In Caenorhabditis elegans, the insulin/IGF pathway participates in the decision to initiate dauer development. Dauer is a diapause stage that is triggered by environmental stresses, such as a lack of nutrients. Insulin/IGF receptor mutants arrest constitutively in dauer, an effect that can be suppressed by mutations in other elements of the insulin/IGF pathway or by a reduction in the activity of the nuclear hormone receptor
daf-12. We have isolated a
pkc-1 mutant that acts as a novel suppressor of the dauer phenotypes caused by insulin/IGF receptor mutations. Interactions between insulin/IGF mutants and the
pkc-1 suppressor mutant are similar to those described for
daf-12 or the DAF-12 coregulator
din-1. Moreover, we show that the expression of the DAF-12 target
daf-9, which is normally elevated upon a reduction in insulin/IGF receptor activity, is suppressed in a
pkc-1 mutant background, suggesting that
pkc-1 could link the
daf-12 and insulin/IGF pathways.
pkc-1 has been implicated in the regulation of peptide neurosecretion in C.elegans. Although we demonstrate that
pkc-1 expression in the nervous system regulates dauer formation, our results suggest that the requirement for
pkc-1 in neurosecretion is independent of its role in modulating insulin/IGF signalling.
pkc-1 belongs to the novel protein kinase C (nPKC) family, members of which have been implicated in insulin resistance and diabetes in mammals, suggesting a conserved role for
pkc-1 in the regulation of the insulin/IGF pathway.