Journal
MOLECULAR CELL
Volume 70, Issue 1, Pages 34-+Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2018.02.017
Keywords
-
Categories
Funding
- Fondazione Umberto Veronesi (FUV) Fellowship
- AIRC [15631]
- Telethon [GGP15227]
- MIUR
- Spanish Ministry of Economy and Competitiveness [BFU2016-75058-P]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available