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Group B streptococcus (GBS) strains with the highest ability to bind to human fibrinogen belong to the highly invasive clonal complex (CC) 17. To investigate the fibrinogen-binding mechanisms of CC17 strains, we determined the prevalence of fibrinogen-binding genes ( fbsA  and  fbsB ), and  fbs  regulator genes ( rogB  encoding an  fbsA  activator,  rovS  encoding an  fbsA  repressor and  rgf  encoding a two-component system [TCS] whose role on  fbs  genes was not determined yet) in a collection of 134 strains representing the major CCs of the species. We showed that specific gene combinations were related to particular CCs; only CC17 strains contained the  fbsA ,  fbsB , and  rgf  genes combination. Non polar  rgfAC  deletion mutants of three CC17 serotype III strains were constructed. They showed a 3.2- to 5.1-fold increase of  fbsA  transcripts, a 4.8- to 6.7-fold decrease of  fbsB  transcripts, and a 52% to 68% decreased fibrinogen-binding ability, demonstrating that the RgfA/RgfC TCS inhibits the  fbsA  gene and activates the  fbsB  gene. The relative contribution of the two  fbs  genes in fibrinogen-binding ability was determined by constructing isogenic  fbsA ,  fbsB , deletion mutants of the three CC17 strains. The ability to bind to fibrinogen was reduced by 49% to 57% in  ΔfbsA  mutants, and by 78% to 80% in  ΔfbsB  mutants, suggesting that FbsB protein plays a greater role in the fibrinogen-binding ability of CC17 strains. Moreover, the relative transcription level of  fbsB  gene was 9.2- to 12.7-fold higher than that of  fbsA  gene for the three wild type strains. Fibrinogen-binding ability could be restored by plasmid-mediated expression of  rgfAC ,  fbsA , and  fbsB  genes in the corresponding deletion mutants. Thus, our results demonstrate that a specific combination of  fbs  genes and  fbs  regulator genes account for the high fibrinogen-binding ability of CC17 strains that may participate to their enhanced invasiveness for neonates as compared to strains of other CCs.

Two-Component System RgfA/C Activates the fbsB Gene Encoding Major Fibrinogen-Binding Protein in Highly Virulent CC17 Clone Group B Streptococcus