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首页> 外文期刊>Cell metabolism >Regulation of yeast chronological life span by TORC1 via adaptive mitochondrial ROS signaling.
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Regulation of yeast chronological life span by TORC1 via adaptive mitochondrial ROS signaling.

机译：通过自适应线粒体ROS信号由TORC1调节酵母的时间寿命。

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摘要

Here we show that yeast strains with reduced target of rapamycin (TOR) signaling have greater overall mitochondrial electron transport chain activity during growth that is efficiently coupled to ATP production. This metabolic alteration increases mitochondrial membrane potential and reactive oxygen species (ROS) production, which we propose supplies an adaptive signal during growth that extends chronological life span (CLS). In strong support of this concept, uncoupling respiration during growth or increasing expression of mitochondrial manganese superoxide dismutase significantly curtails CLS extension in tor1Delta strains, and treatment of wild-type strains with either rapamycin (to inhibit TORC1) or menadione (to generate mitochondrial ROS) during growth is sufficient to extend CLS. Finally, extension of CLS by reduced TORC1/Sch9p-mitochondrial signaling occurs independently of Rim15p and is not a function of changes in media acidification/composition. Considering the conservation of TOR-pathway effects on life span, mitochondrial ROS signaling may be an important mechanism of longevity regulation in higher organisms.
机译：在这里，我们显示具有减少的雷帕霉素（TOR）信号靶标的酵母菌株在生长过程中具有更高的整体线粒体电子传输链活性，可以有效地与ATP产生偶联。这种代谢改变增加了线粒体膜电位和活性氧（ROS）的产生，我们建议在生长过程中提供适应性信号，从而延长时间寿命（CLS）。在此概念的有力支持下，生长过程中的呼吸解耦或线粒体锰超氧化物歧化酶表达的增加显着降低了tor1Delta菌株的CLS延伸，并用雷帕霉素（抑制TORC1）或甲萘醌（产生线粒体ROS）治疗野生型菌株生长期间足以延长CLS。最后，通过减少的TORC1 / Sch9p-线粒体信号传导而进行的CLS延伸独立于Rim15p发生，并且与培养基酸化/组成的变化无关。考虑到TOR途径对生命的影响的保守性，线粒体ROS信号可能是高等生物中长寿调节的重要机制。

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