EBNA2 Drives Formation of New Chromosome Binding Sites and Target Genes for B-Cell Master Regulatory Transcription Factors RBP-jκ and EBF1
Fig 5
EBNA2-dependent transcription factor redistribution in chromatin occupancy.
EREB2.5 cells were treated with (+) or without (-) estradiol (E2) for 24 or 48 hrs and then assayed by ChIP for binding to EBF1 (A and B), RBP-jκ (C and D), or EBNA2 (E and F) at cellular (A, C, E) or EBV genome sites (B, D, F). Actin genomic region (cellular) or Qp (EBV) was used as negative binding control for EBF1, RBP-jκ, ορ EBNA2 ChIP. (G) ChIP binding for CTCF, PU.1, or PAX5 in EREB2.5 cells treated (blue) or untreated (red) with E2 for 48 hrs. PPP1R1B or KCTD17 genomic region was negative binding control PU.1 or PAX5, respectively. Asterisk indicates p < 0.05. (H) Western blot showing protein levels for EBF1, RBP-jκ, EBNA2, Actin, and CTCF in EREB2.5 cells at 24 and 48 hrs after E2 withdrawal.