Comparison of Francisella tularensis genomes reveals evolutionary events associated with the emergence of human pathogenic strains View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-06-05

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

ABSTRACT

BackgroundFrancisella 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.ResultsComparison 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.ConclusionThe 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. More... »

PAGES

r102

Journal

TITLE

Genome Biology

ISSUE

6

VOLUME

8

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/gb-2007-8-6-r102

DOI

http://dx.doi.org/10.1186/gb-2007-8-6-r102

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1032674768

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17550600


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