Abstract: Programmed cell death (PCD) is an active and genetically controlled process that results in cell death in a multicellular organism. PCD plays important roles in plant development and defense and can be induced by increased reactive oxygen species (ROS) in mitochondria. Previous studies by Jiayang Li’s group in the Institute of Genetics and Developmental Biology, Chinese Academy of Sciences identified a cell death mutant, mod1, in Arabidopsis. Although the authors suggested that signal communication between chloroplast and mitochondrion contributes to PCD in mod1, the underlying mechanisms remain elusive. Recently, by screening the suppressors of mod1, they cloned three new suppressor genes, plNAD-MDH, DiT1 and mMDH1, which encode a plastid-localized NAD-dependent malate dehydrogenase, a chloroplastic dicarboxylate transporter, and a mitochondrial malate dehydrogenase, respectively. Mutations in these three genes each can suppress ROS accumulation and PCD in mod1. Functional analyses of these genes demonstrated that malate is transported from chloroplasts to mitochondria and triggers ROS generation and PCD in plant. This study expands our knowledge of intracellular communications between organelles and provides new understanding of molecular mechanisms of PCD in plants, which is an important progress in this field.

Key words: chloroplast, mitochondrion, malate, reactive oxygen species, programmed cell death