Paudel Sujan, Franco Yaritza, Zhao Mei, Dutta Bhabesh, Kvitko Brian H
Department of Plant Pathology, University of Georgia, Athens, GA, U.S.A.
Department of Microbiology, University of Georgia, Athens, GA, U.S.A.
Mol Plant Microbe Interact. 2025 May;38(3):427-439. doi: 10.1094/MPMI-10-24-0129-R. Epub 2025 May 15.
Slippery skin of onion caused by pv. (Bga) is a common bacterial disease reported from onion-growing regions around the world. Despite the increasing attention in recent years, our understanding of the virulence mechanisms of this pathogen remains limited. In this study, we characterized the predicted genetic determinants of virulence in Bga strain 20GA0385 using a reverse genetics approach. Using the closely related rice pathogen as a reference, comparative genomics analysis was performed to identify Bga candidate virulence factors and regulators. Marked and unmarked deletion mutants were generated using allelic exchange, and the mutants were functionally validated using in vitro and in vivo assays. The role of mutants in pathogenic phenotypes was analyzed using onion foliar/seedling necrosis assays, the red scale necrosis assay, and in planta bacterial population counts. The phytotoxin toxoflavin was a major contributor to foliar necrosis and bacterial populations, whereas the type II and type III secretion systems (T2SS/T3SS) were dispensable for foliar symptoms. In onion scale tissue, the T2SS single mutant and its double and triple mutant derivatives all contributed to scale lesion area. Neither the lipocyclopeptide icosalide, toxoflavin, nor T3SS was required for scale symptoms. Our results suggest that the quorum sensing system in Bga regulates toxoflavin, T2SS, and T3SS, contributing to onion symptom production. We show that different virulence factors contribute to onion tissue-specific virulence patterns in Bga and that decreases in scale symptoms often do not result in decreased Bga populations in onion tissue. [Formula: see text] Copyright © 2025 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
由洋葱致病疫霉(Bga)引起的洋葱表皮滑皮病是一种在世界各地洋葱种植区均有报道的常见细菌性疾病。尽管近年来受到越来越多的关注,但我们对这种病原体的致病机制仍了解有限。在本研究中,我们使用反向遗传学方法对Bga菌株20GA0385中预测的致病遗传决定因素进行了表征。以密切相关的水稻病原体为参考,进行了比较基因组学分析,以鉴定Bga候选致病因子和调节因子。使用等位基因交换产生了有标记和无标记的缺失突变体,并通过体外和体内试验对突变体进行了功能验证。使用洋葱叶片/幼苗坏死试验、红色鳞片坏死试验和植物体内细菌数量计数分析了突变体在致病表型中的作用。植物毒素毒黄素是叶片坏死和细菌数量的主要促成因素,而II型和III型分泌系统(T2SS/T3SS)对叶片症状并非必需。在洋葱鳞片组织中,T2SS单突变体及其双突变和三突变衍生物均对鳞片病斑面积有影响。鳞片症状既不需要脂环肽异珊瑚内酯、毒黄素,也不需要T3SS。我们的结果表明,Bga中的群体感应系统调节毒黄素、T2SS和T3SS,促成洋葱症状的产生。我们表明,不同的致病因子导致Bga中洋葱组织特异性的致病模式,并且鳞片症状的减轻通常不会导致洋葱组织中Bga数量的减少。[公式:见正文] 版权所有© 2025作者。这是一篇根据CC BY-NC-ND 4.0国际许可分发的开放获取文章。