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

doi:10.1016/j.neuron.2006.07.010

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

Research output: Contribution to journal › Article › peer-review

214 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 language	English (US)
Pages (from-to)	409-416
Number of pages	8
Journal	Neuron
Volume	51
Issue number	4
DOIs	https://doi.org/10.1016/j.neuron.2006.07.010
State	Published - Aug 17 2006
Externally published	Yes

ASJC Scopus subject areas

General Neuroscience

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10.1016/j.neuron.2006.07.010

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@article{1e5c611844114ddea6e933d480a5a735,

title = "RGS Expression Rate-Limits Recovery of Rod Photoresponses",

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.",

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

note = "Funding Information: This work was funded by NIH grants EY014047 (M.E.B.), EY013811 (C.K.C.), EY011900 (T.G.W.), and EY012859 (V.Y.A.); Research to Prevent Blindness (C.K.C.), the E. Matilda Ziegler Foundation (M.E.B.), the UC Davis MD/PHD program (C.M.K.), NIH Vision Core Grant EY12576 to UC Davis, and equipment funds from the Department of Psychiatry and Behavioral Sciences, the School of Medicine, and the Section of Neurobiology, Physiology and Behavior at UC Davis. We thank Dr. Tom Blankenship (UC Davis) for performing light and electron microscopy, Drs. Melvin Simon, Rehwa Lee, and David Garbers for generously supplying antibodies, and Drs. Denis A. Baylor, King-Wai Yau, and Edward G. Jones for helpful comments on the manuscript. ",

year = "2006",

month = aug,

day = "17",

doi = "10.1016/j.neuron.2006.07.010",

language = "English (US)",

volume = "51",

pages = "409--416",

journal = "Neuron",

issn = "0896-6273",

publisher = "Cell Press",

number = "4",

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TY - JOUR

T1 - RGS Expression Rate-Limits Recovery of Rod Photoresponses

AU - Krispel, Claudia M.

AU - Chen, Desheng

AU - Melling, Nathan

AU - Chen, Yu Jiun

AU - Martemyanov, Kirill A.

AU - Quillinan, Nidia

AU - Arshavsky, Vadim Y.

AU - Wensel, Theodore G.

AU - Chen, Ching Kang

AU - Burns, Marie E.

N1 - Funding Information: This work was funded by NIH grants EY014047 (M.E.B.), EY013811 (C.K.C.), EY011900 (T.G.W.), and EY012859 (V.Y.A.); Research to Prevent Blindness (C.K.C.), the E. Matilda Ziegler Foundation (M.E.B.), the UC Davis MD/PHD program (C.M.K.), NIH Vision Core Grant EY12576 to UC Davis, and equipment funds from the Department of Psychiatry and Behavioral Sciences, the School of Medicine, and the Section of Neurobiology, Physiology and Behavior at UC Davis. We thank Dr. Tom Blankenship (UC Davis) for performing light and electron microscopy, Drs. Melvin Simon, Rehwa Lee, and David Garbers for generously supplying antibodies, and Drs. Denis A. Baylor, King-Wai Yau, and Edward G. Jones for helpful comments on the manuscript.

PY - 2006/8/17

Y1 - 2006/8/17

N2 - 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.

AB - 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.

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U2 - 10.1016/j.neuron.2006.07.010

DO - 10.1016/j.neuron.2006.07.010

M3 - Article

C2 - 16908407

AN - SCOPUS:33746898592

SN - 0896-6273

VL - 51

SP - 409

EP - 416

JO - Neuron

JF - Neuron

IS - 4

ER -

RGS Expression Rate-Limits Recovery of Rod Photoresponses

Abstract

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