期刊
NUCLEUS
卷 5, 期 3, 页码 203-210出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/nucl.29085
关键词
transcription coupled nucleotide excision repair (TC-NER); transcription restart; chromatin remodeling; HIRA; DOT1l; FACT; SPT16
类别
资金
- Netherlands Organization for Scientific Research project (TOP ALW) [854.11.002]
- Netherlands Organization for Scientific Research project (ZonMW TOP) [912.08.031, 917.96.120]
- Netherlands Organization for Scientific Research project (Horizon Zenith) [93511042]
- Erasmus MC fellowship
- ERC advanced grant
During transcription, RNA polymerase may encounter DNA lesions, which causes stalling of transcription. To overcome the RNA polymerase blocking lesions, the transcribed strand is repaired by a dedicated repair mechanism, called transcription coupled nucleotide excision repair (TC-NER). After repair is completed, it is essential that transcription restarts. So far, the regulation and exact molecular mechanism of this transcriptional restart upon genotoxic damage has remained elusive. Recently, three different chromatin remodeling factors, HIRA, FACT, and Dot1L, were identified to stimulate transcription restart after DNA damage. These factors either incorporate new histones or establish specific chromatin marks that will gear up the chromatin to subsequently promote transcription recovery. This adds a new layer to the current model of chromatin remodeling necessary for repair and indicates that this specific form of transcription, i.e., the transcriptional restart upon DNA damage, needs specific chromatin remodeling events.
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