Nature Genetics
37, 153 - 159 (2005)
Published online: 9 January 2005; | doi:10.1038/ng1499
The complete genome sequence of Francisella tularensis, the causative agent of tularemiaPär Larsson1, Petra C F Oyston2, Patrick Chain3, May C Chu4, Melanie Duffield2, Hans-Henrik Fuxelius5, Emilio Garcia3, Greger Hälltorp5, Daniel Johansson1, Karen E Isherwood2, Peter D Karp6, Eva Larsson1, Ying Liu7, Stephen Michell2, Joann Prior2, Richard Prior2, Stephanie Malfatti3, Anders Sjöstedt8, Kerstin Svensson1, Nick Thompson9, Lisa Vergez3, Jonathan K Wagg6, Brendan W Wren10, Luther E Lindler7, Siv G E Andersson5, Mats Forsman1
& Richard W Titball2, 101
Swedish Defence Research Agency, SE-901 82 Umeå, Sweden. 2
Defence Science and Technology Laboratory, Salisbury SP4 0JQ, UK. 3
Biology and Biotechnology Research Program, Lawrence Livermore National Laboratory, California 94550, USA. 4
Division of Vector-Borne Infectious Diseases, Centers for Disease Control and Prevention, Fort Collins, Colorado, USA. 5
Department of Molecular Evolution, University of Uppsala, S-752 36 Uppsala, Sweden. 6
Bioinformatics Research Group, SRI International, Menlo Park, California 94025, USA. 7
Walter Reed Army Institute of Research, Silver Spring, Maryland 20910, USA. 8
Department of Clinical Microbiology, Umeå University, SE-901 85 Umeå, Sweden. 9
Welcome Trust Sanger Institute, Cambridge CB10 1SA, UK. 10
Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London WC1E 7HT, UK.
Correspondence should be addressed to Richard W Titball rtitball@dstl.gov.uk
Francisella tularensis is one of the most infectious human pathogens known. In the past, both the former Soviet Union and the US had programs to develop weapons containing the bacterium. We report the complete genome sequence of a highly virulent isolate of F. tularensis (1,892,819 bp). The sequence uncovers previously uncharacterized genes encoding type IV pili, a surface polysaccharide and iron-acquisition systems. Several virulence-associated genes were located in a putative pathogenicity island, which was duplicated in the genome. More than 10% of the putative coding sequences contained insertion-deletion or substitution mutations and seemed to be deteriorating. The genome is rich in IS elements, including IS630 Tc-1 mariner family transposons, which are not expected in a prokaryote. We used a computational method for predicting metabolic pathways and found an unexpectedly high proportion of disrupted pathways, explaining the fastidious nutritional requirements of the bacterium. The loss of biosynthetic pathways indicates that F. tularensis is an obligate host-dependent bacterium in its natural life cycle. Our results have implications for our understanding of how highly virulent human pathogens evolve and will expedite strategies to combat them.
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