Mechanistic basis for the failure of cone transducin to translocate: why cones are never blinded by light.

Journal Article (Journal Article)

The remarkable ability of our vision to function under ever-changing conditions of ambient illumination is mediated by multiple molecular mechanisms regulating the light sensitivity of rods and cones. One such mechanism involves massive translocation of signaling proteins, including the G-protein transducin, into and out of the light-sensitive photoreceptor outer segment compartment. Transducin translocation extends the operating range of rods, but in cones transducin never translocates, which is puzzling because cones typically function in much brighter light than rods. Using genetically manipulated mice in which the rates of transducin activation and inactivation were altered, we demonstrate that, like in rods, transducin translocation in cones can be triggered when transducin activation exceeds a critical level, essentially saturating the photoresponse. However, this level is never achieved in wild-type cones: their superior ability to tightly control the rates of transducin activation and inactivation, responsible for avoiding saturation by light, also accounts for the prevention of transducin translocation at any light intensity.

Full Text

Duke Authors

Cited Authors

  • Lobanova, ES; Herrmann, R; Finkelstein, S; Reidel, B; Skiba, NP; Deng, W-T; Jo, R; Weiss, ER; Hauswirth, WW; Arshavsky, VY

Published Date

  • May 19, 2010

Published In

Volume / Issue

  • 30 / 20

Start / End Page

  • 6815 - 6824

PubMed ID

  • 20484624

Pubmed Central ID

  • PMC2883257

Electronic International Standard Serial Number (EISSN)

  • 1529-2401

Digital Object Identifier (DOI)

  • 10.1523/JNEUROSCI.0613-10.2010


  • eng

Conference Location

  • United States