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Comparative genomic analysis of three Leishmania species that cause diverse human disease |
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| Authors: | Peacock Christopher S Seeger Kathy Harris David Murphy Lee Ruiz Jeronimo C Quail Michael A Peters Nick Adlem Ellen Tivey Adrian Aslett Martin Kerhornou Arnaud Ivens Alasdair Fraser Audrey Rajandream Marie-Adele Carver Tim Norbertczak Halina Chillingworth Tracey Hance Zahra Jagels Kay Moule Sharon Ormond Doug Rutter Simon Squares Rob Whitehead Sally Rabbinowitsch Ester Arrowsmith Claire White Brian Thurston Scott Bringaud Frédéric Baldauf Sandra L Faulconbridge Adam Jeffares Daniel Depledge Daniel P Oyola Samuel O Hilley James D Brito Loislene O Tosi Luiz R O Barrell Barclay Cruz Angela K |
| Affiliation: | Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire CB10 1SA, UK. csp@sanger.ac.uk |
| 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 approximately 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. |
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