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首页> 外文期刊>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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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：猪病原体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 的表达编码了一种聚-β-1,6- N -乙酰基-d-氨基葡萄糖（PGA）细胞外基质。与在聚苯乙烯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 A中PGA表达和生物膜形成的调控。胸膜肺炎，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 rseA 和 hns两个基因的突变。 em>，这导致粘附菌落表型的形成。在其他细菌中，包括 Enterobacteriaceae ，H-NS充当全局基因调节剂，而RseA是胞外应激反应σ因子σ E 的负调节剂。 A的转录分析。胸膜肺炎的rseA 和 hns 突变体表明，σ E 和H-NS均独立调节 pga 操纵子的表达。 pga 操纵子的转录是在没有H-NS的情况下从σ E 启动子启动的，而σ E 的上调足以取代H-NS，使转录继续进行。在 A中。胸膜肺炎，H-NS不能作为全局基因调节剂，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 操纵子的正调控表明，生物膜的形成是 A中胞质外应激反应的一部分。胸膜肺炎。

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