Comparative genomics reveal the mechanism of the parallel evolution of O157 and non-O157 enterohemorrhagic Escherichia coli

Abstract

Among the various pathogenic Escherichia coli strains, enterohemorrhagic E. coli (EHEC) is the most devastating. Although serotype O157:H7 strains are the most prevalent, strains of different serotypes also possess similar pathogenic potential. Here, we present the results of a genomic comparison between EHECs of serotype O157, O26, O111, and O103, as well as 21 other, fully sequenced E. coli/Shigella strains. All EHECs have much larger genomes (5.5-5.9 Mb) than the other strains and contain surprisingly large numbers of prophages and integrative elements (IEs). The gene contents of the 4 EHECs do not follow the phylogenetic relationships of the strains, and they share virulence genes for Shiga toxins and many other factors. We found many lambdoid phages, IEs, and virulence plasmids that carry the same or similar virulence genes but have distinct evolutionary histories, indicating that independent acquisition of these mobile genetic elements has driven the evolution of each EHEC. Particularly interesting is the evolution of the type III secretion system (T3SS). We found that the T3SS of EHECs is composed of genes that were introduced by 3 different types of genetic elements: an IE referred to as the locus of enterocyte effacement, which encodes a central part of the T3SS; SpLE3-like IEs; and lambdoid phages carrying numerous T3SS effector genes and other T3SS-related genes. Our data demonstrate how E. coli strains of different phylogenies can independently evolve into EHECs, providing unique insights into the mechanisms underlying the parallel evolution of complex virulence systems in bacteria.bacteriophage ͉ genome evolution ͉ type III secretion system

Diversity of CRISPR loci in Escherichia coli

“…However, such a similarity cannot be due to a common origin, since Shigella species derive from lineages that are independent of B2 (Fricke et al, 2008;Ogura et al, 2009;Pupo et al, 2000;Turner et al 2006). Moreover, the closely related ECOR strains carry a complete CRISPR2/CAS-E system (our unpublished results) and the deletions in CRISPR2.1/CAS-E are unrelated, entailing distinct genes and sequences (Supplementary Fig.…”

In Vitro and In Vivo Model Systems for Studying Enteropathogenic Escherichia coli Infections

“…Adult volunteers have been used to verify the roles of intimin, EspB, and bundle-forming pili (BFP) in EPEC pathogenesis (Donnenberg et al 1993;Bieber et al 1998;Tacket et al 2000). BFP is an EPEC-specific virulence factor but intimin and EspB are found in the genomes of diverse A/E pathogen species (Tauschek et al 2002;Iguchi et al 2009;Ogura et al 2009;Petty et al 2010). Intimin and EspB are essential for A/E lesion formation in tissue culture (Foubister et al 1994;Abe et al 1997) and intestinal damage in rabbits and mice infected with REPEC (Abe et al 1998;Marchès et al 2000) or C. rodentium, respectively (Schauer and Falkow 1993;Newman et al 1999;Deng et al 2004).…”

“…The seven LEE-encoded type III secreted (T3S) effectors as well as some of the Nle effectors are well conserved across A/E pathogen species, whereas the number and type of other Nle effectors varies significantly (Dean and Kenny 2009). The prototypic EPEC strain E2348/69 encodes 23 effectors Deng et al 2012), whereas certain serotypes of EHEC encode as many as 41 (Tobe et al 2006;Ogura et al 2009). Likewise, there is considerable variation in the numberof effectors found among A/E animal pathogens such as Citrobacter rodentium , which colonizes mice (Luperchio and Schauer 2001).…”

Efa-1/LifA mediates intestinal colonization of calves by enterohaemorrhagic Escherichia coli O26 : H– in a manner independent of glycosyltransferase and cysteine protease motifs or effects on type III secretion

“…3c). The efa-1/lifA gene is encoded immediately downstream of the LEE4 operon in some non-O157 EHEC strains (Ogura et al, 2009), and even where such linkage does not occur, efa-1/lifA is carried by LEE-positive strains at a high frequency. The reasons why efa-1/lifA mutations affect expression and secretion of type III secreted proteins in some EHEC strains but not others require further investigation.…”