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Science 15 July 2005:
Vol. 309. no. 5733, pp. 404 - 409
DOI: 10.1126/science.1112181
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Research Articles

Comparative Genomics of Trypanosomatid Parasitic Protozoa

Najib M. El-Sayed,1,2*{dagger} Peter J. Myler,3,4,5*{dagger} Gaëlle Blandin,1 Matthew Berriman,6 Jonathan Crabtree,1 Gautam Aggarwal,3 Elisabet Caler,1 Hubert Renauld,6 Elizabeth A. Worthey,3 Christiane Hertz-Fowler,6 Elodie Ghedin,1,2 Christopher Peacock,6 Daniella C. Bartholomeu,1 Brian J. Haas,1 Anh-Nhi Tran,7 Jennifer R. Wortman,1 U. Cecilia M. Alsmark,8 Samuel Angiuoli,1 Atashi Anupama,3 Jonathan Badger,1 Frederic Bringaud,9 Eithon Cadag,3 Jane M. Carlton,1 Gustavo C. Cerqueira,1,10 Todd Creasy,1 Arthur L. Delcher,1 Appolinaire Djikeng,1 T. Martin Embley,8 Christopher Hauser,1 Alasdair C. Ivens,6 Sarah K. Kummerfeld,11 Jose B. Pereira-Leal,11 Daniel Nilsson,7 Jeremy Peterson,1 Steven L. Salzberg,1 Joshua Shallom,1 Joana C. Silva,1 Jaideep Sundaram,1 Scott Westenberger,1{ddagger} Owen White,1 Sara E. Melville,12 John E. Donelson,13 Björn Andersson,7 Kenneth D. Stuart,3,4 Neil Hall6{dagger}§

A comparison of gene content and genome architecture of Trypanosoma brucei, Trypanosoma cruzi, and Leishmania major, three related pathogens with different life cycles and disease pathology, revealed a conserved core proteome of about 6200 genes in large syntenic polycistronic gene clusters. Many species-specific genes, especially large surface antigen families, occur at nonsyntenic chromosome-internal and subtelomeric regions. Retroelements, structural RNAs, and gene family expansion are often associated with syntenic discontinuities that—along with gene divergence, acquisition and loss, and rearrangement within the syntenic regions—have shaped the genomes of each parasite. Contrary to recent reports, our analyses reveal no evidence that these species are descended from an ancestor that contained a photosynthetic endosymbiont.

1 The Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA.
2 Department of Microbiology and Tropical Medicine, George Washington University, Washington, DC 20052, USA.
3 Seattle Biomedical Research Institute, 307 Westlake Avenue North, Seattle, WA 98109–2591, USA.
4 Department of Pathobiology, University of Washington, Seattle, WA 98195, USA.
5 Division of Biomedical and Health Informatics, University of Washington, Seattle, WA 98195, USA.
6 Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK.
7 Center for Genomics and Bioinformatics, Karolinska Institutet, Berzelius väg 35, S-171 77 Stockholm, Sweden.
8 School of Biology, The Devonshire Building, University of Newcastle, Newcastle upon Tyne NE1 7RU, UK.
9 Laboratoire de Génomique Fonctionnelle des Trypanosomatides, UMR-CNRS 5162, Université Victor Segalen Bordeaux II, 33076 Bordeaux cedex, France.
10 Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, CEP 31270-901, Belo Horizonte, MD, Brazil.
11 Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 2QH, UK.
12 Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, UK.
13 Department of Biochemistry, University of Iowa, 4-403 Bowen Science Building, Newton Road, Iowa City, IA 52242, USA.

* These authors contributed equally to this work.

{ddagger} Present address: Department of Microbiology, Immunology, and Molecular Genetics, University of California, Los Angeles, CA 90095, USA.

§ Present address: The Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA.

{dagger} To whom correspondence should be addressed. E-mail: nelsayed{at}tigr.org (N.M.E.-S.); peter.myler{at}sbri.org (P.J.M.); nhall{at}tigr.org (N.H.)

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