The RAG2 C terminus suppresses genomic instability and lymphomagenesis

Ludovic Deriano, Julie Chaumeil, Marc Coussens, Asha Multani, YiFan Chou, Alexander V. Alekseyenko, Sandy Chang, Jane A. Skok and David B. Roth ()
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Ludovic Deriano: New York University School of Medicine
Julie Chaumeil: New York University School of Medicine
Marc Coussens: New York University School of Medicine
Asha Multani: The M.D. Anderson Cancer Center
YiFan Chou: New York University School of Medicine
Alexander V. Alekseyenko: Center for Health Informatics and Bioinformatics, New York University School of Medicine
Sandy Chang: Yale University School of Medicine
Jane A. Skok: New York University School of Medicine
David B. Roth: New York University School of Medicine

Nature, 2011, vol. 471, issue 7336, 119-123

Abstract: RAG2's tail adds stability Misrepair of DNA double-strand breaks produced by the V(D)J recombinase (the RAG1/RAG2 proteins) at immunoglobulin (Igh) and T-cell receptor (Tcr) loci has been implicated in pathogenesis of lymphoid malignancies. In this paper, the authors show that the RAG2 C-terminus is critical for maintaining genomic stability, despite being dispensable for V(D)J recombination. Rag2c/c p53−/− mice, unlike Rag1c/c p53−/− and p53−/− animals, rapidly develop thymic lymphomas bearing complex chromosomal translocations, amplifications and deletions involving the Tcrα/δ and Igh loci. These results reveal a new 'genome guardian' role for RAG2 and suggest that similar defects in end release and end persistence might underlie genomic instability and lymphomagenesis in Rag2c/c p53−/− and Atm−/− mice.

Date: 2011
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DOI: 10.1038/nature09755

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