| First Author | Wang Z | Year | 2005 |
| Journal | J Biol Chem | Volume | 280 |
| Issue | 26 | Pages | 24293-300 |
| PubMed ID | 15851469 | Mgi Jnum | J:100845 |
| Mgi Id | MGI:3589723 | Doi | 10.1074/jbc.M502588200 |
| Citation | Wang Z, et al. (2005) Enhanced shutoff of phototransduction in transgenic mice expressing palmitoylation-deficient rhodopsin. J Biol Chem 280(26):24293-300 |
| abstractText | Palmitoylation is a reversible, post-translational modification observed in a number of G-protein-coupled receptors. To gain a better understanding of its role in visual transduction, we produced transgenic knock-in mice that expressed a palmitoylation-deficient rhodopsin (Palm(-/-)). The mutant rhodopsin was expressed at wild-type levels and showed normal cellular localization to rod outer segments, indicating that neither rhodopsin stability nor its intracellular trafficking were compromised. But Palm(-/-) rods had briefer flash responses and reduced sensitivity to flashes and to steps of light. Upon exposure to light, rhodopsin became phosphorylated at a faster rate in mutant than in wild-type retinas. Since quench of rhodopsin begins with its phosphorylation, these results suggest that palmitoylation may modulate rod photoreceptor sensitivity by permitting rhodopsin to remain active for a longer period. |
