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Nucleic Acids Research 2005 33(21):6733-6742; doi:10.1093/nar/gki983
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Published online 27 November 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oxfordjournals.org

Article

Lack of MSH2 involvement differentiates V(D)J recombination from other non-homologous end joining events

Mani Larijani*, Ahmad Zaheen, Darina Frieder, Yuxun Wang1, Gillian E. Wu2, Winfried Edelmann1 and Alberto Martin

Department of Immunology, University of Toronto Medical Sciences Building 5265, Toronto, Canada, M5S 1A8 1Department of Cell Biology, Albert Einstein College of Medicine 1300 Morris Park Avenue Bronx, NY 10461, USA 2Faculty of Science and Engineering, York University Toronto, Ontario, Canada, M3J 1P3

*To whom correspondence should be addressed. Tel: +1 416 978 4235; Fax: +1 416 978 1938; Email: mani.larijani{at}utoronto.ca

Received October 21, 2005. Revised November 9, 2005. Accepted November 9, 2005.

V(D)J recombination and class switch recombination are the two DNA rearrangement events used to diversify the mouse and human antibody repertoires. While their double strand breaks (DSBs) are initiated by different mechanisms, both processes use non-homologous end joining (NHEJ) in the repair phase. DNA mismatch repair elements (MSH2/MSH6) have been implicated in the repair of class switch junctions as well as other DNA DSBs that proceed through NHEJ. MSH2 has also been implicated in the regulation of factors such as ATM and the MRN (Mre11, Rad50, Nbs1) complex, which are involved in V(D)J recombination. These findings led us to examine the role of MSH2 in V(D)J repair. Using MSH2–/– and MSH2+/+ mice and cell lines, we show here that all pathways involving MSH2 are dispensable for the generation of an intact pre-immune repertoire by V(D)J recombination. In contrast to switch junctions and other DSBs, the usage of terminal homology in V(D)J junctions is not influenced by MSH2. Thus, whether the repair complex for V(D)J recombination is of a canonical NHEJ type or a separate microhomology-mediated-end joining (MMEJ) type, it does not involve MSH2. This highlights a distinction between the repair of V(D)J recombination and other NHEJ reactions.

Correspondence may also be addressed to Alberto Martin. Tel: +1 416 978 4230; Fax: +1 416 978 1938; Email: alberto.martin{at}utoronto.ca


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