Authors: Malone EA; Inoue T; Thomas JH
Abstract: Based on environmental cues, the nervous system of Caenorhabditis elegans 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 semi-dominant mutation daf-28(sa191) is Daf-c but has no apparent effect on dauer recovery. We use this unique aspect of daf-28(sa191) 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(sa191) 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-1, identified previously by mutations that extend life span. We find that age-1 alleles are also Daf-c at 27 degrees.Keywords: Alleles; Animals; Caenorhabditis elegans/*genetics/*growth & development; *Epistasis, Genetic; Mutation
Date: July 1, 1996
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Malone EA, Inoue T, Thomas JH (1996) Genetic analysis of the roles of daf-28 and age-1 in regulating Caenorhabditis elegans dauer formation. Genetics 143: 1193-205.