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Comments on T Inoue et al. (1999) International C. elegans Meeting "Characterization of suppressors of daf-1, daf-8 and daf-14." (0)
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T Inoue, & JH Thomas (1999). Characterization of suppressors of daf-1, daf-8 and daf-14 presented in International C. elegans Meeting. Unpublished information; cite only with author permission.
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.
