In the sensory system of C. elegans, the candidate odorant receptor gene str-2 is strongly expressed in one of the two AWC neurons and weakly in both ASI neurons. Asymmetric AWC expression results from suppression of str-2 expression by a Ca2+/MAPK signaling pathway in one of the AWC neurons early in development. Here we show that the same Ca2+/MAPK pathway promotes str-2 expression in the AWC and ASI neurons together with multiple cell-autonomous and noncell-autonomous G-protein-signaling pathways. In first-stage larvae and adult animals, signals mediated by the Galpha subunits ODR-3, GPA-2, GPA-5, and GPA-6 and a Ca2+/MAPK pathway involving the Ca2+ channel subunit UNC-36, the CaMKII UNC-43, and the MAPKK kinase NSY-1 induce strong str-2 expression. Cell-specific rescue experiments suggest that ODR-3 and the Ca2+/MAPK genes function in the AWC neurons, but that GPA-5 and GPA-6 function in the AWA and ADL neurons, respectively. In Dauer larvae, the same network of genes promotes strong str-2 expression in the ASI neurons, but ODR-3 functions in AWB and ASH and GPA-6 in AWB. Our results reveal a complex signaling network, encompassing signals from multiple cells, that controls the level of receptor gene expression at different developmental stages.

*Calcium Signaling, *Gene Expression Regulation, *MAP Kinase Signaling System, Animals, Caenorhabditis elegans Proteins/*genetics/metabolism, Caenorhabditis elegans/*genetics/metabolism, GTP-Binding Protein alpha Subunits/genetics/*metabolism, Receptors, Odorant/genetics/metabolism
dx.doi.org/10.1534/genetics.106.058750, hdl.handle.net/1765/14025
Genetics (Print): a periodical record of investigations bearing on heredity and variation
Erasmus MC: University Medical Center Rotterdam

Lans, H, & Jansen, G. (2006). Noncell- and cell-autonomous G-protein-signaling converges with Ca2+/mitogen-activated protein kinase signaling to regulate str-2 receptor gene expression in Caenorhabditis elegans. Genetics (Print): a periodical record of investigations bearing on heredity and variation, 173(3), 1287–1289. doi:10.1534/genetics.106.058750