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Mammalian SIRT1 limits replicative life span in response to chronic genotoxic stress.

Abstract：

:The Saccharomyces cerevisiae chromatin silencing factor Sir2 suppresses genomic instability and extends replicative life span. In contrast, we find that mouse embryonic fibroblasts (MEFs) deficient for SIRT1, a mammalian Sir2 homolog, have dramatically increased resistance to replicative senescence. Extended replicative life span of SIRT1-deficient MEFs correlates with enhanced proliferative capacity under conditions of chronic, sublethal oxidative stress. In this context, SIRT1-deficient cells fail to normally upregulate either the p19(ARF) senescence regulator or its downstream target p53. However, upon acute DNA damage or oncogene expression, SIRT1-deficient cells show normal p19(ARF) induction and cell cycle arrest. Together, our findings demonstrate an unexpected SIRT1 function in promoting replicative senescence in response to chronic cellular stress and implicate p19(ARF) as a downstream effector in this pathway.

journal_name

Cell Metab

journal_title

Cell metabolism

authors

Chua KF,Mostoslavsky R,Lombard DB,Pang WW,Saito S,Franco S,Kaushal D,Cheng HL,Fischer MR,Stokes N,Murphy MM,Appella E,Alt FW

doi

10.1016/j.cmet.2005.06.007

keywords:

subject

Has Abstract

pub_date

2005-07-01 00:00:00

pages

67-76

issue

1

eissn

1550-4131

issn

1932-7420

pii

S1550-4131(05)00172-5

journal_volume

2

pub_type

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