ArticleNucleic acids research2023
Sustained pigmentation causes DNA damage and invokes translesion polymerase Polκ for repair in melanocytes.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 3 citations in OpenAlex.
- microRNA miR-31-5p confers protection to melanin-deficient vitiligo keratinocytes against UV-B induced DNA damage by activating autophagy machinery.Scientific reports · 2026Article
- Disruption of the reciprocal inhibitory relationship between cell proliferation and melanogenesis in pet murine melanoma cells by ultraviolet radiation.Frontiers in veterinary science · 2026Article
- Infrared radiation alleviates damage to epidermal melanocytes induced by ultraviolet irradiation: potential for improving the efficacy of phototherapy for vitiligo lesions.Frontiers in bioengineering and biotechnology · 2026Article
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Report of the 47th annual conference and the golden jubilee year meeting of the Environmental Mutagen Society of India (EMSI) and international conference on environmental and molecular mutagenesis: genomic integrity and implication to human health, Tamil Nadu, India, January 29-31, 2025.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanin protects skin cells from ultraviolet radiation-induced DNA damage. However, intermediates of eumelanin are highly reactive quinones that are potentially genotoxic. In this study, we systematically investigate the effect of sustained elevation of melanogenesis and map the consequent cellular repair response of melanocytes. Pigmentation increases γH2AX foci, DNA abasic sites, causes replication stress and invokes translesion polymerase Polκ in primary human melanocytes, as well as mouse melanoma cells. Confirming the causal link, CRISPR-based genetic ablation of tyrosinase results in depigmented cells with low Polκ levels. During pigmentation, Polκ activates replication stress response and keeps a check on uncontrolled proliferation of cells harboring melanin-damaged DNA. The mutational landscape observed in human melanoma could in part explain the error-prone bypass of DNA lesions by Polκ, whose absence would lead to genome instability. Thereby, translesion polymerase Polκ is a critical response of pigmenting melanocytes to combat melanin-induced DNA alterations. Our study illuminates the dark side of melanin and identifies (eu)melanogenesis as a key missing link between tanning response and mutagenesis, mediated via the necessary evil translesion polymerase, Polκ.
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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.