Wednesday, 2 April 2014

Misison Impossible

Supplementary material

It's true: dogs are colour blind. That doesn't mean they see in black and white, but that they can't distinguish red from green for lack of the proper photoreceptors. That is not a specifically canine problem, mind you: most mammals are in the same boat. We humans are very lucky to belong to the Old World primates category; thanks to a fortuitous mutation event described below, we gained an extra gene for colour perception that gives us trichromatic ("three colours") instead of dichromatic ("two colours") vision. And so we can better appreciate the work of Vincent van Gogh.

Light perception by the brain relies on the stimulation of certain nerve cells called photoreceptors located in the retina, acting as the film for the eye's camera. We have two main types of photoreceptors: they are called rods and cones, based on their shape, and despite a shared mechanism of action they have somewhat different roles. Photons must hit these photoreceptors for them to send the appropriate signal down a chain of nerve cells, and only certain wavelengths will do: we cannot, for example, see x-rays even if they are also part of the electromagnetic spectrum, just like visible light.

Here's how photoreceptors manage to convert photons into electric current that the brain can understand.

Each of these specialized cells contains a large stack of internal disks that form from folds in the plasma membrane. In cones, the folds remain connected to the plasma membrane but in rods they come loose inside the cell, forming what looks like a pile of pita bread. Each of these disks is studded with proteins called opsins. These proteins associate with a molecule called 11-cis retinal, which our body makes from vitamin A. That's why carrots are said to be good for our eyes, their bright orange colour revealing the presence of large amounts of beta-carotene, a vitamin A precursor.

In the rods, cells that allow us to see in dim light and are responsible for peripheral vision, the association between the opsin and the retinal is called rhodopsin. In the cones, cells that allow us to distinguish between colours, that association is called photopsin or iodopsin. The two types of photoreceptors are not distributed the same way in the retina: cones are less numerous (6-7 millions of them per eye) and are concentrated in a region of the eye called the macula, just opposing the pupil, while rods are more abundant (125 millions per eye) and cover a larger area, which also makes them responsible for our peripheral vision. That rods are more sensitive to light explains why a star seen from the corner of the eye at night seems to disappear when we try to focus on it: it's just not bright enough for the cones located at the back of the eye.

In the dark, each photoreceptor contains plenty of cyclic GMP, which by attaching to plasma membrane sodium channels allows Na+ ions to come and go, depolarizing the cell. This depolarization affects voltage-dependent calcium channels that also allow Ca2+ into the cell. This calcium causes the fusion of glutamate-containing vesicles with the plasma membrane, letting this neurotransmitter out, and when it contacts the glutamate receptors of the nearby bipolar cells it essentially tells the brain "I ain't seein' nuthin' at the moment".

When photons hit rhodopsin or photopsin, their energy is absorbed and induce a change in 11-cis retinal which adopts an all-trans conformation. This modification in turn activates a nearby G protein called transducin, which then triggers a phosphodiesterase. This enzyme turns cGMP into 5'-GMP, causing the sodium channels to close. The cell begins to hyperpolarize, the voltage-sentitive calcium channels close, and glutamate is no longer released. This interruption of the "nothing to report" signal is interpreted by the brain as "this photoreceptor has just been hit by photons!"

The opsin found in cones and in rods is not all the same. In fact, from what must have been some kind of ancestral opsin, successive events of gene duplication followed by sequence divergence has given the animal world access to a wide choice of different photosensitive proteins. The most useful property of all these proteins is that they do not have the same sensitivity to specific wavelengths, thus allowing us to tell the difference between a few of them (which we interpret as different colours).

The opsin called RHO is found in human rods. It is has an activation peak at 495 nm. Its gene is found on chromosome 3.

The cone opsins are the following:

  • OPN1SW, also called "blue opsin", covers a range from 400 to 500 nm with an excitation peak at 420 nm. Its gene is on chromosome 7.
  • OPN1MW, also called"green opsin", covers a ranbge from 450 to 630 nm with an excitation peak at 534 nm. Its gene is on the X chromosome, right after the gene for the red opsin. A small detail: in some people (who have a perfectly normal vision) this gene is repeated and there are two copies of the green opsin gene following the gene for the red one.
  • OPN1LW, also called the "red opsin", covers a range from 500 to 700 nm with an axcitation peak at 564nm. As we've just said, it is on the chromosome X, right before the gene for the green opsin.

Each cone expresses only one type of"coloured" opsin and will therefore specialize in a certain peak of excitability. There will be cones more easily triggered by red, blue or green wavelengths and it is the difference in relative stimulation among all our cones that tells the brain whether it's looking at something that's more blue, red or green. The rods, since they come in only one variety, only say "light". Because rods are lousy receptors for red light, since their excitability peak is sort of in the green, we can use a dim red light to preserve our night vision when we go out at night to observe the stars. The red light will not cause our rods to adapt to the presence of light.

As we've just mentioned, our different opsins come from the divergence of an ancestral gene. Looking at different branches of the tree of life we'll see how millions of years of evolution led to the development of several distinct opsins that give a wide range of colour perception. Chondricthyans, cartilaginous fish that include the sharks, the rays and the chimerae, rely on one rod opsin and four cone opsins: ultraviolet, red, green and blue. Bony fishes have even more, with one red, one ultraviolet, two blues and three greens on top of the rod opsin. Our own mammalian ancestors lost the green and blue opsins, leaving only the ultraviolet and the red opsin on top of the rod opsin; this may have happened due to a prolonged period of nocturnal lifestyle (and if I had to share the world with dinosaurs, I'd probably try to be as inconspicuous as possible, living in burrows and coming out only at night). What's the point of distinguishing many colours when you live in the dark, right?

"But", you'll ask, "what's this ultraviolet thing? I do see the colour blue, and I don't see the ultraviolet!" Which is perfectly true: our UV opsin has changed over time, and its peak excitability is now at a longer wavelength, giving us a "new" blue opsin. And that's where most mammals are today, including the dog, with a dichromatic vision. But we primates were pretty lucky: many of us evolved thrichromatic vision again. Our red opsin gene was duplicated on the X chromosome, and the new copy accumulated mutations that changed its peak excitability to a shorter wavelength, giving us a new green opsin. That happened to the ancestor of all Old World primates. When either the red gene or the green gene is mutated, we lose the ability to distinguish between red and green; this is a condition called daltonism. It's more frequent among boys than girls because the former only have one X chromosome and one inactive gene will do the trick; for a girl to be affected, both copies of the same gene would have to be affected (since she has two X chromosomes). Girls have a back-up, boys don't. That's only true for red-green colour blindness: the gene for our blue opsin is on chromosome 7, of which both boys and girls have two copies.

New world world monkeys can also be trichromatic, because some of their red alleles have mutated to get closer to green,which doesn't demand a lot of modifications, actually. Males can therefore have a red or green allele on their X chromosome, and although they'll still be dichromatic they won't be for the same reason as their neighbour. Some females will be lucky enough to have a green allele on one X and a red one on the other, and will have trichromatic vision (a great advantage to tell a ripe apple from a sour one). Howler monkeys (Alouatta and Aotus) are fully trichromatic: the green allele was translocated on the X, not far from the red allele, and so these monkeys are in a situation similar to ours (altgough they got there by a different way).

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