ArticleCell cycle (Georgetown, Tex.)2011
The DNA repair endonuclease XPG interacts directly and functionally with the WRN helicase defective in Werner syndrome.
Article in Cell cycle (Georgetown, Tex.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 0 citations in OpenAlex.
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- DNA damage and repair in age-related inflammation.Nature reviews. Immunology · 2023Review
- XPG in the Nucleotide Excision Repair and Beyond: a study on the different functional aspects of XPG and its associated diseases.Molecular biology reports · 2022Review
- XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022Review
- Transcriptional Stress Induces Chromatin Relocation of the Nucleotide Excision Repair Factor XPG.International journal of molecular sciences · 2021Article
- Skin Abnormalities in Disorders with DNA Repair Defects, Premature Aging, and Mitochondrial Dysfunction.The Journal of investigative dermatology · 2021Review
- Decoding Cancer Variants of Unknown Significance for Helicase-Nuclease-RPA Complexes Orchestrating DNA Repair During Transcription and Replication.Frontiers in molecular biosciences · 2021Article
- Function and Molecular Mechanism of the DNA Damage Response in Immunity and Cancer Immunotherapy.Frontiers in immunology · 2021Review
- An efficient chemical screening method for structure-based inhibitors to nucleic acid enzymes targeting the DNA repair-replication interface and SARS CoV-2.Methods in enzymology · 2021Article
- Human XPG nuclease structure, assembly, and activities with insights for neurodegeneration and cancer from pathogenic mutations.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Review
- Werner Syndrome Protein and DNA Replication.International journal of molecular sciences · 2018Review
- The MRE11-RAD50-NBS1 Complex Conducts the Orchestration of Damage Signaling and Outcomes to Stress in DNA Replication and Repair.Annual review of biochemistry · 2018Review
- Article
- Werner syndrome: Clinical features, pathogenesis and potential therapeutic interventions.Ageing research reviews · 2017Review
- The Ku-binding motif is a conserved module for recruitment and stimulation of non-homologous end-joining proteins.Nature communications · 2016Article
- Non-catalytic Roles for XPG with BRCA1 and BRCA2 in Homologous Recombination and Genome Stability.Molecular cell · 2016Article
- Replication stress induced site-specific phosphorylation targets WRN to the ubiquitin-proteasome pathway.Oncotarget · 2016Article
- Nonenzymatic role for WRN in preserving nascent DNA strands after replication stress.Cell reports · 2014Article
- Cell-autonomous progeroid changes in conditional mouse models for repair endonuclease XPG deficiency.PLoS genetics · 2014Article
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11 authors at 1 institution in 1 country.
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Abstract
XPG is a structure-specific endonuclease required for nucleotide excision repair (NER). XPG incision defects result in the cancer-prone syndrome xeroderma pigmentosum, whereas truncating mutations of XPG cause the severe postnatal progeroid developmental disorder Cockayne syndrome. We show that XPG interacts directly with WRN protein, which is defective in the premature aging disorder Werner syndrome, and that the two proteins undergo similar subnuclear redistribution in S phase and colocalize in nuclear foci. The co-localization was observed in mid- to late S phase, when WRN moves from nucleoli to nuclear foci that have been shown to contain both protein markers of stalled replication forks and telomeric proteins. We mapped the interaction between XPG and WRN to the C-terminal domains of each, and show that interaction with the C-terminal domain of XPG strongly stimulates WRN helicase activity. WRN also possesses a competing DNA single-strand annealing activity that, combined with unwinding, has been shown to coordinate regression of model replication forks to form Holliday junction/chicken foot intermediate structures. We tested whether XPG stimulated WRN annealing activity, and found that XPG itself has intrinsic strand annealing activity that requires the unstructured R- and C-terminal domains but not the conserved catalytic core or endonuclease activity. Annealing by XPG is cooperative, rather than additive, with WRN annealing. Taken together, our results suggest a novel function for XPG in S phase that is, at least in part, performed coordinately with WRN, and which may contribute to the severity of the phenotypes that occur upon loss of XPG.
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