Color Vision Synthesis

Human color vision is broken down into 3 pigment sequencing of genomic and DNA clones that encode the apoproteins of these 3 pigments the; deduced amino acid show 41 +/- percent identity w/ rhodopsin. Red and Green 96% mutual but only 45% with blue. Green varies among color-normal individuals and together w/ a single red pigment gene, is proposed to reside in a head-to-tail down array with the X chromosome. Absorption spectra of cone photo pigments over the spectral range of 530 to 562 nm are a principal cause of individual differences in color vision within and across other primates. Nucleotide sequences were determined for 8 primate photo pigment cones. Normal mice Failed to discriminate yellow vs. red lights when the light intensities were set to give equal activation of their middle wavelength receptor. Mice with the human long wavelength and the mouse middle

One suggestion proposed by Doctor Neitz in his “Trichromatic color vision in New World monkeys’ paper is that at some point in the past apes acquired trichromacy and then passed it down through the females, random mutations created a variant of receptor sites, that were located on the X chromosome producing 2 receptor types and only certain female apes acquired trichromatic vision. Therefore it is possible that, due to an anomaly the brain can adapt to said anomaly and use it as a modification rather a defect. For the mice one medium receptor was replaced with a long human receptor, 3 color receptors blue; red; green. Furthermore, there are multitudes of these 3 types of cones; a red-green deficiency is a result of too little red cones. The color perceived are merely a result of a combination of the different color receiving rods to perceive more colors we’d need cones that perceive either larger (longer) wavelengths or smaller (shorter)