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 SW15-dependent transcriptional activation of the Saccharomyces cerevisiae HO gene. 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 swi5 suppressor, RGR1. The RGR1 gene was identified originally as a negative regulator of SUC2. Epistasis analysis indicates that six swi5 suppressor genes function in four distinct pathways, with RPD3 and SIN3 in one pathway, RGR1 and SIN4 in a second pathway, and SDI4 and SIN5 each in distinct pathways. Finally, we show that complete suppression of the swi5 defect in HO expression by sin5 requires the wild-type ACE2 gene. This suggests that one function of SIN5 is to prevent ACE2, a SWI5 homolog, from activating HO expression.
Stillman
D J
DJ
Department of Cellular, Viral, and Molecular Biology, University of Utah Medical Center, Salt Lake City 84132.
Dorland
S
S
Yu
Y
Y
D004843:Epistasis, Genetic; D015966:Gene Expression Regulation, Fungal; D005800:Genes, Fungal; D016153:Genes, Suppressor; D005816:Genetic Complementation Test; D009154:Mutation; D012441:Saccharomyces cerevisiae / Q000235:genetics*; D015534:Trans-Activators
D015534:Trans-Activators