ArticleNucleic acids research2024
Differential processing of RNA polymerase II at DNA damage correlates with transcription-coupled repair syndrome severity.
Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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Who cites it
14 citing papers in PubMed.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- Oxidative stress triggers RNAPII arrest through PARylation and DNA damage.Nature communications · 2026Article
- Genome instability is increased during DNA replication in the presence of the CPD UV photoproduct in transcriptionally active genes.iScience · 2026Article
- Amino-acids-mTORC1-driven DDA1 phosphorylation promotes DNA repair and glioblastoma progression.Cell communication and signaling : CCS · 2026Article
- PAF1C restores transcription after DNA damage independently of promoting histone mark deposition.EMBO reports · 2026Article
- Integrator subunit INTS12 links ribotoxic stress to transcription-coupled nucleotide excision repair.Nature structural & molecular biology · 2026Article
- LMO7-mediated POLR2A degradation promotes cellular senescence through the MDM4/p53/p21 axis.Cell death & disease · 2026Article
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- Hierarchical mechanisms control the clearance of DNA lesion-stalled RNA polymerase II.Nature communications · 2026Article
- RNA polymerase II degradation triggered by DNA repair occurs in trans and independently of how the lesion is recognized.Nucleic acids research · 2026Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- The molecular basis of human transcription-coupled DNA repair.Nature cell biology · 2025Review
- Transcription-coupled repair of crosslinking DNA damage.DNA repair · 2025Review
- RNA Polymerase II Activity Control of Gene Expression and Involvement in Disease.Journal of molecular biology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
DNA damage severely impedes gene transcription by RNA polymerase II (Pol II), causing cellular dysfunction. Transcription-Coupled Nucleotide Excision Repair (TC-NER) specifically removes such transcription-blocking damage. TC-NER initiation relies on the CSB, CSA and UVSSA proteins; loss of any results in complete TC-NER deficiency. Strikingly, UVSSA deficiency results in UV-Sensitive Syndrome (UVSS), with mild cutaneous symptoms, while loss of CSA or CSB activity results in the severe Cockayne Syndrome (CS), characterized by neurodegeneration and premature aging. Thus far the underlying mechanism for these contrasting phenotypes remains unclear. Live-cell imaging approaches reveal that in TC-NER proficient cells, lesion-stalled Pol II is swiftly resolved, while in CSA and CSB knockout (KO) cells, elongating Pol II remains damage-bound, likely obstructing other DNA transacting processes and shielding the damage from alternative repair pathways. In contrast, in UVSSA KO cells, Pol II is cleared from the damage via VCP-mediated proteasomal degradation which is fully dependent on the CRL4CSA ubiquitin ligase activity. This Pol II degradation might provide access for alternative repair mechanisms, such as GG-NER, to remove the damage. Collectively, our data indicate that the inability to clear lesion-stalled Pol II from the chromatin, rather than TC-NER deficiency, causes the severe phenotypes observed in CS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.