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Clinical isolates of the porcine pathogenActinobacillus 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 inA. pleuropneumoniae , we screened a bank of transposon mutants of the nonadherent serovar 1 strain S4074T and identified mutations in two genes,rseA andhns , which resulted in the formation of the adherent colony phenotype. In other bacteria, including theEnterobacteriaceae , H-NS acts as a global gene regulator, and RseA is a negative regulator of the extracytoplasmic stress response sigma factor σE . Transcription profiling ofA. pleuropneumoniae rseA andhns mutants revealed that both σE and H-NS independently regulate expression of thepga operon. Transcription of thepga 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. InA. pleuropneumoniae , H-NS does not act as a global gene regulator but rather specifically regulates biofilm formation via repression of thepga operon. Positive regulation of thepga operon by σE indicates that biofilm formation is part of the extracytoplasmic stress response inA. pleuropneumoniae .

Regulation of pga Operon Expression and Biofilm Formation in Actinobacillus pleuropneumoniae by σ E and H-NS

Regulation of pga Operon Expression and Biofilm Formation in Actinobacillus pleuropneumoniae by σ ^E and H-NS