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Antimicrobial Agents and Chemotherapy, May 2002, p. 1535-1539, Vol. 46, No. 5
0066-4804/02/$04.00+0 DOI: 10.1128/AAC.46.5.1535-1539.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Joel H. Weiner,2 and Susan M. Rosenberg1,3,4*
Departments of Molecular and Human Genetics,1 Biochemistry and Molecular Biology,3 Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas 77030-3411,4 Department of Biochemistry, University of Alberta, Edmonton, Alberta T6G 2H7 Canada2
Received 5 September 2001/ Returned for modification 25 November 2001/ Accepted 9 February 2002
In some enterobacterial pathogens, but not in Escherichia coli, loss-of-function mutations in the ampD gene are a common route to ß-lactam antibiotic resistance. We constructed an assay system for studying mechanism(s) of enterobacterial ampD mutation using the well-developed genetics of E. coli. We integrated the Enterobacter ampRC genes into the E. coli chromosome. These cells acquire spontaneous recombination- and SOS response-independent ß-lactam resistance mutations in ampD. This chromosomal system is useful for studying mutation mechanisms that promote antibiotic resistance.
Present address: Department of Cell Biology, Johns Hopkins School of Medicine, Baltimore, MD 21205.
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