Prolonged G(q) activity triggers fly rhodopsin endocytosis and degradation, and reduces photoreceptor sensitivity
Document Type
Journal ArticlePublication Date
2007-12-12Keywords
AnimalsAnimals, Genetically Modified
Arrestins
Drosophila Proteins
*Drosophila melanogaster
Dynamins
Endocytosis
GTP-Binding Protein alpha Subunits, Gq-G11
Light
Membrane Proteins
Phospholipase C beta
Photoreceptor Cells, Invertebrate
Recombinant Fusion Proteins
Rhodopsin
Second Messenger Systems
Trans-Activators
Neuroscience and Neurobiology
Metadata
Show full item recordAbstract
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 G(q) 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 G(q)-stimulated Rh1 endocytosis does not require phospholipase C, a known effector of G(q), 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.Source
EMBO J. 2007 Dec 12;26(24):4966-73. Epub 2007 Nov 22. Link to article on publisher's siteDOI
10.1038/sj.emboj.7601929Permanent Link to this Item
http://hdl.handle.net/20.500.14038/38008PubMed ID
18034157Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1038/sj.emboj.7601929