SOD2 functions downstream of Sch9 to extend longevity in yeast.

Authors: Fabrizio P; Liou LL; Moy VN; Diaspro A; Valentine JS; Gralla EB; Longo VD
Year: 2003
Journal: Genetics
Abstract: 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 sch9Delta 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.
Reference

Integration:

Created on Nov. 5, 2012, 4:45 p.m.
Not linked
Integrated: False

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Species: Budding yeast

Experiments: 0
Interventions:

CTT1 overexpression

COQ3 deletion

MSN2 MSN4 double mutation

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