首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A cell-cell signaling sensor is required for virulence and insect transmission of Xylella fastidiosa
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A cell-cell signaling sensor is required for virulence and insect transmission of Xylella fastidiosa

机译:需要一种细胞信号传感器来对小木杆菌的毒力和昆虫传播

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Cell-cell signaling in Xylella fastidiosa, a xylem-colonizing plant pathogenic bacterium, mediated by a fatty acid Diffusible Signaling Factor (DSF), is required to colonize insect vectors and to suppress virulence to grape. Here, we show that a hybrid two-component regulatory protein RpfC is involved in negative regulation of DSF synthesis by RpfF in X. fastidiosa. X. fastidiosa rpfC mutants hyperexpress rpfF and overproduce DSF and are deficient in virulence and movement in the xylem vessels of grape. The expression of the genes encoding the adhesins FimA, HxfA, and HxfB is much higher in rpfC mutants, which also exhibit a hyper-attachment phenotype in culture that is associated with their inability to migrate in xylem vessels and cause disease. rpfF mutants deficient in DSF production have the opposite phenotypes for all of these traits. RpfC is also involved in the regulation of other signaling components including rpfG, rpfB, a GGDEF domain protein that may be involved in intracellular signaling by modulating the levels of cyclic-di-GMP, and the virulence factors tolC and pgIA required for disease. rpfC mutants are able to colonize the mouth-parts of insect vectors and wild-type strains but are not transmitted as efficiently to new host plants, apparently because of their high levels of adhesiveness. Because of the conflicting contributions of adhesiveness and other traits to movement within plants and vectoring to new host plants, X. fastidiosa apparently coordinates these traits in a population-size-dependent fashion involving accumulation of DSF.
机译:需通过脂肪酸扩散信号因子(DSF)介导的木质部定植植物病原细菌Xylella fastidiosa中的细胞信号转导才能定居昆虫载体并抑制对葡萄的毒力。在这里,我们显示杂种两组分调控蛋白RpfC参与了X. fastidiosa中RpfF对DSF合成的负调控。 X. fastidiosa rpfC突变体过度表达rpfF并过度产生DSF,并且在葡萄木质部容器中缺乏毒力和运动能力。在rpfC突变体中,编码粘附素FimA,HxfA和HxfB的基因的表达要高得多,而rpfC突变体在培养物中也表现出超附着表型,这与它们无法在木质部血管中迁移并导致疾病有关。缺乏DSF产生的rpfF突变体具有所有这些性状的相反表型。 RpfC还参与其他信号传导成分的调节,包括rpfG,rpfB,可通过调节环二GMP的水平参与细胞内信号传导的GGDEF域蛋白,以及疾病所需的毒力因子tolC和pgIA。 rpfC突变体能够在昆虫载体和野生型菌株的口部定居,但显然不能高效地传播给新的宿主植物,这显然是因为它们具有很高的粘附性。由于粘附性和其他性状对植物内运动和向新宿主植物的转移的贡献相互矛盾,因此,X。fastidiosa显然以依赖种群大小的方式协调这些性状,涉及DSF的积累。

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