No abstract

Surfactin is a signal to trigger biofilm formation against harsh environments. Generally, harsh environments can result in change of the cellular redox state to induce biofilm formation, but we know little about whether the cellular redox state influences biofilm formation via surfactin. Here, the reductant glucose could reduce surfactin and enhance biofilm formation by a surfactin-independent way. The oxidant H2O2 led to a decrease of surfactin accompanying with weakened biofilm formation. Spx and PerR were both necessary for surfactin production and biofilm formation. H2O2 improved surfactin production but inhibited biofilm formation by a surfactin-independent manner in Δspx, while it reduced surfactin production without obvious influence on biofilm formation in ΔperR. The ability against H2O2 stress was enhanced in Δspx, but weakened in ΔperR. Thereby, PerR was favorable for resisting oxidative stress, while Spx played a negative role in this action. Knockout and compensation of rex also supported that the cells could form biofilm by a surfactin-independent way. Collectively, surfactin is not a unique signal to trigger biofilm formation, and the cellular redox state can influence biofilm formation by a surfactin- dependent or independent way in B. amyloliquefaciens.

Surfactin is a signal to trigger biofilm formation against harsh environments. Generally, harsh environments can result in change of the cellular redox state to induce biofilm formation, but we know little about whether the cellular redox state influences biofilm formation via surfactin. Here, the reductant glucose could reduce surfactin and enhance biofilm formation by a surfactin‐indirect way. The oxidant H2O2 led to a decrease of surfactin accompanying with weakened biofilm formation. Spx and PerR were both necessary for surfactin production and biofilm formation. H2O2 improved surfactin production but inhibited biofilm formation by a surfactin‐indirect manner in Δspx, while it reduced surfactin production without obvious influence on biofilm formation in ΔperR. The ability against H2O2 stress was enhanced in Δspx, but weakened in ΔperR. Thereby, PerR was favorable for resisting oxidative stress, while Spx played a negative role in this action. Knockout and compensation of rex also supported that the cells could form biofilm by a surfactin‐indirect way. Collectively, surfactin is not a unique signal to trigger biofilm formation, and the cellular redox state can influence biofilm formation by a surfactin‐direct or ‐indirect way in Bacillus amyloliquefaciens WH1.