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Autophagy mediates the mitotic senescence transition

By Andrew R.J. Young, Masako Narita, Manuela Ferreira, Kristina Kirschner, Mahito Sadaie, Jeremy F.J. Darot, Simon Tavaré, Satoko Arakawa, Shigeomi Shimizu, Fiona M. Watt and Masashi Narita

Abstract

As a stress response, senescence is a dynamic process involving multiple effector mechanisms whose combination determines the phenotypic quality. Here we identify autophagy as a new effector mechanism of senescence. Autophagy is activated during senescence and its activation is correlated with negative feedback in the PI3K–mammalian target of rapamycin (mTOR) pathway. A subset of autophagy-related genes are up-regulated during senescence: Overexpression of one of those genes, ULK3, induces autophagy and senescence. Furthermore, inhibition of autophagy delays the senescence phenotype, including senescence-associated secretion. Our data suggest that autophagy, and its consequent protein turnover, mediate the acquisition of the senescence phenotype

Topics: Research Communication
Publisher: Cold Spring Harbor Laboratory Press
OAI identifier: oai:pubmedcentral.nih.gov:2666340
Provided by: PubMed Central
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