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- W1998852095 abstract "Reactive oxygen species (ROS) play complex roles in aging, having both damaging effects and signaling functions. Transiently elevating mitochondrial stress, including mitochondrial ROS (mtROS), elicits beneficial responses that extend lifespan. However, these adaptive, longevity-signaling pathways remain poorly understood. We show here that Tel1p and Rad53p, homologs of the mammalian DNA damage response kinases ATM and Chk2, mediate a hormetic mtROS longevity signal that extends yeast chronological lifespan. This pathway senses mtROS in a manner distinct from the nuclear DNA damage response and ultimately imparts longevity by inactivating the histone demethylase Rph1p specifically at subtelomeric heterochromatin, enhancing binding of the silencing protein Sir3p, and repressing subtelomeric transcription. These results demonstrate the existence of conserved mitochondria-to-nucleus stress-signaling pathways that regulate aging through epigenetic modulation of nuclear gene expression." @default.
- W1998852095 created "2016-06-24" @default.
- W1998852095 creator A5027656934 @default.
- W1998852095 creator A5079476247 @default.
- W1998852095 creator A5085739157 @default.
- W1998852095 date "2013-06-01" @default.
- W1998852095 modified "2023-10-16" @default.
- W1998852095 title "Epigenetic Silencing Mediates Mitochondria Stress-Induced Longevity" @default.
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- W1998852095 doi "https://doi.org/10.1016/j.cmet.2013.04.003" @default.
- W1998852095 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3694503" @default.
- W1998852095 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23747251" @default.
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