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Article
Subject Categories: Membranes & Transport | Signal Transduction
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 Han, Keith Reddig and Hong-Sheng Li
Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA, USA

To whom correspondence should be addressed
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; Published online 22 November 2007.
Abstract
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
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