DSF inactivator RpfB homologous FadD upregulated in Bradyrhizobium japonicum under iron limiting conditions

Abstract

AbstractPhytopathogenic bacteriaXanthomonas campestrispv.campestris(Xcc) causes black rot and other plant diseases.Xccsenses diffusible signal factor (DSF) as a quorum-sensing (QS) signal that mediates mainly iron uptake and virulence. RpfB deactivates DSF in this DSF–QS circuit. We examined differential gene expression profiles ofBradyrhizobium japonicumunder low versus high iron conditions and found thatfadDandirrwere upregulated under low iron (log2 fold change 0.825 and 1.716, respectively). In addition to having similar protein folding patterns and functional domain similarities, FadD shared 58% sequence similarity with RpfB ofXcc. The RpfB–DSF and FadD–DSF complexes had SWISSDock molecular docking scores of − 8.88 kcal/mol and − 9.85 kcal/mol, respectively, and the 100 ns molecular dynamics simulation results were in accord with the docking results. However, significant differences were found between the binding energies of FadD–DSF and RpfB–DSF, indicating possible FadD-dependent DSF turnover. The protein–protein interaction network showed that FadD connected indirectly with ABC transporter permease (ABCtp), which was also upregulated (log2 fold change 5.485). We speculate that the low iron condition may be a mimetic environmental stimulus forfadDupregulation inB. japonicumto deactivate DSF, inhibit iron uptake and virulence of DSF-producing neighbors. This finding provides a new option of usingB. japonicumor a genetically improvedB. japonicumas a potential biocontrol agent againstXcc, with the added benefit of plant growth-promoting properties.