Journal
NEURON
Volume 51, Issue 4, Pages 409-416Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2006.07.010
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Funding
- NEI NIH HHS [R01 EY014047, EY011900, EY12576, EY013811, EY012859, EY014047, R01 EY014047-05] Funding Source: Medline
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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 FIGS complex (RGS9-1(.)G beta 5L(.)R9AP) dramatically accelerates response recovery. Our results show that G protein deactivation is normally at feast 2.5 times slower than rhodopsin deactivation, resolving a long-standing controversy concerning the mechanism underlying the recovery of rod visual transduction.
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