一个开拓性线虫效应器通过与III类过氧酶相互作用来抑制植物反应性氧物种的爆发
Lin Rui1,2, Tong-Yue Wen1,2, Yi-Jun Qiu1,2
1Co-Innovation Center for Sustainable Forestry in Southern China, College of Forestry, Nanjing Forestry University, Nanjing, China.
Plant, cell & environment
|May 29, 2024
概括
布尔萨菲伦克斯 (Bursaphelenchus xylophilus) 使用BxPIE1效应器通过抑制活性氧物种 (ROS) 生产来抑制松树的防御. 这一发现揭示了针对松病的新型线虫毒性机制.
科学领域:
- 植物病理学 植物病理学
- 遗体学 遗体学 是一个学科.
- 分子生物学分子生物学
背景情况:
- 由Bursaphelenchus xylophilus引起的松病对森林生态系统构成重大威胁.
- 植物通常使用活性氧物种 (ROS) 来防御线虫感染,但线虫效应器操纵ROS的机制尚不清楚.
研究的目的:
- 为了识别和描述参与操纵植物ROS代谢的Bursaphelenchus xylophilus效应物.
- 阐明一种新型效应因子BxPIE1在与Pinus thunbergii的寄生相互作用中的作用.
主要方法:
- 在B. xylophilus. 中对BxPIE1的基因沉默.
- 蛋白质与蛋白质相互作用测试以确定BxPIE1的相互作用伙伴.
- 在受感染的植物中测量ROS的产生和与病变发生相关的 (PR) 基因表达.
- 对线虫繁殖和疾病进展的评估.
主要成果:
- 沉默BxPIE1降低了线虫的繁殖和疾病严重程度,伴随着PtPR-3和PtPR-9的表达增加.
- 发现BxPIE1与Pinus thunbergii III类过氧化酶 (PtPrx3) 相互作用,这种酶产生H2O2.2.
- BxPIE1通过PtPrx3抑制了H2O2生成,这种抑制被ascorbate逆转,表明ROS清理恢复了毒性.
结论:
- BxPIE1是B. xylophilus的一个关键的毒性因子.
- BxPIE1通过与PtPrx3.3相互作用来抑制ROS的产生来抑制松树免疫力.
- 这项研究揭示了一种新的线虫策略,在松病进展期间克服植物防御.
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