DNA excision-repair processes in human cells can eliminate the cytotoxic and mutagenic consequences of ultraviolet irradiation
Abstract
The ability of DNA excision-repair processes in diploid human fibroblasts to eliminate potentially cytotoxic and mutagenic lesions induced by UV radiation (254 nm) was demonstrated in two ways: (1) Cells with normal rates of excision were compared with cells with an intermediate rate of excision (XP2BE) and cells with an excision rate less than or equal to 1% that of normal (XP12BE) for sensitivity to the killing and mutagenic action of UV radiation. The normal cells proved resistant to doses of UV which reduced the survival of the XP cells to 14% and 0.7%, respectively, and increased the frequency of mutations to 8-azaguanine resistance in the XP cells 5- to 10-fold over background. (2) Cells in confluence were irradiated with cytotoxic and mutagenic doses of UV and allowed to carry out excision repair. After various lengths of time they were replated at lower densities to allow for expression of mutations to 6-thioguanine resistance and/or at cloning densities to assay survival. Normal cells and XP cells with reduced rates of excision repair (from complementation groups C and D) exhibited a gradual increase in survival from an initial level of 15--20% to 100% if held approximately 20 h in confluence. In contrast, XP12BE cells showed no increase from an initial survival of 20% even when held for 7 days. Normal cells irradiated in confluence but prevented from replicating for 7 days exhibited background mutation frequencies, whereas the mutation frequency in XP12BE cells did…
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Defects in GGR are associated with enhanced UV-induced mutagenesis in XP-C cells.
“Because cancer, especially in skin, is associated with mutagenesis (9, 10), we hypothesized that, unlike defects in GGR, which are associated with enhanced UV-induced mutagenesis in XP-C cells (11), the”
From Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency (2016) · cites this paper as [11]
These results validate the use of duplex sequencing for the detection of UV-induced mutagenesis.
“These results are consistent with previous reports of UV-induced mutagenesis in reporter genes (11, 13 -15) and validate our use of duplex sequencing for the detection of UV-induced mutagenesis.”
From Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency (2016) · cites this paper as [11]
UV-induced mutations in the HPRT gene that conferred resistance to 6-thioguanine were greatly enhanced in XP cells from both excision-defective and polymerase-defective groups.
“Maher showed that UV-induced mutations in the hypoxanthine phosphoribosyl transferase ( HPRT ) gene that conferred resistance to 6-thioguanine (6-TG) were greatly enhanced in XP cells from both excision-defective and polymerase-defective groups (11, 12).”
From Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency (2016) · cites this paper as [11]
No citation lists for this paper
No citation lists for this paper yet — checked again daily.
References 24 · Cited by 242
- Authors
- Maher, V. M., Dorney, D. J., Mendrala, A. L., Konze-Thomas, B., & McCormick, J. J.
- Affiliations
- Michigan State University (US)
- Venue
- Mutation Research
- Publisher
- Elsevier BV
- Published
- 1979-09
- Volume
- 62
- Issue
- 2
- Pages
- 311-323
- ISSN
- 0027-5107 (ISSN-L)
- OpenAlex
- W2013735942
- Cited by
- 242
- References
- 24
- Citations by year
- 2023: 1 · 2022: 1 · 2021: 1 · 2020: 1 · 2017: 1 · 2016: 5 · 2015: 2 · 2014: 2 · 2012: 2
- FWCI
- 12.78
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Mutation research. Fundamental and molecular mechanisms of mutagenesis (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA 21247, CA 21253)
- Deutsche Forschungsgemeinschaft
- U.S. Department of Energy (4659)
- 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 › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- excision repair, xeroderma pigmentosum, ultraviolet radiation, UV mutagenesis, human fibroblasts, 8-azaguanine resistance, 6-thioguanine resistance, cell survival, complementation groups
- MeSH terms
- Cell Line, Cells, Cultured, DNA, DNA Repair, Humans, Lesch-Nyhan Syndrome, Skin, Ultraviolet Rays, Xeroderma Pigmentosum
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
