DNA repair in an active gene: Removal of pyrimidine dimers from the DHFR gene of CHO cells is much more efficient than in the genome overall

Bohr, V

doi:10.1016/0092-8674(85)90150-3

Cited by 1,237DNA Repair MechanismsCarcinogens and Genotoxicity AssessmentEffects of Radiation Exposure

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DNA repair in an active gene: Removal of pyrimidine dimers from the DHFR gene of CHO cells is much more efficient than in the genome overall

Bohr, V·1985·Cell

DOI 10.1016/0092-8674(85)90150-3

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Abstract

DNA repair was measured in the dihydrofolate reductase gene in Chinese hamster ovary cells, amplified for the gene, by quantitating pyrimidine dimers with a specific UV-endonuclease. More than two thirds of the dimers had been removed from a 14.1 kb restriction fragment of the gene by 26 hr after irradiation (20 J/m2), while little removal was detected in fragments upstream of the gene and only 15% were removed from the genome overall. This suggests that damage processing can vary according to function or activity of affected sequences, which has general implications for correlations of DNA repair with survival and mutagenesis. Perhaps preferential repair of vital sequences facilitates UV-resistance of these cells despite low overall repair levels.

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XPA is an indispensable factor for both transcription-coupled NER and global genome NER.
“XPA is an indispensable factor both for transcription-coupled NER and global genome NER [7], [8].”
From UV-Induced Nuclear Import of XPA Is Mediated by Importin-α4 in An ATR-Dependent Manner (2013) · cites this paper as [7]
Two subpathways of NER exist: transcription-blocking lesions in the transcribed strand of active genes are repaired quickly by transcription-coupled NER, whereas the rest of the genome, including the nontranscribed strand of active genes, is repaired more slowly by global genome NER.
“Two subpathways of NER exist: transcription-blocking lesions in the transcribed strand (TS) of active genes are repaired quickly by transcription-coupled NER (TC-NER), whereas the rest of the genome, including the nontranscribed strand (NTS) of active genes, is repaired more slowly by global genome NER (GG-NER) (8, 33, 34, 44, 54).”
From A Role for Checkpoint Kinase-Dependent Rad26 Phosphorylation in Transcription-Coupled DNA Repair in Saccharomyces cerevisiae (2010) · cites this paper as [8]

