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Is the SRY gene the sole responsible of biological male sex?
It's very well known that the Y chromosome is what determines maleness, but more specifically this seems to happen thanks to the SRY gene located on it. Some individuals have an XX karyotype, but because of unequal crossing-over between X and Y chromosomes during meiosis in the father, one of the X chromosomes ends up containing the SRY gene, and the individual develops into a male (De La Chapelle Syndrome).
So I was wondering, is the SRY gene all that's really needed for an individual to be, unquestionably, a male? It's kinda odd how XX males have male genitalia but are classified as intersex solely because their karyotype is a typical feminine one (which should be irrelevant given how they also possess the SRY gene).

No. The SRY gene is an RNA inhibitor gene. If its target is altered to not match, you get an XY female.

To my knowledge, the SRY gene is the only gene that cause variance in sex determination in humans. Of course, many genes are then involved in sex determination cascade but none these genes have variance in humans. Because environmental variance has no impact on gene determination in humans (to my knowledge and despite a few highly criticized articles) and therefore, nothing else than the SRY gene explains the sex determination.
The genes that are involved in the cascade of sex determination are not necessarily on the sexual chromosomes. On the Y chromosome, there are some genes that are male beneficial (beneficial for the male function) but these genes are not involved in the sex determining system.
In all species, the sex is determined by the environment and/or the genes. The best way to look at it is by reaction norms. On the below picture, think of the x-axis as being the temperature. Then, if you ask the question "Does the temperature influence the probability to develop into one sex or another?" One should answer. "It depends on the range of temperature you're looking at!" If you look at only very high temperature (far right) or very low temperature (far left), only the genotype explains the sex determination. If you look at mid-range of temperature, then both the genotype and the environment determines the sex.

N. Perrin and L. Beukeboom are writing what is probably going to be a very good book that will obviously interest you. I think the book is going to be publish in 2014 only. Here is the amazon link to pre-command it.

Check out this recent article in Science (AOP).
They say that two genes- Sry and Eif2s3y are sufficient to provide the entire functionality of the Y chromosome. Alhough, there is reduced number of spermatids in these mice (Genotype :XO-Sry-Eif2s3y), the viable ones are able to give rise to healthy offsprings.

The question did not have to do with male functionalities but with sex determination system. What matters for this question are the loci which variance bring some variance in sex determination.

read the article.. it is quite interesting.. what it says is that two genes can suffice for the entire Y chromosome (in the process of sex determination and also to retain the ability to reproduce).

From what I read of the abstract, it doesn't seem that the gene Eif2s3y has some polymorphism in nature. Therefore, this gene does not influence the variance in sex determination. But when I read the OP's question again, I realize that I might have misunderstood his point. This article seem very interesting indeed and might answer to OP's question.


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Are these cats calico?
Calico cats are cats that have 3 fur colors and are always female or males two X chromosomes.
I've seen many cats that will have 2 fur colors (one of them is usually white) and another, third, color which is a darker shade of one of the other colors. As exampled in the pictures below (taken from the internet). Are those considered Calico cats?

(source: mirror.co.uk)

I don't know much about calico cats, but from those pictures nobody can tell you for sure if they are female. One of the upper two closely resembles a male (and fertile) cat I know.

The relation to female was only through Calico cats. I don't really care about their gender.

I'd say, those could as well be normal tabby cats. Calicos are more often those with big brown and black patches on white. Or at least they have a distinctive amount of visible bright brown in their coat.

@skymninge, are tabby cats considered to be Calicos, and can they be of both genders?

Tabby is just another name for the color. Like Calico, it is not a breed. http://en.wikipedia.org/wiki/Tabby_cat Some Calicos could also said to be tabbys. Like Calicos, they can be of both genders. (It's just that most calicos are female, not all of them.)

they don't look like calicos to me. their patches don't form as stripes really.

We call this a White Calico with Tabby patches in my area.

I think you are misunderstanding "color" here. When applied to cats, it doesn't literally mean a color shade as used in color theory, but "coat color" which can in fact also be a "coat pattern".
The cats above are two-colored, not three-colored. One color is white. The other color is what is called "tabby" in English and is a pattern of dark spots arranged in regular stripes on a lighter background. These spots are not considered a third color in cats.

This is a calico cat. Her three coat colors are white, orange, and grey tabby. See how the orange and grey are irregularly interspersed, this is the pattern of paternal and maternal chromosome expression on her body. Again, the grey and black patches within the tabby part are regularly placed. They don't make two separate colors, grey and black, but a single coat coloring, grey tabby. There are also other color combinations in calico cats, for example white-orange-black, and they are more straightforward to recognize.

note two patterns is quite common in cats as some coat color genes can be affected by temprature.

Tortoiseshell cats (which is the normal name for Calico style cats in Europe) arise due to a gene on the X chromosome. Some patches are ginger, and some tabby due to the deactivation of one X chromosome in each cell at an early stage of development. This produces a tortoiseshell-like pattern.
What you see in these tabby cats with the white colouring is due to temperature dependence, this gives the patterning on the feet/nose etc. Tortoiseshell cats looks quite different, where the different coloured patches of fur are random.

Adding to this massively late, but while the cats in the first pictures are "just" black tabbies with minor white spotting, the cat in the second picture may actually be a diluted caliby! A diluted caliby (calico-tabby) is a black, orange and white cat with a tabby gene and a double dilution gene! This makes them a blue, cream and white tabby, shortly known as caliby. Unless the light is playing tricks on me, you can see a cream-colored patch on her right cheek that indicates the presence of ginger/cream.
As almost all cats that possess both a black and a ginger color are female, with only very rare exceptions, the second cat in this case would likely be female. Note that the color white is not a sex-linked color and does not indicate any gender! Important is the presence of both a black-based and a ginger-based color!
And a tiny crash course on the cats in the first picture: To tell the true color of a tabby cat, look at the stripes, especially at the tail tip. You can see their base color is clearly black, whereas the rest of their body has various shades of black due to the agouti gene, which gives each individual hair little stripes and creates the tabby pattern through that! If the cat is a torbie (tortoiseshell tabby, black + orange tabby) you will notice patches where the stripes are ginger instead of black.

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Is it safe to look at infrared LEDs?
What happens if one looks directly at infrared LEDs? Sometimes I see this kind of LED at night as red dots and I'm also courious about it.
I was wondering what would happen if one looks directly to these LEDs, because we see them everywhere like in remote controls, CCTV cameras, sensors, etc.
What is the difference between infrared and visible light to our eyes?
(I mean why is it impossible to look directly to visible light while we can look to infrared?)

