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The Journal of Neuroscience, August 6, 2003, 23(18):6965-6971

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Prolonged Photoresponses and Defective Adaptation in Rods of G{beta}5-/- Mice

Claudia M. Krispel,1,2 Ching-Kang Chen,3 Melvin I. Simon,4 and Marie E. Burns1,2

1Center for Neuroscience and 2Department of Psychiatry, University of California, Davis, Davis, California 95616, 3Department of Ophthalmology, Eccles Institute of Human Genetics, University of Utah, Salt Lake City, Utah 84112, and 4Division of Biology, California Institute of Technology, Pasadena, California 91125

Timely deactivation of G-protein signaling is essential for the proper function of many cells, particularly neurons. Termination of the light response of retinal rods requires GTP hydrolysis by the G-protein transducin, which is catalyzed by a protein complex that includes regulator of G-protein signaling RGS9-1 and the G-protein {beta} subunit G{beta}5-L. Disruption of the G{beta}5 gene in mice (G{beta}5-/-) abolishes the expression of G{beta}5-L in the retina and also greatly reduces the expression level of RGS9-1. We examined transduction in dark- and light-adapted rods from wild-type and G{beta}5-/- mice. Responses of G{beta}5-/- rods were indistinguishable in all respects from those of RGS9-/- rods. Loss of G{beta}5-L (and RGS9-1) had no effect on the activation of the G-protein cascade, but profoundly slowed its deactivation and interfered with the speeding of incremental dim flashes during light adaptation. Both RGS9-/- and G{beta}5-/- responses were consistent with another factor weakly regulating GTP hydrolysis by transducin in a manner proportional to the inward current. Our results indicate that a complex containing RGS9-1-G{beta}5-L is essential for normal G-protein deactivation and rod function. In addition, our light adaptation studies support the notion than an additional weak GTPase-accelerating factor in rods is regulated by intracellular calcium and/or cGMP.

Key words: phototransduction; G-protein; transducin; adaptation; RGS; calcium; cGMP

Received Feb. 26, 2003; revised Jun. 3, 2003; accepted Jun. 5, 2003.




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