期刊
CELL REPORTS
卷 9, 期 6, 页码 2011-2017出版社
CELL PRESS
DOI: 10.1016/j.celrep.2014.11.044
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资金
- Cancer Research UK [C1470/A12430]
- Biotechnology and Biological Sciences Research Council [BB/M004236/1]
- Medical Research Council (MRC) [G0801130]
- Portuguese Fundacao para a Ciencia e Tecnologia (FCT) [PTDC/SAU-OBD/66438/2006, PTDC/BIA-BCM/099367/2008]
- FCT postdoctoral fellowship
- MRC-Doctoral Training Account PhD studentship
- Research Councils UK
- BBSRC [BB/M004236/1] Funding Source: UKRI
- MRC [G0801130] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/M004236/1] Funding Source: researchfish
- Medical Research Council [G0801130] Funding Source: researchfish
- Fundação para a Ciência e a Tecnologia [PTDC/BIA-BCM/099367/2008, PTDC/SAU-OBD/66438/2006] Funding Source: FCT
Eukaryotic cells use two principal mechanisms for repairing DNA double-strand breaks (DSBs): homologous recombination (HR) and nonhomologous end-joining (NHEJ). DSB repair pathway choice is strongly regulated during the cell cycle. Cyclin-dependent kinase 1 (Cdk1) activates HR by phosphorylation of key recombination factors. However, a mechanism for regulating the NHEJ pathway has not been established. Here, we report that Xlf1, a fission yeast XLF ortholog, is a key regulator of NHEJ activity in the cell cycle. We show that Cdk1 phosphorylates residues in the C terminus of Xlf1 over the course of the cell cycle. Mutation of these residues leads to the loss of Cdk1 phosphorylation, resulting in elevated levels of NHEJ repair in vivo. Together, these data establish that Xlf1 phosphorylation by Cdc2(Cdk1) provides a molecular mechanism for downregulation of NHEJ in fission yeast and indicates that XLF is a key regulator of end-joining processes in eukaryotic organisms.
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