H3K27me3 ChIP-Seq in LCLs cells with conditionally activated EBNA3C

Epstein-Barr virus (EBV) is a herpesvirus that establishes lifelong asymptomatic infection in up to 95% of the human population. In vitro EBV infection of resting B lymphocytes drives them to proliferate as lymphoblastoid cell lines (LCLs). EBV expresses limited genes, which include six nuclear proteins (EBNAs), three integral membrane proteins (LMPs), and more than 30 micro RNAs in LCLs. EBNA3C, one of the six nuclear proteins, is transcription factor and regulates host cell genes. The growth effects of EBNA3C appear to be primarily due to suppression of the CDKN2A gene products, p16INK4A and p14ARF. Conditional inactivation of EBNA3C results in increasing p16 expression and this is accompanied by the substantial reduction of the repressive H3K27me3 modification at the CDKN2A promoter and cell cycle arrest. To further elucidate the relationship between EBNA3C and H3K27me3 modification, we profiled H3K27me3 by ChIP-seq in CDKN2A knockout EBNA3CHT LCLs in the presence (4HT+) or absence (4HT-) of 4-hydroxytamoxifen, with a total of 4 biological replicates per condition. We profiled H3K27me3 by ChIP-seq in CDKN2A knockout EBNA3CHT LCLs in the presence (4HT+) or absence (4HT-) of 4-hydroxytamoxifen, with a total of 4 biological replicates per condition.