DNA double-strand break repair is essential for maintenance of genome stability. Recent work has implicated a host of chromatin regulators in the DNA-damage response, and although several functional roles have been defined, the mechanisms that control their recruitment to DNA lesions remain unclear. Here we find that efficient double-strand break recruitment of the INO80, SWR-C, NuA4, SWI/SNF and RSC enzymes is inhibited by the non-homologous end-joining machinery, and that their recruitment is controlled by early steps of homologous recombination. Strikingly, we find no significant role for H2A.X phosphorylation in the recruitment of chromatin regulators, but rather their recruitment coincides with reduced levels of H2A.X phosphorylation. Our work indicates that cell cycle position has a key role in DNA repair pathway choice and that recruitment of chromatin regulators is tightly coupled to homologous recombination.