@article {585336,
	title = {The Epstein-Barr Virus Regulome in Lymphoblastoid Cells},
	journal = {Cell Host Microbe},
	volume = {22},
	number = {4},
	year = {2017},
	month = {2017 Oct 11},
	pages = {561-573.e4},
	abstract = {Epstein-Barr virus (EBV) transforms B cells to continuously proliferating lymphoblastoid cell lines (LCLs), which represent an experimental model for EBV-associated cancers. EBV nuclear antigens (EBNAs) and LMP1 are EBV transcriptional regulators that are essential for LCL establishment, proliferation, and survival. Starting with the 3D genome organization map of LCL, we constructed a comprehensive EBV regulome encompassing 1,992 viral/cellular genes and enhancers. Approximately 30\% of genes essential for LCL growth were linked to EBV enhancers. Deleting EBNA2 sites significantly reduced their target gene expression. Additional EBV super-enhancer (ESE) targets included MCL1, IRF4, and EBF. MYC ESE looping to the transcriptional stat site of MYC was dependent on EBNAs. Deleting MYC ESEs greatly reduced MYC expression and LCL growth. EBNA3A/3C altered CDKN2A/B spatial organization to suppress senescence. EZH2 inhibition decreased the looping at the CDKN2A/B loci and reduced LCL growth. This study provides a comprehensive view of the spatial organization of chromatin during EBV-driven cellular transformation.},
	issn = {1934-6069},
	doi = {10.1016/j.chom.2017.09.001},
	author = {Jiang, Sizun and Zhou, Hufeng and Liang, Jun and Gerdt, Catherine and Wang, Chong and Ke, Liangru and Schmidt, Stefanie C S and Narita, Yohei and Ma, Yijie and Wang, Shuangqi and Colson, Tyler and Gewurz, Benjamin and Li, Guoliang and Kieff, Elliott and Zhao, Bo}
}
