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Antimicrobial Agents and Chemotherapy, November 2004, p. 4250-4255, Vol. 48, No. 11
0066-4804/04/$08.00+0 DOI: 10.1128/AAC.48.11.4250-4255.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Complex Multiple Antibiotic and Mercury Resistance Region Derived from the r-det of NR1 (R100)
Sally R. Partridge1 and
Ruth M. Hall2*
Department of Biological Sciences, Macquarie University,1
School of Molecular and Microbial Biosciences, The University of Sydney, Sydney, New South Wales, Australia2
Received 17 December 2003/
Returned for modification 17 May 2004/
Accepted 23 July 2004
The sequence of the 45.2-kb multidrug and mercury resistance region of pRMH760, a large plasmid from a clinical isolate of Klebsiella pneumoniae collected in 1997 in Australia, was completed. Most of the modules found in the resistance determinant (r-det), or Tn2670, region of NR1 (also known as R100), isolated from a Shigella flexneri strain in Japan in the late 1950s, were present in pRMH760 but in a different configuration. The location was also different, with the Tn2670-derived region flanked by the transposition module of Tn1696 and a mercury resistance module almost identical to one found in the plasmid pDU1358. This arrangement is consistent with a three-step process. First, the r-det was circularized via homologous recombination between the IS1 elements and reincorporated at a new location, possibly in a different plasmid, via homologous recombination between the 5'-conserved (5'-CS) or 3'-CS of the In34 integron in the r-det and the same region of a second class 1 integron in a Tn1696 relative. Subsequently, resolvase-mediated recombination between the res sites in the r-det and a second mercury resistance transposon removed one end of the Tn1696-like transposon and part of the second transposon. Other events occurring within the r-det-derived portion have also contributed to the formation of the pRMH760 resistance region. Tn2 or a close relative that includes the blaTEM-1b gene had moved into the Tn21 mercury resistance module with subsequent deletion of the adjacent sequence, and all four 38-bp inverted repeats corresponding to Tn21 family transposon termini have been interrupted by an IS4321-like element.
* Corresponding author. Mailing address: School of Molecular and Microbial Biosciences, Biochemistry and Microbiology Building G08, The University of Sydney, Sydney, NSW 2006, Australia. Phone: 61-2-9351 6014. Fax: 61-2-9351 45714. E-mail:
Ruth.Hall{at}mmb.usyd.edu.au.
Antimicrobial Agents and Chemotherapy, November 2004, p. 4250-4255, Vol. 48, No. 11
0066-4804/04/$08.00+0 DOI: 10.1128/AAC.48.11.4250-4255.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
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