well as proteinopathies (although these can be caused by DNA mutations; see below) such as Alzheimer's disease. Telomere shortening can also be considered to be a form of aging-associated degeneration, but it is almost certainly not a central mechanism underlying any of the more noticeable aspects of the symptomatology of physiological aging due to its easily reversible nature (i.e. otherwise we would already have seen "immortals" appear due to random germline mutations causing overexpression of telomerase within stem cells).
While the accumulation of genomic DNA mutations eventually leads to carcinogenesis, cancer is actually a relatively unlikely consequence of this process, since multiple key mutations in several oncogenes/tumor suppressor genes tend to be necessary for transformation. As such, a much more likely (initial) consequence of the accumulation of DNA mutations would be the random inhibition of cellular functions by knock-out and modification of actively transcribed genes (or random activation of silent genes). This would explain why in old age, the body tends to be 'worn out' in general; if nearly all cells have some degree of dysfunction, we would naturally expect to see the body as a whole to perform poorly as well.
Also, even when enough mutations have accumulated to potentially cause cancer, usually, this ends up triggering the anti-cancer defenses of a cell and turn them senescent. When stem cells become senescent, they stop dividing. This would neatly explain why wounds and infections heal much slower in older individuals. In fact, it has been shown that hematopoietic stem cells lose their regeneration capacity over time, and that this is correlated with the accumulation of DNA mutations (Rossi et al. 2007).
In addition, random DNA mutations can also conceivably trigger proteopathies (e.g. Alzheimer's disease or idiopathic prion disease), since for many of these you only need one gene producing a 'bad version' of a protein to cause aggregation and cell death. Both prion proteins and amyloid-beta tend to be infectious (Jaunmuktane et al. 2015), so it is entirely possible that a single mutation in a single cell could trigger large-scale degeneration.
So, to stop aging, you would at least need to fix DNA damage periodically, and this would more or less prevent cancer as a by-product. However, I imagine it would be hard to repair the DNA damage in each and every cell in the body with a single treatment (e.g. with some kind of a viral correction therapy where the treatment is administered by intravenous injection, it would be extremely unlikely for the therapeutic agent to reach all cells every time, since there is a limit to how concentrated you can make it). As such, it would still be possible for a cancer to arise at some point, and in this sense, it is entirely possible for us to end up in a situation where we are able to reverse all aspects of biological aging, and yet people still die of aggressive cancers every now and then.
References:
Jaunmuktane, Zane, et al. "Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy." Nature 525.7568 (2015): 247.
Rossi, D.J., Bryder, D., Seita, J., Nussenzweig, A., Hoeijmakers, J. and Weissman, I.L., 2007. Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with age. Nature, 447(7145), p.725.

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text:
Meaning of "primers IL-2" in a scientific article
From an article ("Amelioration of Experimental Autoimmune Encephalomyelitis in Lewis Rats by FTY720 Treatment", 2003):

We performed PCR amplification in a 100-μl reaction mixture containing 200 μM of each of the regular dNTPs, 10 pmol of each primer, and 2.5 U of TaqDNA polymerase (TaKaRa) using primers IL-2 (300 base pairs; bp), 5′-CAGCTGTTGCT GGACTTACAGG-3′ and 5′-CACAGTTGATGGCTCATCATCG-3′; IL-6 (294 bp), 5′-GACTTCACAGAGGATACCC-3′ and 5′-TAAGTTGTTCTTCACAAACTCC-3′; INF-γ (310 bp), 5′-GGATATCTGGAGGAACTGGCAAAAG-3′ and 5′-GCTAGATT CTGGTGACAGCTGGTG-3′; β-actin (461 bp) 5′-CATCGTGGGCCGCTCTAGGCA-3′ and 5′-CCGGCCAGCCAAGTCCAGACGC-3′.

I'm not completely sure: do they mean that the primers are "specific to the IL-2 gene"?
Do they mean "5′-CAGCTGTTGCT GGACTTACAGG-3′ and 5′-CACAGTTGATGGCTCATCATCG-3′ are primers that are specific to the IL-2 gene"?

Looks like they're missing a semi-colon so yes, primers; IL-2...

