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Genome screen identifies mechanism of Mitochondria-Insulin signalling crosstalk in the regulation of the UPRmt

AutorHernando-Rodríguez, Blanca; Jarit-Cabanillas, Aitor; Kaderali, Lars; Artal-Sanz, Marta
Fecha de publicación2017
CitaciónVI Spanish Worm Meeting (2017)
ResumenDepletion of the mitochondrial prohibitin complex (PHB) shows an opposite effect on aging: it shortens lifespan in wild-type worms while it dramatically extends the longevity of the already long-lived insulin/IGF-1 signaling (IIS) pathway mutants. Moreover, PHB depletion induces a strong mitochondrial unfolded protein response (UPRmt) in wild-type animals while this response is remarkably reduced in IIS mutants. Interestingly, some of the described UPRmt components are not required for the activation of the response upon PHB depletion. We present data from RNAi screens identifying new pathways involved in the regulation of the PHB-mediated mitochondrial stress response. In addition of transcription, protein synthesis and protein processing, we described conserved signal transduction pathways, such as MAPK signaling and TGF-ß signaling pathways, as essential modulators of the mitochondrial stress response. Furthermore we report pathways regulating the UPRmt in an insulin-dependent manner. Our results suggest a difference in metabolism between PHB-depleted worms and PHB-depleted;IIS mutants and place carbohydrate and lipid metabolism as possible mechanisms contributing to the differential effect of PHB depletion in the aging phenotype of wild-type and metabolically compromised animals.
DescripciónResumen del trabajo presentado al VI Spanish Worm Meeting, celebrado en Valencia del 9 al 10 de marzo de 2017.
URIhttp://hdl.handle.net/10261/163860
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