项目名称: E3泛素连接酶StPUB17及其靶标在马铃薯晚疫病抗病免疫应答中的作用机制
项目编号: No.31471550
项目类型: 面上项目
立项/批准年度: 2015
项目学科: 食品科学、农学基础与作物学
项目作者: 田振东
作者单位: 华中农业大学
项目金额: 85万元
中文摘要: 马铃薯是我国第四大粮食作物,晚疫病是生产中为害最严重的病害。培育抗性品种是防治晚疫病的经济、有效途径。R基因介导的抗性是马铃薯最基本、最重要的抗性,但是R 基因容易被快速变异的病原菌克服,了解R 基因介导的抗病机制是有效利用R 基因的理论基础。泛素降解通路在植物抗病免疫应答中起着至关重要的作用。我们前期研究显示马铃薯U-box E3 泛素连接酶StPUB17参与R基因介导的晚疫病抗性,可能是一个正调控因子。本项目将进一步系统分析StPUB17与R基因介导的 HR 反应及抗性的关系;确定其在细胞中的定位,筛选鉴定与其作用的靶蛋白及调节因子;分析其参与和调控的抗病信号网络,构建StPUB17-靶标底物-互作蛋白模型,阐明StPUB17泛素降解通路在马铃薯晚疫病抗性中的分子机制、揭示R基因抗病信号的传导过程。研究结果将为通过调节抗病信号传导途径和有效利R基因来改良晚疫病抗性提供理论依据和新思路。
中文关键词: 马铃薯;E3-泛素连接酶;StPUB17;晚疫病;抗病机理
英文摘要: Potato is the fourth most important food crop in China. Late blight caused by Phytophthora infestans is the most devastating disease of potato almost everywhere potatoes are grown. R gene controled resistance is a critical basis for potato against P. infestans. But it can be easily overcome by new virulent strains. It is pivotal to understand resistance mechanisms controlled by R genes for effectively using it. The ubiquitin-proteasome degradation plays essential roles in plant innate immunity. Previously, we found that potato U-box E3 ubiquitin ligase StPUB17, as a positive regulator, plays an important roles in the potato late blight resistance in previous research. In this program, combined with the molecular biology and physiological and biochemical analysis, we will further elucidate the relationship among hypersensitive response (HR), StPUB17 ubiquitin degradation and late blight resistance; determine it's cell locolization, screen and identify interacting proteins and degradation targets of StPUB17 and then construct StPUB17-target protein-interacting protein model and explore the mechanism of how StPUB17 plays it's role in R gene mediated resistance signal pathway. The findings in this project will deepen our understanding of the molecular basis of the plant resistance and provide new strategy to improve resistance using R genes effectively in potatoes for sustaining control of late blight disease.
英文关键词: potato;E3-ubiquitin ligase;StPUB17;late blight;Mechanism of resistance