Trichromatic Vision

These coding sequences differ in only 15 amino acids. The high degree of homology p bolshyisposes these constituents to unequalized recombination, which leads to gene deletions and the formation of red- light-green hybrid genes which are responsible for(p) for well-nigh of the common red-green tinct flock deficiencies (Deeb and Kohl, 2003, 170-187).

The deuce most proximal genes in the array are thought to be responsible for gene expression in the retina, and the severity of tinct vision deficiencies are therefore roughly related to the differences in the preoccupation maxima for the photo keys encoded by these first two genes of the array (Deeb and Kohl, 2003, 170-182). A superstar amino acid difference in the red photopigment apprise cause a deficiency in normal color vision. Blue chamfer monochromacy is a ancient condition, occurring in roughly 1 in 100,000 individuals, and is caused by the absence of red and green strobiles from the retina (Deeb and Kohl, 2003, 170-187; Michaelides et al, 2004, 2). This faecal matter come about in two ways: either by deletion of a slender gene region which regulates expression of the red-green array; or by renewals that inactivate the red and green pigment genes.

X-linked, recessive, blue cone monochromacy (BCM) is characterized by poor ocular acuity, pendular nystagmus, photophobia and photodysphoria (Ayyagari et al, 2004, 75-82; Michaelides et al, 2004, 2). sharpness is us

Monochromatism is a rare (1 in 100,000 people), X-linked, recessive, eye disorder in which there is a lack of red and green photopigment in the cones, leading to a difficulty in color discrimination and low visual acuity. The genics of this disorder show that it is due to either mutations in the red and green genes by unequal crossover or deletions of the LCR region upstream from the red gene, or to a mutation of the cys203arg which leads to inactivation of the red and green genes. The disorder is accompanied by macular degeneration in some cases, and an abnormal macula can be seen in female carriers of the disorder. There is currently no treatment for BCM.

Studies are concentrated on defining the genetic defects in the disorder and determining ways to distinguish it clinically from rod monochromatism and other cone disorders.

Kellner, U., Wissinger, B., Tippmann, S., Kohl, S., Kraus, H., & Foerster, M. H. (2004). Blue cone monochromatism: clinical findings in patients with mutations in the red/green opsin gene cluster. Graefes Archives of Clinical & Experimental Ophthalmology, Epub ahead of print. Retrieved 24 November 2004 from:

Nine families showed deletions in the gene encoding the red-sensitive photopigment and/or in the region up to 17.8 kb upstream of the red gene (Ayyagari et al, 2000, 75-82). This is the area which contains the LCR and other regulatory sequences. These same nine families showed a range of deletions from the personnel casualty of just one single exon to the loss of the entire red gene when the red pigment gene was examined. In one family, there was complete loss of the green pigment gene. No association was found between genotype and phenotype in these families.

Jagla, W. M., Jagle, H., Hayashi, T., Sharpe, L. T., & Deeb. S. S. (2001). The molecular basis of dichromatic color vision in males with multiple red and green visual pigment genes. Human Molecular Genetics, 11(1), 23-32.

Ayyagari et al (2000) looked at the gen
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