期刊
MOLECULAR CELL
卷 70, 期 1, 页码 34-+出版社
CELL PRESS
DOI: 10.1016/j.molcel.2018.02.017
关键词
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资金
- Fondazione Umberto Veronesi (FUV) Fellowship
- AIRC [15631]
- Telethon [GGP15227]
- MIUR
- Spanish Ministry of Economy and Competitiveness [BFU2016-75058-P]
UV-induced photoproducts are responsible for the pathological effects of sunlight. Mutations in nucleotide excision repair (NER) cause severe pathologies characterized by sunlight sensitivity, coupled to elevated predisposition to cancer and/or neurological dysfunctions. We have previously shown that in UV-irradiated non-cycling cells, only a particular subset of lesions activates the DNA damage response (DDR), and this requires NER and EXO1 activities. To define the molecular mechanism acting at these lesions, we demonstrate that Y family TLS polymerases are recruited atNER- and EXO1-positive lesion sites in non-S phase cells. The coordinated action of EXO1 and Y family TLS polymerases promotes checkpoint activation, leads to lesion repair, and is crucial to prevent cytotoxic double-strand break (DSB) formation.
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