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Why does the butterfly have a cocoon stage in its life cycle?
Why does the butterfly have a cocoon stage in its life cycle? It could have simply grown up within the egg/cocoon, and emerged as a butterfly. Instead it is first an egg, then a worm, then a chrysalis, and finally after some time a butterfly.

It's not just butterflies; many insects (e.g. bees, wasps, fleas, ants) go through a similar complete metamorphosis during their life cycle.

@BruceAlderman: Agreed. What could have been the motivation for such a life-cycle?

Fyi, if one wanted to be technical, the  pupal stage of butterflies is called a chrysalis not a cocoon.

In addition to the list provided by @BruceAlderman, beetles also undergo complete metamorphosis.

Holometaboly is believed to have evolved only once (Labandeira, 2011), but is arguably the most successful mode of development we know of in terms of species richness (Kristensen, 1999 - PDF link). Insects which have adopted this method are far more diverse than their hemimetabolous counterparts. A conservative estimate by Hammond (1992) is that holometabolous insects comprise more than 60% of all living organisms.
The subclass Pterygota (winged insects) is divided into (super orders) endopterygota (wings develop interiorly) which are holometabolous, and the exopterygota (external wing development) which are hemimetabolous.
Hemimetabolous insects (usually) develop from an egg to an adult through a series of immature forms (known as nymphs or instars) which are slightly modified (and usually slightly larger) forms of the preceding form. There are exceptions to this mode within the exopterygota including asexual parthenogenesis which is common in aphids. The general life cycle is well illustrated in the Dermaptera (earwigs). All stages inhabit the same ecological niche and so maintain the same general body plan.

Image file from Wikimedia Commons here
Although hemimetaboly is a more gradual process than holometaboly, it happens in a small number (often four or five nymphal instars) of discrete steps rather than the more continuous development of other animals such as mammals. Although all insects fall into either the exopterygote or endopterygote categories (i.e. wings either develop externally or internally), there are examples of intermediate processes which lie somewhere between hemi- and holometaboly. A notable example are the Cicadas. Cicadas are Hemiperans (true bugs) which lie in the exopterygota and so are, by default hemimetabolous. However there is a considerable difference between their immature and mature stages:

Illustration by Debbie Hadley, using drawings from Insects - Their Ways and Means of Living by Robert Evans Snodgrass, U.S. Bureau of Entomology. These drawings are in the public domain. From here.
During the immature stages, the larva (or nymph) will burrow underground, sometimes for many years. This requires strong front appendages, which they also use when they surface to grip onto a surface whilst they shed their final skin to become an adult. This differential niche exploitation is likely to have given rise to the morphological differences between immature and mature life stages.
Exploiting different niches during different developmental stages not only reduces intra-specific competition between young and adult, it also enables the insect to be more specialised to fulfill their specific role, which changes as they develop. The role of the immature is to grow, they do not yet need to be able to reproduce or disperse; whereas the role of the adult is to find a mate and reproduce. Young often develop below ground where there are fewer predators, adults often fly to enhance dispersal (further reducing competition and also decreasing inbreeding). These two activities call for vastly different body designs.
Some other common holometabolous insect orders are Coleoptera (beetles), Hymenoptera (bees, wasps, and ants), and Diptera (true flies), whereas hemimetabolous groups include Orthoptera (grasshoppers, crickets etc.), Mantodea (praying mantids), and Blattaria (cockroaches).
As for the chrysalis which Lepidoptera (butterflies and moths) have evolved to surround their pupal stage, the main role is likely to be protection. Larvae (caterpillars) are a highly nutritious and energetic food source and thus have adapted defensive mechanisms such as mimicry, warning colours, and dropping to the ground when disturbed. This drop would damage the metamorphosing pupa (the most vulnerable stage as it is usually relatively immobile), as the cuticle softens to allow for cell-rearrangement.
The process of insect development is regulated by juvenile hormone (JH), see Konopova et al, (2011) for more on this.
References

Hammond, P. (1992) Species Inventory. Global Biodiversity (ed B. Groombridge), pp. 17–39. Chapman and Hall, London.
Konopova, B., Smykal, V. & Jindra, M. (2011) Common and Distinct Roles of Juvenile Hormone Signaling Genes in Metamorphosis of Holometabolous and Hemimetabolous Insects. PLoS ONE, 6, e28728.
Kristensen, N.P. (1999) Phylogeny of endopterygote insects, the most successful lineage of living organisms. European Journal of Entomology, 96, 237–253.
Labandeira, C.C. (2011) Evidence for an Earliest Late Carboniferous Divergence Time and the Early Larval Ecology and Diversification of Major Holometabola Lineages. Entomologica Americana, 117, 9–21.

The cocoon phase allows lepidopterans (and other holometabolous insects) to reorganize their body and undertake the dramatic metamorphosis from larvae to adult in a safe environment. Cocoons and pupae are typically attached to branches by silk (oftentimes after climbing high into the canopy), thereby removing them from many predatory interactions and providing a protected environment to breakdown the larval body and develop into the adult phase.
In my mind, the main adaptive significance of the cocoon/pupal phase is to provide an environment within which the animal can metamorphose while reducing exposure to both predators and any harsh elements.

The butterfly is the reproductive stage while the larvae all it does is eat an accumulates energy to be succesfull during the reproductive phase.
In terms of adaptation this life cycle would be much more efficent.

I’m not convinced – it certainly requires a much more complex regulation and gene setup. I’m not sure that this optimises the adaptation of the organism.

I agree it requires complex genetics, but that does not imply higher energy cost or low efficiency.

Could you expand on why it would be more efficient, or toss a link? I'm inclined to concur with Konrad's comment.

I talk about efficiency as in survival fitness. What I meant is that maybe the metabolic expense of such life-cycle it's compensated by the adaptation capabilities provided. I have no proof of this, I's just a though.


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Are there examples of the green beard effect in humans?
Green-beard effects are genes that:

Produce an effect that can be detected
Produce preference to others with the same effect

Are there any examples of this in humans?

Could you expand you question to make it more accessible to users, and thus easier to answer? What 'samples' are you interested in? Do you have an example? Thanks.

So... essentially you are looking for examples of dominant alleles with a clear phenotype? I do not understand your examples, though: racism, wars etc. are all but "easy" situations that definitely cannot be explained [just] in terms of genetics. Also, when you write "sample" do you mean "example"? I am asking because sample has a different meaning.

Essensially I am still confused. I feel that altruism toward those who are similar are very much a like altruism toward family  members. Yes, it may not be pure genetic. Then what? How, mathematically, those traits reproduce? Does every such traits come with a complementary trait to like those with the traits? Still some part is mathematically missing.

You cannot reduce everything to genetics. Ambient plays a role of paramount importance in all those situations. There are certainly a series (definitely not one) of genes that can influence how much altruist or racist or violent you are, but the education you are given and the culture in which you grow in are much more powerful in shaping your behaviour.

I've reverted all the later changes, they confused the matter more than they helped in my opinion.

Your examples are way too broad. A green-beard effect only applies to the effects of a single gene or group of linked genes, not to just any trait. Racism and your Mongol war example are too complex to be explained by this effect. In reality examples will mostly be found in single-celled organisms where expression of a single protein can have whole-organism effects such as causing aggregation, or in larger organisms where some highly visible effect is possible such as a colour change.
There are very few real known examples of the green-beard effect, but four are listed on the Wikipedia page:

The killing of red ant queens carrying a particular allele by workers with a different allele (Keller & Ross, 1998)
Altruism in social amoeba resulting from homophilic adhesion of a protein (Queller et al., 2003)
A multi-locus example in which similarly-coloured male lizards protect one another (Sinervo et al., 2006)
A neat example in yeast whereby individuals sharing an allele for a particular locus selectively aggregate, preventing those without the allele from benefiting by proxy from their trait (Smukalla et al., 2008)

References

 Keller L, Ross KG. 1998. Selfish genes: a green beard in the red fire ant. Nature 394: 573–575.
 Queller DC, Ponte E, Bozzaro S, Strassmann JE. 2003. Single-Gene Greenbeard Effects in the Social Amoeba Dictyostelium Discoideum. Science 299: 105–106.
 Sinervo B, Chaine A, Clobert J, Calsbeek R, Hazard L, Lancaster L, McAdam AG, Alonzo S, Corrigan G, Hochberg ME. 2006. Self-recognition, color signals, and cycles of greenbeard mutualism and altruism. Proc Natl Acad Sci U S A 103: 7372–7377.
 Smukalla S, Caldara M, Pochet N, Beauvais A, Guadagnini S, Yan C, Vinces MD, Jansen A, Prevost MC, Latgé J-P, et al.. 2008. FLO1 Is a Variable Green Beard Gene that Drives Biofilm-like Cooperation in Budding Yeast. Cell 135: 726–737.

Nice answer, just wanted to point out that obviously "altruism" in the amoeba cannot be extrapolated to altruism in men (not that you are saying that, but I can see such a comment coming)

@nico yes that's a good point, in this case it literally means sticking together

I asked why people are altruistic toward those who are similar to them, and they said green beard. Then here you said green beard don't work for humans.

Who is 'they'? The green beard effect simply describes one possible explanation for evolution of simple cases of altruism. It may or may not apply to humans, but no human example is known.

Perhaps you're talking about Winawer's answer here?. He doesn't mention humans, and specifically says it's more likely in bacteria, and that it probably isn't that widespread.

