{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Verschuren J"],"funding":["Ministerie van Volksgezondheid, Welzijn en Sport","Ministerie van Volksgezondheid, Welzijn en Sport (Dutch Ministry of Health, Welfare and Sport)"],"pagination":["2495"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11906846"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["To counteract the damaging effects of DNA interstrand crosslinks (ICLs), cells have evolved various specialized ICL repair pathways. However, how ICL repair impacts genetic integrity remains incompletely understood. Here, we determined the mutagenic consequences of psoralen ICL repair in the animal model C. elegans and identify two mutagenic repair mechanisms: (i) translesion synthesis through POLH and REV1/3-mediated bypass, leading to single nucleotide polymorphisms (SNVs), and (ii) end joining via POLQ or HELQ action resulting in deletions. While we found no role for the Fanconi anemia genes FANCD2 and FANCI, disruption of TRAIP, which triggers unloading of the CMG helicase at sites of blocked replication, led to a strikingly altered repair profile, suggesting a role for DNA replication"],"journal":["Nature communications"],"pubmed_title":["FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations."],"pmcid":["PMC11906846"],"funding_grant_id":["OP.393"],"pubmed_authors":["Knipscheer P","Verschuren J","Tijsterman M","van Bostelen I","Verkennis AEE","van Schendel R"],"additional_accession":[]},"is_claimable":false,"name":"FAN1-mediated translesion synthesis and POLQ/HELQ-mediated end joining generate interstrand crosslink-induced mutations.","description":"To counteract the damaging effects of DNA interstrand crosslinks (ICLs), cells have evolved various specialized ICL repair pathways. However, how ICL repair impacts genetic integrity remains incompletely understood. Here, we determined the mutagenic consequences of psoralen ICL repair in the animal model C. elegans and identify two mutagenic repair mechanisms: (i) translesion synthesis through POLH and REV1/3-mediated bypass, leading to single nucleotide polymorphisms (SNVs), and (ii) end joining via POLQ or HELQ action resulting in deletions. While we found no role for the Fanconi anemia genes FANCD2 and FANCI, disruption of TRAIP, which triggers unloading of the CMG helicase at sites of blocked replication, led to a strikingly altered repair profile, suggesting a role for DNA replication","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2026-05-29T16:50:36.369Z","creation":"2025-04-06T23:56:02.023Z"},"accession":"S-EPMC11906846","cross_references":{"pubmed":["40082407"],"doi":["10.1038/s41467-025-57764-z"]}}