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. 2011 Aug 25;7(8):e1002204. doi: 10.1371/journal.ppat.1002204

Figure 13. Model of c-di-GMP-mediated control of type 3 fimbriae expression and biofilm formation in K. pneumoniae.

Figure 13

Signals resulting in increased/decreased intracellular concentration of c-di-GMP, via changes in the relative activities of DGCs (carrying a GGDEF domain [YfiN]) and PDEs (carrying an EAL domain [MrkJ]), direct the DNA-binding activity of the c-di-GMP receptor MrkH (carrying a PilZ domain). High c-di-GMP levels promote biofilm formation through MrkH:c-di-GMP-dependent transcriptional activation of the mrkABCDF operon encoding type 3 fimbriae. The major pilin subunit MrkA is bound by the MrkB chaperone in the periplasm to activate it for polymerization by the usher translocase MrkC. Once sufficiently elongated, the fimbriae would emerge through the extracellular capsule layer (represented by grey shading surrounding the cell). Conversely, low c-di-GMP levels promote biofilm dispersal and the planktonic state through a decrease in activated MrkH:c-di-GMP availability. Whether the LuxR-like regulator MrkI acts on mrkABCDF gene expression, or the expression of other factors influencing type 3 fimbriae polymerization or capsule polysaccharide production remains to be determined.