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Mol Cell. 2011 May 6;42(3):390-400. doi: 10.1016/j.molcel.2011.03.021.

Absence of mitochondrial translation control proteins extends life span by activating sirtuin-dependent silencing.

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  • 1Department of Cell and Molecular Biology, University of Gothenburg, Medicinaregatan 9C, 413 90 Göteborg, Sweden. antonio.caballero_reyes@kcl.ac.uk

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 sov1Δ 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.

Copyright © 2011 Elsevier Inc. All rights reserved.

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PMID:
21549315
[PubMed - indexed for MEDLINE]
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