ArticleNucleic acids research2014
UV light-induced DNA lesions cause dissociation of yeast RNA polymerases-I and establishment of a specialized chromatin structure at rRNA genes.
Article in Nucleic acids research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- Psoralen Crosslinking-Chromatin Endogenous Cleavage Assay to Examine Histone DNA Interactions of Active and Inactive rRNA Genes.Methods in molecular biology (Clifton, N.J.) · 2025Article
- RNA polymerase pausing, stalling and bypass during transcription of damaged DNA: from molecular basis to functional consequences.Nucleic acids research · 2022Review
- Transcription of ncRNAs promotes repair of UV induced DNA lesions in Saccharomyces cerevisiae subtelomeres.PLoS genetics · 2022Article
- Establishment and Maintenance of Open Ribosomal RNA Gene Chromatin States in Eukaryotes.Methods in molecular biology (Clifton, N.J.) · 2022Review
- In vivo chromatin organization on native yeast telomeric regions is independent of a cis-telomere loopback conformation.Epigenetics & chromatin · 2020Article
- A SUMO-dependent pathway controls elongating RNA Polymerase II upon UV-induced damage.Scientific reports · 2019Article
- Analyses of rRNA gene chromatin in cell cycle arrestedData in brief · 2019Article
- Mechanistic insights in transcription-coupled nucleotide excision repair of ribosomal DNA.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Yeast HMO1: Linker Histone Reinvented.Microbiology and molecular biology reviews : MMBR · 2017Review
- Cellular sensitivity to UV-irradiation is mediated by RNA polymerase I transcription.PloS one · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cytotoxicity of UV light-induced DNA lesions results from their interference with transcription and replication. DNA lesions arrest elongating RNA polymerases, an event that triggers transcription-coupled nucleotide excision repair. Since arrested RNA polymerases reduce the accessibility of repair factors to DNA lesions, they might be displaced. The fate of arrested RNA polymerases-II at DNA lesions has been extensively studied, yielding partially contradictory results. Considerably less is known about RNA polymerases-I that transcribe nucleosomes-depleted rRNA genes at very high rate. To investigate the fate of arrested RNA polymerases-I at DNA lesions, chromatin-immunoprecipitation, electron microscopy, transcription run-on, psoralen-cross-linking and chromatin-endogenous cleavage were employed. We found that RNA polymerases-I density increased at the 5'-end of the gene, likely due to continued transcription initiation followed by elongation and pausing/release at the first DNA lesion. Most RNA polymerases-I dissociated downstream of the first DNA lesion, concomitant with chromatin closing that resulted from deposition of nucleosomes. Although nucleosomes were deposited, the high mobility group-box Hmo1 (component of actively transcribed rRNA genes) remained associated. After repair of DNA lesions, Hmo1 containing chromatin might help to restore transcription elongation and reopening of rRNA genes chromatin.
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