PMID: 9442495Jan 1, 1997Paper

Massive reduction in methicillin resistance by transposon inactivation of the normal PBP2 in a methicillin-resistant strain of Staphylococcus aureus

Microbial Drug Resistance : MDR : Mechanisms, Epidemiology, and Disease
Mariana G PinhoH de Lencastre

Abstract

Screening of a large transposon library constructed in the background of a highly and homogeneously methicillin-resistant Staphylococcus aureus (MRSA) strain (methicillin MIC 1,600 micrograms/ml) for Tn551 mutants with reduced resistance, identified mutant RUSA130 with a methicillin MIC of 12 micrograms/ml. Cloning in E. coli followed by sequencing located the Tn551 insert omega 703 near the C-terminal of the PBP2 gene. Penicillin-binding assays with mutant RUSA130 showed the presence of normal amounts of penicillin-binding protein 2A (PBP2A) but the absence of PBP2. These observations suggest that the mecA gene product PBP2A is not the sole catalyst of peptidoglycan synthesis in MRSA growing in the presence of beta-lactam antibiotics, since an intact PBP2 is also essential for the optimal expression of methicillin resistance in MRSA.

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Citations

Sep 19, 2003·International Journal of Antimicrobial Agents·Malthe M KristiansenLeonard Amaral
Aug 23, 2001·Proceedings of the National Academy of Sciences of the United States of America·M G PinhoA Tomasz
Sep 10, 2003·Microbial Drug Resistance : MDR : Mechanisms, Epidemiology, and Disease·R G SobralA Tomasz
Mar 6, 2004·Microbial Drug Resistance : MDR : Mechanisms, Epidemiology, and Disease·Yuki KatayamaHenry F Chambers
May 20, 1999·Microbial Drug Resistance : MDR : Mechanisms, Epidemiology, and Disease·S W Wu, H De Lencastre
Sep 29, 2006·Antimicrobial Agents and Chemotherapy·S GardeteA Tomasz
Jul 5, 2005·Expert Opinion on Investigational Drugs·H LabischinskiB Wieland
Jun 4, 2015·Annual Review of Biochemistry·Sharon J Peacock, Gavin K Paterson
Oct 9, 2001·Nature Medicine·J V Höltje
Jun 6, 1998·Journal of Bacteriology·A Wada, H Watanabe
Oct 26, 1999·Biochemical and Biophysical Research Communications·H MurakamiT Ohta

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