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Genes 2017, 8(1), 33;

Replication Fork Protection Factors Controlling R-Loop Bypass and Suppression

Terry Fox Laboratory, British Columbia Cancer Agency, 675 West 10th Ave., Vancouver, BC V5Z1L3, Canada
Author to whom correspondence should be addressed.
Academic Editor: Frédéric Chédin
Received: 28 October 2016 / Revised: 2 January 2017 / Accepted: 9 January 2017 / Published: 14 January 2017
(This article belongs to the Special Issue R-loop Biology in Eukaryotes)
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Replication–transcription conflicts have been a well-studied source of genome instability for many years and have frequently been linked to defects in RNA processing. However, recent characterization of replication fork-associated proteins has revealed that defects in fork protection can directly or indirectly stabilize R-loop structures in the genome and promote transcription–replication conflicts that lead to genome instability. Defects in essential DNA replication-associated activities like topoisomerase, or the minichromosome maintenance (MCM) helicase complex, as well as fork-associated protection factors like the Fanconi anemia pathway, both appear to mitigate transcription–replication conflicts. Here, we will highlight recent advances that support the concept that normal and robust replisome function itself is a key component of mitigating R-loop coupled genome instability. View Full-Text
Keywords: R-loop; DNA replication stress; DNA repair; transcription–replication conflict R-loop; DNA replication stress; DNA repair; transcription–replication conflict

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Chang, E.Y.-C.; Stirling, P.C. Replication Fork Protection Factors Controlling R-Loop Bypass and Suppression. Genes 2017, 8, 33.

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