2.50
Hdl Handle:
http://hdl.handle.net/10541/70326
Title:
Replication fork barriers: pausing for a break or stalling for time?
Authors:
Labib, Karim; Hodgson, Ben
Abstract:
Defects 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.
Affiliation:
Cancer Research UK, Paterson Institute for Cancer Research, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK. klabib@picr.man.ac.uk
Citation:
Replication fork barriers: pausing for a break or stalling for time? 2007, 8 (4):346-53 EMBO Rep.
Journal:
EMBO Reports
Issue Date:
Apr-2007
URI:
http://hdl.handle.net/10541/70326
DOI:
10.1038/sj.embor.7400940
PubMed ID:
17401409
Type:
Article
Language:
en
ISSN:
1469-221X
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
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.en
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

Related articles on PubMed

All Items in Christie are protected by copyright, with all rights reserved, unless otherwise indicated.