The gene for the alpha-subunit of retinal rod transducin is on mouse chromosome 9.
Mice carrying the autosomal recessive rd gene experience total degeneration of the photoreceptor cells of the retina by 3 to 4 weeks of life. Biochemical studies of the rd retina have demonstrated a lesion in cyclic guanosine monophosphate (cGMP) metabolism due to depressed rod-specific cGMP-phosphodiesterase (cGMP-PDE) activity. The depressed activity could result from, among other things, a lesion in the cGMP-PDE enzyme itself or in any of a number of proteins in the rod that regulate it. We have used a cDNA clone for the alpha-subunit of bovine rod transducin (T alpha 1) to map the corresponding gene, Gnat-1, to mouse chromosome 9 with a panel of Chinese hamster-mouse somatic cell hybrid DNAs. Transducin, a heterotrimeric G protein, is involved in the stimulation of cGMP-PDE when light hits the rod photoreceptors. Since the primary defect in rd disease occurs in a gene(s) on mouse chromosome 5, our results suggest that Gnat-1 is not the rd gene.[1]References
- The gene for the alpha-subunit of retinal rod transducin is on mouse chromosome 9. Danciger, M., Kozak, C.A., Farber, D.B. Genomics (1989) [Pubmed]
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