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When has an organism evolved enough to be called a new species?
Imagine that we take a population of horses, split them in half and place them in completely different environments. The two species will evolve separate from each other and because the environment is different, the outcome of evolution will be different.
But at what point can you say that these horses have evolved into two different species?
(I do know that they would probably go extinct if we conducted this exact experiment, but this experiment is just to give an example)

I think LuketheDuke's answer is an oversimplification of the biological species concept (possibly resulting from the dictionary having a poor definition). The definition he gives is one of many which are in current use, and is made redundant by many types of organism.
It is important to recognise that because reproduction is not the same process in all organisms, genetic differentiation between individuals occurs in different ways for different groups.
Let's take the definition given in LuketheDuke's answer...

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but are not able to breed with members of another species.

Under this definition, lions and tigers (see ligers and tiglons, which are sterile hybrids between the two) would be considered one species, as would donkeys and horses (see mules and hinnys, again sterile hybrids). There are hundreds of other examples of pairs of animal species which can hybridise to produce sterile offspring.
However, these animal hybrids usually only take place with human intervention, by delibrate breeding efforts. Thus we could extend the previous definition to include them...

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but do not breed freely with members of another species in the wild.

That last part takes care of the ligers and tiglons. But what if we consider plants? Under the definition I just gave, most grasses (around 11,000 species) would have to be considered as one species. In the wild, most grasses will freely pollinate related species and produce hybrid seed, which germinates. You might then think we could just modify the definition to specify that the offspring must be fertile (i.e. able to reproduce with one another)...

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but do not breed freely with members of another species in the wild to produce fertile progeny.

Unfortunately, the situation is still more complicated (we've barely started!). Often wild hybridisation events between plants lead to healthy, fertile offspring. In fact common wheat (Triticum aestivum) is a natural hybrid between three related species of grass. The offspring are able to breed freely with one another.
Perhaps we could account for this by taking into account whether the populations usually interbreed, and whether they form distinct populations...

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of populations or meta-populations of related individuals that resemble one another, are able to breed among themselves, but do tend not to breed freely with members of another species in the wild to produce fertile progeny.

This accounts for the grasses, but it still leaves a messy area when you have a hybridisation which establishes - until the hybrid population is segregated away from the parent populations it is unclear whether they still count as the same species.
We could probably live with this situation, except for the fact that bacteria refuse to conform to it at all. Bacteria of the same species, or even very different species, can freely transfer genes from one to the other in conjugation, which combined with fission can result in perfectly replicable hybrids. This is such a common occurence that it breaks even the 'tend to' part of the previous definition, and members of a population can be doing this almost constantly, which negates the segregation requirement.
Richard Dawkins had a go at defining around this, by stating that...

two organisms are conspecific if and only if they have the same number of chromosomes and, for each chromosome, both organisms have the same number of nucleotides

This partly gets around the bacterial problem and means that bacteria which result from conjugation are a new species. Unfortunately under this definition we might as well not ever bother trying to classify bacteria as billions of new species would be created every day - something which the medical profession might have something to say about. This definition would also mean that those with genetic diseases like trisomy 21 are not human. The final nail in the coffin of this attempt is that there are many species, including frogs and plants, which are very certainly considered a single species by taxonomists but which have some variety in the presence of small accessory chromosomes, which occur in different combinations between individuals.
Let's consider one last option. We now live in the era of genomics where data about genomes of thousands of organisms is accumulating rapidly. We could try to use that data to build a species definition based upon similarity at the nucleotide level. This is often used for bacteria, by considering organisms with less than 97% nucleotide similarity to be different species.
The major point I've been trying to make, though, is that species is not a natural concept. Humans need to be able to classify organisms in order to be able to structure our knowledge about them and make it accessible to people trying to link ideas together. But the natural world doesn't care about our definitions. Ultimately the species concept is different for different groups of organisms and will continue to change over time as our analytical methods and the requirements of our knowledge change. Note that I've deliberately skipped over many historical species concept ideas.
The direct answer to your horse question is "it depends how you want to define a horse".

So you're saying that it is incorrect to say that the horses are no longer the same species when they can no longer successfully breed (successfully here meaning 'producing fertile offspring'), as stated in my answer? I would say this is 'correct', even if it is a simplification. If the example had been bacteria (that do not 'breed' per se) then I would not have given this definition.

That being said, yours is a very interesting and informative answer. But it does not really answer the question. If you were to test whether the horses had sufficiently divereged to become 2 new species, would the test not be to see if they could successfully breed?

@LukeTheDuke yes I'm saying that's incorrect. Firstly because the definition you gave doesn't specify that 'successfully' means 'producing fertile offspring'. And secondly because there are many situations in which two populations of horses can't breed to produce fertile offspring, for example if they are geographically separated. Accounting for those to things, we could get a workable definition for a horse.
For horses, then, we could say they were no longer the same species if, when cohabiting, they did not breed to produce fertile offspring.

@LukeTheDuke I hope it's clear that I don't think you've done anything wrong, but that the dictionary gives an insufficient definition.

Not a problem, as you say there is no definitive way to draw the line between species, but the line is much easier to draw in animals like a horse. Yours should be the 'correct' answer for this, as the title to the question is not about horses, but species as a rule (the horses were just an example). But therein lies the problem - using one definition (the 'classical' definition?) we can distinguish between 2 closely related animals, but this same definition is not adequate for other organisms. Is it possible to clarify your answer to include separate definitions for plants/animals/bateria?

Sure thing, when I get home this evening I'll add a summary at the end of appropriate definitions for major groups.

Wow, I didn't imagine it would be this hard to draw a line between two species (should I even call them species now?).

Hence why you end up with huge discussions about whether there are human races etc. Words like species, races etc. are just words, they are mutable and it is pretty much impossible to provide a biologically funded universal definition. Hence why definitions usually say things like 'should be considered' or 'differences[...]warrant'

As another example of why the dictionary definition is not always applicable; the two breeds of dog, great dane and chihuahua are unable to breed successfully but are still considered to be the same species due to their genetic similarity.

Amongst taxonomists - who define and name species - there are 'lumpers' and 'splitters' who choose larger taxa with more diversity, and smaller with less respectively. The problem exists even for professionals where it ultimately becomes a personal preference.

I registered to the site just to say that this is a great answer.

The story of the ability to interbreed is even more complicated than the ambiguity posed by horses, donkeys, lions and tigers. In California and Mexico, there are a series of species of lizards which form a geographical 'horseshoe'. Neighboring lizards can interbreed, but species at either end of the horseshoe cannot breed. In other words, lizards at the ends of the horseshoe are clearly of different species, but any pair of geographically close groups of lizards can be argued to be the same species. There's no place to draw the line to say where one species ends, and the next begins.
I think that this lies at the heart of the question... the concept of a species is an artificial construct. By and large, there are large enough separations of space and time that the lines are easy to draw, but during the split, the lines are in no way clear.

The biological definition of a species on Dictionary.com is as follows;

The major subdivision of a genus or subgenus, regarded as the basic category of biological classification, composed of related individuals that resemble one another, are able to breed among themselves, but are not able to breed with members of another species.

So what we take from this is that a species, by definition, are those individuals/organisms that can successfully breed together. It is worth pointing out that some members of closely related species can breed together (e.g. a male horse and a female donkey can produce a 'mule'), but these animals are not fertile, so this is not considered 'successful' breeding, and the two organisms (in this case the horse and the donkey) are of different (if closely related) species.
In your example, the populations of horses would be said to have sufficiently diverged from one-another when they can no longer successfully breed.

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Examples of intracellular parasites of medical or economic importance?
What are examples of intracellular parasites of medical or economic importance? I have read that Xanthomonas oryzae is an intracellular parasite in rice that produces proteins able to cause changes in the gene regulation of the rice cells in order to feed off the sugars produced by the rice cells.
I would like to know of other examples of intracellular parasites of medical or economic importance that would be potentially (even if not tested) able to interact with the host's genome in a similar manner.

All viruses are obligate intracellular parasites... I would closely watch that because they could soon become a very useful tool for medicine :)

As Armatus pointed out above, all viruses are obligately intracellular, and their medical and economic importance cannot be overstated.
Many bacterial species live intracellularly. The arthropod specific Wolbachia has a wide variety of consequences for its host, including alteration of reproduction and sex ratios, induction of reproductive isolation possibly driving speciation, and conferring protection from some viral infections.
Eukaryotes can be intracellular parasites as well: Malaria is a well-known example. Toxoplasma gondii is another intracellular parasite that uses cats as a primary host, but can use other warm-blooded animals (such as humans, rats, and birds) as intermediate hosts. T. gondii infection has been shown to induce behavioral changes in rats, causing an attraction to cats (thereby increasing the chance that the parasite will infect the cat and sexually reproduce). There is also some evidence that T. gondii infection in humans causes behavioral and psychological changes such as decreased reaction times, and links to depression and suicide.


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How high is the energy yield of photovoltaics compared to photosynthesis?
I'm not an expert in plant physiology. I was wondering if, per square centimeter, leaves are converting more or less energy than photovoltaic systems. Can this be estimated? How?

In areas where our technology is advanced, you often get us doing better than nature because natural selection only does 'as good as necessary so as not to be outcompeted' whereas our technology can actually do 'as good as practically possible' :)

Your question could use some clarification. As stated, the premise is wrong because neither leaves nor PV cells produce energy. They can capture or store energy, they can also reflect or absorb and release energy. What pools or fluxes of energy are you interested in comparing? a common comparison is "quantum efficiency", but it is not clear if this is the comparison that you are looking for.

