| Literature DB >> 12910271 |
Julian Parkhill1, Mohammed Sebaihia, Andrew Preston, Lee D Murphy, Nicholas Thomson, David E Harris, Matthew T G Holden, Carol M Churcher, Stephen D Bentley, Karen L Mungall, Ana M Cerdeño-Tárraga, Louise Temple, Keith James, Barbara Harris, Michael A Quail, Mark Achtman, Rebecca Atkin, Steven Baker, David Basham, Nathalie Bason, Inna Cherevach, Tracey Chillingworth, Matthew Collins, Anne Cronin, Paul Davis, Jonathan Doggett, Theresa Feltwell, Arlette Goble, Nancy Hamlin, Heidi Hauser, Simon Holroyd, Kay Jagels, Sampsa Leather, Sharon Moule, Halina Norberczak, Susan O'Neil, Doug Ormond, Claire Price, Ester Rabbinowitsch, Simon Rutter, Mandy Sanders, David Saunders, Katherine Seeger, Sarah Sharp, Mark Simmonds, Jason Skelton, Robert Squares, Steven Squares, Kim Stevens, Louise Unwin, Sally Whitehead, Bart G Barrell, Duncan J Maskell.
Abstract
Bordetella pertussis, Bordetella parapertussis and Bordetella bronchiseptica are closely related Gram-negative beta-proteobacteria that colonize the respiratory tracts of mammals. B. pertussis is a strict human pathogen of recent evolutionary origin and is the primary etiologic agent of whooping cough. B. parapertussis can also cause whooping cough, and B. bronchiseptica causes chronic respiratory infections in a wide range of animals. We sequenced the genomes of B. bronchiseptica RB50 (5,338,400 bp; 5,007 predicted genes), B. parapertussis 12822 (4,773,551 bp; 4,404 genes) and B. pertussis Tohama I (4,086,186 bp; 3,816 genes). Our analysis indicates that B. parapertussis and B. pertussis are independent derivatives of B. bronchiseptica-like ancestors. During the evolution of these two host-restricted species there was large-scale gene loss and inactivation; host adaptation seems to be a consequence of loss, not gain, of function, and differences in virulence may be related to loss of regulatory or control functions.Entities:
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Year: 2003 PMID： 12910271 DOI： 10.1038/ng1227
Source DB: PubMed Journal: Nat Genet ISSN： 1061-4036 Impact factor: 38.330