LED: Light-emitting diode

Infrared wavelengths are EM waves of longer wavelengths than visible light. Also, visible waves are more energetic than IR waves.
Because of this, Visible light has the ability to excite organic receptor molecules in our eyes called Rods and Cones. These molecules stimulate cell responses and in turn excite cell responses in our nerves called an Action Response. Still unclear to most scientists is how the brain composes these action responses into an image, though a great deal of research is being done to date.
The reason why "nothing happens" when we aim infrared lights into our eyes (which I still wouldn't suggest) is that the photoreceptor molecules that we use to see don't have the necessary bonding configuration to accept the energy from these impinging EM waves.
 However, don't go thinking that nothing happens. Infrared radiation is a type of radiation that is usually a measurable heat source. IR is one of the broader parts of the EM spectrum. My point is to say, that when you "radiate" some thing with an IR source:
1) You don't know if it is also radiating other EM waves unless you know the specs.
2) You're still exciting molecules with that energy even if it isn't causing a seen effect. I highly doubt anything will happen unless you have a very high powered IR source. You shouldn't really ever focus high power lasers of any source onto your body, because higher intensities could inflict damage.

To Learn more about IR radiation:
http://coolcosmos.ipac.caltech.edu/cosmic_classroom/ask_astronomer/faq/radiation.shtml
IR (InfraRed)
EM (ElectroMagnetic)

I was aware that it's not a good idea to aim a source or IR directly to the eyes. Sometimes I see in the street CFTV cameras at night and I can clearly see the IR LEDs as red dots, how could this happen as IR is not seen?

As I mentioned, You never know if a source is only radiating one wavelength. The red exists because those "IR LEDs" also have radiation that is in the visible spectrum.  Red (visible) light is closest to IR radiation in the EM spectrum.  See the spectrum here. This only applies for radiation that is being emitted not detected. http://www.pion.cz/_sites/pion/upload/images/a14cf10a5583d19f7cfdebd63cf64382_electromagnetic-spectrum.png

Wait, wait wait wait. Those CFTV camera's have a red light only to let you know that it's recording...The outgoing red light has nothing to do with the light that is being absorbed, aka the IR light. The IR light for the camera is generated from your body, as thermal radiation.

I added a picture of the IR LEDs as I mentioned in the comments to better illustrate the question. The red dots aren't of the LED that indicates that the device is powered on.

This is an old question, but those IR LEDs are actually Near IR, just below the visible light cutoff. The ones that make a faint visible red are probably around 800 nm. There are others around 900 nm that don't make any visible light.

Hi, I work with desktop devices that features IR audio distribution. I am supposed to keep the devices in front of me, such that the 4 ir emitters used for audio distribution is in direct contact towards my face, neck and shoulder. The problem is, after this project, i am sometimes feeling itching feeling in my one eyes as long as i am sitting with this device. Can you advise on this ?

here's a similar question. some studies say that it may cause cataracts if you see enough of them, also the eye may receive a lot of a wavelength while dilated. that's a technical thing about sunglasses, if a sunglass dilates your pupil but IR flashes through the seams, technically it's not perfect. Could there be any effects from low powered infrared being used to track eye movements long term?

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On the definition of gDCW (gram dry cell weight)
I need some clarification on the concept of gram dry cell weight.
The unit acronym gDCW stands for gram dry cell weight. My interpretation is that 1 gDCW is equivalent to 1 gram of dry cells, but I am not sure. Is this accurate?
For example, the dry cell weight of mouse cells is roughly 300 pico grams. Therefore, in this case, one gram of dry mouse cells contains $10^{12}/300$ mouse cells (1 picogram $=10^{-12}$ grams). And if one says that there are 0.6 mmol of alanine per gDCW of mouse cells, this means that the total alanine content of $10^{12}/300$ mouse cells is 0.6 mmol. Is this accurate?


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

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

Question

"What examples of group-selection are there?"

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

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

Forward Example (trait whose presence benefits the group)

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

Reverse Example (trait whose absence benefits the group)

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

Links

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Shigeta, we are still eagerly waiting :)


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Sodium levels and blood pressure

Why does low Na+ levels cause hypotension (low blood pressure).
  Alternatively, why does excessive intake of Na+ cause
  hypertension or high blood pressure?

From what I understand, there are two different mechanisms at play. Renin secretion from kidneys occur during low salt levels in blood and hence, under low sodium concentration, high amount of Renin secretion from kidneys should actually raise the blood pressure, via the Renin-Angiotensin loop, constricting the arteries. Under high sodium concentrations, low renin secretion should be accompanied by low pressure. If the osmotic entry of water into blood raising the blood volume and thus pressure, plays a role here, will not, on increase of blood volume, decreased Vasopressin increase urinary output and thus control the blood volume, not allowing it to cause any body changes? Why isn't the first effect (renin) significant here as compared to the second (osmotic entry).

Renin angiotensin is for regaining homeostasis. If you have lost salts, blood pressure and blood volume will decrease due to loss of fluids. But the renin angiotensin mechanism will try to undo this by stimulating uptake of Na and water.But still, they can not fully compensate for loss of Na , INTAKE of Na is NECESSARY.

By the way, the main stimulus for triggering renin angiotensin is Blood volume and pressure rather than Osmolarity of blood. In conditions like hemorrhage where blood loss occurs but there is no change in osmolarity, Renin-Angiotensin will still respond ( but ADH(vasopressin) will not as ADH responds only to change in osmolarity.)

@biogirl Thank you. This helped to a considerable extent. :)

I think it will help you a lot if you read these topics from Tortora and Derrickson or other physiology books.

Renin angiotensin is for regaining homeostasis. If you have lost salts, blood pressure and blood volume will decrease due to loss of fluids. But the renin angiotensin mechanism will try to undo this by stimulating uptake of Na+ and water. But still, they can not fully compensate for loss of Na+, INTAKE of Na+ is NECESSARY.
By the way, the main stimulus for triggering renin angiotensin is Blood volume and pressure rather than Osmolarity of blood. In conditions like hemorrhage where blood loss occurs but there is no change in osmolarity, Renin-Angiotensin will still respond (but ADH(vasopressin) will not as ADH responds only to change in osmolarity.)     —  biogirl


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Excretion of various wastes and water requirement
A common fact is that Ammonia, Urea and Uric acid are the most common excreted metabolites and their removal needs varying amount of water, highest for ammonia (hence suited only for aquatic animals) and lowest for uric acid (suited for desert animals). Why is this so? Is it because of different solubility of these compounds in water or their toxicity? If it is the latter, how would excess water reduce the toxicity of a compound? This is a bit over-simplistic question, but I want to understand the tradeoffs involved in selecting the mode of excretion, ammonotelic, ureotelic, uricotelic.

you can also look at it in a molecular point of view.. Uric acid has more atoms of nitrogen (4) per mole; then comes urea (2) and then ammonia (1)

Ammonia is more water soluble and also more toxic than either urea or uric acid but it is energetically less expensive. So, in regions where deficiency of water is not a problem, ammonia is an excretory product. Where water is scarce urea or uric acid is the excretory product but it is energetically more expensive to manufacture them. So, you can see an obvious trade off between energy expenditure and water conservation.
You can refer to any introductory biology book like campbell for further reading.
UPDATE :
Ammonia    : Most toxic , Easily Soluble , Less Energy Requirement
Urea       :Moderately toxic , Moderately soluble , More energy requirement(As needed to be processed from ammonia
Uric Acid:Least toxic , Least soluble , Highest energy requirement ( As needed to be processed from ammonia )
It is obvious now what tradeoffs are involved.
The only tradeoff not deducible from above is that of the eggs/youngs. In birds, eggs are not permeable for water so the best option is to excrete waste in form of uric acid so that high concentration of waste does not build up. Uric acid is excreted in form of solid palette which can stay in the egg without any harm.
We can also think of tadpoles which live exclusively in water and so they excrete ammonia but the frogs live both in land and water and so while on land they excrete urea as dessication is the main problem there.

it would be nice if you provide some references (or explain a little bit).

