Parkhill Julian, 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
The Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, CB10 1SA, UK.
Nat Genet. 2003 Sep;35(1):32-40. doi: 10.1038/ng1227. Epub 2003 Aug 10.
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.
百日咳博德特氏菌、副百日咳博德特氏菌和支气管败血博德特氏菌是密切相关的革兰氏阴性β-变形菌,它们定殖于哺乳动物的呼吸道。百日咳博德特氏菌是一种近期进化起源的严格人类病原体,是百日咳的主要病因。副百日咳博德特氏菌也可引起百日咳,而支气管败血博德特氏菌可在多种动物中引起慢性呼吸道感染。我们对支气管败血博德特氏菌RB50(5,338,400 bp;5,007个预测基因)、副百日咳博德特氏菌12822(4,773,551 bp;4,404个基因)和百日咳博德特氏菌Tohama I(4,086,186 bp;3,816个基因)的基因组进行了测序。我们的分析表明,副百日咳博德特氏菌和百日咳博德特氏菌是支气管败血博德特氏菌样祖先的独立衍生物。在这两个宿主限制性物种的进化过程中,发生了大规模的基因丢失和失活;宿主适应性似乎是功能丧失而非获得的结果,毒力差异可能与调控或控制功能的丧失有关。