期刊
FEBS JOURNAL
卷 284, 期 14, 页码 2133-2147出版社
WILEY
DOI: 10.1111/febs.14048
关键词
chromatin; DNA damage response; DNA double-strand breaks; gene silencing; noncoding RNAs; RNA Polymerase II; transcription
资金
- Fondazione Cariplo [2014-1215, 2014-0812]
- Fondazione Italiana per la Ricerca sul Cancro, AIRC [12971]
- Human Frontier Science Program [RGP 0014/2012]
- Cariplo Foundation [2010.0818]
- Marie Curie Initial Training Networks [FP7 PEOPLE 2012 ITN (CodAge)]
- Fondazione Telethon [GGP12059]
- Worldwide Cancer Research [14-1331]
- Progetti di Ricerca di Interesse Nazionale (PRIN)
- Italian Ministry of Education Universities
- Research EPIGEN
- InterOmics Projects
- European Research Council advanced grant [322726]
- European Research Council (ERC) [322726] Funding Source: European Research Council (ERC)
The fine modulation of transcriptional activity around DNA lesions is essential to carefully regulate the crosstalk between the activation of the DNA damage response, DNA repair and transcription, particularly when the lesion occurs next to actively transcribed genes. Recently, several studies have been carried out to investigate how DNA lesions impact on local transcription, but the emerging model remains incomplete. Transcription of genes around damaged DNA is actively downregulated by the DNA damage response through different mechanisms, which appear specific to the chromatin context, the type of DNA damage or its complexity. Intriguingly, emerging evidence also indicates that transcription of noncoding RNAs (ncRNAs) is induced at sites of DNA damage, producing small ncRNAs that are, in turn, required for a full DNA damage response activation. We discuss here these recent findings, highlighting the major unresolved questions in the field, and propose ways to reconcile these apparently contradictory observations.
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