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

Abstract:

: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.

journal_name

Neuron

journal_title

Neuron

authors

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

doi

10.1016/s0896-6273(04)00252-1

subject

Has Abstract

pub_date

2004-05-27 00:00:00

pages

581-93

issue

4

eissn

0896-6273

issn

1097-4199

pii

S0896627304002521

journal_volume

42

pub_type

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