NADPH氧化酶的S-基化调节植物免疫中的细胞死亡
Byung-Wook Yun1, Angela Feechan, Minghui Yin
1Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JH, UK.
Nature
|October 4, 2011
概括
氧化修改了囊二醇 (S-nitrosothiols),以促进植物的免疫反应. 高水平的S-nitrosothiol通过抑制NADPH氧化酶来限制这些反应,这种机制在真核生物中得到保护.
科学领域:
- 植物免疫力 植物免疫力
- 蜂信号传输是如何进行的
- 转毒生物学 转毒生物学
背景情况:
- 免疫反应涉及氧化还原状态的变化,但信号机制尚不清楚.
- 植物微生物防御包括氧化 (NO) 和活性氧中间体 (ROI).
- NO和ROI涉及过敏反应 (HR),一种植物细胞死亡机制.
研究的目的:
- 阐明协调植物免疫中NO和ROI合成的分子机制.
- 研究S-nitrosothiols (SNO) 在过敏反应中的作用.
- 确定S-化在调节植物免疫信号传递中的作用.
主要方法:
- 基因分析,以研究在没有酸和ROI的情况下S-nitrosothiol的功能.
- 研究了调节过敏反应的负反循环.
- 在Cys 890检查了NADPH氧化酶 (AtRBOHD) 的S-化及其功能后果.
主要成果:
- S-nitrosothiols促进过敏反应独立于酸和ROI.
- 高度的S-nitrosothiol会触发一个负反循环,限制HR.
- 在Cys 890的AtRBOHD的S-化抑制了ROI合成,控制了HR的大小.
- 基因Cys 890的突变破坏了S-尼特罗斯醇介导的AtRBOHD活性调节.
- 调节性半氨酸在人类和中的NADPH氧化酶中被保存.
结论:
- S-尼托醇是植物免疫反应的关键调节剂,调节过敏反应.
- NADPH氧化酶的S-基化提供了控制植物细胞死亡的负反机制.
- 这种依赖于S-化酶的调节机制在动物的免疫反应中得到保留.
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