SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast Export

@article{citeulike:3290404, 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 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.}, author = {Fabrizio, Paola and Liou, Lee-Loung and Moy, Vanessa N. and Diaspro, Alberto and Selverstone and Gralla, Edith B. and Longo, Valter D.}, citeulike-article-id = {3290404}, citeulike-linkout-0 = {http://www.genetics.org/cgi/content/abstract/163/1/35}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/12586694}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=12586694}, day = {1}, journal = {Genetics}, keywords = {longevity, mice, pathway, signalling, sod2, yeast, yvonne}, month = {January}, number = {1}, pages = {35--46}, posted-at = {2008-09-18 20:57:01}, priority = {2}, title = {SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast}, url = {http://www.genetics.org/cgi/content/abstract/163/1/35}, volume = {163}, year = {2003} }

TY - JOUR ID - citeulike:3290404 L3 - citeulike-article-id:3290404 N2 - 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. IS - 1 JF - Genetics EP - 46 TI - SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast VL - 163 SP - 35 KW - longevity KW - mice KW - pathway KW - signalling KW - sod2 KW - yeast KW - yvonne AU - Fabrizio, Paola AU - Liou, Lee-Loung AU - Moy, Vanessa AU - Diaspro, Alberto AU - Selverstone AU - Gralla, Edith AU - Longo, Valter PY - 2003/01/01/ UR - http://www.genetics.org/cgi/content/abstract/163/1/35 ER -