Abstract
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 (DiT1) and MITOCHONDRIAL MALATE 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.
Highlights
Programmed cell death (PCD), a genetically controlled process of cell suicide, is a fundamental event of life, and originated before the advent of eukaryotes.[1]
To identify the signal transported from chloroplasts to induce Reactive oxygen species (ROS) production in mitochondria, we describe a screen for new mod[1] suppressors derived from ethyl methanesulfonate (EMS) mutagenized Arabidopsis M2 seeds
SOM410 encodes a plastid-localized NAD-dependent malate dehydrogenase To understand the nature and functions of the genes mutated in these soms, we systematically mapped and cloned these genes
Summary
Programmed cell death (PCD), a genetically controlled process of cell suicide, is a fundamental event of life, and originated before the advent of eukaryotes.[1]. Suggest that CTM communication plays an important role in Compared with mod[1], the malate concentration in the chloroplasts of mod[1] som[410] was significantly decreased and restored to the wild-type level, reflecting the deficiency in conversion from regulating redox homeostasis and thereby affecting plant growth in response to different photoperiod conditions and that the impairment in the CTM communication could reduce the OAA to malate as a result of the SOM410 mutation (Fig. 5b).
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