Rtt107 BRCT3/4 and 5/6 domains mediated recruitment to double-stranded breaks.
Rad9 BRCT domains were able to functionally replace Rtt107 BRCT5/6 domains.
Slx4 but not Dpb11 was dependent on Rtt107 for its recruitment to DNA lesions.
Fusing Rtt107 BRCT5/6 domains to Slx4 alleviated some phenotypes of rtt107Δ mutants.