This was helpful, and settles the tradeoffs part. But, Can you elaborate on why ammonia is the most toxic, and uric acid the least?

@satwik pasani Well, I asked this here at stack exchange but couldn't get an answer.

By the way, I do remember reading about ammonia toxicity in Lehninger biochemistry. I will try finding more about it !

One more thing, I haven't ever even thought about  why  uric acid is less toxic. Interesting question ! Will search it out.


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Punnett Square Help
In fruit flies, red eyes are dominant over white eyes. Show a cross between two white-eye fruit flies.
My question is...
How do I know if the white-eye fruit flies are homozygous or heterozygous?

This looks like a homework question, you should take a look at the policy on asking homework questions - it is important to demonstrate an attempt at an answer and make sure it is tagged as homework http://meta.biology.stackexchange.com/questions/266/homework-policy-for-faq

Just to add an extended perspective to all of the answers submitted so far.
The classic white-eye phenotype in Drosophila is associated with a gene, white (or w) that is carried on the X chromosome (females XX, males XY) i.e. it is a sex-linked phenotype. Male white-eyed flies are therefore technically not homozygous, they are hemizygous since they only have one X chromosome and thus one copy of the gene.
There are other white-eyed phenotypes due to segregation of two genes (brown and scarlet) - this is the standard two-factor cross example in many genetics courses. In this case (no sex linkage is involved) a white-eyed fly is homozygous for the recessive allele at both loci.

In order for any recessive trait to be expressed, it must be homozygous for that recessive trait. If an individual was heterozygous, the recessive allele would be masked by the dominant allele, giving it the dominant phenotype.
Therefore, since white eyes are recessive, fruit flies with white eyes will always be homozygous (aa) for that recessive trait. A fruit fly that is heterozygous (Aa) for this trait would have red eyes.

In fruit flies, red eyes are dominant over white eyes.

Red is dominant (A) which means we can deduce that white is recessive (a). Therefore AA individuals are red eye, and so to are Aa because the dominant red allele overrides the white recessive allele. Then the only way a fly can be white eyed is with aa.

Show a cross between two white-eye fruit flies.

Both white eyed flies are aa so all four possible outcomes are aa in a single locus punnet square.

Because red is dominant over white, in order for the flies to express the recessive white eye trait they must be homozygous for the recessive white allele - I.e (no pun intended) rr.

If the question allows you to assume that eye-colour is a typical gene with two alleles, then we can figure out the answer. If flies' eye-colour has two alleles - dominant and recessive - then the phenotype will be dominant (red - A) or recessive (white - a). Dominant traits need only one dominant allele, so the genotype can be Aa or AA. The only other combination is aa, and that codes for the recessive phenotype of white eyes. There can be no heterozygous white eyed fly.

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How HIV Affects and Its Treatment using Combination Therapy
Can someone please help me with the following questions. I've written my specific questions right after the text question.

Human immunodeficiency virus (HIV) is a retrovirus. Its genome is a single (+) stranded RNA that is packaged with the reverse transcriptase enzyme within a protein capsid. This is further packaged into an envelope that is derived from the plasma membrane of the host cell in which the virus had replicated. The surface of the envelope is covered with the envelope glycoprotein, called gp120 & gp41.
a) HIV specifically infects the T-helper (TH) cells of the human immune system. If the HIV enters the host cell by means of host receptor recognizing a viral protein, what would be the most likely ligand and its corresponding receptor during HIV infection?
b) Some individuals are resistant to HIV infection even after repeated exposure. Assuming that these individuals express a normal level of the functional receptor that you have recognized above, how can you explain their resistance to HIV?
c) In recent years, therapies have been developed to fight AIDS using nucleotide analogs. The drug used to combat AIDS is Azidothymine (AZT). The structure of AZT is very similar to thymidine except that in AZT, the 3’-OH group on the deoxyribose sugar is replaced by an azido (N3) group. Which process of the life cycle of HIV do you think is inhibited by AZT?
d) Combination therapy is the new treatment strategy for treating HIV patients.
i. Why is combination therapy more successful in preventing the emergence of the disease resistant clones?
ii. If the combination therapy involves a drug that prevents…
1) HIV binding to the target cell, what protein does this target?
2) Integration of HIV genome into host cell genome, what protein does this target?
3) The cleaving of viral polypeptide into individual proteins, what protein does this target?
e) If the AIDS patient were given combination therapy, would the patient still be able to transmit the HIV virus to his/ her partner (Yes/ No)? Explain your choice.
**
a) No idea.
b) Maybe their T-helper cells have some sort of mutation that makes it impossible for HIV to bind to them?
c) I'm thinking "formation of HIV RNA" because in the absence of 3' -OH bonds, phosphodiester bonds cannot form.
d)
    i. It kind of makes sense because a virus being resistant to multiple drugs would be very unlikely but maybe there's some definite reason why?
ii. No clue. Is this talking about proteins of the virus or of the host? Also, enzymes are also proteins, right?

Is this a homework question? If so, use the tag.

a) HIV uses a certain receptor that's expressed widely on T helper cells. As this is homework I suggest looking at the wikipedia article to look this up for yourself. It is under tropism.
b) You mentioned mutation. That's very true but this question is excluding people with that mutation called the delta 32 mutation. Thus HIV can infect these people, but what happens to any virus in the context of infection? How does the human body deal with viral infections. Is there any variation that would account for why some people can be resistant to HIV and others not be?
c) Yes! Well done :) You're thinking along the right lines. Look up the drug on wikipedia and look up it's mechanism.
d) i) Yeah exactly that. But more than that. There's optimal HIV which in the absence of drugs does the best job at infecting. If we give a drug then HIV has to mutate away from optimal HIV to stay alive, but it's weaker. Give multiple drugs and it can't mutate away from all of them because if it did it would be so far from optimal it would be a rubbish virus.
ii) 1) It could affect the HIV binding receptor protein or the protein with which it binds on the host cell. So both! Logic would dictate we would use self receptor blockade because at least they're more conserved but I'm sure both are probably used. Enzymes and receptors are both proteins.
2 + 3) Look up the lifecycle of HIV
e) Theoretically possible. He might not take the drugs. If he takes the drugs unlikely because the virus basically becomes undetectable. Look this up, it should be on wikipedia again.


