The Genome Sequence of Trypanosoma cruzi , Etiologic Agent of Chagas Disease

American Association for the Advancement of Science (AAAS) - Tập 309 Số 5733 - Trang 409-415 - 2005
Najib M. El-Sayed1,2,3,4,5, Peter J. Myler1,3,4, Daniella Castanheira Bartholomeu1,2,3,4,5, Daniel Nilsson1,2,3,4,5, Gautam Aggarwal1,2,3,4,5, Anh-Nhi Tran1,2,3,4,5, Elodie Ghedin1,2,3,4,5, Elizabeth A. Worthey1,2,3,4,5, Arthur L. Delcher1,2,3,4,5, Gaëlle Blandin1,2,3,4,5, Scott J Westenberger1,6,3,4,5, Elisabet Caler1,2,3,4,5, Gustavo Cerqueira1,2,3,4,5, Carole Branche1,2,3,4,5, Brian J. Haas1,2,3,4,5, Atashi Anupama1,2,3,4,5, Erik Arner1,2,3,4,5, Lena Åslund1,2,3,4,5, Philip Attipoe1,2,3,4,5, Esteban J. Bontempi1,2,3,4,5, Frédéric Bringaud1,2,3,4,5, Peter Burton1,2,3,4,5, Eithon Cadag1,2,3,4,5, David A. Campbell1,2,6,4,5, Mark Carrington1,2,3,4,5, Jonathan Crabtree1,2,3,4,5, Hamid Darban1,2,3,4,5, José Franco da Silveira1,2,3,4,5, Pieter de Jong1,2,3,4,5, Kimberly M. Edwards1,2,3,4,5, Paul T. Englund7,1,2,4,5, Gholam Fazelina1,2,3,4,5, Tamara V. Feldblyum1,2,3,4,5, Marcela Ferella1,2,3,4,5, Alberto C.C. Frasch1,2,3,4,5, Keith Gull1,2,3,4,5, David Horn1,2,3,4,5, Lihua Hou1,2,3,4,5, Yi‐Ting Huang1,2,3,4,5, Ellen Kindlund1,2,3,4,5, Michele M. Klingbeil1,2,3,4,5, Sindy Kluge1,2,3,4,5, Hean Koo1,2,3,4,5, Daniela R. Lacerda1,2,3,4,5, Mariano J. Levin1,2,3,4,5, Hernán Lorenzi1,2,3,4,5, Tin Louie1,2,3,4,5, Carlos Renato Machado1,2,3,4,5, Richard McCulloch1,2,3,4,5, Alan Mckenna1,2,3,4,5, Yumi Mizuno1,2,3,4,5, Jeremy C. Mottram1,2,3,4,5, Siri Nelson1,2,3,4,5, Stephen Ochaya1,2,3,4,5, Kazutoyo Osoegawa1,2,3,4,5, Grace Pai1,2,3,4,5, Marilyn Parsons1,3,4,5, Martin Pentony1,2,3,4,5, Ulf Pettersson1,2,3,4,5, Mihai Pop1,2,3,4,5, José Luis Ramı́rez1,2,3,4,5, Joel Rinta1,2,3,4,5, Laura Robertson1,2,3,4,5, Steven L. Salzberg1,2,3,4,5, Daniel O. Sánchez1,2,3,4,5, Amber Seyler1,2,3,4,5, Reuben Sunil Kumar Sharma1,2,3,4,5, Jyoti Shetty1,2,3,4,5, Anjana J. Simpson1,2,3,4,5, Ellen Sisk1,2,3,4,5, Martti T. Tammi1,2,3,4,5, Rick L. Tarleton8,1,2,4,5, Santuza Maria Ribeiro Teixeira1,2,3,4,5, Susan Van Aken1,2,3,4,5, Christy Vogt1,2,3,4,5, Pauline N. Ward1,2,3,4,5, Bill Wickstead1,2,3,4,5, Jennifer R. Wortman1,2,3,4,5, Owen White1,2,3,4,5, Claire M. Fraser1,2,3,4,5, Kenneth Stuart1,3,4,5, Björn Andersson1,2,3,4,5
1Department of Medical Education and Biomedical Informatics, University of Washington, Seattle, WA 98195, USA
2Department of Microbiology and Tropical Medicine, George Washington University, Washington, DC 20052, USA
3Department of Parasite Genomics, The Institute for Genomic Research, Rockville, MD 20850, USA
4Department of Pathobiology, School of Public Health and Community Medicine, University of Washington, Seattle, WA 98195, USA
5Seattle Biomedical Research Institute, Seattle, WA 98109, USA
6Department of Microbiology, Immunology and Molecular Genetics, University of California, Los Angeles, CA 90095, USA
7Department of Biological Chemistry, Johns Hopkins University, School of Medicine, Baltimore, MD 21205, USA
8Center for Tropical and Emerging Global Diseases, Department of Cellular Biology, University of Georgia, Athens, GA 30602, USA

Tóm tắt

Whole-genome sequencing of the protozoan pathogen Trypanosoma cruzi revealed that the diploid genome contains a predicted 22,570 proteins encoded by genes, of which 12,570 represent allelic pairs. Over 50% of the genome consists of repeated sequences, such as retrotransposons and genes for large families of surface molecules, which include trans-sialidases, mucins, gp63s, and a large novel family (>1300 copies) of mucin-associated surface protein (MASP) genes. Analyses of the T. cruzi, T. brucei , and Leishmania major (Tritryp) genomes imply differences from other eukaryotes in DNA repair and initiation of replication and reflect their unusual mitochondrial DNA. Although the Tritryp lack several classes of signaling molecules, their kinomes contain a large and diverse set of protein kinases and phosphatases; their size and diversity imply previously unknown interactions and regulatory processes, which may be targets for intervention.

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We thank our colleagues in the T. cruzi Genome Network (TcGN) and the trypanosomatid research community for their continued support and encouragement. In particular we thank the members of the Tritryp Sequencing Consortium for their help with comparative genome annotation; J. Donelson and S. Melville for a critical review of this manuscript; A. Kerhornou for his help with GPI anchor predictions; as well as O. Campetella I. Dórso V. Campo G. Montagna and F. Aguero for their help with the surface protein analyses. Funding for this project was provided by grants from the National Institute for Allergy and Infectious Diseases (NIAID) to N.M.E.-S. (AI45038) K.D.S. and P.J.M. (AI045039) and B.A. (AI45061); the M. J. Murdoch Charitable Trust to the Seattle Biomedical Research Institute; the Beijer Foundation to B.A. M.J.L. and A.C.F. are Howard Hughes Medical Institute International Research Scholars. G.C.C. is supported in part by CNPq Brazil. We also express our gratitude to NIAID Burroughs Wellcome Fund (BWF) the Wellcome Trust and WHO (Tropical Disease Research) for providing funds for several TcGN and Tritryp meetings. Special thanks to C. Hertz-Fowler and P. Mooney at the Wellcome Trust Sanger Institute (WTSI) for coordinating data exchange with The Institute for Genomic Research (TIGR) and to A. Tivey and M. Aslett for loading and updating the T. cruzi data in GeneDB at WTSI. This Whole-Genome Shotgun project has been deposited at the DNA Databank of Japan (DDBJ) the European Molecular Biology Laboratory (EMBL) and GenBank under the project accession AAHK00000000. The version described in this paper is the first version AAHK01000000. All data sets and genome annotations are also available through GeneDB at www.genedb.org.

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American Association for the Advancement of Science (AAAS)

Tập 309 Số 5733

409-415

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