ArticleProceedings of the National Academy of Sciences of the United States of America2024
High UV damage and low repair, but not cytosine deamination, stimulate mutation hotspots at ETS binding sites in melanoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 5 citations in OpenAlex.
- UV damage mapping reveals different impacts of yeast XPD mutations on global genomic and transcription-coupled DNA repair.The Journal of biological chemistry · 2026Article
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.Nucleic acids research · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Nature communications · 2026Article
- Molecular basis of UV lesion binding and repair inhibition by ETS-family transcription factors.bioRxiv : the preprint server for biology · 2026Article
- Genome-wide maps of CPD deamination in yeast reveal the impact of DNA sequence context and nucleosome architecture on cytosine deamination rates.Genome research · 2026Article
- High-throughput characterization of transcription factors that modulate UV damage formation and repair at single-nucleotide resolution.Research square · 2025Article
- Reannotation of cancer mutations based on expressed RNA transcripts reveals functional non-coding mutations in melanoma.American journal of human genetics · 2025Article
- Nucleotide excision repair of aflatoxin-induced DNA damage within the 3D human genome organization.Nucleic acids research · 2024Article
- Deciphering the dynamic code: DNA recognition by transcription factors in the ever-changing genome.TranscriptionReview
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Noncoding mutation hotspots have been identified in melanoma and many of them occur at the binding sites of E26 transformation-specific (ETS) proteins; however, their formation mechanism and functional impacts are not fully understood. Here, we used UV (Ultraviolet) damage sequencing data and analyzed cyclobutane pyrimidine dimer (CPD) formation, DNA repair, and CPD deamination in human cells at single-nucleotide resolution. Our data show prominent CPD hotspots immediately after UV irradiation at ETS binding sites, particularly at sites with a conserved TTCCGG motif, which correlate with mutation hotspots identified in cutaneous melanoma. Additionally, CPDs are repaired slower at ETS binding sites than in flanking DNA. Cytosine deamination in CPDs to uracil is suggested as an important step for UV mutagenesis. However, we found that CPD deamination is significantly suppressed at ETS binding sites, particularly for the CPD hotspot on the 5' side of the ETS motif, arguing against a role for CPD deamination in promoting ETS-associated UV mutations. Finally, we analyzed a subset of frequently mutated promoters, including the ribosomal protein genes
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