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Zhang, X. ; Schuhmachers, P.* ; Mourao, A. ; Giansanti, P.* ; Murer, A.* ; Thumann, S. ; Kuklik-Roos, C. ; Beer, S. ; Hauck, S.M. ; Hammerschmidt, W. ; Kuppers, R.* ; Kuster, B.* ; Raab, M.* ; Strebhardt, K.* ; Sattler, M. ; Münz, C.* ; Kempkes, B.

PLK1-dependent phosphorylation restrains EBNA2 activity and lymphomagenesis in EBV-infected mice.

EMBO Rep.:e53007 (2021)

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While Epstein-Barr virus (EBV) establishes a life-long latent infection in apparently healthy human immunocompetent hosts, immunodeficient individuals are at particular risk to develop lymphoproliferative B-cell malignancies caused by EBV. A key EBV protein is the transcription factor EBV nuclear antigen 2 (EBNA2), which initiates B-cell proliferation. Here, we combine biochemical, cellular, and in vivo experiments demonstrating that the mitotic polo-like kinase 1 (PLK1) binds to EBNA2, phosphorylates its transactivation domain, and thereby inhibits its biological activity. EBNA2 mutants that impair PLK1 binding or prevent EBNA2 phosphorylation are gain-of-function mutants. They exhibit enhanced transactivation capacities, accelerate the proliferation of infected B cells, and promote the development of monoclonal B-cell lymphomas in infected mice. Thus, PLK1 coordinates the activity of EBNA2 to attenuate the risk of tumor incidences in favor of the establishment of latency in the infected but healthy host.

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Publication type Article: Journal article

Document type Scientific Article

Corresponding Author

Keywords B-lymphomagenesis ; Ebna2 ; Ebv ; Plk1 ; Humanized Mice; Epstein-barr-virus; Polo-like Kinase; Nuclear-protein-2 Acidic Domain; Box Domain; Physical Interaction; Plk1; Binding; Target; Hyperphosphorylation; Transactivation

ISSN (print) / ISBN 1469-221X

e-ISSN 1469-3178

Journal EMBO Reports

Quellenangaben Article Number: e53007

Publisher EMBO Press

Publishing Place 111 River St, Hoboken 07030-5774, Nj Usa

Non-patent literature Publications

Reviewing status Peer reviewed

Institute(s) Research Unit Gene Vector (AGV)
Institute of Structural Biology (STB)
CF Metabolomics & Proteomics (CF-MPC)

Grants Swiss National Science Foundation
Cancer Research Switzerland
China-Scholarship-Council