Document Type
Article
Publication Date
8-2021
Publication Title
Pathogens
Disciplines
Biology | Parasitic Diseases
Abstract
Trypanosoma brucei causes human African trypanosomiasis and regularly switches its major surface antigen, Variant Surface Glycoprotein (VSG), to evade the host immune response. Such antigenic variation is a key pathogenesis mechanism that enables T. brucei to establish long-term infections. VSG is expressed exclusively from subtelomere loci in a strictly monoallelic manner, and DNA recombination is an important VSG switching pathway. The integrity of telomere and subtelomere structure, maintained by multiple telomere proteins, is essential for T. brucei viability and for regulating the monoallelic VSG expression and VSG switching. Here we will focus on T. brucei TRF and RAP1, two telomere proteins with unique nucleic acid binding activities, and summarize their functions in telomere integrity and stability, VSG switching, and monoallelic VSG expression. Targeting the unique features of TbTRF and TbRAP10 s nucleic acid binding activities to perturb the integrity of telomere structure and disrupt VSG monoallelic expression may serve as potential therapeutic strategy against T. brucei.
DOI
10.3390/pathogens10080967
Version
Publisher's PDF
Recommended Citation
Li, Bibo Ph.D. and Zhao, Yanxiang, "Regulation of Antigenic Variation by Trypanosoma brucei Telomere Proteins Depends on Their Unique DNA Binding Activities" (2021). Biological, Geological, and Environmental Faculty Publications. 253.
https://engagedscholarship.csuohio.edu/scibges_facpub/253
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.
Volume
10
Issue
8
Comments
This work is supported by NIH, AI066095 (PI, B.L.), Research Grants Council Hong
Kong, PolyU 151062/18M (PI, Y.Z.), and Shenzhen Basic Research Program, JCYJ20170818104619974
(PI, Y.Z.).