From the description, yes, those primers are supposed to be specific for the IL-2 gene. The way they would be used would be on mRNA, not DNA, so you could use them to quantify the level of IL-2 transcription. However, there seems to be some glitch in there, because while the first sequence (5′-CAGCTGTTGCT GGACTTACAGG-3′) matches rat IL-2 mRNA starting at 120 in the sequence,  the second one (CACAGTTGATGGCTCATCATCG) does not match any IL-2; a BLAST search only turns up random and irrelevant matches.
This may be an error in the paper (copying and pasting the wrong primer, which is extremely common, unfortunately); it may have been an error in design (someone used the wrong primer and got lucky results that seemed to match what they expect); or I may be doing something wrong, which I'm not going to try to troubleshoot any more than this.
(Edit, as @VonBeche points out in comments the reverse primer is almost a match at 398, with a one-nucleotide mismatch that screwed up my search -- possibly allelic variant, but equally possibly a mistake)

The reverse primer starts at 398. Nice trick for blasting specific sequences like this: set the species to rat (or whatever you need). Especially with short you'll find too much uselessness otherwise.

Annoyingly it's not a perfect match (A/C at 9) so my grep on the sequence didn't find it.

@iayork, That's why we have BLAT ; )


text:
What does orbital mean in orbital frontal cortex?
Orbital frontal cortex is where decisions are made.
What does the word orbital there mean?
I looked around in wikipedia and never find it.

This belongs to Stack's English section. But surely you know the term orb. As a wild guess, judging from the 'al' in front'al', or later/lateral, I would say the postfix 'al' indicates position-relatedness.

I think it's more of a fit for here than English.SE

Orbitofrontal cortex: the area of the cerebral cortex located at the base of the frontal lobes above the orbits (or eye sockets), involved especially in social and emotional behaviour.

Very good. But that's what orbitofrontal cortex mean. I am asking what orbito means. THe below answer seems to be better.

I thought that part of the brain is behind the eyes rather than above the eye.

Did you not ask what it means in the context of orbital frontal cortex? The definition I posted explains it, or does it not? the area [...] above the orbits (or eye sockets).

The boney component of the anatomical orbitstrong text (in lay terms the eye socket) is the area bordered by the zygomatic, frontal, maxilla, sphenoid, palatine, lacrimal and ethmoid bones.

The use of the word orbit (red) in orbitofrontal cortex refers to the positioning of this part of the frontal cortex (green) being directly behind the orbit:

Quick search on etymonline for Orbital:

orbital (adj.):
1540s with reference to eye sockets;
1839 with reference to heavenly bodies;
from orbit
(n.) + -al (1).

So my best guess is that it's related to eyes.

why -1? +1 from me. This seesm to be the one making sense.

cheers @JimThio, thought I was doing something wrong till now :)


text:
What evolutionary explanations are there for death?
I know death and cancer doesn't hurt humans' reproductive success. It's not helping either.
Why do we die? Why dying humans (all of us) are common? What's the point of dying?

Not everything has an evolutionary advantage...

Cancer does hurt human's reproductive success; and evolution does fight with it.

Most cancers are post-reproductive, so fitness (strictly speaking) is 0 at that point.

This is kind of relevant to a senescence question on SE I was just came across.
A book referred to in that question, Geriatric Medicine: An Evidence Based Approach by Cassel, said biologists argue that senescence is an evolutionary byproduct rather than a bestowed advantage and is probably a result of "interaction of many genes with the environment".

@nico is correct, and he's not likely saying so with any religious zeal... for example, genetic drift is a powerful evolutionary force that has no obvious "advantage" per se. I've edited your title to remove that suggestion. but +1 anyway since it's an interesting question.

This post is very much related to your question and the answers offer a good overview of the reasons to the question "why we age? why we die?"

An organism that spends a great deal of energy and resources protecting itself from a very rare form of damage will be out competed by ones that do not but instead spend those resources increasing its chances of mating or on its offspring.

Death is not only for humans. All 'complicated enough' organisms die (with a notable exception of Hydra, though you may argue when it comes to the complexity). It is is easier to create a new organism from scratch than to repair both internal factors (free radicals, metabolic by-products, ...) and external (physical damage, exposure to toxins, ...).
Underlying causes of death actually can be evolutionary beneficial. For example, shortening of telomeres offers protection against cancer (on a cellular level), but also bounds lifespan.
So actually they may be evolutionary competition (within the same species) of young and old. Mutations helping young but harming older may be preferred to the opposite ones.

