ArticleNature communications2020
Continuous transcription initiation guarantees robust repair of all transcribed genes and regulatory regions.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed.
- Comparative analysis of the transcriptome and methylome in distinct trophoblast populations at the time of embryo implantation in mares.BMC genomics · 2026Article
- IncRNA-ZFAS1, an Emerging Gate-Keeper in DNA Damage-Dependent Transcriptional Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cockayne syndrome B protein is implicated in transcription and associated chromatin dynamics in homeostatic and genotoxic conditions.Aging cell · 2025Article
- Rapid P-TEFb-dependent transcriptional reorganization underpins the glioma adaptive response to radiotherapy.Nature communications · 2024Article
- Gene architecture is a determinant of the transcriptional response to bulky DNA damages.Life science alliance · 2024Article
- Enhanced frequency of transcription pre-initiation complexes assembly after exposure to UV irradiation results in increased repair activity and reduced probabilities for mutagenesis.Nucleic acids research · 2023Article
- Review
- Histone H2Bub dynamics in the 5' region of active genes are tightly linked to the UV-induced transcriptional response.Computational and structural biotechnology journal · 2023Article
- A novel, rapid and sensitive flow cytometry method reveals degradation of promoter proximal paused RNAPII in the presence and absence of UV.Nucleic acids research · 2022Article
- Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022Review
- A new technique for genome-wide mapping of nucleotide excision repair without immunopurification of damaged DNA.The Journal of biological chemistry · 2022Article
- Cellular fractionation reveals transcriptome responses of human fibroblasts to UV-C irradiation.Cell death & disease · 2022Article
- Current Analytical Strategies in Studying Chromatin-Associated-Proteome (Chromatome).Molecules (Basel, Switzerland) · 2021Review
- aniFOUND: analysing the associated proteome and genomic landscape of the repaired nascent non-replicative chromatin.Nucleic acids research · 2021Article
- Genomic Characterization of Cisplatin Response Uncovers Priming of Cisplatin-Induced Genes in a Resistant Cell Line.International journal of molecular sciences · 2021Article
- Exons and introns exhibit transcriptional strand asymmetry of dinucleotide distribution, damage formation and DNA repair.NAR genomics and bioinformatics · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inhibition of transcription caused by DNA damage-impaired RNA polymerase II (Pol II) elongation conceals a local increase in de novo transcription, slowly progressing from Transcription Start Sites (TSSs) to gene ends. Although associated with accelerated repair of Pol II-encountered lesions and limited mutagenesis, it is still unclear how this mechanism is maintained during genotoxic stress-recovery. Here we uncover a widespread gain in chromatin accessibility and preservation of the active H3K27ac mark after UV-irradiation. The concomitant increase in Pol II escape from promoter-proximal pause (PPP) sites of most active genes, PROMPTs and enhancer RNAs favors unrestrained initiation, as evidenced by the synthesis of nascent RNAs including start RNAs. Accordingly, drug-inhibition of PPP-release replenishes levels of pre-initiating Pol II at TSSs after UV. Our data show that such continuous engagement of Pol II molecules ensures maximal transcription-driven repair throughout expressed genes and regulatory loci. Importantly, revealing this unanticipated regulatory layer of UV-response provides physiological relevant traction to the emerging concept that Pol II initiation rate is determined by pause-release dynamics.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.