Two Frameshift Products Involved in the Transposition of Bacterial Insertion Sequence IS629

Chen, Chang-Chieh; Hu, Shiau-Ting

doi:10.1074/jbc.m602437200

Cited by 10 publications

(16 citation statements)

References 39 publications

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“…ISPmi1 shares a common genetic organization with members of the IS51 group, in which a potential tetrameric frameshift motif is accompanied by an elaborate frameshift stimulator, the apical loopinternal loop pseudoknot. Conserved structural elements similar to those in IS3411 and IS629 have been demonstrated experimentally to be involved in the control of gene expression by translational frameshifting, and the OrfAB transposase is indeed synthesized via PRF-1 on the predicted motif (5,16).…”

Section: Discussionmentioning

confidence: 99%

“…OrfAB was a fusion protein with an identity of 58% to IS51 (M14365), which has transposase activity produced by the Ϫ1 programmed ribosomal frameshift (PRF-1) (4). A predicted Ϫ1 translational frameshift signal (TTTTG) associated with an apical loop-internal loop pseudoknot was deduced near the 3Ј end of orfA and the 5Ј end of orfB, suggesting the existence of frameshifted products that could be responsible for transposition of this new IS element (5,16).…”

Section: Cloning Of Qnrcmentioning

confidence: 99%

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New Plasmid-Mediated Quinolone Resistance Gene, qnrC , Found in a Clinical Isolate of Proteus mirabilis

Wang

Guo

et al. 2009

Antimicrob Agents Chemother

296

158

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Since the discovery of qnrA in 1998, two additional qnr genes, qnrB and qnrS, have been described. These three plasmid-mediated genes contribute to quinolone resistance in gram-negative pathogens worldwide. A clinical strain of Proteus mirabilis was isolated from an outpatient with a urinary tract infection and was susceptible to most antimicrobials but resistant to ampicillin, sulfamethoxazole, and trimethoprim. Plasmid pHS10, harbored by this strain, was transferred to azide-resistant Escherichia coli J53 by conjugation. A transconjugant with pHS10 had low-level quinolone resistance but was negative by PCR for the known qnr genes, aac(6)-Ib-cr and qepA. The ciprofloxacin MIC for the clinical strain and a J53/pHS10 transconjugant was 0.25 g/ml, representing an increase of 32-fold relative to that for the recipient, J53. The plasmid was digested with HindIII, and a 4.4-kb DNA fragment containing the new gene was cloned into pUC18 and transformed into E. coli TOP10. Sequencing showed that the responsible 666-bp gene, designated qnrC, encoded a 221-amino-acid protein, QnrC, which shared 64%, 42%, 59%, and 43% amino acid identity with QnrA1, QnrB1, QnrS1, and QnrD, respectively. Upstream of qnrC there existed a new IS3 family insertion sequence, ISPmi1, which encoded a frameshifted transposase. qnrC could not be detected by PCR, however, in 2,020 strains of Enterobacteriaceae. A new quinolone resistance gene, qnrC, was thus characterized from plasmid pHS10 carried by a clinical isolate of P. mirabilis.Plasmid-mediated quinolone resistance was first described for a ciprofloxacin-resistant strain of Klebsiella pneumoniae in 1998 (15). The responsible gene, qnr (later named qnrA), was located on plasmid pMG252, which encodes multidrug resistance proteins. qnrB and qnrS were discovered in 2005 and 2006, respectively, and mediated similar levels of ciprofloxacin resistance (9, 11). Qnr proteins belong to the pentapeptide repeat protein (PRP) family and protect DNA gyrase and topoisomerase IV from quinolone inhibition (26,27,28). qnr genes show a high level of diversity; there are at least 6 qnrA, 20 qnrB, and 3 qnrS alleles reported, with one or more amino acid alterations within each family (12; http://www.lahey.org /qnrStudies). More recently, qnrD was found in Salmonella isolates (3). qnr genes are widely distributed in clinical Enterobacteriaceae isolates around the world and are usually associated with mobile elements (21). There were also qnr-like genes found on the chromosomes of Vibrio vulnificus, Vibrio parahaemolyticus, Photobacterium profundum, Stenotrophomonas maltophilia, and gram-positive genera such as Enterococcus, Listeria, Clostridium, and Bacillus (1,17,22,24). The wide distribution of qnr genes in different species of Enterobacteriaceae and their high degree of diversity raise the concern that there might be more qnr genes that have not yet been discovered. In this study, a new plasmid-mediated quinolone resistance gene, qnrC, was found on and cloned from a transferable plasmid, pHS10, in a clinical ...

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Section: Discussionmentioning

confidence: 99%

Section: Cloning Of Qnrcmentioning

confidence: 99%

New Plasmid-Mediated Quinolone Resistance Gene, qnrC , Found in a Clinical Isolate of Proteus mirabilis

