ArticleNature communications2024
Hyper-recombination in ribosomal DNA is driven by long-range resection-independent RAD51 accumulation.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- A system-level metastable model of cancer evolution: integrating replication stress, cell cycle deregulation and chromosomal instability.Annals of medicine · 2026Review
- Elucidating structure-function relationships in the mammalian nucleolus.Nature reviews. Molecular cell biology · 2026Review
- RAD54L coordinates the nucleolar DNA damage response to maintain rDNA stability.The EMBO journal · 2026Article
- A small molecule disrupts G4-STAT1 interaction and synergizes with olaparib to drive cancer cell death.Nucleic acids research · 2026Article
- Ribosome biogenesis is increased in hepatocellular carcinoma and represents a potential therapeutic target.NAR cancer · 2026Article
- A Double-Edged Role for SIRT7 in Cancer: Can Anti-Cancer Immunity Tip the Balance?Pharmaceuticals (Basel, Switzerland) · 2025Review
- C8orf33 dictates DNA double-strand break repair choice by modulating KAT8-mediated H4K16 acetylation.Cell death & disease · 2025Article
- Nucleolar Organization in Response to Transcriptional Stress.Cancer science · 2025Review
- A High-Throughput ImmunoHistoFluorescence (IHF) Method for Sub-Nuclear Protein Analysis in Tissue.Cells · 2025Article
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
Ribosomal DNA (rDNA) encodes the ribosomal RNA genes and represents an intrinsically unstable genomic region. However, the underlying mechanisms and implications for genome integrity remain elusive. Here, we use Bloom syndrome (BS), a rare genetic disease characterized by DNA repair defects and hyper-unstable rDNA, as a model to investigate the mechanisms leading to rDNA instability. We find that in Bloom helicase (BLM) proficient cells, the homologous recombination (HR) pathway in rDNA resembles that in nuclear chromatin; it is initiated by resection, replication protein A (RPA) loading and BRCA2-dependent RAD51 filament formation. However, BLM deficiency compromises RPA-loading and BRCA1/2 recruitment to rDNA, but not RAD51 accumulation. RAD51 accumulates at rDNA despite depletion of long-range resection nucleases and rDNA damage results in micronuclei when BLM is absent. In summary, our findings indicate that rDNA is permissive to RAD51 accumulation in the absence of BLM, leading to micronucleation and potentially global genomic instability.
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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.