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诱导CBF表达1通过直接激活酸信号,促进增强寒冷免疫力
Shaoqin Li1,2, Li He3, Yongping Yang1,2
1CAS Key Laboratory of Tropical Plant Resources and Sustainable Use, Xishuangbanna Tropical Botanical Garden, Chinese Academy of Sciences, Kunming, Yunnan 650223, China.
寒冷压力通过ICE1蛋白质增强疾病抵抗力来提高植物免疫力. ICE1将寒冷信号与酸 (SA) 途径联系起来,激活像PR1.1这样的防御基因.
科学领域:
- 植物生物学 植物生物学
- 分子植物病理学 分子植物病理学
- 植物免疫学 植物免疫学
背景情况:
- 植物的免疫反应受到环境压力的调节,包括寒冷.
- 酸 (SA) 信号通路对于植物免疫是至关重要的.
- 在工厂防御中协调冷应力和SA信号的机制尚未完全理解.
研究的目的:
- 研究低温信号如何与SA途径相互作用以调节植物免疫力.
- 为了确定关键的分子参与者参与寒冷增强的疾病耐药性.
主要方法:
- 阿拉比多普西斯·塔利亚纳的抗病能力测试针对Pseudomonas syringae pv. 番茄 DC3000 在冷应力下.
- 研究了CBF表达1的诱导者 (ICE1) 和与致病相关的基因1的非表达者 (NPR1) 的作用.
- 评估了蛋白质与蛋白质相互作用 (ICE1-NPR1,ICE1-TGA3) 和与病原发生相关的基因1 (PR1) 的转录激活.
主要成果:
- 低温增强了阿拉比多普西斯病的耐药性,依赖于ICE1.1.
- ICE1与NPR1发生了物理相互作用,NPR1是SA通路的关键调节器.
- NPR1增强了ICE1与PR1促进体的结合及其转录激活.
- 寒冷压力促进了ICE1,NPR1和TGA3之间的相互作用,促进了PR1的激活.
结论:
- ICE1作为关键的调节节点,连接冷激活和SA调节的植物免疫.
- 寒冷和SA信号通过ICE1合作,增强植物对病原体的防御能力.
- 这项研究阐明了整合环境线索和荷尔蒙信号在植物免疫中的新机制.
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