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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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.
| Item Type: | Articles |
|---|---|
| Status: | Published |
| Refereed: | Yes |
| 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: | 0890-9369 |
| ISSN (Online): | 1549-5477 |
| Published Online: | 11 March 2009 |
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