Genome-Wide Mapping of E2F1 Transcription Factor Binding Sites Across Human and Epstein-Barr virus (EBV) Chromosomes

E2F1, the first member of E2F family transcription factors, plays a central role in cell cycle progression, DNA-damage response and apoptosis. Accumulating evidence indicates that E2F1 regulates replication of several DNA viruses. We and others previously described deregulated E2F1 expression during Epstein-Barr virus (EBV) induced B-cell transformation and its role in survival of transformed B-lymphocytes in response to DNA-damage signals. In addition, global transcriptomic analyses (GSE235941, GSE237484) reveal that E2F1 expression is transcriptionally activated during EBV latent infection in B-lymphocytes but suppressed during lytic-cycle reactivation. However, the precise regulations by which E2F1 sustains EBV latent to lytic switch remains unanswered. Given that E2F activity is often deregulated by infection with DNA viruses, the main objective of our study was to investigate the genome-wide occupancy of E2F1 on both cellular and viral gene promoters, driving EBV pathogenesis. Overall design: Chromatin immunoprecipitation was performed using E2F1 specific antibody (KH95, Invitrogen) in two in vitro EBV transformed lymphoblastoid cell lines (LCL#1 and LCL#89) followed by sequencing analyses on the Illumina HiSeq2500 platform.