Comparison of Francisella tularensis genomes reveals evolutionary events associated with the emergence of human pathogenic strains |
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Authors: | Laurence Rohmer Christine Fong Simone Abmayr Michael Wasnick Theodore J Larson Freeman Matthew Radey Tina Guina Kerstin Svensson Hillary S Hayden Michael Jacobs Larry A Gallagher Colin Manoil Robert K Ernst Becky Drees Danielle Buckley Eric Haugen Donald Bovee Yang Zhou Jean Chang Ruth Levy Regina Lim Will Gillett Don Guenthener Allison Kang Scott A Shaffer Greg Taylor Jinzhi Chen Byron Gallis David A D'Argenio Mats Forsman Maynard V Olson David R Goodlett Rajinder Kaul Samuel I Miller Mitchell J Brittnacher |
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Affiliation: | Department of Genome Sciences, University of Washington, Campus Box 357710, 1705 NE Pacific street Seattle, Washington 98195, USA. lrohmer@u.washington.edu |
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Abstract: |
Background Francisella tularensis subspecies tularensis and holarctica are pathogenic to humans, whereas the two other subspecies, novicida and mediasiatica, rarely cause disease. To uncover the factors that allow subspecies tularensis and holarctica to be pathogenic to humans, we compared their genome sequences with the genome sequence of Francisella tularensis subspecies novicida U112, which is nonpathogenic to humans. Results Comparison of the genomes of human pathogenic Francisella strains with the genome of U112 identifies genes specific to the human pathogenic strains and reveals pseudogenes that previously were unidentified. In addition, this analysis provides a coarse chronology of the evolutionary events that took place during the emergence of the human pathogenic strains. Genomic rearrangements at the level of insertion sequences (IS elements), point mutations, and small indels took place in the human pathogenic strains during and after differentiation from the nonpathogenic strain, resulting in gene inactivation. Conclusion The chronology of events suggests a substantial role for genetic drift in the formation of pseudogenes in Francisella genomes. Mutations that occurred early in the evolution, however, might have been fixed in the population either because of evolutionary bottlenecks or because they were pathoadaptive (beneficial in the context of infection). Because the structure of Francisella genomes is similar to that of the genomes of other emerging or highly pathogenic bacteria, this evolutionary scenario may be shared by pathogens from other species. |
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