Viral oncogene EBNALP regulates YY1 DNA binding and alters host 3D genome organization

ABSTRACT: The Epstein-Barr virus (EBV) nuclear antigen leader protein (EBNALP) is essential for the immortalization of naïve B lymphocytes (NBLs). However, the mechanisms remain elusive. To understand EBNALP's role in B cell transformation, we compare NBLs infected with wild-type EBV and an EBNALP-null mutant EBV using multi-omics techniques. EBNALP inactivation alters enhancer-promoter interactions, resulting in decreased CCND2 and increased CASP1 and BCL2L11 expression. Mechanistically, EBNALP interacts with and colocalizes with the looping factor YY1. Depletion of EBNALP reduces YY1 DNA binding and enhancer-promoter interactions, similar to effects observed with YY1 depletion. Furthermore, EBNALP colocalizes with DPF2, a protein that binds to H3K14ac and H4K16ac. CRISPR depletion of DPF2 reduces

SUBMITTER: Chong Wang 

PROVIDER: S-SCDT-10_1038-S44319-024-00357-6 | biostudies-other |

REPOSITORIES: biostudies-other