Happel A M, Swanson M S, Winston F
Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115.
Genetics. 1991 May;128(1):69-77. doi: 10.1093/genetics/128.1.69.
The Saccharomyces cerevisiae SNF2, SNF5 and SNF6 genes were initially identified as genes required for expression of SUC2 and other glucose repressible genes. The Suc- defect in all three of these classes of mutants is suppressed by mutations in the SPT6 gene. Since mutations in SPT6 had also been identified as suppressors of Ty and solo delta insertion mutations at the HIS4 and LYS2 loci, we have examined Ty transcription in snf2, snf5 and snf6 mutants and have found that Ty transcription is abolished or greatly reduced. The snf2, snf5 and snf6 defect for Ty transcription, like the defect for SUC2 transcription, is suppressed by spt6 mutations. In contrast to other mutations that abolish or greatly reduce Ty transcription (in the SPT3, SPT7 and SPT8 genes), mutations in these SNF genes do not cause suppression of insertion mutations. This result suggests that the SNF2, SNF5 and SNF6 gene products act by a distinct mechanism from the SPT3, SPT7 and SPT8 gene products to promote transcription of Ty elements. This result also suggests that a reduction of Ty transcription is not always sufficient for activation of adjacent gene expression.
酿酒酵母的SNF2、SNF5和SNF6基因最初被鉴定为SUC2和其他葡萄糖可阻遏基因表达所需的基因。这三类突变体中的所有Suc - 缺陷都被SPT6基因中的突变所抑制。由于SPT6中的突变也已被鉴定为HIS4和LYS2位点处Ty和单独δ插入突变的抑制因子,我们研究了snf2、snf5和snf6突变体中的Ty转录,发现Ty转录被消除或大大减少。snf2、snf5和snf6在Ty转录方面的缺陷,与SUC2转录缺陷一样,被spt6突变所抑制。与其他消除或大大减少Ty转录的突变(如SPT3、SPT7和SPT8基因中的突变)不同,这些SNF基因中的突变不会导致插入突变的抑制。这一结果表明,SNF2、SNF5和SNF6基因产物通过与SPT3、SPT7和SPT8基因产物不同的机制来促进Ty元件的转录。这一结果还表明,Ty转录的减少并不总是足以激活相邻基因表达。