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Regulation of yeast replicative life span by TOR and Sch9 in response to nutrients

机译:TOR和Sch9对营养物质的响应调节酵母复制寿命

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Calorie restriction increases life span in many organisms, including the budding yeast Saccharomyces cerevisiae. From a large-scale analysis of 564 single-gene-deletion strains of yeast, we identified 10 gene deletions that increase replicative life span. Six of these correspond to genes encoding components of the nutrient-responsive TOR and Sch9 pathways. Calorie restriction of tor1 Delta or sch9 Delta cells failed to further increase life span and, like calorie restriction, deletion of either SCH9 or TOR1 increased life span independent of the Sir2 histone deacetylase. We propose that the TOR and Sch9 kinases define a primary conduit through which excess nutrient intake limits longevity in yeast.
机译:热量限制会延长许多生物的寿命,包括发芽的酵母酿酒酵母。通过对564个单基因缺失酵母菌株的大规模分析,我们确定了10个基因缺失,这些基因缺失可延长复制寿命。其中六个对应于编码营养响应性TOR和Sch9途径组分的基因。限制tor1或sch9 Delta细胞的热量无法进一步延长寿命,并且像限制卡路里一样,删除SCH9或TOR1可以延长寿命,而与Sir2组蛋白脱乙酰基酶无关。我们建议TOR和Sch9激酶定义一条主要管道,过量的营养摄入通过该管道限制酵母的寿命。

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