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

Journal article
Authors Antonio Caballero
Ana Ugidos
Beidong Liu
David Öling
Kristian Kvint
Xinxin Hao
Cora Mignat
Laurence Nachin
Mikael Molin
Thomas Nyström
Published in Molecular cell
Volume 42
Issue 3
Pages 390-400
ISSN 1097-4164
Publication year 2011
Published at Department of Cell and Molecular Biology
Pages 390-400
Language en
Subject categories Biological Sciences, Cell and molecular biology, Molecular biology, Cell Biology, Microbiology


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.

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