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Epinephrine vs. Adrenaline
Both names are widely used, with what appears to me as a slight prevalence of “epinephrine” in scientific literature and an overwhelming prevalence of “adrenaline” in popular media.
Are there any well-documented and/or well-motivated guidelines for the usage of these terms?

epinephrine is common in medical practice.. in general biology the molecule is usually referred to as adrenaline. and the receptors are also called adrenergic receptors.

@WYSIWYG epinephrine is certainly common in American medical practice, it's not universal across the entire profession however.

AFAIK, they're the same molecule, so the nomenclature is interchangeable. Despite the answer by @TheChymera, I see Epinephrine used more often nowadays in publications.

Apparently I asked too soon. Summarizing my recent findings, I conclude that adrenaline is the better term.
To be more explicit, here is why:

The US National Library of Medicine recommends “epinephrine”, this is however mainly due to historical reasons (adrenaline used to be a trademark name in the USA).
This quite comprehensive paper on the issue presents a series of arguments for the use of “adrenaline”. These include: Better compatibility with other languages (where epinephrine is not at all in use); Better integration with other biological terms (adrenergic receptors, adrenal gland, adrenectomy, etc.); Better historical accuracy (epinephrine used to be the name for a neurochemically inactive crude extract from the adrenal glands).

I find the arguments of the referenced publication convincing, though I would recomend you read them in full.

Epinephrine and norepinephrine is used in the US mainly. This is where the term epi-pen comes from. Everywhere else we tend to use Adrenaline and noradrenaline. Epinephrine is typically only used in literature arising from the US or US English speaking countries. In most countries they use adrenaline and also include Epinephrine so our American cousins don't miss our publications. Adrenaline is the better term as it is more widely understood by scientists, health professionals and the public. However at the end of the day they're the same thing.


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

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

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

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

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

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


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Is there a limit to acceptable brightness for plants?
Can overly bright artificial light harm plants? Is it possible to achieve a level of brightness so high that it does more harm than good to plants?
If sunlight can be filtered of infrared light spectrum, so the plants don't burn from high temperature, but if it's possible, then that too.

Have you done any initial research/litterature searches? If so, it is useful if you post this info.

The wikipedia page on photosynthetic efficiency has some useful insight here:

Photosynthesis increases linearly with light intensity at low intensity, but at higher intensity this is no longer the case. Above about 10,000 lux or ~100 watts/square meter the rate no longer increases. Thus, most plants can only utilize ~10% of full mid-day sunlight intensity. (5)

and

If photosynthesis is inefficient, excess light energy must be dissipated to avoid damaging the photosynthetic apparatus. Energy can be dissipated as heat (non-photochemical quenching), or emitted as chlorophyll fluorescence.

So, briefly, yes. Too much light can harm plants.
To answer the second question: yes, there exist filters for a large variety of wavelengths of light. You could certainly filter out infrared light, just as most sunglasses filter out some UV light wavelengths. However, just filtering out infrared light would not filter out all photons that could cause damage; likewise, all wavelengths of light have the capacity to heat up what they hit, not just infrared wavelengths.


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

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

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

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

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

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

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

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

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


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Why don't we have more cone cells (bigger fovea)?
Background
Apart from being able to sense color, cone cells are able to perceive finer detail and more rapid changes in images, because their response times to stimuli are faster than those of rods.
The fovea centralis is where cone cells are most concentrated and is responsible for sharp central vision (foveal vision), which is necessary in humans for reading, driving, and any activity where visual detail is of primary importance.
Question
It is hard to imagine what it would be like to be missing the fovea centralis, and even harder to imagine what it would be like to have one the size of the entire retina! In any case it seems that having a bigger fovea centralis would be beneficial for survival, so why do we have so much peripheral vision?

Fovea has very high resolution , color vision but low light sensitivity. So, if we consider the fact that most mammals are nocturnal doesn't this make sense ?

See this

We use central vision for a lot more things today than in the past. Peripheral vision is most important in navigation, so those who lose their central field retain the ability to navigate around objects. It is important that this is fast and sensitive in the dark as well as light. It isn't important for it to be in colour; this would mean it would be less sensitive in the dark and colour isn't important in navigation and also it would take longer. Navigation is of vital importance as it can be the difference between survival or death in the flight or fight response. Similarly it is important in the fight part, being able to see a foe.
Let's our foveas were bigger, well we would lose the above. What would we gain? The ability to see more at full resolution and colour. It's impossible for us to concentrate on more than we can see in our central field already. in fact we dart our gaze around to focus on many things because we can't focus on multiple things at once. By this I mean thinking about what we see not processing it. Of course we would also require a much larger brain to be able to process it all, processing the central field takes a lot of brain matter.
So in conclusion, it's not helpful.


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Does avocado and orange have a common ancestor?
While I'm eating my orange, I felt as if I was eating avocado. It might be genetic manipulations perhaps but it made me think if they have a common evolutionary ancestor. Is there?

Yes, they have a common ancestor just like any other living things! Here is a website that presents very accuerately the tree of life: http://tolweb.org/tree/

Actually, what I tried to ask was that if they have a relationship as humans and chimpanzees do. Should I said "close"?

Yes saying "How closely related are they?", "when lived the common ancester of.." or "when did the speciation between the two lineages occur?". But, of course I clearly understood what you meant in your question.

Here is a website that presents very accuerately the tree of life: tolweb.org/tree
Yes, they have a common ancestor just like any other living things! How closely related are they?
Both species are:

Eukaryotes (cells with a nucleus)
Archaeplastidae (plants)
Angiosperms (flowering plants)

Then, they split their way! Here is the tolweb.org page that correspond to this speciation: http://tolweb.org/Angiosperms/20646
The avocado is in the Laurales family: http://tolweb.org/Laurales/20672
The orange is in the Rutacea (sapindales, rosids, eudicots) family: http://tolweb.org/Sapindales/21051.
You can use the left arrow on the tree of these pages to come back through times and see the different speciation event that seperate both species.
While the orange is a eudicots, the avocado is part of the magnolids. The oldest fossil records of an angiosperm lived about 132MYA (see Crane et al., 2004). So the two species diverge for quite a long time! In order to give a comparison, they are as distant than humans and rabbits (it is a rough personal estimation, I don't have any reference for that!)
Note: The orange is called Citrus sinensis in latin. The species originated in China. The avocado is called Persea americana and it originated in central american (as their names indicate).
I don't know what make you feel that they are closely related. Maybe someone might say some words about their chemical compounds (and their flavour) but at first glance these two fruits taste very differently to me. Or maybe they have some remarkably similar phenotypic traits due to convergence evolution... I don't quite know about that!

