Deficient plastidic fatty acid synthesis triggers cell death by modulating mitochondrial reactive oxygen species  被引量:16

Deficient plastidic fatty acid synthesis triggers cell death by modulating mitochondrial reactive oxygen species

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作  者:Jian Wu Yuefeng Sun Yannan Zhao Jian Zhang Lilan Luo Meng Li Jinlong Wang Hong Yu Guifu Liu Liusha Yang Guosheng Xiong Jian-Min Zhou Jianru Zuo Yonghong Wang Jiayang Li 

机构地区:[1]State Key Laboratory of Plant Genomics and National Center for Plant Gene Research (Beij'ing), Institute of Genetics and Devel-opmental Biology, Chinese Academy of Sciences, Beijing 100101, China [2]Department of Pathology and Cell Biology, University ofSouth Florida, Tampa, FL 33612, USA

出  处:《Cell Research》2015年第5期621-633,共13页细胞研究(英文版)

基  金:We thank Xinnian Dong (Duke University) for critically reading the manuscript and Weicai Yang (Institute of Genetics and Developmental Biology, Chinese Academy of Sciences) for providing the pWM101 vector. This work was supported by grants from the National Natural Science Foundation of China (30830009, 91335204) and the Chinese Academy of Sciences.

摘  要:Programmed cell death (PCD) is of fundamental importance to development and defense in animals and plants. In plants, a well-recognized form of PCD is hypersensitive response (HR) triggered by pathogens, which involves the generation of reactive oxygen species (ROS) and other signaling molecules. While the mitochondrion is a master reg- ulator of PCD in animals, the chloroplast is known to regulate PCD in plants. Arabidopsis Mosaic Death 1 (MOD1), an enoyl-acyl carrier protein (ACP) reductase essential for fatty acid biosynthesis in chloroplasts, negatively regulates PCD in Arabidopsis. Here we report that PCD in modl results from accumulated ROS and can be suppressed by mu- tations in mitochondrial complex I components, and that the suppression is confirmed by pharmaceutical inhibition of the complex 1-generated ROS. We further show that intact mitochondria are required for full HR and optimum disease resistance to the Pseudomonas syringae bacteria. These findings strongly indicate that the ROS generated in the electron transport chain in mitochondria plays a key role in triggering plant PCD and highlight an important role of the communication between chloroplast and mitochondrion in the control of PCD in plants.

关 键 词:cell death PPR protein ETC ROS MITOCHONDRIA CHLOROPLASTS Arabidopsis thaliana 

分 类 号:Q255[生物学—细胞生物学] S852.2[农业科学—基础兽医学]

 

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