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

Man Liu, Jamie L. Duke, Daniel J. Richter, Carola G. Vinuesa, Christopher C. Goodnow, Steven H. Kleinstein and David G. Schatz ()
Additional contact information
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
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
Steven H. Kleinstein: Yale University School of Medicine, New Haven, Connecticut 06510, USA
David G. Schatz: Department of Immunobiology,

Nature, 2008, vol. 451, issue 7180, 841-845

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.

Date: 2008
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DOI: 10.1038/nature06547

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