ArticleGenes & development2014
A cell cycle-regulated Slx4-Dpb11 complex promotes the resolution of DNA repair intermediates linked to stalled replication.
Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 94 citations in OpenAlex.
- Dual-site phosphorylation of SLX4 stabilizes the SLX4-MUS81 interface to promote mitotic SMX assembly and genome protection.Nucleic acids research · 2026Article
- Slx4 and Fun30/SMARCAD1 coordinate S-phase checkpoint regulation and replication fork protection in response to Top1-DNA crosslinks.Nucleic acids research · 2026Article
- CIP2A mediates mitotic recruitment of SLX4/MUS81/XPF to resolve replication stress-induced DNA lesions.Nature communications · 2025Article
- The CIP2A-TOPBP1 axis facilitates mitotic DNA repair via MiDAS and MMEJ.Nature communications · 2025Article
- TopBP1 coordinates DNA repair synthesis in mitosis via recruitment of the nuclease scaffold SLX4.Communications biology · 2025Article
- The Slx4-Rad1-Rad10 nuclease differentially regulates deletions and duplications induced by a replication fork barrier.PLoS genetics · 2025Article
- The Yeast HMGB Protein Hmo1 Is a Multifaceted Regulator of DNA Damage Tolerance.International journal of molecular sciences · 2025Article
- Proteomic Profiling of Endothelial Cells Exposed to Mitomycin C: Key Proteins and Pathways Underlying Genotoxic Stress-Induced Endothelial Dysfunction.International journal of molecular sciences · 2024Article
- Implications of ubiquitination and the maintenance of replication fork stability in cancer therapy.Bioscience reports · 2023Review
- Comprehensive Interactome Mapping of the DNA Repair Scaffold SLX4 Using Proximity Labeling and Affinity Purification.Journal of proteome research · 2023Article
- Regulation of Mus81-Eme1 structure-specific endonuclease by Eme1 SUMO-binding and Rad3ATR kinase is essential in the absence of Rqh1BLM helicase.PLoS genetics · 2022Article
- SUMO-mediated recruitment allows timely function of the Yen1 nuclease in mitotic cells.PLoS genetics · 2022Article
- Phosphoproteomics reveals a distinctive Mec1/ATR signaling response upon DNA end hyper-resection.The EMBO journal · 2021Article
- Structural parameters of palindromic repeats determine the specificity of nuclease attack of secondary structures.Nucleic acids research · 2021Article
- Review
- Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020Review
- Article
- SLX4 interacts with RTEL1 to prevent transcription-mediated DNA replication perturbations.Nature structural & molecular biology · 2020Article
- Review
- Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A key function of the cellular DNA damage response is to facilitate the bypass of replication fork-stalling DNA lesions. Template switch reactions allow such a bypass and involve the formation of DNA joint molecules (JMs) between sister chromatids. These JMs need to be resolved before cell division; however, the regulation of this process is only poorly understood. Here, we identify a regulatory mechanism in yeast that critically controls JM resolution by the Mus81-Mms4 endonuclease. Central to this regulation is a conserved complex comprising the scaffold proteins Dpb11 and Slx4 that is under stringent control. Cell cycle-dependent phosphorylation of Slx4 by Cdk1 promotes the Dpb11-Slx4 interaction, while in mitosis, phosphorylation of Mms4 by Polo-like kinase Cdc5 promotes the additional association of Mus81-Mms4 with the complex, thereby promoting JM resolution. Finally, the DNA damage checkpoint counteracts Mus81-Mms4 binding to the Dpb11-Slx4 complex. Thus, Dpb11-Slx4 integrates several cellular inputs and participates in the temporal program for activation of the JM-resolving nuclease Mus81.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.