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首页> 外文期刊>PLoS Genetics >A Regulated Response to Impaired Respiration Slows Behavioral Rates and Increases Lifespan in Caenorhabditis elegans
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A Regulated Response to Impaired Respiration Slows Behavioral Rates and Increases Lifespan in Caenorhabditis elegans

机译：对呼吸受损的受调节反应减缓行为率和增加秀丽隐杆线虫的寿命

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When mitochondrial respiration or ubiquinone production is inhibited in Caenorhabditis elegans, behavioral rates are slowed and lifespan is extended. Here, we show that these perturbations increase the expression of cell-protective and metabolic genes and the abundance of mitochondrial DNA. This response is similar to the response triggered by inhibiting respiration in yeast and mammalian cells, termed the “retrograde response”. As in yeast, genes switched on in C. elegans mitochondrial mutants extend lifespan, suggesting an underlying evolutionary conservation of mechanism. Inhibition of fstr-1, a potential signaling gene that is up-regulated in clk-1 (ubiquinone-defective) mutants, and its close homolog fstr-2 prevents the expression of many retrograde-response genes and accelerates clk-1 behavioral and aging rates. Thus, clk-1 mutants live in “slow motion” because of a fstr-1/2–dependent pathway that responds to ubiquinone. Loss of fstr-1/2 does not suppress the phenotypes of all long-lived mitochondrial mutants. Thus, although different mitochondrial perturbations activate similar transcriptional and physiological responses, they do so in different ways.
机译：当在八角杆菌中抑制线粒体呼吸或泛醌产量时，行为率减缓，延长了寿命。在这里，我们表明这些扰动增加了细胞保护和代谢基因的表达和线粒体DNA的丰度。这种反应类似于通过抑制酵母和哺乳动物细胞呼吸而引发的响应，称为“逆行反应”。如在酵母中，基因在C.秀丽隐杆线虫细胞突变体中开启了延长了寿命，暗示了机制的潜在进化守恒。 FSTR-1的抑制，在CLK-1（缺乏缺陷型）突变体中上调的潜在信号基因及其关闭同源物FSTR-2可防止许多逆行响应基因的表达，并加速CLK-1行为和老化费率。因此，由于FSTR-1/2依赖性途径，CLK-1突变体居住在“慢动作”中，其响应泛醌。 FSTR-1/2的丧失不会抑制所有长寿命的线粒体突变体的表型。因此，虽然不同的线粒体扰动激活了类似的转录和生理反应，但它们以不同的方式这样做。

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