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Antimicrobial Agents and Chemotherapy, March 2004, p. 1028-1031, Vol. 48, No. 3
0066-4804/04/$08.00+0 DOI: 10.1128/AAC.48.3.1028-1031.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
and Ben Adler*
Bacterial Pathogenesis Research Group, Department of Microbiology, Monash University, Victoria 3800, Australia
Received 1 August 2003/ Returned for modification 23 October 2003/ Accepted 5 November 2003
The Shigella resistance locus (SRL) pathogenicity island (PAI) in Shigella spp. mediates resistance to streptomycin, ampicillin, chloramphenicol, and tetracycline. It can be excised from the chromosome via site-specific recombination mediated by the P4-related int gene. Here, we show that SRL PAI attP is capable of RecA-independent, site-specific, int-mediated integration into two bacterial tRNA attB sites.
Present address: Department of Microbiology and Immunology, University of Leicester, Leicester LE1 9HN, United Kingdom.
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