温暖的温度通过拦截N-hydroxypipecolic酸生物合成来抑制植物系统性获得的抵抗力
Alyssa Shields1, Lingya Yao2,3,4, Christina A M Rossi1
1Department of Biology, Wilfrid Laurier University, Waterloo, Ontario, N2L 3C5, Canada.
The Plant journal : for cell and molecular biology
|August 4, 2025
概括
气候变暖通过减少N-hydroxypipecolic acid (NHP) 生物合成来抑制植物的系统免疫力. 这项研究揭示了温度如何影响植物防御,为开发适应气候的作物提供了洞察力.
科学领域:
- 植物免疫和气候变化的相互作用.
- 分子植物病理学 分子植物病理学
- 植物激素信号传递器
背景情况:
- 气候变暖影响了植物的免疫反应,包括模式触发免疫 (PTI),效应器触发免疫 (ETI) 和酸 (SA) 在感染地点的产生.
- 温度对系统性植物免疫力的影响在很大程度上仍然不清楚.
研究的目的:
- 为了研究温度升高对Arabidopsis thaliana.的病原体触发系统性获得性耐药性 (SAR) 的影响.
- 阐明了SAR受温度介导的抑制背后的分子机制.
主要方法:
- 在正常和高温下对阿拉比多普西斯SAR诱导基因表达的比较分析.
- 对SAR代谢物的量化N-基酸 (NHP) 和酸 (Pip) 水平.
- 对NHP和SA生物合成基因表达的分析 (ALD1,FMO1,ICS1).
- 识别调节热敏NHP生物合成的转录因子 (CBP60g,SARD1).
主要成果:
- 病原体触发的SAR在阿拉比多普西斯的高温下被抑制,伴随着SAR诱导基因的全球下调.
- 抑制的SAR与NHP的生物合成减少相关,NHP是一种关键的SAR代谢物,由于ALD1和FMO1基因的下调.
- 外源性应用NHP或Pip在高温下恢复了疾病保护,证实了NHP途径的作用.
- 在温暖的温度下,SA生物合成基因ICS1的表达也被局部和全身抑制.
- 一个涉及CBP60g和SARD1的转录网络被确定为控制热敏NHP生物合成.
结论:
- 高温通过抑制NHP生物合成,损害了本地和全身植物免疫力.
- 这些发现强调了NHP途径在温度介导的植物防御调节中的关键作用.
- 这项研究为工程气候弹性植物免疫系统提供了基础.
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