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首页> 美国卫生研究院文献>Journal of Bacteriology >Regulation of pga Operon Expression and Biofilm Formation in Actinobacillus pleuropneumoniae by σE and H-NS
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Regulation of pga Operon Expression and Biofilm Formation in Actinobacillus pleuropneumoniae by σE and H-NS

机译：σE和H-NS对胸膜肺炎放线杆菌pga操纵子表达和生物膜形成的调控

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摘要

Clinical isolates of the porcine pathogen Actinobacillus pleuropneumoniae often form adherent colonies on agar plates due to expression of an operon, pgaABCD, encoding a poly-β-1,6-N-acetyl-d-glucosamine (PGA) extracellular matrix. The adherent colony phenotype, which correlates with the ability to form biofilms on the surfaces of polystyrene plates, is lost following serial passage in broth culture, and repeated passage of the nonadherent variants on solid media does not result in reversion to the adherent colony phenotype. In order to investigate the regulation of PGA expression and biofilm formation in A. pleuropneumoniae, we screened a bank of transposon mutants of the nonadherent serovar 1 strain S4074T and identified mutations in two genes, rseA and hns, which resulted in the formation of the adherent colony phenotype. In other bacteria, including the Enterobacteriaceae, H-NS acts as a global gene regulator, and RseA is a negative regulator of the extracytoplasmic stress response sigma factor σE. Transcription profiling of A. pleuropneumoniae rseA and hns mutants revealed that both σE and H-NS independently regulate expression of the pga operon. Transcription of the pga operon is initiated from a σE promoter site in the absence of H-NS, and upregulation of σE is sufficient to displace H-NS, allowing transcription to proceed. In A. pleuropneumoniae, H-NS does not act as a global gene regulator but rather specifically regulates biofilm formation via repression of the pga operon. Positive regulation of the pga operon by σE indicates that biofilm formation is part of the extracytoplasmic stress response in A. pleuropneumoniae.
机译：猪病原性胸膜肺炎放线杆菌的临床分离株通常会在琼脂平板上形成粘附菌落，这是由于操纵子pgaABCD的表达，该操纵子编码一种聚β-1,6-N-乙酰基-d-葡萄糖胺（PGA）细胞外基质。与在聚苯乙烯平板表面上形成生物膜的能力相关的粘附菌落表型在肉汤培养中连续传代后消失，并且非粘附变体在固体培养基上的重复传代不会导致回复到粘附菌落表型。为了研究胸膜肺炎链球菌中PGA表达和生物膜形成的调控，我们筛选了一组非粘附性血清型1菌株S4074 T 的转座子突变体，并鉴定了两个基因rseA和hns的突变，这导致粘附菌落表型的形成。在包括肠杆菌科细菌在内的其他细菌中，H-NS充当全局基因调节剂，而RseA是胞浆外应激反应σ因子σ E 的负调节剂。胸膜肺炎链球菌rseA和hns突变体的转录谱分析表明，σ E 和H-NS均独立调节pga操纵子的表达。在没有H-NS的情况下，pga操纵子的转录是从σ E 启动子开始的，而σ E 的上调足以取代H-NS，从而实现转录继续。在胸膜肺炎链球菌中，H-NS并不充当全局基因调节剂，而是通过抑制pga操纵子来特异性调节生物膜的形成。 σ E 对pga操纵子的正向调控表明，生物膜的形成是胸膜肺炎放线杆菌胞外应激反应的一部分。

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