Phosphoproteomic dataset comparing wild type, bob1-1 and bob1-1dbf4∆ cells in M-phase arrested S.cerevisiae.

DNA double-strand breaks (DSBs) can be repaired by several pathways. In eukaryotes, repair pathway choice – the cellular decision making underlying DSB repair – occurs at the level of DSB resection and is controlled by the cell cycle. Upon cell cycle-dependent activation, cyclin-dependent kinases (CDKs) phosphorylate resection proteins and thereby stimulate DSB resection and repair by homologous recombination (HR). We uncovered a novel role for the Dbf4-dependent kinase Cdc7 (DDK) in regulating HR and DNA end resection. We therefore analyzed phosphorylation substrates of DDK by phosphoproteomics, where we compared wild type, bob1-1 and bob1-1dbf4∆ cells in M-phase arrested S.cerevisiae.