@article{oai:nagoya.repo.nii.ac.jp:00030336,
 author = {Nakazawa, Yuka and Hara, Yuichiro and Oka, Yasuyoshi and Komine, Okiru and van den Heuvel, Diana and Guo, Chaowan and Daigaku, Yasukazu and Isono, Mayu and He, Yuxi and Shimada, Mayuko and Kato, Kana and Jia, Nan and Hashimoto, Satoru and Kotani, Yuko and Miyoshi, Yuka and Tanaka, Miyako and Sobue, Akira and Mitsutake, Norisato and Suganami, Takayoshi and Masuda, Akio and Ohno, Kinji and Nakada, Shinichiro and Mashimo, Tomoji and Yamanaka, Koji and Luijsterburg, Martijn S. and Ogi, Tomoo},
 issue = {6},
 journal = {Cell},
 month = {Mar},
 note = {Transcription-coupled nucleotide excision repair (TC-NER) is initiated by the stalling of elongating RNA polymerase II (RNAPIIo) at DNA lesions. The ubiquitination of RNAPIIo in response to DNA damage is an evolutionarily conserved event, but its function in mammals is unknown. Here, we identified a single DNA damage-induced ubiquitination site in RNAPII at RPB1-K1268, which regulates transcription recovery and DNA damage resistance. Mechanistically, RPB1-K1268 ubiquitination stimulates the association of the core-TFIIH complex with stalled RNAPIIo through a transfer mechanism that also involves UVSSA-K414 ubiquitination. We developed a strand-specific ChIP-seq method, which revealed RPB1-K1268 ubiquitination is important for repair and the resolution of transcriptional bottlenecks at DNA lesions. Finally, RPB1-K1268R knockin mice displayed a short life-span, premature aging, and neurodegeneration. Our results reveal RNAPII ubiquitination provides a two-tier protection mechanism by activating TC-NER and, in parallel, the processing of DNA damage-stalled RNAPIIo, which together prevent prolonged transcription arrest and protect against neurodegeneration., ファイル公開：2021-03-19},
 pages = {1228--1244.e24},
 title = {Ubiquitination of DNA Damage-Stalled RNAPII Promotes Transcription-Coupled Repair},
 volume = {180},
 year = {2020}
}