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March 25, 2007
The kaleidoscope in our eyes
Long-time readers of this blog will remember that last summer I received a deluge of email from people taking the "reverse" colorblind test on my webpage. This happened because someone dugg the test, and a Dutch magazine featured it in their 'Net News' section. For those of you who haven't been wasting your time on this blog for quite that long, here's a brief history of the test:
In April of 2001, a close friend of mine, who is red-green colorblind, and I were discussing the differences in our subjective visual experiences. We realized that, in some situations, he could perceive subtle variations in luminosity that I could not. This got us thinking about whether we could design a "reverse" colorblindness test - one that he could pass because he is color blind, and one that I would fail because I am not. Our idea was that we could distract non-colorblind people with bright colors to keep them from noticing "hidden" information in subtle but systematic variations in luminosity.
Color blind is the name we give to people who are only dichromatic, rather than the trichromatic experience that 'normal' people have. This difference is most commonly caused by a genetic mutation that prevents the colorblind retina from producing more than two kinds of photosensitive pigment. As it turns out, most mammals are dichromatic, in roughly the same way that colorblind people are - that is, they have a short-wave pigment (around 400 nm) and a medium-wave pigment (around 500 nm), giving them one channel of color contrast. Humans, and some of our closest primate cousins, are unusual for being trichromatic. So, how did our ancestors shift from being di- to tri-chromatic? For many years, scientists have believed that the gene responsible for our sensitivity in the green part of the spectrum (530 nm) was accidentally duplicated and then diverged slightly, producing a second gene yielding sensitivity to slightly longer wavelengths (560 nm; this is the red-part of the spectrum. Amazingly, the red-pigment differs from the green by only three amino acids, which is somewhere between 3 and 6 mutations).
But, there's a problem with this theory. There's no reason a priori to expect that a mammal with dichromatic vision, who suddenly acquired sensitivity to a third kind of color, would be able to process this information to perceive that color as distinct from the other two. Rather, it might be the case that the animal just perceives this new range of color as being one of the existing color sensations, so, in the case of picking up a red-sensitive pigment, the animal might perceive reds as greens.
As it turns out, though, the mammalian retina and brain are extremely flexible, and in an experiment recently reported in Science, Jeremy Nathans, a neuroscientist at Johns Hopkins, and his colleagues show that a mouse (normally dichromatic, with one pigment being slightly sensitive to ultraviolet, and one being very close to our medium-wave, or green sensitivity) engineered to have the gene for human-style long-wave or red-color sensitivity can in fact perceive red as a distinct color from green. That is, the normally dichromatic retina and brain of the mouse have all the functionality necessary to behave in a trichromatic way. (The always-fascinating-to-read Carl Zimmer, and Nature News have their own takes on this story.)
So, given that a dichromatic retina and brain can perceive three colors if given a third pigment, and a trichromatic retina and brain fail gracefully if one pigment is removed, what is all that extra stuff (in particular, midget cells whose role is apparently to distinguish red and green) in the trichromatic retina and brain for? Presumably, enhanced dichromatic vision is not quite as good as natural trichromatic vision, and those extra neural circuits optimize something. Too bad these transgenic mice can't tell us about the new kaleidoscope in their eyes.
But, not all animals are dichromatic. Birds, reptiles and teleost fish are, in fact, tetrachromatic. Thus, after mammals branched off from these other species millions of years ago, they lost two of these pigments (or, opsins), perhaps during their nocturnal phase, where color vision is less functional. This variation suggests that, indeed, the reverse colorblind test is based on a reasonable hypothesis - trichromatic vision is not as sensitive to variation in luminosity as dichromatic vision is. But why might a deficient trichromatic system (retina + brain) would be more sensitive to luminal variation than a non-deficient one? Since a souped-up dichromatic system - the mouse experiment above - has most of the functionality of a true trichromatic system, perhaps it's not all that surprising that a deficient trichromatic system has most of the functionality of a true dichromatic system.
A general explanation for both phenomena would be that the learning algorithms of the brain and retina organize to extract the maximal amount of information from the light coming into the eye. If this happens to be from two kinds of color contrast, it optimizes toward taking more information from luminal variation. It seems like a small detail to show scientifically that a deficient trichromatic system is more sensitive to luminal variation than a true trichromatic system, but this would be an important step to understanding the learning algorithm that the brain uses to organize itself, developmentally, in response to visual stimulation. Is this information maximization principle the basis of how the brain is able to adapt to such different kinds of inputs?
G. H. Jacobs, G. A. Williams, H. Cahill and J. Nathans, "Emergence of Novel Color Vision in Mice Engineered to Express a Human Cone Photopigment", Science 315 1723 - 1725 (2007).
P. W. Lucas, et al, "Evolution and Function of Routine Trichromatic Vision in Primates", Evolution 57 (11), 2636 - 2643 (2003).
posted March 25, 2007 10:51 AM in Evolution | permalink
Comments
Interesting, as I am not colour blind but I am able to see most patterns in the colour card tests. We did an experiment at university many years ago now where we tried to determine what a normal person would see and what a colour blind person would see.
It turned out that I and another person were the only two to see both sets of patterns in each of the test cards. We used about 100 cards.
In the test examples you provided, I could see the six (not clearly at first) though the top section was more hidden. In the second, I could see the circle but also saw a distinct W in the centre of the sircle which didn't show up in your answer images.
As I say interesting.
Posted by: Bruce Rennie at March 28, 2007 07:05 AM
There is strong suggestive evidence that many women are effectively tetrachromatic. In particular, Verrelli and Tishkoff find that "subtle changes in L-cone opsin wavelength absorption may have been adaptive during human evolution." One possible explanation for this is an advantage to women who are tetrachromatic due to distinct "red" opsin genes on their two X chromosomes.
Posted by: Steve Mount at April 5, 2007 09:42 PM
That's very interesting. In my mind, though, effective tetrachromatic vision would seem to require that the distance (i.e., the degree of contrast) between peak sensitivities of the two L-cone opsins to be roughly comparable to the distance between the peaks for the L- and M-cones, or the M- and the S-cones. Otherwise, it's not clear to me that having two kinds L-cone opsins would result in any appreciable gain in chromatic contrast sensitivity... but, maybe I'm misunderstanding the evidence. An alternative explanation might be that two L-cone opsins being present in non-trivial frequencies in the human population is from neutral selection effects or a historical accident... Still, I agree it's strange.
Posted by: Aaron at April 5, 2007 10:24 PM