Visualization and quantification of rDNA instabilities in mammalian cells and mouse models

Nucleic Acids Res. 2026 Jan 14;54(2):gkaf1523. doi: 10.1093/nar/gkaf1523.

Abstract

Ribosomal DNA (rDNA) encodes the 18S, 5.8S, and 28S rRNA, accounting for ∼70% of cellular transcription. Despite its essential role and links to cancer and aging, quantifying rDNA instability in mammals remains challenging due to its repetitive organization and inherent heterogeneity. Here, we developed a murine rDNA FISH probe and genomic tools tailored for laboratory mouse strains. The results confirmed rDNA cluster locations, revealed substantial inter- and intra-strain as well as intercellular heterogeneity in rDNA organization within inbred mice and unstressed cells, and identified sources of spontaneous and replication-associated DNA double-strand breaks in the rDNA transcription termination region. Using mouse embryonic stem cells, we showed that BRCA1-mediated homologous recombination promotes rDNA instability, the non-homologous end joining factor XRCC1, but not Ku, suppresses intra-cluster deletions, and ATM kinase preserves rDNA cluster stability. Together, these findings establish a platform and tools for studying rDNA instability in animal models relevant to aging and cancer research.

MeSH terms

  • Animals
  • Ataxia Telangiectasia Mutated Proteins / genetics
  • Ataxia Telangiectasia Mutated Proteins / metabolism
  • BRCA1 Protein / genetics
  • BRCA1 Protein / metabolism
  • DNA Breaks, Double-Stranded
  • DNA, Ribosomal* / genetics
  • DNA, Ribosomal* / metabolism
  • Genomic Instability*
  • Homologous Recombination
  • In Situ Hybridization, Fluorescence
  • Ku Autoantigen / genetics
  • Ku Autoantigen / metabolism
  • Mice
  • X-ray Repair Cross Complementing Protein 1 / genetics
  • X-ray Repair Cross Complementing Protein 1 / metabolism

Substances

  • DNA, Ribosomal
  • Ataxia Telangiectasia Mutated Proteins
  • X-ray Repair Cross Complementing Protein 1
  • BRCA1 Protein
  • Atm protein, mouse
  • Ku Autoantigen