Does energy used to evaporate water count? Or the energy required to physically transport water from the soil to the air? PV cells don't evaporate or transport water. These are not accounted for in standard measures of quantum efficiency.

@David. Thanks, fixed the point: of course energy can not be produced/created. My curiosity indulges in the application: could we ever use plants for domestic energy requirements?. It seems photovoltaic are much better, do you agree?

I don't think either could meet domestic energy requirements alone, at least not in the near future. Your question could be improved with better definitions; it still says "converting", without saying to what. See, for example, quantum efficiency and quantum yield.

According to wikipedia, plants typically convert around 5% of the energy of the sunlight that hit the leaves into energy usable by the plant.  Sugarcane seems to be the best, it converts up to 8% of the energy into actual biomass.
The best solar panels on the market, according to the Independent, convert 21% of energy from sunlight into usable electricity.  Experimental prototypes do much better, and there are some that get over 40%.  Wikipedia has a nice graph of the most efficient solar cell prototypes.

By the way, the Forbes article is only the best poly-crystalline, not the best PV in general. Poly is typically less efficient than mono. There are mono panels on the market that are better than 16%

Good point!  Replaced that with another link and a bigger number.

Photovoltaics made from organic sources, like Graphene, (OPVs) have the potential for efficiencies exceeding 24% in a stacked structure. A theoretical max efficiency has not been  proposed, but it is expected to be less than silicon. The main benefit of OPVs is the rock-bottom price and the ability to make very tiny panels.


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Do you know of any disease where HLA / MHC association discovery has led to better treatment or management?
If we discover an association between a disease and a particular HLA type (MHC class I or class II molecule) then it may provide us with some insight into the disease in a very basic way. However, will it provide us with a therapeutic target? Or second best, will it provide us with information that is useful for diagnosis or management? I am looking for examples. Do you know of any?
The most obvious is in transplantation where one would use HLA typing to match donor to recipient but that is not the same as using knowledge of an HLA type to target, treat, diagnose, prognosticate.

I don't know any true disease associations, but since this question still has no answers, I'll offer one...
One class of associations you might be missing is difference in drug response. Patients with HLA-B*5701 are known to be hypersensitive to abacavir. Genetic screens are available to screen for this allele, and this information is used clinically.

Bone marrow transplant for leukemia and multiple myeloma.
Uses extensive HLA typing like you said are you looking for additional diseases?

That is just a matching process so that the graft does not attack the host. I am seeking an association between some form of a HLA which makes for a therapeutic target.

Actually it can help by curing specific types of cancer e.g. Chimeric Antigen Receptor–Modified T Cells in Chronic Lymphoid Leukemia. But ofc. it does not help in every case. You can live without B-cells, but you cannot live without liver...
So yes it can be used by designing a therapy for a disease, if that's the question.


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How does one measure the length of telomeres?
My questions are:

What techniques are available for doing so?
Are they destructive ?
What is their accuracy ?

Again, not an expert, but I found this article seems to say it pretty well:
Telomere's are most commonly measured by qPCR of the repetitive regions with degenerate oligomer sequences such as "TTAGGG and CCCTAA repeats"  Although articles like this one appear to advance measurements in vertebrates, this reference from 2011 implies two techniques continue to be most common:
1) qPCR with the appropriate oligos and then running them on an agarose gel
2) Southern blot of a restriction digest that leaves the telomeres intact
Clearly sequencing techniques don't do well with repetitive sequences such as this, so in general this still seems like the most common method.
This would indeed be quite destructive, at least for the cells used, though a biopsy would be enough, though apparently micrograms of DNA are required.  Kind of a large amount.
The accuracy would then be limited to that of the gel or blot.  That would generally be a percentage of total length, I think 2% might be obtainable, but I'm not sure about that part.


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Do both TSG and Proto-oncogenes have to suffer mutations to cause cancer?
I'm having a conceptual nightmare trying to understand when a group of cells may become cancerous and the more resources I consult the more confused I seem to get.
In order for a cell to become cancerous, does it have to mutate to knock out tumour suppressor genes and have a proto-oncogene become an oncogene?
I'm  currently working on the basis that that is the case, or at least that a mutated TSG on its own will not cause uncontrolled division.  However wikipedia seems to suggest that an oncogene alone can cause uncontrolled division with a functional TSG in place.
It could be a flaw in the idea I have that tumour suppressor genes only trigger apoptosis once a cell has started to divide rapidly, are they actually carrying it out to a regular schedule independent of oncogene presence?

There is a nice nature paper by Dr. Micheal Stratton et al. that I think might be a good place to start.
I think answering you question is complex, because different cancers will actually have different mechanisms that trigger their onset and aggressiveness and as such some have more complex mutational landscapes than others.
A good question to ask yourself is : what is a driver mutation and what is a passenger mutation. A driver mutation is usually what is driving the cancer, and it can be a proto-oncogene or TSG. Passenger mutations don't really have as much of an impact and result from the destructive tendencies of the driver mutations.

The typical idea is that several "hits" are required. The difference between proto-oncogene and TSG is mainly in their heritability - TSG mutations are usually recessive (because a heterozygote will still express sufficient suppressor, e.g. p53) whereas proto-oncogenes are dominant (if a consitutively active agent e.g. Ras is present, it doesn't matter if the other allele is under normal control).
A single "hit" in this way (TSG or proto-oncogene) may just cause the cell to die, which isn't a bad thing (in fact, TSG such as p53 often work by inducing apoptosis because proliferative errors make them accumulute). A tumour only results when a single cell accumulates sufficient mutations and genomic damage to gain a reproductive advantage over the cells in its vicinity.
However, you are asking about cancer, which is not simply a tumour. Tumours are any sort of abnormal growth, i.e. neoplasms, but they can be benign! This means they stay in their tumour capsule, do not grow at a fast rate and do not invade or metastasise other tissues. The distinct characteristics that define a cancer are very well-known and were published in a well recognised paper by Weinberg & Hanahan, 2002, "The Hallmarks of Cancer".
The six primary hallmarks of cancer. The first two are the ones most people know, but the other ones are just as essential for

Independence from external growth signals: Cancer cells produce their on autocrine growth factors or have mutated signal pathways active without GF receptor stimulation (Oncogenes).
Resistance to anti-growth signals: Cancer cells do not respond to growth-inhibitory factors from outside or inside (Tumour suppressor genes).
Evasion of apoptosis: Cancer cells resist signals which cause normal cells to die (apoptose) (these are also tumour suppressor genes).
Limitless replication / Evasion of cell senescence: Apart from stem cells, all normal cells can only replicate their genome a certain number of times before the ends of the chromosomes known as telomeres are too short, disintegrate and cause the cell to enter senescence or die. Cancer cells express telomerase, which extends telomeres and maintains replicative potential.
Sustained angiogenesis: Tumours and cancers form massive cell heaps. Tumours may stall growth because blood vessels do not grow into the heap and supply the cells with the nutrients needed to proliferate. Cancer cells have found a way to induce blood vessel growth (VEGF) and sustain it in order to maintain nutrient supply.
Invasion and metastasis: This is the crucial, most distinguishing difference between benign neoplasm (tumour) and malign neoplasm (cancer). Cancer cells degrade the extracellular matrix around them (by secreting metallo-matrix-proteases, MMP), which allows them to move away from where they are and invade into neighbouring tissues. They can also spill into blood vessels this way (especially if the neoplasm is well-vascularised thanks to hallmark number 5), where they can travel to other sites in the body and grow new cancerous tumours in other locations.

There are four more emerging hallmarks and enabling characteristics (immune evasion, inflammation induction, modification of energy metabolism, genomic instability), which allow better cancer growth and make a cancer more dangerous if it acquires them, but these are outside the scope of this answer.


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Shouldn't evolution have taken care of baldness already?
It is my understanding that the hair on the head is there to protect us from sunburn.  I've never seen a bald animal, so isn't evolution in charge of addressing these type of things?
How is it that evolution gave us a thumb, but hasn't found a way to keep the hair on our heads?

Your question doesn't provide very compelling evidence for reduced fitness due to baldness.

Because we use hats?

There are tons of bald animals. Fish immediately come to mind. Then there are naked mole rats and lots of other critters. Also, your last sentence can be used to ask the equivalent question “why didn’t evolution give chimps thumbs?” – This is simply not how evolution works.

fish never grow hair, they don't get bald within their lifespan  I don't see any correlation between a fish and my question.

@Rafael.IT The correlation is that fish have (some of) the same supposed disadvantages due to their hairlessness, so according to the argument they should have evolved hair by now. But if you don’t like this example, take the other ones, where animals have lost their ancestors’ hair. Actually, nico’s comment above is excellent (and not at all a joke!): we evolved the ability to manufacture hats. This is an adaptation to combat the disadvantages of baldness.

research claiming bald men get less cancer: http://news.bbc.co.uk/2/hi/health/8569826.stm

the article actually talks about the level of testosterone, baldness is  consequence of high testosterone but the baldness itself holds no correlation with  cancer

If testosterone causes both baldness and cancer then that is a push towards baldness and cancer correlation. The article states baldness to cancer correlation.

using that premise you can link pretty much anything you want, for instance if high testosterone causes that men have more sex than usual would that mean that sex causes cancer?

