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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.
Open accessAbstract
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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“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]
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“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]
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“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]
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“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]
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“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]
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“Although both 6-4PPs and CPDs are removed presumably by the same NER proteins, the relative repair efficiency of both of these lesions varies considerably in mammalian cells.”
From Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair (2010) · cites this paper as [211]
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Cited by
Sorted by citations
Molecular Mechanisms of Ultraviolet Radiation‐Induced DNA Damage and Repair
Rastogi, R. P., Richa, Kumar, A., Tyagi, M. B., & Sinha, R. P. (2010) · Journal of Nucleic Acids · doi:10.4061/2010/592980 · Cited by 1,329
“…been observed that the large structural distortion induced by the (6-4) lesion may ensure a favorable recognition by the repair enzyme, which may possibly elucidate the correlation with the elevated repair rate of the T-T (6-4) adduct than of the T-T Dewar product and the T-T cis-syn dimer [76].”
BackgroundMolecular mechanism of nucleotide excision repair
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Self-citation
Metadata
- 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
- Published
- 1995-01-01
- Volume
- 14
- Issue
- 2
- Pages
- 360-367
- ISSN
- 0261-4189 (ISSN-L)
- 1460-2075
- 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
- 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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