{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Mangione RM"],"funding":["Ligue Contre le Cancer","Fondation ARC pour la Recherche sur le Cancer","Fondation ARC pour la Recherche sur le Cancer (ARC Foundation for Cancer Research)","Agence Nationale de la Recherche","Fondation pour la Recherche Médicale (Foundation for Medical Research in France)","Agence Nationale de la Recherche (French National Research Agency)","Fondation pour la Recherche Médicale","U.S. Department of Health & Human Services | National Institutes of Health (NIH)","BioSPC PhD program Université Paris Cité","NIGMS NIH HHS","U.S. Department of Health & Human Services | National Institutes of Health"],"pagination":["2401"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11893903"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["While DNA:RNA hybrids contribute to multiple genomic transactions, their unscheduled formation is a recognized source of DNA lesions. Here, through a suite of systematic screens, we rather observed that a wide range of yeast mutant situations primarily triggering DNA damage actually leads to hybrid accumulation. Focusing on Okazaki fragment processing, we establish that genic hybrids can actually form as a consequence of replication-born discontinuities such as unprocessed flaps or unligated Okazaki fragments. Strikingly, such \"post-lesion\" DNA:RNA hybrids neither detectably contribute to genetic instability, nor disturb gene expression, as opposed to \"pre-lesion\" hybrids formed upon defective mRNA biogenesis, e.g., in THO complex mutants. Post-lesion hybrids similarly arise in distinct ge"],"journal":["Nature communications"],"pubmed_title":["DNA lesions can frequently precede DNA:RNA hybrid accumulation."],"pmcid":["PMC11893903"],"funding_grant_id":["ANR-18-IDEX-0001","GM50237","FDT202304016590","R35 GM118180","ANR-21-CE12-0040","EQU202003010245","PJA20181208112","RS21/75-21","ANR-18-CE12-003","ANR-11-LABX-0071"],"pubmed_authors":["de Almeida SF","Pierce S","Mangione RM","Goncalves C","Reid RJD","Lancrey A","Lautier O","Zheng M","Palancade B","Scaglione S","de Sousa Morgado C","Gaillard PH","Martin RM","Penzo A","Stirling PC","Kumar A","Rothstein R"],"additional_accession":[]},"is_claimable":false,"name":"DNA lesions can frequently precede DNA:RNA hybrid accumulation.","description":"While DNA:RNA hybrids contribute to multiple genomic transactions, their unscheduled formation is a recognized source of DNA lesions. Here, through a suite of systematic screens, we rather observed that a wide range of yeast mutant situations primarily triggering DNA damage actually leads to hybrid accumulation. Focusing on Okazaki fragment processing, we establish that genic hybrids can actually form as a consequence of replication-born discontinuities such as unprocessed flaps or unligated Okazaki fragments. Strikingly, such \"post-lesion\" DNA:RNA hybrids neither detectably contribute to genetic instability, nor disturb gene expression, as opposed to \"pre-lesion\" hybrids formed upon defective mRNA biogenesis, e.g., in THO complex mutants. Post-lesion hybrids similarly arise in distinct ge","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-06-01T18:02:04.644Z","creation":"2025-04-04T00:21:44.243Z"},"accession":"S-EPMC11893903","cross_references":{"pubmed":["40064914"],"doi":["10.1038/s41467-025-57588-x"]}}