Evidence map›Paper›PMID 34563793›Full record

ArticleMutation research

Biochemical and photochemical mechanisms that produce different UV-induced mutation spectra.

Tomohiko Sugiyama, Brianna Keinard, Griffin Best, Mahima R Sanyal

Abstract read
In one paragraph

Article in Mutation research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. UVA-light-induced mutagenesis in the exome of human nucleotide excision repair-deficient cells.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2025
    Article
  5. Patterns of spontaneous and induced genomic alterations inApplied and environmental microbiology · 2025
    Article
  6. The Surprising Diversity of UV-Induced Mutations.Advanced genetics (Hoboken, N.J.) · 2024
    Article
  7. Biochemical analysis of HDNA repair · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Tomohiko SugiyamaDepartment of Biological Sciences; Molecular and Cellular Biology Graduate Program, Ohio University, Athens, OH, 45701, USA. Electronic address: sugiyama@ohio.edu.
Brianna KeinardDepartment of Biological Sciences.
Griffin BestDepartment of Biological Sciences.
Mahima R SanyalDepartment of Biological Sciences; Molecular and Cellular Biology Graduate Program, Ohio University, Athens, OH, 45701, USA.

Funding

NGS-based analysis of mutation signatures during the translesion synthesisR15ES029723 · NIEHS · OHIO UNIVERSITY ATHENS · PI SUGIYAMA, TOMOHIKO · 2020 to 2020
$453k
NGS-based analysis of mutation signatures during the translesion synthesisR15GM116098 · NIGMS · OHIO UNIVERSITY ATHENS · PI SUGIYAMA, TOMOHIKO · 2015 to 2015
$370k
NIEHS NIH HHS R15 ES029723NIGMS NIH HHS R15 GM116098
6 · The paper itself

Abstract

Although UV-induced mutagenesis has been studied extensively, the precise mechanisms that convert UV-induced DNA damage into mutations remain elusive. One well-studied mechanism involves DNA polymerase (Pol) η and ζ, which produces C > T transitions during translesion synthesis (TLS) across pyrimidine dimers. We previously proposed another biochemical mechanism that involves multiple UV-irradiations with incubation in the dark in between. The incubation facilitates spontaneous deamination of cytosine in a pyrimidine dimer, and the subsequent UV irradiation induces photolyase-independent (direct) photoreversal that converts cytosine into monomeric uracil residue. In this paper, we first demonstrate that natural sunlight can induce both mutational processes in vitro. The direct photoreversal was also reproduced by monochromatic UVB at 300 nm. We also demonstrate that post-irradiation incubation in the dark is required for both mutational processes, suggesting that cytosine deamination is required for both the Pol η/ζ-dependent and the photoreversal-dependent mechanisms. Another Y-family polymerase Pol ι also mediated a mutagenic TLS on UV-damaged templates when combined with Pol ζ. The Pol ι-dependent mutations were largely independent of post-irradiation incubation, indicating that cytosine deamination was not essential for this mutational process. Sunlight-exposure also induced C > A transversions which were likely caused by oxidation of guanine residues. Finally, we constructed in vitro mutation spectra in a comparable format to cancer mutation signatures. While both Pol η-dependent and photoreversal-dependent spectra showed high similarities to a cancer signature (SBS7a), Pol ι-dependent mutation spectrum has distinct T > A/C substitutions, which are found in another cancer signature (SBS7d). The Pol ι-dependent T > A/C substitutions were resistant to T4 pyrimidine dimer glycosylase-treatment, suggesting that this mutational process is independent of cis-syn pyrimidine dimers. An updated model about multiple mechanisms of UV-induced mutagenesis is discussed.

Indexed as

DNA RepairCytosineDNADNA DamageDNA-Directed DNA PolymeraseDNA, Single-StrandedHumansIsoenzymesMutationNeoplasmsPyrimidine DimersSaccharomyces cerevisiaeSunlightUltraviolet RaysUracilCytosineDNADNA-Directed DNA PolymeraseDNA, Single-StrandedIsoenzymesPyrimidine DimersUracilDirect photoreversalSkin cancerSolar radiationTranslesion synthesis

Identifiers

PMID34563793
PMCPMC8671204

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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.