Department of Plant Pathology, University of California, Davis, California, USA.
Department of Plant Pathology, Kearney Agricultural Research and Extension Center, Parlier, California, USA.
Microbiol Spectr. 2024 Oct 3;12(10):e0132424. doi: 10.1128/spectrum.01324-24. Epub 2024 Sep 3.
To gain insights into the diversity of sensu lato affecting sweet cherry in California, we sequenced and analyzed the phylogenomic and genomic architecture of 86 fluorescent pseudomonads isolated from symptomatic and asymptomatic cherry tissues. Fifty-eight isolates were phylogenetically placed within the species complex and taxonomically classified into five genomospecies: pv. , , , , and . We annotated components of the type III secretion system and phytotoxin-encoding genes and correlated the data with pathogenicity phenotypes. Intact probable regulatory protein HrpR was annotated in the genomic sequences of all isolates of pv. , , , and . Isolates of had atypical probable regulatory protein HrpR. Syringomycin and syringopeptin-encoding genes were annotated in isolates of all genomospecies except for and . All isolates of pv. caused cankers, leaf spots, and fruit lesions in the field. In contrast, all isolates of and and some isolates of caused only cankers. Isolates of genomospecies could not cause any symptoms suggesting phytotoxins are essential for pathogenicity. On detached immature cherry fruit pathogenicity assays, isolates of all five genomospecies produced symptoms (black-dark brown lesions). However, symptoms of isolates of genomospecies were significantly ( < 0.01) less severe than those of other genomospecies. We also mined for genes conferring resistance to copper and kasugamycin and correlated these data with antibiotic sensitivity tests.
Comprehensive identification of phytopathogens and an in-depth understanding of their genomic architecture, particularly virulence determinants and antibiotic-resistant genes, are critical for several practical reasons. These include disease diagnosis, improved knowledge of disease epidemiology, pathogen diversity, and determination of the best possible management strategies. In this study, we provide the first report of the presence and pathogenicity of genomospecies and in California sweet cherry. More importantly, we report a relatively high level of resistance to copper among the population of pv. (47.5%). This implies copper cannot be effectively used to control bacterial blast and bacterial canker of sweet cherries. On the other hand, no isolates were resistant to kasugamycin, an indication that kasugamycin could be effectively used for the control of bacterial blast and bacterial canker. Our findings are important to improve the management of bacterial blast and bacterial canker of sweet cherries in California.
为了深入了解影响加利福尼亚甜樱桃的广义意义上的病原体的多样性，我们对从有症状和无症状樱桃组织中分离出的 86 株荧光假单胞菌进行了测序和分析，以构建系统发育基因组学图谱并分析其基因组结构。58 株分离物在系统发育上位于 种复合体中，并在分类上分为五个基因组种： 、 、 、 和 。我们注释了 III 型分泌系统组件和植物毒素编码基因，并将数据与致病性表型相关联。在 、 、 和 的所有分离物的基因组序列中都注释了完整的可能调节蛋白 HrpR。 的分离物具有非典型的可能调节蛋白 HrpR。在除了 和 之外的所有基因组种的分离物中都注释了菌毒症素和菌毒症肽编码基因。所有 pv. 分离物在田间都能引起溃疡、叶斑和果实病斑。相比之下，所有 和 的分离物以及 的一些分离物仅能引起溃疡。基因组种 的分离物不能引起任何症状，表明植物毒素对致病性是必需的。在离体未成熟樱桃果实致病性测定中，所有五个基因组种的分离物均产生症状（黑-深棕色病斑）。然而，基因组种 分离物的症状明显（<0.01）比其他基因组种的症状轻。我们还挖掘了对抗铜和井冈霉素的抗性基因，并将这些数据与抗生素敏感性测试相关联。
全面识别植物病原体并深入了解其基因组结构，特别是毒力决定因素和抗生素抗性基因，从几个实际原因来看都是至关重要的。这些原因包括疾病诊断、更好地了解疾病流行病学、病原体多样性以及确定最佳管理策略。在这项研究中，我们首次报告了基因组种 和 在加利福尼亚甜樱桃中的存在和致病性。更重要的是，我们报告了 pv. （47.5%）对铜的相对高水平抗性。这意味着铜不能有效地用于控制甜樱桃的细菌性溃疡和细菌性溃疡病。另一方面，没有分离物对井冈霉素有抗性，这表明井冈霉素可以有效地用于控制细菌性溃疡和细菌性溃疡病。我们的研究结果对于改善加利福尼亚甜樱桃细菌性溃疡和细菌性溃疡病的管理非常重要。
