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أعرض في EDS

Dual role of proliferating cell nuclear antigen monoubiquitination in facilitating Fanconi anemia-mediated interstrand crosslink repair.

التفاصيل البيبلوغرافية
العنوان: Dual role of proliferating cell nuclear antigen monoubiquitination in facilitating Fanconi anemia-mediated interstrand crosslink repair.
المؤلفون: Shah R; Department of Tumor Biology and Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands., Aslam MA; Department of Tumor Biology and Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.; Department/Institute of Molecular Biology and Biotechnology, Bahauddin Zakariya University, Bosan Road, 60800 Multan, Pakistan., Spanjaard A; Department of Tumor Biology and Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands., de Groot D; Department of Tumor Biology and Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands., Zürcher LM; Department of Tumor Biology and Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands., Altelaar M; Proteomics Facility, The Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands.; Biomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research, Utrecht Institute for Pharmaceutical Sciences, Utrecht University and Netherlands Proteomics Centre, Utrecht, Padualaan 8, 3584 CH Utrecht, The Netherlands., Hoekman L; Proteomics Facility, The Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands., Pritchard CEJ; Mouse Clinic for Cancer and Aging Transgenic Facility, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands., Pilzecker B; Department of Tumor Biology and Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands., van den Berk PCM; Department of Tumor Biology and Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands., Jacobs H; Department of Tumor Biology and Immunology, The Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands.
المصدر: PNAS nexus [PNAS Nexus] 2024 Jun 18; Vol. 3 (7), pp. pgae242. Date of Electronic Publication: 2024 Jun 18 (Print Publication: 2024).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Oxford University Press on behalf of the National Academy of Sciences Country of Publication: England NLM ID: 9918367777906676 Publication Model: eCollection Cited Medium: Internet ISSN: 2752-6542 (Electronic) Linking ISSN: 27526542 NLM ISO Abbreviation: PNAS Nexus Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Oxford] : Oxford University Press on behalf of the National Academy of Sciences, [2022]-
مستخلص: The Fanconi anemia (FA) repair pathway governs repair of highly genotoxic DNA interstrand crosslinks (ICLs) and relies on translesion synthesis (TLS). TLS is facilitated by REV1 or site-specific monoubiquitination of proliferating cell nuclear antigen (PCNA) (PCNA-Ub) at lysine 164 (K164). A Pcna K164R/K164R but not Rev1 -/- mutation renders mammals hypersensitive to ICLs. Besides the FA pathway, alternative pathways have been associated with ICL repair (1, 2), though the decision making between those remains elusive. To study the dependence and relevance of PCNA-Ub in FA repair, we intercrossed Pcna K164R/+ ; Fancg -/+ mice. A combined mutation ( Pcna K164R/K164R ; Fancg -/- ) was found embryonically lethal. RNA-seq of primary double-mutant (DM) mouse embryonic fibroblasts (MEFs) revealed elevated levels of replication stress-induced checkpoints. To exclude stress-induced confounders, we utilized a Trp53 knock-down to obtain a model to study ICL repair in depth. Regarding ICL-induced cell toxicity, cell cycle arrest, and replication fork progression, single-mutant and DM MEFs were found equally sensitive, establishing PCNA-Ub to be critical for FA-ICL repair. Immunoprecipitation and spectrometry-based analysis revealed an unknown role of PCNA-Ub in excluding mismatch recognition complex MSH2/MSH6 from being recruited to ICLs. In conclusion, our results uncovered a dual function of PCNA-Ub in ICL repair, i.e. exclude MSH2/MSH6 recruitment to channel the ICL toward canonical FA repair, in addition to its established role in coordinating TLS opposite the unhooked ICL.
(© The Author(s) 2024. Published by Oxford University Press on behalf of National Academy of Sciences.)
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فهرسة مساهمة: Keywords: Fanconi anemia; PCNA monoubiquitination; interstrand crosslink; mismatch repair; replication stress
تواريخ الأحداث: Date Created: 20240703 Latest Revision: 20240704
رمز التحديث: 20240704
مُعرف محوري في PubMed: PMC11217772
DOI: 10.1093/pnasnexus/pgae242
PMID: 38957451
قاعدة البيانات: MEDLINE
الوصف
تدمد:2752-6542
DOI:10.1093/pnasnexus/pgae242