Prolonged photoresponses and defective adaptation in rods of Gβ5 -/- mice

Claudia M. Krispel, Ching Kang Chen, Melvin I. Simon, Marie E. Burns

Research output: Contribution to journalArticlepeer-review

77 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)6965-6971
Number of pages7
JournalJournal of Neuroscience
Issue number18
StatePublished - Aug 6 2003
Externally publishedYes


  • Adaptation
  • Calcium
  • G-protein
  • Phototransduction
  • RGS
  • Transducin
  • cGMP

ASJC Scopus subject areas

  • General Neuroscience


Dive into the research topics of 'Prolonged photoresponses and defective adaptation in rods of Gβ5 -/- mice'. Together they form a unique fingerprint.

Cite this