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首页> 外文期刊>Applied Microbiology >Hha Controls Escherichia coli O157:H7 Biofilm Formation by Differential Regulation of Global Transcriptional Regulators FlhDC and CsgD
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Hha Controls Escherichia coli O157:H7 Biofilm Formation by Differential Regulation of Global Transcriptional Regulators FlhDC and CsgD

机译：Hha通过差异调节全局转录调节因子FlhDC和CsgD来控制大肠杆菌O157：H7生物膜形成

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Although molecular mechanisms promoting adherence of enterohemorrhagic Escherichia coli (EHEC) O157:H7 on epithelial cells are well characterized, regulatory mechanisms controlling biofilm formation are not fully understood. In this study, we demonstrate that biofilm formation in EHEC O157:H7 strain 86-24 is highly repressed compared to that in an isogenic hha mutant. The hha mutant produced large quantities of biofilm compared to the wild-type strain at 30°C and 37°C. Complementation of the hha mutant reduced the level of biofilm formation to that of the wild-type strain, indicating that Hha is a negative regulator of biofilm production. While swimming motility and expression of the flagellar gene fliC were significantly reduced, the expression of csgA (encoding curlin of curli fimbriae) and the ability to bind Congo red were significantly enhanced. The expression of both fliC and csgA and the phenotypes of motility and curli production affected by these two genes, respectively, were restored to wild-type levels in the complemented hha mutant. The csgA deletion abolished biofilm formation in the hha mutant and wild-type strain, and csgA complementation restored biofilm formation to these strains, indicating the importance of csgA and curli in biofilm formation. The regulatory effects of Hha on flagellar and curli gene expression appear to occur via the induction and repression of FlhDC and CsgD, as demonstrated by reduced flhD and increased csgD transcription in the hha mutant, respectively. In gel shift assays Hha interacted with flhDC and csgD promoters. In conclusion, Hha regulates biofilm formation in EHEC O157:H7 by differential regulation of FlhDC and CsgD, the global regulators of motility and curli production, respectively.
机译：尽管促进肠出血性大肠杆菌（EHEC）O157：H7粘附在上皮细胞上的分子机制已得到很好的表征，但控制生物膜形成的调控机制尚未完全明了。在这项研究中，我们证明与同基因hha突变体相比，EHEC O157：H7菌株86-24中的生物膜形成受到高度抑制。与在30°C和37°C的野生型菌株相比，hha突变体产生了大量生物膜。 hha突变体的补充使生物膜形成的水平降低至野生型菌株的水平，表明Hha是生物膜产生的负调节剂。游泳运动和鞭毛基因fliC的表达显着降低时，csgA（编码卷曲菌毛的卷曲蛋白）的表达和结合刚果红的能力显着增强。在互补的hha突变体中，分别受这两个基因影响的fliC和csgA的表达以及运动性和卷曲产生的表型被恢复到野生型水平。 csgA缺失消除了hha突变体和野生型菌株中的生物膜形成，并且csgA互补作用使这些菌株恢复了生物膜形成，表明csgA和curli在生物膜形成中的重要性。 Hha对鞭毛和curli基因表达的调节作用似乎是通过FlhDC和CsgD的诱导和抑制而发生的，分别通过在hha突变体中减少的flhD和增加的csgD转录来证明。在凝胶迁移分析中，Hha与flhDC和csgD启动子相互作用。总之，Hha通过分别调节FlhDC和CsgD（运动性和卷曲生产的全球调节剂）的差异调节EHEC O157：H7中生物膜的形成。

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