A number of mutations in chemosensory behavior are known to affect the ciliary growth of chemosensory neurons, and usually these neurons are completely or partially defective in fluorescein dyes uptake by amphid and phasmid neurons (Hedgecock at al., 1985; Perkins at al., 1986; Starich at al., 1994). An important chemosensory behavior is dauer formation (Cassada and Russell, 1975), which has been analyzed both at genetic and cellular levels (Riddle, 1988; Bergman and Horvitz, 1991). By taking advantage of various alleles of
osm-3, we have shown the FITC uptake by ADF neurons in eight alleles of
osm-3, that display variable penetrance and expressivity. We earlier showed that dauer formation behavior is mediated through ADF chemosensory neurons and the FITC uptake by ADF neurons in various alleles of
osm-3 is directly proportional to the dauer formation behavior (Shakir et al., 1993), providing a convenient approach to define the role of ADF chemosensory neurons in dauer formation behavior. The advantage of the genetic approach is that it can be applied to a very large number of individuals, which is often essential for behavioral studies. We are now analyzing various mutants in genes interacting in the dauer formation pathway, and their interaction with the
osm-3 mutation. Most of the unc mutants usually can concentrate fluorescein dyes in amphid and phasmid neurons, but we find that
unc-119 (
e2498) mutants fail in FITC dye uptake in amphid and phasmid neurons. Since,
unc-119 is affecting dauer formation behavior (Maduro and Pilgrim, 1995), and is defective in chemosensory behavior (our results), we are examining the
unc-119::lacZ fusion gene expression in various
osm-3 alleles to reveal the interaction of
unc-119 and
osm-3 genes in neurons affecting dauer formation and chemosensory behavior.