Please use this identifier to cite or link to this item:
標題: Inactivation of mrcA gene derepresses the basal-level expression of L1 and L2 beta-lactamases in Stenotrophomonas maltophilia
作者: Lin, C.W.
Lin, H.C.
Huang, Y.W.
Chung, T.C.
Yang, T.C.
關鍵字: S. maltophilia;penicillin-binding proteins;PBPs;penicillin-binding proteins;escherichia-coli;induction;resistance;ampc
Project: Journal of Antimicrobial Chemotherapy
期刊/報告no:: Journal of Antimicrobial Chemotherapy, Volume 66, Issue 9, Page(s) 2033-2037.
Objectives: To characterize the relationship between inactivation of the mrcA gene and beta-lactamase expression and beta-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 KJ Delta mrcA was constructed to investigate the role of this putative penicillin-binding protein 1a (PBP1a) in beta-lactamase expression and beta-lactam resistance. The Delta ampR, Delta ampNG, Delta ampDI and Delta creBC alleles were introduced into KJ Delta mrcA, and KJ Delta DI Delta BC and KJ Delta DI Delta mrcA Delta BC were also constructed for comparison. All the mutants and their corresponding parent strains were assayed for beta-lactamase activities and MICs of beta-lactams. Results: Inactivation of mrcA caused basal L1/L2 beta-lactamase production to increase by similar to 100-fold, but made little difference to cefuroxime-induced beta-lactamase activity and the MICs of beta-lactams. The Delta mrcA-derived basal beta-lactamase hyperproduction was ampR and ampN-ampG dependent. Simultaneous inactivation of ampD(I) and mrcA did not augment beta-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 beta-lactamase hyperproduction in a Delta ampD(I) or Delta mrcA background. Conclusions: Inactivation of mrcA, predicted to encode PBP1a, causes basal L1/L2 beta-lactamase hyperproduction in S. maltophilia.
ISSN: 0305-7453
DOI: 10.1093/jac/dkr276
Appears in Collections:期刊論文

Show full item record

Google ScholarTM




Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.