Dissemination of pheU- and pheV-located genomic islands among enteropathogenic (EPEC) and enterohemorrhagic (EHEC) E. coli and their possible role in the horizontal transfer of the locus of enterocyte effacement (LEE)

Rumer, Leonid; Jores, Joerg; Kirsch, Petra; Cavignac, Yolaine; Zehmke, Karen; Wieler, Lothar H.

doi:10.1078/1438-4221-00229

Cited by 27 publications

(29 citation statements)

References 31 publications

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“…Due to the different insertion sites in certain E. coli strains of different serotypes, it was assumed that the LEE was possibly taken up several times from an unknown origin during evolution (6,58,60). However, the unexpected high level of identity (on average, 99.5% identity at the DNA level) between the LEE core regions of B6 (O26:K60) and 9812 (O128:H2) that are integrated in different tRNA loci clearly points to LEE transfer between different strains which had also been suggested previously (e.g., references 28, 31, 50, 60, and 65).…”

Section: Discussionmentioning

confidence: 99%

Comparative Analysis of the Locus of Enterocyte Effacement and Its Flanking Regions

Müller¹,

Benz²,

Liebchen³

et al. 2009

Infect Immun

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The attaching-and-effacing (A/E) phenotype mediated by factors derived from the locus of enterocyte effacement (LEE) is a hallmark of clinically important intestinal pathotypes of Escherichia coli, including enteropathogenic (EPEC), atypical EPEC (ATEC), and enterohemorrhagic E. coli strains. Epidemiological studies indicate that the frequency of diarrhea outbreaks caused by ATEC is increasing. Hence, it is of major importance to further characterize putative factors contributing to the pathogenicity of these strains and to gain additional insight into the plasticity and evolutionary aspects of this emerging pathotype. Here, we analyzed the two clinical ATEC isolates B6 (O26:K60) and 9812 (O128:H2) and compared the genetic organizations, flanking regions, and chromosomal insertion loci of their LEE with those of the LEE of other A/E pathogens. Our analysis shows that the core LEE is largely conserved-particularly among genes coding for the type 3 secretion system-whereas genes encoding effector proteins display a higher variability. Chromosomal insertion loci appear to be restricted to selC, pheU, and pheV. In contrast, striking differences were found between the 5-and 3-associated flanking regions reflecting the different histories of the various strains and also possibly indicating different lines in evolution.

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Section: Discussionmentioning

confidence: 99%

Comparative Analysis of the Locus of Enterocyte Effacement and Its Flanking Regions

Müller¹,

Benz²,

Liebchen³

et al. 2009

Infect Immun

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“…The genomes of the Shiga toxin-producing E. coli (STEC) strains Sakai, EDL933, and EC4115 carry a large deletion encompassing pheV and the adjacent kps capsular and gsp type II secretion loci. However, the pheV tRNA gene is included in a nonsyntenic locus and is known to be a hot spot for insertion of the locus for enterocyte effacement (LEE) (50,51). The afa-8 locus on a pheV genomic island has been described previously (52), although the associated int gene is like intP4-2, not intP4-1, and the VR50 afa locus is quite divergent from afa-8 (see below).…”

Section: Phenotypic Characteristics Of E Coli Vr50 E Coli Vr50 (Ormentioning

confidence: 99%

Molecular Analysis of Asymptomatic Bacteriuria Escherichia coli Strain VR50 Reveals Adaptation to the Urinary Tract by Gene Acquisition

