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Reference: Caballero A, et al. (2011) Absence of mitochondrial translation control proteins extends life span by activating sirtuin-dependent silencing. Mol Cell 42(3):390-400

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Abstract


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 mitochondrial 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 sov1Delta 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.CI - Copyright (c) 2011 Elsevier Inc. All rights reserved.

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Journal Article
Authors
Caballero A, Ugidos A, Liu B, Oling D, Kvint K, Hao X, Mignat C, Nachin L, Molin M, Nystrom T
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