The Journal of Experimental Medicine
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Published 6 May 2002. doi:10.1084/jem.20011858
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© Rockefeller University Press, 0022-1007/2002/5/1193/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 9, May 6, 2002 1193-1198

Brief Definitive Report

 The Activation-induced Deaminase Functions in a Postcleavage Step of the Somatic Hypermutation Process

F. Nina Papavasiliou1 and David G. Schatz2

1 Laboratory of Lymphocyte Biology, The Rockefeller University, New York, NY 10021
2 Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520

Address correspondence to F. Nina Papavasiliou, Laboratory of Lymphocyte Biology, The Rockefeller University, Box 39, 1230 York Ave., New York, NY 10021. Phone: 212-327-7857; Fax: 212-327-7319; E-mail: papavasiliou{at}rockefeller.edu

Activation of B cells by antigen fuels two distinct molecular modifications of immunoglobulin (Ig) genes. Class-switch recombination (CSR) replaces the Igµ heavy chain constant region with a downstream constant region gene, thereby altering the effector function of the resulting antibodies. Somatic hypermutation (SHM) introduces point mutations into the variable regions of Ig genes, thereby changing the affinity of antibody for antigen. Mechanistic overlap between the two reactions has been suggested by the finding that both require the activation-induced cytidine deaminase (AID). It has been proposed that AID initiates both CSR and SHM by activating a common nuclease. Here we provide evidence that cells lacking AID, or expressing a dominant negative form of the protein, are still able to incur DNA lesions in SHM target sequences. The results indicate that an intact cytidine deaminase motif is required for AID function, and that AID acts downstream of the initial DNA lesions in SHM.

Key Words: somatic hypermutation • AID • DNA double-strand breaks • B lymphocyte • Ig gene


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