Chemotaxis to water-soluble chemicals such as sodium ion is an important behavior of Caenorhabditis elegans for seeking food, and ASE chemosensory neurons have a major role in this behavior. We isolated mutants defective in chemotaxis to sodium acetate. We show here that among them
ks86 had a mutation in the
ceh-36 gene.
ceh-36 :: gfp reporter constructs were expressed in ASE and AWC neurons. In a mutant of the
che-1 gene, which encodes another transcription factor and is required for specification of ASE neurons, expression of the
ceh-36 :: gfp reporter in ASE is lost. This indicates that the
ceh-36 gene functions downstream of the
che-1 gene in ASE. In the
ceh-36(
ks86) mutant, expression of the
tax-2 gene encoding a cyclic nucleotide-gated channel was reduced in ASE and AWC. This affords an explanation for defects of the
ceh-36 mutant in the chemotaxis mediated by ASE and AWC. When a
ceh-36 cDNA was expressed in an adult
ceh-36 mutant by a heat shock promoter, chemotaxis to sodium acetate was recovered. These results suggest that
ceh-36 is required for functions, and not for development, of ASE.