The fly CAMTA transcription factor potentiates deactivation of rhodopsin, a G protein-coupled light receptor.
Cell
; 127(4): 847-58, 2006 Nov 17.
Article
em En
| MEDLINE
| ID: mdl-17110341
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Rodopsina
/
Transativadores
/
Células Fotorreceptoras de Invertebrados
/
Proteínas de Drosophila
/
Drosophila
Tipo de estudo:
Prognostic_studies
Limite:
Animals
Idioma:
En
Revista:
Cell
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Estados Unidos