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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/128968
Título

pkc-1 regulates daf-2 insulin/IGF signalling-dependent control of dauer formation in Caenorhabditis elegans

AutorMonje, José Manuel ; Brokate-Llanos, Ana María ; Pérez-Jiménez, Mercedes M. ; Fidalgo, Manuel A.; Muñoz, Manuel J.
Palabras claveProtein kinase C
C. elegans
Dauer
Insulin
Nuclear hormone
Longevity
Fecha de publicación2011
EditorBlackwell Publishing
CitaciónAging Cell 10(6): 1021-1031 (2011)
ResumenIn 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.
URIhttp://hdl.handle.net/10261/128968
DOI10.1111/j.1474-9726.2011.00747.x
Identificadoresdoi: 10.1111/j.1474-9726.2011.00747.x
issn: 1474-9718
e-issn: 1474-9726
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