Who is to say that having living Humans isn't hurting our reproductive success? Older non-reproducing humans cost the human network valuable resources and take up a sizeable portion of our living niche. Metabolically unstreamlined aged organisms are certainly not the most efficient and could potentially get in the way of better suited young'uns.

It's naive group-selection argument. Like "I'd sacrifice myself when I get old so that others could produce more children". But if one would live longer and help his own grandchildren - he would spread his genes better even if it would hurt the society.

@MartaCz-C: how does helping grandchildren spread genes? The only way for an old person to continue spreading his/her own gene is to have kids which would actually be bad.

@nico if person X have even 15 children but non of them have their own children through their lifespan, then genes of person X did not spread at all. One of measures of fitness is number of grandchildren.

@MartaCz-C: sure, but my question is about "helping his own granchildren". The fact of helping them in no way means you are spreading your own genes. The fact of having granchildren means you spread your own genes in the past which... well is the purpose of reproduction.

@nico Helping your relatives spread their genes is equal to spreading your own genes (if you multiply your effort in helping others by the percentage of consanguinity). That's what I mean but maybe I use wrong terminology.

+1 for effort. Flawed because it underestimate gene selfishness.

From a systemic point of view, if we wish to evolutionarily induce our descendants (descendants of the current human race on the whole) to live longer lives, we would need to pro-create later.
If the whole of human race enforced a statute that prohibits pro-creation before the age of 40, then two pronged dynamics would happen

only adults fit enough to pro-create after 40 would produce off-springs.
only off-springs born to parents older than 40 who are fit enough would survive.

Since, there is a high tendency of abnormality and low survival of off-springs born to parents of older ages, absence of resource contention and genetic dynamics would encourage the initial propagation of the rare few fit off-springs.
Hence, unnatural "natural selection" would encourage the propagation of humans of longer life-spans. Perhaps, a natural disaster or viral outbreak could discourage humans from pro-creating before age 40. Perhaps, high rates of abortion. So long as the human race does not die out due to such restrictions. Perhaps, to the satisfaction of conspiracy lovers, a secretive organisation carries out a plan every 100K years to raise the bar for child-bearing age.
Therefore, it might be less of a question of advantage and more of the effects of motivation. That current status where

high motivation for humans to pro-create early in life.
low motivation for humans to have more children as they wise-up by being tired of raising kids too early.

Therefore, since no such secret organisation exists, there is infinitesimally little motivation for the existence of a "super-virus" type of humans to exist.
There is no motivation for super-humans to exist, because the distribution of life-spans have crowded out the food and survival resources of any possible primeval super-human.

Do you have proof of your first part in your answer? I know it holds for fruit flies, but that doesn't mean it holds for humans.

There is no evolutionary advantage to dying.
So you question should be rephrased as to why organism die at all? Why hasn't evolution come up with an immortal animal that lives forever?
Well nature has actually done that https://en.wikipedia.org/wiki/Turritopsis_dohrnii Behold the immortal jellyfish.
So if we do have immortal jellyfish.. why aren't there immortal mice?
A possible answer is because mice get eaten by cats (and wolves, foxes, owls, toads, humans, etc) The idea goes like this... there is no point having genes that makes you immortal if the probability of you being eaten within 1 year approaches 100%. In fact, in such a situation, you would want genes that will allow you to have as many babies as possible before that one year is up, even if those genes result in your death (ie cancer from cells that are growing too fast in that rush to be an adult, heart problem, muscle degeneration, poor immune system.. because the body has redirected all energy from repair to reproduction). Such a trade off is worth while, as you aren't going to be alive long enough to see the downside of those bad genes.
So if this idea is correct... if an animal has fewer predators (or none at all), the animal would live longer. And yes, we actually do see such examples.
A famous example are the Opossums of Sapelo Island. The Possums were isolated on a predator free island 9000 years ago and now live 25%-50% longer than their mainland cousins. The difference is hereditary.
https://books.google.com/books?id=yYwHDAAAQBAJ&pg=PT62&lpg=PT62&dq=Sapelo+Island+opossum+long+lived&source=bl&ots=4AHZcnd8_L&sig=9Wgka1-bVl1xzJTX2F-AJhF0Y-g&hl=en&sa=X&ved=0ahUKEwi506Kq7_7QAhUI6YMKHS3FBQ84ChDoAQgZMAA#v=onepage&q=Sapelo%20Island%20opossum%20long%20lived&f=false
Another possible example is that between bats and mice. Both are small animals of similar weight. And in general the smaller the animal, the faster it breeds and the shorter its life span. Bats are a noted exception from this the rule. Bats live a very long life span or their mass. Lifespan in the wild rangers from 10 years to 40 years depending on species. Compare that to 1 year for a mouse. The difference? Not metabolism... Not mass.. Not climate. But predators. Mice have many predators. Bats very few.

