Bordetella pertussis is the bacterial agent of the human disease such as whooping cough. In many bacteria, the extracellular function sigma factor σE is central to the response to envelope stress, and its activity is negatively controlled by the RseA anti-sigma factor. In this study, the role of RseA in B. pertussis envelope stress responses was investigated. Compared with the wild-type strain, an rseA mutant showed elevated resistance to envelope stress and enhanced growth at 25 °C. rpoH and other predicted σE target genes demonstrated increased transcription in the rseA mutant compared with the wild-type parent. Transcription of those genes was also increased in wild-type B. pertussis and Escherichia coli under envelope stress, whereas no stress-induced increase in transcription was observed in the rseA mutant. rseA inactivation was also associated with altered levels of certain proteins in culture supernatant fluids, which showed increased adenylate cyclase toxin (CyaA) levels. The increased CyaA in the mutant was correlated with an apparent increased stability of the extracellular toxin and increased production of CyaA-containing outer membrane vesicles. Consistent with this, compared with the wild-type strain, rseA mutant cells produced increased numbers of large surface-associated vesicles.
Keywords: Bordetella pertussis; RpoE; RseA; adenylate cyclase; envelope stress; σE.
© 2013 Federation of European Microbiological Societies.