The Fly Camta Transcription Factor Potentiates Deactivation of Rhodopsin, a G Protein-coupled Light Receptor.
From: Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Cell
- Publish Date: Nov 2006
- ISSN: 0092-8674
- Volume: 127
- Issue: 4
- Pages: 847-58
- Medium: Print
- Language: English
- Citation (JAMA): Han Junhai, Gong Ping, Reddig Keith, et al. The Fly Camta Transcription Factor Potentiates Deactivation of Rhodopsin, a G Protein-coupled Light Receptor.. Cell Nov 2006;127:847-58
Abstract
Control of membrane-receptor activity is required not only for the accuracy of sensory responses, but also to protect cells from excitotoxicity. Here we report the isolation of two noncomplementary fly mutants with slow termination of photoresponses. Genetic and electrophysiological analyses of the mutants revealed a defect in the deactivation of rhodopsin, a visual G protein-coupled receptor (GPCR). The mutant gene was identified as the calmodulin-binding transcription activator (dCAMTA). The known rhodopsin regulator Arr2 does not mediate this visual function of dCAMTA. A genome-wide screen identified five dCAMTA target genes. Of these, overexpression of the F box gene dFbxl4 rescued the mutant phenotypes. We further showed that dCAMTA is stimulated in vivo through interaction with the Ca(2+) sensor calmodulin. Our data suggest that calmodulin/CAMTA/Fbxl4 may mediate a long-term feedback regulation of the activity of Ca(2+)-stimulating GPCRs, which could prevent cell damage due to extra Ca(2+) influx.
Mesh Headings (Keywords): Animals, Arrestins, Base Sequence, Calmodulin, Drosophila, Drosophila Proteins, F-Box Proteins, Gene Expression Regulation, Molecular Sequence Data, Mutation, Photoreceptors, Invertebrate, Phototransduction, Promoter Regions (Genetics), Protein Binding, RNA, Messenger, Rhodopsin, Trans-Activators
Check for Full Text / PubMed Unique Identifier (PMID): 17110341
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