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Inhibition of peroxisome fission but not mitochondrial fission increases yeast chronological lifespan

机译:抑制过氧化物酶体裂变但不抑制线粒体裂变可增加酵母的时间寿命

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摘要

Mitochondria are key players in aging and cell death. It has been suggested that mitochondrial fragmentation, mediated by the Dnm1/Fis1 organelle fission machinery, stimulates aging and cell death. This was based on the observation that Saccharomyces cerevisiae Δdnm1 and Δfis1 mutants show an enhanced lifespan and increased resistance to cell death inducers. However, the Dnm1/Fis1 fission machinery is also required for peroxisome division. Here we analyzed the significance of peroxisome fission in yeast chronological lifespan, using yeast strains in which fission of mitochondria was selectively blocked. Our data indicate that the lifespan extension caused by deletion of FIS1 is mainly due to a defect in peroxisome fission and not caused by a block in mitochondrial fragmentation. These observations are underlined by our observation that deletion of FIS1 does not lead to lifespan extension in yeast peroxisome deficient mutant cells.
机译:线粒体是衰老和细胞死亡的关键因素。有人建议,由Dnm1 / Fis1细胞器分裂机制介导的线粒体碎片刺激衰老和细胞死亡。这是基于以下观察结果:酿酒酵母Δdnm1和Δfis1突变体显示出更长的寿命并增加了对细胞死亡诱导剂的抗性。但是,过氧化物酶体的分裂也需要Dnm1 / Fis1裂变机制。在这里,我们使用线粒体裂变被选择性阻断的酵母菌株,分析了过氧化物酶体裂变在酵母时间序列寿命中的重要性。我们的数据表明,由FIS1缺失引起的寿命延长主要归因于过氧化物酶体裂变的缺陷,而不是由线粒体断裂的阻滞引起的。这些观察结果是我们的观察结果所强调的,即删除FIS1不会导致酵母过氧化物酶体缺陷型突变细胞的寿命延长。

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