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PMID: 12910271 Published · ppublish English Comparative Study Journal Article Research Support, Non-U.S. Gov't

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

Nature genetics ·Vol. 35 ·No. 1 ·2003-09-00 ·Pages 32-40

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

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.

MeSH Terms
Base Sequence Bordetella/genetics,metabolism,pathogenicity Bordetella bronchiseptica/genetics,metabolism,pathogenicity Bordetella pertussis/genetics,metabolism,pathogenicity DNA, Bacterial Genome, Bacterial Molecular Sequence Data Sequence Analysis, DNA Species Specificity
Chemicals
DNA, Bacterial
Authors & Affiliations
53 authors, click to expand affiliations / ORCID
Parkhill Julian
The Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK. [email protected]
Sebaihia Mohammed
Preston Andrew
Murphy Lee D
Thomson Nicholas
Harris David E
Holden Matthew T G
Churcher Carol M
Bentley Stephen D
Mungall Karen L
Cerdeño-Tárraga Ana M
Temple Louise
James Keith
Harris Barbara
Quail Michael A
Achtman Mark
Atkin Rebecca
Baker Steven
Basham David
Bason Nathalie
Cherevach Inna
Chillingworth Tracey
Collins Matthew
Cronin Anne
Davis Paul
Doggett Jonathan
Feltwell Theresa
Goble Arlette
Hamlin Nancy
Hauser Heidi
Holroyd Simon
Jagels Kay
Leather Sampsa
Moule Sharon
Norberczak Halina
O'Neil Susan
Ormond Doug
Price Claire
Rabbinowitsch Ester
Rutter Simon
Sanders Mandy
Saunders David
Seeger Katherine
Sharp Sarah
Simmonds Mark
Skelton Jason
Squares Robert
Squares Steven
Stevens Kim
Unwin Louise
Whitehead Sally
Barrell Bart G
Maskell Duncan J
Article Info
Journal
Nature genetics
Abbr.
Nat Genet
ISSN
1061-4036
Published
2003-09-00
Epub
2003-00-10
Pages
32-40
Language
English
Region
United States
NLM ID
9216904
Subset
IM
Databases
GENBANK
BX470248, BX470249, BX470250
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