title: pkc-1 regulates daf-2 insulin/IGF signalling-dependent control of dauer formation in Caenorhabditis elegans.
abstract: 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.
authors.affiliation: Centro Andaluz de Biología del Desarrollo (CABD), CSIC/Universidad Pablo de Olavide, Seville, Spain.
authors.forename: José M
authors.initials: JM
authors.lastname: Monje
authors.forename: Ana M
authors.initials: AM
authors.lastname: Brokate-Llanos
authors.forename: Mercedes M
authors.initials: MM
authors.lastname: Pérez-Jiménez
authors.forename: Manuel A
authors.initials: MA
authors.lastname: Fidalgo
authors.forename: Manuel J
authors.initials: MJ
authors.lastname: Muñoz
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D030801:Animals, Genetically Modified; D017173:Caenorhabditis elegans / Q000235:genetics / Q000378:metabolism*; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism; D003577:Cytochrome P-450 Enzyme System / Q000235:genetics / Q000378:metabolism; D005786:Gene Expression Regulation / Q000502:physiology*; D005838:Genotype; D006801:Humans; D007328:Insulin / Q000378:metabolism; D008018:Life Cycle Stages / Q000235:genetics*; D008136:Longevity / Q000235:genetics*; D009154:Mutation; D010641:Phenotype; D011493:Protein Kinase C / Q000235:genetics / Q000378:metabolism; D011972:Receptor, Insulin / Q000235:genetics / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction / Q000235:genetics*; D013002:Somatomedins / Q000235:genetics / Q000378:metabolism*; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism
chemical_list: D029742:Caenorhabditis elegans Proteins; C410905:DAF-12 protein, C elegans; C492744:Din-1 protein, C elegans; D007328:Insulin; D018160:Receptors, Cytoplasmic and Nuclear; D013002:Somatomedins; D014157:Transcription Factors; D003577:Cytochrome P-450 Enzyme System; C486228:DAF-9 protein, C elegans; D011972:Receptor, Insulin; D011493:Protein Kinase C