One key concept to bear in mind is "mutational load".  Over time, individuals accumulate mutations - for example, older fathers pass on more mutations than younger ones.  Undesirable mutations need to be removed by natural selection each generation at at least the same rate as they accumulate, or a "mutational meltdown" occurs.  The length of time between generations needs to be set so that the number of mutations purged by deaths is equal to the number that are introduced by mutation.  Here is a rather interesting study providing some evidence for this point of view.
Note that infertility is "lethal" in genetic terms, so this concept in and of itself does not explain why a woman who passes menopause needs to die at any age.  It seems easy to add further speculation here, so I'll leave that to the reader.

The evolutionary explanation is quite simple. Without death, evolution couldn't take place in the first place at all.
Who knows that jellyfish are immortal? Did they continuously evolve from one cell (without reproduction)? I don't think so. Who knows if today present jellyfish were already alive 1000 000 years ago (i.e. without parents)? I think this is the case for any living creature.
That's why telomeres get shorter and shorter when growing older. In the case of cancer, these telomeres stay the same with each division of the parent cell, so it grows wildly. Which all species would probably do so too.


text:
What are some examples of genes that code for multiple proteins?
The title pretty much says it all. It is widely taught that a gene in a eukaryotic system could produce more than one protein due to post-transcriptional modification, but I do not believe I have come across any specific examples of this. Are any such systems known? Or is this more theoretical?

The top hit for a Google search for "alternative splicing" is the Wikipedia article on alternative splicing, which includes several examples. I can't imagine that any textbook that covers alternative splicing would not also offer examples.

Are you talking about post-transcriptional modification or do you mean alternative splicing?

The answer is not simple - @shigeta mentioned a few mechanisms leading to single gene-to-multi protein relationships - and the answer is certainly not short (there are thousands of these genes).
But anyway "alternative splicing" seems to be the primary mechanism according to this article, so rather than listing all alternatively splicing genes, here are the databases (+links):
Alternative splicing gene database (click on blue for link):
EDAS: EST derived alternative splicing database
U12DB: A database of U12 spliceosomal introns
FASTdb: Friendly Alternative Splicing and Transcript database
BIPASS: Bioinformatics Pipeline for Alternative Splicing
ASAP II: Alternative Splicing Database
ASTD: Alternative Splicing and Transcript Diversity database
H-DBAS: Human database of alternative splicing
Hollywood: Alternatively spliced mRNA database
Ecgene: Genome annotation for alternative splicing
SpliceMiner: Collection of splice variants for human genes

There are a large number of ways a protein variant can be produced by post translational modification.  The question may seem obvious, but its really quite broad.
I can start this out.  I doubt I know all the ways a single transcript can produce variant proteins.   A detailed description might be more like a review article than an answer here.
First, there are very rare cases of eukaryotic polycistronic mRNA: mRNA which code for more than one protein.  In this case, after translation, the mRNA are processed to make multiple monocistronic RNA.
Then there are proteins with molecules added by covalent bonding to the protein.  Glycoproteins are notoriously variable. Many other small molecules can be bonded to a protein to make a variant of this sort: ubiquitinization, N-acetylation, SUMO domains, lysine methylation are just a few of the more common covalent modifications of proteins.
There are RNA editing which removes some of the coding RNA to make alternative splice RNA.
The list goes on and on. So does any of this come close to what you wanted to know?

Just for balance, here is an example of a single protein being constructed from two primary gene products (two separate genes involved) via protein splicing.


text:
Is there a PSI-BLAST for nucleotide sequences?
I understand that one can translate a nucleotide sequence and run PSI-BLAST on the protein (proteins if you take the 6 reading frames), but I'm looking for distant homology for bacterial small RNAs (typically 50-200 nucleotides long and noncoding).
If there is no such resource, what are the main obstacles to this implementation?

why not blastn?

have you tried the HMMER program yet? Theoretically it is very similar to PSI-BLAST in that it is a profile method but bolted with a more rigorous probabilistic framework + it is used to search for remote homologues

if either of my answers have actually "answered" your question please click "accept" (tick) - this both improves the site and is good etiquette