As a supplement to your answer, here's link to a more user-friendly resource TimeTree: http://www.timetree.org/index.php?found_taxon_a=2711%7Corange&found_taxon_b=3435%7Cavocado&action=


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Cancer history on environment-cancer relationship
I am interested to know how environment-cancer relationship knowledge has developed.
I know that all began when Muller first proved that mutation could be induced via ionizing radiation, X rays in the case, and hypothesized for the first time the role that this could have on carcinogenesis. Do you know further data and the main or most significant events that leaded from that point until the current state of the art? (like when smoking and cancer were proved related)
(all factors enhancing risk would be included in the query, as human behavioral aspects (such as diet), work environment...)

Actually, "soot wart" was identified by Percival Pott in 1775. It is the first reported occupational cancer (it is a squamous cell carcinoma of the skin of the scrotum). It was shown in 1922 that an active ingredient of coal soot was a carcinogen. I'm not sure of an expansive, technical text on environmental cancers, but you may want to check out
"The Emperor of All Maladies: A Biography of Cancer" which covers the origins of man's understanding of cancer starting with the ancient Greeks, progressing to mention Percival Pott, and then moving on to modern day science and medicine. This book won the Pulitzer in nonfiction a few years ago and is well worth your time.


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Why and how does complexity usually tend to increase through time?
The question of complexity is classic in the very first lectures of evolutionary biology where the teacher usually tries to tell the students that complexity does not necessarily increase and that humans are not more complex than other organisms.
My questions are:

Why does complexity tend to increase through evolutionary time?
What are the different hypotheses to explain this pattern?

When writing "Mass extinction" on google image, we find many graphs displaying the number of families (or other taxa) through evolutionary times with the five mass extinctions. What would it look like to draw such graph replacing the family richness in the y-axis by :

Mean complexity among all living things?
Complexity of the most complex taxon?

I suppose that anyone who wishes to answer to this post will necessarily need to define the words "complexity". He or she might define it in terms of number of genes, number of metabolic pathways, length of DNA sequence, number of cell types, some kind of index taken from information theory. When asking my questions I had in mind a definition close to "number of genes" or "number of metabolic pathways".

I'm not putting this as an answer because I have no references, if I find any we'll see. I can see two reasons why complexity would increase in evolution (not the only two possibilities mind). 1) Plain diffusion: as life diversifies a range of complexity develops, and since life started at the lower bound the upper bound can only go up. And 2) the environment is complex, being able to act in specific ways in specific circumstances can promote survival, complex behavior means complex structure, so complexity is adaptive in some(many) cases, so evolution will promote complexity in those cases.

Having posted that I'm not convinced "complexity" as defined by "number of genes" or "number of metabolic pathways" HAS increased that much since, say, the Cambrian. "Number of genes" is probably capped by mechanisms like Müller's Ratchet anyway, and most of the ways around that haven't changed since Eukaryotes became a thing. We all know how potatoes have more genes than humans and such trivia. Metabolic pathways might be another story depending on how it's defined (C4 does date from the Oligocene), but what we perceive as "complexity" in Eukaryotes isn't about metabolic pathways.

I have just putted a revised edition to the answer of your question but I fear you (biologists) may take it to be "too philosophical" for you people so I will put it simply here-the reason (the answer to question why) complexity is increasing is the more complex organisms inhabit an ecosystem the more niches for ever more complex organisms they create and the mechanism of complexity increase (the answer to the question how) is the drive of these new complex organism to adapt to the new niches provided by the previous complex organisms. How is this answer?

@Yordan Yordanov, This answer, like many like it, insufficiently answers the question.  It's basically saying the 'need' or 'benefit' of more complexity creates more complexity.  This isn't a valid mechanism.  The 'benefit' of my smart phone being smarter does not explain the mechanism for making it smarter.  I feel a better answer needs to be given.

I think I can understand your point. You're referring to my second point the answer to the question how, right? I think everybody can agree on the first point the answer to the question why is it provides self-sustaining process-more complex organisms make more niches for other more complex organisms and it is this organisms-ecosystem interaction which causes the proliferation of complexity through time. Just like the smarter your smartphone gets, the smarter you want it. It is a self-sustaining process, you see? The moment you want smarter phone and the conditions allow it to get smarter it

is you who provide "the drive" for the smartening of your phone-you say you will pay money for smarter phone, so the company producing it wants to invest in technology to make it smarter and the result is the development of ever more smarter phones. I call this self-sustaining process (philosophically you can define it by saying-it is the reason for itself). My point it complexity generation is also such self-sustaining process-the more it generates the conditions for more of it arise. So once a certain amount of organizational features is reached the accumulation of new ones becomes

self-sustaining and the process can go on forever or until the conditions of the environment allow it. It is the reason behind complexity. The second part is the more "tricky" one and I agree may be I had to develop it further in my answer but as you can see it is already well too long. "The trick" consists of making the definition of complexity itself dependent on adaptability of the organism. If we define complexity as the increase of variation driving adaptability with the emergence of new organization, then it is organization itself driving the ability to make new organization.

Your smartphone isn't alive but can you consider would it have had the organization it has today if there weren't many generations of "ancestors" before it where all the features needed to make it as smart as it is today weren't tested. You can also say your smart phone now is a testing ground for the smart phones of the future, too. Nobody knows where the smart phone's design would go but you can bet it will be based on the models we use today. How is that not a reasonable argument? Then, it's the same for Life and complexity-trying to adapt to new environments organisms must try many new

organizational features and sometimes the new environment they adapt to forces them to generate ever more new organizational features which in turn can form the environment to provide space for more new organizational features and so on in a self-sustaining process like the one I discussed answering the first part of the question however by including the adaptability argument I can in a way "close" the question by dissolving it with the definition of complexity(yes, I know, such thinking isn't very popular in biology). How that isn't an answer?

@Yordan Yordanov,  Not quite.  I'd summarize your first half more succinctly: more complexity comes because there's always room for more complexity.  That may be 'the drive', but that's not a mechanism.  Pontificating at length on the smartphone analogy misses the point:  ENGINEERS are the mechanism.  Remi.B asks an excellent question, and this "because there's room for improvement" style answer again doesn't identify the mechanism.

I don't think Remi.B's question is good at all and I think I provided good enough (although somewhat too long) answer to it. He actually asks a whole bunch of questions and at the end of it all puts what can be considered basically a philosophical question about the definition of complexity all with the rest. I think this is definitely not what you do when you want to know more about complexity in biology. And I think I manages to answer his main point. Yes, it is true I can expand more on the mechanism point and write something about the particular instances of complexity he is mentioning

but there can you imagine how huge would this answer get. I am at a dilemma here-if I write all I know about the issue my answer would go in the size of a small book (no, not even a paper sized answer will be enough) and the creators of this platform had explicitly stated it isn't for extended discussions or vague and/or long answers. Even my answer now as it is too long. Yesterday I tried writing shorter answer but someone just told me it isn't succinct the way it was. If I'm going to answer all of Remi.B's question than this is definitely not the right platform! And I can't do anything

about it. The way I see it there are 2 ways out of the situation-either Remi.B would come and make this question shorter and more precise (e.g. for example, with talking about a particular instance of complexity like the number of genes, of metabolic pathways, the mean complexity among all living things, the complexity of the most complex taxon, etc.) or he can try "breaking up" this question into a series of questions (I even suggest creating special tag-complexity) each dealing with an individual issue of complexity. Then we can all answer them in paragraphs with reasonable length.

