通过改性宿主蛋白复合体激活平衡的植物辅助NLR
Shijia Huang1,2, Junli Wang3, Ridan Song4
1Research Center for Industries of the Future and School of Life Sciences, Westlake University, Hangzhou, China.
Nature
|February 12, 2025
概括
植物免疫受体,核酸结合丰富的重复受体 (NLR),感知病原体. 这项研究揭示了EDS1-SAG101复合物如何激活NRG1A以及NRG1C如何抑制这种植物免疫路径.
科学领域:
- 植物免疫力
- 分子生物学
- 结构生物学
背景情况:
- 核酸结合丰富的重复受体 (NLR) 是植物免疫的关键调节者,检测病原体效应物.
- 在Arabidopsis中,传感器NLRs充当NADase,产生触发免疫信号的第二信使.
- 增强疾病易感性1 (EDS1) - 老化相关基因101 (SAG101) 复合体识别了这些第二信使以激活下游组件.
研究的目的:
- 阐明EDS1-SAG101复合体激活NRG1A的结构基础.
- 了解NRG1C抑制植物免疫反应的机制.
- 揭示控制植物免疫通路的激活和限制的分子相互作用.
主要方法:
- 用冷电子显微镜 (cryo-EM) 确定EDS1-SAG101-NRG1A复合物的结构.
- 结构比较以确定第二次信使结合时的形状变化.
- 生物化学测试以评估EDS1-SAG101,NRG1A和NRG1C之间的结合相互作用.
主要成果:
- 化EM显示激活的EDS1-SAG101结合了NRG1A的富含白的重复域,形成了一个稳定的复合体.
- 第二个信使结合诱导EDS1-SAG101的构造变化,这些变化被NRG1A识别,导致其全激活.
- 抑制性NRG1C蛋白与NRG1A在与激活的EDS1-SAG101结合方面进行竞争,从而有效地隔离了该复合体.
结论:
- 该研究通过识别修饰EDS1-SAG101复合体来发现NRG1A激活的机制.
- 通过对EDS1-SAG101的竞争性结合,NRG1C通过阻止NRG1A的激活来抑制免疫反应.
- 这些发现为植物免疫信号通路的调节提供了关键的见解.
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