Marine biologist Sonja Kleinlogel and quantum physicist Andrew White have found that the mantis shrimp from the Great Barrier Reef in Australia can see eleven or twelve primary colours, rather than the three that humans can see (red, yellow, and blue, and their combinations):

Most animals can tell how fast the electric field in a light wave is oscillating, which is perceived as colour. (Blue light oscillates faster than green, which is faster than red). The direction of the oscillation is known as polarisation: many animals, from budgerigars to ants have some form of polarisation vision.

Most life forms see this polarization of the light wave's electric field only as lighter or darker patches. But the electric field of light is not still. It can go from swinging back and forth to travelling in a circle. The sensitive mantis shrimp eye can measure four linear and two circular polarizations at once, according to the researchers, so the shrimp know both the direction and the degree of polarization of the light. Presumably, the shrimp would detect these as if they were different colours. What benefit does such a high degree of sensitivity to colour offer the shrimp?

Prof. White notes, "Some of the animals they like to eat are transparent, and quite hard to see in sea-water - except they're packed full of polarising sugars - I suspect they light up like Christmas trees as far as these shrimp are concerned."

The evolution of the eye

Eye origin has long been a puzzle in evolution because a number of quite different complex systems exist. Biochemist Michael Denton of the University of Otago in New Zealand thinks that just about every conceivable means of seeing (forming an optical image) has been used by life forms:

These include the familiar camera-type of eye found in vertebrates, molluscs, and various invertebrates; the reflecting eye of the scallop pecten and the crustacean Gigantocypris, which form an image by reflection from a concave mirror onto a retina situated ast the focal point of the mirror; and the three different types of compound eye of the insects and arthropods. One type of compound eye found in diurnal insects os made up of a hexagonal array of tiny lenslets, each of which has its own photoreceptor cell that receives light only from its own lenslet. A second type (the superposition type) is found in nocturnal insects, again made up of a hexagonal array of tiny lenslets which bend the light rays so that light is focused by refraction through many le3nslets to one point in the photoreceptor layer. A third type is also a superposition eye, but in this case the light is focused by reflection from a series of tiny square mirror-lined units onto the photo-receptor layer ... Finally, there is even what appears to be a scanning eye, utilized by a small marine crustacean which scans an image formed b y a simple lens by rapidly moving a single photoreceptor back and forth across the image. (Nature's Destiny, New York: Free Press, 1998, pp. 307-8)

In addition, Denton notes, there is a "near-infinite variety" of simple eyes that do not form an image, such as the photosensitive pigments of Protozoa (one-celled life forms) and the simpler photoreceptor eyes of spiders.

What are "simple" eyes?

When biologists refer to "simple" eyes, they mean that the eye mechanism itself is simple. However, in addition to a mechanism to detect light, a visual system must have a means of transforming light signals into nervous system signals that produce information. Only if information is produced and acted on is a visual system complete. The process of transforming light into information is complex, even when the structure of the eye is simple. Biochemist Michael Behe explains the process for the human eye:

When light strikes the retina a photon is absorbed by an organic molecule called 11-cis-retinal, causing it to rearrange within picoseconds to trans-retinal. The change in shape of retinal forces a corresponding change in shape of the protein, rhodopsin, to which it is tightly bound. As a consequence of the protein's metamorphosis, the behavior of the protein changes in a very specific way. The altered protein can now interact with another protein called transducin. Before associating with rhodopsin, transducin is tightly bound to a small organic molecule called GDP, but when it binds to rhodopsin the GDP dissociates itself from transducin and a molecule called GTP, which is closely related to, but critically different from, GDP, binds to transducin.

The exchange of GTP for GDP in the transducinrhodopsin complex alters its behavior. GTP-transducinrhodopsin binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When bound by rhodopsin and its entourage, the phosphodiesterase acquires the ability to chemically cleave a molecule called cGMP. Initially there are a lot of cGMP molecules in the cell, but the action of the phosphodiesterase lowers the concentration of cGMP. Activating the phosphodiesterase can be likened to pulling the plug in a bathtub, lowering the level of water.

A second membrane protein which binds cGMP, called an ion channel, can be thought of as a special gateway regulating the number of sodium ions in the cell. The ion channel normally allows sodium ions to flow into the cell, while a separate protein actively pumps them out again. The dual action of the ion channel and pump proteins keeps the level of sodium ions in the cell within a narrow range. When the concentration of cGMP is reduced from its normal value through cleavage by the phosphodiesterase, many channels close, resulting in a reduced cellular concentration of positively charged sodium ions. This causes an imbalance of charges across the cell membrane which, finally, causes a current to be transmitted down the optic nerve to the brain: the result, when interpreted by the brain, is vision.

If the biochemistry of vision were limited to the reactions listed above, the cell would quickly deplete its supply of 11-cis-retinal and cGMP while also becoming depleted of sodium ions. Thus a system is required to limit the signal that is generated and restore the cell to its original state; there are several mechanisms which do this. Normally, in the dark, the ion channel, in addition to sodium ions, also allows calcium ions to enter the cell; calcium is pumped back out by a different protein in order to maintain a constant intracellular calcium concentration. However, when cGMP levels fall, shutting down the ion channel and decreasing the sodium ion concentration, calcium ion concentration is also decreased. The phosphodiesterase enzyme, which destroys cGMP, is greatly slowed down at lower calcium concentration. Additionally, a protein called guanylate cyclase begins to resynthesize cGMP when calcium levels start to fall. Meanwhile, while all of this is going on, metarhodopsin II is chemically modified by an enzyme called rhodopsin kinase, which places a phosphate group on its substrate. The modified rhodopsin is then bound by a protein dubbed arrestin, which prevents the rhodopsin from further activating transducin. Thus the cell contains mechanisms to limit the amplified signal started by a single photon.

Trans-retinal eventually falls off of the rhodopsin molecule and must be reconverted to 11-cis-retinal and again bound by opsin to regenerate rhodopsin for another visual cycle. To accomplish this trans-retinal is first chemically modified by an enzyme to transretinol, a form containing two more hydrogen atoms. A second enzyme then isomerizes the molecule to 11-cis-retinol. Finally, a third enzyme removes the previously added hydrogen atoms to form 11-cis-retinal, and the cycle is complete.

Charles Darwin described the eye as one of the "organs of extreme perfection" and considered it a problem for his theory of natural selection. Indeed, the eye gave him a "cold shudder." He thought, however, that an eye like the human eye might arise from simpler structures, like the photosensitive spot of the worm. The difficulty with his explanation is, as we have seen, that the process of vision, as well as the structure, is complex, and it is not clear that the process can be less complex. Mathematician David Berlinski phrases the problem like "this":

Like vibrations passing through a spider's web, changes to any part of the eye, if they are to improve vision, must bring about changes throughout the optical system. Without a correlative increase in the size and complexity of the optic nerve, an increase in the number of photoreceptive membranes can have no effect. A change in the optic nerve must in turn induce corresponding neurological changes in the brain. If these changes come about simultaneously, it makes no sense to talk of a gradual ascent of Mount Improbable. If they do not come about simultaneously, it is not clear why they should come about at all.

We know that vision got started during the Cambrian era and some have argued that it actually explains the Cambrian explosion. Whatever the merits of such a thesis, the origin of vision itself  requires explanation.