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Deficient plastidic fatty acid synthesis triggers cell death by modulating mitochondrial reactive oxygen species
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 and Jiayang Li
Cell Research
Abstract
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 regulator 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 mod1results from accumulated ROS and can be suppressed by mutations in mitochondrial complex I components, and that the suppression is confirmed by pharmaceutical inhibition of the complex I-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. Keywords: cell death; PPR protein; ETC; ROS; mitochondria; chloroplasts;Arabidopsis thaliana
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DOI:10.1038/cr.2015.46 |
论文题目: |
Deficient plastidic fatty acid synthesis triggers cell death by modulating mitochondrial reactive oxygen species |
英文论文题目: |
Deficient plastidic fatty acid synthesis triggers cell death by modulating mitochondrial reactive oxygen species |
第一作者: |
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 and Jiayang Li |
英文第一作者: |
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 and Jiayang Li |
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2015-04-29 |
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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 regulator 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 mod1results from accumulated ROS and can be suppressed by mutations in mitochondrial complex I components, and that the suppression is confirmed by pharmaceutical inhibition of the complex I-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. Keywords: cell death; PPR protein; ETC; ROS; mitochondria; chloroplasts;Arabidopsis thaliana |
英文摘要: |
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 regulator 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 mod1results from accumulated ROS and can be suppressed by mutations in mitochondrial complex I components, and that the suppression is confirmed by pharmaceutical inhibition of the complex I-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. Keywords: cell death; PPR protein; ETC; ROS; mitochondria; chloroplasts;Arabidopsis thaliana |
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Cell Research |
英文刊物名称: |
Cell Research |
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其它备注: |
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 and Jiayang Li. Deficient plastidic fatty acid synthesis triggers cell death by modulating mitochondrial reactive oxygen species. Cell Research. DOI:10.1038/cr.2015.46 |
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