No, absolutely not. but it would push sex towards being correlated with cancer.

@isJustMe it would also mean there was a selective advantage to being vulnerable to that form of cancer,  no trait exists in a vacuum.

Can you demonstrate any reason baldness should be selected against?

As is typical for questions about fitness, this question has more than one valid answer.
The essential question @AndrewSalmon is answering is the right one:
"If evolution eliminates disadvantages, why can xyz trait still be seen the population?"
Here is a more complete list,
1) The trait is not eliminated by evolution since it is manifested after reproduction.  The classic example of this sort of trait is senescence.  Why do we grow old and die?  Clearly it doesn't stop us from having offspring.  I generally don't find this sort of answer informative. Its not a bad argument for the traits of bipolar and schitzophrenic tendencies which can manifest as a chronic mental condition, often in the 30s after many people have children.
These traits are fairly common (1 in 6) in the population.
It is usually arguable that these traits are of some sort of advantage from some perspective (including my examples).  In this case @Andrew argues this.  I'm not sure I agree, but you can read his post for the argument.
2) Pleiotropy. The idea that the negative trait evidences more than one trait.  In this case one might say that baldness is tied with another trait that is beneficial.  Some say that the cause of male pattern baldness, which is an excess of testosterone, would be tied in with other masculine signals, which can often outweigh disadvantages of being bald and trying to find a mate.  A trait like baldness could also for instance be tied to a desirable trait in women, causing it to persist in men as a result of the advantage of say, less hairy women.  I probably wouldn't take this stand either, though its conceivable.
3) "Neutral variant" The third explanation that I will put out is that baldness simply isn't a trait with enough disadvantage (if any) that it should be removed from the gene pool.  While there is evidence that baldness is a disadvantage come friday night, to say that a trait is disadvantageous we have to see, in the long run - over the lifetime - really is a disadvantage.  I think I would agree with those who say that while some women do not find bald men attractive, its not enough to stop them from having kids, which is all evolution cares about.
And if you happen to be balding probably what you should care about, guys!
If evolution should eliminate male baldness, then why not eliminate sterility, homeliness, impotence, poverty, obesity, being dull, living with your parents and adolescent awkwardness?  These are probably even more important obstacles to finding a mate? All of these traits are beneficial traits that are maladapted to modern life or genetic accidents.  Evolution can't get rid of them at all I think.
For an even more complete discussion of the general subject, see Dawkin's "The Extended Phenotype".  Baldness is not discussed however.

It needs to be pointed out homelessness, poverty, and living with your parents do not have genetic components so they make bad examples, evolution cannot do anything about them.

The closest research I can find with a little poking is this paper.  The results are somewhat inconclusive, because AGA (the technical term for male pattern baldness) has many separate genetic components.  Nonetheless, there appears to be evidence that AGA is under positive selective pressure in Europeans and possibly Asians.  That is, there appears to be a fitness advantage to baldness in some circumstances.  However, there are other possibilities, for example, it may be that an adjacent gene is being selected for and this gene is coming along for the ride.
Note that AGA is less frequent in Africans than Europeans, which suggests that indeed there may be selective pressure against baldness in sunnier climates for the reason you suggest.  Note that in cold climates, on the other hand, there can be selection for increased UV exposure to avoid Vitamin D deficiency (the evolution of lighter skin).

+1 The fact about africans having less tendecy to baldness is interesting

The linked paper says "Epidemiological data for African populations is sparse, but it has been reported that males without AGA are four times more frequent in Africa than in Europe" citing a paper from 1970.

Care to explain the downvote? Did I get something wrong?

I voted up man, must be someone else

Yeah, sorry, I didn't think it was you.

Or it is simply under less negative selection in populations living in places with lower UV incidence.

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


text:
Is the function of adjacent genes correlated?
Do genes that occupy a similar locus on the genome have correlated function, specifically in human beings? It is my understanding that adjacent genes are inherited together, and so location plays a role there. However it terms of function, I don't know to what extent location plays a role. Furthermore, if say two adjacent genes have the same expression, does this necessarily mean that their function is correlated, or is that interpretation stretch?

Trivial and maybe a bit tongue-in-cheek comment: that cannot be true, otherwise any gene in the genome would be correlated to its neighbour, hence all of the genes would be correlated to each other :)

@nico But it is true to some extent, at least when looking at co-regulation.

That only says they can't be perfectly corollated. Otherwise corollation would drop off exponentially with distance.

@Konrad Rudolph: I know, I was just joking. Anyway distance on genomic map does not mean distance in space...

You might look into the homeotic genes. They are involved in patterning embryos during development. Interestingly, in vertebrates especially, their pattern of expression on the anterior-posterior axis of the embryo (and the proximal-distal axis of the developing limb) is the same as their order on the chromosome. They are said to be colinear, though no one really knows why.

In bacteria, this is often true.  This is because more than one gene is often transcribed onto a single RNA.  This grouping of genes is called an operon.  It is usually true that these have a related function because they are being translated to protein in very much the same proportion - a convenient way to regulate the function as a whole.
Once you get into eukaryotes this is no longer true (except for v. rare cases most of which are viral genes), one mRNA transcript contains just one translation region.  This is true even for yeast and other single celled organisms.  Gene regulation can be correlated, but the relationship on the genome has little to do with it.
There is some importance to the genomic relationship of two genes because of the crossing over that occurs in meiosis, but this is more of a relationship that is important in speciation and evolution, it doesn't have any recognized importance to how the genes act within the eukaryotic cell.

A group of tightly linked genes that are involved in similar molecular pathway is called a supergene.
For the pleasure to formulate a slight opposition to @shigeta's answer, I will give some examples of supergenes in eukaryotes.

In Primula, heterostyly is controlled by a supergene.
In Papilio memno, mimicry is controlled by a supergene.
In some species of ants, some social behaviour is caused by a supergene.
Sexual chromosomes (and this is quite common) can be considered as supergenes.

Globally speaking, every locus that is under antagonist sexual in different sex/castes/ecotype/whatever is likely to start forming a supergene as soon as another locus that has antagonist effect appears in its vicinity because the presence of two such genes on the same chromosomal region will select for arrest of recombination.
But of course, those represent exceptions (however common these exceptions might be) but in general, I don't think you should expect that adjacent genes would have similar functions.


text:
What's the state of the art in designing and creating your own life forms?
What's the state of the art for solving the following problem. You imagine a set of features that you want a life-form to have. Just to take an arbitrary example, say you want your life-form to have a) a strong sense of smell, b) the ability to fly and c) a comfortable couch shaped saddle on its back. What's the sequence of steps you need to take so that you can create this life-form in the lab?
I realize that we are probably far away from solving this very general problem. But perhaps there are some smaller subproblems that we do know how to solve.
For example, as far as I gather, you can probably make any living being fluorescent green in color by inserting into its genome the gene responsible for expressing the Green Fluorescent Protein. So may be if we limit the set of features one is allowed to choose from, the above problem can be solved. So my first question of the set of questions is:
1)  What features can be easily inserted into almost any organism easily?
Next, I imagine that to design and create an artificial life-form will consist of three steps:

Figure out which proteins will give rise to those feaures,
Design a genome that will express those proteins in the right quantities and
Implant that genome into a cell and actually let the being grow.

2)  Is the above sequence of steps correct, or am I missing something?
3)  What is the state of the art for each of these steps?
Finally, in light of the recent spur in the open source biology groups and DIYbio enthusiasts, I feel that there might be some very simple but really cool things related to my question that you can already do in your garage. For example, may be there is some very simple single-cell life-form that's so well understood that you can add or subtract tons of features from it with a budget of a few hundred dollars. So my final question is:
4) What is the cheapest experiment you can perform at your own home without access to a biology lab which involves changing the genome of a living organism in a way that's functionally visible? (An arbitrary example: Can you create an apple that's blue in color with a budget of $500? By create, I mean you should be able to hold the blue apple in your hand.)

You may want to try splitting this into multiple questions (along the delineations you've already set up).  It will keep the answers better organized.

This would seem to be far too localised: the situation will inevitably change every year. And you've asked several questions in one, which is very strongly discouraged.

@EnergyNumbers: I doubt that the situation of creating your transgenic life form in your garage with $500 will change anytime soon...

Addressing what you can do in your garage: Infusing E.coli (one of the best-undestood bacteria out there) with GFP requires: a) E.coli with appropriate medium obviously, b) antibiotic-medium to select for the transformed strains, c) a pGLO plasmid or equivalent, which contains GFP in an operon E.coli normally uses to digest arabinose (ara operon), d) calcium chloride for heatshocking them, e) UV light to see them glow; plus utensils for transferring the bacteria. Might be doable with $500 actually; but this only regards bacteria, which take up and integrate DNA happily.

@Armatus: hmmm... even just the competent cells + medium would probably be ~$500.

@nico huh? E. coli can be considered free, and media is about $20/kg dry (e.g. malt extract)

@David: hmmmm... and what is the transfection efficiency of naturally found E. Coli (I don't really want to know where you would find it :P)? I was specifically speaking about competent cells. As for the media, LB goes at around 100-120 euros/kg (powder). Again, even if that was almost free, the cheapest Taq would also be at least 50 euros (not a big amount), he would need restriction enzymes, ligases, a spectrophotometer, a thermocycler, micropipettes etc etc.

