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Journal of Bacteriology, September 2008, p. 5797-5805, Vol. 190, No. 17
0021-9193/08/$08.00+0     doi:10.1128/JB.00468-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Evolution of the Rhodococcus equi vap Pathogenicity Island Seen through Comparison of Host-Associated vapA and vapB Virulence Plasmids{triangledown} ,{dagger}

Michal Letek,1,2,3,{ddagger} Alain A. Ocampo-Sosa,2,3,{ddagger} Mandy Sanders,4 Ursula Fogarty,3 Tom Buckley,3 Desmond P. Leadon,3 Patricia González,1,3 Mariela Scortti,1,2,5 Wim G. Meijer,6 Julian Parkhill,4 Stephen Bentley,4 and José A. Vázquez-Boland1,2,5*

Division of Microbial Pathogenesis, Centre for Infectious Diseases, Ashworth Laboratories, King's Buildings, University of Edinburgh, Edinburgh EH9 3JT, United Kingdom,1 Bacterial Molecular Pathogenesis Group, Faculty of Medical and Veterinary Sciences, University of Bristol, Bristol, United Kingdom,2 Irish Equine Centre, Johnstown, Naas, Ireland,3 Pathogen Genomics, Wellcome Trust Sanger Institute, Genome Campus, Hinxton, United Kingdom,4 Grupo de Patogenómica Bacteriana, Instituto de Biología Molecular y Genómica, Universidad de León, León, Spain,5 School of Biomolecular and Biomedical Science, University College Dublin, Dublin, Ireland6

Received 6 April 2008/ Accepted 18 June 2008

The pathogenic actinomycete Rhodococcus equi harbors different types of virulence plasmids associated with specific nonhuman hosts. We determined the complete DNA sequence of a vapB+ plasmid, typically associated with pig isolates, and compared it with that of the horse-specific vapA+ plasmid type. pVAPB1593, a circular 79,251-bp element, had the same housekeeping backbone as the vapA+ plasmid but differed over an {approx}22-kb region. This variable region encompassed the vap pathogenicity island (PAI), was clearly subject to selective pressures different from those affecting the backbone, and showed major genetic rearrangements involving the vap genes. The pVAPB1593 PAI harbored five different vap genes (vapB and vapJ to -M, with vapK present in two copies), which encoded products differing by 24 to 84% in amino acid sequence from the six full-length vapA+ plasmid-encoded Vap proteins, consistent with a role for the specific vap gene complement in R. equi host tropism. Sequence analyses, including interpolated variable-order motifs for detection of alien DNA and reconstruction of Vap family phylogenetic relationships, suggested that the vap PAI was acquired by an ancestor plasmid via lateral gene transfer, subsequently evolving by vap gene duplication and sequence diversification to give different (host-adapted) plasmids. The R. equi virulence plasmids belong to a new family of actinobacterial circular replicons characterized by an ancient conjugative backbone and a horizontally acquired niche-adaptive plasticity region.

* Corresponding author. Mailing address: Division of Microbial Pathogenesis, Centre for Infectious Diseases, Ashworth Laboratories, King's Buildings, University of Edinburgh, Edinburgh EH9 3JT, United Kingdom. Phone: 44 (0)131 651 3619. Fax: 44 (0)131 650 6564. E-mail: v.boland{at}ed.ac.uk

{triangledown} Published ahead of print on 7 July 2008.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} These authors are alphabetically arranged and contributed equally to the work.

Journal of Bacteriology, September 2008, p. 5797-5805, Vol. 190, No. 17
0021-9193/08/$08.00+0     doi:10.1128/JB.00468-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.





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