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Regulation of antigenic variation by a DOT1B/RNaseH2 complex in Trypanosoma brucei

Subject Area Parasitology and Biology of Tropical Infectious Disease Pathogens
Term from 2019 to 2023
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 430676033
 
Final Report Year 2025

Final Report Abstract

Antigenic variation is one of the most sophisticated strategies used by pathogens, such as Trypanosoma Trypanosoma, Borrelia or Neisseria, to escape the immune system of their hosts. Trypanosomes periodically changes the expression of protective variant surface glycoproteins (VSGs) to evade the immune system of their mammalian hosts. One route to change VSG expression is the transcriptional activation of a previously silent VSG expression site (ES), a subtelomeric region containing the VSG genes. Homologous recombination of a different VSG from a large reservoir into the active ES represents another route. Many molecular details of these processes are still elusive. We could demonstrate that the conserved histone methyltransferase DOT1B is involved in transcriptional silencing of active ES and influences ES switching kinetics. The molecular machinery that enables DOT1B to execute these regulatory functions remains elusive, however. To better understand DOT1B- mediated regulatory processes, we purified DOT1B-associated proteins using complementary biochemical approaches. We identified several novel DOT1B-interactors. One of these was the Ribonuclease H2 complex, previously shown to resolve RNA-DNA hybrids, maintain genome integrity, and play a role in antigenic variation. Our study revealed that DOT1B depletion results in an increase in RNA-DNA hybrids, accumulation of DNA damage and recombination-based ES switching events. Surprisingly, a similar pattern of VSG deregulation was observed in Ribonuclease H2 mutants. We propose that both proteins act together in resolving R-loops to ensure genome integrity and contribute to the tightly regulated process of antigenic variation.

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