title: Inactivation of mrcA gene derepresses the basal-level expression of L1 and L2 β-lactamases in Stenotrophomonas maltophilia.
abstract: OBJECTIVE
  To characterize the relationship between inactivation of the mrcA gene and β-lactamase expression and β-lactams resistance in Stenotrophomonas maltophilia KJ and to investigate the involvement of ampR, ampN-ampG, ampD(I) and creBC in this.
  
  
  METHODS
  The mrcA deletion mutant KJΔmrcA was constructed to investigate the role of this putative penicillin-binding protein 1a (PBP1a) in β-lactamase expression and β-lactam resistance. The ΔampR, ΔampNG, ΔampDI and ΔcreBC alleles were introduced into KJΔmrcA, and KJΔDIΔBC and KJΔDIΔmrcAΔBC were also constructed for comparison. All the mutants and their corresponding parent strains were assayed for β-lactamase activities and MICs of β-lactams.
  
  
  RESULTS
  Inactivation of mrcA caused basal L1/L2 β-lactamase production to increase by ∼100-fold, but made little difference to cefuroxime-induced β-lactamase activity and the MICs of β-lactams. The ΔmrcA-derived basal β-lactamase hyperproduction was ampR and ampN-ampG dependent. Simultaneous inactivation of ampD(I) and mrcA did not augment β-lactamase production over and above that seen in an ampD(I) mutant alone. Furthermore, we could find no evidence for a role of the creBC two-component regulatory system in β-lactamase hyperproduction in a ΔampD(I) or ΔmrcA background.
  
  
  CONCLUSIONS
  Inactivation of mrcA, predicted to encode PBP1a, causes basal L1/L2 β-lactamase hyperproduction in S. maltophilia.
authors: Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung 404, Taiwan.
authors: Cheng-Wen
authors: CW
authors: Lin
authors: Hsin-Chieh
authors: HC
authors: Lin
authors: Yi-Wei
authors: YW
authors: Huang
authors: Tung-Ching
authors: TC
authors: Chung
authors: Tsuey-Ching
authors: TC
authors: Yang
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology; D017931:DNA Primers; D004790:Enzyme Induction / Q000187:drug effects / Q000235:genetics; D004926:Escherichia coli / Q000235:genetics / Q000378:metabolism; D005798:Genes, Bacterial / Q000235:genetics*; D007769:Lactams / Q000494:pharmacology; D008826:Microbial Sensitivity Tests; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics; D010957:Plasmids / Q000235:genetics; D018085:Regulon; D020615:Stenotrophomonas maltophilia / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism*; D001618:beta-Lactamases / Q000096:biosynthesis* / Q000235:genetics*
chemical_list: D000900:Anti-Bacterial Agents; D017931:DNA Primers; D007769:Lactams; C088032:beta-lactamase L1; C425104:beta-lactamase L2; D001618:beta-Lactamases