程序性细胞死亡是一种受遗传调控的细胞死亡方式，在植物的生长发育和抵御生物与非生物胁迫过程中均发挥重要作用。研究显示，叶绿体和线粒体在植物程序性细胞死亡中起到关键作用，且细胞器之间的信号交流也在这一过程中发挥重要功能，但目前对其信号交流的关键因子还知之甚少，是亟待解决的科学问题。mosaic death 1 (mod1)是我们实验室此前克隆的一个拟南芥细胞死亡突变体。MOD1基因编码一个质体定位的烯酰-ACP还原酶。研究表明，MOD1功能降低导致其底物NADH在叶绿体中大量积累，进而使得大量携带着还原力的苹果酸通过苹果酸-草酰乙酸穿梭途径由叶绿体进入线粒体中，导致线粒体中NADH水平的升高，进而引发活性氧的产生和细胞死亡的发生。本项目拟在前期研究的基础上，系统深入解析参与叶绿体和线粒体之间信号转导的关键组分，从而揭示高等植物细胞器互作在程序性细胞死亡中发挥重要功能的分子机理。

Programmed cell death (PCD), a genetically controlled process of cell suicide, is now realized essential for plant development and survival by regulating organogenesis, biotic and abiotic stress responses through its diverse functions in developmental patterning, cell differentiation, cell number homeostasis, and hypersensitive response (HR). Chloroplasts and mitochondria are central regulators in plant PCD, and the communication between the organelles plays a pivotal role in this process, however the signals between chloroplasts and mitochondria remain to be elucidated. Our previous studies have shown that the mosaic death 1 (mod1) in Arabidopsis thaliana is a cell death mutant, which has an elevated ROS levels in multiple organs. The MOD1 gene encodes an enoyl-acyl carrier protein (ACP) reductase, a subunit of fatty acid synthesis complex that catalyzes the de novo biosynthesis of fatty acids in plastids, and its deficiency leads to PCD. The deficiency in MOD1 will favorably lead to the accumulation of the reducing equivalent NADH in the chloroplast and then drive the transport of reducing power in the form of malate from chloroplasts to mitochondria to trigger ROS generation and initiate PCD. To understand the ROS-inducing signals transported from plastids to mitochondria, in this project we plan to clone key genes regulating communication between plastids and mitochondria, and elucidate the underlying regulatory mechanisms of organelle communication in plant PCD.