@nico: Can't all E.coli be induced competent under heat shock? Just need calcium chloride additionally. Also I thought you can buy the pGLO plasmid pre-prepared.

To put GFP into E.coli you would also need an autoclave or some other way to sterilize your medium and IPTG for induction in most cases. Naturally found E. coli would probably not be suitable, not even speaking on the difficulty of isolating them specifically (and the dangers if you accidentally isolate one of the dangerous strains). You probably would need to get some E. coli K12 and the plasmid from a friendly academic lab to be able to do this on a budget.

State of the art questions have the obvious defect that they are temporal. The answers to this question are now six years old — hardly 'state of the art'. Time to retire this question.

The problem is of course very complex so take my answers as simplifications.
Most transgenesis so far has been done on unicellular beings (bacteria, yeast), which we can change as much as we want fairly "easily", plants, insects and some mammals. Notably, for the latter case, mice are the species which has been used the most for transgenesis, as they are cheap (compared to, say, using pigs), do not take lots of space, have big litters and a quick reproductive cycle (~20 days). Aside from mice we've seen GFP rats, pigs, dogs, cats, sheep and probably there is more, but I will mostly restrict my answers to mice (as far as I know there are big technical difficulties in applying transgenics procedures to something bigger than a mouse, but to be honest I could not explain you the details on this as I have never done it).

What features can be easily inserted into almost any organism easily?

Well, essentially, it is easy to give rise to monogenic traits (i.e. traits that depend on a single gene). Generally speaking, when you want to have more traits, or need more than 1 gene to have the trait you create single transgenics and then breed them together.
So, if your phenotype depends on the presence of gene A and B you will generate a (mouse) line expressing A, one expressing B, you breed them together and, if you are lucky, a part of the pups will be expressing both.

Next, I imagine that to design and create an artificial life-form will consist of three steps: 1. Figure out which proteins will give rise to those feaures, 2. Design a genome that will express those proteins in the right quantities and 3. Implant that genome into a cell and actually let the being grow.
Is the above sequence of steps correct, or am I missing something?

No, that is not how it is done!
There has been, to my knowledge, only one (very impressive) attempt to do that, a project led by Craig Venter at Celera Genomics. The project resulted in the creation of the first synthetic life form, named Mycoplasma laboratorium (see also the original paper on Science). Doing this for a multicellular being is, presently, science-fiction.
What normally you would do is to insert or remove just the piece of DNA you need in the genome.
There are different approaches to do that: for instance, you can start from embryonic stem cells, from fertilized oocytes or from spermatozoa.
This is the general process for making a transgenic mouse:

Source: https://web.archive.org/web/20161212170103/http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/T/TransgenicAnimals.html
Now, depending on how you inject your gene you can distinguish between transgenics and knock-in mice. In a transgenic mouse you insert the gene somewhere in the genome and, although there are method to understand where it ended up you generally do not know.
Knock-in animals, instead, target a specific region of the genome. This is usually used in order to change an existing gene, to improve its function or to remove its function (knock-out animals). This process, called gene targeting relies on the biological process called homologous recombination.
So, why don't we just synthesize a new genome each time?
Aside from Venter's dream, the process would:

have incredibly high cost
be extremely complicated technically
be extremely long (mostly for reason 2)
suffer from the problem that there is so much we do not know about genome regulation in a bacteria, let alone in a mouse! You have to think that the genome is not just a series of genes one after another: there is a big part of regulatory regions that define things like the 3D form of the genome, which determines when and how much genes are accessible for transcription, when and where they are activated and so on. Also, more and more attention is now drawn to something called epigenetics marks, modifications of the DNA, or its associated proteins that can also modulate its transcription.

What is the cheapest experiment you can perform at your own home without access to a biology lab which involves changing the genome of a living organism in a way that's functionally visible? (An arbitrary example: Can you create an apple that's blue in color with a budget of $500? By create, I mean you should be able to hold the blue apple in your hand.)

Quick answer: no you cannot.

Health authorities will be not very happy if you start to produce transgenic organisms in your garage
The sole cost of the reagents which you will need to create the transgene will be >$500. You would then need various machines (e.g. a thermocycler, probably a spectrophotometer, a hood, etc etc.).
I personally don't have a clue how one creates a transgenic plant, but I suspect it is not much easier than an animal. And definitely you don't want a mouse colony in your garage, do you?

An easy experiment you can do is extracting (fairly unpurified) DNA with stuff you have at home. More than that it gets really complicated.

In principle a very good answer, but I think there are some points where science can actually do a bit more than you describe - I'll try to write up an additional answer with these points later :)

This answer is mostly meant to be an addition to nico's answer, which while  correct and on the point, does not completely cover what we can do nowadays.

1) What features can be easily inserted into almost any organism
  easily?

The short version of nico's answer here is 'any monogenic trait', which is basically the GFP example.
I would however say that - with additional, sometimes years of work of course - synthetic biology is at a point, where we can make a single cell perform pretty much any non too complicated task (ballpark something you can describe in one simple sentence): the creation of regulatory networks that react to a certain extra-cellular signal is totally possible, as is the generation of multiple proteins (genes) as output. (These two video's might give an idea, I couldn't find a good source right now that isn't overly specific.)
However, this is still very far away from things like sense of smell, flying or making certain body parts, all of which require the coordinated interplay of many different cells.

2)
  Next, I imagine that to design and create an artificial life-form will
  consist of three steps:

Figure out which proteins will give rise to those feaures
Design a genome that will express those proteins in the right quantities and
Implant that genome into a cell and actually let the being grow.

nico mostly focused on the problem with the second and third point: we don't make genomes - we change them. For adding or changing single genes this has only recently become relatively easy (this is what CRISPR is for), and even adding multiple things in one big block is doable. But at some point you need to start doing this iteratively, which comes with its own set of further complications.
However even with the first point there can be a problem: what if there is no single one protein that makes the function you want? Often you'll need multiple proteins interacting or you need to start combining multiple functions into one protein (which opens the box of protein design - I'm just not gonna go into that though)

4) What is the cheapest experiment you can perform at your own home
  without access to a biology lab which involves changing the genome of
  a living organism in a way that's functionally visible? (An arbitrary
  example: Can you create an apple that's blue in color with a budget of
  $500? By create, I mean you should be able to hold the blue apple in
  your hand.)

This may actually be the only point, where I think nico's answer is not really spot on.
He's right that there are considerable safety, legal and equipment barriers, but still 'open bio science' is a thing: from (mostly local) open wetlab spaces to 3D-printable laboratory equipment there is a lot of possibility out there. That being said, its is very illegal in most countries to make GMOs (which the blue apple would likely be) without the corresponding licenses etc.

Very good points Nicolai, and I definitely agree with you! Indeed it's incredible how fast things have changed since I wrote my original answer... thank you for improving on it!


text:
Why hasn't mother nature made us aware of our lizard brain?
In many personal improvement books I've read, people make a distinction between 2 parts of our brain:

the logical brain, dealing with logic, judgement, thinking; what makes Humans different than Animals
the lizard brain inherited from our ancestors, dealing with emotions and instincts, which takes shortcuts to react to the immediate problems, such as a saber tiger croping up to eat us.

The facts are, the lizard brain sometimes take actions/decisions without making the logical brain aware of that, which is at the origin of many brain biases.
I am wondering if there's a sound reason why Mother Nature didn't evolve us so that we would be made aware of our lizard brain decisions after the fact (i.e. a kind of summary for our logical brain). I mean, is there's something physical or an evolutionary reason that would prevent that?

The reason is that the “lizard brain” doesn’t exist, it’s pseudo-science sauce, as are almost all self-improvement books. In reality, the brain is much more complex than that.

I just looked this up. I am blown away by all the websites on lizard people. How can anyone believe David Icke.

@GabrielFair the Lizard Brain is not the same as David Icke's reptilian theory. The Lizard Brain thing seems to be just a simplistic way of describing a separate 'primitive' part of the brain (which doesn't exist), whereas David Icke thinks lizards secretly rule the world. While they are both stupid, I think Icke's ideas are insane, while the Lizard Brain thing is a basic misunderstanding.

@KonradRudolph you should make that an actual answer, so we can vote it up for visibility

-1 mother nature does not evolve us. That is a religious rather than a scientific view

I guess the problem lie in the wording: sorry but English in not my mother tongue and I am not in biology. Still, I'm surprised that this question has been closed as "non constructive". How can I improve this question? Maybe by removing the allusions to the lizard brain?

Two upvotes for this question?

