Transposon Mutagenesis of Pseudomonas syringae Pathovars syringae and morsprunorum to Identify Genes Involved in Bacterial Canker Disease of Cherry.
Transposon Mutagenesis of Pseudomonas syringae Pathovars syringae and morsprunorum to Identify Genes Involved in Bacterial Canker Disease of Cherry.
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DOI：
10.3390/microorganisms9061328
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发表时间：
2021-06-18
期刊：
影响因子：
4.5
通讯作者：
Arnold DL
中科院分区：
文献类型：
--
作者：
Neale HC;Hulin MT;Harrison RJ;Jackson RW;Arnold DL
李细菌性溃疡病是由李假单胞菌（Pseudomonasalumingae，P.s.）引起的一种病害，主要危害樱桃、桃、杏、李等核果类果树。来自两种致病变种的菌株-P.s. PV. Pss）和P.s. PV. morsprunorum小种1（PsmR 1）和2（PsmR 2）-在三个遗传学上遥远的分支中会聚地进化以感染李属。细菌通过伤口和叶痕进入木质组织，引起黑色坏死溃疡。症状也发生在开花、果实和叶子上。很少有人知道的机制P.S.用于在树宿主如李属植物中定居。在此，我们在一株P.s.并在未成熟的樱桃果实上筛选突变体以寻找毒力的变化。检测到毒性降低或增强的突变体（242），并通过体外筛选进一步表征生物膜形成、群集能力和叶和切枝上的致病性。总共选择了18个影响毒力的基因，这些基因涉及多种功能，包括运动性、III型分泌、膜转运、氨基酸合成、DNA修复和初级代谢。有趣的是，效应基因hopAU 1的突变导致Psm R2的毒力增加。
Bacterial canker of Prunus, affecting economically important stone fruit crops including cherry, peach, apricot and plum, is caused by the plant pathogen Pseudomonas syringae (P.s.). Strains from two pathovars—P.s. pv. syringae (Pss) and P.s. pv. morsprunorum race 1 (PsmR1) and 2 (PsmR2)—in three phylogenetically distant clades have convergently evolved to infect Prunus. The bacteria enter woody tissues through wounds and leaf scars, causing black necrotic cankers. Symptoms are also produced on blossom, fruit and leaves. Little is known about the mechanisms P.s. uses to colonise tree hosts such as Prunus. Here, we created transposon (Tn) mutant libraries in one strain of P.s. from each of the three clades and screened the mutants on immature cherry fruit to look for changes in virulence. Mutants (242) with either reduced or enhanced virulence were detected and further characterised by in vitro screens for biofilm formation, swarming ability, and pathogenicity on leaves and cut shoots. In total, 18 genes affecting virulence were selected, and these were involved in diverse functions including motility, type III secretion, membrane transport, amino acid synthesis, DNA repair and primary metabolism. Interestingly, mutation of the effector gene, hopAU1, led to an increase in virulence of Psm R2.