I need a bit more tinkering time

First check if your RNA sequences are described by existing covariance models (CMs) available in Rfam. You can do this using the Infernal package to search the Rfam database of CMs. For those RNA sequences which match an Rfam CM, you can then use that CM to search the sequence databases for additional matches.
For those that do not match an Rfam CM, you will want to build your own models. In order to do this you need to identify homologues for each sequence which you can use to produce an alignment from which a model can be built. In order to do this you will want to use a method which is RNA aware and uses a rigorous search method. For example from the FASTA suite, which has an RNA mode which adjusts the scoring accordingly:

Smith and Waterman for local/local alignment (e.g. SSEARCH)
Needleman–Wunsch for global/global alignment (e.g. GGSEARCH)
Hybrid alignment for global/local alignment (e.g. GLSEARCH)

Your coverage requirements and the nature of the database being searched will determine the most suitable method to use for the sequence similarity search. Combining the best search method with appropriate selection of the database to search, for example the European Nucleotide Archive (ENA) provide a set of non-protein coding sequences (ftp://ftp.ebi.ac.uk/pub/databases/ena/non-coding/) derived from the annotations in EMBL-Bank that could be a good starting point your search. Will improve the sensitivity of your search.
Given the set of homologous sequences you need to produce a multiple sequence alignment (MSA) to generate a model from. To do this you will want to use an RNA aware MSA tool, for example R-COFFEE or Clustal Omega in order to produce an alignment which attempts to take into account the folding of the RNA molecules.
Given the alignment you can create a CM using Infernal or an HMM using HMMER, and use this to search the sequence database (cmsearch or hmmsearch) to find additional homologues in the database.

If you have a non-coding gene sequence (e.g. regulatory sequence) this answer should hold your solution:
Background theory

Firstly you must realize that PSI-BLAST is built for detecting "romote homologues",  (i.e. those that have a very "distant evolutionary relationship" to your query) - from a database of sequences. It is therefore known to be a "sensitive" analysis which can recruit distantly related matches but has a small chance of recruiting some false matches - "rogue homologues".
Secondly PSI-BLAST is known as a "profile method" that is it uses multiple sequences that are cumulatively recruited with each "psi-blast iteration", to build an empirical profile of amino acid residues along the positions of your query. This is in the same family of analyses as "Hidden markov models" (HMMs) in that HMMs use multiple sequences to build an empirical profile that is able to recruit distant homologous, except the "profile" includes probabilistic pathways to all the recruited sequences.

My Answer
I suggest you use a software package called HMMER. Indeed this method shares critical theoretical similarity to PSI-BLAST as well as functionality in your case (searching for remote nucleotide sequence matches in a database vs. a nucleotide query), it also does not assume your sequence is protein-coding - here is the wiki description:

HMMER is a free and commonly used software package for sequence
  analysis written by Sean Eddy.1 Its general usage is to identify
  homologous protein or nucleotide sequences. It does this by comparing
  a profile-HMM to either a single sequence or a database of sequences.

Other possible answers
If you are afraid of using HMMER, then here is a list of all alignment software tools represented in a table that allows you to focus on only those that use nucleotide sequence as input:
http://en.wikipedia.org/wiki/List_of_sequence_alignment_software

Assuming you are using PSI-BLAST to recruit coding homologous nucleotide sequences to your query nucleotide sequence.
Here's a work-around using PSI-BLAST itself:

Translate your nucleotide sequence into amino acid sequence
Run psi-blast to recruit matching homologous protein sequences
Store the names or database IDs (e.g. genbank accession numbers) of the best matching proteins
Acquire nucleotide sequences of your matches by searching the IDs against a nucleotide database

Extra details:

This type of alignment is called a "codon alignment" (as opposed to DNA alignment or protein alignment)
This assumes your DNA protein codes for a protein whose functionality is constrained by evolution
You must remove all introns from your sequence prior to aligning
Your first codon must be a start codon (ATG)
Your last codon must be a stop codon.

