RGS Expression Rate-Limits Recovery of Rod Photoresponses

Claudia M. Krispel, Desheng Chen, Nathan Melling, Yu Jiun Chen, Kirill A. Martemyanov, Nidia Quillinan, Vadim Y. Arshavsky, Theodore G. Wensel, Ching Kang Chen, Marie E Burns

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181 Scopus citations

Abstract

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·Gβ5L·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.

Original languageEnglish (US)
Pages (from-to)409-416
Number of pages8
JournalNeuron
Volume51
Issue number4
DOIs
StatePublished - Aug 17 2006

ASJC Scopus subject areas

  • Neuroscience(all)

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    Krispel, C. M., Chen, D., Melling, N., Chen, Y. J., Martemyanov, K. A., Quillinan, N., Arshavsky, V. Y., Wensel, T. G., Chen, C. K., & Burns, M. E. (2006). RGS Expression Rate-Limits Recovery of Rod Photoresponses. Neuron, 51(4), 409-416. https://doi.org/10.1016/j.neuron.2006.07.010