程序性细胞死亡(PCD)是生物体受遗传调控的自主细胞死亡现象, 在植物生长发育和抵抗环境胁迫中起重要作用。PCD的发生可受线粒体中活性氧(ROS)诱导。中国科学院遗传与发育生物学研究所李家洋研究组早期的研究发现了1个拟南芥(Arabidopsis thaliana)细胞死亡突变体mod1, 并暗示植物细胞中存在叶绿体与线粒体之间的信号交流调控PCD, 但其中的具体作用机制尚不清楚。最近, 他们通过大规模筛选mod1突变体的抑制突变体, 克隆了3个新的抑制基因plNAD- MDH、DiT1和mMDH1。此3个基因分别编码质体定位的NAD依赖的苹果酸脱氢酶、叶绿体被膜定位的二羧酸转运蛋白1和线粒体定位的苹果酸脱氢酶1, 突变后都可抑制mod1中ROS的积累及PCD的发生。通过对这些基因进行深入的功能分析, 他们论证了苹果酸从叶绿体到线粒体的转运对线粒体中ROS的产生及随后PCD的诱导起重要作用。该研究拓展了我们对植物细胞中细胞器间交流的认识, 为我们深入理解植物PCD发生机制提供了新线索, 是该领域的一项突破性进展。

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.