植物免疫需要NPR1通过S-化和 thioredoxins的结构变化[纠正]
Yasuomi Tada1, Steven H Spoel, Karolina Pajerowska-Mukhtar
1Department of Biology, Post Office Box 90338, Duke University, Durham, NC 27708, USA.
概括
植物的免疫反应涉及氧化还原变化. 酸酸 (S-nitrosoglutathione,GSNO) 和氨酸 (thioredoxins,TRXs) 反对调节NPR1蛋白,NPR1蛋白是白酸 (salicylic acid,SA) 介导的防御中的一个关键参与者,影响疾病抵抗力.
科学领域:
- 植物免疫力 植物免疫力
- 分子信号传递是分子信号传递.
- 转毒生物学 转毒生物学
背景情况:
- 在免疫反应期间观察到氧化状态的变化,但信号机制尚不清楚.
- 在植物中,氧化还原变化调节NPR1构造,NPR1构造是白酸 (SA) 中介防御基因的关键调节器.
- 通过二硫化物键,NPR1存在于细胞质中的寡合体,影响其活性.
研究的目的:
- 阐明控制植物免疫中的NPR1功能的氧化还原依赖信号机制.
- 调查S-化和硫素在调节NPR1寡合和活性中的作用.
主要方法:
- 研究了S-尼特罗斯谷 (GSNO) 对NPR1寡合化的作用.
- 检查了 thioredoxins (TRXs) 在 NPR1 寡合物到单合物过渡中的作用.
- 利用NPR1cysteine-156和TRXs的突变分析来评估疾病耐药性.
主要成果:
- 通过GSNO在氨酸-156处S-化NPR1促进其寡合化,保持蛋白质平衡.
- 铁素 (TRXs) 催化SA诱导的NPR1寡合物的解离成单体.
- 影响NPR1cysteine-156或TRXs的突变损害了NPR1-介导的抗病能力.
结论:
- 植物免疫中的NPR1功能是由GSNO (促进寡合化) 和TRX (促进单合化) 的对立作用调节的.
- 这些发现确定了病原体诱导的氧化还原变化和植物防御途径中的基因调节之间的联系.
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