Abstract Based on environmental cues, the nervous system of Caenorhabditis ekgans regulates formation of the dauer larva, an alternative larval form specialized for long-term survival under harsh conditions. Mutations that cause constitutive or defective dauer formation (Daf-c or Daf-d) have been identified and the genes ordered in a branched pathway. Most Daf-c mutations also affect recovery from the dauer stage. The semidominant mutation daf-28(sa191) is Daf-c but has no apparent effect on dauer recovery. We use this unique aspect of daf28(sal91) to characterize the effects of several Daf-d and synthetic Daf-c mutations on dauer recovery. We present double mutant analysis that indicates that daf-28(saI91) acts at a novel point downstream in the genetic pathway for dauer formation. We also show that daf-28(sa191) causes a modest increase (12-13%) in life span. The phenotypes and genetic interactions of daf-28(sa191) are most similar to those of daf-2 and daf-23 mutations, which also cause a dramatic increase in life span. We present mapping and complementation data that suggest that daf-23 is the same gene as age-I, identified previously by mutations that extend life span. We find that age-l alleles are also Daf-c at 27°.

Malone, E. A., Inoue, T., & Thomas, J. H. (1996). Genetic Analysis of the Roles of daf28 and age-1 in Regulating Caenorhabditis elegans Dauer Formation. Genetics, 143(3), 1193–1205.