| First Author | Danciger M | Year | 1989 |
| Journal | Genomics | Volume | 4 |
| Issue | 2 | Pages | 215-7 |
| PubMed ID | 2737680 | Mgi Jnum | J:9850 |
| Mgi Id | MGI:58307 | Doi | 10.1016/0888-7543(89)90303-0 |
| Citation | Danciger M, et al. (1989) The gene for the alpha-subunit of retinal rod transducin is on mouse chromosome 9. Genomics 4(2):215-7 |
| abstractText | 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. |
