(Below N is a link to NCBI taxonomic web page and E link to ESTHER at designed phylum.) > cellular organisms: NE > Bacteria: NE > Proteobacteria: NE > Betaproteobacteria: NE > Burkholderiales: NE > Alcaligenaceae: NE > Bordetella: NE > Bordetella bronchiseptica: NE
Warning: This entry is a compilation of different species or line or strain with more than 90% amino acid identity. You can retrieve all strain data
(Below N is a link to NCBI taxonomic web page and E link to ESTHER at designed phylum.) Bordetella bronchiseptica RB50: N, E.
Bordetella bronchiseptica OSU553: N, E.
Bordetella bronchiseptica 99-R-0433: N, E.
Bordetella bronchiseptica 253: N, E.
LegendThis sequence has been compared to family alignement (MSA) red => minority aminoacid blue => majority aminoacid color intensity => conservation rate title => sequence position(MSA position)aminoacid rate Catalytic site Catalytic site in the MSA MATAIASDGVRLHYETTGAGTPIVFVHEFAGNLRSWEPQVRHFARQYQCI RFNARGYPPSEVPESVSAYSQAQAVRDIVAVMDAVGAAKAHVVGLSMGGF AALHLGLTHPERALSLCVAGAGYGAEPGRRDLFRQESETSARLLLELGMP AFAERYTQGPTRMPFLRADPLGFAEFVALMKTHSALGSANTQLGVQRERP SLYELEEQLGRLTVPTLILNGDEDWPCLAPGLMLKRVIPSAALSVIPNCG HTINLEASEAFNRVLGDFMAQAASGRWPQRDPRAMADTITGMSGGKS
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.