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Biofilm formation is important for infection by many pathogens.  Bordetella bronchiseptica  causes respiratory tract infections in mammals and forms biofilm structures in nasal epithelium of infected mice. We previously demonstrated that cyclic di-GMP is involved in biofilm formation in  B .  bronchiseptica . In the present work, based on their previously reported function in  Pseudomonas fluorescens , we identified three genes in the  B .  bronchiseptica  genome likely involved in c-di-GMP-dependent biofilm formation:  brtA ,  lapD  and  lapG . Genetic analysis confirmed a role for BrtA, LapD and LapG in biofilm formation using microtiter plate assays, as well as scanning electron and fluorescent microscopy to analyze the phenotypes of mutants lacking these proteins.  In vitro  and  in vivo  studies showed that the protease LapG of  B .  bronchiseptica  cleaves the N-terminal domain of BrtA, as well as the LapA protein of  P .  fluorescens , indicating functional conservation between these species. Furthermore, while BrtA and LapG appear to have little or no impact on colonization in a mouse model of infection, a  B .  bronchiseptica  strain lacking the LapG protease has a significantly higher rate of inducing a severe disease outcome compared to the wild type. These findings support a role for c-di-GMP acting through BrtA/LapD/LapG to modulate biofilm formation, as well as impact pathogenesis, by  B .  bronchiseptica

Homologs of the LapD-LapG c-di-GMP Effector System Control Biofilm Formation by Bordetella bronchiseptica