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Nucleic Acids Research 2006 34(8):2269-2279; doi:10.1093/nar/gkl258
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Published online 2 May 2006

© The Author 2006. 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@oxfordjournals.org

Article

Mobile D-loops are a preferred substrate for the Bloom's syndrome helicase

Csanád Z. Bachrati, Rhona H. Borts1 and Ian D. Hickson*

Cancer Research UK Laboratories, Weatherall Institute of Molecular Medicine, University of Oxford, John Radcliffe Hospital Oxford, OX3 9DS, UK 1 Department of Genetics, University of Leicester Leicester LE1 7RH, UK

*To whom correspondence should be addressed. Tel: +44 1865 222 417; Fax: +44 1865 222 431; Email: ian.hickson{at}cancer.org.uk

Received January 9, 2006. Revised February 1, 2006. Accepted March 31, 2006.

The Bloom's syndrome helicase, BLM, is a member of the highly conserved RecQ family, and possesses both DNA unwinding and DNA strand annealing activities. BLM also promotes branch migration of Holliday junctions. One role for BLM is to act in conjunction with topoisomerase III{alpha} to process homologous recombination (HR) intermediates containing a double Holliday junction by a process termed dissolution. However, several lines of evidence suggest that BLM may also act early in one or more of the recombination pathways to eliminate illegitimate or aberrantly paired DNA joint molecules. We have investigated whether BLM can disrupt DNA displacement loops (D-loops), which represent the initial strand invasion step of HR. We show that mobile D-loops created by the RecA recombinase are a highly preferred substrate for BLM with the invading strand being displaced from the duplex. We have identified structural features of the D-loop that determine the efficiency with which BLM promotes D-loop dissociation. We discuss these results in the context of models for the role of BLM as an ‘anti-recombinase’.


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