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首页> 外文期刊>Eukaryotic cell >Increased Respiration in the sch9Δ Mutant Is Required for Increasing Chronological Life Span but Not Replicative Life Span
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Increased Respiration in the sch9Δ Mutant Is Required for Increasing Chronological Life Span but Not Replicative Life Span

机译：需要增加sch9Δ突变体中的呼吸作用，以增加时序寿命，而不是复制性寿命

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Loss of the protein kinase Sch9p increases both the chronological life span (CLS) and the replicative life span (RLS) of Saccharomyces cerevisiae by mimicking calorie restriction, but the physiological consequences of SCH9 deletion are poorly understood. By transcriptional profiling of an sch9Δ mutant, we show that mitochondrial electron transport chain genes are upregulated. Accordingly, protein levels of electron transport chain subunits are increased and the oxygen consumption rate is enhanced in the sch9Δ mutant. Deletion of HAP4 and CYT1, both of which are essential for respiration, revert the sch9Δ mutant respiratory rate back to a lower-than-wild-type level. These alterations of the electron transport chain almost completely blocked CLS extension by the sch9Δ mutation but had a minor impact on the RLS. SCH9 thus negatively regulates the CLS and RLS through inhibition of respiratory genes, but a large part of its action on life span seems to be respiration independent and might involve increased resistance to stress. Considering that TOR1 deletion also increases respiration and that Sch9p is a direct target of TOR signaling, we propose that SCH9 is one of the major effectors of TOR repression of respiratory activity in glucose grown cells.
机译：蛋白激酶Sch9p的丢失通过模仿卡路里限制而延长了酿酒酵母的时间寿命（CLS）和复制寿命（RLS），但是 SCH9 删除了解甚少。通过sch9Δ突变体的转录谱，我们表明线粒体电子传输链基因被上调。因此，sch9Δ突变体中电子传输链亚基的蛋白质水平增加，耗氧率提高。对呼吸必不可少的 HAP4 和 CYT1 删除后，会将sch9Δ突变呼吸频率恢复为低于野生状态的水平。类型级别。电子传输链的这些改变几乎完全通过sch9Δ突变阻止了CLS的延伸，但对RLS的影响较小。因此， SCH9 通过抑制呼吸基因来负调控CLS和RLS，但是其对生命的作用很大一部分似乎与呼吸无关，并且可能增加了对压力的抵抗力。考虑到 TOR1 缺失也会增加呼吸作用，并且Sch9p是TOR信号的直接靶点，我们建议 SCH9 是TOR抑制葡萄糖中呼吸活性的主要作用因子之一生长的细胞。

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