Explain the inheritance of colour blindness
in human beings.
Answers
Answer:
It is well established that colour-blindness and haemophilia are due to sex-linked genes. These genes appear to manifest themselves in all males who carry them. In women the gene for haemophilia is probably always recessive, the cases of alleged haemophilia in heterozygous women being very doubtful.
Explanation:
There are three types of inherited or congenital color vision deficiencies: monochromacy, dichromacy, and anomalous trichromacy. Monochromacy, also known as "total color blindness", is the lack of ability to distinguish colors (and thus the person views everything as if it were on a black and white television); caused by cone defect or absence. Monochromacy occurs when two or all three of the cone pigments are missing and color and lightness vision is reduced to one dimension.
Rod monochromacy (achromatopsia) is an exceedingly rare, nonprogressive inability to distinguish any colors as a result of absent or nonfunctioning retinal cones. It is associated with light sensitivity (photophobia), involuntary eye oscillations (nystagmus), and poor vision.
Cone monochromacy is a rare total color blindness that is accompanied by relatively normal vision, electroretinogram, and electrooculogram. Cone monochromacy can also be a result of having more than one type of dichromatic color blindness. People who have, for instance, both protanopia and tritanopia are considered to have cone monochromacy. Since cone monochromacy is the lack of/damage of more than one cone in retinal environment, having two types of dichromacy would be an equivalent
Dichromacy is hereditary. Protanopia and deuteranopia are hereditary and sex-linked, affecting predominantly males.
Protanopia is caused by the complete absence of red retinal photoreceptors. Protans have difficulties distinguishing between blue and green colors and also between red and green colors. It is a form of dichromatism in which the subject can only perceive light wavelengths from 400 nm to 650 nm, instead of the usual 700 nm. Pure reds cannot be seen, instead appearing black; purple colors cannot be distinguished from blues; more orange-tinted reds may appear as dim yellows, and all orange–yellow–green shades of too long a wavelength to stimulate the blue receptors appear as a similar yellow hue. It is present in 1% of males.
Deuteranopia affects hue discrimination in a similar way to protanopia, but without the dimming effect. Again, it is found in about 1% of the male population.[15]
Tritanopia is a very rare color vision disturbance in which only the red and the green cone pigments are present, with a total absence of blue retinal receptors. Blues appear greenish, yellows and oranges appear pinkish, and purple colors appear deep red. It is related to chromosome 7; thus unlike protanopia and deuteranopia, tritanopia and tritanomaly are not sex-linked traits and can be acquired rather than inherited and can be reversed in some cases.
Anomalous trichromacy is a common type of inherited color vision deficiency, occurring when one of the three cone pigments is altered in its spectral sensitivity.
Protanomaly is a mild color vision defect in which an altered spectral sensitivity of red retinal receptors (closer to green receptor response) results in poor red–green hue discrimination. It is hereditary, sex-linked, and present in 1% of males. In contrast to other defects, in this case the L-cone is present but malfunctioning, whereas in protanopia the L-cone is completely missing.
Deuteranomaly, caused by a similar shift in the green retinal receptors, is by far the most common type of color vision deficiency, mildly affecting red–green hue discrimination in 5% of European males. It is hereditary and sex-linked. In contrast to deuteranopia, the green-sensitive cones are not missing but malfunctioning.
Tritanomaly is a rare, hereditary color vision deficiency affecting blue–green and yellow–red/pink hue discrimination. It is related to chromosome 7. In contrast to tritanopia, the S-cone is malfunctioning but not missing.