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Multi-faceted regulation of mitochondria by TOR.

机译：TOR对线粒体的多方面调节。

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Nutrient-sensing pathways and mitochondrial respiration both have evolutionary conserved roles in aging and longevity. In our recent publi cation, "Extension of chronological life span by reduced TOR signaling requires down-regulation of Sch9p and involves increased mitochondrial OXPHOS complex density" in Aging (www. impactaging.com), we have solidified a mecha nistic and multi-faceted connection between these two aging-associated processes. Building upon our previous study, which showed that reduced signaling through the nutrient-sensing, target of rapamycin (TOR) pathway extends yeast chronological life span in a mitochondrial respiration-dependent fashion, we found that a unique form of mitochondrial regulation is at play. Specifically, the enhanced respiration is mediated by an increased number of oxida-tive phosphorylation (OXPHOS) complexes per organelle, as opposed to increasing the total amount of mitochondria per cell. We speculate that this increase in complex density promotes a unique arrangement of OXPHOS complexes in the inner membrane that allows for a mode of respiration that is less prone to production of damaging reactive oxygen species (ROS), which, in turn, contributes significantly to the extension of yeast chronological life span. One interesting possibility, raised by Finkel, is that the increased OXPHOS complex density may facilitate forma tion of so-called OXPHOS "supercomplexes," which could be one way to allow increased respiration without a concpmitant increase in ROS formation. In the proteomic approach we used in our study to begin to uncover the role of the TOR pathway in controlling mitochondrial activity, we not only uncovered the aforemen tioned effects on OXPHOS complex density, but also that reduced TOR signaling affects mitochondrial composition on multiple levels. Notably, one protein that helps rid the cell of the nitric oxide (NO), Yhblp, is in increased abundance, suggesting the intriguing possibility that TOR regulates mitochondrial NO-dependent processes as part of its stronghold on the organ elle. Finally, our results provide new evidence for a "mitochondrial preconditioning" effect on yeast aging.
机译：营养感应途径和线粒体呼吸在衰老和长寿中均具有进化保守的作用。在我们最近的出版物中，“通过降低TOR信号来延长时间寿命，需要下调Sch9p的含量，并增加线粒体OXPHOS复合物的密度”（www。impactaging.com），我们已经建立了一个机制多面这两个与老化​​相关的过程之间的联系。在我们之前的研究的基础上，该研究表明通过营养敏感的雷帕霉素（TOR）途径靶标减少的信号传导以线粒体呼吸依赖的方式延长了酵母的时间寿命，我们发现线粒体调控的独特形式正在发挥作用。具体而言，与增加每个细胞的线粒体总量相反，增强的呼吸作用是通过每个细胞器中氧化磷酸化（OXPHOS）复合物数量的增加来介导的。我们推测，复合物密度的这种增加促进了内膜中OXPHOS复合物的独特排列，从而使呼吸方式更不易产生破坏性的活性氧（ROS），从而大大促进了活性氧的产生。延长酵母按时间顺序的寿命。 Finkel提出的一种有趣的可能性是，增加的OXPHOS复合物密度可以促进形成所谓的OXPHOS“超级复合物”，这可能是允许呼吸增加而ROS形成没有明显增加的一种方式。在我们的研究中使用的蛋白质组学方法开始揭示TOR途径在控制线粒体活性中的作用，我们不仅发现了对OXPHOS复合物密度的上述影响，而且还发现减少的TOR信号传导在多个水平上影响线粒体的组成。值得注意的是，一种有助于消除细胞中一氧化氮（NO）的蛋白质Yhblp的丰度增加，这表明TOR调节线粒体NO依赖性过程是其在器官上的据点的一种有趣的可能性。最后，我们的结果为酵母的衰老提供了“线粒体预处理”效果的新证据。

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