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Comparative analysis of the genome sequences of Bordetella pertussis, Bordetella parapertussis and Bordetella bronchiseptica. 2003
Julian Parkhill, and
Mohammed Sebaihia, and
Andrew Preston, and
Lee D Murphy, and
Nicholas Thomson, and
David E Harris, and
Matthew T G Holden, and
Carol M Churcher, and
Stephen D Bentley, and
Karen L Mungall, and
Ana M Cerdeño-Tárraga, and
Louise Temple, and
Keith James, and
Barbara Harris, and
Michael A Quail, and
Mark Achtman, and
Rebecca Atkin, and
Steven Baker, and
David Basham, and
Nathalie Bason, and
Inna Cherevach, and
Tracey Chillingworth, and
Matthew Collins, and
Anne Cronin, and
Paul Davis, and
Jonathan Doggett, and
Theresa Feltwell, and
Arlette Goble, and
Nancy Hamlin, and
Heidi Hauser, and
Simon Holroyd, and
Kay Jagels, and
Sampsa Leather, and
Sharon Moule, and
Halina Norberczak, and
Susan O'Neil, and
Doug Ormond, and
Claire Price, and
Ester Rabbinowitsch, and
Simon Rutter, and
Mandy Sanders, and
David Saunders, and
Katherine Seeger, and
Sarah Sharp, and
Mark Simmonds, and
Jason Skelton, and
Robert Squares, and
Steven Squares, and
Kim Stevens, and
Louise Unwin, and
Sally Whitehead, and
Bart G Barrell, and
Duncan J Maskell
The Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK. parkhill@sanger.ac.uk
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.
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