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水稻中的OsCUL3a通过降解OsNPR1负向调控细胞死亡和免疫反应。

OsCUL3a Negatively Regulates Cell Death and Immunity by Degrading OsNPR1 in Rice.

作者信息

Liu Qunen, Ning Yuese, Zhang Yingxin, Yu Ning, Zhao Chunde, Zhan Xiaodeng, Wu Weixun, Chen Daibo, Wei Xiangjin, Wang Guo-Liang, Cheng Shihua, Cao Liyong

机构信息

State Key Laboratory of Rice Biology, China National Rice Research Institute, Hangzhou 311400 China.

State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China.

出版信息

Plant Cell. 2017 Feb;29(2):345-359. doi: 10.1105/tpc.16.00650. Epub 2017 Jan 18.

Abstract

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 () is important for the regulation of cell death and immunity. The rice lesion mimic mutant 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 and pv We cloned the gene via a map-based strategy and found that the lesion mimic phenotype of is associated with the early termination of OsCUL3a protein. Interaction assays showed that OsCUL3a interacts with both OsRBX1a and OsRBX1b to form a multisubunit 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 mutant than in the wild type. Furthermore, the double mutant does not exhibit the lesion mimic phenotype of the mutant. Our data demonstrate that OsCUL3a negatively regulates cell death and immunity by degrading OsNPR1 in rice.

摘要

基于Cullin3的RING E3泛素连接酶(CRL3)由Cullin3(CUL3)、RBX1和BTB蛋白组成,参与植物免疫,但CUL3在此过程中的功能很大程度上未知。在此,我们表明水稻()对细胞死亡和免疫的调节很重要。水稻类病变突变体在flg22和几丁质诱导的活性氧积累、病程相关基因表达以及对和pv的抗性方面均显著增加。我们通过图位克隆策略克隆了基因,发现的类病变表型与OsCUL3a蛋白的提前终止有关。相互作用分析表明,OsCUL3a与OsRBX1a和OsRBX1b相互作用,在水稻中形成多亚基CRL。引人注目的是,OsCUL3a与OsNPR1相互作用并使其降解,OsNPR1在水稻中作为细胞死亡的正调控因子发挥作用。OsNPR1蛋白在突变体中的积累比野生型中更多。此外,双突变体不表现出突变体的类病变表型。我们的数据表明,OsCUL3a通过降解水稻中的OsNPR1对细胞死亡和免疫进行负调控。

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本文引用的文献

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Pathogen Tactics to Manipulate Plant Cell Death.病原体操控植物细胞死亡的策略。
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