The C. elegans EGF receptor homolog, LET-23, signals through the Ras/MAPK pathway to specify cell fates during development, and signals through a PLC-<font face=symbol>g</font>/IP3 pathway in the adult spermatheca to regulate ovulation. We have been investigating a novel role for LET-23 in the regulation of behavior. We have found that expression of LIN-3/EGF from a heat-shock inducible promoter at any stage inhibits pharyngeal pumping and movement, and that induction of this sleep-like state by LIN-3 is dependent on LET-23, PLC-<font face=symbol>g</font>(
plc-3), DAG-binding proteins, and regulators of synaptic vesicle release. We have determined the site of action for LET-23 in this pathway to be the ALA neuron, which has not been previously ascribed a function. We find that LET-23 is expressed in ALA, and that disruption of ALA function, by genetic methods (
ceh-17(lf) or
deg-3(gf) mutants) or by laser ablation, abolishes the effects of LIN-3 on feeding and movement. In addition, ALA-ablated animals show movement defects that are not attributable to loss of EGFR signaling, suggesting an additional EGFR-independent role of this neuron in regulating locomotion. Quiescent states in C. elegans occur during dauer, lethargus, oxygen deprivation, and satiety. We have analyzed the phenotypes of
let-23 and
plc-3 mutants in these states and have observed an increase in pharyngeal pumping and movement specifically during lethargus. Here we present the results of these quiescence studies, our site of action analysis for LET-23, and our analysis of both the EGF-dependent and EGF-independent functions of the ALA neuron in the regulation of behavior.