But I can talk so much more about the issues mentioned here that this comment section will get the size of a book here, so I suggest you if you would like to continue the discussion on the topic to go into special chat room for the issue. Do you agree?

If you want to join the discussion you can go here http://chat.stackexchange.com/rooms/54964/complexity-in-nature

I've voted to close because it is not clear what is meant by complexity. Complexity has specific definitions in different subfields of biology. I think you need to pick one and stick with it in order to get a good answer. The top voted accepted answer is more of an explanation of complexity definitions rather than an answer to the question.

@James I totally disagree. Perhaps a lexicon update would help us all, no matter how meta...

This is actually a very interesting yet difficult question to give a single precise answer to. I will try and summarize for you a "meta answer":
Complexity Science Some consider complexity not to be a Biological topic as such, since it is a property that accumulates in non-biological systems e.g. economics, technology, music, language - in fact anything that "evolves" through time. This new field of science is called "Complexity Science" or "Complex Systems" and is primarily a field of mathematics or information theory: Complex systems
Complexity in Biology What I can say is that these kinds of questions have started an almost new field in Biology, called "diversity evolution", here is a very interesting paper: Diversity Evolution.
Defining Complexity You were right to mention Complexity first needs to be defined, and as an early field of science this is where much focus has been recently. There are quite a few definitions but it is perhaps too controversial to list any particulars... HERE is a whole UCL lecture dedicated to defining Complexity!
Topics of Complexity Science I have written enough, so perhaps this lovely diagram of the topics of Complexity Science will be of some help:

Thanks for your answer. From your answer I understand how broad is the science of complexity and I understand that the tendency for complexity to increase does not exist only in biological evolution but also in the evolution of music, technology, economics and other. It is very interesting. It does not answer to why complexity tends to increase (in the biological system) and how it evolved through the past time. I realize that the question might be a hard one! I'll wait to see if someone have some hypotheses for this increase and for past patterns.

"economics, technology, music, language" are all biologic, since they exist inside biological organisms. If you want to talk about complexity outside of biological realm, you can consider physics, chemistry, minerals, crystals, etc.

