Article abstract
Nature Genetics 39, 839 - 847 (2007)
Published online: 17 June 2007 | doi:10.1038/ng2053
Comparative genomic analysis of three Leishmania species that cause diverse human disease
Christopher S Peacock1, Kathy Seeger1, David Harris1, Lee Murphy1, Jeronimo C Ruiz2, Michael A Quail1, Nick Peters1, Ellen Adlem1, Adrian Tivey1, Martin Aslett1, Arnaud Kerhornou1, Alasdair Ivens1, Audrey Fraser1, Marie-Adele Rajandream1, Tim Carver1, Halina Norbertczak1, Tracey Chillingworth1, Zahra Hance1, Kay Jagels1, Sharon Moule1, Doug Ormond1, Simon Rutter1, Rob Squares1, Sally Whitehead1, Ester Rabbinowitsch1, Claire Arrowsmith1, Brian White1, Scott Thurston1, Frédéric Bringaud3, Sandra L Baldauf4, Adam Faulconbridge4, Daniel Jeffares1, Daniel P Depledge4, Samuel O Oyola4, James D Hilley5, Loislene O Brito2, Luiz R O Tosi2, Barclay Barrell1, Angela K Cruz2, Jeremy C Mottram5, Deborah F Smith4 & Matthew Berriman1
Abstract
Leishmania parasites cause a broad spectrum of clinical disease. Here we report the sequencing of the genomes of two species of Leishmania: Leishmania infantum and Leishmania braziliensis. The comparison of these sequences with the published genome of Leishmania major reveals marked conservation of synteny and identifies only
200 genes with a differential distribution between the three species. L. braziliensis, contrary to Leishmania species examined so far, possesses components of a putative RNA-mediated interference pathway, telomere-associated transposable elements and spliced leader–associated SLACS retrotransposons. We show that pseudogene formation and gene loss are the principal forces shaping the different genomes. Genes that are differentially distributed between the species encode proteins implicated in host-pathogen interactions and parasite survival in the macrophage.
- Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK.
- Departmento de Biologia Celular e Molecular e Bioagentes Patogênicos, Faculdade de Medicina, de Ribeirão Preto, Universidade de São Paulo, Avenida Bandeirantes 3900, CEP 14049-900 Ribeirão Preto, São Paulo, Brazil.
- Laboratoire de Génomique Fonctionnelle des Trypanosomatides, Universitité Victoir Segalen Bordeaux II, UMR-5162 CNRS, 33076 Bordeaux Cedex, France.
- Immunology and Infection Unit, Department of Biology, University of York, York YO10 5YW, UK.
- Wellcome Centre for Molecular Parasitology and Division of Infection & Immunity, Glasgow Biomedical Research Centre, University of Glasgow, 120 University Place, Glasgow G12 8TN, UK.
Correspondence to: Christopher S Peacock1 e-mail: csp@sanger.ac.uk
Correspondence to: Matthew Berriman1 e-mail: mb4@sanger.ac.uk
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