ArticleNucleic acids research2015
Roles of PCNA ubiquitination and TLS polymerases κ and η in the bypass of methyl methanesulfonate-induced DNA damage.
Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 49 citations in OpenAlex.
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- Chromatin assembly factor 1 subunit A promotes TLS pathway by recruiting E3 ubiquitin ligase RAD18 in cancer cells.Cell death & disease · 2025Article
- Molecular dependencies and genomic consequences of a global DNA damage tolerance defect.Genome biology · 2024Article
- ATAD5-BAZ1B interaction modulates PCNA ubiquitination during DNA repair.Nature communications · 2024Article
- Human translesion DNA polymerases ι and κ mediate tolerance to temozolomide in MGMT-deficient glioblastoma cells.DNA repair · 2024Article
- Dual role of proliferating cell nuclear antigen monoubiquitination in facilitating Fanconi anemia-mediated interstrand crosslink repair.PNAS nexus · 2024Article
- REV7: a small but mighty regulator of genome maintenance and cancer development.Frontiers in oncology · 2024Review
- A C57BL/6J Fancg-KO Mouse Model Generated by CRISPR/Cas9 Partially Captures the Human Phenotype.International journal of molecular sciences · 2023Article
- Reprotoxic Effect of Tris(2,3-Dibromopropyl) Isocyanurate (TBC) on Spermatogenic Cells In Vitro.Molecules (Basel, Switzerland) · 2023Article
- Mammalian life depends on two distinct pathways of DNA damage tolerance.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- RFWD3 and translesion DNA polymerases contribute to PCNA modification-dependent DNA damage tolerance.Life science alliance · 2022Article
- Division of labor within the DNA damage tolerance system reveals non-epistatic and clinically actionable targets for precision cancer medicine.Nucleic acids research · 2022Article
- RIP140 regulatesCancer drug resistance (Alhambra, Calif.) · 2022Article
- Determination of DNA lesion bypass using a ChIP-based assay.DNA repair · 2021Article
- Versatile cell-based assay for measuring DNA alkylation damage and its repair.Scientific reports · 2021Article
- Rad18 mediates specific mutational signatures and shapes the genomic landscape of carcinogen-induced tumorsNAR cancer · 2021Article
- The Widely Used Antihelmintic Drug Albendazole is a Potent Inducer of Loss of Heterozygosity.Frontiers in pharmacology · 2021Article
- The HLTF-PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate.Oncogenesis · 2020Article
- UBB pseudogene 4 encodes functional ubiquitin variants.Nature communications · 2020Article
- DNA damage tolerance in stem cells, ageing, mutagenesis, disease and cancer therapy.Nucleic acids research · 2019Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Translesion synthesis (TLS) provides a highly conserved mechanism that enables DNA synthesis on a damaged template. TLS is performed by specialized DNA polymerases of which polymerase (Pol) κ is important for the cellular response to DNA damage induced by benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), ultraviolet (UV) light and the alkylating agent methyl methanesulfonate (MMS). As TLS polymerases are intrinsically error-prone, tight regulation of their activity is required. One level of control is provided by ubiquitination of the homotrimeric DNA clamp PCNA at lysine residue 164 (PCNA-Ub). We here show that Polκ can function independently of PCNA modification and that Polη can function as a backup during TLS of MMS-induced lesions. Compared to cell lines deficient for PCNA modification (Pcna(K164R)) or Polκ, double mutant cell lines display hypersensitivity to MMS but not to BPDE or UV-C. Double mutant cells also displayed delayed post-replicative TLS, accumulate higher levels of replication stress and delayed S-phase progression. Furthermore, we show that Polη and Polκ are redundant in the DNA damage bypass of MMS-induced DNA damage. Taken together, we provide evidence for PCNA-Ub-independent activation of Polκ and establish Polη as an important backup polymerase in the absence of Polκ in response to MMS-induced DNA damage.
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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.