I think there is a way to tackle the issue however it requires a lot of work on the "edges" of what we consider science and philosophy (and their interaction with each other). I can propose you a suggestion but it is my own research, so it can be quite controversial and please, bare with me.
First the big question here-what is complexity can have multiple answers upon the definition you use. But definitions aren't the subject of biology but of philosophy. And in philosophy whole fields of study can simply dissolve if their definitions prove unsatisfactory. So, one can argue there isn't anything like complexity in Nature and every single time this word is used we can find some problem defined in the terms of some science where the word complexity is missing. One can argue if we can do this for all cases the word complexity is used, then, there truly isn't such a thing like complexity in Nature, but rather it is an artificial human language construct and as such has no objective base in reality. I refer to such cases as "denial by definition".
Pay attention that even the very word "Life" itself can be the subject of "denial by definition" and if it is indeed denied, then how about the rest of biology? So, the "denial by definition" can be serious issue for many problems in biology, not just complexity. In order to avoid it the only way to proceed would be to find one or more universal characteristics behind what we can call complexity having common origins. It is the origins which are important because they can provide us with a common mechanism behind the process and thus give us a way to put "flesh" on the word complexity by denoting the same effect under different circumstances. If you can make such a dictionary definition of complexity than you can relate it directly to the mechanism creating such effects and show its use is more than a convenient semantic coincidence but there are some real scientific implications for your question.
Now, such an effect should have its defining cases-these circumstances when what you are trying to show exists as more than just a convenient word and emerges as a real world characteristic of the system. Then the problem is transferred from one of philosophy to one of science and you can have your definition of complexity. Then, complexity is equated to what characteristics emerge in the system with the advent of new processes taking place in it. I believe such a solution to the problem of the definition of complexity provides best use for science because it turns the problem of defining complexity into the problem of the emergence of properties when new mechanisms appear in the system. I know may be the philosophy is too much for you but can you understand me?
If we follow through these assumptions then complexity arises in the system only when we can show direct link between the emergence of new characteristics of the systems (things that can describe it) and new processes in it. Then we can conditionally define "simplicity" as the state when both the characteristics of the system and its organization are unchanged, some "unrelated states" when the system can accumulate new characteristics or organization without one changing the other and complexity only when change in the characteristics relates to change in the organization and vice versa. I know this definition may sound quite "obscure" for biology because it doesn't specifically prescribe genes, or proteins or metabolic pathways or anything for that matter but, please, consider some examples. If a new metabolic pathway arises do the number of genes remain the same? What about their organization? What about the way their organization is itself organized? However, if an animal adapts for a new environment does it always implies some "fundamental" changes in its anatomy and physiology or does the simple change of "minor details" suffice to make it fit for its new niche? In the first case you can say there is a remarkable increase in complexity, while in the second you can claim just "a simple adaptation". In order to connect the increase in adaptive variation and the organization generating it one needs to know the mechanism beyond both, which as you can see returns us back to the point already discussed in the "denial by definition" problem. If there is an increase in the number and/or interconnectedness of such mechanisms one can make the point the two are pretty much connected with each other and prove the point such a definition can be taken as the definition of complexity in biology. Then, the "denial by definition" argument automatically dissolves by itself and such a definition of complexity can be accepted as a working one. On the other hand if there isn't any relationship between the generation of new mechanisms in the living world and an increase in the connection between variation and organization we should be able to see examples of increased variation without new organizational features and the vice versa. However, I think we can easily prove that in the living world in order to increase the potential variation any lifeform can have, the number of its organizational features should also increase and the vice versa. Can you imagine spiders evolving into diverse families and species without their ability to weave webs? Or the evolution of the higher plants without the evolution of leaves? Or the evolution of new bacteria without the evolution of new metabolic pathways? And so on and on. I believe you can readily see the point that every time adaptive variation becomes able to widen its scope one can see the corresponding emergence of new organizational features. I believe you can easily make the case for the opposite argument, too-that new organizational features always increase the ability of the organism to vary and therefore to take over new niches. I wouldn't be giving examples for the sake of shortness here but I believe you can see my point. New organizations widens variation and new variation allows better adaptability. Of course, new organization isn't always required by the organism to adapt to new niches, but new organization always arises and stays in evolution to make the organism fit for new niches. My argument is that this relation is the mechanism connecting adaptive variation and the increase in the number of organizational features and it by itself is the definition of complexity one should adopt in biology. Thus, complexity can be defined as the increase in organization driving the increase in the potential (here potential is key word because one can make the case new organisms with new organizational features can have lesser ability to vary than their ancestors, and in fact we can see that there is the trend the more "complex" the organism is the more are those features which remain conservative through its further evolution, but if we consider the overall ability of the new organism to evolve ever newer and newer forms we can see more complexity actually generates more variation because the ability of the ancestor to vary was limited by its organizational features while the evolution of newer features means they can add more possible routes evolution can use-"the trick" isn't to consider the overall ability of the ancestor to evolve on many potential routes but the net gain available to vary more organizational features give on the routes of its descendants which has to be greater than the ancestor according to this definition) variation which can be used to adapt to new niches. If I have to "translate" it in a more "layman" (e.g. non-philosopher) terms complexity is the increase of possible routes evolution can take on when new organizational features emerge. It means the emergence of new organization have to always generate more variation which can be used to adapt to new niches and the ability of the organism to widen its adaptability must always come with the emergence of new organizational features. If we adopt this definition then organization and adaptation become fundamentally linked by definition and we don't have to search for the cause of either any more. The significance of this definition is that then this isn't mere "play of words" to define complexity any more, this is viable scientific hypothesis! We can prove the statement: " Every time new organizational feature appears more variation increasing the ability of an organism to adapt is also generated and the vice versa." by observation of our data. If you can provide even a single example of an organizational feature appearing "just by accident" with no extra ability to vary generated by it, then, you have your proof the above statement is wrong! One can argue philosophy is mere "play of words" where you can choose different conflicting "opinions" about a certain question and make the case they can be both correct depending on your point of view, but science isn't. It means the moment you can make a statement that can be put to the test by observations of reality this isn't philosophy any more-it's science! Do you understand my point?
If this definition of complexity allows us to make statements about the observable universe, then, this isn't any more some "philosophical definition", it is verifiable scientific hypothesis which can be put to the test. It means we were able to "export" a question out of philosophy and "import" it into science. And this is an achievement!
Then, this definition can serve as the base for viable scientific investigation. Now, the questions is "Why and how complexity usually tends to increase through time?", right? (This is the last revision I'm using here-I don't remember exactly what was the previous one but I'm certain the topic is still about the reason (why) and the mechanism (how) complexity is increasing through time. Correct me if I'm wrong, please.) Therefore, our investigation requires what we deem as complexity to be able to increase through time for a reason (the "why" part) and with some common mechanism (the "how" part). Do you agree? The definition I already made the case for connects the increase in complexity (as the appearance of new organizational features) with the variability of the organism which in turn serves as the source of adaptability. Therefore, the reason why new organizational features should appear in the organism (and therefore, define this as an increase in complexity) is its adaptability. If the above hypothesis that the appearance of new organizational features and the generation of new variability for new adaptability holds (which is how we defined complexity), then, the reason for the appearance of more complexity (by definition) is the very environment the organism needs to adapt to. The reason fro complexity is none other than the reason for evolution itself-the drive to always increase its number. But in the particular case for complexity it is the fact that the environments presents to the organization of the organism new challenges its current form isn't able to adapt to. This is why the organism evolves some extra organizational features  it can use to cope with these challenges. Now, I know may be this isn't the answer you were looking for when you specify about the genes or the proteins or whatever, but it is a viable answer of the question you posted. The term "new organizational feature" can represent wide range of possibilities-may be a new gene, may be new metabolic pathway, may be some new mechanism for the regulation of gene expression, may be the development of some new organ or gland in the organism, may be the development of new hormone and so on. As you can see the list is endless but this is exactly what the answer of your question is. Different environments force organisms to develop different organizational features which we deem as an increase in complexity. It is us who think of complexity as some "global move" of Life to more and more organization, but are you sure that Life itself thinks the same way (we if assume that evolution is intelligent)? Put yourself in the shoes of the evolving organism. Why do you need to evolve? Because you "feel like" you have to become more "organized" or because you simply must in order to survive the new environment? What do you think evolution would answer you if it could speak? It is us who think complexity is some "grand move" of Life to become more and more organized! From the point of view of the organism themselves Life is just Life as "usual". They simply want to survive and reproduce any way possible. Some of those ways involve "minor changes" well within the organizational features of the organisms themselves under their current level of organization, but some require what we (not the organisms themselves) can call as "giant leaps" or "quantum jumps" in evolution. Do you think the first fish to start to evolve into a land based animal wanted to walk? Or it simply wanted to be able to move on the ground to be able to escape drying ponds? What about the first reptile to be able to evolve into birds? Do you think it wanted to fly or to escape predators in the air? How about the first ape to become human? What did it want-to become an intelligent being able to change the world or to be able to gather into more compact and well organized groups to find food and fend off predators better? I think the examples are endless here, too. The point is the environment itself sometimes requires organisms to get new organizational features to survive in it, not that there is some "grand mechanism" or "tendency" of Life to get more "organized". If such "great tendency" is to be assigned then it has to be to the environment itself, not to the organisms! One can make the case the more organisms an ecosystems has and the more are their interactions among themselves the more new niches this ecosystems can offer to new organisms which in turn can develop new organizational features which can produce new organisms which can offer yet other new organisms more new niches and so on in an ever expanding self-sustaining process. Here is a nice reason for complexity, isn't it? The argument can be further extended for organization itself. If new organization (which is required by the diversifying environment) can bring about more diverse environment which can in turn bring about the emergence of niches requiring even more organized organisms and so on in a self-sustaining manner, then, in a way the mechanism to bring about ever more complexity in the world. But, remember, this is not depending on the organism itself, but on its environment. The question of "Why does complexity usually tends to increase through time?" is transformed into the question "Does the ecosystem itself require increase in complexity to develop further?" which as you can see are 2 very different questions. Then the focus fall not on complexity by definition but on the environment as a whole. And this is one very different question. And it is one we can have the answer to if we can know enough about the ecosystem this organism is in. Once again you can see how "superficially" "philosophical" questions can be transformed into distinctly different scientific questions if we can clarify our definitions and follow through the consequences of those. This is a particular approach I myself have developed but it isn't something accepted by the community, so you are free to disagree with my approach and answer.
As far as the mechanism part of your question is concerned I already "touched" on it when I defined complexity.By the very definition I expounded whenever there is an increase in complexity (e.g. the appearance of novel organizational features) there is an increase in adaptability it brings on. Therefore, the more complexity an organism accumulates the better it can adapt to particular conditions. The increase in adaptation means novel features it has and the novel features it has define complexity, therefore, one can argue adaptation driven by the accumulation of novel organizational features IS the mechanism of complexity increase. This is a "classical" case of the "denial by definition" argument I put on previously! If you say complexity increase is the adaptation by accumulation of organizational features, then the entire question "What is the mechanism of complexity increase?" which in turn can be equated to your question "How does complexity usually tend to increase through time?" simply dissolves or to put it in layman's terms-makes no sense at all.
I know it may seem like "too much philosophy" for biology but the thing is the arguments I put forward actually make sense if taken together and if you want to come to a satisfactory answer to your question (which itself isn't asked in a clear-minded manner according to me), then you need to take the steps I already described and "translate" it into questions which can be answered in more rigorous manner and if they are done (as I suggest here) may be you can agree you have your answer?
To conclude this all too long reply I would like to reflect on personal experience with both philosophers and biologists. My experience has been that both the philosophers don't want to reflect on the science biologists are trying to put on with their questions and the biologists don't want to reflect on the arguments philosophers are trying to put on when reflecting on the biological questions. In my mind this is what "the tragedy" of modern biology is part of because philosophy may be is able to provide answers biologists may find useful but they just aren't listening to them. On the other hand if biologist can "export" difficult to tackle in the modern biological paradigm questions to philosophy, than, may be, philosophers can bring on understanding and possible explanations biologists are just missing! It can be very fruitful relationship! But in order to do it one just has to listen to what the other has to say and this "listening" isn't something either side do very well in my mind. Thank you very much if you managed to endure long enough to get to here, I didn't intended to make this answer so long but as you can see the argument isn't easy to follow either.
Thank you very much for your patience.

