期刊
MOLECULAR CELL
卷 42, 期 3, 页码 390-400出版社
CELL PRESS
DOI: 10.1016/j.molcel.2011.03.021
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资金
- Swedish Natural Research Council (VR)
- Knut and Alice Wallenberg Foundation
- Foundation for Strategic Research in Sweden
- Goran Gustafsson Foundation
- EC
- Spanish Ministry of Education and Science
- Spanish Fundacion Ramon Areces
Altered mitochondrial functionality can extend organism life span, but the underlying mechanisms are obscure. Here we report that inactivating SOV1, a member of the yeast mitochondria, translation control (MTC) module, causes a robust Sir2-dependent extension of replicative life span in the absence of respiration and without affecting oxidative damage. We found that SOV1 interacts genetically with the cAMP-PKA pathway and the chromatin remodeling apparatus. Consistently, Sov1p-deficient cells displayed reduced cAMP-PKA signaling and an elevated, Sir2p-dependent, genomic silencing. Both increased silencing and life span extension in sov1 Delta cells require the PKA/Msn2/4p target Pnc1p, which scavenges nicotinamide, a Sir2p inhibitor. Inactivating other members of the MTC module also resulted in Sir2p-dependent life span extension. The data demonstrate that the nuclear silencing apparatus senses and responds to the absence of MTC proteins and that this response converges with a pathway for life span extension elicited by reducing TOR signaling.
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