Figure 1

Model for the HtpB/HsbRAD, GacS/GacA/Rsm and CrsRA/RpoS signaling network. (A) Unphosphorylated form of HsbR triggers HsbA phosphorylation through its kinase/Anti-σ factor domain (A/KS). Once phosphorylated HsbA binds HsbD diguanylate cyclase and triggers c-di-GMP production which is rsmY inducer²⁷. RsmY production induces biofilm formation by sequestering/inhibiting RsmA. Phosphorylated form of HsbR triggers HsbA dephosphorylation through its phosphatase domain (PP2C). Once dephosphorylated HsbA binds FlgM anti-σ factor and trigger swimming motility thought FliA σ-factor²⁵. HsbA dephosphorylation shutdown biofilm formation by inhibiting HsbD c-di-GMP production. Dashed lines suggest a probable indirect regulation. (B) Phosphorylation of CsrA by the CsrR kinase/Anti-σ factor domain (A/KS) leads to dissociation of the CsrA-CsrR complex and a subsequent stable sequestration of RpoS sigma factor by CsrR. Dephosphorylation of CsrA by the CsrR phosphatase domain (PP2C) leads to formation of the CsrA-CsrR complex and a release of the RpoS sigma factor.