Stillman D J, Dorland S, Yu Y
Department of Cellular, Viral, and Molecular Biology, University of Utah Medical Center, Salt Lake City 84132.
Genetics. 1994 Mar;136(3):781-8. doi: 10.1093/genetics/136.3.781.
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.
我们研究了能够克服酿酒酵母HO基因对SWI5依赖性转录激活需求的突变。我们发现RPD3基因与SDI2基因相同，SIN4基因与TSF3和SDI3基因相同。我们还鉴定出了一个新的swi5抑制基因RGR1。RGR1基因最初被鉴定为SUC2的负调控因子。上位性分析表明，六个swi5抑制基因在四条不同的途径中发挥作用，RPD3和SIN3在一条途径中，RGR1和SIN4在第二条途径中，SDI4和SIN5分别在不同的途径中。最后，我们表明sin5对HO表达中swi5缺陷的完全抑制需要野生型ACE2基因。这表明SIN5的一个功能是阻止与SWI5同源的ACE2激活HO表达。
