PT  - JOURNAL ARTICLE
AU  - Krispel, Claudia M.
AU  - Chen, Ching-Kang
AU  - Simon, Melvin I.
AU  - Burns, Marie E.
TI  - Prolonged Photoresponses and Defective Adaptation in Rods of  Gβ5<sup>-/-</sup> Mice
AID  - 10.1523/JNEUROSCI.23-18-06965.2003
DP  - 2003 Aug 06
TA  - The Journal of Neuroscience
PG  - 6965--6971
VI  - 23
IP  - 18
4099  - http://www.jneurosci.org/content/23/18/6965.short
4100  - http://www.jneurosci.org/content/23/18/6965.full
SO  - J. Neurosci.2003 Aug 06; 23
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.