Abstract：
:We have previously found that UV irradiation promotes RNA polymerase II (RNAPII) hyperphosphorylation and subsequent changes in alternative splicing (AS). We show now that UV-induced DNA damage is not only necessary but sufficient to trigger the AS response and that photolyase-mediated removal of the most abundant class of pyrimidine dimers (PDs) abrogates the global response to UV. We demonstrate that, in keratinocytes, RNAPII is the target, but not a sensor, of the signaling cascade initiated by PDs. The UV effect is enhanced by inhibition of gap-filling DNA synthesis, the last step in the nucleotide excision repair pathway (NER), and reduced by the absence of XPE, the main NER sensor of PDs. The mechanism involves activation of the protein kinase ATR that mediates the UV-induced RNAPII hyperphosphorylation. Our results define the sequence UV-PDs-NER-ATR-RNAPII-AS as a pathway linking DNA damage repair to the control of both RNAPII phosphorylation and AS regulation.
journal_name
Cell Repjournal_title
Cell reportsauthors
Muñoz MJ,Nieto Moreno N,Giono LE,Cambindo Botto AE,Dujardin G,Bastianello G,Lavore S,Torres-Méndez A,Menck CFM,Blencowe BJ,Irimia M,Foiani M,Kornblihtt ARdoi
10.1016/j.celrep.2017.02.066subject
Has Abstractpub_date
2017-03-21 00:00:00pages
2868-2879issue
12issn
2211-1247pii
S2211-1247(17)30281-4journal_volume
18pub_type
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