EPISTASIS ANALYSIS OF SUPPRESSOR MUTATIONS THAT ALLOW HO EXPRESSION IN THE ABSENCE OF THE YEAST SW15 TRANSCRIPTIONAL ACTIVATOR

We have examined mutations which overcome the requirement for SWI5-dep endent transcriptional activation of the Saccharomyces cerevisiae HO g ene. We show that the RPD3 gene is the same as SDI2, and that SIN4 is the same as the TSF3 and SDI3 genes. We have also identified a new swi 5 suppressor, RGR1. The RGR1 gene was identified originally as a negat ive regulator of SUC2. Epistasis analysis indicates that six swi5 supp ressor genes function in four distinct pathways, with RPD3 and SIN3 in one pathway, RGR1 and SIN4 in a second pathway, and SDI4 and SIN5 eac h in distinct pathways. Finally, we show that complete suppression of the swi5 defect in HO expression by sin5 requires the wild-type ACE2 g ene. This suggests that one function of SIN5 is to prevent ACE2, a SWI 5 homolog, from activating HO expression.