The three-dimensional structure of Epstein-Barr virus genome varies by latency type and is regulated by PARP1 enzymatic activity [ChIP-Seq]

PARP does have an essential role in the regulation of global EBV episome chromatin structure. We have functionally characterized the effect of PARP enzymatic inhibition on total episomal structure and we mapped intragenomic contact changes after PARP inhibition to global binding of the chromatin looping factors CTCF and cohesin across the EBV genome. The altered expression profile after the structural rearrangement induced by PARP inhibition supports the model where PARP1 helps maintain EBV latency programs. Overall design: Two biological replicates of both LCL and Mutu control cell and olaparib [2.5 uM] treated cells. Chromatin immunoprecipitation (ChIP) was performed using RAD21 antibody or sonicate chromatin (input) were used to make ChIP-seq libraries. For peak calling we compare the RAD21 enrichment to the input signal