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Nucleic Acids Research, 2003, Vol. 31, No. 16 4856-4863
© 2003 Oxford University Press

The sequence and analysis of Trypanosoma brucei chromosome II

Najib M. A. El-Sayed*,1,2, Elodie Ghedin1,2, Jinming Song1, Annette MacLeod3, Frederic Bringaud4, Christopher Larkin1, David Wanless1, Jeremy Peterson1, Lihua Hou1, Sonya Taylor5, Alison Tweedie3, Nicolas Biteau4, Hanif G. Khalak1, Xiaoying Lin1, Tanya Mason1, Linda Hannick1, Elisabet Caler1, Gaëlle Blandin1, Daniella Bartholomeu1, Anjana J. Simpson1, Samir Kaul1, Hong Zhao1, Grace Pai1, Susan Van Aken1, Teresa Utterback1, Brian Haas1, Hean L. Koo1, Lowell Umayam1, Bernard Suh1, Caroline Gerrard6, Vanessa Leech6, Rong Qi7, Shiguo Zhou7, David Schwartz7, Tamara Feldblyum1, Steven Salzberg1, Andrew Tait3, C. Michael R. Turner5, Elisabetta Ullu8, Owen White1, Sara Melville6, Mark D. Adams1, Claire M. Fraser1,2 and John E. Donelson9

1 The Institute for Genomic Research, Rockville, MD 20850, USA, 2 Department of Microbiology and Tropical Medicine, George Washington University, Washington, DC 20052, USA, 3 Wellcome Centre for Molecular Parasitology, University of Glasgow, Glasgow, G11 6NU, UK, 4 Laboratoire de Parasitologie Moléculaire, Université Victor Segalen Bordeaux II, UMR5016-CNRS, 33076 Bordeaux, France, 5 Division of Infection and Immunity, Institute of Biological and Life Science, University of Glasgow, Glasgow, G12 8QQ, UK, 6 Department of Pathology, University of Cambridge, Cambridge, CB2 1QP, UK, 7 Departments of Genetics and Chemistry, University of Wisconsin, Madison, WI 53706, USA, 8 Departments of Medicine and Cell Biology, Yale University, New Haven, CT 06520, USA and 9 Department of Biochemistry, University of Iowa, Iowa City, IA 52242, USA

*To whom correspondence should be addressed at: The Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA. Tel: +1 301 838 0200; Fax: +1 301 838 0208; Email: nelsayed{at}tigr.org
Present addresses:
Jinming Song, Aventis Pharmaceuticals, Bridgewater, NJ 08807, USA
Xiaoying Lin, Rong Qi and Mark D. Adams, Celera Genomics, Rockville, MD 20850, USA
+AC007864–AC007866, AC007862, AC073246, AC079606, AC012647, AC008031, AC008368, AC009463, AE017150

We report here the sequence of chromosome II from Trypanosoma brucei, the causative agent of African sleeping sickness. The 1.2-Mb pairs encode about 470 predicted genes organised in 17 directional clusters on either strand, the largest cluster of which has 92 genes lined up over a 284-kb region. An analysis of the GC skew reveals strand compositional asymmetries that coincide with the distribution of protein-coding genes, suggesting these asymmetries may be the result of transcription-coupled repair on coding versus non-coding strand. A 5-cM genetic map of the chromosome reveals recombinational ‘hot’ and ‘cold’ regions, the latter of which is predicted to include the putative centromere. One end of the chromosome consists of a 250-kb region almost exclusively composed of RHS (pseudo)genes that belong to a newly characterised multigene family containing a hot spot of insertion for retroelements. Interspersed with the RHS genes are a few copies of truncated RNA polymerase pseudogenes as well as expression site associated (pseudo)genes (ESAGs) 3 and 4, and 76 bp repeats. These features are reminiscent of a vestigial variant surface glycoprotein (VSG) gene expression site. The other end of the chromosome contains a 30-kb array of VSG genes, the majority of which are pseudogenes, suggesting that this region may be a site for modular de novo construction of VSG gene diversity during transposition/gene conversion events.


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