Modulation of Enhancer Looping and Differential Gene Targeting by Epstein-Barr Virus Transcription Factors Directs Cellular Reprogramming
Figure 7
EBNA 2 and EBNA 3 protein binding at the ITGAL promoter in EBV-infected cells.
(A) EBNA 2 (green) and EBNA 3 (red) sequencing reads from immunoprecipitated Mutu III DNA plotted as in Figure 3. Panels B–E show ChIP-QPCR carried out in Mutu III cells and panels F–I show data from the PER253 B95.8 LCL. Precipitated DNA was analysed using primer sets located at the binding sites (sets B, D, and F) or regions adjacent to the binding sites (sets A, C, and E). Binding signals at the CTBP2 binding site in the same ChIP experiments are shown as a positive control and primers spanning the transcription start site of the cellular gene PPIA provide a background binding control (indicated by dotted lines). (B) and (F) ChIP using anti-EBNA 2 antibodies. (C) and (G) ChIP using anti-EBNA 3A antibodies. (D) and (H) ChIP using anti-EBNA 3B antibodies. (E) and (I) ChIP using anti-EBNA 3C antibodies. Percentage input signals, after subtraction of no antibody controls, are shown as the mean −/+ range of two independent ChIP experiments.