Transcriptional repression facilitates RNA:DNA hybrid accumulation at DNA double-strand breaks

  • Nat Cell Biol. 2025 Jun;27(6):992-1005. doi: 10.1038/s41556-025-01669-y.
Florian Saur  #  1 ,  Emma Lesage  #  1 ,  Lea Pradel  1 ,  Sarah Collins  1 ,  Anne-Laure Finoux  1 ,  Emile Alghoul  1 ,  Benjamin Le Bozec  1 ,  Vincent Rocher  1 ,  Romane Carette  1 ,  Nadine Puget  1 ,  Marie Couralet  1 ,  Melanie Petiot  1 ,  Thomas Clouaire  2  3 ,  Aline Marnef  4 ,  Gaëlle Legube  5
Affiliations
  • 1. MCD, Centre de Biologie Intégrative (CBI), CNRS, Université de Toulouse UT, Toulouse, France.
  • 2. MCD, Centre de Biologie Intégrative (CBI), CNRS, Université de Toulouse UT, Toulouse, France. [email protected].
  • 3. Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France. [email protected].
  • 4. MCD, Centre de Biologie Intégrative (CBI), CNRS, Université de Toulouse UT, Toulouse, France. [email protected].
  • 5. MCD, Centre de Biologie Intégrative (CBI), CNRS, Université de Toulouse UT, Toulouse, France. [email protected].
  • # Contributed equally.
Abstract

RNA:DNA hybrids accumulate at DNA double-strand breaks (DSBs) and were shown to regulate homologous recombination repair. The mechanism responsible for the formation of these non-canonical RNA:DNA structures remains unclear although they were proposed to arise consequently to RNA polymerase II or III loading followed by DSB-induced de novo transcription at the break site. Here, we found no evidence of RNA polymerase recruitment at DSBs. Rather, strand-specific R-loop mapping revealed that RNA:DNA hybrids are mainly generated at DSBs occurring in transcribing loci, from the hybridization of pre-existing RNA to the 3' overhang left by DNA end resection. We further identified the H3K4me3 reader spindlin 1 and the transcriptional regulator PAF1 as factors promoting RNA:DNA hybrid accumulation at DSBs, through their role in mediating transcriptional repression in cis to DSBs. Altogether, we provide evidence that RNA:DNA hybrids accumulate at DSBs occurring in transcribing loci as a result of DSB-induced transcriptional shut down.

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