RT Journal Article SR Electronic T1 Trypanosoma brucei PolIE suppresses telomere recombination JF bioRxiv FD Cold Spring Harbor Laboratory SP 2021.05.07.443201 DO 10.1101/2021.05.07.443201 A1 Maiko Tonini A1 M. A. G. Rabbani A1 Marjia Afrin A1 Bibo Li YR 2021 UL http://biorxiv.org/content/early/2021/05/08/2021.05.07.443201.abstract AB Telomeres are essential for genome integrity and stability. In T. brucei that causes human African trypanosomiasis, the telomere structure and telomere proteins also influence the virulence of the parasite, as its major surface antigen involved in the host immune evasion is expressed exclusively from loci immediately upstream of the telomere repeats. However, telomere maintenance mechanisms are still unclear except that telomerase-mediated telomere synthesis is a major player. We now identify PolIE as an intrinsic telomere complex component. We find that depletion of PolIE leads to an increased amount of telomere/subtelomere DNA damage, an elevated rate of antigenic variation, and an increased amount of telomere T-circles and C-circles, indicating that PolIE suppresses telomere recombination and helps maintain telomere integrity. In addition, we observe much longer telomere G-rich 3’ overhangs in PolIE-depleted cells, which is not dependent on telomerase. Furthermore, the level of telomere DNA synthesis is slightly increased in PolIE-depleted cells, which is dependent on telomerase. Therefore, we identify PolIE as a major player for telomere maintenance in T. brucei.Competing Interest StatementThe authors have declared no competing interest.