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Published 24 May 2004. doi:10.1083/jcb.200403021
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 165, Number 4, 459-464
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53BP1 is required for class switch recombination



Irene M. Ward1, Bernardo Reina-San-Martin4, Alexandru Olaru5, Kay Minn1, Koji Tamada2, Julie S. Lau2, Marilia Cascalho3, Lieping Chen2, Andre Nussenzweig6, Ferenc Livak5, Michel C. Nussenzweig4, and Junjie Chen1

1 Division of Oncology Research, Mayo Clinic, Rochester, MN 55905
2 Division of Immunology, Mayo Clinic, Rochester, MN 55905
3 Transplantation Biology, Mayo Clinic, Rochester, MN 55905
4 Laboratory of Molecular Immunology, Howard Hughes Medical Institute, The Rockefeller University, New York, NY 10021
5 Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201
6 Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892

Address correspondence to Junjie Chen, 1306 Guggenheim, Mayo Clinic, 200 First St., SW, Rochester, MN 55905. Tel.: (507) 538-1545. Fax: (507) 284-3906. email: Chen.junjie{at}mayo.edu

53BP1 participates early in the DNA damage response and is involved in cell cycle checkpoint control. Moreover, the phenotype of mice and cells deficient in 53BP1 suggests a defect in DNA repair (Ward et al., 2003b). Therefore, we asked whether or not 53BP1 would be required for the efficient repair of DNA double strand breaks. Our data indicate that homologous recombination by gene conversion does not depend on 53BP1. Moreover, 53BP1-deficient mice support normal V(D)J recombination, indicating that 53BP1 is not required for "classic" nonhomologous end joining. However, class switch recombination is severely impaired in the absence of 53BP1, suggesting that 53BP1 facilitates DNA end joining in a way that is not required or redundant for the efficient closing of RAG-induced strand breaks. These findings are similar to those observed in mice or cells deficient in the tumor suppressors ATM and H2AX, further suggesting that the functions of ATM, H2AX, and 53BP1 are closely linked.

Key Words: NHEJ; ATM; H2AX; V(D)J recombination; DNA repair

Abbreviations used in this paper: CSR, class switch recombination; DSB, double strand break; HR, homologous recombination; I, intronic; IR, ionizing radiation; NHEJ, nonhomologous end joining; PFGE, pulse field gel electrophoresis; TCR, T cell receptor.


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