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dc.contributor.authorLabib, Karim
dc.contributor.authorHodgson, Ben
dc.date.accessioned2009-06-12T14:00:34Z
dc.date.available2009-06-12T14:00:34Z
dc.date.issued2007-04
dc.identifier.citationReplication fork barriers: pausing for a break or stalling for time? 2007, 8 (4):346-53 EMBO Rep.en
dc.identifier.issn1469-221X
dc.identifier.pmid17401409
dc.identifier.doi10.1038/sj.embor.7400940
dc.identifier.urihttp://hdl.handle.net/10541/70326
dc.description.abstractDefects in chromosome replication can lead to translocations that are thought to result from recombination events at stalled DNA replication forks. The progression of forks is controlled by an essential DNA helicase, which unwinds the parental duplex and can stall on encountering tight protein-DNA complexes. Such pause sites are hotspots for recombination and it has been proposed that stalled replisomes disassemble, leading to fork collapse. However, in both prokaryotes and eukaryotes it now seems that paused forks are surprisingly stable, so that DNA synthesis can resume without recombination if the barrier protein is removed. Recombination at stalled forks might require other events that occur after pausing, or might be dependent on features of the surrounding DNA sequence. These findings have important implications for our understanding of the regulation of genome stability in eukaryotic cells, in which pausing of forks is mediated by specific proteins that are associated with the replicative helicase.
dc.language.isoenen
dc.subject.meshAnimals
dc.subject.meshChromosomes
dc.subject.meshDNA Replication
dc.subject.meshEscherichia coli
dc.subject.meshRecombination, Genetic
dc.subject.meshSaccharomycetales
dc.subject.meshSchizosaccharomyces
dc.titleReplication fork barriers: pausing for a break or stalling for time?en
dc.typeArticleen
dc.contributor.departmentCancer Research UK, Paterson Institute for Cancer Research, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK. klabib@picr.man.ac.uken
dc.identifier.journalEMBO Reportsen
html.description.abstractDefects in chromosome replication can lead to translocations that are thought to result from recombination events at stalled DNA replication forks. The progression of forks is controlled by an essential DNA helicase, which unwinds the parental duplex and can stall on encountering tight protein-DNA complexes. Such pause sites are hotspots for recombination and it has been proposed that stalled replisomes disassemble, leading to fork collapse. However, in both prokaryotes and eukaryotes it now seems that paused forks are surprisingly stable, so that DNA synthesis can resume without recombination if the barrier protein is removed. Recombination at stalled forks might require other events that occur after pausing, or might be dependent on features of the surrounding DNA sequence. These findings have important implications for our understanding of the regulation of genome stability in eukaryotic cells, in which pausing of forks is mediated by specific proteins that are associated with the replicative helicase.


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