A molecular mechanism for how sigma factor AlgT and transcriptional regulator AmrZ inhibit twitching motility inPseudomonas aeruginosa

Pseudomonas aeruginosaisolates from cystic fibrosis patients are often mucoid (due to the overexpression of exopolysaccharide alginate) yet lost motility. It remains unclear about howP. aeruginosacoordinately regulates alginate production and the type IV pili-driven twitching motility. Here we showed that sigma 22 factor (AlgT/U), an activator of alginate biosynthesis, repressed twitching motility by inhibiting the expression of pilin (PilA) through the intermediate transcriptional regulator AmrZ, which directly bound to the promoter region ofpilAin both mucoid strain FRD1 and non-mucoid strain PAO1. Four conserved AmrZ-binding sites were found inpilApromoters among 10P. aeruginosastrains although their entirepilApromoters had low identity. AmrZ has been reported to be essential for twitching in PAO1. We found that AmrZ was also required for twitching in mucoid FRD1, yet a high level of AmrZ inhibited twitching motility. This result was consistent with the phenomenon that twitching is frequently repressed in mucoid strains, in which the expression of AmrZ was highly activated by AlgT. Additionally, AlgT also inhibited the transcription ofpilMNOPoperon, which is involved in efficient pilus assembly. Our data elucidated a mechanism for how AlgT and AmrZ coordinately controlled twitching motility inP. aeruginosa.

Automated summary

Pseudomonas aeruginosa isolates from cystic fibrosis patients are often mucoid and lose motility. The study revealed the coordinated regulation of alginate production and twitching motility by AlgT and AmrZ in P. aeruginosa.