Wu Jian, Sun Yuefeng, Zhao Yannan, Zhang Jian, Luo Lilan, Li Meng, Wang Jinlong, Yu Hong, Liu Guifu, Yang Liusha, Xiong Guosheng, Zhou Jian-Min, Zuo Jianru, Wang Yonghong, Li Jiayang
State Key Laboratory of Plant Genomics and National Center for Plant Gene Research (Beijing), Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China.
1] State Key Laboratory of Plant Genomics and National Center for Plant Gene Research (Beijing), Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China [2] Current address: Department of Pathology and Cell Biology, University of South Florida, Tampa, FL 33612, USA.
Cell Res. 2015 May;25(5):621-33. doi: 10.1038/cr.2015.46. Epub 2015 Apr 24.
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 mod1 results 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.
程序性细胞死亡（PCD）对于动植物的发育和防御至关重要。在植物中，一种广为人知的PCD形式是由病原体触发的超敏反应（HR），这涉及活性氧（ROS）和其他信号分子的产生。虽然线粒体是动物PCD的主要调节因子，但已知叶绿体可调节植物中的PCD。拟南芥花叶死亡1（MOD1）是叶绿体中脂肪酸生物合成所必需的烯酰 - 酰基载体蛋白（ACP）还原酶，它对拟南芥中的PCD起负调节作用。在此我们报告，mod1中的PCD是由积累的ROS引起的，并且可以被线粒体复合体I组分的突变所抑制，并且这种抑制通过对复合体I产生的ROS的药物抑制得到证实。我们进一步表明，完整的线粒体对于完全的HR和对丁香假单胞菌的最佳抗病性是必需的。这些发现强烈表明线粒体电子传递链中产生的ROS在触发植物PCD中起关键作用，并突出了叶绿体与线粒体之间的通讯在控制植物PCD中的重要作用。
