Parallel independent evolution of pathogenicity within the genus Yersinia
Reuter, S
Connor, TR
Barquist, L
Walker, D
Feltwell, T
Harris, SR
Fookes, M
Hall, ME
Petty, NK
Fuchs, TM
Corander, J
Dufour, M
Ringwood, T
Savin, C
Bouchier, C
Martin, L
Miettinen, M
Shubin, M
Riehm, JM
Laukkanen-Ninios, R
Sihvonen, LM
Siitonen, A
Skurnik, M
Falcão, JP
Fukushima, H
Scholz, HC
Prentice, MB
Wren, BW
Parkhill, J
Carniel, E
Achtman, M
McNally, A
Thomson, NR
- Publication Type:
- Journal Article
- Citation:
- Proceedings of the National Academy of Sciences of the United States of America, 2014, 111 (18), pp. 6768 - 6773
- Issue Date:
- 2014-05-06
Closed Access
Filename | Description | Size | |||
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2013002896OK.pdf | 822.17 kB | Adobe PDF |
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Full metadata record
Field | Value | Language |
---|---|---|
dc.contributor.author | Reuter, S | en_US |
dc.contributor.author | Connor, TR | en_US |
dc.contributor.author | Barquist, L | en_US |
dc.contributor.author | Walker, D | en_US |
dc.contributor.author | Feltwell, T | en_US |
dc.contributor.author | Harris, SR | en_US |
dc.contributor.author | Fookes, M | en_US |
dc.contributor.author | Hall, ME | en_US |
dc.contributor.author |
Petty, NK https://orcid.org/0000-0001-6528-9886 |
en_US |
dc.contributor.author | Fuchs, TM | en_US |
dc.contributor.author | Corander, J | en_US |
dc.contributor.author | Dufour, M | en_US |
dc.contributor.author | Ringwood, T | en_US |
dc.contributor.author | Savin, C | en_US |
dc.contributor.author | Bouchier, C | en_US |
dc.contributor.author | Martin, L | en_US |
dc.contributor.author | Miettinen, M | en_US |
dc.contributor.author | Shubin, M | en_US |
dc.contributor.author | Riehm, JM | en_US |
dc.contributor.author | Laukkanen-Ninios, R | en_US |
dc.contributor.author | Sihvonen, LM | en_US |
dc.contributor.author | Siitonen, A | en_US |
dc.contributor.author | Skurnik, M | en_US |
dc.contributor.author | Falcão, JP | en_US |
dc.contributor.author | Fukushima, H | en_US |
dc.contributor.author | Scholz, HC | en_US |
dc.contributor.author | Prentice, MB | en_US |
dc.contributor.author | Wren, BW | en_US |
dc.contributor.author | Parkhill, J | en_US |
dc.contributor.author | Carniel, E | en_US |
dc.contributor.author | Achtman, M | en_US |
dc.contributor.author | McNally, A | en_US |
dc.contributor.author | Thomson, NR | en_US |
dc.date.issued | 2014-05-06 | en_US |
dc.identifier.citation | Proceedings of the National Academy of Sciences of the United States of America, 2014, 111 (18), pp. 6768 - 6773 | en_US |
dc.identifier.issn | 0027-8424 | en_US |
dc.identifier.uri | http://hdl.handle.net/10453/27923 | |
dc.description.abstract | 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. | en_US |
dc.relation.ispartof | Proceedings of the National Academy of Sciences of the United States of America | en_US |
dc.relation.isbasedon | 10.1073/pnas.1317161111 | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Yersinia | en_US |
dc.subject.mesh | Yersinia enterocolitica | en_US |
dc.subject.mesh | Evolution, Molecular | en_US |
dc.subject.mesh | Phylogeny | en_US |
dc.subject.mesh | Virulence | en_US |
dc.subject.mesh | Species Specificity | en_US |
dc.subject.mesh | Genome, Bacterial | en_US |
dc.subject.mesh | Metabolic Networks and Pathways | en_US |
dc.title | Parallel independent evolution of pathogenicity within the genus Yersinia | en_US |
dc.type | Journal Article | |
utslib.citation.volume | 18 | en_US |
utslib.citation.volume | 111 | en_US |
utslib.for | 110316 Pathology (excl. Oral Pathology) | en_US |
pubs.embargo.period | Not known | en_US |
pubs.organisational-group | /University of Technology Sydney | |
pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
pubs.organisational-group | /University of Technology Sydney/Strength - ithree - Institute of Infection, Immunity and Innovation | |
utslib.copyright.status | closed_access | |
pubs.issue | 18 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 111 | en_US |
Abstract:
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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