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Venema, J., van Hoffen, A., Karcagi, V., Natarajan, A. T., van Zeeland, A. A., & Mullenders, L. H. F. (1991) · Molecular and Cellular Biology · doi:10.1128/mcb.11.8.4128 · Cited by 319
Cockayne syndrome group B protein enhances elongation by RNA polymerase II
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DNA REPAIR GENES AND PROTEINS OF SACCHAROMYCES CEREVISIAE
Prakash, S., Sung, P., & Prakash, L. (1993) · Annual Review of Genetics · doi:10.1146/annurev.ge.27.120193.000341 · Cited by 303
Slow Repair of Pyrimidine Dimers at p53 Mutation Hotspots in Skin Cancer
Tornaletti, S., & Pfeifer, G. P. (1994) · Science · doi:10.1126/science.8128225 · Cited by 296
Oxidatively induced DNA damage: Mechanisms, repair and disease
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TP53 mutations in human skin cancers
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“TCR repairs a subset of lesions, including UV-lesions, on the transcribed strand of active genes while GGR repairs those lesions on the rest of the genome [Bohr et al., 1985; Le Page et al., 2000; Mellon et al., 1987].”
Background
Deficient repair of the transcribed strand of active genes in Cockayne's syndrome cells
van Hoffen, A., Natarajan, A. T., Mayne, L. V., van Zeeland, A. A., Mullenders, L. H. F., & Venema, J. (1993) · Nucleic Acids Research · doi:10.1093/nar/21.25.5890 · Cited by 291
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“of cell viability, and (2) polymorphisms may induce detrimental”
Background
DNA Repair: Enzymatic Mechanisms and Relevance to Drug Response
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Mechanisms of DNA Repair by Photolyase and Excision Nuclease (Nobel Lecture)
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Human Transcription-Repair Coupling Factor CSB/ERCC6 Is a DNA-stimulated ATPase but Is Not a Helicase and Does Not Disrupt the Ternary Transcription Complex of Stalled RNA Polymerase II
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Analysis of Gene-Specific DNA Damage and Repair Using Quantitative Polymerase Chain Reaction
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The Cockayne syndrome B protein, involved in transcription‐coupled DNA repair, resides in an RNA polymerase II‐containing complex
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“…et al., 1992), a clear link exists4Corresponding author between transcription and repair efficiency (Bohr, 1991).e-mail: HOEIJMAKERS@GEN.FGG.EUR.NL Bohr et al. (1985) were the first to show that active RNA A.J.van Gool and E.Citterio contributed equally to this work polymerase II-transcribed…”
Background
NUCLEOTIDE EXCISION REPAIR
Sancar, A., & Tang, M. (1993) · Photochemistry and Photobiology · doi:10.1111/j.1751-1097.1993.tb09233.x · Cited by 262
Oxidatively induced DNA damage and its repair in cancer
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RAD26, the functional S. cerevisiae homolog of the Cockayne syndrome B gene ERCC6.
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The Induction and Repair of DNA Photodamage in the Environment
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Transcription‐coupled repair removes both cyclobutane pyrimidine dimers and 6‐4 photoproducts with equal efficiency and in a sequential way from transcribed DNA in xeroderma pigmentosum group C fibroblasts.
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The XPD variant alleles are associated with increased aromatic DNA adduct level and lung cancer risk
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“GG 3.3 1.7 (51) 3.0 1.4 (13) 6.1 (1) 3.3 1.6 (65) GA 2.8 1.7 (15) 3.8 1.7 (59) 4.0 1.4 (13) 3.6 1.7 (87) AA 4.1 1.4 ( 2 ) 3.3 1.5 (3) 3.4 1.6 (14) 3.4 1.5 (19)”
BackgroundInfluential
The genetic control of direct-repeat recombination in Saccharomyces: the effect of rad52 and rad1 on mitotic recombination at GAL10, a transcriptionally regulated gene.
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Self-citation
How DNA lesions are turned into powerful killing structures: Insights from UV-induced apoptosis
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“On the other hand, GGR can remove (6-4)PPs from the genome much faster than CPDs [36] which is probably related to the fact that the XPC-HR23B complex”
Effect of DNA lesions on transcription elongation
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Preferential DNA secondary structure mutagenesis in the lagging strand of replication in E. coli
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DNA Repair Mechanisms and the Bypass of DNA Damage in Saccharomyces cerevisiae
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“TC-NER was discovered in mammalian cells, where repair of CPDs is faster in the expressed DHFR gene than in transcriptionally silent downstream sequences (Bohr et al. 1985).”
Background
Powerful Skin Cancer Protection by a CPD-Photolyase Transgene
Jans, J., Schul, W., Sert, Y.-G., Rijksen, Y., Rebel, H., Eker, A. P. M., Nakajima, S., van Steeg, H., de Gruijl, F. R., Yasui, A., et al. (2005) · Current Biology · doi:10.1016/j.cub.2005.01.001 · Cited by 227
DNA repair and the role of chromatin structure
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Multiple Mechanisms Confining RNA Polymerase II Ubiquitylation to Polymerases Undergoing Transcriptional Arrest
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“Several types of DNA lesions in the transcribed strand of active genes are removed much more quickly than in the nontranscribed strand or in the genome overall, via a process called transcription-coupled nucleotide excision repair (TC-NER) (Bohr et al., 1985; Svejstrup, 2002).”
BackgroundInfluential
The residual repair capacity of xeroderma pigmentosum complementation group C fibroblasts is highly specific for transcriptionally active DNA
Venema, J., van Hoffen, A., Natarajan, A. T., van Zeeland, A. A., & Mullenders, L. H. F. (1990) · Nucleic Acids Research · doi:10.1093/nar/18.3.443 · Cited by 224
Damage, Repair, and Mutagenesis in Nuclear Genes after Mouse Forebrain Ischemia–Reperfusion
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“The amount of zero class and the frequency of Fpg protein-sensitive sites (FPGSS) in the actin genes were calculated as described previously (Bohr et al., 1985; Mellon et al., 1987).”
Method
Effect of gamma rays at the dihydrofolate reductase locus: Deletions and inversions
Urlaub, G., Mitchell, P. J., Käs, E., Chasin, L. A., Funanage, V. L., Myoda, T. T., & Hamlin, J. L. (1986) · Somatic Cell and Molecular Genetics · doi:10.1007/bf01671941 · Cited by 222
Dial 9-1-1 for p53: Mechanisms of p53 Activation by Cellular Stress
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Site-specific DNA repair at the nucleosome level in a yeast minichromosome
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Biological consequences of oxidative stress-induced DNA damage in Saccharomyces cerevisiae
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CSB Is a Component of RNA Pol I Transcription
Bradsher, J., Auriol, J., Proietti‐De‐Santis, L., Iben, S., Vonesch, J., Grummt, I., & Egly, J. (2002) · Molecular Cell · doi:10.1016/s1097-2765(02)00678-0 · Cited by 221
Escherichia coli mfd mutant deficient in "mutation frequency decline" lacks strand-specific repair: in vitro complementation with purified coupling factor.
Selby, C. P., Witkin, E. M., & Sancar, A. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.24.11574 · Cited by 215
UV-induced formation of pyrimidine dimers in nucleosome core DNA is strongly modulated with a period of 10.3 bases.
Gale, J. M., Nissen, K. A., & Smerdon, M. J. (1987) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.84.19.6644 · Cited by 210
Molecular and Cellular Effects of Ultraviolet Light-Induced Genotoxicity
Griffiths, H. R., Mistry, P., Herbert, K. E., & Lunec, J. (1998) · Critical Reviews in Clinical Laboratory Sciences · doi:10.1080/10408369891234192 · Cited by 210

Authors: Bohr, V
Affiliations: Stanford University (US)
Corresponding author: Bohr, V
ORCID: Bohr, V
Venue: Cell
Publisher: Elsevier BV
Published: 1985-02
Volume: 40
Issue: 2
Pages: 359-369
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/0092-8674(85)90150-3
OpenAlex: W1984353960
Cited by: 1,237
References: 34
Citations by year: 2026: 11 · 2025: 17 · 2024: 15 · 2023: 14 · 2022: 12 · 2021: 17 · 2020: 18 · 2019: 11 · 2018: 18 · 2017: 13 · 2016: 23 · 2015: 9 · 2014: 24 · 2013: 24 · 2012: 22
FWCI: 15.13
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute of General Medical Sciences (GM 09901)
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: DNA repair, pyrimidine dimers, dihydrofolate reductase gene, UV-induced DNA damage, UV endonuclease, UV resistance, CHO cells, mutagenesis, cell survival
MeSH terms: Animals, Base Sequence, Cell Line, Cell Survival, Cricetulus, DNA Repair, Endodeoxyribonucleases, Female, Cricetinae, Multienzyme Complexes, N-Glycosyl Hydrolases, Pyrimidine Dimers, Tetrahydrofolate Dehydrogenase

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DNA repair in an active gene: Removal of pyrimidine dimers from the DHFR gene of CHO cells is much more efficient than in the genome overall

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