Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene

MELLON, I

doi:10.1016/0092-8674(87)90151-6

Cited by 1,228DNA Repair MechanismsDNA and Nucleic Acid ChemistryCarcinogens and Genotoxicity Assessment

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Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene

MELLON, I·1987·Cell

DOI 10.1016/0092-8674(87)90151-6

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Abstract

We find a dramatic difference in the efficiency of removal of UV-induced pyrimidine dimers from the transcribed and nontranscribed strands of the dihydrofolate reductase (DHFR) gene in cultured hamster and human cells. In hamster cells, 80% of the dimers are removed from the transcribed strand in 4 hr, but little repair occurs in the nontranscribed strand even after 24 hr. In human cells, repair is significantly faster in the transcribed strand than in the other strand. Furthermore, in the 5' flanking region of the human DHFR gene, selective rapid repair occurs in the opposite DNA strand relative to the transcribed strand of the DHFR gene. This strand is thought to serve as a template for transcription of a divergent transcript. These results have important implications for excision repair pathways and mutagenesis in mammalian cells.

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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 [8]
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 [34]

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Authors: MELLON, I.
Affiliations: Stanford University (US)
Corresponding author: MELLON, I
ORCID: MELLON, I
Venue: Cell
Publisher: Elsevier BV
Published: 1987-10
Volume: 51
Issue: 2
Pages: 241-249
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/0092-8674(87)90151-6
OpenAlex: W2059901912
Cited by: 1,228
References: 38
Citations by year: 2026: 11 · 2025: 10 · 2024: 13 · 2023: 18 · 2022: 16 · 2021: 18 · 2020: 20 · 2019: 13 · 2018: 22 · 2017: 18 · 2016: 28 · 2015: 19 · 2014: 26 · 2013: 23 · 2012: 29
FWCI: 11.43
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Funders: American Cancer Society
National Cancer Institute (CA35744)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Keywords: DNA repair, pyrimidine dimers, UV-induced DNA damage, transcribed strand, dihydrofolate reductase gene, excision repair, divergent transcription, 5'-flanking region, hamster cells, human cells, mutagenesis
MeSH terms: Animals, Cell Line, Cricetulus, DNA Damage, DNA Repair, Female, Genes, Cricetinae, Humans, Tetrahydrofolate Dehydrogenase, Transcription, Genetic

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Selective removal of transcription-blocking DNA damage from the transcribed strand of the mammalian DHFR gene

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