ChIP-exo of HH514-16 treated with NaB or left untreated

How Krüppel-associated box-domain zinc finger protein (KRAB-ZFP) transcriptional repressors recruit TRIM28/KAP1 to recognizes target sequences or foreign genomes is unclear. Here, we used Epstein-Barr virus-infected cells in which a KRAB-ZFP, SZF1, silences lytic/replicative-phase genes of the virus to determine how the ZFP-footprints on cell and viral genomes to target pericentromeric regions. We observed that it uses non-consensus sites to target viral genes. This heterochromatin machinery employed by the host silences and regulate an invader without deregulating itself. Overall design: We treated HH514-16 Burkitt Lyphoma cells with NaB to induced the lytic phase of the life cyle of EBV or left untreated. After 24hrs, the cells were harvested, stained with reference EBV-seropositive and EBV-seronegative serum, washed, and sorted by Fluorescence Activated Cell Sorting (FACS) into EBV lytic and latent/refractory cell populations. We next performed ChIP-exo and barcoded library for each sample treatment. The sequencing reads were processed by Peconic Genomics for peak-calling. Reads were mapped to GRC hg38 assembly of human genome and EBV reference genome (NC_007605). Peaks were called and identified using default parameters of the GeneTrack and GEM algorithms.