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通过转录组分析深入了解辣椒对丁香假单胞菌的 bs5 抗性机制。

Insights into bs5 resistance mechanisms in pepper against Xanthomonas euvesicatoria through transcriptome profiling.

机构信息

Department of Plant Pathology, University of Florida, Gainesville, FL, USA.

Southwest Florida Research & Education Center, University of Florida, Immokalee, FL, USA.

出版信息

BMC Genomics. 2024 Jul 23;25(1):711. doi: 10.1186/s12864-024-10604-8.

DOI:10.1186/s12864-024-10604-8
PMID:39044136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11267861/
Abstract

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.

CONCLUSION

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.

摘要

背景

由四种不同的黄单胞菌引起的辣椒细菌性斑点病(BSP),主要是 X. euvesicatoria(Xe),对辣椒种植构成了重大挑战。寄主抗性被认为是控制 BSP 的最重要方法,可提供长期保护和可持续性。虽然多年来对 BSP 的抗性育种主要集中在显性 R 基因上,但隐性抗性的基因导入已成为育种计划的一个较新焦点。隐性抗性的分子相互作用仍知之甚少。

结果

在这项研究中,通过两种不同的辣椒品系(Xe 抗性品系 ECW50R,其含有 bs5,一个隐性抗性基因,可抵抗所有辣椒 Xe 种群;Xe 敏感品系 ECW)进行 Xe 菌株 P6 侵染的转录组分析,阐明了防御反应。结果在 0、1、2 和 4 天接种后(dpi)总共发现了 3357 个上调和 4091 个下调基因,在 2 dpi 时观察到最多的差异表达基因(DEGs)。途径分析突出了关键途径中的 DEGs,如植物-病原体相互作用、MAPK 信号通路、植物激素信号转导和光合作用-天线蛋白,以及半胱氨酸和蛋氨酸代谢。值得注意的是,观察到与病原体相关分子模式触发的免疫(PTI)相关基因的上调,包括 FLS2、Ca 依赖性途径、Rboh 和活性氧(ROS)生成等成分。支持这些结果,Xe 细菌悬浮液渗透到 ECW50R 叶片中导致可观察到的过氧化氢积累,而没有电解质泄漏的快速增加,提示不存在效应物触发的免疫(ETI)。此外,该研究证实 bs5 不会破坏效应子传递系统,因为在 bs5 背景下,非毒性基因与其相应的显性抗性基因之间存在不亲和相互作用。

结论

总的来说,这些发现为 Xe 引起的辣椒中 bs5 介导的抗性的分子机制提供了深入的了解,并表明 ECW50R 中存在强大的防御机制,主要通过 PTI 介导。鉴于 bs5 提供了早期强烈的抗性响应,将这种抗性与其他显性抗性基因结合将增强对 BSP 的抗性耐久性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/da8b4ceb1616/12864_2024_10604_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/919837aad3a2/12864_2024_10604_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/9ee4790e183d/12864_2024_10604_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/dd9ae885042d/12864_2024_10604_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/da8b4ceb1616/12864_2024_10604_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/919837aad3a2/12864_2024_10604_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/6a1cf4e52be8/12864_2024_10604_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/9ee4790e183d/12864_2024_10604_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/dd9ae885042d/12864_2024_10604_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d20/11267861/da8b4ceb1616/12864_2024_10604_Fig7_HTML.jpg

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