Mammalian Transcription-Coupled Excision Repair
Open accessAbstract
Transcriptional arrest caused by DNA damage is detrimental for cells and organisms as it impinges on gene expression and thereby on cell growth and survival. To alleviate transcriptional arrest, cells trigger a transcription-dependent genome surveillance pathway, termed transcription-coupled nucleotide excision repair (TC-NER) that ensures rapid removal of such transcription-impeding DNA lesions and prevents persistent stalling of transcription. Defective TC-NER is causatively linked to Cockayne syndrome, a rare severe genetic disorder with multisystem abnormalities that results in patients' death in early adulthood. Here we review recent data on how damage-arrested transcription is actively coupled to TC-NER in mammals and discuss new emerging models concerning the role of TC-NER-specific factors in this process.
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Upon damage occurrence, the ligase is inactivated by COP9 signalosome (CSN) that deneddylates Cullin 4A.
“However, upon damage occurrence the ligase is inactivated by constitutive photomorphogenesis 9 (COP9) signalosome (CSN) that deneddylates Cullin 4A.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
TC-NER is the repair closely connected with actively transcribed genes.
“TC-NER is the repair closely connected with actively transcribed genes.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
TC-NER protects cells from apoptosis and cell cycle arrest in case of robust DNA damage response.
“Thus, TC-NER protects the cells from apoptosis and cell cycle arrest in case of robust DNA damage response.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
CSA together with DDB1, Cullin 4A and RBX proteins works as an E3-ubiquitin ligase.
“CSA together with DDB1, Cullin 4A and E3 ubiquitin-protein ligase RBX1 (RBX) proteins works as a E3-ubiquitin ligase.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
In contrast to other generally mutagenic repair mechanisms such as TLS, TC-NER resolves lesions with high rapidness and fidelity.
“In contrast to other generally mutagenic repair mechanisms such as translesion synthesis (TLS), TC-NER resolves lesions with high rapidness and fidelity.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
TC-NER is initiated in response to stalling of RNA polymerase II at sites of damage.
“TC-NER is initiated in response to stalling of RNA polymerase II (RNAPII) at the sites of damage.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
Transcriptional arrest following DNA damage interferes with gene expression, influencing cell growth and survival.
“This is of particular importance, given the fact that transcriptional arrest following DNA damage interfere with gene expression influencing cell growth and survival.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
CSA is crucial for recruitment of other TC-NER components.
“CSA is also crucial for recruitment of other TC-NER components described further below.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
Stalling of RNAPII at sites of UV damage immediately activates TC-NER.
“Stalling of RNAPII at sites of UV damage immediately activates TC-NER.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
Repair begins with recruitment of CSA(ERCC8) and CSB(ERCC6) to lesions.
“The repair begins with the recruitment of CSA(ERCC8) and CSB(ERCC6) to the lesions [97].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
Blocked transcription complexes are extremely cytotoxic structures.
“Moreover, blocked transcription complexes are extremely cytotoxic structures.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
Down-regulation or mutation in XAB2, USP7, or HMGN1 results in impaired repair of lesions in transcribed strands and leads to apoptosis of cells harboring damage.
“Down-regulation or mutation in the former factors results in impaired repair of lesions in transcribed strands and lead to apoptosis of cells harboring damage [97].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
TC-NER prevents formation of mutant transcripts and is pivotal for cellular homeostasis.
“This prevents formation of mutant transcripts and is pivotal for the cellular homeostasis.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
XAB2 interacts with XPA protein and RNAPII, playing a role as a scaffold for other TC-NER components.
“XAB2 interacts with XPA protein and RNAPII, playing role as a scaffold for other TC-NER components.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
CSB protein is a DNA-dependent ATPase and nucleosome remodeling enzyme involved in transcriptional control of genes following UV irradiation.
“On the other hand, CSB protein is a DNA-dependent ATPase and nucleosome remodeling enzyme involved in transcriptional control of genes following UV irradiation.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [97]
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References 121 · Cited by 184
- Authors
- Vermeulen, W., & Fousteri, M.
- Affiliations
- Erasmus MC (NL)
- Alexander Fleming Biomedical Sciences Research Center (GR)
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2013-08-01
- Volume
- 5
- Issue
- 8
- Pages
- a012625-a012625
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC3721277
- OpenAlex
- W2162365619
- Cited by
- 184
- References
- 121
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 5 · 2023: 13 · 2022: 9 · 2021: 17 · 2020: 12 · 2019: 10 · 2018: 14 · 2017: 20 · 2016: 26 · 2015: 19 · 2014: 27 · 2013: 3 · 2012: 1
- Type
- posted content
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- RePub (Erasmus University Rotterdam) (submittedVersion, other-oa)
- Funders
- European Commission (253544)
- ZonMw
- FP7 Ideas: European Research Council (309612)
- 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 › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- transcription-coupled repair, transcriptional arrest, DNA damage, Cockayne syndrome, genomic surveillance, DNA repair proteins
- MeSH terms
- Animals, Chromatin, Cockayne Syndrome, DNA Damage, DNA Repair, Mammals, Models, Genetic, Transcription, Genetic
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