Animals regulate their development in response to changing environmental conditions and their internal metabolic status. This developmental plasticity is mediated by changes in gene expression, but the exact mechanisms by which environmental signals are transduced and integrated with internal status to affect developmental programs are poorly understood. C. elegans responds to conditions of overcrowding, limited food and high temperature by arresting development as a dauer larva. High levels of secreted ascaroside pheromone serve as the primary signal to trigger entry into the dauer stage (Golden & Riddle, 1982; Jeong et al., 2005; Butcher et al., 2008). We and others previously showed that pheromone exposure down-regulates expression of a
daf-7 TGF-b and a subset of putative G-protein coupled chemosensory receptor genes such as
str-3 in the ASI neurons; this downregulation influences dauer formation (Nolan et al., 2002; Peckol et al., 1999; Kim et al., 2009). To identify the signaling pathways and genes required for this pheromone-regulated gene expression and dauer formation, we performed a genetic screen and also examined candidate genes (Kim et al., 2009). These analyses showed that the
cmk-1 (CaM kinase I) and
ckk-1(CaM kinase kinase) genes are required to downregulate
str-3 GPCR expression upon pheromone exposure. As expected,
cmk-1 mutants are also defective in the pheromone-mediated dauer decision. Additionally, we found that
crh-1 (CREB) is required for
str-3 expression even in the absence of pheromone. Surprisingly, CMK-1 and CRH-1 act non-autonomously in the ASE/AWC chemosensory neurons to regulate
str-3 expression in the ASI neurons, suggesting that
cmk-1 and/or
crh-1 may act in these neurons to transmit environmental signals to ASI. The phenotypic analyses of double mutants indicate that the CMK-1 and CRH-1 may act in parallel pathways. Current experiments are aimed at identifying the sensory cues that regulate
str-3 expression, and investigating the mechanisms by which information is transmitted from the AWC/ASE to the ASI neurons.