Article

  • The EMBO Journal (2007) 26, 4966 - 4973
  • doi:10.1038/sj.emboj.7601929

Published online: 22 November 2007

Prolonged Gq activity triggers fly rhodopsin endocytosis and degradation, and reduces photoreceptor sensitivity

Junhai Han1, Keith Reddig1 and Hong-Sheng Li1

  1. Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA, USA

Correspondence to:

Hong-Sheng Li, Department of Neurobiology, University of Massachusetts Medical School, 364 Plantation Street, Worcester, MA 1605, USA. Tel.: +1 508 856 6702; Fax: +1 508 856 6070; E-mail: Hong-Sheng.Li@umassmed.edu

Received 16 May 2007; Accepted 26 October 2007


Rapid deactivation of the Drosophila light receptor rhodopsin, through a visual arrestin Arr2 and a pathway that involves a transcription factor dCAMTA, is required for timely termination of light responses in the photoreceptor neuron. Here we report that this process is also critical for maintenance of the photoreceptor sensitivity. In both dCAMTA- and arr2-mutant flies, the endocytosis of the major rhodopsin Rh1 was dramatically increased, which was mediated by a Gq protein that signals downstream of rhodopsin in the visual transduction pathway. Consequently, the Rh1 level was downregulated and the photoreceptor became less sensitive to light. Remarkably, the Gq-stimulated Rh1 endocytosis does not require phospholipase C, a known effector of Gq, but depends on a tetraspanin protein. Our work has identified an arrestin-independent endocytic pathway of G protein-coupled receptor in the fly. This pathway may also function in mammals and mediate an early feedback regulation of receptor signaling.

  • Keywords:

    • CAMTA,
    • endocytosis,
    • GPCR,
    • G protein,
    • tetraspanin