Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence

S. T. Cole (), R. Brosch, J. Parkhill, T. Garnier, C. Churcher, D. Harris, S. V. Gordon, K. Eiglmeier, S. Gas, C. E. Barry, F. Tekaia, K. Badcock, D. Basham, D. Brown, T. Chillingworth, R. Connor, R. Davies, K. Devlin, T. Feltwell, S. Gentles, N. Hamlin, S. Holroyd, T. Hornsby, K. Jagels, A. Krogh, J. McLean, S. Moule, L. Murphy, K. Oliver, J. Osborne, M. A. Quail, M.-A. Rajandream, J. Rogers, S. Rutter, K. Seeger, J. Skelton, R. Squares, S. Squares, J. E. Sulston, K. Taylor, S. Whitehead and B. G. Barrell ()
Additional contact information
S. T. Cole: Unité de Génétique Moléculaire Bactérienne
R. Brosch: Unité de Génétique Moléculaire Bactérienne
J. Parkhill: Sanger Centre, Wellcome Trust Genome Campus
T. Garnier: Unité de Génétique Moléculaire Bactérienne
C. Churcher: Sanger Centre, Wellcome Trust Genome Campus
D. Harris: Sanger Centre, Wellcome Trust Genome Campus
S. V. Gordon: Unité de Génétique Moléculaire Bactérienne
K. Eiglmeier: Unité de Génétique Moléculaire Bactérienne
S. Gas: Unité de Génétique Moléculaire Bactérienne
C. E. Barry: Tuberculosis Research Unit, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health
F. Tekaia: Unité de Génétique Moléculaire des Levures
K. Badcock: Sanger Centre, Wellcome Trust Genome Campus
D. Basham: Sanger Centre, Wellcome Trust Genome Campus
D. Brown: Sanger Centre, Wellcome Trust Genome Campus
T. Chillingworth: Sanger Centre, Wellcome Trust Genome Campus
R. Connor: Sanger Centre, Wellcome Trust Genome Campus
R. Davies: Sanger Centre, Wellcome Trust Genome Campus
K. Devlin: Sanger Centre, Wellcome Trust Genome Campus
T. Feltwell: Sanger Centre, Wellcome Trust Genome Campus
S. Gentles: Sanger Centre, Wellcome Trust Genome Campus
N. Hamlin: Sanger Centre, Wellcome Trust Genome Campus
S. Holroyd: Sanger Centre, Wellcome Trust Genome Campus
T. Hornsby: Sanger Centre, Wellcome Trust Genome Campus
K. Jagels: Sanger Centre, Wellcome Trust Genome Campus
A. Krogh: Center for Biological Sequence Analysis, Technical University of Denmark
J. McLean: Sanger Centre, Wellcome Trust Genome Campus
S. Moule: Sanger Centre, Wellcome Trust Genome Campus
L. Murphy: Sanger Centre, Wellcome Trust Genome Campus
K. Oliver: Sanger Centre, Wellcome Trust Genome Campus
J. Osborne: Sanger Centre, Wellcome Trust Genome Campus
M. A. Quail: Sanger Centre, Wellcome Trust Genome Campus
M.-A. Rajandream: Sanger Centre, Wellcome Trust Genome Campus
J. Rogers: Sanger Centre, Wellcome Trust Genome Campus
S. Rutter: Sanger Centre, Wellcome Trust Genome Campus
K. Seeger: Sanger Centre, Wellcome Trust Genome Campus
J. Skelton: Sanger Centre, Wellcome Trust Genome Campus
R. Squares: Sanger Centre, Wellcome Trust Genome Campus
S. Squares: Sanger Centre, Wellcome Trust Genome Campus
J. E. Sulston: Sanger Centre, Wellcome Trust Genome Campus
K. Taylor: Sanger Centre, Wellcome Trust Genome Campus
S. Whitehead: Sanger Centre, Wellcome Trust Genome Campus
B. G. Barrell: Sanger Centre, Wellcome Trust Genome Campus

Nature, 1998, vol. 393, issue 6685, 537-544

Abstract: Abstract Countless millions of people have died from tuberculosis, a chronic infectious disease caused by the tubercle bacillus. The complete genome sequence of the best-characterized strain of Mycobacterium tuberculosis, H37Rv, has been determined and analysed in order to improve our understanding of the biology of this slow-growing pathogen and to help the conception of new prophylactic and therapeutic interventions. The genome comprises 4,411,529 base pairs, contains around 4,000 genes, and has a very high guanine + cytosine content that is reflected in the biased amino-acid content of the proteins. M. tuberculosis differs radically from other bacteria in that a very large portion of its coding capacity is devoted to the production of enzymes involved in lipogenesis and lipolysis, and to two new families of glycine-rich proteins with a repetitive structure that may represent a source of antigenic variation.

Date: 1998
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DOI: 10.1038/31159

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