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Breaking down cell cycle checkpoints and DNA repair during antigen receptor gene assembly

Oncogene volume 26, pages 7759–7764 (2007)Cite this article

Abstract

Double-strand breaks (DSBs) are intermediates in several physiological processes including V(D)J and class switch recombination. They are also potent substrates for chromosomal translocations that arise as by-products of antigen receptor gene assembly in lymphocytes. ATM is one among several key proteins involved in the detection, signaling and repair of DNA breaks. Despite redundancies in DSB signaling pathways, it has recently been demonstrated that ATM deficient lymphocytes can survive and proliferate several generations in vitro and in vivo despite harboring terminally deleted chromosomes produced by V(D)J recombination. In this review, we discuss how two complementary genome maintenance functions mediated by ATM prevent lymphocytes from adapting to persistent DNA damage.

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Authors and Affiliations

  1. Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA

    E Callén & A Nussenzweig

  2. Laboratory of Molecular Immunology, The Rockefeller University, New York, NY, USA

    M C Nussenzweig

  3. Howard Hughes Medical Institute, New York, NY, USA

    M C Nussenzweig

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  1. E Callén
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Correspondence to E Callén.

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Callén, E., Nussenzweig, M. & Nussenzweig, A. Breaking down cell cycle checkpoints and DNA repair during antigen receptor gene assembly. Oncogene 26, 7759–7764 (2007). https://doi.org/10.1038/sj.onc.1210873

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