Dauer formation is controlled in part by a TGF-beta related signal transduction pathway. Mutations in some of these components (
daf-1, -4, -7, -8, and -14 ) lead to constitutive dauer formation under dauer non-inducing conditions. In order to identify additional components of the dauer pathway, we isolated 36 independent mutations that suppress the Daf-c phenotype of
daf-1,
daf-8 or
daf-14 . We tentatively classify the mutations into three categories: 1) alleles of
daf-3,
daf-5 and
daf-12 . These genes were previously identified in screens for suppressors of
daf-4 and
daf-7 . Many of these alleles suppress dauer formation completely, even under dauer inducing conditions. 2)
sa315 . This unique mutation suppresses the Daf-c phenotype strongly, with a small fraction of animals forming partial dauers. Interactions of this mutation with various Daf-c genes are somewhat similar to those of
daf-16,
daf-18, and
akt-1(dm) , perhaps indicating a defect in the
daf-2/age-1 insulin receptor pathway. Curiously,
sa315 maps to the same genetic interval as
age-1 . We are currently testing to see if this is an unusual allele of
age-1 . The third class of mutations suppress the Daf-c phenotype of
daf-1, -8 or -14 incompletely (90-99% suppressed at 25C), and where tested, also weakly suppress
daf-4 and/or
daf-7 . So far, mapping and complementation tests among these suppressors have revealed three new genes. These genes were not found in previous screens probably because the suppression is relatively weak. Currently, we are characterizing further these suppressors. As part of this analysis, we are cloning
scd-1 , one of the incomplete suppressor genes.
scd-1 suppresses all pleiotropies of
daf-8, -7, and -14 but does not suppress
daf-11, suggesting that it may be a novel component of the TGF-beta-related signal transduction mechanism.