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    Replication fork barriers: pausing for a break or stalling for time?

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    Authors
    Labib, Karim
    Hodgson, Ben
    Affiliation
    Cancer Research UK, Paterson Institute for Cancer Research, University of Manchester, Wilmslow Road, Manchester M20 4BX, UK. klabib@picr.man.ac.uk
    Issue Date
    2007-04
    
    Metadata
    Show full item record
    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.
    Citation
    Replication fork barriers: pausing for a break or stalling for time? 2007, 8 (4):346-53 EMBO Rep.
    Journal
    EMBO Reports
    URI
    http://hdl.handle.net/10541/70326
    DOI
    10.1038/sj.embor.7400940
    PubMed ID
    17401409
    Type
    Article
    Language
    en
    ISSN
    1469-221X
    ae974a485f413a2113503eed53cd6c53
    10.1038/sj.embor.7400940
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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