Telomere Maintenance in Trypanosoma brucei 

Seminar Details

Host: Dr. Jorge Cruz-Reyes

Time: 4:00-5:00 pm

Location: BCBP 108

Seminar Abstract

Telomeres are nucleoprotein complexes at chromosome ends and are essential for genome integrity and chromosome stability in eukaryotic cells. For Trypanosoma brucei that causes sleeping sickness in humans, the telomere complex also plays critical roles in antigenic variation, a process where T. brucei sequentially expresses distinct VSGs, its major surface antigen, to evade the host’s immune response. VSGs are expressed exclusively from subtelomeric region in a strictly monoallelic manner. As telomere DNA serves as a docking site for telomere proteins that are required for normal parasite proliferation and long-term infections, we are investigating telomere maintenance mechanisms in T. brucei. We have shown that telomere elongation by telomerase (including both a protein and an RNA component) is the predominant mechanism of telomere maintenance in T. brucei. However, the telomere end processing mechanisms appear distinct from those described in yeasts and mammals. T. brucei does not seem to have OB-fold containing telomere-specific proteins. Rather, T. brucei uses PolIE, an A type DNA polymerase, and PPL2, a translesion DNA polymerase, to regulate telomerase action and to coordinate telomere G- and C-rich strand syntheses. These findings reveal unique essential features of T. brucei telomere complex, paving the way for future development of anti-parasite agents.