Is the IS 1-flanked r-Determinant of the R Plasmid NR1 a Transposon?

Iida, Shigeru; Hänni, Christine; Echarti, C.; Arber, Werner

doi:10.1099/00221287-126-2-413

Cited by 16 publications

(9 citation statements)

References 36 publications

(47 reference statements)

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“…The organization of the YSH6000 SRL deletants suggests that a similar recombination event may have taken place between the two flanking SRL IS1 elements, thus leaving a single copy of an IS1 element on the chromosome. Interestingly, after mobilization to P1, Tn2671 was subsequently mobilized to E. coli recipients and then to the genome of phage P7, demonstrating the existence of a natural mechanism for spread of antibiotic resistance genes (23). This highlights the potential of the SRL to spread to other genomes, independent of mechanisms involving the MRDE or SRL PAI deletions.…”

Section: Discussionmentioning

confidence: 89%

Nested Deletions of the SRL Pathogenicity Island of Shigella flexneri 2a

et al. 2001

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In this study, we determined the boundaries of a 99-kb deletable element of Shigella flexneri 2a strain YSH6000. The element, designated the multiple-antibiotic resistance deletable element (MRDE), had recently been found to contain a 66-kb pathogenicity island (PAI)-like element (designated the SRL PAI) which carries the Shigella resistance locus (SRL), encoding resistance determinants to streptomycin, ampicillin, chloramphenicol, and tetracycline. The YSH6000 MRDE was found to be flanked by two identical IS91 elements present at the S. flexneri homologs of the Escherichia coli genes putA and mdoA on NotI fragment D. Sequence data from two YSH6000-derived MRDE deletants, YSH6000T and S2430, revealed that deletion of the MRDE occurred between the two flanking IS91 elements, resulting in a single IS91 element spanning the two original IS91 loci. Selection for the loss of tetracycline resistance confirmed that the MRDE deletion occurred reproducibly from the same chromosomal site and also showed that the SRL PAI and the SRL itself were capable of independent deletion from the chromosome, thus revealing a unique set of nested deletions. The excision frequency of the SRL PAI was estimated to be 10 ؊5 per cell in the wild type, and mutation of a P4-like integrase gene (int) at the left end of the SRL PAI revealed that int mediates precise deletion of the PAI.

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Section: Discussionmentioning

confidence: 89%

Nested Deletions of the SRL Pathogenicity Island of Shigella flexneri 2a

et al. 2001

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“…This structure illustrates how resistance genes in MRR can have several levels of mobility as the aadA1a gene cassette could move independently (either mediated by IntI1 or by homologous recombination in the CS), as part of In2 (if the necessary Tni proteins are provided), as part of Tn 21 (transposition of the entire transposon or one‐ended transposition, TnpR‐mediated site specific recombination or homologous recombination of segments). The whole of Tn 2670 can also move as a composite transposon (Iida et al ., 1981) or as a circle generated by homologous recombination (Silver et al ., 1980).…”

Section: Examples Of Mrr Structures Evolution and Relationshipsmentioning

confidence: 99%

Analysis of antibiotic resistance regions in Gram-negative bacteria

2011

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Antibiotic resistance in Gram-negative bacteria is often due to the acquisition of resistance genes from a shared pool. In multiresistant isolates these genes, together with associated mobile elements, may be found in complex conglomerations on plasmids or on the chromosome. Analysis of available sequences reveals that these multiresistance regions (MRR) are modular, mosaic structures composed of different combinations of components from a limited set arranged in a limited number of ways. Components common to different MRR provide targets for homologous recombination, allowing these regions to evolve by combinatorial evolution, but our understanding of this process is far from complete. Advances in technology are leading to increasing amounts of sequence data, but currently available automated annotation methods usually focus on identifying ORFs and predicting protein function by homology. In MRR, where the genes are often well characterized, the challenge is to identify precisely which genes are present and to define the boundaries of complete and fragmented mobile elements. This review aims to summarize the types of mobile elements involved in multiresistance in Gram-negative bacteria and their associations with particular resistance genes, to describe common components of MRR and to illustrate methods for detailed analysis of these regions.

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“…The RTF contains genes for conjugative transfer (tra) and replication (rep) functions but also includes the transposon Tn10, which contains the tetA(B) tetracycline resistance determinant (30). The r-det includes the other antibiotic resistance markers of NR1 and a mercury resistance (mer) determinant and is essentially equivalent to the transposon Tn2670, which includes both copies of IS1 (13,16). Tn2670 (Fig.…”

mentioning

confidence: 99%

“…Tn2670 is an active transposon (13,16), and in NR1, it is flanked by a 9-bp target site duplication characteristic of insertion of IS1. However, RecA-dependent homologous recombination between the IS1a and IS1b elements of Tn2670 can form an extrachromosomal, covalently closed circular molecule containing a single copy of IS1 (3,4,29).…”

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confidence: 99%

Complex Multiple Antibiotic and Mercury Resistance Region Derived from the r-det of NR1 (R100)

Partridge

Hall

2004

Antimicrob Agents Chemother

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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 bla TEM-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.

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Is the IS 1-flanked r-Determinant of the R Plasmid NR1 a Transposon?

Cited by 16 publications

References 36 publications

Nested Deletions of the SRL Pathogenicity Island of Shigella flexneri 2a

Nested Deletions of the SRL Pathogenicity Island of Shigella flexneri 2a

Analysis of antibiotic resistance regions in Gram-negative bacteria

Complex Multiple Antibiotic and Mercury Resistance Region Derived from the r-det of NR1 (R100)

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