C. elegans dauer formation (daf) genes are involved in surface antigen switching at the L1 molt. Dauer-constitutive (ts daf-c) mutants express an L1-specific surface antigen on all larval stages (Srf heterochronic expression, SHE).
srf-6 II mutants show SHE but are not ts Daf-c. Epistasis between ts daf-c mutations and dauer-defective (daf-d) mutations suggests that daf-c genes control dauer formation and surface antigen switching through bifurcating pathways. Most daf mutations affect both processes, but ts daf-c mutations in
daf-2 and daf-d mutations in
daf-12 do not affect surface antigen switching. In addition,
daf-11 mutants are only partially penetrant for SHE. All these effects on SHE are gene-specific, rather than allele-specific. ts daf-c mutants exhibit SHE even under non-dauer-inducing conditions. Under dauer-inducing conditions, all daf-c genotypes except for
daf-2 expressed L1-specific antigen at the L2d stage. However, surprisingly, no daf-c dauer larvae expressed the antigen. Interaction between
srf-6 or daf-c mutants and a
srf-2 mutant defective in L1-specific antigen expression was studied. Results with a ts daf-c mutant,
daf-1, indicated that SHE required wild-type activity in
srf-2. In contrast, the
srf-2 defect was partially suppressed by a
srf-6 mutation, suggesting more direct genetic interaction.