Dpb11 coordinates Mec1 kinase activation with cell cycle-regulated Rad9 recruitment.

作者: Boris Pfander , John F X Diffley

DOI: 10.1038/EMBOJ.2011.345

关键词:

摘要: Eukaryotic cells respond to DNA damage by activating checkpoint signalling pathways. Checkpoint signals are transduced a protein kinase cascade that also requires non-kinase mediator proteins. One such is the Saccharomyces cerevisiae Dpb11 protein, which binds and activates apical kinase, Mec1. Here, we show ternary complex of Dpb11, Mec1 another key Rad9 required for efficient phosphorylation in vitro, activation vivo. Phosphorylation cyclin-dependent (CDK) on two residues generates binding site tandem BRCT repeats thereby recruitment into complex. via therefore, does not efficiently occur during G1 phase when CDK inactive. Thus, coordinates signal transduction both temporally spatially, ensuring initiator specifically activated proximity one its critical substrates.

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