Abstract
After UV irradiation, the transcriptionally active MATα locus in Saccharomyces cerevisiae is preferentially repaired compared with the inactive HMLα locus. The effect of rad mutations from three different epistasis groups on differential repair was investigated. Three mutants, rad9, radio, and rad24, were impaired in the removal of UV dimers from the inactive HMLα locus, whereas they had generally normal repair of the active MATol locus. Since RAD9 is necessary for G2 arrest after UV irradiation, we propose that the G2 stage plays a role in making the dimers accessible for repair, at least in the repressed HMLol locus.