Sensory signals regulate multiple developmental and behavioral circuits in C. elegans, providing a genetically tractable system in which to investigate the mechanisms underlying the acquisition and integration of sensory information. kin-29 mutants are defective in the expression of a set of chemoreceptor genes, and exhibit characteristics associated with altered sensory signaling, including increased lifespan, decreased body size, and deregulated entry into the dauer developmental stage. kin-29 encodes a Ser/Thr kinase with similarity to the MARK and AMPK/SNF1 family of kinases. We show that KIN-29 acts cell-autonomously and non-cell-autonomously in sensory neurons to regulate chemoreceptor expression, body size, and the dauer decision, suggesting that kin-29 function is essential for the correct acquisition and transduction of sensory information.
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