JB Accepts, published online ahead of print on 6 November 2009

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J. Bacteriol. doi:10.1128/JB.01144-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The Citrobacter rodentium genome sequence reveals convergent evolution with human pathogenic Escherichia coli

Nicola K. Petty, Richard Bulgin, Valerie F. Crepin, Ana M. Cerdeño-Tárraga, Gunnar N. Schroeder, Michael A. Quail, Nicola Lennard, Craig Corton, Andrew Barron, Louise Clark, Ana L. Toribio, Julian Parkhill, Gordon Dougan, Gad Frankel, and Nicholas R. Thomson^*

Pathogen Genomics, The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK; Centre for Molecular Microbiology and Infection, Division of Cell and Molecular Biology, Imperial College London, London SW7 2AZ, UK

^* To whom correspondence should be addressed. Email: nrt{at}sanger.ac.uk.

Citrobacter rodentium (formally C. freundii Biotype 4280) is a highly infectious pathogen that causes colitis and transmissible colonic hyperplasia in mice. In common with enteropathogenic and enterhemorrhagic Escherichia coli (EPEC and EHEC respectively), C. rodentium exploits a type III secretion system (T3SS) to induce attaching and effacing (A/E) lesions that are essential for virulence. Here we report the fully annotated genome sequence of the 5.3 Mb chromosome and four plasmids harboured by C. rodentium strain ICC168. The genome sequence revealed key information about the phylogeny of C. rodentium and identified 1585 C. rodentium-specific (without orthologues in EPEC or EHEC) coding sequences, 10 prophage-like regions and 17 genomic islands, including the LEE region, which encodes a T3SS and effector proteins. Among the 29 T3SS effectors found in C. rodentium are all the core 22 effectors of EPEC strain E2348/69. In addition, we identified a novel C. rodentium effector, named EspS. C. rodentium harbours two type VI secretion systems (T6SS) (CTS1 and CTS2), while EHEC contains only one T6SS (EHS). Our analysis suggests that C. rodentium and EPEC/EHEC have converged on a common host infection strategy through access to a common pool of mobile DNA, and that C. rodentium has lost gene functions associated with a previous pathogenic niche.