GSE75385
Combinatorial Control of RBP-jk and EBF1 Chromosome Occupancy induced by viral co-activator EBNA2 [expression array]
Gene expression programs depend on sequence-specific DNA binding transcription factors, but the mechanisms that control the selective binding of these factors in a chromosomal and genomic context remain enigmatic.   Here, we show that two master regulators of B-cell fate, namely EBF1 and RBP-jk, show variable genome-wide chromosome distribution in two related B-lymphocyte lines carrying different forms of Epstein-Barr Virus (EBV) latency.  The latency-type specific EBV-encoded EBNA2 colocalized with RBP-jk and EBF1 at induced binding sites.  Colocalization of EBF1, RBP-jk, and EBNA2 correlated with transcriptional activation.  Conditional expression or repression of EBNA2 lead to a rapid alteration in RBP-jk and EBF1 binding.  Biochemical and shRNA depletion studies provide evidence for cooperative assembly at co-occupied sites.  These findings reveal that non-DNA binding cofactors can facilitate combinatorial interactions to induce new patterns of transcription factor occupancy and gene programming Overall design: Examination of EBNA2/EBF1/EBP-jk binding and gene expression differences in MutuI and LCL cell lines