4) We also identify DDK to be required for STR-Dna2 mediated resection elongation via phosphorylation of Dna2.

3) We find DDK to be required for efficient Sae2-MRX mediated resection initiation, via phosphorylation of Sae2 and consequent stimulation of the Sae2-MRX nucleolytic activity.

2) We observe an impairment in DNA end resection in both yeast and human cells upon depletion/inhibition of DDK, and consistently, identify resection proteins Sae2 and Dna2 to be targeted by DDK.

1) We find DDK to be required for DSB repair via HR in budding yeast, and by using phospho-proteomics, identify a widespread involvement of DDK in phosphorylating DNA repair proteins.

Tweetorial: Previous work had shown that CDK mediates activation of DNA end resection and this is important for homologous recombination (HR)-mediated DSB repair. Here, we identify a novel role of the DDK kinase in the control of resection and HR, suggesting dual kinase control.