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Glaser, L.V. ; Rieger, S. ; Thumann, S. ; Beer, S. ; Kuklik-Roos, C. ; Martin, D.E.* ; Maier, K.C.* ; Harth-Hertle, M.L. ; Grüning, B.* ; Backofen, R.* ; Krebs, S.* ; Blum, H.* ; Zimmer, R.* ; Erhard, F.* ; Kempkes, B.

EBF1 binds to EBNA2 and promotes the assembly of EBNA2 chromatin complexes in B cells.

PLoS Pathog. 13, e1006664:e1006664 (2017)
Publ. Version/Full Text Postprint Research data DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Epstein-Barr virus (EBV) infection converts resting human B cells into permanently proliferating lymphoblastoid cell lines (LCLs). The Epstein-Barr virus nuclear antigen 2 (EBNA2) plays a key role in this process. It preferentially binds to B cell enhancers and establishes a specific viral and cellular gene expression program in LCLs. The cellular DNA binding factor CBF1/CSL serves as a sequence specific chromatin anchor for EBNA2. The ubiquitous expression of this highly conserved protein raises the question whether additional cellular factors might determine EBNA2 chromatin binding selectively in B cells. Here we used CBF1 deficient B cells to identify cellular genes up or downregulated by EBNA2 as well as CBF1 independent EBNA2 chromatin binding sites. Apparently, CBF1 independent EBNA2 target genes and chromatin binding sites can be identified but are less frequent than CBF1 dependent EBNA2 functions. CBF1 independent EBNA2 binding sites are highly enriched for EBF1 binding motifs. We show that EBNA2 binds to EBF1 via its N-terminal domain. CBF1 proficient and deficient B cells require EBF1 to bind to CBF1 independent binding sites. Our results identify EBF1 as a co-factor of EBNA2 which conveys B cell specificity to EBNA2.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Virus Nuclear Antigen-2; Lymphocyte Growth Transformation; Rbp-j-kappa; Transcription Factors; Gene-expression; Induce Expression; Estrogen Action; Notch Pathway; Genome-wide; Protein
ISSN (print) / ISBN 1553-7366
e-ISSN 1553-7374
Journal PLoS Pathogens
Quellenangaben Volume: 13, Issue: 10, Pages: e1006664 Article Number: e1006664 Supplement: ,
Publisher Public Library of Science (PLoS)
Publishing Place San Francisco
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Research Unit Gene Vector (AGV)