直接无处不在的模式识别受体FLS2减弱了植物天生的免疫力
Dongping Lu1, Wenwei Lin, Xiquan Gao
1Department of Biochemistry and Biophysics, Texas A&M University, College Station, TX 77843, USA.
概括
植物免疫受体FLAGELLIN-SENSING 2 (FLS2) 是由E3泛基因酶PUB12和PUB13调节的. 这些由BAK1激活的酶向FLS2进行降解,减弱植物对鞭毛虫的免疫反应.
科学领域:
- 植物免疫力 植物免疫力
- 分子植物病理学 分子植物病理学
- 信号传导传导是指信号的传导.
背景情况:
- 模式识别受体 (PRRs) 在检测病原体相关的分子模式时启动先天免疫反应.
- 阿拉比多普西斯PRR FLAGELLIN-SENSING 2 (FLS2) 识别了细菌的鞭毛蛋白,通过其共同受体BAK1.1激活下游免疫信号.
- 控制FLS2介导免疫信号减弱的机制在很大程度上仍未被阐明.
研究的目的:
- 为了研究负责减弱Arabidopsis.FLAGELLIN-SENSING 2 (FLS2) 激活的分子机制.
- 确定参与FLS2受体综合体营业额的关键调节者.
主要方法:
- 同免疫沉测试检测蛋白质与蛋白质相互作用.
- 立化试验用于评估FLS2的多立化.
- 在鞭毛素处理后对FLS2降解的分析.
- 对Arabidopsis突变的表型分析 (pub12,pub13) 作为对flagellin的反应.
主要成果:
- 弗拉格林治疗诱导了U-box E3泛素酶PUB12和PUB13的招募到FLS2受体综合体.
- BAK1酸化PUB12和PUB13,这对于它们与FLS2.2.的关联至关重要.
- PUB12和PUB13催化了FLS2的多基化,促进了其降解.
- 缺乏PUB12和PUB13的突变体表现出对鞭毛蛋白的增强免疫反应.
结论:
- 一个涉及BAK1-介导的酸化和E3酶的招募 (PUB12/13) 的新型调节途径控制了FLS2的无处不在和降解.
- 这种机制提供了直接控制FLS2受体周转率,导致植物免疫信号的减弱.
- 这些发现揭示了一个独特的电路,用于微调植物的先天免疫力.
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