The Journal of Experimental Medicine
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Published online July 2, 2007
doi:10.1084/jem.20070255
The Journal of Experimental Medicine, Vol. 204, No. 7, 1717-1727
The Rockefeller University Press, 0022-1007 $30.00
© 2007 Soulas-Sprauel et al.
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ARTICLE

 Role for DNA repair factor XRCC4 in immunoglobulin class switch recombination

Pauline Soulas-Sprauel1,2, Gwenaël Le Guyader1,2, Paola Rivera-Munoz1,2, Vincent Abramowski1,2, Christelle Olivier-Martin3, Cécile Goujet-Zalc3, Pierre Charneau4, and Jean-Pierre de Villartay1,2,5

1 Institut National de la Santé et de la Recherche Médicale, U768, Paris, F-75015, France
2 Université Paris-Descartes, Faculté de Médecine René Descartes, Site Necker, IFR 94, Paris, F-75015, France
3 Service d'Expérimentation Animale et de Transgénèse, UPS44, Centre National de la Recherche Scientifique, Villejuif, F-94801, France
4 Institut Pasteur, Groupe de Virologie Moléculaire et Vectorologie, Paris, F-75015, France
5 Assistance Publique-Hôpitaux de Paris, Hôpital Necker Enfants Malades, Service d'Immunologie et d'Hématologie Pédiatrique, Paris, F-75015, France

CORRESPONDENCE J.P. de Villartay: devillar{at}necker.fr

V(D)J recombination and immunoglobulin class switch recombination (CSR) are two somatic rearrangement mechanisms that proceed through the introduction of double-strand breaks (DSBs) in DNA. Although the DNA repair factor XRCC4 is essential for the resolution of DNA DSB during V(D)J recombination, its role in CSR has not been established. To bypass the embryonic lethality of XRCC4 deletion in mice, we developed a conditional XRCC4 knockout (KO) using LoxP-flanked XRCC4 cDNA lentiviral transgenesis. B lymphocyte restricted deletion of XRCC4 in these mice lead to an average two-fold reduction in CSR in vivo and in vitro. Our results connect XRCC4 and the nonhomologous end joining DNA repair pathway to CSR while reflecting the possible use of an alternative pathway in the repair of CSR DSB in the absence of XRCC4. In addition, this new conditional KO approach should be useful in studying other lethal mutations in mice.

Abbreviations used: AID, activation-induced cytidine deaminase; CP, cortical plate; CSR, class switch recombination; DSB, double-strand break; E, embryonic day; GT, germline transcript; NHEJ, nonhomologous end joining; RAG, recombination-activating gene; TAP, tandem affinity purification.


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