背景:辣椒的细菌斑点(BSP),由四种不同的黄单胞菌引起,主要是X.euvesicatoria(XE),在辣椒种植中提出了重大挑战。宿主抗性被认为是控制BSP的最重要方法,提供长期保护和可持续性。尽管多年来对BSP的抗性育种主要集中在显性R基因上,隐性抗性的渗入一直是育种计划的最新重点。隐性抗性背后的分子相互作用仍然知之甚少。
结果:在这项研究中,进行了转录组学分析,以阐明由两种不同的辣椒系引起的Xe种族P6感染引发的防御反应:含有bs5的Xe抗性系ECW50R,bs5是一种隐性抗性基因,可赋予所有辣椒Xe种族抗性,和Xe敏感线ECW。结果显示,在接种后(dpi)0、1、2和4天,共有3357个上调基因和4091个下调基因,在2dpi时观察到最高数量的差异表达基因(DEGs)。路径分析强调了植物-病原体相互作用等关键途径中的DEGs,MAPK信号通路,植物激素信号转导,和光合作用-天线蛋白,随着半胱氨酸和蛋氨酸的代谢。值得注意的是,观察到与PAMP触发免疫(PTI)相关的基因上调,包括像FLS2,钙依赖性途径,Rboh,和活性氧(ROS)的产生。为了支持这些结果,用Xe的细菌悬浮液渗透ECW50R叶子导致可观察到的过氧化氢积累,而电解质泄漏没有迅速增加,提示缺乏效应物触发免疫(ETI)。此外,该研究证实bs5不会破坏效应物递送系统,bs5背景中无毒力基因与其相应的显性抗性基因之间的不相容相互作用证明了这一点。
结论:总体而言,这些发现为bs5介导的辣椒抗Xe的分子机制提供了见解,并提出了ECW50R中强大的防御机制,主要通过PTI介导。鉴于bs5提供早期强烈的抗性反应,将这种抗性与其他显性抗性基因组合将增强对BSP的抗性的持久性。
BACKGROUND: Bacterial spot of pepper (BSP), caused by four different Xanthomonas species, primarily X. euvesicatoria (Xe), poses a significant challenge in pepper cultivation. Host resistance is considered the most important approach for BSP control, offering long-term protection and sustainability. While breeding for resistance to BSP for many years focused on dominant R genes, introgression of recessive resistance has been a more recent focus of breeding programs. The molecular interactions underlying recessive resistance remain poorly understood.
RESULTS: In this study, transcriptomic analyses were performed to elucidate defense responses triggered by Xe race P6 infection by two distinct pepper lines: the Xe-resistant line ECW50R containing bs5, a recessive resistance gene that confers resistance to all pepper Xe races, and the Xe-susceptible line ECW. The results revealed a total of 3357 upregulated and 4091 downregulated genes at 0, 1, 2, and 4 days post-inoculation (dpi), with the highest number of differentially expressed genes (DEGs) observed at 2 dpi. Pathway analysis highlighted DEGs in key pathways such as plant-pathogen interaction, MAPK signaling pathway, plant hormone signal transduction, and photosynthesis - antenna proteins, along with cysteine and methionine metabolism. Notably, upregulation of genes associated with PAMP-Triggered Immunity (
PTI) was observed, including components like FLS2, Ca-dependent pathways, Rboh, and reactive oxygen species (ROS) generation. In support of these results, infiltration of ECW50R leaves with bacterial suspension of Xe led to observable hydrogen peroxide accumulation without a rapid increase in electrolyte leakage, suggestive of the absence of Effector-Triggered Immunity (ETI). Furthermore, the study confirmed that bs5 does not disrupt the effector delivery system, as evidenced by incompatible interactions between avirulence genes and their corresponding dominant resistant genes in the bs5 background.
CONCLUSIONS: Overall, these findings provide insights into the molecular mechanisms underlying bs5-mediated resistance in pepper against Xe and suggest a robust defense mechanism in ECW50R, primarily mediated through
PTI. Given that bs5 provides early strong response for resistance, combining this resistance with other dominant resistance genes will enhance the durability of resistance to BSP.