Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 115, Issue 29, Pages E6770-E6779Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1716581115
Keywords
human ribosomal DNA; nucleotide excision repair; RNAP1 transcription; UV lesions; nucleolar organization
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Funding
- La Ligue Nationale Contre le Cancer
- l'Agence Nationale de la Recherche (ANR FreTNET) [ANR10-BLAN-1231-01]
- l'Agence Nationale de la Recherche (ANR DyReCT) [ANR-14-CE10-0009]
- Association pour la Recherche sur le Cancer [ARC PJA 20131200188]
- Agence Nationale de la Recherche (ANR) [ANR-14-CE10-0009] Funding Source: Agence Nationale de la Recherche (ANR)
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Nucleotide excision repair (NER) guarantees genome integrity against UV light-induced DNA damage. After UV irradiation, cells have to cope with a general transcriptional block. To ensure UV lesions repair specifically on transcribed genes, NER is coupled with transcription in an extremely organized pathway known as transcription-coupled repair. In highly metabolic cells, more than 60% of total cellular transcription results from RNA polymerase I activity. Repair of the mammalian transcribed ribosomal DNA has been scarcely studied. UV lesions severely block RNA polymerase I activity and the full transcription-coupled repair machinery corrects damage on actively transcribed ribosomal DNAs. After UV irradiation, RNA polymerase I is more bound to the ribosomal DNA and both are displaced to the nucleolar periphery. Importantly, the reentry of RNA polymerase I and the ribosomal DNA is dependent on the presence of UV lesions on DNA and independent of transcription restart.
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