ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks
Author: ["Ali Jazayeri","Jacob Falck","Claudia Lukas","Jiri Bartek","Graeme C. M. Smith","Jiri Lukas","Stephen P. Jackson"]
Publication: Nature Cell Biology
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Abstract
It is generally thought that the DNA-damage checkpoint kinases, ataxia-telangiectasia mutated (ATM) and ATM- and Rad3-related (ATR), work independently of one another. Here, we show that ATM and the nuclease activity of meiotic recombination 11 (Mre11) are required for the processing of DNA double-strand breaks (DSBs) to generate the replication protein A (RPA)-coated ssDNA that is needed for ATR recruitment and the subsequent phosphorylation and activation of Chk1. Moreover, we show that efficient ATM-dependent ATR activation in response to DSBs is restricted to the S and G2 cell cycle phases and requires CDK kinase activity. Thus, in response to DSBs, ATR activation is regulated by ATM in a cell-cycle dependent manner.
Cite this article
Jazayeri, A., Falck, J., Lukas, C. et al. ATM- and cell cycle-dependent regulation of ATR in response to DNA double-strand breaks. Nat Cell Biol 8, 37–45 (2006). https://doi.org/10.1038/ncb1337
