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芸薹属植物 EDS1 基因的生物信息学和功能分析及其对芸薹根肿菌侵染的响应。

Bioinformatics and functional analysis of EDS1 genes in Brassica napus in response to Plasmodiophora brassicae infection.

机构信息

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.

出版信息

Plant Sci. 2024 Oct;347:112175. doi: 10.1016/j.plantsci.2024.112175. Epub 2024 Jul 8.

Abstract

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.

摘要

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。

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