The Rice Dynamin-Related Protein OsDRP1E Negatively Regulates Programmed Cell Death by Controlling the Release of Cytochrome c from Mitochondria.
The Rice Dynamin-Related Protein OsDRP1E Negatively Regulates Programmed Cell Death by Controlling the Release of Cytochrome c from Mitochondria.
复制标题
水稻动力相关蛋白 OsDRP1E 通过控制线粒体释放细胞色素 c 负调控程序性细胞死亡
DOI：
10.1371/journal.ppat.1006157
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发表时间：
2017-01
期刊：
影响因子：
6.7
通讯作者：
Wang GL
中科院分区：
文献类型：
--
作者：
Li Z;Ding B;Zhou X;Wang GL
由线粒体介导的细胞程序性死亡（PCD）已成为植物生长发育和对非生物和生物胁迫响应的重要机制。然而，细胞色素c在PCD期间从线粒体移位到胞质溶胶的作用仍不清楚。在这里，我们证明，水稻动力蛋白相关蛋白1 E（OsDRP 1 E）负调控PCD通过控制线粒体结构和细胞色素c的释放。我们利用图位克隆的方法从水稻拟病斑突变体dj-lm中分离到OsDRP 1 E，并证实OsDRP 1 E中的E409 V突变导致水稻细胞自发死亡。病原菌接种试验表明，dj-lm显著提高了对真菌和细菌病原菌的抗性。对E409 V突变的功能分析表明，突变蛋白削弱了OsDRP 1 E的自缔合和高阶复合物的形成;这反过来又降低了OsDRP 1 E的GTdR活性。此外，共聚焦显微镜显示，E409 V突变损害了OsDRP 1 E的定位到线粒体。E409 V突变显著影响线粒体嵴的形态发生，并导致细胞色素c从线粒体异常释放到细胞质中。综上所述，我们的研究结果表明，OsDRP 1 E定位蛋白的功能作为一个负调节细胞色素c的释放和PCD的植物。植物已经发展出过敏反应（HR），其在感染部位周围显示快速程序性细胞死亡（PCD），这反过来限制病原体入侵并限制病原体的传播。尽管在过去的十年中，许多研究报道了PCD在不同病理系统中的表征，但PCD如何启动以及它如何调节宿主抗性的分子机制仍然不清楚。病变模拟突变体表现出自发的HR样细胞死亡没有病原体入侵，是解剖PCD途径的理想遗传材料。在这项研究中，我们的特点是病变模拟基因OsDRP 1 E，负调控植物PCD通过控制细胞色素c从线粒体释放。我们的研究结果表明，E409 V点突变的动力蛋白相关蛋白OsDRP 1 E影响线粒体嵴的形态发生，导致细胞色素c释放到细胞质中。该研究为动力蛋白相关蛋白在植物免疫中的功能提供了新的见解。
Programmed cell death (PCD) mediated by mitochondrial processes has emerged as an important mechanism for plant development and responses to abiotic and biotic stresses. However, the role of translocation of cytochrome c from the mitochondria to the cytosol during PCD remains unclear. Here, we demonstrate that the rice dynamin-related protein 1E (OsDRP1E) negatively regulates PCD by controlling mitochondrial structure and cytochrome c release. We used a map-based cloning strategy to isolate OsDRP1E from the lesion mimic mutant dj-lm and confirmed that the E409V mutation in OsDRP1E causes spontaneous cell death in rice. Pathogen inoculation showed that dj-lm significantly enhances resistance to fungal and bacterial pathogens. Functional analysis of the E409V mutation showed that the mutant protein impairs OsDRP1E self-association and formation of a higher-order complex; this in turn reduces the GTPase activity of OsDRP1E. Furthermore, confocal microscopy showed that the E409V mutation impairs localization of OsDRP1E to the mitochondria. The E409V mutation significantly affects the morphogenesis of cristae in mitochondria and causes the abnormal release of cytochrome c from mitochondria into cytoplasm. Taken together, our results demonstrate that the mitochondria-localized protein OsDRP1E functions as a negative regulator of cytochrome c release and PCD in plants. Plants have developed a hypersensitive response (HR) that shows rapid programed cell death (PCD) around the infection site, which in turn limits pathogen invasion and restricts the spread of pathogens. Although many studies reported the characterization of PCD in different pathosystems in the last decade, the molecular mechanisms on how PCD is initiated and how it regulates host resistance are still unclear. Lesion mimic mutants exhibit spontaneous HR-like cell death without pathogen invasion and are ideal genetic materials for dissecting the PCD pathway. In this study, we characterized the lesion mimic gene OsDRP1E that negatively regulates plant PCD through the control of cytochrome c release from mitochondria. Our results suggest that the E409V point mutation in the dynamin-related protein OsDRP1E affects the morphogenesis of mitochondrial cristae that leads to the cytochrome c release into cytoplasm. This study provides new insights into the function of dynamin-related proteins in plant immunity.