Open AccessRole of Bordetella pertussis RseA in the cell envelope stress response and adenylate cyclase toxin release
Author(s) -
Hanawa Tomoko,
Yonezawa Hideo,
Kawakami Hayato,
Kamiya Shigeru,
Armstrong Sandra K.
Publication year - 2013
Publication title -
pathogens and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.983
H-Index - 105
ISSN - 2049-632X
DOI - 10.1111/2049-632x.12061
Subject(s) - adenylate cyclase toxin , bordetella pertussis , sigma factor , cell envelope , biology , mutant , pertussis toxin , microbiology and biotechnology , wild type , escherichia coli , biochemistry , bacteria , g protein , gene , signal transduction , rna polymerase , genetics
Bordetella pertussis is the bacterial agent of the human disease such as whooping cough. In many bacteria, the extracellular function sigma factor σ E 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 σ E 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.