In order to identify the genes associated with behavioral plasticity in sensory neurons, we screened for the mutants that are defective in adaptation/saturation to odorants. A screen was conducted to identify the mutants that did not fail to chemotaxis toward a point source of odorant in a field of same odorant. From approximately 8000 EMS mutagenized animals, we isolated 11 mutants that exhibited defects in adaptation/saturation to the AWC-sensed odorants and 1 mutant that exhibited defect in adaptation to the AWA-sensed odorants. We cloned the Ndr kinase family
sax-1 gene that suppressed the phenotype of one of the mutants. Genetic analysis indicated that the mutated gene is identical with the
sax-1 gene. These results suggest that SAX-1 is essential for olfactory adaptation/saturation.