UVA-induced cyclobutane pyrimidine dimers form predominantly at thymine-thymine dipyrimidines and correlate with the mutation spectrum in rodent cells

Rochette, P. J.

doi:10.1093/nar/gkg402

Cited by 231DNA Repair MechanismsCarcinogens and Genotoxicity AssessmentSkin Protection and Aging

UVA-induced cyclobutane pyrimidine dimers form predominantly at thymine-thymine dipyrimidines and correlate with the mutation spectrum in rodent cells

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Rochette, P. J.·2003·Nucleic Acids Research

DOI 10.1093/nar/gkg402PMC PMC156735

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Abstract

Ligation-mediated PCR was employed to quantify cyclobutane pyrimidine dimer (CPD) formation at nucleotide resolution along exon 2 of the adenine phosphoribosyltransferase (aprt) locus in Chinese hamster ovary (CHO) cells following irradiation with either UVA (340-400 nm), UVB (295-320 nm), UVC (254 nm) or simulated sunlight (SSL; lambda > 295 nm). The resulting DNA damage spectrum for each wavelength region was then aligned with the corresponding mutational spectrum generated previously in the same genetic target. The DNA sequence specificities of CPD formation induced by UVC, UVB or SSL were very similar, i.e., in each case the overall relative proportion of this photoproduct forming at TT, TC, CT and CC sites was approximately 28, approximately 26, approximately 16 and approximately 30%, respectively. Furthermore, a clear correspondence was noted between the precise locations of CPD damage hotspots, and of 'UV signature' mutational hotspots consisting primarily of C-->T and CC-->TT transitions within pyrimidine runs. However, following UVA exposure, in strong contrast to the above situation for UVC, UVB or SSL, CPDs were generated much more frequently at TT sites than at TC, CT or CC sites (57% versus 18, 11 and 14%, respectively). This CPD deposition pattern correlates well with the strikingly high proportion of mutations recovered opposite TT dipyrimidines in UVA- irradiated CHO cells. Our results directly implicate the CPD as a major promutagenic DNA photoproduct induced specifically by UVA in rodent cells.

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UVA radiation has been shown since the 1970s to induce CPDs in bacteria, mammalian cells and human skin.
“In fact, UVA radiation has been shown since the 1970s, first in bacteria (29) and then in mammalian cells (32,55,(80)(81)(82)(83)(84) and human skin (61,65,(85)(86)(87), to be also able to induce CPDs.”
From Photoinduced Damage to Cellular DNA: Direct and Photosensitized Reactions† (2012) · cites this paper as [83]

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Authors: Rochette, P. J.
Affiliations: Centre hospitalier universitaire de Québec (CA)
Corresponding author: Rochette, P. J.
ORCID: Rochette, P. J.
Venue: Nucleic Acids Research
Publisher: Oxford University Press (OUP)
Published: 2003-06-01
Volume: 31
Issue: 11
Pages: 2786-2794
ISSN: 0305-1048 (ISSN-L)
1362-4962
DOI: 10.1093/nar/gkg402
PMC: PMC156735
OpenAlex: W2078531129
Cited by: 231
References: 53
Citations by year: 2025: 8 · 2024: 4 · 2023: 9 · 2022: 10 · 2021: 6 · 2020: 7 · 2019: 11 · 2018: 13 · 2017: 5 · 2016: 13 · 2015: 11 · 2014: 14 · 2013: 14 · 2012: 11
FWCI: 3.80
Type: journal article
Language: en
Open access: green
europepmc.org
Locations: Nucleic Acids Research (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Health Sciences › Medicine › Dermatology › Skin Protection and Aging
Keywords: cyclobutane pyrimidine dimers, UVA, UV-induced DNA damage, mutation spectrum, adenine phosphoribosyltransferase, DNA photoproducts, C>T transitions, photomutagenesis, simulated sunlight, UV-B radiation, UV-C
MeSH terms: Adenine Phosphoribosyltransferase, Animals, DNA Damage, DNA Mutational Analysis, Exons, Cricetinae, Mutation, Pyrimidine Dimers, Ultraviolet Rays, Polymerase Chain Reaction, Mutagenesis, CHO Cells

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UVA-induced cyclobutane pyrimidine dimers form predominantly at thymine-thymine dipyrimidines and correlate with the mutation spectrum in rodent cells

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