Department of Plant Pathology, University of Georgia, Athens, GA, U.S.A.
Department of Plant Pathology, University of Georgia, Tifton, GA, U.S.A.
Mol Plant Microbe Interact. 2023 Jun;36(6):381-391. doi: 10.1094/MPMI-11-22-0246-R. Epub 2023 Jun 28.
is an unusual bacterial pathogen that lacks typical virulence determinants yet causes extensive necrosis in onion foliage and bulb tissues. The onion necrosis phenotype is dependent on the expression of the phosphonate toxin, pantaphos, which is synthesized by putative enzymes encoded by the HiVir (high virulence) gene cluster. The genetic contributions of individual genes in HiVir-mediated onion necrosis remain largely unknown, except for the first gene, (phosphoenolpyruvate mutase, ), whose deletion resulted in the loss of onion pathogenicity. In this study, using gene-deletion mutation and complementation, we report that, of the ten remaining genes, to are also strictly required for the HiVir-mediated onion necrosis and in-planta bacterial growth, whereas to partially contributed to these phenotypes. As the HiVir gene cluster is a common genetic feature shared among the onion-pathogenic . strains that could serve as a useful diagnostic marker of onion pathogenicity, we sought to understand the genetic basis of HiVir-positive yet phenotypically deviant (non-pathogenic) strains. We identified and genetically characterized inactivating single nucleotide polymorphisms in the essential genes of six phenotypically deviant . strains. Finally, inoculation of cell-free spent medium of the isopropylthio-β-galactoside (IPTG)-inducible promoter (P)-driven HiVir strain caused . -characteristic red onion scale necrosis as well as cell death symptoms in tobacco. Co-inoculation of the spent medium with essential mutant strains restored in-planta populations of the strains to the wild-type level, suggesting that necrotic tissues are important for the proliferation of . in onion. [Formula: see text] Copyright © 2023 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
是一种不寻常的细菌病原体，缺乏典型的毒力决定因素，但会导致洋葱叶片和鳞茎组织广泛坏死。洋葱坏死表型依赖于膦酸盐毒素 pantaphos 的表达，该毒素由 HiVir（高毒力）基因簇编码的假定酶合成。除了第一个基因 （磷酸烯醇丙酮酸变位酶）外，HiVir 介导的洋葱坏死和体内细菌生长的个别基因的遗传贡献在很大程度上仍然未知，该基因的缺失导致洋葱致病性丧失。在这项研究中，我们使用基因缺失突变和互补，报告说，在剩下的十个基因中， 到 对于 HiVir 介导的洋葱坏死和体内细菌生长也是严格必需的，而 到 部分贡献了这些表型。由于 HiVir 基因簇是洋葱致病菌中共同的遗传特征 菌株，可以作为洋葱致病性的有用诊断标记，我们试图了解 HiVir 阳性但表型异常（非致病性）菌株的遗传基础。我们鉴定并遗传表征了六个表型异常的 菌株中必需的 基因中的单核苷酸多态性。最后，异丙基硫代-β-半乳糖苷（IPTG）诱导启动子（P）驱动的 HiVir 菌株的无细胞耗尽培养基的接种导致. 特征性的红洋葱鳞片坏死以及烟草中的细胞死亡症状。耗尽培养基与必需的 突变体菌株共接种可将菌株在体内的种群恢复到野生型水平，表明坏死组织对于. 在洋葱中的增殖很重要。 [公式：见正文] 版权所有 © 2023 作者。这是一份在 CC BY-NC-ND 4.0 国际许可下分发的开放获取文章。
