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Genetics, Vol. 163, 35-46, January 2003, Copyright © 2003

SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast

Paola Fabrizioa, Lee-Loung Lioub, Vanessa N. Moyb, Alberto Diasproc, Joan Selverstone Valentineb, Edith Butler Grallab, and Valter D. Longoa
a Andrus Gerontology Center and Department of Biological Sciences, University of Southern California, Los Angeles, California 90089-0191,
b Department of Chemistry and Biochemistry, University of California, Los Angeles, California 90095
c Department of Physics, University of Genoa, 16146 Genoa, Italy

Corresponding author: Valter D. Longo, University of Southern California, 3715 McClintock Ave., Los Angeles, CA 90089-0191., vlongo{at}usc.edu (E-mail)

Communicating editor: M. JOHNSTON

Signal transduction pathways inactivated during periods of starvation are implicated in the regulation of longevity in organisms ranging from yeast to mammals, but the mechanisms responsible for life-span extension are poorly understood. Chronological life-span extension in S. cerevisiae cyr1 and sch9 mutants is mediated by the stress-resistance proteins Msn2/Msn4 and Rim15. Here we show that mitochondrial superoxide dismutase (Sod2) is required for survival extension in yeast. Deletion of SOD2 abolishes life-span extension in sch9{Delta} mutants and decreases survival in cyr1:mTn mutants. The overexpression of Sods—mitochondrial Sod2 and cytosolic CuZnSod (Sod1)—delays the age-dependent reversible inactivation of mitochondrial aconitase, a superoxide-sensitive enzyme, and extends survival by 30%. Deletion of the RAS2 gene, which functions upstream of CYR1, also doubles the mean life span by a mechanism that requires Msn2/4 and Sod2. These findings link mutations that extend chronological life span in S. cerevisiae to superoxide dismutases and suggest that the induction of other stress-resistance genes regulated by Msn2/4 and Rim15 is required for maximum longevity extension.




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