Just to echo what others have said here, the term lizard brain is a remnant of "recapitulation theory" which rigorously proposed that the embryo develops through more primitive animals.  This is an intriguing idea when looking at embryos - early stage embryos of flies, birds, fish and primates really do resemble each other.  So the idea was that our lower brain, near the spinal chord was the brain of a lizard, whereas the prefrontal cortex, which is highly developed in humans compared to lizards, birds etc was 'added later' and represents a 'human brain'.  This idea is flawed because it basically assumed that the lizard part of us never evolved and was based on a linear idea of phylogeny, as opposed to Darwin's idea of evolutionary trees where lizards and insect continue to evolve.  In evolution there are no 'lower animals'.
In practice, the parts of the brain we have in common with lizards do handle more physiologically autonomous functions (heart rate, etc).  While cortex and prefrontal cortex do show greater activity in emotional and rational decision making.  This is now more of a rule of thumb, not a rigorous statement or a theory of development, merely the result that structures that were developed later tend to have newer functions.  A good discussion of this can be found in Gould's "Ontogeny and Philogeny".
Your question also asks why we can't rationally understand our lower brain functions...
Awareness itself is not an intrinsic property of the brain.  Some aspects of the rational mind and articulate self consciousness are so far fairly unique amongst brains.
I should mention at this point that I do not mean that conscious thought is unique to humans - its clear that primates are aware that they exist and have empathy for feelings of others. Its likely that other animals have similar amazing abilities we think of as human.
Just the same, the level of development in humans is distinctly unique.  Insofar as it is a unique development, not a typical brain function, we should understand that it is far from all encompassing.  Given all this, its not surprising that the physiological functions of the brain such as regulation of breathing, many hormonal levels, stress are not conscious.  I usually only know I've run too far and too hard because I can feel my chest heave - its actually only something I'm aware of because my brain is receiving signals from my chest that its heaving and my heart is beating rapidly.
The limits of our consciousness are the subject of much study now.  From cognitive psychology and behavioral economics we've been surprised over and over in the past 20 years how there are limits to the amount of information we can process at a time and, how limited we are in being rational to the point that we can make foolish decisions, and lastly how much of those decisions are made subconciously, only to be rationalized later by our thoughts.
I will give three examples.
1) Experiments in cognitive psych show that as subjects turn over cards in a deck, our pulse and respiration indicate they know that the deck is stacked before they consciously know.
2) Psychologist/Philosopher Joshua Greene is famous for observing that moral decisions are made in parallel in more than one region of the brain before the decision is rationally made.  This is a great radiolab podcast on this story.
3) Behavioral economists have shown that we don't even know a good deal when we see it.  We are often convinced by cues in the environment about the profitability of our decisions which comes from pre-set processes embodied in our minds.  Studies showing what happens when we pay CEOs too much money, manipulate decision making by offering too many choices and how poor people are more generous than wealthy ones.
This discussion goes back to Descartes, who felt we could be fooling ourselves to the point that we might even be deluding ourselves to believe in mathematics.
If there are ever times when people do things that don't make sense, we have often found that the faults go back to the limitations of our brains.   If you have never had that experience ... "Ill have what @Sylvain's having"!
Looking at references for cognitive dissonance, optical illusions will tell you a dozen more fascinating stories.  Highly recommend it :)

Whilst there is some interesting info in here, I think you should point out the fallacy in the original question (i.e. the lizard brain is not a thing).

added it - good point.


text:
Do men have significant hormonal cycles?
I know there's a similar question here. But that discussion dissolved into lunar cycle and a correlation with it.  I want to find more towards the original question of is there a periodic hormone cycle in men.
The links i have read suggest that there's probably a daily one for sure. But few hint at monthly ones too.
 That link seems to have very shaky science, but my biology is too weak for me to find the actual studies. Anyone else with more informed opinions? Any studies tracking purely hormone levels in men over a period of couple of months/years?
[EDIT]
   I understand it's clear there are cycles within the day or around the 24-hr mark now. I still am looking for studies focusing on longer term cycles like week,months etc.

I found this -

Celec et al. (2003) Circatrigintan cycle of salivary testosterone in human male. Biological Rhythm Research 34: 305-315
Conclusion. We believe that this is the first study demonstrating the existence of circatrigintan and circavigintan rhythms of testosterone in human males. Our findings might have implications in human physiology and pathophysiology.

(circatrigintan = ~30 day period; circavigintan = ~20 day period
also:

Celec et al (2006) Infradian rhythmic variations of salivary estradiol and progesterone in healthy men Biological Rhythm Research 37: 37-44
Discussion. We believe that this is the first study to describe a 12-day (duodecimal) rhythm of salivary estradiol in men. This finding might be of importance for physiological and pathophysiological research though the pattern needs to be investigated in larger studies.

However these papers have not been widely cited so their significance is unclear. The citing articles do not lead to a body of literature on this topic.
Finally, the entire text of this book:

INTRODUCING BIOLOGICAL RHYTHMS A Primer on the Temporal Organization of Life,
with Implications for Health,Society,Reproduction and the Natural Environment
Willard L. Koukkari and Robert B. Sothern. (2006) Springer, New York.

is available here. There is a long discussion of infradian rhythms in men starting at page 273.

Short answer: yes.
Although clearly the infradian changes in steroid hormones in females are quite "obvious", other changes are less evident, but happen nonetheless in males as well as in females.
Most of the hormones produced by endocrine organs such as the hypothalamus (a region at the base of the brain) or the hypophisis are not secreted in a continuous manner but rather in pulses. The exact frequency/amplitude etc. of these pulses can be different depending on the species considered, but (as fare as we know) the undelying mechanism are fairly conserved.*
In general, you can find circadian (~24 h), ultradian (<24h) and infradian (>24h) rhythms.
For instance these graphs show the concentration of cortisol, aldosteron and renin in a man, showing a strong circadian rhythm.

From: Charloux et al. - Am J Physiol Endocrinol Metab 1999
You can see that on top of the circadian rhythm, an ultradian pulsatility (every ~2-3h) is also quite clear.
Another example is that of GH (growth hormone): here you see secretion of GH in an healthy women (top) and an healthy men (bottom)

From: van den Bergh et al. - J Clin Endocrinol Metab. 1996
Many other hormones show this type of rhythmicity in males, such as testosterone, LH, GnRH, and probably many other.
I am not aware of long term studies on this matter.

* Actually, the mechanisms underlying pulsatility are still poorly understood.

Thanks for the answer, though I was looking for some studies/answer focusing on (>24 hr) rhythms. Yours is still new information to me.

authors: Дмитро Попович


text:
Is pure (100% H20, (near to no) solutes) water toxic to living organisms?

Possible Duplicate:
Death because of distilled water consumption

I know about the effects and myths about drinking distilled and/or deionized water. I'm not asking about such substances.
I wonder if a semi-immediate effect of drinking, say 1L pure 100% H2O is deadly or harmful.
My intuition says yes: either the reverse osmosis effect also present in distilled water is amplified so much that critical systems shut down due to extremely low concentrations in the organs/cells/... or the reverse happens, where the water is absorbed into cells making them burst, leading to among other things (massive) internal bleeding.
I'm particularly interested in scientific studies (if any) that were done (link to publication would be very welcome, my Web of Knowledge search-fu doesn't seem to work for this subject).

I don't know much about this subject but here are a few links you might find helpful.
http://purchon.com/wordpress/biology/?page_id=173
http://www.sciforums.com/showthread.php?s=d463b981152a76c85345e9164df85b9e&t=55440&page=2

@Kevin: Close, but not quite. The commercially available distilled water is not pure enough for what I mean. Unfortunately, I am unable to find any decent "purity classification" other than this little table that forgets to mention any solute concentrations whatsoever.

The distilled water you find in a chemistry lab is pretty much as pure as it gets... For a classification see the Wikipedia purified water article. Even if you were to ask about perfectly pure water with no solutes whatsoever I don't see how the answer would be different from that of the other question.


text:
Why do only two sexes exist for animals?
Why, from the natural selection point of view, do only two sexes exist for animals?

What avantage would you see in more than 2 sexes?

Mushrooms have a lot of sexes. So where is the advantage for them?

Fungi have a completely different type of reproductive cycle when compared to vertebrates. For instance they often switch between haploid and diploid during their life cycle. To be honest I am not sure of what you consider "a lot of sexes" in mushrooms. Could you elaborate (my microbiology courses are very far away in time...)

The meaning of my comment is: If i can say that more then two sexes does not bring any advantage then i can ask: where is the advantage of having only two sex?

Having sexual reproduction has several advantage over asexual reproduction. Having 2 different genders (rather than 3 or 4) is the easiest way to have sexual reproduction. Which bring us to my original question: 2 genders (sexual reproduction) is better than 1 (asexual reproduction). What would be the advantage of 3 rather than 2?

His question is actually a big one in biology. Why is there sex at all? It seems obvious but it goes a lot deeper than you would think.

Chance. Evolving another gender is hard, especially if you are a large multi-cellular animal, losing a gender is easy. Single celled animals do sometimes have more than one sex however.

@nico The benefit is that if there are $n >1$ sexes, than it is possible to mate with $1 - \frac{1}{n}$ of the remaining population for any given individual -- this approaches 100% as $n$ goes to infinity. For $n = 2$ this is a measly 50%.

Is there evidence for this statement? "More than two would confer no further genetic benefit for either repair or diversity, and would likely introduce complexity and inefficiency." – kmm Sep 30 '15 at 2:37 Evidence? No. Just logical reasoning. – Anthony X Sep 30 '15 at 2:46
2 I don't think you can say whether or not additional sexes would be beneficial or not, without some theoretical or empirical basis. Just because a trait hasn't evolved, doesn't mean that it wouldn't be beneficial if it did (e.g., wheels). – kmm Sep 30 '15 at 12:15

@TinaGallant - Please do no re-port other users comments as "answers". They are here anyway and are not answering anything.

I've upvoted as I think this is a good question, but I would ask you to add some content to show that you've done some research into the purpose of sex and the systems used by other organisms beforehand.

I'm voting to close this question. It shows neither research on the subject or presents any arguments or explanation for their being a problem. It appears many people think there is a problem, but this is extremely broad. If they wish the question to remain open they should modify the question so that it is appropriate.

