RT Journal Article SR Electronic T1 Prolonged Photoresponses and Defective Adaptation in Rods of Gβ5-/- Mice JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 6965 OP 6971 DO 10.1523/JNEUROSCI.23-18-06965.2003 VO 23 IS 18 A1 Krispel, Claudia M. A1 Chen, Ching-Kang A1 Simon, Melvin I. A1 Burns, Marie E. YR 2003 UL http://www.jneurosci.org/content/23/18/6965.abstract AB 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 β subunit Gβ5-L. Disruption of the Gβ5 gene in mice (Gβ5-/-) abolishes the expression of Gβ5-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 Gβ5-/- mice. Responses of Gβ5-/- rods were indistinguishable in all respects from those of RGS9-/- rods. Loss of Gβ5-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 Gβ5-/- 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-Gβ5-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.