Phosphoproteomic Datasets for Mec1/ATR Signaling Upon Hyper-Resection

The Mec1/ATR kinase is crucial for genome maintenance, although the mechanisms by which it controls DNA repair pathways remain elusive. Here we uncovered a role for Mec1/ATR in controlling homologous recombination (HR) factors in response to hyper-resection of DNA ends. Cells lacking RAD9, a checkpoint activator and an inhibitor of resection, exhibit Mec1-dependent hyper-phosphorylation of proteins associated with single strand DNA transactions, including the ssDNA binding protein Rfa2, the translocase/ubiquitin ligase Uls1 and the HR-regulatory Sgs1-Top3-Rmi1 (STR) complex. Extensive Mec1-dependent phosphorylation of the STR complex, mostly on the Sgs1 helicase subunit, promotes an interaction between STR and the DNA repair scaffolding protein Dpb11.