Comprehensive genomic analysis of Trypanosoma rangeli reveals key insights into the biology and evolution of this non-virulent American mammalian trypanosome
Maia, G. A.; Matos, G. M.; Silva, A. C. d.; Pereira, C. A.; Pontes, C. L. M.; Lückemeyer, D. D.; Carmo, R. A. d.; Moreira, R. S.; Pereira, T. K. d. S.; Rosar, A. d. S.; Brascher, T. C.; Maciel, G. R.; Silveira Filho, J. F. d.; Steindel, M.; Stoco, P. H.; Wagner, G.; Andersson, B.; Grisard, E. C.
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BackgroundTrypanosoma rangeli is a non-virulent hemoflagellate protozoan parasite that infects mammals, including humans, in Central and South America. It is primarily transmitted through the bites of triatomine bugs and shares an overlapping geographical distribution with T. cruzi, as well as triatomine vectors and mammalian hosts, and various shared surface antigens. The life cycle of T. rangeli differs from those of other human-infecting trypanosomes, such as T. cruzi and T. brucei, and the molecular mechanisms underlying host-parasite and host-vector interactions are not well understood, demanding improved molecular and genomic resources. ResultsThe use of a hybrid approach to sequence and assemble the T. rangeli genome, complemented by transcriptomics and proteomics for functional gene annotation, led to the generation of the near-complete genome sequence of the parasite. Detailed intra- and inter-specific comparative genomics allowed analysis of polymorphisms, genome structure and improved resolution of genes coding for important surface molecules such as Mucins, TASV and GP63. ConclusionsThe improved T. rangeli genome assembly, combined with comparative genomics has yielded novel biological insights. These included the first description of a metalloprotease activity, attributed to specific GP63 genes that are absent in Leishmania species. In addition, a TASV gene family that is absent in T. cruzi was identified, which indicates a possible role in the T. rangeli infection process.
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