Graduate School of Biological Sciences, Nara Institute of Science and Technology, 8916-5 Takayama, Ikoma, Nara 630-0192, Japan.
FEBS Lett. 2012 Jul 30;586(16):2411-6. doi: 10.1016/j.febslet.2012.05.056. Epub 2012 Jun 12.
The proline metabolism intermediate Δ(1)-pyrroline-5-carboxylate (P5C) induces cell death in animals, plants and yeasts. To elucidate how P5C triggers cell death, we analyzed P5C metabolism, mitochondrial respiration and superoxide anion generation in the yeast Saccharomyces cerevisiae. Gene disruption analysis revealed that P5C-mediated cell death was not due to P5C metabolism. Interestingly, deficiency in mitochondrial respiration suppressed the sensitivity of yeast cells to P5C. In addition, we found that P5C inhibits the mitochondrial respiration and induces a burst of superoxide anions from the mitochondria. We propose that P5C regulates cell death via the inhibition of mitochondrial respiration.
脯氨酸代谢中间产物 Δ(1)-吡咯啉-5-羧酸（P5C）会诱导动物、植物和酵母细胞死亡。为了阐明 P5C 如何引发细胞死亡，我们分析了酵母酿酒酵母中 P5C 代谢、线粒体呼吸和超氧阴离子生成。基因敲除分析表明，P5C 介导的细胞死亡不是由于 P5C 代谢。有趣的是，线粒体呼吸缺陷抑制了酵母细胞对 P5C 的敏感性。此外，我们发现 P5C 抑制线粒体呼吸并诱导线粒体中超氧阴离子的爆发。我们提出，P5C 通过抑制线粒体呼吸来调节细胞死亡。
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