{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Li C"],"funding":["National Natural Science Foundation of China"],"pagination":["e112756"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10068331"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["42(7)"],"pubmed_abstract":["DNA double-strand breaks (DSBs) are one of the most toxic forms of DNA damage, which threatens genome stability. Homologous recombination is an error-free DSB repair pathway, in which the evolutionarily conserved SMC5/6 complex (SMC5/6) plays essential roles. The PAF1 complex (PAF1C) is well known to regulate transcription. Here we show that SMC5/6 recruits PAF1C to facilitate DSB repair in plants. In a genetic screen for DNA damage response mutants (DDRMs), we found that the Arabidopsis ddrm4 mutant is hypersensitive to DSB-inducing agents and is defective in homologous recombination. DDRM4 encodes PAF1, a core subunit of PAF1C. Further biochemical and genetic studies reveal that SMC5/6 recruits PAF1C to DSB sites, where PAF1C further recruits the E2 ubiquitin-conjugating enzymes UBC1/2, which interact with the E3 ubiquitin ligases HUB1/2 to mediate the monoubiquitination of histone H2B at DSBs. These results implicate SMC5/6-PAF1C-UBC1/2-HUB1/2 as a new axis for DSB repair through homologous recombination, revealing a new mechanism of SMC5/6 and uncovering a novel function of PAF1C."],"journal":["The EMBO journal"],"pubmed_title":["The SMC5/6 complex recruits the PAF1 complex to facilitate DNA double-strand break repair in Arabidopsis."],"pmcid":["PMC10068331"],"funding_grant_id":["31970311","32000372","32270306"],"pubmed_authors":["Li C","Guo Y","Yan S","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"The SMC5/6 complex recruits the PAF1 complex to facilitate DNA double-strand break repair in Arabidopsis.","description":"DNA double-strand breaks (DSBs) are one of the most toxic forms of DNA damage, which threatens genome stability. Homologous recombination is an error-free DSB repair pathway, in which the evolutionarily conserved SMC5/6 complex (SMC5/6) plays essential roles. The PAF1 complex (PAF1C) is well known to regulate transcription. Here we show that SMC5/6 recruits PAF1C to facilitate DSB repair in plants. In a genetic screen for DNA damage response mutants (DDRMs), we found that the Arabidopsis ddrm4 mutant is hypersensitive to DSB-inducing agents and is defective in homologous recombination. DDRM4 encodes PAF1, a core subunit of PAF1C. Further biochemical and genetic studies reveal that SMC5/6 recruits PAF1C to DSB sites, where PAF1C further recruits the E2 ubiquitin-conjugating enzymes UBC1/2, which interact with the E3 ubiquitin ligases HUB1/2 to mediate the monoubiquitination of histone H2B at DSBs. These results implicate SMC5/6-PAF1C-UBC1/2-HUB1/2 as a new axis for DSB repair through homologous recombination, revealing a new mechanism of SMC5/6 and uncovering a novel function of PAF1C.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Apr","modification":"2026-06-21T03:15:08.076Z","creation":"2025-04-06T22:49:11.793Z"},"accession":"S-EPMC10068331","cross_references":{"pubmed":["36815434"],"doi":["10.15252/embj.2022112756"]}}