Trypanosoma brucei ATR Links DNA Damage Signaling during Antigenic Variation with Regulation of RNA Polymerase I-Transcribed Surface Antigens.

摘要: Trypanosoma brucei evades mammalian immunity by using recombination to switch its surface-expressed variant surface glycoprotein (VSG), while ensuring that only one of many subtelomeric multigene VSG expression sites are transcribed at a time. DNA repair activities have been implicated in the catalysis switching recombination, not transcriptional control. How is signaled guide appropriate reaction or integrate into parasite growth unknown. Here, we show loss ATR, damage-signaling protein kinase, lethal, causing nuclear genome instability and increased through VSG-localized damage. Furthermore, ATR leads transcription silent mixed VSGs on cell surface, effects associated with altered localization RNA polymerase I VEX1. This work shows acts antigenic variation both damage signaling antigen