ArticleNucleic acids research2004
Enhanced mutagenic potential of 8-oxo-7,8-dihydroguanine when present within a clustered DNA damage site.
Article in Nucleic acids research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 99 citations in OpenAlex.
- The role of DNA polymerase I in tolerating single-strand breaks generated at clustered DNA damage in Escherichia coli.Scientific reports · 2024Article
- AOP report: Development of an adverse outcome pathway for oxidative DNA damage leading to mutations and chromosomal aberrations.Environmental and molecular mutagenesis · 2022Article
- Molecular Mechanisms Associated with Clustered Lesion-Induced Impairment of 8-oxoG Recognition by the Human Glycosylase OGG1.Molecules (Basel, Switzerland) · 2021Article
- Arabidopsis thaliana PrimPol is a primase and lesion bypass DNA polymerase with the biochemical characteristics to cope with DNA damage in the nucleus, mitochondria, and chloroplast.Scientific reports · 2021Article
- Genome-Wide Analysis of Cadmium-Induced, Germline Mutations in a Long-TermEnvironmental health perspectives · 2021Article
- Fluorescence anisotropy study of radiation-induced DNA damage clustering based on FRET.Analytical and bioanalytical chemistry · 2021Article
- Mutagenic Effects of a 2-Deoxyribonolactone-Thymine Glycol Tandem DNA Lesion in Human Cells.Biochemistry · 2020Article
- The Influence of (5'Cells · 2019Article
- 8-Oxo-7,8-dihydro-2'-deoxyguanosine and abasic site tandem lesions are oxidation prone yielding hydantoin products that strongly destabilize duplex DNA.Organic & biomolecular chemistry · 2017Article
- Disruption of PARP1 function inhibits base excision repair of a sub-set of DNA lesions.Nucleic acids research · 2015Article
- Xeroderma Pigmentosum Group A Suppresses Mutagenesis Caused by Clustered Oxidative DNA Adducts in the Human Genome.PloS one · 2015Article
- Bcl2 inhibits recruitment of Mre11 complex to DNA double-strand breaks in response to high-linear energy transfer radiation.Nucleic acids research · 2015Article
- Increased mutability and decreased repairability of a three-lesion clustered DNA-damaged site comprised of an AP site and bi-stranded 8-oxoG lesions.International journal of radiation biology · 2014Article
- Reduced repair capacity of a DNA clustered damage site comprised of 8-oxo-7,8-dihydro-2'-deoxyguanosine and 2-deoxyribonolactone results in an increased mutagenic potential of these lesions.Mutation research · 2014Article
- Replication fork collapse is a major cause of the high mutation frequency at three-base lesion clusters.Nucleic acids research · 2013Article
- Article
- Delayed repair of radiation induced clustered DNA damage: friend or foe?Mutation research · 2011Review
- Clustered DNA lesion repair in eukaryotes: relevance to mutagenesis and cell survival.Mutation research · 2011Review
- Hierarchy of lesion processing governs the repair, double-strand break formation and mutability of three-lesion clustered DNA damage.Nucleic acids research · 2010Article
- Apex1 can cleave complex clustered DNA lesions in cells.DNA repair · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The formation of clustered DNA damage sites is a unique feature of ionizing radiation. Recent studies have shown that the repair of lesions within clusters may be compromised, but little is understood about the mutagenic consequences of such damage sites. Using a plasmid-based method, damaged DNA containing uracil positioned at 1-5 bp separations from 8-oxo-7,8-dihydroguanine on the complementary strand was transfected into wild-type Escherichia coli or into strains lacking the DNA glycosylases Fpg and MutY. Mutation frequencies were found to be significantly higher for clustered damage sites than for single lesions. The loss of MutY gave a large relative increase in mutation frequency and a strain lacking both Fpg and MutY showed even higher mutation frequencies, up to nearly 40% of rescued plasmid. In these strains, the mutation frequency decreases with increasing spacing of the uracil from the 8-oxo-7,8-dihydroguanine site. Sequencing of plasmid DNA carrying clustered damage, following rescue from bacteria, showed that almost all of the mutations are GC-->TA transversions. The data suggest that at clustered damage sites, depending on lesion spacing, the action of Fpg is compromised and post-replication processing of lesions by MutY is the most important mechanism for protection against mutagenesis.
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