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MRE11-RAD50-NBS1 promotes Fanconi Anemia R-loop suppression at transcription–replication conflicts
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Journal Article
MRE11-RAD50-NBS1 promotes Fanconi Anemia R-loop suppression at transcription–replication conflicts
2019
Overview
Ectopic R-loop accumulation causes DNA replication stress and genome instability. To avoid these outcomes, cells possess a range of anti-R-loop mechanisms, including RNaseH that degrades the RNA moiety in R-loops. To comprehensively identify anti-R-loop mechanisms, we performed a genome-wide trigenic interaction screen in yeast lacking
RNH1
and
RNH201
. We identified >100 genes critical for fitness in the absence of RNaseH, which were enriched for DNA replication fork maintenance factors including the MRE11-RAD50-NBS1 (MRN) complex. While MRN has been shown to promote R-loops at DNA double-strand breaks, we show that it suppresses R-loops and associated DNA damage at transcription–replication conflicts. This occurs through a non-nucleolytic function of MRE11 that is important for R-loop suppression by the Fanconi Anemia pathway. This work establishes a novel role for MRE11-RAD50-NBS1 in directing tolerance mechanisms at transcription–replication conflicts.
Accumulations of R-loops can lead to genome instability. Here the authors reveal a role for the MRN complex in suppressing R-loops and associated DNA damage at transcription–replication conflicts.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 14
/ 14/1
/ 14/63
/ 42
/ 45
/ 45/15
/ 49
/ 49/40
/ Acid Anhydride Hydrolases - genetics
/ Acid Anhydride Hydrolases - metabolism
/ Anemia
/ Cell Cycle Proteins - genetics
/ Cell Cycle Proteins - metabolism
/ DNA
/ DNA-Binding Proteins - genetics
/ DNA-Binding Proteins - metabolism
/ Fitness
/ Genomes
/ Genomic Instability - genetics
/ Humanities and Social Sciences
/ Humans
/ MRE11 Homologue Protein - genetics
/ MRE11 Homologue Protein - metabolism
/ Nuclear Proteins - metabolism
/ R-Loop Structures - genetics
/ R-loops
/ RNA
/ Schizosaccharomyces - genetics
/ Science
/ Transcription, Genetic - genetics
/ Yeast
