Nucleic Acids Research Advance Access originally published online on May 5, 2007
Nucleic Acids Research 2007 35(11):3551-3560; doi:10.1093/nar/gkm243
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Nucleic Acids Research, 2007, Vol. 35, No. 11 3551-3560
© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Molecular Biology |
Involvement of DNA polymerase µ in the repair of a specific subset of DNA double-strand breaks in mammalian cells
1Genetic instability and Cancer group, Institute of Pharmacology and Structural Biology, University Paul Sabatier, UMR CNRS 5089, 205 route de Narbonne, 31077 Toulouse cedex and 2Département de Radiobiologie et Radiopathologie, 60-68 av. Général Leclerc, UMR 217 CNRS-CEA, 92265 Fontenay aux Roses cedex, France
*To whom correspondence should be addressed. Tel: +33 5 6117 5861; Fax: +33 5 6117 5994; Email: Yvan.Canitrot{at}ipbs.fr Correspondence may also be addressed to Jean-Sébastien Hoffmann. Tel: +33 5 6117 5975; Fax: +33 5 6117 5994; Email: jseb{at}ipbs.fr
Received February 27, 2007. Revised April 2, 2007. Accepted April 3, 2007.
The repair of DNA double-strand breaks (DSB) requires processing of the broken ends to complete the ligation process. Recently, it has been shown that DNA polymerase µ (polµ) and DNA polymerase 
(pol) are both involved in such processing during non-homologous end joining in vitro. However, no phenotype was observed in animal models defective for either polµ and/or pol. Such observations could result from a functional redundancy shared by the X family of DNA polymerases. To avoid such redundancy and to clarify the role of polµ in the end joining process, we generated cells over-expressing the wild type as well as an inactive form of polµ (polµD). We observed that cell sensitivity to ionizing radiation (IR) was increased when either polµ or polµD was over-expressed. However, the genetic instability in response to IR increased only in cells expressing polµD. Moreover, analysis of intrachromosomal repair of the I-SceI-induced DNA DSB, did not reveal any effect of either polµ or polµD expression on the efficiency of ligation of both cohesive and partially complementary ends. Finally, the sequences of the repaired ends were specifically affected when polµ or polµD was over-expressed, supporting the hypothesis that polµ could be involved in the repair of a DSB subset when resolution of junctions requires some gap filling.
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