Malate transported from chloroplast to mitochondrion triggers production of ROS and PCD in Arabidopsis thaliana
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 mod1 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 (D/T1) and MITOCHONDRIAL MALATE DEHYDROGENASE 1 (mMDHl) 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 ma late-induced PCD pathway in plant and animal systems, revolutionizing our understanding of the communication between organelles.
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We thank Jian-Min ZhouInstitute of Genetics and Developmental Biology,Chinese Academy of Sciencesfor critical comments on the manuscript,Weicai YangInstitute of Genetics and Developmental Biology,Chinese Academy of Sciencesfor providing binary vector pWM101 and assistance in isolating mitochondrN877710;som328-2N362639;dit2.1-1N663245;dit2.1-2N669411;dit2.2-1N661169;dit2.2-2N655976;IsdlN542687seeds. This work was supported by the National Natural Science Foundation of China31521001,31661143025;the Strategic Priority Research Program of the Chinese Academy of SciencesXDB13030300
2018-08-29（万方平台首次上网日期，不代表论文的发表时间）
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448-461
