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Transmitted by the tsetse fly, Trypanosoma brucei is a protozoan parasite that causes sleeping sickness in human and nagana in cattle. While infecting the bloodstream and central nervous system, T. brucei evades the immune system by altering its major surface antigen, Variant Surface Glycoproteins (VSGs), which forms a thick coat on its cell membrane. The expression sites for VSGs are at the sub-telomeric regions of T. brucei chromosomes. Telomeres, DNA-protein complexes located at the end of chromosomes, provide chromosome stability by preventing degradation of the chromosome ends. The telomere complex also regulates the sub-telomeric VSG expression and switching in T. brucei. To eradicate T. brucei, further understanding of how the telomere complex regulates VSG expression and switching is needed. TbTIF2 (TRF-Interacting Factor 2), a telomere-specific protein, was discovered to be essential for cell viability and the suppression of VSG switching in T. brucei. To better understand the telomere complex and the mechanisms of TbTIF2 function, we have performed a yeast 2- hybrid screen and identified a number of proteins that may interact with TbTIF2. The goal of our current study is to validate the TbTIF2-interacting candidates. We have subcloned several promising TbTIF2-interacting factors. We are currently testing these candidates for their interaction with TbTIF2 using yeast 2-hybrid analysis.

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Validating TbTIF2-interacting Candidates

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