Comparative analysis of the genome sequences of Bordetella pertussis, Bordetella parapertussis and Bordetella bronchiseptica

J Parkhill*, M Sebaihia, A Preston, LD Murphy, N Thomson, DE Harris, MTG Holden, CM Churcher, SD Bentley, KL Mungall, AM Cerdeno-Tarraga, L Temple, K James, B Harris, MA Quail, M Achtman, R Atkin, S Baker, D Basham, N BasonI Cherevach, T Chillingworth, M Collins, A Cronin, P Davis, J Doggett, T Feltwell, A Goble, N Hamlin, H Hauser, S Holroyd, K Jagels, S Leather, S Moule, H Norberczak, S O'Neil, D Ormond, C Price, E Rabbinowitsch, S Rutter, M Sanders, D Saunders, K Seeger, S Sharp, M Simmonds, J Skelton, R Squares, S Squares, K Stevens, L Unwin, S Whitehead, BG Barrell, DJ Maskell

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

794 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)32-40
Number of pages9
JournalNature Genetics
Volume35
Issue number1
DOIs
Publication statusPublished - Sept 2003

Keywords

  • RESPIRATORY EPITHELIAL-CELLS
  • FIMBRIAL SUBUNIT GENE
  • III SECRETION
  • FILAMENTOUS HEMAGGLUTININ
  • ESCHERICHIA-COLI
  • VIRULENCE
  • TOXIN
  • POLYSACCHARIDES
  • PATHOGENICITY
  • PATHOGENESIS

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