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Comparative genomic analysis of three Leishmania species that cause diverse human disease
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
Institution: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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