Replication Fork Protection Factors Controlling R-Loop Bypass and Suppression
AbstractReplication–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
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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.
Chang EY-C, Stirling PC. Replication Fork Protection Factors Controlling R-Loop Bypass and Suppression. Genes. 2017; 8(1):33.Chicago/Turabian Style
Chang, Emily Y.-C.; Stirling, Peter C. 2017. "Replication Fork Protection Factors Controlling R-Loop Bypass and Suppression." Genes 8, no. 1: 33.
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