{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Elango R"],"funding":["Howard Hughes Medical Institute","NCI NIH HHS","NIGMS NIH HHS"],"pagination":["801-812"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9941964"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(8)"],"pubmed_abstract":["Vertebrate replication forks arrested at interstrand DNA cross-links (ICLs) engage the Fanconi anemia pathway to incise arrested forks, 'unhooking' the ICL and forming a double strand break (DSB) that is repaired by homologous recombination (HR). The FANCP product, SLX4, in complex with the XPF (also known as FANCQ or ERCC4)-ERCC1 endonuclease, mediates ICL unhooking. Whether this mechanism operates at replication fork barriers other than ICLs is unknown. Here, we study the role of mouse SLX4 in HR triggered by a site-specific chromosomal DNA-protein replication fork barrier formed by the Escherichia coli-derived Tus-Ter complex. We show that SLX4-XPF is required for Tus-Ter-induced HR but not for error-free HR induced by a replication-independent DSB. We additionally uncover a role for SL"],"journal":["Nature structural & molecular biology"],"pubmed_title":["The structure-specific endonuclease complex SLX4-XPF regulates Tus-Ter-induced homologous recombination."],"pmcid":["PMC9941964"],"funding_grant_id":["R01 CA095175","R01 GM134425","R35 CA263813","R01 CA204127"],"pubmed_authors":["Scully R","Lach FP","Willis NA","Nicholson K","Elango R","Smogorzewska A","Duffey EE","Panday A"],"additional_accession":[]},"is_claimable":false,"name":"The structure-specific endonuclease complex SLX4-XPF regulates Tus-Ter-induced homologous recombination.","description":"Vertebrate replication forks arrested at interstrand DNA cross-links (ICLs) engage the Fanconi anemia pathway to incise arrested forks, 'unhooking' the ICL and forming a double strand break (DSB) that is repaired by homologous recombination (HR). The FANCP product, SLX4, in complex with the XPF (also known as FANCQ or ERCC4)-ERCC1 endonuclease, mediates ICL unhooking. Whether this mechanism operates at replication fork barriers other than ICLs is unknown. Here, we study the role of mouse SLX4 in HR triggered by a site-specific chromosomal DNA-protein replication fork barrier formed by the Escherichia coli-derived Tus-Ter complex. We show that SLX4-XPF is required for Tus-Ter-induced HR but not for error-free HR induced by a replication-independent DSB. We additionally uncover a role for SL","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2025-04-22T09:57:37.397Z","creation":"2025-02-18T22:57:22.047Z"},"accession":"S-EPMC9941964","cross_references":{"pubmed":["35941380"],"doi":["10.1038/s41594-022-00812-9"]}}