Abstract
BackgroundThe protozoan parasite Trypanosoma cruzi, causative agent of Chagas disease, depends upon a cell surface-expressed trans-sialidase (ts) to avoid activation of complement-mediated lysis and to enhance intracellular invasion. However these functions alone fail to account for the size of this gene family in T. cruzi, especially considering that most of these genes encode proteins lacking ts enzyme activity. Previous whole genome sequencing of the CL Brener clone of T. cruzi identified ~1400 ts variants, but left many partially assembled sequences unannotated.ResultsIn the current study we reevaluated the trans-sialidase-like sequences in this reference strain, identifying an additional 1779 full-length and partial ts genes with their important features annotated, and confirming the expression of previously annotated “pseudogenes” and newly annotated ts family members. Multiple EM for Motif Elicitation (MEME) analysis allowed us to generate a model T. cruzi ts (TcTS) based upon the most conserved motif patterns and demonstrated that a common motif order is highly conserved among ts family members. Using a newly developed pipeline for the analysis of recombination within large gene families, we further demonstrate that TcTS family members are undergoing frequent recombination, generating new variants from the thousands of functional and non-functional ts gene segments but retaining the overall structure of the core TcTS family members.ConclusionsThe number and variety as well as high recombination frequency of TcTS family members supports strong evolutionary pressure, probably exerted by immune selection, for continued variation in ts sequences in T. cruzi, and thus for a unique immune evasion mechanism for the large ts gene family.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-3037-z) contains supplementary material, which is available to authorized users.
Highlights
The protozoan parasite Trypanosoma cruzi, causative agent of Chagas disease, depends upon a cell surface-expressed trans-sialidase to avoid activation of complement-mediated lysis and to enhance intracellular invasion
Identification of previously unannotated T. cruzi trans-sialidases (TcTS) sequences Prior to beginning analysis of the TcTS family, we first made sure that we had identified the complete complement of TcTS genes for the reference CL Brener clone of T. cruzi
A preliminary remapping of whole genome shotgun (WGS) reads selected because of their homology to TcTS gene sequences to the assembled genome revealed that a large number of these TcTS-like reads mapped to regions with no annotated genes
Summary
The protozoan parasite Trypanosoma cruzi, causative agent of Chagas disease, depends upon a cell surface-expressed trans-sialidase (ts) to avoid activation of complement-mediated lysis and to enhance intracellular invasion. These functions alone fail to account for the size of this gene family in T. cruzi, especially considering that most of these genes encode proteins lacking ts enzyme activity. The first complete genome sequence for the protozoan parasite T. cruzi was reported in 2005, along with the genomes of the related parasites Trypanosoma brucei and Leishmania major. It is further postulated that these gene families have expanded in response to immune pressure, presumably by duplication, recombination and mutation of the ancestral founding family members
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