Abstract
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.