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The Yku70–Yku80 complex contributes to regulate double-strand break processing and checkpoint activation during the cell cycle

By Michela Clerici, Davide Mantiero, Ilaria Guerini, Giovanna Lucchini and Maria Pia Longhese

Abstract

DNA double-strand breaks (DSBs) are repaired by non-homologous end joining (NHEJ) or homologous recombination (HR). HR requires 5′ DSB end degradation that occurs in the presence of cyclin-dependent kinase (CDK) activity. Here, we show that a lack of any of the NHEJ proteins Yku (Yku70–Yku80), Lif1 or DNA ligase IV (Dnl4) increases 5′ DSB end degradation in G1 phase, with ykuΔ cells showing the strongest effect. This increase depends on MRX, the recruitment of which at DSBs is enhanced in ykuΔ G1 cells. DSB processing in G2 is not influenced by the absence of Yku, but it is delayed by Yku overproduction, which also decreases MRX loading on DSBs. Moreover, DSB resection in ykuΔ cells occurs independently of CDK activity, suggesting that it might be promoted by CDK-dependent inhibition of Yku

Topics: Scientific Report
Publisher: Nature Publishing Group
OAI identifier: oai:pubmedcentral.nih.gov:2515202
Provided by: PubMed Central
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