AmpG is required for BlaXc beta-lactamase expression in Xanthomonas campestris pv. campestris str. 17

Abstract The cwhromosomal ampRXc-blaXc module is essential for the β-lactam resistance of Xanthomonas campestris pv. campestris. BlaXc β-lactamase is expressed at a high basal level in the absence of an inducer and its expression can be further induced by β-lactam. In enterobacteria, ampG encodes an inner membrane facilitator involved in the recycling of murein degradation compounds. An isogenic ampG mutant (XcampG) of X. campestris pv. campestris str. 17 (Xc17) was constructed to investigate the link between murein recycling and blaXc expression. Our data demonstrate that (1) XcampG is susceptible to β-lactam antibiotics; (2) AmpGXc is essential for expression of blaXc; (3) AmpGs of Xc17, Stenotrophomonas maltophilia KJ (SmKJ) and Escherichia coli DH5α can complement the defect of XcampG; (4) overexpression of AmpGXc significantly increased blaXc expression; and (5) AmpGXc from Xc17 is able to restore β-lactamase induction of the ampNXc-ampGXc double mutant of SmKJ. In Xc17, ampGXc can be expressed from the promoter residing in the intergenic region of ampNXc-ampGXc and the expression is independent of β-lactam induction. AmpN, which is required for β-lactamases induction in SmKJ, is not required for the β-lactam antibiotic resistance of Xc17.