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¹ Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Department of Cancer Biology. Institut National de la Santé et de la Recherche Médicale U964-Centre National de la Recherche Scientifique UMR7104, Université de Strasbourg, 67404 Illkirch, France
² Poly(ADP-ribosyl)ation et Intégrité du Génome, IREBS-FRE3211 Centre National de la Recherche Scientifique, Université de Strasbourg, Ecole Supérieure de Biotechnologie de Strasbourg, 67412 Illkirch, France

CORRESPONDENCE Bernardo Reina-San-Martin: reinab{at}igbmc.fr

Immunoglobulin class switch recombination (CSR) is initiated by DNA breaks triggered by activation-induced cytidine deaminase (AID). These breaks activate DNA damage response proteins to promote appropriate repair and long-range recombination. Aberrant processing of these breaks, however, results in decreased CSR and/or increased frequency of illegitimate recombination between the immunoglobulin heavy chain locus and oncogenes like c-myc. Here, we have examined the contribution of the DNA damage sensors Parp1 and Parp2 in the resolution of AID-induced DNA breaks during CSR. We find that although Parp enzymatic activity is induced in an AID-dependent manner during CSR, neither Parp1 nor Parp2 are required for CSR. We find however, that Parp1 favors repair of switch regions through a microhomology-mediated pathway and that Parp2 actively suppresses IgH/c-myc translocations. Thus, we define Parp1 as facilitating alternative end-joining and Parp2 as a novel translocation suppressor during CSR.

© 2009 Robert et al.
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