冠氨酸调节了ABI1介导的口腔开口,以通过进口β蛋白SAD2促进细菌病原体感染
Lu Liu1, Yanzhi Liu2, Xuehan Ji1
1State Key Laboratory of Agrobiotechnology and MOA Key Laboratory for Monitoring and Green Management of Crop Pests, China Agricultural University, Beijing, China.
The Plant journal : for cell and molecular biology
|April 29, 2024
概括
细菌冠状酸 (COR) 通过劫持SAD2蛋白来将ABI1移动到细胞核中,重视酸 (ABA) 免疫信号,从而重新打开植物胃口.
科学领域:
- 植物免疫力 植物免疫力
- 植物与微生物的相互作用
- 分子植物病理学 分子植物病理学
背景情况:
- 胃体免疫对于防御细菌病原体至关重要.
- 来自病原体的植物毒素,如冠状腺素 (COR),破坏植物激素信号传递,如酸 (ABA),以促进感染.
- 对于COR对抗ABA信号传递和重新打开胃口的确切机制尚不清楚.
研究的目的:
- 阐明细菌冠状素 (COR) 对抗植物中酸 (ABA) 信号的分子机制.
- 研究SAD2蛋白在植物对COR和ABA信号的反应中的作用.
主要方法:
- 在COR治疗后研究了ABI1蛋白的亚细胞局部化.
- 使用sad2突变来评估在ABI1核进口中SAD2的需求.
- 在野生类型和突变植物中分析了ABA敏感性.
主要成果:
- 冠状腺素 (COR) 治疗诱导了植物核中ABI1的积累,ABI1是ABA信号的负调节器.
- 作为对COR的反应,ABI1的核积累取决于进口β家族蛋白 SAD2.
- 失去了SAD2的功能损害了ABI1的核进口,改变了植物对ABA的敏感性.
结论:
- 研究表明,细菌COR通过利用宿主蛋白SAD2来对抗植物口腔免疫,以促进ABI1.1的核进口.
- 这种机制解释了病原体如何重新打开胃口以促进感染,回答了植物病原体相互作用的一个关键问题.
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