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.

van Hoffen, A.; Venema, J.; Meschini, R.; van Zeeland, A.A.; Mullenders, L.H.

doi:10.1002/j.1460-2075.1995.tb07010.x

Cited by 242DNA Repair MechanismsNuclear Structure and FunctionCarcinogens and Genotoxicity Assessment

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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van Hoffen, A., Venema, J., Meschini, R., van Zeeland, A.A., Mullenders, L.H.·1995·The EMBO Journal

DOI 10.1002/j.1460-2075.1995.tb07010.xPMC PMC398090

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Abstract

We investigated the contribution of the global and the transcription-coupled nucleotide excision repair pathway to the removal of structurally different DNA lesions. The repair kinetics of UV-induced cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (6-4PPs) were determined in an active and inactive gene in normal human fibroblasts and in xeroderma pigmentosum group C (XP-C) fibroblasts. Previously we have shown that in normal human cells exposed to a UV dose of 10 J/m2 repair of CPDs takes place via two pathways: global repair and transcription-coupled repair, the latter being responsible for accelerated repair of CPDs in the transcribed strand of active genes. So far, no clear evidence for transcription-coupled repair of 6-4PPs has been presented. Here we demonstrate that 6-4PPs really form a target for transcription-coupled repair. In XP-C cells, exposed to 30 J/m2 and only capable of performing transcription-coupled repair, CPDs as well as 6-4PPs are removed selectively and with similar kinetics from the transcribed strand of the adenosine deaminase (ADA) gene. The non-transcribed strand of the ADA gene and the inactive 754 gene are hardly repaired. In contrast to XP-C cells, normal cells exposed to 30 J/m2 lack strand-specific repair of both 6-4PPs and CPDs, suggesting that transcription-coupled repair is overruled by global repair, probably due to severe inhibition of transcription at this high UV dose. The much more rapid repair of 6-4PPs compared with CPDs in normal cells may be related to higher affinity of the global repair system for the former lesion. In XP-C cells the similarity of the rate of repair of both 6-4PPs and CPDs in the transcribed strand at 30 J/m2 indicates that transcription-coupled repair of photolesions takes place in a sequential way. Our results strongly suggest that the significance of transcription-coupled repair for removal of lesions depends on the type of lesion and on the dose employed.

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GGR is the most preferred and efficient pathway for removing 6-4PPs.
“This indicates that the GGR is the most preferred and efficient pathway for 6-4PP removal [211].”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [211]
The Introduction says global repair removes 6-4PPs faster than transcription-coupled repair in normal human cells, at least at higher UV doses. The Discussion cautions that transcription-coupled repair may dominate at low doses. The claim omits those conditions and presents global repair as universally preferred. (LLM, conf=0.87)
Experimental — accuracy not yet measured
In human XP-C cells, where 6-4PP removal occurs through the TCR pathway, repair appears threefold slower than in normal cells.
“In human XP-C cells, where the removal of 6-4PP takes place through the TCR pathway, the repair seems to be threefold slower as compared to normal cells.”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [211]
The Results section (page not available) reports that XP-C fibroblasts removed 6-4PPs from the active ADA gene much more slowly than normal fibroblasts. The Discussion identifies transcription-coupled repair as the pathway in XP-C cells. The paper does not establish a threefold difference in repair rate: it reports 33% removal after 24 hours in XP-C cells versus 100% within 8 hours in normal cells, which are different extents of repair. (LLM, conf=0.86)
Experimental — accuracy not yet measured
In human and hamster cells, elimination of 6-4PP is at least fivefold faster than elimination of CPDs.
“It has been established that in human and hamster cells, the elimination of 6-4PP is at least fivefold faster than that of CPDs [211].”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [211]
The Results section (page unavailable) reports that 6-4PPs were repaired approximately fivefold faster than CPDs in normal human fibroblasts at the tested UV dose. The paper does not establish that rate for hamster cells, and its Discussion reports similar repair kinetics for the two lesions in human XP-C cells. Thus, the claim overgeneralizes the cell types and states an approximate rate as a minimum. (LLM, conf=0.88)
Experimental — accuracy not yet measured
XPC is the only XP factor not essential for TCR and is restricted to GGR.
“XPC is the sole XP factor not essential for TCR and is restricted to GGR [211].”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [211]
The Introduction says XP-C fibroblasts retain transcription-coupled repair (TCR), and the Discussion contrasts their TCR-only repair with normal cells’ TCR and global repair. This supports that XPC is not essential for TCR and is associated with global repair, but the paper does not establish that XPC is the sole XP factor with that distinction. (LLM, conf=0.84)
Experimental — accuracy not yet measured
6-4PPs are removed much faster from the genome than CPDs, possibly because of differences in affinity of the damage sensor hHR23B-XPC.
“For instance, 6-4PPs are removed much faster from the genome than CPDs, possibly because of disparity in affinity of the damage sensor hHR23B-XPC.”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [211]
The Introduction and results on repair in specific sequences (page not supplied) report that 6-4PPs are repaired much faster than CPDs in normal human fibroblasts. The Discussion reports similar repair kinetics for the two lesions in XP-C fibroblasts. Our copy does not support the proposed explanation involving differential affinity of hHR23B-XPC. (LLM, conf=0.88)
Experimental — accuracy not yet measured

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The xeroderma pigmentosum group C gene leads to selective repair of cyclobutane pyrimidine dimers rather than 6-4 photoproducts
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Authors: van Hoffen, A., Venema, J., Meschini, R., van Zeeland, A. A., & Mullenders, L. H.
Affiliations: Leiden University (NL)
ORCID: Meschini, R.
Venue: The EMBO Journal
Publisher: Springer Science and Business Media LLC
Published: 1995-01-01
Volume: 14
Issue: 2
Pages: 360-367
ISSN: 0261-4189 (ISSN-L)
1460-2075
DOI: 10.1002/j.1460-2075.1995.tb07010.x
PMC: PMC398090
OpenAlex: W1889725400
Cited by: 242
References: 38
Citations by year: 2026: 1 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 2 · 2021: 1 · 2020: 1 · 2019: 2 · 2018: 2 · 2017: 1 · 2015: 5 · 2014: 6 · 2013: 4 · 2012: 6
FWCI: 6.69
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: The EMBO Journal (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Universiteit Leiden
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Carcinogens and Genotoxicity Assessment
Keywords: transcription-coupled repair, cyclobutane pyrimidine dimers, 6-4 photoproducts, xeroderma pigmentosum group C, UV-induced DNA damage, repair kinetics, strand-specific repair, UV dose dependence
MeSH terms: Cells, Cultured, DNA, DNA Repair, Endodeoxyribonucleases, Fibroblasts, Humans, Photochemistry, Pyrimidine Dimers, Transcription, Genetic, Ultraviolet Rays, Xeroderma Pigmentosum, Escherichia coli Proteins

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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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