Methionine Restriction and Life-Span Extension

2019 ◽  
pp. 263-266 ◽  
Author(s):  
Robert M. Hoffman
Keyword(s):  
Life Span ◽  
Life Span Extension ◽  
Methionine Restriction

scholarly journals Life-Span Extension in Mice by Preweaning Food Restriction and by Methionine Restriction in Middle Age

2009 ◽  
Vol 64A (7) ◽  
pp. 711-722 ◽  
Author(s):  
L. Sun ◽  
A. A. Sadighi Akha ◽  
R. A. Miller ◽  
J. M. Harper
Keyword(s):  
Life Span ◽  
Food Restriction ◽  
Middle Age ◽  
Life Span Extension ◽  
Methionine Restriction

Methionine restriction beyond life-span extension

2016 ◽  
Vol 1363 (1) ◽  
pp. 68-79 ◽  
Author(s):  
Gene P. Ables ◽  
Julie R. Hens ◽  
Sailendra N. Nichenametla
Keyword(s):  
Life Span ◽  
Life Span Extension ◽  
Methionine Restriction

SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast

Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Paola Fabrizio ◽  
Lee-Loung Liou ◽  
Vanessa N Moy ◽  
Alberto Diaspro ◽  
Joan Selverstone Valentine ◽  
...  
Keyword(s):  
Life Span ◽  
Stress Resistance ◽  
Reversible Inactivation ◽  
Life Span Extension ◽  
Resistance Proteins ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Aconitase ◽  
Chronological Life Span ◽  
Survival Extension ◽  
Mitochondrial Superoxide Dismutase

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 sch9Δ 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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