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The nucleoid-associated proteins H-NS and FIS modulate the DNA supercoiling response of the pel genes, the major virulence factors in the plant pathogen bacterium Dickeya dadantii

机译:核苷相关蛋白H-NS和FIS调节pel基因的DNA超螺旋反应,而pel基因是植物病原菌Dickeya dadantii中的主要毒力因子。

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摘要

Dickeya dadantii is a pathogen infecting a wide range of plant species. Soft rot, the visible symptom, is mainly due to the production of pectate lyases (Pels) that can destroy the plant cell walls. Previously we found that the pel gene expression is modulated by H-NS and FIS, two nucleoid-associated proteins (NAPs) modulating the DNA topology. Here, we show that relaxation of the DNA in growing D. dadantii cells decreases the expression of pel genes. Deletion of fis aggravates, whereas that of hns alleviates the negative impact of DNA relaxation on pel expression. We further show that H-NS and FIS directly bind the pelE promoter and that the response of D. dadantii pel genes to stresses that induce DNA relaxation is modulated, although to different extents, by H-NS and FIS. We infer that FIS acts as a repressor buffering the negative impact of DNA relaxation on pel gene transcription, whereas H-NS fine-tunes the response of virulence genes precluding their expression under suboptimal conditions of supercoiling. This novel dependence of H-NS effect on DNA topology expands our understanding of the role of NAPs in regulating the global bacterial gene expression and bacterial pathogenicity.
机译:Dickeya dadantii是一种病原体,可感染多种植物。软腐病是可见症状,主要是由于果胶裂解酶(Pel)的产生,可破坏植物细胞壁。以前,我们发现pel基因的表达受H-NS和FIS调节,这是两个与核苷酸相关的蛋白(NAP),它们调节DNA拓扑结构。在这里,我们显示了在生长的达达尼丁(D. dadantii)细胞中DNA的松弛降低了pel基因的表达。 fis的缺失加剧,而hns的缺失减轻DNA松弛对pel表达的负面影响。我们进一步显示,H-NS和FIS直接结合pelE启动子,而D. dadantii pel基因对诱导DNA松弛的压力的响应,虽然程度不同,但由H-NS和FIS调节。我们推断,FIS充当抑制基因,抑制DNA松弛对pel基因转录的负面影响,而H-NS则微调了毒力基因的响应,从而排除了它们在超螺旋条件下的最佳表达。 H-NS效应对DNA拓扑结构的这种新型依赖性扩展了我们对NAP在调节全局细菌基因表达和细菌致病性中的作用的理解。

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