Phosphorylation of EXO1 by CDKs 1 and 2 regulates DNA end resection and repair pathway choice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-12

AUTHORS

Nozomi Tomimatsu, Bipasha Mukherjee, Molly Catherine Hardebeck, Mariya Ilcheva, Cristel Vanessa Camacho, Janelle Louise Harris, Matthew Porteus, Bertrand Llorente, Kum Kum Khanna, Sandeep Burma

ABSTRACT

Resection of DNA double-strand breaks (DSBs) is a pivotal step during which the choice between NHEJ and HR DNA repair pathways is made. Although CDKs are known to control initiation of resection, their role in regulating long-range resection remains elusive. Here we show that CDKs 1/2 phosphorylate the long-range resection nuclease EXO1 at four C-terminal S/TP sites during S/G2 phases of the cell cycle. Impairment of EXO1 phosphorylation attenuates resection, chromosomal integrity, cell survival and HR, but augments NHEJ upon DNA damage. In contrast, cells expressing phospho-mimic EXO1 are proficient in resection even after CDK inhibition and favour HR over NHEJ. Mutation of cyclin-binding sites on EXO1 attenuates CDK binding and EXO1 phosphorylation, causing a resection defect that can be rescued by phospho-mimic mutations. Mechanistically, phosphorylation of EXO1 augments its recruitment to DNA breaks possibly via interactions with BRCA1. In summary, phosphorylation of EXO1 by CDKs is a novel mechanism regulating repair pathway choice. More... »

PAGES

3561

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms4561

DOI

http://dx.doi.org/10.1038/ncomms4561

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008266362

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24705021


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