线粒体基因组表达的抑制通过依赖综合应激反应而非线粒体未折叠蛋白反应的细胞信号传导触发CHOP-10的激活。
Inhibition of mitochondrial genome expression triggers the activation of CHOP-10 by a cell signaling dependent on the integrated stress response but not the mitochondrial unfolded protein response.
作者信息
Michel Sebastien, Canonne Morgane, Arnould Thierry, Renard Patricia
机构信息
Laboratory of Biochemistry and Cell Biology (URBC), NAmur Research Institute for LIfe Sciences (NARILIS), University of Namur (UNamur), 61 rue de Bruxelles, 5000 Namur, Belgium.
Laboratory of Biochemistry and Cell Biology (URBC), NAmur Research Institute for LIfe Sciences (NARILIS), University of Namur (UNamur), 61 rue de Bruxelles, 5000 Namur, Belgium.
出版信息
Mitochondrion. 2015 Mar;21:58-68. doi: 10.1016/j.mito.2015.01.005. Epub 2015 Jan 30.
Mitochondria-to-nucleus communication, known as retrograde signaling, is important to adjust the nuclear gene expression in response to organelle dysfunction. Among the transcription factors described to respond to mitochondrial stress, CHOP-10 is activated by respiratory chain inhibition, mitochondrial accumulation of unfolded proteins and mtDNA mutations. In this study, we show that altered/impaired expression of mtDNA induces CHOP-10 expression in a signaling pathway that depends on the eIF2α/ATF4 axis of the integrated stress response rather than on the mitochondrial unfolded protein response.
线粒体与细胞核的通讯，即逆行信号传导，对于响应细胞器功能障碍来调节核基因表达至关重要。在已描述的对线粒体应激作出反应的转录因子中，CHOP-10可被呼吸链抑制、未折叠蛋白在线粒体中的积累以及线粒体DNA突变激活。在本研究中，我们表明线粒体DNA表达的改变/受损会在一条依赖于综合应激反应的eIF2α/ATF4轴而非线粒体未折叠蛋白反应的信号通路中诱导CHOP-10的表达。
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