College of Plant Science and Technology, Huazhong Agricultural University, Wuhan, China; Department of Crop Science, Faculty of Agriculture, University of Benin, Benin City, Nigeria.
Center for Plant Science Innovation and Department of Biochemistry, University of Nebraska-Lincoln, Lincoln NE68588, USA; Department of Crop Science, Faculty of Agriculture, University of Benin, Benin City, Nigeria.
Plant Sci. 2024 Oct;347:112175. doi: 10.1016/j.plantsci.2024.112175. Epub 2024 Jul 8.
Enhanced Disease Susceptibility 1 (EDS1) is a key regulator of plant-pathogen-associated molecular pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) responses. In the Brassica napus genome, we identified six novel EDS1 genes, among which four were responsive to clubroot infection, a major rapeseed disease resistant to chemical control. Developing resistant cultivars is a potent and economically viable strategy to control clubroot infection. Bioinformatics analysis revealed conserved domains and structural uniformity in Bna-EDS1 homologs. Bna-EDS1 promoters harbored elements associated with diverse phytohormones and stress responses, highlighting their crucial roles in plant defense. A functional analysis was performed with Bna-EDS1 overexpression and RNAi transgenic lines. Bna-EDS1 overexpression boosted resistance to clubroot and upregulated defense-associated genes (PR1, PR2, ICS1, and CBP60), while Bna-EDS1 RNAi increased plant susceptibility, indicating suppression of the defense signaling pathway downstream of NBS-LRRs. RNA-Seq analysis identified key transcripts associated with clubroot resistance, including phenylpropanoid biosynthesis. Activation of SA regulator NPR1, defense signaling markers PR1 and PR2, and upregulation of MYC-TFs suggested that EDS1-mediated clubroot resistance potentially involves the SA pathway. Our findings underscore the pivotal role of Bna-EDS1-dependent mechanisms in resistance of B. napus to clubroot disease, and provide valuable insights for fortifying resistance against Plasmodiophora brassicae infection in rapeseed.
增强型疾病易感性 1(EDS1)是植物-病原体相关分子模式触发免疫(PTI)和效应子触发免疫(ETI)反应的关键调节剂。在油菜基因组中,我们鉴定了六个新的 EDS1 基因,其中四个对根肿病感染有反应,根肿病是一种主要的油菜病害,抗化学控制。培育抗性品种是控制根肿病感染的有效且经济可行的策略。生物信息学分析显示 Bna-EDS1 同源物具有保守结构域和结构一致性。Bna-EDS1 启动子含有与多种植物激素和应激反应相关的元件,突出了它们在植物防御中的关键作用。通过 Bna-EDS1 过表达和 RNAi 转基因系进行了功能分析。Bna-EDS1 过表达增强了对根肿病的抗性,并上调了防御相关基因(PR1、PR2、ICS1 和 CBP60),而 Bna-EDS1 RNAi 增加了植物的易感性,表明 NBS-LRRs 下游防御信号通路受到抑制。RNA-Seq 分析鉴定了与根肿病抗性相关的关键转录本,包括苯丙烷生物合成。SA 调节因子 NPR1、防御信号标记物 PR1 和 PR2 的激活以及 MYC-TFs 的上调表明,EDS1 介导的根肿病抗性可能涉及 SA 途径。我们的研究结果强调了 Bna-EDS1 依赖性机制在油菜抵抗根肿病中的关键作用,并为增强油菜对 Plasmodiophora brassicae 感染的抗性提供了有价值的见解。