The insulin/IGF pathway negatively regulates dauer formation decision and. longevity. We have found that
pkc-1 mutants suppress the dauer constitutive. and longevity phenotypes of some alleles of
daf-2. Those alleles have been. classified as class I, which are also suppressed by mutations in the. nuclear hormone receptor gene
daf-12.. We have found several similarities with
daf-12:. Both are able to suppress
daf-2 mutants without relocating the fork head. transcription factor
daf-16 out of the nucleus. Both are able to suppress
daf-2 mutants without repressing the expression. of
sod-3, a direct target of DAF-16.. Differently to
daf-12, mutations in
pkc-1 does not suppress the dauer. formation of the TGF-B pathway mutants, in fact is enhanced.. These two apparently contradictory results, enhancement of the dauer. formation of the TGF-B pathway and suppression of the dauer formation of. the Insulin/IGF pathway, can be explained if
pkc-1 participates in both. pathways, in one working as positive regulator and in the other as negative. regulator. In agreement with this idea, we have demonstrated, by
pkc-1. complementation using different promoters, that these two functions are. physically separated.. It has been reported that PKC-1 has a role in several processes like. thermotaxis, high osmolarity avoidance and it is necessary for dense core. vesicles secretion, then we propose
pkc-1(
pv12) as the first mutant. affected in neurosecretion that suppresses longevity and dauer formation. phenotypes of the insulin pathway mutants.