ArticleNucleic acids research2019
FACT subunit Spt16 controls UVSSA recruitment to lesion-stalled RNA Pol II and stimulates TC-NER.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 48 citations in OpenAlex.
- Mechanisms of transcription-coupled repair and DNA damage surveillance in health and disease.Nature reviews. Molecular cell biology · 2026Review
- DGCR8 regulates multiple processes of transcription coupled nucleotide excision repair.Scientific reports · 2026Article
- Review
- PARP1 and PARylation facilitate transcription-coupled DNA repair by stabilizing the CSB-RNAPII complex.Nucleic acids research · 2025Article
- Transcription-coupled repair: tangled up in convoluted repair.The FEBS journal · 2025Review
- Beyond Chaperoning: The Multifaceted Role of FACT in Chromatin Transactions.International journal of molecular sciences · 2025Review
- Histone variant H2A.Z is needed for efficient transcription-coupled NER and genome integrity in UV challenged yeast cells.PLoS genetics · 2024Article
- The FABD domain is critical for the oncogenicity of BCR/ABL in chronic myeloid leukaemia.Cell communication and signaling : CCS · 2024Article
- DNA Repair in Nucleosomes: Insights from Histone Modifications and Mutants.International journal of molecular sciences · 2024Review
- Live-cell imaging of endogenous CSB-mScarletI as a sensitive marker for DNA-damage-induced transcription stress.Cell reports methods · 2024Article
- ASH1L-MRG15 methyltransferase deposits H3K4me3 and FACT for damage verification in nucleotide excision repair.Nature communications · 2023Article
- Genome-wide mapping of protein-DNA damage interaction by PADD-seq.Nucleic acids research · 2023Article
- FACT subunit SUPT16H associates with BRD4 and contributes to silencing of interferon signaling.Nucleic acids research · 2022Article
- Phosphorylation of the FACT histone chaperone subunit SPT16 affects chromatin at RNA polymerase II transcriptional start sites in Arabidopsis.Nucleic acids research · 2022Article
- Active DNA damage eviction by HLTF stimulates nucleotide excision repair.Molecular cell · 2022Article
- Targets Exploration of Hydroxychloroquine for Pigmentation and Cell Protection Effect in Melanocytes: The Clue for Vitiligo Treatment.Drug design, development and therapy · 2022Article
- Dissecting regulatory pathways for transcription recovery following DNA damage reveals a non-canonical function of the histone chaperone HIRA.Nature communications · 2021Article
- Elongation factor ELOF1 drives transcription-coupled repair and prevents genome instability.Nature cell biology · 2021Article
- SMARCAD1-mediated active replication fork stability maintains genome integrity.Science advances · 2021Article
- FACT subunit SUPT16H associates with BRD4 and contributes to silencing of antiviral interferon signaling.bioRxiv : the preprint server for biology · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription-coupled nucleotide excision repair (TC-NER) is a dedicated DNA repair pathway that removes transcription-blocking DNA lesions (TBLs). TC-NER is initiated by the recognition of lesion-stalled RNA Polymerase II by the joint action of the TC-NER factors Cockayne Syndrome protein A (CSA), Cockayne Syndrome protein B (CSB) and UV-Stimulated Scaffold Protein A (UVSSA). However, the exact recruitment mechanism of these factors toward TBLs remains elusive. Here, we study the recruitment mechanism of UVSSA using live-cell imaging and show that UVSSA accumulates at TBLs independent of CSA and CSB. Furthermore, using UVSSA deletion mutants, we could separate the CSA interaction function of UVSSA from its DNA damage recruitment activity, which is mediated by the UVSSA VHS and DUF2043 domains, respectively. Quantitative interaction proteomics showed that the Spt16 subunit of the histone chaperone FACT interacts with UVSSA, which is mediated by the DUF2043 domain. Spt16 is recruited to TBLs, independently of UVSSA, to stimulate UVSSA recruitment and TC-NER-mediated repair. Spt16 specifically affects UVSSA, as Spt16 depletion did not affect CSB recruitment, highlighting that different chromatin-modulating factors regulate different reaction steps of the highly orchestrated TC-NER pathway.
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