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Comparative Genomics of Trypanosomatid Parasitic Protozoa
Najib M. El-Sayed,1,2*Peter J. Myler,3,4,5*Gaëlle Blandin,1Matthew Berriman,6Jonathan Crabtree,1Gautam Aggarwal,3Elisabet Caler,1Hubert Renauld,6Elizabeth A. Worthey,3Christiane Hertz-Fowler,6Elodie Ghedin,1,2Christopher Peacock,6Daniella C. Bartholomeu,1Brian J. Haas,1Anh-Nhi Tran,7Jennifer R. Wortman,1U. Cecilia M. Alsmark,8Samuel Angiuoli,1Atashi Anupama,3Jonathan Badger,1Frederic Bringaud,9Eithon Cadag,3Jane M. Carlton,1Gustavo C. Cerqueira,1,10Todd Creasy,1Arthur L. Delcher,1Appolinaire Djikeng,1T. Martin Embley,8Christopher Hauser,1Alasdair C. Ivens,6Sarah K. Kummerfeld,11Jose B. Pereira-Leal,11Daniel Nilsson,7Jeremy Peterson,1Steven L. Salzberg,1Joshua Shallom,1Joana C. Silva,1Jaideep Sundaram,1Scott Westenberger,1Owen White,1Sara E. Melville,12John E. Donelson,13Björn Andersson,7Kenneth D. Stuart,3,4Neil Hall6
A comparison of gene content and genome architecture of Trypanosomabrucei, Trypanosoma cruzi, and Leishmania major, three relatedpathogens with different life cycles and disease pathology,revealed a conserved core proteome of about 6200 genes in largesyntenic polycistronic gene clusters. Many species-specificgenes, especially large surface antigen families, occur at nonsyntenicchromosome-internal and subtelomeric regions. Retroelements,structural RNAs, and gene family expansion are often associatedwith syntenic discontinuities that—along with gene divergence,acquisition and loss, and rearrangement within the syntenicregions—have shaped the genomes of each parasite. Contraryto recent reports, our analyses reveal no evidence that thesespecies are descended from an ancestor that contained a photosyntheticendosymbiont.
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.
Present address: Department of Microbiology, Immunology, andMolecular Genetics, University of California, Los Angeles, CA90095, USA.
Present address: The Institute for Genomic Research, 9712 MedicalCenter Drive, Rockville, MD 20850, USA.
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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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. 
To whom correspondence should be addressed. E-mail: 
