Dysregulation of RNA Pol activity at CTCF binding sites in EBV LCL ?CTCF mutant

We used Precision Nuclear Run-on followed by Deep Sequencing (PRO-Seq) to investigate RNA Polymerase (Pol) activity during Epstein-Barr Virus (EBV) reactivation and its link to CTCF in latently EBV infected ymphoblastoid cell lines (LCLs). Nuclei were harvested from WT LCLs or LCLs containing an 18bp deletion at the LMP CTCF binding site (DCTCF) treated with DMSO or induced to reactivate with the small molecule C60 for 24h. Relative to WT, DCTCF displayed disrupted transcriptional activity at other CTCF sites during latency and this phenotype correlated with an inability to reactivate from latency. Overall design: PRO-Seq data from 14h DMSO or C60 treated WT EBV LCLs and DCTCF EBV LCLs containing 2 biological replicates per condition. All samples contain Drosophila spike-in.