Wang

Guo

et al. 2009

Antimicrob Agents Chemother

296

158

View full text Add to dashboard Cite

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“…When IS629's OrfB overexpresses, its transposase (OrfAB), which is obtained by a Ϫ1 frameshift signal, is repressed. As a consequence, the expected transposition is inhibited (43). Genomes having a high copy number of IS629 will also overexpress OrfB, and IS629 transposition will be reduced or inhibited.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous Presence of Insertion Sequence Excision Enhancer and Insertion Sequence IS 629 Correlates with Increased Diversity and Virulence in Shiga Toxin-Producing Escherichia coli

et al. 2015

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cAlthough new serotypes of enterohemorrhagic Escherichia coli (EHEC) emerge constantly, the mechanisms by which these new pathogens arise and the reasons emerging serotypes tend to carry more virulence genes than other E. coli are not understood. An insertion sequence (IS) excision enhancer (IEE) was discovered in EHEC O157:H7 that promoted the excision of IS3 family members and generating various genomic deletions. One IS3 family member, IS629, actively transposes and proliferates in EHEC O157:H7 and enterotoxigenic E. coli (ETEC) O139 and O149. The simultaneous presence of the IEE and IS629 (and other IS3 family members) may be part of a system promoting not only adaptation and genome diversification in E. coli O157:H7 but also contributing to the development of pathogenicity among predominant serotypes. Prevalence comparisons of these elements in 461 strains, representing 72 different serotypes and 5 preassigned seropathotypes (SPT) A to E, showed that the presence of these two elements simultaneously was serotype specific and associated with highly pathogenic serotypes (O157 and top non-O157 Shiga toxin-producing Escherichia coli [STEC]) implicated in outbreaks and sporadic cases of human illness (SPT A and B). Serotypes lacking one or both elements were less likely to have been isolated from clinical cases. Our comparisons of IEE sequences showed sequence variations that could be divided into at least three clusters. Interestingly, the IEE sequences from O157 and the top 10 non-O157 STEC serotypes fell into clusters I and II, while less commonly isolated serotypes O5 and O174 fell into cluster III. These results suggest that IS629 and IEE elements may be acting synergistically to promote genome plasticity and genetic diversity among STEC strains, enhancing their abilities to adapt to hostile environments and rapidly take up virulence factors. Shiga toxin-producing Escherichia coli (STEC) strains are important food pathogens responsible for serious human disease worldwide (1-3). Although new STEC serotypes constantly emerge (4), the mechanisms by which these strains acquire virulence are not entirely understood. Elements such as phages, pathogenicity islands (PAIs), and plasmids can introduce new virulence genes (such as those for producing Shiga toxin) that contribute to the pathogenic potential of strains, but the existence of horizontal transfer is not sufficient to explain the subsequent evolution of these strains or why some strains carry more virulence genes than others.Karmali et al. (5) classified STEC into seropathotypes (SPT) from A to E in descending order of virulence. Serotypes that are frequently linked to outbreaks and severe disease, for example, hemolytic-uremic syndrome (HUS), are classified as SPT A. Serotypes in SPT B are also associated with outbreaks and severe disease, but these associations occur less frequently in SPT B serotypes than those in SPT A serotypes. Serotypes associated with sporadic cases of HUS, but not known to be responsible for outbreaks, are classified as SPT C, and ...

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“…X51586, also identified as IS1203v) is a 1.31 kb, non-replicative IS featuring a pair of inverted repeat sequences and two ORFs (orfA and orfB) that overlap by a single base pair (Matsutani & Ohtsubo, 1990). It belongs to the IS3 family whose transposition activity is regulated by frame shifts and a cis-acting regulator (Chen & Hu, 2006;Kusumoto et al, 2011). IS629 is the most prevalent IS in the E. coli O157 : H7 genome, while being rare in E. coli O55:H7, the proposed ancestor of E. coli O157 : H7 (Rump et al, 2011a).…”

Section: Introductionmentioning

confidence: 99%

Phylogenetic characterization of Escherichia coli O157 : H7 based on IS629 distribution and Shiga toxin genotype

et al. 2014

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Shiga toxin (stx)-producing Escherichia coli O157 : H7 is a prominent food-borne pathogen. Symptoms in human infections range from asymptomatic to haemorrhagic colitis and haemolytic uraemic syndrome, and there is a need for methods that yield information that can be used to better predict clinical and epidemiological outcomes. IS629 is an insertion sequence notable for its prevalence and variable distribution in the chromosome of E. coli O157 : H7, which has been exploited for subtyping and strain characterization. In particular, IS629 distribution is closely aligned with the major phylogenetic lineages that are known to be distinctive in their genome structure and virulence potential. In the present study, a comprehensive subtyping method in which IS629-typing was combined with stx genotyping was developed using a conventional PCR approach. This method consisted of a set of 32 markers based on the unique distribution of IS629 in the three major phylogenetic lineages of E. coli O157 : H7 and six additional markers to determine the stx genotype, a key virulence signature associated with each lineage. The analysis of IS629 loci variation with the 32 markers allowed us to determine the IS629 distribution profile (IDP), phylogenetic lineage and genetic relatedness of the 31 E. coli O157 : H7 strains examined. An association between IDP typing and stx genotype was observed. The use of both IDP and the stx genotype for strain characterization provided confirmative and complementary data in support of lineage placement of closely related strains. In addition, IS629/stx profiles were in agreement with strain segregation based on LSPA-6 (lineage-specific polymorphism assay) and PFGE subtyping, demonstrating its potential as a subtyping and strain tracking method.

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Two Frameshift Products Involved in the Transposition of Bacterial Insertion Sequence IS629

Cited by 10 publications

References 39 publications

New Plasmid-Mediated Quinolone Resistance Gene, qnrC , Found in a Clinical Isolate of Proteus mirabilis

New Plasmid-Mediated Quinolone Resistance Gene, qnrC , Found in a Clinical Isolate of Proteus mirabilis

Simultaneous Presence of Insertion Sequence Excision Enhancer and Insertion Sequence IS 629 Correlates with Increased Diversity and Virulence in Shiga Toxin-Producing Escherichia coli

Phylogenetic characterization of Escherichia coli O157 : H7 based on IS629 distribution and Shiga toxin genotype

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