内在的亡途径调解了C. elegans中对线粒体ROS的亲长寿反应
Callista Yee1, Wen Yang1, Siegfried Hekimi1
1Department of Biology, McGill University, Montreal, QC H3A 1B1, Canada.
Cell
|May 13, 2014
概括
线粒体ROS信号传递通过激活细胞亡途径来延长C. elegans的寿命,而不是诱导细胞死亡,而是触发保护性基因表达并促进压力下的生存.
科学领域:
- 细胞生物学 细胞生物学
- 衰老的研究研究.
- 线粒体功能 线粒体功能
背景情况:
- 在C. elegans电子运输链突变体中,长寿的增加与线粒体的活性氧物种 (mtROS) 信号传递有关.
- 本质性亡途径是一种参与细胞对压力和损伤反应的保存机制.
研究的目的:
- 阐明调解C. elegans电子运输链突变物长寿的信号通路.
- 调查内在亡途径在对mtROS升高的反应中的作用.
- 确定通过亡途径传递mtROS信号是否可以促进独立于亡的生存.
主要方法:
- 利用C. elegans电子运输链突变物 (isp-1和noo-6) 来研究长寿和mtROS信号传递.
- 研究了内在亡途径组件 (CED-9/Bcl2,CED-4/Apaf1,CED-3/Casp9) 和CED-13的参与.
- 分析了基因表达模式,以应对升高的mtROS.
主要成果:
- 长寿C. elegans突变体中的mtROS信号由内在的亡途径传递,涉及CED-13.
- 通过mtROS激活这种通路不会诱导亡,但会触发一种独特的基因表达模式.
- 这种基因表达调制增强了抗压能力,促进了生物的生存,从而延长了寿命.
结论:
- 通过亡途径感知mtROS可以引起独立于亡的保护机制.
- 亡途径的非亡功能在mtROS升高的条件下有助于延长寿命.
- 澄清了线粒体,ROS,亡和衰老之间的复杂关系.
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