Ok, but the problem with this is it assumes conservation based on the coded protein sequence, not the nucleotide sequence. I suppose it will get some of the distant homologs, but:
a) it wouldn't be optimal
b) it might be weirdly biased (if that matters)

Firstly for your peace of mind, this strategy - called "codon alingment" is a standard for your type of situation as long as the sequence is protein coding: http://bit.ly/18odX27. The only situation I can see where this will "go wrong" is if you are using non-coding DNA (e.g. regulatory sequence). Indeed you must remove all introns before running the "codon alignment" as I mentioned above. The starting codon must be 'ATG' (i.e. start codon) and the last codon must code for a "stop codon"

W.r.t the assumption of conservation at protein level: indeed I make that assumption, and this is a valid assumption given that the dna sequence you are using DOES code for a protein and whose functionality is constrained to the protein level (i.e. the protein has a function that benefits the host)

That's exactly the situation I'm facing.  My bacterial small RNA genes of interest are indeed noncoding.

oh dear, I feared that may be the case...! I will see what I can come up with for you

I have posted a new answer dealing with your case of "non-coding" sequence query


text:
What are the differences between HPRD and BIOGRID databases?
What are the differences between HPRD and BIOGRID protein-protein interactions databases?

What are their purposes? Why do we need two different databases?
How is data collected into each one?
How different are they in the interactions they contain?
Is one considered more reliable than the other?
Which one is more commonly used when benchmarking models?
Are there any other commonly used PPI databases?

Do you mean in funding or functionality? Your question is very general. Both projects have different purposes. The latter seems to be more specific, interaction repository with data compiled through comprehensive curation efforts, while the former more general about proteins. In some cases HPRD is better, while BIOGRID in other depending on the situation. Reliability again depends on your issue. It is often the case that BIOGRID can be more reliable in its specific cases, while HPRD can provide some overview well.

I've added some details to my question. I'm not sure what you mean by more general/specific.

i've covered major differences in my answer, but most importantly HPRD focusses on high-quality manually curated Human data and BIOGRID is for multiple species

Short Answer
In a nutshell, there are two major differences:

Species range: BioGRID integrates multiple species' protein-protein interaction (PPI) data, whereas HPRD focuses mainly on Human data.
Functionality: HPRD has some GUI tools that can interact directly with it's database (e.g. BLAST - for searching proteins and their binding partners via sequence alignment) whereas BioGRID is mostly just a database.

Long Answer
In bold are the unique features of each database.
About HPRD:

The Human Protein Reference Database represents a
  centralized platform to visually depict and integrate information
  pertaining to domain architecture, post-translational modifications,
  interaction networks and disease association for each protein in the
  human proteome. All the information in HPRD has been manually
  extracted from the literature by expert biologists who read, interpret
  and analyze the published data. HPRD has been created using an object
  oriented database in Zope, an open source web application server, that
  provides versatility in query functions and allows data to be
  displayed dynamically.
FAQ HPRD: Why did you decide to develop yet another database instead of integrating other existing databases?"
  We believe that biological databases are still in their early stages
  and no protein database can be considered as an established standard.
  We feel that a variety of databases trying to solve problems in
  diverse ways provide the biologists the possibility of choosing their
  favorite. Our approach is radically different from existing databases
  and we want to offer biologists the possibility of choosing instead of
  imposing one database by default. Besides, most of the databases are
  automated and ours is manually curated to avoid errors. We are also
  trying to provide information that few other databases provide.

About Biogrid:

The Biological General Repository for Interaction Datasets (BioGRID)
  is a public database that archives and disseminates genetic and
  protein interaction data from model organisms and humans
  (thebiogrid.org). BioGRID currently holds over 720,000 interactions
  curated from both high-throughput datasets and individual focused
  studies, as derived from over 41,000 publications in the primary
  literature. Complete coverage of the entire literature is maintained
  for budding yeast (S. cerevisiae), fission yeast (S. pombe) and thale
  cress (A. thaliana), and efforts to expand curation across multiple
  metazoan species are underway. Current curation drives are focused on
  particular areas of biology to enable insights into conserved networks
and pathways that are relevant to human health. The BioGRID 3.2 web
  interface contains new search and display features that enable rapid
  queries across multiple data types and sources. BioGRID provides
  interaction data to several model organism databases, resources such
  as Entrez-Gene, SGD, TAIR, FlyBase and other interaction
  meta-databases. The entire BioGRID 3.2 data collection may be
  downloaded in multiple file formats, including IMEx compatible PSI MI
  XML. For developers, BioGRID interactions are also available via a
  REST based Web Service and Cytoscape plugin. All BioGRID documentation
  is available online in the BioGRID Wiki.