ArticleProceedings of the National Academy of Sciences of the United States of America2020
The 6-4 photoproduct is the trigger of UV-induced replication blockage and ATR activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 63 citations in OpenAlex.
- UV photodamage pathways and the evolutionary selection of thymine over uracil in early genetic systems.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The cutaneous microbiome as a dynamic photoprotective interface against solar radiation.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2026Review
- DGCR8 regulates multiple processes of transcription coupled nucleotide excision repair.Scientific reports · 2026Article
- Differential effects of mercury compounds on mutagenicity, genotoxicity and repair of UV-DNA damage.Toxicology · 2025Article
- Chromatin context shapes DNA damage formation and nucleotide excision repair dynamics in Caenorhabditis elegans.Nucleic acids research · 2025Article
- DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025Review
- Light-Induced Transcription in Zebrafish Targets Mitochondrial Function and Heme Metabolism.Antioxidants (Basel, Switzerland) · 2025Article
- Far-ultraviolet light causes direct DNA damage in human lung cells and tissues.Scientific reports · 2025Article
- Post-replicative lesion processing limits DNA damage-induced mutagenesis.Nucleic acids research · 2025Article
- Medicinal Plant Extracts Targeting UV-Induced Skin Damage: Molecular Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Investigation on possible resistance ofmicroPublication biology · 2025Article
- Synergistic effects of retinol and retinyl palmitate in alleviating UVB-induced DNA damage and promoting the homologous recombination repair in keratinocytes.Frontiers in pharmacology · 2025Article
- An overview of benefits and risks of chronic melanocortin-1 receptor activation.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Review
- Generation and characterization of CRISPR-Cas9-mediated XPC gene knockout in human skin cells.Scientific reports · 2024Article
- Senataxin Attenuates DNA Damage Response Activation and Suppresses Senescence.Antioxidants (Basel, Switzerland) · 2024Article
- How Do ROS Induce NETosis? Oxidative DNA Damage, DNA Repair, and Chromatin Decondensation.Biomolecules · 2024Review
- The photoreactivation of 6 - 4 photoproducts in chloroplast and nuclear DNA depends on the amount of the Arabidopsis UV repair defective 3 protein.BMC plant biology · 2024Article
- Article
- Activation of Peroxisome Proliferator-Activated Receptor-β/δ (PPARβ/δ) in Keratinocytes by Endogenous Fatty Acids.Biomolecules · 2024Article
- Human CST complex restricts excessive PrimPol repriming upon UV induced replication stress by suppressing p21.Nucleic acids research · 2024Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The most prevalent human carcinogen is sunlight-associated ultraviolet (UV), a physiologic dose of which generates thousands of DNA lesions per cell, mostly of two types: cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). It has not been possible, in living cells, to precisely characterize the respective contributions of these two lesion types to the signals that regulate cell cycle progression, DNA replication, and cell survival. Here we coupled multiparameter flow cytometry with lesion-specific photolyases that eliminate either CPDs or 6-4PPs and determined their respective contributions to DNA damage responses. Strikingly, only 6-4PP lesions activated the ATR-Chk1 DNA damage response pathway. Mechanistically, 6-4PPs, but not CPDs, impeded DNA replication across the genome as revealed by microfluidic-assisted replication track analysis. Furthermore, single-stranded DNA accumulated preferentially at 6-4PPs during DNA replication, indicating selective and prolonged replication blockage at 6-4PPs. These findings suggest that 6-4PPs, although eightfold fewer in number than CPDs, are the trigger for UV-induced DNA damage responses.
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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.