ArticleNature communications2022
A POLD3/BLM dependent pathway handles DSBs in transcribed chromatin upon excessive RNA:DNA hybrid accumulation.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Multi-omics profiling reveals homologous recombination repair hyperactivation as a therapeutic vulnerability in neuroendocrine cervical carcinoma.Signal transduction and targeted therapy · 2026Article
- DDX3X regulates DNA repair pathway choice at double-strand breaks via RNA-DNA hybrid formation.Cell death and differentiation · 2026Article
- HELZ is a RNA-DNA helicase that resolves R loops to facilitate homologous recombination repair.Nature communications · 2026Article
- The multiple layers of RNA response in double-strand break repair.Experimental & molecular medicine · 2025Review
- Break-induced replication is activated to repair R-loop-associated double-strand breaks in SETX-deficient cells.Cell reports · 2025Article
- Identification of SUMOylation modifiers involved in lung adenocarcinoma progression and Osimertinib resistance by integrated bioinformatics analysis.Scientific reports · 2025Article
- Transcriptional repression facilitates RNA:DNA hybrid accumulation at DNA double-strand breaks.Nature cell biology · 2025Article
- Discovery of novel serum peptide biomarkers for cholangiocarcinoma recurrence through MALDI-TOF MS and LC-MS/MS peptidome analysis.Scientific reports · 2025Article
- POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024Review
- Hyper-recombination in ribosomal DNA is driven by long-range resection-independent RAD51 accumulation.Nature communications · 2024Article
- Developmental progression of DNA double-strand break repair deciphered by a single-allele resolution mutation classifier.Nature communications · 2024Article
- PSIP1/LEDGF reduces R-loops at transcription sites to maintain genome integrity.Nature communications · 2024Article
- Evidence that Alzheimer's Disease Is a Disease of Competitive Synaptic Plasticity Gone Awry.Journal of Alzheimer's disease : JAD · 2024Review
- Break-induced RNA-DNA hybrids (BIRDHs) in homologous recombination: friend or foe?EMBO reports · 2023Review
- Article
- R-Loops in Genome Instability and Cancer.Cancers · 2023Review
- Mechanisms of insertions at a DNA double-strand break.Molecular cell · 2023Article
- Antecedent chromatin organization determines cGAS recruitment to ruptured micronuclei.Nature communications · 2023Article
- Transcriptional regulation and chromatin dynamics at DNA double-strand breaks.Experimental & molecular medicine · 2022Review
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Authors and funding
17 authors at 2 institutions in 3 countries.
Funding
Abstract
Transcriptionally active loci are particularly prone to breakage and mounting evidence suggests that DNA Double-Strand Breaks arising in active genes are handled by a dedicated repair pathway, Transcription-Coupled DSB Repair (TC-DSBR), that entails R-loop accumulation and dissolution. Here, we uncover a function for the Bloom RecQ DNA helicase (BLM) in TC-DSBR in human cells. BLM is recruited in a transcription dependent-manner at DSBs where it fosters resection, RAD51 binding and accurate Homologous Recombination repair. However, in an R-loop dissolution-deficient background, we find that BLM promotes cell death. We report that upon excessive RNA:DNA hybrid accumulation, DNA synthesis is enhanced at DSBs, in a manner that depends on BLM and POLD3. Altogether our work unveils a role for BLM at DSBs in active chromatin, and highlights the toxic potential of RNA:DNA hybrids that accumulate at transcription-associated DSBs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.