{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Heuze J"],"funding":["Institut Universitaire de France (IUF)","Fondation ARC pour la Recherche sur le Cancer","Agence Nationale de la Recherche (ANR)","Agence Nationale de la Recherche","Centre National de la Recherche Scientifique (CNRS)","College of Natural Resources and Sciences, Humboldt State University","Fondation pour la Recherche Médicale (FRM)","Institut Universitaire de France","Fondation pour la Recherche Médicale","French Ministry of Research and Higher Education","Fondation ARC pour la Recherche sur le Cancer (ARC)"],"pagination":["e113104"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10690446"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["42(23)"],"pubmed_abstract":["R-loops represent a major source of replication stress, but the mechanism by which these structures impede fork progression remains unclear. To address this question, we monitored fork progression, arrest, and restart in Saccharomyces cerevisiae cells lacking RNase H1 and H2, two enzymes responsible for degrading RNA:DNA hybrids. We found that while RNase H-deficient cells could replicate their chromosomes normally under unchallenged growth conditions, their replication was impaired when exposed to hydroxyurea (HU) or methyl methanesulfonate (MMS). Treated cells exhibited increased levels of RNA:DNA hybrids at stalled forks and were unable to generate RPA-coated single-stranded (ssDNA), an important postreplicative intermediate in resuming replication. Similar impairments in nascent DNA re"],"journal":["The EMBO journal"],"pubmed_title":["RNase H2 degrades toxic RNA:DNA hybrids behind stalled forks to promote replication restart."],"pmcid":["PMC10690446"],"funding_grant_id":["ANR‐18‐IDEX‐0001","ANR-18-IDEX-0001","ANR‐16‐CE12‐0022‐01","ANR-16-CE12-0022-01","ANR-17-EURE-0013","ANR-21-CE12-0040-01","ANR‐21‐CE12‐0040‐01","ANR‐19‐CE12‐0016‐01","ANR-19-CE12-0016-01","ANR-20-CE12-0016-01","ANR‐20‐CE12‐0016‐01","ANR‐17‐EURE‐0013","ANR‐22‐CE12‐0031‐01","ANR‐19‐CE12‐0023‐03","ANR-19-CE12-0023-03","ANR-22-CE12-0031-01"],"pubmed_authors":["Libri D","Kemiha S","Poli J","Vilarrubias AT","Lengronne A","Lin YL","Aouadi E","Barthe A","Pasero P","Heuze J","Aiello U"],"additional_accession":[]},"is_claimable":false,"name":"RNase H2 degrades toxic RNA:DNA hybrids behind stalled forks to promote replication restart.","description":"R-loops represent a major source of replication stress, but the mechanism by which these structures impede fork progression remains unclear. To address this question, we monitored fork progression, arrest, and restart in Saccharomyces cerevisiae cells lacking RNase H1 and H2, two enzymes responsible for degrading RNA:DNA hybrids. We found that while RNase H-deficient cells could replicate their chromosomes normally under unchallenged growth conditions, their replication was impaired when exposed to hydroxyurea (HU) or methyl methanesulfonate (MMS). Treated cells exhibited increased levels of RNA:DNA hybrids at stalled forks and were unable to generate RPA-coated single-stranded (ssDNA), an important postreplicative intermediate in resuming replication. Similar impairments in nascent DNA re","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Dec","modification":"2026-07-14T20:42:43.009Z","creation":"2025-04-04T07:40:57.433Z"},"accession":"S-EPMC10690446","cross_references":{"pubmed":["37855233"],"doi":["10.15252/embj.2022113104"]}}