Malate transported from chloroplast to mitochondrion triggers production of ROS and PCD in Arabidopsis thaliana  

作　　者：Yannan Zhao Lilan Luo Jiesi Xu Peiyong Xin Hongyan Guo Jian Wu Lin Bai Guodong Wang Jinfang Chu Jianru Zuo Hong Yu Xun Huang Jiayang Li 

机构地区：[1]State Key Laboratory of Plant Genomics and National Center for Plant Gene Research, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China [2]University of Chinese Academy of Sciences, Beijing 100049, China [3]State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China [4]Department of Plant Science, Weizmann Institute of Science, Rehovot 7610001, Israel

出　　处：《Cell Research》2018年第4期448-461,共14页细胞研究（英文版）

基　　金：We thank Jian-Min Zhou （Institute of Genetics and Developmental Biology, Chinese Academy of Sciences） for critical comments on the manuscript, Weicai Yang （Institute of Genetics and Developmental Biology, Chinese Academy of Sciences） for providing binary vector pWM101 and assistance in isolating mitochondria and chloroplasts, Qijun Chen （China Agricultural University） for providing CRISPR/Cas9 binary vector pHEE2A-TRI, and Nottingham Arabidopsis Stock Centre （NASC） for providing som787-2 （N877710）, som328-2 （N362639）, dit2.1-1 （N663245）, dit2.1-2 （N669411）, dit2.2-1 （N661169）, dit2.2-2 （N655976）, and Isdl （N542687） seeds. This work was supported by the National Natural Science Foundation of China （31521001, 31661143025）, and the Strategic Priority Research Program of the Chinese Academy of Sciences （XDB13030300）.

摘　　要：Programmed cell death （PCD） is a fundamental biological process. Deficiency in MOSAIC DEATH 1 （MOD1）, a plastid-localized enoyl- ACP reductase, leads to the accumulation of reactive oxygen species （ROS） and PCD, which can be suppressed by mitochondrial complex I mutations, indicating a signal from chloroplasts to mitochondria. However, this signal remains to be elucidated. In this study, through cloning and analyzing a series of modl suppressors, we reveal a comprehensive organelle communication pathway that regulates the generation of mitochondrial ROS and triggers PCD. We show that mutations in PLASTIDIAL NAD-DEPENDENT MALATE DEHYDROGENASE （plNAD-MDH）, chloroplastic DICARBOXYLATE TRANSPORTER 1 （DiT1） and MITOCHONDRIAL MALA TE DEHYDROGENASE 1 （mMDH1） can each rescue the ROS accumulation and PCD phenotypes in mod1, demonstrating a direct communication from chloroplasts to mitochondria via the malate shuttle. Further studies demonstrate that these elements play critical roles in the redox homeostasis and plant growth under different photoperiod conditions. Moreover, we reveal that the ROS level and PCD are significantly increased in malate-treated HeLa cells, which can be dramatically attenuated by knockdown of the human gene MDH2, an ortholog of Arabidopsis mMDH1. These results uncover a conserved malate-induced PCD pathway in plant and animal systems, revolutionizing our understanding of the communication between Organelles.

关 键 词：Cell death Molecular biology ORGANELLES 

分 类 号：Q255[生物学—细胞生物学] X173[环境科学与工程—环境科学]