The results of this study indicate the existence of a strong interaction between ethyl methanesulfonate (EMS) and ultraviolet light (UV) for cell killing in the yeast Saccharomyces cerevisiae. Conversely, mutation and gene conversion frequencies observed for the combined treatment of EMS and UV do not deviate significantly from that expected on the basis of simple additivity. Studies involving repair-deficient mutants (rad mutants) reveal that the synergistic interaction for cell killing depends on RAD52 function (recombinational repair), but not on RAD3 function (excision repair). On the basis of this analysis, the interaction between EMS and UV in S. cerevisiae might arise from the inhibition of double-strand break repair by one, or both agents.