The Siderophore Pyoverdine of Pseudomonas syringae pv. tabaci 6605 Is an Intrinsic Virulence Factor in Host Tobacco Infection

The Siderophore Pyoverdine of Pseudomonas syringae pv. tabaci 6605 Is an Intrinsic Virulence Factor in Host Tobacco Infection
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DOI:
10.1128/jb.00689-09
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发表时间:
2010-01-01
影响因子:
3.2
通讯作者:
Ichinose, Yuki
Ichinose, Yuki
中科院分区:
生物学3区
文献类型:
--
作者:
Taguchi, Fumiko;Suzuki, Tomoko;Ichinose, Yuki

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目的:探讨铁载体吡哆醇介导的铁摄取在植物病原菌紫丁香假单胞菌毒力中的作用。Tabaci 6605,三个预测的与吡喃甲啶合成相关的基因pvdJ、pvdL和fpvA发生突变。PvdJ、pvdL和fpvA基因分别编码酪氨酸侧链多肽合成酶III的L-苏氨酸-L-丝氨酸组分、发色团合成酶和依赖于TonB的铁蛋白受体。Delta pvdJ和Delta pvdL突变体不能在缺铁条件下的无机盐葡萄糖介质中产生吡哆醇。此外,Delta pvdJ和Delta pvdL突变体产生烟草毒素、胞外多糖和酰基高丝氨酸内酯的能力较低,从而降低了对寄主烟草的毒力。相反,所有突变体都加快了蜂群能力,增加了生物表面活性物质的产生,这表明吡喃呋喃可能对蜂群运动和生物表面活性物质的产生产生了负面的控制。接种突变菌株的烟叶表面扫描电子显微镜显示,这些突变株周围只有少量的胞外聚合物基质,表明成熟的生物膜被破坏。Delta pvdL突变株对抗生素的耐受性显著提高,而Delta心理突变株在AHL生产中存在缺陷。这些结果证明了紫丁假单胞菌群体感应系统的建立和吡喃佛定的合成。Tabaci 6605是寄主烟草侵染毒力所必需的,AHL可能负向调节对抗生素的耐受性。
To investigate the role of iron uptake mediated by the siderophore pyoverdine in the virulence of the plant pathogen Pseudomonas syringae pv. tabaci 6605, three predicted pyoverdine synthesis-related genes, pvdJ, pvdL, and fpvA, were mutated. The pvdJ, pvdL, and fpvA genes encode the pyoverdine side chain peptide synthetase III L-Thr-L-Ser component, the pyoverdine chromophore synthetase, and the TonB-dependent ferripyoverdine receptor, respectively. The Delta pvdJ and Delta pvdL mutants were unable to produce pyoverdine in mineral salts glucose medium, which was used for the iron-depleted condition. Furthermore, the Delta pvdJ and Delta pvdL mutants showed lower abilities to produce tabtoxin, extracellular polysaccharide, and acyl homoserine lactones (AHLs), which are quorum-sensing molecules, and consequently had reduced virulence on host tobacco plants. In contrast, all of the mutants had accelerated swarming ability and increased biosurfactant production, suggesting that swarming motility and biosurfactant production might be negatively controlled by pyoverdine. Scanning electron micrographs of the surfaces of tobacco leaves inoculated with the mutant strains revealed only small amounts of extracellular polymeric matrix around these mutants, indicating disruption of the mature biofilm. Tolerance to antibiotics was drastically increased for the Delta pvdL mutant, as for the Delta psyI mutant, which is defective in AHL production. These results demonstrated that pyoverdine synthesis and the quorum-sensing system of Pseudomonas syringae pv. tabaci 6605 are indispensable for virulence in host tobacco infection and that AHL may negatively regulate tolerance to antibiotics.