Parallel independent evolution of pathogenicity within the genus Yersinia.

Sandra Reuter; Thomas R Connor; Lars Barquist; Danielle Walker; Theresa Feltwell; Simon R Harris; Maria Fookes; Miquette E Hall; Nicola K Petty; Thilo M Fuchs; +23 more... Jukka Corander; Muriel Dufour; Tamara Ringwood; Cyril Savin; Christiane Bouchier; Liliane Martin; Minna Miettinen; Mikhail Shubin; Julia M Riehm; Riikka Laukkanen-Ninios; Leila M Sihvonen; Anja Siitonen; Mikael Skurnik; Juliana Pfrimer Falcão; Hiroshi Fukushima; Holger C Scholz; Michael B Prentice; Brendan W Wren ORCID logo; Julian Parkhill; Elisabeth Carniel; Mark Achtman; Alan McNally; Nicholas R Thomson ORCID logo; (2014) Parallel independent evolution of pathogenicity within the genus Yersinia. Proceedings of the National Academy of Sciences of the United States of America, 111 (18). pp. 6768-6773. ISSN 0027-8424 DOI: 10.1073/pnas.1317161111
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The genus Yersinia has been used as a model system to study pathogen evolution. Using whole-genome sequencing of all Yersinia species, we delineate the gene complement of the whole genus and define patterns of virulence evolution. Multiple distinct ecological specializations appear to have split pathogenic strains from environmental, nonpathogenic lineages. This split demonstrates that contrary to hypotheses that all pathogenic Yersinia species share a recent common pathogenic ancestor, they have evolved independently but followed parallel evolutionary paths in acquiring the same virulence determinants as well as becoming progressively more limited metabolically. Shared virulence determinants are limited to the virulence plasmid pYV and the attachment invasion locus ail. These acquisitions, together with genomic variations in metabolic pathways, have resulted in the parallel emergence of related pathogens displaying an increasingly specialized lifestyle with a spectrum of virulence potential, an emerging theme in the evolution of other important human pathogens.

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