کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2038515 1072376 2006 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
The Fly CAMTA Transcription Factor Potentiates Deactivation of Rhodopsin, a G Protein-Coupled Light Receptor
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی بیوشیمی، ژنتیک و زیست شناسی مولکولی (عمومی)
پیش نمایش صفحه اول مقاله
The Fly CAMTA Transcription Factor Potentiates Deactivation of Rhodopsin, a G Protein-Coupled Light Receptor
چکیده انگلیسی

SummaryControl 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 Ca2+ sensor calmodulin. Our data suggest that calmodulin/CAMTA/Fbxl4 may mediate a long-term feedback regulation of the activity of Ca2+-stimulating GPCRs, which could prevent cell damage due to extra Ca2+ influx.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: - Volume 127, Issue 4, 17 November 2006, Pages 847–858
نویسندگان
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