Transducin activation state controls its light-dependent translocation in rod photoreceptors

Abstract

Light-dependent redistribution of transducin between the rod outer segments (OS) and other photoreceptor compartments including the inner segments (IS) and synaptic terminals (ST) is recognized as a critical contributing factor to light and dark adaptation. The mechanisms of light-induced transducin translocation to the IS/ST and its return to the OS during dark adaptation are not well understood. We have probed these mechanisms by examining light-dependent localizations of the transducin-α subunit (Gtα) in mice lacking the photoreceptor GAP-protein RGS9, or expressing the GTPase-deficient mutant GtαQ200L. An illumination threshold for the Gtα movement out of the OS is lower in the RGS9 knock-out mice, indicating that the fast inactivation of transducin in the wild-type mice limits its translocation to the IS/ST. Transgenic GtαQ200L mice have significantly diminished levels of proteins involved in cGMP metabolism in rods, most notably the PDE6 catalytic subunits, and severely reduced sensitivity to light. Similarly to the native Gtα, the GtαQ200L mutant is localized to the IS/ST compartment in light-adapted transgenic mice. However, the return of GtαQ200L to the OS during dark adaptation is markedly slower than normal. Thus, the light-dependent translocations of transducin are controlled by the GTP-hydrolysis on Gtα, and apparently, do not require Gtα interaction with RGS9 and PDE6. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.