Journal
GENES
Volume 8, Issue 1, Pages -Publisher
MDPI
DOI: 10.3390/genes8010033
Keywords
R-loop; DNA replication stress; DNA repair; transcription-replication conflict
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Funding
- Canadian Cancer Society [703263]
- CIHR [MOP-136982]
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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.
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