Modulation of Enhancer Looping and Differential Gene Targeting by Epstein-Barr Virus Transcription Factors Directs Cellular Reprogramming
Figure 9
EBNA 3 protein binding at the BCL2L11 promoter in EBV-infected cells.
(A) EBNA 3 sequencing reads from immunoprecipitated Mutu III DNA plotted as in Figure 3. Panels B–D show ChIP-QPCR carried out in Mutu III cells and panels F–G show data from the PER253 B95.8 LCL. Precipitated DNA was analysed using primer sets located at the binding site (set B) or regions on either side of the binding site (sets A and C). 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 (E) ChIP using anti-EBNA 3A antibodies. (C) and (F) ChIP using anti-EBNA 3B antibodies. (D) and (G) ChIP using anti-EBNA 3C antibodies. Percentage input signals, after subtraction of no antibody controls, are shown as the mean −/+ range of two independent experiments.