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Molecular and Cellular Biology, January 2008, p. 154-164, Vol. 28, No. 1
0270-7306/08/$08.00+0     doi:10.1128/MCB.00816-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Transcription-Associated Recombination Is Dependent on Replication in Mammalian Cells ^,

Institute for Cancer Studies, Medical School, University of Sheffield, Beech Hill Road, Sheffield S10 2RX,¹ Radiation Oncology & Biology, Radiobiology Research Institute, Churchill Hospital, Headington, Oxford OX3 7LJ, United Kingdom,² Department of Genetics, Microbiology and Toxicology, Arrhenius Laboratory, Stockholm University, S-106 91 Stockholm, Sweden³

Received 9 May 2007/ Returned for modification 11 June 2007/ Accepted 17 October 2007

Transcription can enhance recombination; this is a ubiquitous phenomenon from prokaryotes to higher eukaryotes. However, the mechanism of transcription-associated recombination in mammalian cells is poorly understood. Here we have developed a construct with a recombination substrate in which levels of recombination can be studied in the presence or absence of transcription. We observed a direct enhancement in recombination when transcription levels through the substrate were increased. This increase in homologous recombination following transcription is locus specific, since homologous recombination at the unrelated hprt gene is unaffected. In addition, we have shown that transcription-associated recombination involves both short-tract and long-tract gene conversions in mammalian cells, which are different from double-strand-break-induced recombination events caused by endonucleases. Transcription fails to enhance recombination in cells that are not in the S phase of the cell cycle. Furthermore, inhibition of transcription suppresses induction of recombination at stalled replication forks, suggesting that recombination may be involved in bypassing transcription during replication.

Published ahead of print on 29 October 2007.

Supplemental material for this article may be found at http://mcb.asm.org/.

^# These authors contributed equally to this study.

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