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RAD52 resolves replication-transcription collisions to mitigate R-loop induced genome instability

GSE266483 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2024/07/11 Platform GPL24676
Summary
Collisions of transcription and replication machinery on the same DNA strand can pose a significant threat to genomic stability. These collision occur in part due to of RNA-DNA hybrids termed R-loops, in which a newly synthesized RNA molecule hybridizes with the DNA template strand. This study investigated the novel role of RAD52, a known DNA repair factor, in preventing collisions by managing R-loop formation and resolution. We show that RAD52 deficiency increases R-loop accumulation, exacerbating collisions and resulting in elevated DNA damage. Further, RAD52's ability to interact with the transcription machinery, coupled with its capacity to facilitate R-loop dissolution, highlights its role in preventing collisions. Lastly, we provide the first evidence of an increased mutational burden at conserved R-loop sites in human tumor samples. In summary, this study underscores the importance of RAD52 in orchestrating the delicate balance between replication and transcription processes to prevent collisions and maintain genome stability.
Published in
RAD52 resolves transcription-replication conflicts to mitigate R-loop induced genome instability
Jalan M, Sharma A, Pei X et al. · Nature communications 2024 · PMID 39237529 · doi:10.1038/s41467-024-51784-x
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Also filed as BioProject PRJNA1056281 and SRA study SRP479833. Searching any of these in the dataset finder brings you back here.

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