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Boosting ATM activity alleviates ageing and extends lifespan in a mouse model of progeria.

ABSTRACT: Protein deacetylase SIRT6 and protein kinase ATM both decline during aging, which are of importance in regualtion of glucose metabolism . To explore the mechnisms of SIRT6 and ATM in glycolysis, we analysed the gene expressions in murine embryonic fibroblast cells generated from wildtype, Sirt6-/-, or Atm-/- mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE109280 | GEO | 2018/05/05

REPOSITORIES: GEO

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Boosting ATM activity alleviates ageing and extends lifespan in a mouse model of progeria.

Project description:Boosting ATM activity alleviates ageing and extends lifespan in a mouse model of progeria.

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Boosting ATM activity alleviates aging and extends lifespan in a mouse model of progeria.

Project description:DNA damage accumulates with age (Lombard et al., 2005). However, whether and how robust DNA repair machinery promotes longevity is elusive. Here, we demonstrate that ATM-centered DNA damage response (DDR) progressively declines with senescence and age, while low dose of chloroquine (CQ) activates ATM, promotes DNA damage clearance, rescues age-related metabolic shift, and prolongs replicative lifespan. Molecularly, ATM phosphorylates SIRT6 deacetylase and thus prevents MDM2-mediated ubiquitination and proteasomal degradation. Extra copies of Sirt6 extend lifespan in Atm-/- mice, with restored metabolic homeostasis. Moreover, the treatment with CQ remarkably extends lifespan of Caenorhabditis elegans, but not the ATM-1 mutants. In a progeria mouse model with low DNA repair capacity, long-term administration of CQ ameliorates premature aging features and extends lifespan. Thus, our data highlights a pro-longevity role of ATM, for the first time establishing direct causal links between robust DNA repair machinery and longevity, and providing therapeutic strategy for progeria and age-related metabolic diseases.

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