Table I

Incidence of Congenital Defective Color Vision among Caucasian Males"

Diagnostic category %

Protanopia 1.0

Deuteranopia 1.1

Tritanopia 0.001

Protanomaly 1.0

Deuteranomaly 4.9

Monochromacy 0.003

"The incidence values are based on large-scale surveys of defective color vision and should be considered approximate.

this new pigment is shifted so as to be closer to that of the other (normal) M or L pigment. Depending on which of several atypical genes is present, the spectral separation of the M and L pigments is made either greater or smaller and severity of the color vision defect is correspondingly more or less. Only females that are homozygous for these defective X chromosome opsin genes show classical indications of these red/green color defects, thus explaining why the frequency of defective color vision in females is low. Pedigrees of color vision defects have long indicated that in the usual case sons inherit a color defect from mothers who carry a defective gene but who have normal color vision. The tritan defects similarly result from changes in S opsin genes. Since these represent changes in autosomal genes, the incidences of these defects do not differ for males and females. The biology underlying the complete loss of color vision is not straightforward and, in different cases, is apparently traceable to either photopigment or nervous system alterations.

Surveys indicate that the incidence of defective color vision varies significantly among different population groups. The highest frequencies are found in the United States and Western Europe, where approximately 7-9% of all males show a form of red/green color vision defect. Elsewhere, the incidence is often lower. For instance, several populations have been reported to show comparable defects in only about 1% of the males. These regional/ethnic differences have received various interpretations, perhaps the most popular being that the higher rates of defect are found in those populations in which there has been a relaxation of natural selection pressure against color vision defects. According to this view, those societies that are least altered from their hunter/gatherer origins should have the lowest incidences of defective color

Figure 5 X chromosome gene combinations leading to defective color vision. Arrows represent genes for M and L cone opsins. Illustrated are two examples of unequal recombinations that yield new gene arrays. The dashed lines indicate where crossing over occurs during meiosis. (Left) The unequal crossover yields two new gene arrays, one with an L opsin gene and two copies of the M opsin gene. This genotype is common in individuals having normal color vision. The second result is a deletion of the M cone opsin gene. A male with this genotype would have dichromatic color vision. (Right) The crossovers occur within the gene. This produces new genes whose pigment products will differ from those of the normal M and L opsin genes, and depending on the resultant combination of genes the effects on color vision can be subtle or drastic.

Figure 5 X chromosome gene combinations leading to defective color vision. Arrows represent genes for M and L cone opsins. Illustrated are two examples of unequal recombinations that yield new gene arrays. The dashed lines indicate where crossing over occurs during meiosis. (Left) The unequal crossover yields two new gene arrays, one with an L opsin gene and two copies of the M opsin gene. This genotype is common in individuals having normal color vision. The second result is a deletion of the M cone opsin gene. A male with this genotype would have dichromatic color vision. (Right) The crossovers occur within the gene. This produces new genes whose pigment products will differ from those of the normal M and L opsin genes, and depending on the resultant combination of genes the effects on color vision can be subtle or drastic.

vision. There is no compelling evidence to support this idea, but neither can it be flatly rejected.

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