Regulation of antigenic variation by trypanosoma brucei telomere proteins depends on their unique dna binding activities

Bibo Li, Yanxiang Zhao

Research output: Journal article publicationReview articleAcademic researchpeer-review

1 Citation (Scopus)


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 TbRAP1 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.

Original languageEnglish
Article number967
Issue number8
Publication statusPublished - Aug 2021


  • Antigenic variation
  • DNA binding activity
  • Myb domain
  • RAP1
  • Telomere
  • TRF
  • Trypanosoma brucei
  • VSG

ASJC Scopus subject areas

  • Immunology and Allergy
  • Molecular Biology
  • Immunology and Microbiology(all)
  • Microbiology (medical)
  • Infectious Diseases

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