Nucleic Acids Research Advance Access originally published online on April 30, 2009
Nucleic Acids Research 2009 37(11):3475-3492; doi:10.1093/nar/gkp244
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Nucleic Acids Research, 2009, Vol. 37, No. 11 3475-3492
© 2009 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.
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Replication fork reversal and the maintenance of genome stability
School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK
*To whom correspondence should be addressed. Tel: +44 (0)1224 555183; Fax: +44 (0)1224 555844; Email: p.mcglynn{at}abdn.ac.uk
Received February 26, 2009. Revised March 28, 2009. Accepted March 31, 2009.
The progress of replication forks is often threatened in vivo, both by DNA damage and by proteins bound to the template. Blocked forks must somehow be restarted, and the original blockage cleared, in order to complete genome duplication, implying that blocked fork processing may be critical for genome stability. One possible pathway that might allow processing and restart of blocked forks, replication fork reversal, involves the unwinding of blocked forks to form four-stranded structures resembling Holliday junctions. This concept has gained increasing popularity recently based on the ability of such processing to explain many genetic observations, the detection of unwound fork structures in vivo and the identification of enzymes that have the capacity to catalyse fork regression in vitro. Here, we discuss the contexts in which fork regression might occur, the factors that may promote such a reaction and the possible roles of replication fork unwinding in normal DNA metabolism.
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