| First Author | Krispel CM | Year | 2003 |
| Journal | J Neurosci | Volume | 23 |
| Issue | 18 | Pages | 6965-71 |
| PubMed ID | 12904457 | Mgi Jnum | J:84855 |
| Mgi Id | MGI:2670468 | Doi | 10.1523/JNEUROSCI.23-18-06965.2003 |
| Citation | Krispel CM, et al. (2003) Prolonged photoresponses and defective adaptation in rods of Gbeta5-/- mice. J Neurosci 23(18):6965-71 |
| abstractText | 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 Gbeta5-L. Disruption of the Gbeta5 gene in mice (Gbeta5-/-) abolishes the expression of Gbeta5-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 Gbeta5-/- mice. Responses of Gbeta5-/- rods were indistinguishable in all respects from those of RGS9-/- rods. Loss of Gbeta5-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 Gbeta5-/- 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-Gbeta5-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. |
