Additional genes may affect color vision.

Whether human beings can enjoy wisteria or lilac's gentle hues rests on their genetic inheritance of color vision.

The standard model of color vision, proposed more than 200 years ago, postulates three kinds of photopigments in cone cells on the retina. Sensitive to red, green, and blue light, the three enable one to perceive a rainbow's colors.

This trichromatic theory of vision assumes that people inherit a separate gene for each of the three photopigments. In color blindness, which affects as many as 8 to 10 percent of men, a person may lose the ability to see all colors or merely the capacity to discriminate between certain hues. Standard theory holds that such people lack the gene for one or more pigments or that those genes have failed to work properly.

Now, new evidence suggests a more complex genetic model of color vision.

Molecular geneticist Maureen Neitz and neuroscientist Jay Neitz, both at the Medical College of Wisconsin in Milwaukee, report in the Feb. 17 Science that many men with normal color vision have more pigment genes on their X chromosomes than previously realized.

"It was long assumed that people with normal color vision all have three stereotyped cone pigment genes in common," they say. Recently, scientists have shown that the number of pigment genes in red-green color vision can vary. Now, their results reveal that individual differences in the number of pigment genes "are much larger than have been appreciated," the Neitzes say.

Examining the DNA of 30 men, some normal and some color-blind, they found that men with normal color vision "had as few as two and as many as nine [different] X-linked pigment genes." In fact many men had multiple "long-wavelength" genes for detecting red light -- "often two and as many as four."

These findings have implications for understanding color vision as well as color blindness. "The fact that individuals with multiple long-wave [red light] genes tend to make more intermediate color matches hints that some may be expressing more than one long-wave pigment," they explain. "If that is true, in total they would [make] at least four different cone pigments: two long-wave, a middle-wave, and a short-wave pigment."

This finding contradicts the standard model of color vision "that has held sway for more than 2 centuries, in which the presence of three pigments is proposed to explain human trichromatic color vision," the Neitzes conclude.

"This is an important new finding," says Gerald H. Jacobs, a neuroscientist at the University of California, Santa Barbara. "Their work may lead to a reexamination of the roles of various pigment genes in color vision."

Another set of findings casts new light on the long-accepted explanation of red-green color blindness in British chemist John Dalton (1766--1844).

Dalton, to whom the pink flower Geranium zonale appeared sky blue, decreed that upon his death, his eyes be removed and studied to uncover the defect. His eyes were indeed examined, and scientists concluded that Dalton lacked the retinal pigment for red vision.

However, molecular geneticist David M. Hunt of the University of London and his colleagues recently subjected a tissue sample they obtained from the remains of Dalton's retina to DNA analysis. As it turns out, Hunt's team reports in the Feb. 17 Science, Dalton lacked the gene for pigment sensitive to middle wavelengths, not long wavelengths of light. This deficiency, known as deuteranopia, has a different genetic profile from protanopia, which scientists had blamed for Dalton's problem.

"Molecular biology has finally set history straight," says Hunt.