The Plant Cell:农科院曹立勇研究组和王国梁研究组合作揭示水稻细
2017年1月18日，国际植物科学顶级期刊《The plant Cell》在线发表了中国农业科学院水稻研究所曹立勇课题组和植保所王国梁研究员课题组合作完成的题为“OsCUL3a Negatively Regulates Cell Death and Immunity by Degrading OsNPR1 in Rice”的科研论文，论文揭示了水稻细胞程序性死亡(Programmed cell death, PCD)和免疫调控的新机制。博士研究生刘群恩、宁约瑟副研究员和张迎信副研究员是文章的共同第一作者，曹立勇研究员、程式华研究员以及王国梁研究员为共同通讯作者。
水稻稳产性对保障粮食安全极为重要。稻瘟病和白叶枯病是水稻的主要病害，严重危害水稻安全生产。深入开展水稻抗病性分子机制研究，推动高抗水稻新品种分子改良是解决此问题的根本方法。PCD是植物最典型的防卫应激反应，在抵御病原菌侵染过程中发挥关键作用。水稻体内，泛素/26S蛋白酶体系统参与对PCD和抗病性的紧密调控。OsNPR1蛋白是介导水稻PCD和抗病性关键因子;过表达OsNPR1能显著提升转基因植株对稻瘟病菌和白叶枯病菌的抗性，同时导致自发性细胞死亡表型。但其在水稻体内调控的分子机理尚不清楚。
此项研究在EMS诱变水稻品种ZH11种子而获得的突变体库中发现一个类病斑突变体。该突变体表现出细胞程序性死亡表型，同时显著提高了对稻瘟病菌和白叶枯病菌的抗性。图位克隆和遗传互补实验结果显示，细胞死亡和广谱抗病性表型由OsCUL3a蛋白的提前终止引起。OsCUL3a与OsRBXs在体内互作形成Cullin-Ring类复合亚基E3泛素连接酶并通过靶向降解OsNPR1而负调控水稻细胞程序性死亡和免疫应激反应。本研究首次在遗传和生化水平上对水稻OsCUL3a-OsRBX1类E3泛素连接酶开展系统研究，成果丰富了植物中CUL3蛋白的调控机制。OsCUL3a-OsNPR1蛋白调控水稻程序性细胞死亡和免疫的分子机制研究结果，进一步丰富了影响水稻类病斑突变的分子理论体系，可为高抗水稻分子育种提供新的理论切入点。
原文链接：
OsCUL3a Negatively Regulates Cell Death and Immunity by Degrading OsNPR1 in Rice
原文摘要：
Cullin3-based RING E3 ubiquitin ligases (CRL3), composed of Cullin3 (CUL3), RBX1, and BTB proteins, are involved in plant immunity but the function of CUL3 in the process is largely unknown. Here, we show that rice OsCUL3a is important for the regulation of cell death and immunity. The rice lesion mimic mutant oscul3a displays a significant increase in the accumulation of flg22- and chitin-induced reactive oxygen species, and in pathogenesis-related gene expression as well as resistance to Magnaporthe oryzae and Xanthomonas oryzae pv. oryzae. We cloned the OsCUL3a gene via a map-based strategy and found that the lesion mimic phenotype of oscul3a is associated with the early termination of OsCUL3a protein. Interaction assays showed that OsCUL3a interacts with both OsRBX1a and OsRBX1b to form a multi-subunit CRL in rice. Strikingly, OsCUL3a interacts with and degrades OsNPR1, which acts as a positive regulator of cell death in rice. Accumulation of OsNPR1 protein is greater in the oscul3a mutant than in the wild type. Furthermore, the oscul3a osnpr1 double mutant does not exhibit the lesion mimic phenotype of the oscul3a mutant. Our data demonstrate that OsCUL3a negatively regulates cell death and immunity by degrading OsNPR1 in rice.
作者：曹立勇和王国梁
