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. 2012 Dec;194(23):6537–6547. doi: 10.1128/JB.01168-12

Fig 8.

Fig 8

Model of KinB's role in the regulation of P. aeruginosa virulence. (A) Acute virulence. Acute virulence factors are expressed while chronic virulence factors are repressed. In this state, AlgU is sequestered by MucA, and AlgB exists predominantly in the dephosphorylated state. On detecting appropriate signals, KinB acts predominantly as a phosphatase to maintain AlgB in the dephosphorylated state. (B) Chronic virulence. Chronic virulence factors are expressed while acute virulence factors are repressed. AlgB exists predominantly in the phosphorylated state. AlgB may be phosphorylated by KinB itself (in WT cells), or AlgB may be phosphorylated by another sensor (sensor 2) or small molecules such as acetyl phosphate. AlgB may activate MucA-degrading proteases such as AlgW. AlgW activation could result in the degradation of MucA and the release of AlgU. Alternatively, phosphorylated AlgB may directly upregulate AlgU expression.