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Two levels of protection for the B cell genome during somatic hypermutation

Author

Listed:
  • Man Liu

    (Department of Immunobiology,)

  • Jamie L. Duke

    (Yale University, New Haven, Connecticut 06511, USA)

  • Daniel J. Richter

    (Broad Institute of MIT and Harvard, 7 Cambridge Center, Cambridge, Massachusetts 02141, USA
    Present address: Department of Molecular and Cell Biology, University of California, Berkeley, California 94720-3200, USA.)

  • Carola G. Vinuesa

    (John Curtin School of Medical Research, The Australian National University)

  • Christopher C. Goodnow

    (John Curtin School of Medical Research, The Australian National University
    Australian Phenomics Facility, Canberra, ACT 2601, Australia)

  • Steven H. Kleinstein

    (Yale University School of Medicine, New Haven, Connecticut 06510, USA
    Yale University, New Haven, Connecticut 06511, USA)

  • David G. Schatz

    (Department of Immunobiology,
    Howard Hughes Medical Institute, New Haven, Connecticut 06510, USA)

Abstract

Hypermutation on a leash Somatic hypermutation, the mechanism by which activated B cells in the blood produce a diversity of immunoglobulin genes giving rise to high-affinity antibodies, plays a vital role in protecting the body from infection. Yet it also represents a major risk to genomic stability, with the potential to generate B-cell tumours if unchecked or wrongly directed. The somatic hypermutation reaction is initiated by activation induced deaminase (AID), and it is widely assumed that the risk of inappropriate hypermutation is averted by careful targeting of this enzyme. New work in mice suggests that this is not the case. Rather, AID deaminates a large fraction of the expressed genome, including numerous oncogenes linked to B-cell malignancies. Widespread mutation of the genome is averted in a surprising manner: by gene-specific, error-free DNA repair mediated by base excision and mismatch repair.

Suggested Citation

  • Man Liu & Jamie L. Duke & Daniel J. Richter & Carola G. Vinuesa & Christopher C. Goodnow & Steven H. Kleinstein & David G. Schatz, 2008. "Two levels of protection for the B cell genome during somatic hypermutation," Nature, Nature, vol. 451(7180), pages 841-845, February.
    • Handle: RePEc:nat:nature:v:451:y:2008:i:7180:d:10.1038_nature06547
    DOI: 10.1038/nature06547
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    Cited by:

    1. Jianli Tao & Qi Wang & Carlos Mendez-Dorantes & Kathleen H. Burns & Roberto Chiarle, 2022. "Frequency and mechanisms of LINE-1 retrotransposon insertions at CRISPR/Cas9 sites," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    2. Daniel Malzl & Mihaela Peycheva & Ali Rahjouei & Stefano Gnan & Kyle N. Klein & Mariia Nazarova & Ursula E. Schoeberl & David M. Gilbert & Sara C. B. Buonomo & Michela Virgilio & Tobias Neumann & Rush, 2023. "RIF1 regulates early replication timing in murine B cells," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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