Autophagy mediates the mitotic senescence transition

Young, A. R.J. et al. (2009) Autophagy mediates the mitotic senescence transition. Genes and Development, 23(7), pp. 798-803. (doi: 10.1101/gad.519709) (PMID:19279323) (PMCID:PMC2666340)

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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.

Item Type:Articles
Glasgow Author(s) Enlighten ID:Kirschner, Dr Kristina
Authors: Young, A. R.J., Narita, M., Ferreira, M., Kirschner, K., Sadaie, M., Darot, J. F.J., Tavare, S., Arakawa, S., Shimizu, S., Watt, F. M., and Narita, M.
College/School:College of Medical Veterinary and Life Sciences > School of Cancer Sciences
Journal Name:Genes and Development
Publisher:Cold Spring Harbor Laboratory Press
ISSN (Online):1549-5477
Published Online:11 March 2009

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