Good row of comments... E.g. "not sure of what you consider "a lot of sexes" in mushrooms" (not too many references there to). "Identy" seems to be the key. Horse and donkey may not  be identical enough for meiosis and their crossing over. Not the whole story: there is the male and female of the mule. Refering to mushrooms: if the mule had some, optional, non-sexual reproduction, and assuming not all gametes of horse and donky would suffice, would that correspond to "many sexes of funghi"?

To get a non-circular answer to why humans and other mammals have only two sexes, it's helpful to take a look at our evolutionary history.  While mammals possess several adaptations to a terrestrial life cycle, including internal fertilization and gestation, which require substantial anatomic specialization between males and females, these are all secondary features that evolved long after our aquatic ancestors had acquired two distinct sexes.
Indeed, if we look at animals like fish, which reproduce via external fertilization, it's not at all obvious why they might not have more than two sexes.  After all, for many aquatic animals, mating involves little more than the female and the male releasing their respective gametes into the water, where they meet and fuse to a form new zygote, which can then divide and grow into a new adult.  Seen that way, there seems to be no reason why there could not be more than two "mating types", as in many fungi, such that gametes of any two distinct types could fuse into zygote.
The answer lies in the fact that the male and female gametes aren't actually that similar: the female gametes, or eggs, are typically large cells that contain all the nutrients necessary for the new zygote to develop into a viable individual, whereas the male gametes, or sperm, are tiny and produced in huge numbers.  This asymmetry is known as anisogamy, and modeling its origin has been an important topic in the theoretical study of evolution.
Without going into details on the evolution of anisogamy, once it exists, it clearly forces the mating types to also split into two groups: there's no advantage in two microgametes (sperm) fusing, since the resulting zygote would lack the nutrients it needs to be viable, whereas the fusion of two macrogametes (eggs) would simply be inefficient — eggs, being large, are comparatively rare and expensive, and wasting two of them to produce only one offspring would be suboptimal even if the resulting zygote was viable.  Nor is there really room in such a scheme for gametes of intermediate size: they'd be too small to fuse into a viable zygote with sperm, but too large to be produced in sufficient amounts to be effective in fertilizing eggs.
Of course, there's nothing that would stop a single adult from producing both micro- and macrogametes, but such an adult would not really be a third sex — it would just be male and female at the same time, a mating strategy known as (simultaneous) hermaphroditism, which indeed occurs relatively often in nature.
So, if pretty much all animals are anisogamous, why do fungi remain isogamous (and often have multiple mating types), then?  Well, one explanation is that the main drivers for the evolution of anisogamy — sperm competition and transportation risk — don't really apply to fungi, which mate when two sessile haploid mycelia grow and come into contact with each other.  Since the gametes are not motile, there's no advantage for either/any sex to produce more of them (at the cost of smaller size) in order to increase the chance of successful mating.  Thus, isogamous mating works fine for the lifestyle of fungi, and having multiple mating types is then a useful adaptation to make successful mating between neighboring mycelia more likely.

@emanuele you seem to be asking why there are only 2 sexes for animals, in contrast to fungi which can have many sexes or maybe bacteria which have mobile sex - the ability to donate genetic information can be acquired or lost.
Some animals - worms and fish for instance are hemaphrodites - they can accept sperm or donate them to produce offspring. Fungi are even simpler - the mating is by haploid fusion on the cellular level, since they have single celled life cycles.  The mating type allows mating with any cell that is not of the same mating type.  Its just a matter of how much genome space you want to dedicate to mating and there can be 2 mating types of 10,000 mating types - the only rule is that you can't mate with your own mating type.  Its a simple mechanism to restrict mating with yourself - probably to encourage genetic diversity.
Physiologically, for single celled animals and simple egg layers like fish and worms, you can see why sexual roles might not need to be specialized; its a matter of which gamete you will deposit.  If the egg is no more than an especially fat cell, becoming male is not necessarily a big change.  But when eggs are more complicated structures or live birth becomes an adaptation, the expense of being the gamete donor (male) or recipient (female) becomes a significant commitment and changing roles is not so easy to do in an evolutionary system.
Ultimately, Unlike worms or snakes, committed females are specialized such that turning into a male, with the requisite development of a womb, changes in bone structure, etc is such an elaborate phenomenon that we don't observe it.

Sex reversal, however, is observed for example in fish (notably salmon)

"For animals and humans" -- do you mean mammals? (Snakes and worms are also animals.)

I think the OP is likely asking why mammals only have 2 sexes. This is quite different to asking why we don't spontaneously change sex (as you quite rightly point out, the physiological changes required are too much). But what you don't touch upon is why there are no examples of 3 sexes, for instance, in mammals (that I know of) - I think this would then be a very complete answer.

"Its a simple mechanism to restrict mating with yourself - probably to encourage genetic diversity." - Are there any animals known to exist as hermaphrodites only? Because: self-mating makes sense as an exception to a rule, the rule refering to a whole lot of very diverse ancestors being integrated in that only one, the one and only.

Richard Dawkins describes an elegant solution to the puzzle in his memorable Selfish Gene: in the beginning, all gametes were similar, and many sexes could coexist (like in fungus). But when some lineages began to specialize in different strategies (ESSs, Evolutionarily Stable Strategies), with some increasing and other decreasing the size of the gametes, then there was room for two sexes. Probably a third sex would only compete with one of the others, without space for niche drift, and thus one of them would usually become extinct, driving it back to two sexes again.

This answer focuses on the gametes being different or not. However, think of  donkeys and the horses. 4 sexes of one bastard? It's 2 x 2. Is that, roughly speaking,  the idea of Dawkins...? Can you cite? More comment: Key to me is "identity". Funnily, considering ordinal and cardinal numbers brings up that you end up in two, don't think twice: it's all "right to copy" as long you pay allegiance to the two, there are only two: the original and its copy. Just the two of us. The more you diverge from perfect identy, and what's the use of diploidity if you don't... ("donkeying by numbers")

The purpose of sexual reproduction is to combine the genetic material from the contributing parents to produce a new individual. That combination has the potential to replace genes which may be defective and generally increase diversity in the offspring, improving resistance to certain pathogens. Bottom line: sexual reproduction confers an evolutionary advantage.
Where it occurs, why only two sexes? Simply because two is sufficient to get the job done.
Consider the perspective of one "parent", and the goal to combine genetic material from some other source of the same species in order to produce an offspring having some blend of genetic material. If that "other source" was one randomly selected individual, how does an additional randomly selected source qualitatively change the result? By the principals of statistics, it doesn't. One other source containing some random variation is no more or less random than a combination of two or more such sources. Therefore, to meet the requirements of a random genetic shuffle, two sexes suffice.
If a third sex was required, then three individuals would have to play their respective roles for successful procreation, where only two are required for the two-sex system we understand. If you compare asexual reproduction with two-sex reproduction, you might wonder why asexual reproduction exists at all given the genetic benefits of sex. The answer is in simplicity. No need to find a partner. To go from two sexes to three, there would have to be a benefit to overwhelm or at least balance the added complexity of bringing three partners together instead of just two. As previously discussed, there isn't any. Even if a three-sex system just happened to occur, it would be out-competed by its simpler two-sex rivals.

Is there evidence for this statement? "More than two would confer no further genetic benefit for either repair or diversity, and would likely introduce complexity and inefficiency."

Evidence? No. Just logical reasoning.

I don't think you can say whether or not additional sexes would be beneficial or not, without some theoretical or empirical basis. Just because a trait hasn't evolved, doesn't mean that it wouldn't be beneficial if it did (e.g., wheels).

@kmm As I said in my answer, a third sex adds complexity. We all know how complex partner-seeking and relationships can be when only two sexes are involved. For a trinary sex system to survive, it would have to confer a benefit which would overwhelm the added challenges of fitting in the third "contributor". Since the primary purpose of two sexes is to shuffle genes, and a third contributor isn't going to introduce any more randomness than two is capable of, there's no room left for any benefit from a third component, so it would never survive.

@kmm Also, it's reasonable that in 3.5 billion years of evolution, terrestrial life ought to have had the chance to give a three-sex system a try. If it could succeed, we ought then to be able to find extant examples.


text:
Impact of Alan Turing's approach to morphogenesis
Shortly before his untimely passing, the computing pioneer Alan Turing published his most cited paper The Chemical Basis of Morphogenesis (1952).
The central question for Turing was: how does a spherically symmetric embryo develop into a non-spherically symmetric organism under the action of symmetry-preserving chemical diffusion of morphogens (as Turing calls them, an abstract term for arbitrary molecules relevant to development)? The insight that Turing made is that very small stochastic fluctuations in the chemical distribution can be amplified by diffusion to produce stable (i.e. not time varying except slow increases in intensity; although also potentially time-varying with 3 or more morphogens) patterns that break the spherical symmetry.
The theory is beautifully simple and abstract, and produces very important qualitative results (and also quantitative results through computer simulation, which unfortunately Turing did not get to fully explore). However, even in the definition Turing discusses some potential limitations such as ignoring mechanical factors, and the inability to explain preferences in handedness. The particular models he considers -- a cycle of discrete cells and a circular tissue -- do not seem particularly relevant. As far as I understand, the key feature is his observation of symmetry breaking through small stochastic noise and instability.
What was the most important contribution of Turing's paper to developmental biology? Is his approach still used, or has the field moved on to other models? If his approach is used, how was the handedness problem resolved?

our current understanding of plant morphogenesis seems close to this idea (and there's no problem of handedness). See my answer here.

