Genomic plasticity of the causative agent of melioidosis, <i>Burkholderia pseudomallei</i>

Matthew T. G. Holden(Wellcome Sanger Institute), Richard W. Titball(Defence Science and Technology Laboratory), Sharon J. Peacock(Wellcome Sanger Institute), Ana Cerdeño-Tárraga(Wellcome Sanger Institute), Timothy P. Atkins(Wellcome Sanger Institute), Lisa Crossman(Wellcome Sanger Institute), Tyrone L. Pitt(Wellcome Sanger Institute), Carol Churcher(Wellcome Sanger Institute), Karen Mungall(Wellcome Sanger Institute), Stephen D. Bentley(Wellcome Sanger Institute), Mohammed Sebaihia(Wellcome Sanger Institute), Nicholas R. Thomson(Wellcome Sanger Institute), Nathalie Bason(Wellcome Sanger Institute), Ifor R. Beacham(Wellcome Sanger Institute), Karen Brooks(Wellcome Sanger Institute), Katherine A. Brown(Wellcome Sanger Institute), Nat F. Brown(Wellcome Sanger Institute), Gregory L. Challis(Wellcome Sanger Institute), Inna Cherevach(Wellcome Sanger Institute), T. Chillingworth(Wellcome Sanger Institute), Ann Cronin(Wellcome Sanger Institute), Ben Crossett(Wellcome Sanger Institute), Paul A. Davis(Wellcome Sanger Institute), David DeShazer(Wellcome Sanger Institute), Theresa Feltwell(Wellcome Sanger Institute), Audrey Fraser(Wellcome Sanger Institute), Zahra Hance(Wellcome Sanger Institute), Heidi Hauser(Wellcome Sanger Institute), S. Holroyd(Wellcome Sanger Institute), Kay Jagels(Wellcome Sanger Institute), Karen E. Keith(Wellcome Sanger Institute), Mark Maddison(Wellcome Sanger Institute), Sharon Moule(Wellcome Sanger Institute), Claire Price(Wellcome Sanger Institute), Michael A. Quail(Wellcome Sanger Institute), Ester Rabbinowitsch(Wellcome Sanger Institute), Kim Rutherford(Wellcome Sanger Institute), Mandy Sanders(Wellcome Sanger Institute), Mark Simmonds(Wellcome Sanger Institute), Sirirurg Songsivilai(Wellcome Sanger Institute), Kim Stevens(Wellcome Sanger Institute), Sarinna Tumapa(Wellcome Sanger Institute), Monkgol Vesaratchavest(Wellcome Sanger Institute), Sally Whitehead(Wellcome Sanger Institute), Corin Yeats(Wellcome Sanger Institute), Bart Barrell(Wellcome Sanger Institute), Petra C. F. Oyston(Wellcome Sanger Institute), Julian Parkhill(Wellcome Sanger Institute)
Proceedings of the National Academy of Sciences
September 17, 2004
Cited by 778Open Access
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Abstract

Burkholderia pseudomallei is a recognized biothreat agent and the causative agent of melioidosis. This Gram-negative bacterium exists as a soil saprophyte in melioidosis-endemic areas of the world and accounts for 20% of community-acquired septicaemias in northeastern Thailand where half of those affected die. Here we report the complete genome of B. pseudomallei, which is composed of two chromosomes of 4.07 megabase pairs and 3.17 megabase pairs, showing significant functional partitioning of genes between them. The large chromosome encodes many of the core functions associated with central metabolism and cell growth, whereas the small chromosome carries more accessory functions associated with adaptation and survival in different niches. Genomic comparisons with closely and more distantly related bacteria revealed a greater level of gene order conservation and a greater number of orthologous genes on the large chromosome, suggesting that the two replicons have distinct evolutionary origins. A striking feature of the genome was the presence of 16 genomic islands (GIs) that together made up 6.1% of the genome. Further analysis revealed these islands to be variably present in a collection of invasive and soil isolates but entirely absent from the clonally related organism B. mallei. We propose that variable horizontal gene acquisition by B. pseudomallei is an important feature of recent genetic evolution and that this has resulted in a genetically diverse pathogenic species.


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