I agree that a flimsy definition of complexity is what makes this question a challenge to answer. I think the idea of linking rate of changes in a system to the rate of new characteristics would answer questions about evolution. However, this is hard to quantify objectively & scientifically assess. Not only that but the scale of study required is well beyond what is currently available to scientific interrogation. Ultimately I'm downvoting because the answer isn't succinct, and doesn't attempt to answer the question, but rather comments on the definition of complexity.

@James, I revised my answer. At first I thought it will be one very long to write it here so I tried to present short arguments. But after I saw your comment yesterday I said to myself: "Why the hell shouldn't I write my entire point? If you desire the full argument, then you should get it." and here it is my full argument. I know it may be too long for this site but I downstated my point and used simple language so everybody can understand me. I even bolded the important points. Is this answer succinct? Does it attempt to answer the question?

IMO -1 rating is too harsh, so I corrected it. As for relating philosophers and biologists I think Bruce Alberts in "Molecular Biology of the Cell" captured it the best: "It was innovations in lense grinding, rather than any philosophical advance, allowed Hooke and Levenhook to discover previously unseen cellular world"

The phenomenon of increasing complexity is natural puzzle for everybody studying biology, because "nothing in biology makes sense". Stuart Kauffman shifted the emphasis from complexity to order, and this is IMO the right observation: chaotic systems are more complex in thermodynamic sense, while biological systems occupy a thin niche on the border of chaos. There are many ideas in this book but, unlike the famous manuscript which title Stuart has apparently followed after, there is no satisfactory and compelling answer to that question yet.

Biology arises when some molecules begin copying themselves with a certain amount of error: not too much error, or there would be no heritability; but SOME error, or else there would be no evolution at all. Copying, copying, a few molecules become a multitude, and evolution spreads in all directions, to the more and to the less complex. But when a new level of complexity arises, it usually allows a new size, and a bigger organism can, for instance, eat a smaller organism. Once this level is achieved, it tends to be mantained. Again some copies will lead to smaller lineages, but the big ones have founded a niche that will not disappear by itself (it may take an asteroid). So, looking up close, evolution leads to diversity, not only to higher complexity. But since small complexity already existed, and bigger complexity is something new, we tend to perceive evolution as creating complexity - which is not a false point of view.

I think you are conflating complexity with a necessary increase in size and with speciation, which wasn't the point of the question.

The question was "why and how does complexity increase"? I explained it. Size and speciation are part of the answer. We needed eucariotic cells to get bigger cells. Bigger cells were mantained because they lived in a new niche, where competition couldn't expel them. We needed three germinative layers to have bigger and more complex animals. Size and complexity are like the egg and the chicken, they generate each other.


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

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

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

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

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

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

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

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

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

Quick search on etymonline for Orbital:

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

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

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

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


text:
Mitotic crossover happens in G1?
I was reading this article in wikipedia and came across this :

It has been suggested that recombination takes place during G1, when
  the DNA is in its 2-strand phase, and replicated during DNA synthesis.

If For example - allele A is present on 1 and a is present on 1' and recombination happens such that a is present on 1 and A on 1' and then both get duplicated during S phase.
So how are the daughter cells going to be different from one another and from the mother cell in terms of phenotype? (obviously the alleles around these alleles are going to change)
How can this result in twin spotting in drosophila or any other trait occurring due to coming together of homozygous alleles by mitotic crossovers ?

First off this is called genetic mosaicism and indeed mitotic recombination is a contribution factor.
Mitotic crossover events involve the exchange, by homologous recombination, of regions of chromosomes. 60% of homologous recombination events might occur during G1 and 40% of those event occurs after chromosomes are replicated (see this paper). For twin spotting to occur, you need the homologous recombination to happen on replicated chromosomes (i.e. you need 4 chromatids).
For you question on twin spotting. The following picture illustrates well what are the outcomes of homologous recombination involving two alleles and replicated chromosomes (each line being a chromatid).

If the cell is heterozygous (normal phenotype) for the two recessive alleles, here called y and sn (respectively the "yellow" and "singed bristles" alleles), then two recombination scenarios are possible and differs based on where the recombination occurred. Note that y+ and sn+ are the wild-type alleles and carrying those alleles do not provoke a particular phenotype. The phenotype of the resulting daughter cells are:

Twin spots: Yellow but not singed spots (y/sn+) and singed but not yellow spots (y+/sn) for recombination after the y/sn locus
Single yellow spots: Yellow but not singed spots (y/sn+) and no spots (y+/sn+) for recombination between y and sn

Here the actual picture of what happens:

Therefore this should make clear why daughter cells can show phenotypes that differ from the original parent cell, i.e. the combination of alleles (especially for recessive ones) changes after mitotic crossover events. The twin spot phenotype in Drosophila melanogaster is an excellent example for illustrating that.

Hi! In the answer, you mention that "mitotic recombination occurs after chromosomes are replicated" and it definitely makes much more sense that way. But in the article I have linked, recombination has been said to occur during G1. So is the article inaccurate ?

@biogirl Thanks for pointing that out. I actually incorrectly remembered Lee at al. paper where they concluded that 40% of the mitotic recombination events occur after chromosome are replicated (and not all). This therefore means that indeed 60% of the events might happen during G1. The wiki is correct and lists both possibilities. I updated my answer accordingly.

@biogirl Did the rest of the answer helped you in understanding twin spotting? I am not sure this is really clear.