Worm Breeder's Gazette 11(3): 66
These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.
A genetic pathway for dauer larva formation has been defined by epistatic relationships between dauer-defective and dauer-constitutive genes. The genetic pathway is proposed to correspond to a neural pathway involved in detection of environmental signals by sensory receptors, followed by transduction of signals to neurosecretory cells. According to this hypothesis, genes in the early steps of the genetic pathway may affect the development or function of sensory neurons, and genes in the late steps are involved in the reception of the neurosecretory signal by target tissues, and activation of dauer larva morphogenesis. We wanted to know whether more dauer-defective genes could be isolated in the late steps of the pathway, and whether there is a dauer-defective mutation that can suppress all dauer- constitutive mutants, including daf-2 and daf-4. To isolate dauer- defective mutants, three approaches were taken: one was to select dauer-defective revertants from EMS mutagenized dauer-constitutive parents, another was to select dauer-defective mutants from dauer- inducing pheromone treated mutator strains, and the third was to select revertants from dauer-constitutive mutants in a mutator background. Twenty-two dauer-defective mutants were selected from about 3 million dauer-inducing pheromone treated larvae of the RW7097 mutator strain. Dauer-defective mutants that fail to respond to the dauer-inducing pheromone grow under these conditions, whereas normal worms form dauer larvae. Also three dauer-defective mutant were selected from dauer-constitutive, mutator backgrounds. Chemotaxis assays and FITC uptake were used to identify the mutants with normal amphids. Only six dauer-defective mutants from mutator strains had normal chemotaxis and FITC uptake. Two represent new genes, daf-26 and daf-27, and the others are known genes; one is daf-5, and three are daf-12. After epistasis tests with all the dauer-constitutive mutants in the genetic pathway, the results showed that daf-26 can suppress daf-1, but not daf-2 and daf-4, and daf-27 can suppress daf-4, but not daf-2. Since three independent transposon-insertion alleles of daf-12 were found, this gene was chosen for cloning. [See Figure 1]