DAF-2, DAF-16 AND DAF-23 - GENETICALLY INTERACTING GENES-CONTROLLING DAUER FORMATION IN CAENORHABDITIS-ELEGANS

Under conditions of high population density and low food, Caenorhabdit is elegans forms an alternative third larval stage, called the dauer s tage, which is resistant to desiccation and harsh environments. Geneti c analysis of some dauer constitutive (Daf-c) and dauer defective (Daf -d) mutants has revealed a complex pathway that is likely to function in particular neurons and/or responding tissues. Here we analyze the g enetic interactions between three genes which comprise a branch of the dauer formation pathway that acts in parallel to or downstream of the other branches of the pathway, the Daf-c genes daf-2 and daf-23 and t he Daf-d gene daf-16. Unlike mutations in other Daf-c genes, mutations in both daf-2 and daf-23 cause non-conditional arrest at the dauer st age. Our epistasis analysis suggests that daf-2 and daf-23 are functio ning at a similar point in the dauer pathway. First, mutations in daf- 2 and daf-23 are epistatic to mutations in the same set of Daf-d genes . Second, daf-2 and daf-23 mutants are suppressed by mutations in daf- 16. Mutations in daf-16 do not suppress any of the other Daf-c mutants as efficiently as they suppress daf-2 and daf-23 mutants. Third, doub le mutants between either daf-2 or daf-23 and several other daf-d muta nts exhibit an unusual interaction. Based on these results, we present a model for the function of daf-2, daf-23 and daf-16 in dauer formati on.