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MBC in Press, published online ahead of print February 23, 2005
Mol. Biol. Cell 10.1091/mbc.E04-12-1044

A more recent version of this article appeared on May 1, 2005
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Submitted on December 2, 2004
Revised on February 10, 2005
Accepted on February 11, 2005

Lysophosphatidylcholine-induced Surface Redistribution Regulates Signaling of the Murine G-Protein-coupled Receptor G2A

Li Wang,* Caius G. Radu,* Li V. Yang,{dagger} Laurent A. Bentolila,{ddagger} Mireille Riedinger,{dagger} and Owen N. Witte*{dagger}

*Department of Microbiology, Immunology, and Molecular Genetics, {dagger}Howard Hughes Medical Institute/UCLA, and {ddagger}Department of Chemistry and Biochemistry, University of California Los Angeles, CA 90095

Monitoring Editor: Sandra Schmid

Intracellular trafficking and spatial dynamics of membrane receptors critically regulate receptor function. Using microscopic and subcellular fractionation analysis, we studied the localization of the murine G-protein-coupled receptor G2A (muG2A). Evaluating GFP tagged-exogenously expressed, as well as the endogenous muG2A, we observed that this receptor was spontaneously internalized and accumulated in endosomal compartments, while its surface expression was enhanced and stabilized by LPC treatment. Monensin, a general inhibitor of recycling pathways, blocked LPC-regulated surface localization of muG2A, as well as muG2A-dependent ERK activation and cell migration induced by LPC treatment. Mutation of the conserved DRY motif (R->A) enhanced the surface expression of muG2A, resulting in its resistance to monensin inhibition of ERK activation. Our data suggest that intracellular sequestration and surface expression regulated by LPC, rather than direct agonistic activity control the signaling responses of murine G2A toward LPC.

Address correspondence to: Owen N. Witte (owenw{at}microbio.ucla.edu)




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