Letia Sharon, Bhattacharyya Sabarna, Mendy Badou, Vothknecht Ute C, von Reuss Stephan H, Inada Masaki, Grundler Florian M W, Hasan M Shamim
INRES, Molecular Phytomedicine, University of Bonn, Bonn, Germany.
Plant Cell Biology, Institute for Cellular and Molecular Botany, University of Bonn, Bonn, Germany.
Physiol Plant. 2025 Jul-Aug;177(4):e70386. doi: 10.1111/ppl.70386.
Plant immunity against pathogens is primarily triggered by the perception of pathogen-associated molecular patterns (PAMPs). Ascaroside#18, a nematode-derived pheromone, is the first identified nematode-associated molecular pattern conferring broad-spectrum pathogen resistance. Recently, ascr#18 was shown to be recognised by the leucine-rich repeat receptor NILR1, linked to pattern-triggered immunity (PTI) against nematodes. However, the molecular mechanisms downstream of ascr#18 perception remain largely unknown. Here, we show that ascr#18 triggers an immune response that differs from the typical PTI features, with no reactive oxygen species burst or defence-related growth inhibition. Further analysis indicates that the ascr#18-associated resistance mechanism against cyst nematodes (CN) operates independently of the peroxisomal β-oxidation pathway. Transcriptome profiling of Arabidopsis roots treated with ascr#18 revealed strong effects on the regulation of auxin transport and signalling genes, while classical defence genes remained unchanged. These changes, particularly the downregulation of auxin-related genes, occur independently of NILR1. Analysis of CN feeding sites revealed that ascr#18 pretreatment reduced expression of the auxin influx carrier AUX1 and the auxin-responsive genes SAUR69 and IAA27. Promoter-reporter analysis confirmed reduced AUX1 expression in both nematode-infected and non-infected roots treated with ascr#18. Since nematode establishment and the associated feeding cell development are heavily dependent on the modulation of auxin signalling, our results suggest a novel defence mechanism based on its suppression. This mechanism reduces nematode susceptibility without activating classical PTI responses. Our results provide new insights into how plants fend off biotrophic pathogens and point to ways of developing novel strategies for controlling nematodes and other biotrophic pathogens.
植物对病原体的免疫主要由对病原体相关分子模式（PAMPs）的识别触发。蛔苷#18是一种线虫来源的信息素，是首个被鉴定出的赋予广谱病原体抗性的线虫相关分子模式。最近，ascr#18被富含亮氨酸重复序列的受体NILR1识别，该受体与针对线虫的模式触发免疫（PTI）相关。然而，ascr#18感知下游的分子机制仍 largely未知。在这里，我们表明ascr#18触发的免疫反应不同于典型的PTI特征，没有活性氧爆发或防御相关的生长抑制。进一步分析表明，ascr#18介导的针对胞囊线虫（CN）的抗性机制独立于过氧化物酶体β-氧化途径。用ascr#18处理的拟南芥根的转录组分析显示，其对生长素运输和信号基因的调控有强烈影响，而经典防御基因保持不变。这些变化，特别是生长素相关基因的下调，独立于NILR1发生。对CN取食位点的分析表明，ascr#18预处理降低了生长素流入载体AUX1以及生长素响应基因SAUR69和IAA27的表达。启动子-报告基因分析证实，在经ascr#18处理的线虫感染和未感染的根中，AUX1表达均降低。由于线虫的定殖和相关取食细胞的发育严重依赖于生长素信号的调节，我们的结果表明了一种基于其抑制的新型防御机制。这种机制降低了线虫的易感性，而不激活经典的PTI反应。我们的结果为植物抵御活体营养病原体的方式提供了新的见解，并指出了开发控制线虫和其他活体营养病原体新策略的途径。