et al. 2015

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e Urinary tract infections (UTIs) are among the most common infectious diseases of humans, with Escherichia coli responsible for >80% of all cases. One extreme of UTI is asymptomatic bacteriuria (ABU), which occurs as an asymptomatic carrier state that resembles commensalism. To understand the evolution and molecular mechanisms that underpin ABU, the genome of the ABU E. coli strain VR50 was sequenced. Analysis of the complete genome indicated that it most resembles E. coli K-12, with the addition of a 94-kb genomic island (GI-VR50-pheV), eight prophages, and multiple plasmids. GI-VR50-pheV has a mosaic structure and contains genes encoding a number of UTI-associated virulence factors, namely, Afa (afimbrial adhesin), two autotransporter proteins (Ag43 and Sat), and aerobactin. We demonstrated that the presence of this island in VR50 confers its ability to colonize the murine bladder, as a VR50 mutant with GI-VR50-pheV deleted was attenuated in a mouse model of UTI in vivo. We established that Afa is the island-encoded factor responsible for this phenotype using two independent deletion (Afa operon and AfaE adhesin) mutants. E. coli VR50afa and VR50afaE displayed significantly decreased ability to adhere to human bladder epithelial cells. In the mouse model of UTI, VR50afa and VR50afaE displayed reduced bladder colonization compared to wild-type VR50, similar to the colonization level of the GI-VR50-pheV mutant. Our study suggests that E. coli VR50 is a commensal-like strain that has acquired fitness factors that facilitate colonization of the human bladder. U rinary tract infections (UTIs) are among the most common infectious diseases of humans and a major cause of morbidity. It is estimated that 40 to 50% of all adult women experience at least one UTI episode in their lifetime (1). In addition to welldocumented symptomatic infections, many UTIs are asymptomatic. These infections, referred to as asymptomatic bacteriuria (ABU), represent a carrier state that resembles commensalism and occur in a percentage of the population, depending on age and gender. ABU patients may carry Ͼ10 5 CFU of a single bacterial strain/ml of urine for months or years without significant symptoms.Escherichia coli causes more than 80% of all symptomatic and asymptomatic UTIs. In general, strains that cause symptomatic UTI are collectively described as uropathogenic E. coli (UPEC), while strains that cause asymptomatic UTI are referred to as ABU E. coli. Both UPEC and ABU E. coli strains exhibit a high degree of genetic diversity that is largely attributed to the presence of virulence/fitness genes on mobile genetic elements referred to as pathogenicity islands (PAIs) or genomic islands (GIs) (2, 3). While no single virulence factor is uniquely definitive for UPEC or ABU E. coli, the ability to colonize the urinary tract is enhanced by a number of factors, including fimbriae (e.g., type 1, P, F1C, and Afa), autotransporter proteins (e.g., Ag43, UpaB, and UpaH), cell surface polysaccharides (e.g., O antigen), and siderophores (e.g., ente...

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“…The region unique to APEC-O1 is 1.5 kb in size and contains one ORF coding for a protein of 511 amino acids. Interestingly, the complete pap operon (papI to papG) that encodes the P pilus (4,29), the ireA gene that encodes a siderophore receptor protein of extraintestinal E. coli (23), and the tia invasion determinant gene of enterotoxigenic E. coli (ETEC) (8) reside on PAI I APEC-O1 . The genes involved in the phosphoglycerate transport system (pgtA to pgtP) (25) are also found on this 56-kb DNA stretch.…”

mentioning

confidence: 99%

“…Two such examples are the ireA and tia genes. The ireA gene was first reported in an extraintestinal E. coli isolate that causes sepsis in humans (23). The protein encoded by ireA, the putative siderophore receptor IreA, is involved in iron acquisition and is believed to be a urovirulence factor (23).…”

mentioning

confidence: 99%

“…The ireA gene was first reported in an extraintestinal E. coli isolate that causes sepsis in humans (23). The protein encoded by ireA, the putative siderophore receptor IreA, is involved in iron acquisition and is believed to be a urovirulence factor (23). On the other hand, the tia gene of ETEC shares significant homology with hraI from porcine ETEC and limited homology with the ail locus from Yersinia spp.…”

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confidence: 99%

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The pap Operon of Avian Pathogenic Escherichia coli Strain O1:K1 Is Located on a Novel Pathogenicity Island

2006

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We have identified a 56-kb pathogenicity island (PAI) in avian pathogenic Escherichia coli strain O1:K1 (APEC-O1). This PAI, termed PAI I APEC-O1 , is integrated adjacent to the 3 end of the pheV tRNA gene. It carries putative virulence genes of APEC (pap operon), other E. coli genes (tia and ireA), and a 1.5-kb region unique to APEC-O1. The kps gene cluster required for the biosynthesis of polysialic acid capsule was mapped to a location immediately downstream of this PAI.

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Dissemination of pheU- and pheV-located genomic islands among enteropathogenic (EPEC) and enterohemorrhagic (EHEC) E. coli and their possible role in the horizontal transfer of the locus of enterocyte effacement (LEE)

Cited by 27 publications

References 31 publications

Comparative Analysis of the Locus of Enterocyte Effacement and Its Flanking Regions

Comparative Analysis of the Locus of Enterocyte Effacement and Its Flanking Regions

Molecular Analysis of Asymptomatic Bacteriuria Escherichia coli Strain VR50 Reveals Adaptation to the Urinary Tract by Gene Acquisition

The pap Operon of Avian Pathogenic Escherichia coli Strain O1:K1 Is Located on a Novel Pathogenicity Island

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