Formation of the C. elegans dauer larva is repressed by the chemosensory neurons ADF, ASI, and ASG. Mutant analysis has defined two parallel genetic pathways that control dauer formation. By killing neurons in these mutants, we show that mutations in one of these genetic pathways disrupt dauer repression by ADF, ASI, and ASG. One gene in this pathway is daf-7, which encodes a TGFbeta-related protein. We find that daf-7::GFP fusions are expressed specifically in ASI and that expression is regulated by dauer-inducing sensory stimuli. We also show that a different chemosensory neuron, ASJ, functions in parallel to these neurons to induce dauer formation. Mutations in the second genetic pathway activate dauer formation in an ASJ-dependent manner. Thus, the genetic redundancy in this process is reflected at the neuronal level.