C. elegans modifies both its behaviors and its development in response to chemical cues from its environment. We have identified chemosensory cells required for normal chemotaxis and dauer formation by killing cells with a laser and testing the behavior of the operated animals. Functions for many amphid cell types have been assigned using this approach: Chemotaxis to cAMP, biotin, and Na+ and a- ions: ASE, ADF, ASG, ASI. Chemotaxis to Iysine: ASE, ASG, ASI, ASK. Initiation of dauer formation: ADF, ASG, ASI. Recovery from the dauer stage: ASJ ( and other minor cells). Chemotaxis to the volatile odorants benzaldehyde and butanone: AWC. For responses for which more than one cell type is listed, all named cells must be killed to eliminate the response entirely. However, different cell types contribute to the responses to different extents. For example, killing only ASE greatly decreases the response to cAMP, biotin, and Na+ and Cl- ions, whereas killing ADF, ASG, and ASI without killing ASE does not affect the response substantially. Thus ASE is a more important component of those responses than the other cells. All neurons listed except AWC sense water-soluble molecules and have endings that are exposed to the environment through the opening of the amphid channel. The AWC neurons sense volatile odorants and have endings that are associated with the amphid sensilla and encased within the amphid sheath cell rather than directly exposed to the environment. Thus different types of sensory neurons recognize water- soluble molecules and volatile odorants in C. elegans. These cell types may be analogous to the different neuron types that mediate taste and olfaction in vertebrates and in Drosophila. To elucidate the chemosensory function and development of these cell types, we are isolating mutants that are defective in their abilities to chemotax to particular attractants. Laser ablations, genetics, and behavioral assays are being used to characterize these mutants. Some genes appear to be required for the function of particular cell types. For example, mutations in the odr-l (odr, odorant response) gene (3 alleles) lead to strong defects in chemotaxis to many volatile odorants but not to water-soluble attractants. In serial electron micrographs, the AWC neurons in some odr-l animals appear to have stunted sensory endings. Other mutations affect subsets of the functions of one or more cell types. For example, mutations in
odr-2 V (3 alleles),
odr-3 V (2 alleles), and
odr-4 III (1 allele) each delete the responses to a unique subset of volatile odorants (we have identifled more than 30 volatile attractants). Some of these genes might encode molecules involved in chemoreception and signal transduction.