G protein-coupled receptor kinase function is essential for chemosensation in C. elegans.

Published

Journal Article

G protein-coupled receptors (GPCRs) mediate diverse signaling processes, including olfaction. G protein-coupled receptor kinases (GRKs) are important regulators of G protein signal transduction that specifically phosphorylate activated GPCRs to terminate signaling. Despite previously described roles for GRKs in GPCR signal downregulation, animals lacking C. elegans G protein-coupled receptor kinase-2 (Ce-grk-2) function are not hypersensitive to odorants. Instead, decreased Ce-grk-2 function in adult sensory neurons profoundly disrupts chemosensation, based on both behavioral analysis and Ca(2+) imaging. Although mammalian arrestin proteins cooperate with GRKs in receptor desensitization, loss of C. elegans arrestin-1 (arr-1) does not disrupt chemosensation. Either overexpression of the C. elegans Galpha subunit odr-3 or loss of eat-16, which encodes a regulator of G protein signaling (RGS) protein, restores chemosensation in Ce-grk-2 mutants. These results demonstrate that loss of GRK function can lead to reduced GPCR signal transduction and suggest an important role for RGS proteins in the regulation of chemosensation.

Full Text

Duke Authors

Cited Authors

  • Fukuto, HS; Ferkey, DM; Apicella, AJ; Lans, H; Sharmeen, T; Chen, W; Lefkowitz, RJ; Jansen, G; Schafer, WR; Hart, AC

Published Date

  • May 27, 2004

Published In

Volume / Issue

  • 42 / 4

Start / End Page

  • 581 - 593

PubMed ID

  • 15157420

Pubmed Central ID

  • 15157420

International Standard Serial Number (ISSN)

  • 0896-6273

Digital Object Identifier (DOI)

  • 10.1016/s0896-6273(04)00252-1

Language

  • eng

Conference Location

  • United States