Project description:Abstract: The Kinetoplastida (Euglenozoa) are unicellular flagellates that include the trypanosomatid parasites, most notably Trypanosoma brucei, T.cruzi and Leishmania spp. These organisms cause substantial mortality and morbidity in humans and their livestock worldwide as the causative agents of African sleeping sickness, Chagas disease and leishmaniasis respectively. Draft genome sequences are available for several species of both Trypanosoma and Leishmania. Bodo saltans is a free-living heterotroph found worldwide in freshwater and marine habitats, and it is among the closest bodonid relatives of the trypanosomatids. The purpose of a B. saltans genome sequence is to provide an 'out-group' for comparative genomic analysis of the trypanosomatid parasites. It will provide a model of the ancestral trypanosomatid to distinguish those derived parts of the parasite genomes (i.e., unique trypanosomatid adaptations) from those which are a legacy of the free-living ancestor. To aid annotation of the B.saltans genome sequence, total genomic RNA was extracted on four occasions from the total cellular mass of 160ml of B.saltans cell culture, for the purposes of transcription profiling by high throughput sequencing. Cells were unmodified. B.saltans cells were grown in water at 4oC. Total genomic RNA was extracted from a cell pellet using TRIZOL reagent and ethanol precipitated. Poly A+ mRNA was purified from total RNA using oligo dT dyna bead selection and libraries were created using the Illumina RNA-seq protocol. The samples were sequenced on an Illumina HiSeq 2000. This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/
Project description:The evolution of parasitism is a recurring event in the history of life and a core question in evolutionary biology. Trypanosomatids are important parasites including the human pathogens Trypanosoma brucei, T. cruzi and Leishmania spp., which have evolved complex life cycles to exploit a series of defined host environments after diverging from free-living, phagotrophic bodonids. However, the origins of genomic adaptations for transmission, disease and pathogenesis remain obscure because there has been no genomic comparison of parasitic and free-living species. Addressing this absence, we have produced a genome sequence for Bodo saltans, the closest known non-parasitic relative of trypanosomatids. Here we show how genomic reduction and innovation contributed to the character of trypanosomatid genomes. We find that despite a genetic ‘streamlining’ of diverse physiological functions, including macromolecular degradation and cellular homeostasis, the origin of trypanosomatid parasitism did not lead to a substantial reduction in genome function. Instead, we observe dramatic elaboration of gene families that facilitate host-parasite interactions and pathogenesis. We also show how parasite-specific proteins that characterize the enigmatic cell surfaces of Trypanosoma and Leishmania were derived from the same ancestral proteins, still represented in B. saltans. Our new evidence distinguishes adaptive innovations of trypanosomatids that post-date their parasitic origin from essentially kinetoplastid legacies of a free-living past. It shows that when the labile environment of a phagotrophic ancestor was replaced by the defined conditions of their various hosts, trypanosomatid physiology was reoriented towards host interaction, and ancestral structures were radically transformed to provide adaptations for obligate parasitism.
2018-10-24 | PXD002628 | Pride
Project description:Alpha-proteobacterial endosymbiont of kinetoplastid Bodo saltans