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To evade the host immune system, several pathogens periodically change their cell-surface epitopes. In the African trypanosomes, antigenic variation is achieved by tightly regulating the expression of a multigene family encoding a large repertoire of variant surface glycoproteins (VSGs). Immune evasion relies on two important features: exposing a single type of VSG at the cell surface and periodically and very rapidly switching the expressed VSG. Transcriptional switching between resident telomeric VSG genes does not involve DNA rearrangements, and regulation is probably epigenetic. The histone methyltransferase DOT1B is a nonessential protein that trimethylates lysine 76 of histone H3 in  Trypanosoma brucei . Here we report that transcriptionally silent telomeric  VSG s become partially derepressed when  DOT1B  is deleted, whereas nontelomeric loci are unaffected. DOT1B also is involved in the kinetics of VSG switching: in ΔDOT1B cells, the transcriptional switch is so slow that cells expressing two VSGs persist for several weeks, indicating that monoallelic transcription is compromised. We conclude that DOT1B is required to maintain strict  VSG  silencing and to ensure rapid transcriptional  VSG  switching, demonstrating that epigenetics plays an important role in regulating antigenic variation in  T. brucei .

A Histone Methyltransferase Modulates Antigenic Variation in African Trypanosomes