You may want to look into work on how the first HOX genes trigger differentiation.

This is a very interesting question. Many people have researched this topic, and many still are. But regardless, I had never heard of Alan Turing's contributions, so thank you!
First of all, I cannot actually find who first coined the term morphogen. Though people had hypothesized that chemicals could play a critical role in development through much of the 20th century, I cannot actually find the first person to use morphogen. But the most important paper really came from a guy named Lewis Wolpert, who came up with the model of a gradient of morphogens leading to differential cell fates. The idea being that if some area of an embryo produces a morphogen at a very high concentration, then as you move away from that area, the concentration goes down. So if this morphogen is required at or above a certain threshold for activity, then only those cells with that concentration will have a certain cell fate, while at lower concentrations, the cells can become something different.
But this does not really answer your question. You are asking how a single cell, which is spherically symmetrical, can determine a particular axis. Though most organisms do this is in slightly different ways, the most common feature is that sperm entry point breaks the symmetry. The best way to explain this is to show you a diagram of Xenopus (frog) eggs.

Image from: http://studentreader.com/nieuwkoop-center/
The Xenopus egg, first of all, is inherently not spherically symmetrical. There is a black animal pole, and a white vegetal pole. The sperm can only enter a marrow region of the egg about 30˚ north of the animal/vegetal line. Upon fertilization, an event occurs where the pigmented areas turn toward the sperm entry point, leaving a gray crescent. Nearby the gray crescent, in the vegetal pole, a structure called the organiser develops. This organiser creates many of the morphogens that then pattern the rest of the embryo.
Researchers have studied this a lot in many different organisms, but a few things really remain constant: eggs are not exactly spherically symmetrical, and the sperm entry point provides asymmetry.

Thank you for the answer. Any thoughts on the issue of handed-ness? Because a sperm entry point would still leave the egg achiral.

May I ask you how can I find more information about this topic?

I would think this is very much still "used." 60 years later, we finally have the first experimental support for it:
In this blog article about this journal piece the authors studied the ridges that form on the roof of mouse mouths. They manipulated the signaling molecules that induce their formation and observed changes in line with Turing's theory. Of course, this doesn't preclude other mechanisms from occurring, but supports that of Turing.

Welcome to Bio.SE!  When linking to articles you should summarise the content in your answer in case the article isn't available in the future.

Thanks. It's not my field of biology (so I'm not an expert) but the authors studied the ridges that form on the roof of mouse mouths. They manipulated the signaling molecules that induce their formation and observed changes in line with Turing's theory. Of course, this doesn't preclude other mechanisms from occurring, but supports that of Turing.

While Turing did not include mechanical effects on the differentiaton/patterning in his seminal work, other researchers have expanded on that idea. These do not necessarily change the premises that led Turing to his conclusions, nor make his contribution less relevant today. Adding a dynamic component or mechanics to the substrate in which the diffusion-driven instabilities happen can simply yield more complicated solutions.
Clear examples of this interaction between the reaction-diffusion mechanism and the mechanics or boundary conditions can be found in several places: the formation of palatal ridges in the roof of the mouth in animals, teeth formation across species, bacterial colonies both natural and synthetic and even the issue of boundary conditions has been explored in animal coating patterns.
In the case of handedness, I think this also a question of symmetry breaking, such as with Turing patterns, but happening at different scale. Skeletal primordia are thought to be formed through a Turing-type mechanism. The "issue" with handedness would be that in Turing's formulation all fingers would be equal, but superimposing the patterning already created by the Spemman organizer which polarizes the hand, makes the fingers distinct. So, in essence, a prior symmetry breaking event (which could be caused by a different lateral inhibition process or diffusion-driven instability acting a larger scale) can modulate a downstream developmental process.

Turing patterning has had a large impact in systems biology understandings of morphogenesis. The general idea is that Turing mechanisms can be coupled with other mechanisms to build robust patterning methods.
So while not too many people would say that an entire mechanism is ONLY due to Turing patterning, a lot of regulatory networks can be understand as having the components allow for a Turing patterning mechanism (under certain parameter constraints), and thus they can understand "why" certain interactions exist and predict the behavior of perturbations. Usually there are multiple mechanisms involved in a patterning system so doing some knockouts will not get rid of patterning, but by disturbing the Turing mechanism you will many times see a decrease in the robustness of the patterning.
A lot of systems biology has focused on robustness: what kinds of network motifs allow for robust switch-like behavior? etc. The Turing mechanism is a network motif which allows for robust spatial behaviors.


text:
Do all plants photosynthesize with equal efficiency?
Just what the title states.
Given identical, necessary and favourable conditions (Probably nutrients, humidity, and light but what I mean is all necessary requirements are fulfilled) - Is photosynthesis equally efficient in terms of the amount of sugar/carbohydrates generated by all plants/trees, or are some plants/trees more adept at it?
My background in biology/botany is high-school, so my list of necessary requirements may be lacking for which I crave your indulgence

I think you would have to define the conditions. Even a single plant will vary in photosynthetic output over the course of a single day. Would maximal photosynthetic output be sufficient?

It should also be clarified how exactly you define efficiency. Photosynthesis on a molecular level is likely highly efficient because the pigments exploit a quantum mechanical property called quantum coherence. On a macroscopic level, looking at the overall organism, there must certainly be a range of efficiency when measuring incident photons relative to carbon fixation.

Define efficiency: carbon fixed per unit of what [h2o, nitrogen, light, CO2]? Any way you look at it, the answer will be "no".

@Kevin: Yes, assuming that maximal photosynthetic output refers to the quantity of food available after the process completes

Zhu et al, 2008 provide a review titled "What is the maximum efﬁciency with which photosynthesis can
convert solar energy into biomass?" in the Journal Current Opinion in Biotechnology.

@David that's an excellent paper.

If you mean the efficiency at which plants convert light energy to chemical energy (in sugar or other reduced C compounds) then there is definitely variability between plants, both at the species and individual level. The photosynthetic efficiency WP page gives ranges of between 0.1 and 8% of total solar radiation converted to "biomass", but these values are not cited. In their review, (Zhu et al, 2008) state that the maximum maximum efﬁciency with which photosynthesis can convert solar energy into biomass is 3.5% and 4.3% for C3 and C4 plants (both observed for crops), respectively. Biomass is not a measure of energy, but perhaps they mean potential chemical energy in that biomass.
Its a pretty complicated question though. Photosynthesis is a complex process involving many interdependent chemical reactions and physical processes. All species (or even individuals) of plants have different morphology, physiology, and biochemistry that influences overall photosynthetic efficiency. In addition, they each inhabit different ecological niches and climate space. Therefore, all species or individuals would have a slightly unique maximum potential efficiency. Here are a couple other efficiency related concepts to consider:
There are 2 systems in photosynthesis that work in tandem, the light reaction and the dark reaction.  The light reaction uses light energy, pigments like chlorophyll, and a bunch of electron transport chain proteins to generate ATP and NADPH. These 2 molecules then provide the reducing power for use in the dark reaction (the Calvin Cycle). In the dark reaction, the enzyme RuBisCO joins CO2 and RuBP, creating simple reduced carbon chains which are then used to assemble sugars. This is an over-simplification, as both reactions are very complex systems with lots of biochemical machinery, but this is the basic process used to convert light energy to chemical energy. To operate at peak efficiency, the entire process must not be limited by incoming energy (light), substrate supply (CO2, RuBP), or nutrients used to construct all the needed cellular and molecular machinery (N, P, K, and many others). In reality, there are limits that vary from plant to plant, species to species. For example, a species or individual with a very reflective leaf surface converts less of the light reaching the leaf surface to chemical energy, thus lowering the output of ATP and NADPH. This reduces the chemical energy supplied to the dark reaction and limits the amount of carbon fixed by RuBisCO. So the reflective surface of the leaf, which might be advantageous to the plant in other ways, has a large impact on overall photosynthetic efficiency (compared to a less reflective leaf or leaves).
If you want to search for more information, there are a number of terms that plant physiologists and ecologists use when describing a plant's (or communities of plants) photosynthetic efficiency. Each of these is used in different ways and can have many variations in units.

Light use efficiency: The amount of carbon fixed per unit of light incident.
Water use efficiency: The amount of carbon fixed per unit of water transpired
Nutrient use efficiency: The amount of carbon fixed per unit of nutrient concentration (usually in leaves).

reference:
Zhu, Ort, and Long 2008 "What is the maximum efﬁciency with which photosynthesis can
convert solar energy into biomass?" Current Opinion in Biotechnology.

According to Zhu et al,, 2008 the maximum observed conversion of photosynthetic energy to biomass is 6% at 30C. I am not sure why there is a discrepancy, but Wikipedia has no citation nor reference temperature and Zhu et al do not consider CAM plants or algae.

Great reference that I wish I had seen before posting. If I'm reading it right, the 4.6 and 6% figures are theoretical. They give the highest observed efficiencies as 3.4 and 4.3% (C3 and C4 respectively), so values in the WP article are very high.

Yep, you are correct, I read a good bit of the article, but when it came to writing down the numbers I just grabbed them from the Abstract where they are called "maximum
conversion efficiency of solar energy to biomass", in the text they explain that this is the theoretical max. The numbers you give are short term max reported values (for the record, the C3 value is 3.5%, second line of p 157). I changed your answer.