Nematodes restrict the expresssion of specific surface molecules to a particular time or developmental stage and can switch surface molecules in response to environmental changes. Our study of surface antigen switching in C. elegans has led to the discovery that it is modulated in response to environmental signals, and this response requires functional chemosensory neurons. Previously, we identified a surface antigen switch in which wild type C. elegans is induced to display an L1 surface epitope at a later larval stage (inducible larval display or ILD) when grown under special conditions. We also identified mutations that result in nonconditional display of this epitope on all four larval stages (constitutive larval display or CLD). These include mutations in a new gene,
srf-6 , and in previously identified dauer-constitutive ( daf-c ) genes involved in signal transduction during dauer larva formation. Surface antigen switching and dauer formation are controlled differently. For example,
srf-6 mutations apparently do not affect dauer formation. Examination of double mutants combining
srf-6(
yj13) with ts mutations in daf-c genes suggested that
srf-6 acts in parallel with the TGF- b signaling pathway defined by some daf-c genes, but might act in the same pathway with
daf-11. ILD requires intact sensory cilia. Cilium structure mutations such as
che-3 and
osm-3 resulted in greatly reduced ILD. All sensory cilia are abnormal in
che-3 mutants, while
osm-3 mutations affect only the chemosensory neurons that detect water-soluble substances (taste). A
che-3;
srf-6 double mutant showed no CLD, indicating that intact sensory cilia are required for
srf-6 to affect phenotype. By contrast, mutations that affect olfaction, but not taste, had no effect on ILD. Taken together, these results suggest that ILD requires some ciliated sensory nerve endings, but not the olfactory neurons. In chemotaxis assays,
srf-6(
yj13) showed greatly reduced attraction to both volatile and nonvolatile substances that attract wild type. Taken together, our results are consistent with a model in which
srf-6 activity is required in a chemosensory neuron to inhibit a downstream component that activates expression of the L1 surface epitope at later larval stages.