Please use this identifier to cite or link to this item: http://bura.brunel.ac.uk/handle/2438/13012
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dc.contributor.authorDimude, JU-
dc.contributor.authorMidgley-Smith, SL-
dc.contributor.authorStein, M-
dc.contributor.authorRudolph, C-
dc.date.accessioned2016-07-25T14:20:30Z-
dc.date.available2016-07-25-
dc.date.available2016-07-25T14:20:30Z-
dc.date.issued2016-
dc.identifier.citationGenes, 7(8):40, pp. 1-22, (2016)en_US
dc.identifier.issn2073-4425-
dc.identifier.urihttp://www.mdpi.com/2073-4425/7/8/40-
dc.identifier.urihttp://bura.brunel.ac.uk/handle/2438/13012-
dc.description.abstractDuplication of bacterial chromosomes is initiated via the assembly of two replication forks at a single defined origin. Forks proceed bi-directionally until they fuse in a specialised termination area opposite the origin. This area is flanked by polar replication fork pause sites that allow forks to enter but not to leave. The precise function of this replication fork trap has remained enigmatic, as no obvious phenotypes have been associated with its inactivation. However, the fork trap becomes a serious problem to cells if the second fork is stalled at an impediment, as replication cannot be completed, suggesting that a significant evolutionary advantage for maintaining this chromosomal arrangement must exist. Recently, we demonstrated that head-on fusion of replication forks can trigger over-replication of the chromosome. This over-replication is normally prevented by a number of proteins including RecG helicase and 3’ exonucleases. However, even in the absence of these proteins it can be safely contained within the replication fork trap, highlighting that multiple systems might be involved in coordinating replication fork fusions. Here, we discuss whether considering the problems associated with head-on replication fork fusion events helps us to better understand the important role of the replication fork trap in cellular metabolism.en_US
dc.description.sponsorshipThe authors wish to thank Christian Lesterlin and Ole Skovgaard for critical reading of the manuscript. C.J.R. is supported by a grant from the Biotechnology and Biological Sciences Research Council [BB/K015729/1].en_US
dc.language.isoenen_US
dc.publisherMDPIen_US
dc.subjectTermination of DNA replicationen_US
dc.subjectFork collisionsen_US
dc.subjectRecGen_US
dc.subjectHomologous recombinationen_US
dc.subjectCo-orientation of replication and transcriptionen_US
dc.titleReplication termination: Containing fork fusion-mediated pathologies in escherichia colien_US
dc.typeArticleen_US
dc.identifier.doihttp://dx.doi.org/10.3390/genes7080040-
dc.relation.isPartOfGenes-
pubs.publication-statusPublished-
Appears in Collections:Dept of Life Sciences Research Papers

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