Bordetella are Gram negative respiratory pathogens of animals, birds and humans. A hallmark feature of some Bordetella species is their ability to efficiently survive in the respiratory tract even after vaccination. B. bronchiseptica and B. pertussis form biofilms on abiotic surfaces and in the mouse respiratory tract. The Bps exopolysaccharide is one of the critical determinants for biofilm formation and the survival of Bordetella in the murine respiratory tract. In order to gain a better understanding of regulation of biofilm formation, we sought to study the mechanism by which Bps expression is controlled in Bordetella. Expression of bpsA-D is elevated in biofilms compared with planktonically grown cells. We found that bpsA-D is expressed independent of BvgAS. Subsequently, we identified an ORF BB1771, (designated herein, bpsR) that is located upstream and in the opposite orientation to the bpsA-D locus. BpsR is homologous to the MarR-family of transcriptional regulators. Measurement of bpsA and bpsD transcripts and the Bps polysaccharide levels from the wild-type and the ∆bpsR strains suggested that BpsR functions as a repressor. Consistent with enhanced production of Bps, the bpsR mutant displayed considerably more structured biofilms. We mapped the bpsA-D promoter region and show that purified BpsR protein specifically bound to the bpsA-D promoter. Our results provide mechanistic insights into the regulatory strategy employed by Bordetella for control of the production of the Bps polysaccharide and biofilm formation.
protein, Bordetella, exopolysaccharide, Biofilm
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