Genetic Structure and Distribution of Four Pathogenicity Islands (PAI I536 to PAI IV536) of Uropathogenic Escherichia coli Strain 536

Institut für Molekulare Infektionsbiologie, Universität Würzburg, D-97070 Würzburg, Germany.
Infection and Immunity (Impact Factor: 4.16). 12/2002; 70(11):6365-72. DOI: 10.1128/IAI.70.11.6365-6372.2002
Source: PubMed

ABSTRACT For the uropathogenic Escherichia coli strain 536 (O6:K15:H31), the DNA sequences of three pathogenicity islands (PAIs) (PAI I(536) to PAI III(536)) and their flanking regions (about 270 kb) were determined to further characterize the virulence potential of this strain. PAI I(536) to PAI III(536) exhibit features typical of PAIs, such as (i) association with tRNA-encoding genes; (ii) G+C content differing from that of the host genome; (iii) flanking repeat structures; (iv) a mosaic-like structure comprising a multitude of functional, truncated, and nonfunctional putative open reading frames (ORFs) with known or unknown functions; and (v) the presence of many fragments of mobile genetic elements. PAI I(536) to PAI III(536) range between 68 and 102 kb in size. Although these islands contain several ORFs and known virulence determinants described for PAIs of other extraintestinal pathogenic E. coli (ExPEC) isolates, they also consist of as-yet-unidentified ORFs encoding putative virulence factors. The genetic structure of PAI IV(536), which represents the core element of the so-called high-pathogenicity island encoding a siderophore system initially identified in pathogenic yersiniae, was further characterized by sample sequencing. For the first time, multiple PAI sequences (PAI I(536) to PAI IV(536)) in uropathogenic E. coli were studied and their presence in several wild-type E. coli isolates was extensively investigated. The results obtained suggest that these PAIs or at least large fragments thereof are detectable in other pathogenic E. coli isolates. These results support our view that the acquisition of large DNA regions, such as PAIs, by horizontal gene transfer is an important factor for the evolution of bacterial pathogens.

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Available from: Ulrich Dobrindt, Apr 10, 2014
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    • "This should not disfavor integration events and indeed we find that the frequency of transposases in this region is not significantly different from the rest of the genome (P = 0.77, 2 test). Furthermore, NS regions integrate some well-known pathogenicity islands encoding tyrosine recombinases (Napolitano et al. 2011), for example, PAI-LEE, PAI-I CFT073 , and PAI-III EDL933 (Blum et al. 1994; McDaniel et al. 1995; Dobrindt et al. 2002). Core genes in these regions have sequence compositions similar to the rest of the genome (51% in GC content, P = 0.2, Wilcoxon test) suggesting this is not the cause of a putative integration bias. "
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    Molecular Biology and Evolution 12/2012; 30(4). DOI:10.1093/molbev/mss279 · 14.31 Impact Factor
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    • "Strains CFT073, 536 and UTI89 all contain an island encoding S fimbriae, salmochelin and Ag43 (PAI-CFT073-serX, PAI III UTI89 , PAI III 536 ), but integrated at different chromosomal locations--near serX in CFT073 and UTI89 and near thrW in 536. The Yersinia High Pathogenicity Island (HPI), encoding yersiniabactin, is integrated near the asnT gene in all three sequenced UPEC genomes (HPI CFT073 , PAI IV 536 , PAI IV UTI89 ), but is defective in CFT073 due to mutation [31] [248] [373] [377] [378] [379]. In addition to defining known PAIs, genomics has been used to identify novel regions involved in uropathogenesis. "
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    • "virulence while PAI II and III are implicated both in uro - virulence and in blood stream infections . This might be because PAIs II and III con - tain both blood - interacting elements ( hemolysin , hemagglutinin , hemoglobin protease ) and adhesion proteins the role of which is determinant in uro - epithelial adhesion ( Marre and Hacker , 1987 ; Dobrindt et al . , 2002a ; Wiles et al . , 2008 ) . Deletion of E . coli 536 PAI V has been shown to result in a decreased uropathogenicity ( Schneider et al . , 2004 ) . However , PAI V deletion mutants showed normal resistance to serum ( Schneider et al . , 2004 ) . Consistently , in our model 5 showed the same sep - ticemia lethality as WT eng ."
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