Figure 6.

Mechanisms of NO-induced biofilm dispersal via the NosP domain. Possible NosP signaling pathway in Legionella pneumophila (left, based on Fischer et al. 2019). Binding of NO to LpNosP weakens the interaction between LpNosP and LpNahK and diminishes the inhibitory effect of LpNosP on the autophosphorylation of LpNaHK. LpNaHK can thus transfer the phosphoryl group to the downstream bifunctional LpNaCME, which exhibits reduced DGC activity and increased PDE activity, causing a decrease in the cellular c-di-GMP concentrations, and ultimately leading to biofilm dispersal. SoNosP is a master regulator of the multicomponent No/c-di-GMP signaling network in Shewanella oneidensis (right, based on Nisbett et al. 2019). When the bacteria are not exposed to NO, iron-free SoNosP strongly inhibits the autophosphorylation activity of SoNaHK and SoHaHK, thereby preventing downstream components of the phosphate transport chain from being phosphorylated. However, when NO is present, SoNosP attenuates the inhibitory effect on SoHaHK, enabling the transfer of the phosphoryl group to SoHaCME and enhancing the PDE activity of SoHaCME to induce biofilm dispersion. * indicates that the domain is degraded and lacks catalytic activity. The arrows on the c-di-GMP metabolic domains represent an increase or decrease in activities of the corresponding enzymes.