RGS expression rate-limits recovery of rod photoresponses.

Published

Journal Article

Signaling through G protein-coupled receptors (GPCRs) underlies many cellular processes, yet it is not known which molecules determine the duration of signaling in intact cells. Two candidates are G protein-coupled receptor kinases (GRKs) and Regulators of G protein signaling (RGSs), deactivation enzymes for GPCRs and G proteins, respectively. Here we investigate whether GRK or RGS governs the overall rate of recovery of the light response in mammalian rod photoreceptors, a model system for studying GPCR signaling. We show that overexpression of rhodopsin kinase (GRK1) increases phosphorylation of the GPCR rhodopsin but has no effect on photoresponse recovery. In contrast, overexpression of the photoreceptor RGS complex (RGS9-1.Gbeta5L.R9AP) dramatically accelerates response recovery. Our results show that G protein deactivation is normally at least 2.5 times slower than rhodopsin deactivation, resolving a long-standing controversy concerning the mechanism underlying the recovery of rod visual transduction.

Full Text

Duke Authors

Cited Authors

  • Krispel, CM; Chen, D; Melling, N; Chen, Y-J; Martemyanov, KA; Quillinan, N; Arshavsky, VY; Wensel, TG; Chen, C-K; Burns, ME

Published Date

  • August 17, 2006

Published In

Volume / Issue

  • 51 / 4

Start / End Page

  • 409 - 416

PubMed ID

  • 16908407

Pubmed Central ID

  • 16908407

International Standard Serial Number (ISSN)

  • 0896-6273

Digital Object Identifier (DOI)

  • 10.1016/j.neuron.2006.07.010

Language

  • eng

Conference Location

  • United States