拟南芥MOD1基因突变引发细胞死亡途径中关键基因的鉴定与功能研究

Programmed cell death (PCD), a genetically controlled process of cell suicide, plays important roles in plant growth, development and stress responses. The regulation of plant PCD is extremely complicated, involving the communications of materials, energy and signals among chloroplasts, mitochondria, peroxisomes, ER, and vacuoles. However, the underlying regulation mechanisms are largely unknown. Our previous studies on mosaic death 1 (mod1), an Arabidopsis thaliana PCD mutant triggered by the deficient plastidic fatty acid synthesis, have demonstrated that the ROS accumulation and cell death in mod1 require the transport of malate from chloroplast to mitochondrion and the functional mitochondrial ETC complex I, revealing the important role of the chloroplast-to-mitochondrion communication in mod1-triggered PCD. However, whether other organelle communication or material/energy metabolic pathways are involved in the regulation of PCD in mod1 remains to be elucidated. In this proposal, we plan to identify new components that play key roles in the regulation of PCD in mod1 through genetic screening, gene cloning and functional analyses, and further to dissect the molecular regulation mechanisms of plant PCD, providing theoretical guidance for the application in agriculture.

程序性细胞死亡(programmed cell death, PCD)是一种受遗传调控的细胞死亡方式，在植物生长发育与胁迫响应过程中发挥重要作用。植物PCD调控机制极其复杂，涉及叶绿体、线粒体、过氧化物酶体、内质网和液泡等细胞器之间的物质能量交流，但其分子机制尚不十分清楚。mosaic death 1 (mod1)是一个由质体内脂肪酸合成缺陷造成的拟南芥细胞死亡突变体。前期通过对mod1抑制突变体的研究发现，mod1中细胞死亡的发生是依赖于叶绿体至线粒体的苹果酸运输以及线粒体电子传递链复合体I活性的，说明叶绿体-线粒体交流在mod1细胞死亡中发挥了重要的调控作用。但mod1的细胞死亡过程是否受到其他细胞器或物质能量代谢途径的调控尚不清楚。本项目将通过克隆和研究新的mod1抑制基因，鉴定参与mod1细胞死亡调控的关键元件，阐明植物PCD的分子调控机制，为其在农业生产中的应用提供理论指导。