The 2026 Gordon Research Seminar on DNA Damage, Mutation and Cancer (GRS) will be held in Ventura, California. Apply today to reserve your spot.

The Curie Institute Research CenterThe Institut Curie is a major player in the research and fight against cancer. It consists of a hospital and a Research Center of more than 1000 employees with a str...

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 o

Analysis of the longest-lived mammal, the bowhead whale, reveals an improved ability to repair DNA breaks, mediated by high levels of cold-inducible RNA-binding protein.   

3-year PhD offer in biology to mechanisms of complex rearrangements of the genome.

DNA damage to the somatic genome has been identified as a major cause of ageing. This Perspective provides an overview of current understanding of the role of genome instability in the ageing process and assesses therapeutic strategies targeting the cellular response to DNA damage to delay ageing and prevent associated diseases.

A CRISPR screen reveals a protective role for the RNA/DNA helicase senataxin during V(D)J recombination.