Laurent B C, Treitel M A, Carlson M
Department of Genetics and Development, Columbia University College of Physicians and Surgeons, New York, NY 10032.
Proc Natl Acad Sci U S A. 1991 Apr 1;88(7):2687-91. doi: 10.1073/pnas.88.7.2687.
The SNF2, SNF5, and SNF6 genes of Saccharomyces cerevisiae are required for expression of a variety of differently regulated genes. Previous evidence implicated the SNF5 protein in transcriptional activation, and a DNA-bound LexA-SNF5 fusion protein was shown to activate expression of a nearby promoter. Here, we examine the functional relationship of the SNF2, SNF5, and SNF6 proteins. Activation by DNA-bound LexA-SNF5 fusion protein was greatly reduced in snf2 and snf6 mutants, indicating that activation by LexA-SNF5 requires SNF2 and SNF6 function. An spt6 mutation, which suppresses transcriptional defects caused by snf2, restored activation by LexA-SNF5 in a snf2 mutant. The SNF2 gene was sequenced and encodes a 194-kDa protein that is targeted to the nucleus. DNA-bound LexA-SNF2 fusion protein also activated transcription, dependent on SNF5 and SNF6. These findings suggest that SNF2, SNF5, and SNF6 function interdependently in transcriptional activation, possibly forming a heteromeric complex.
酿酒酵母的SNF2、SNF5和SNF6基因是多种不同调控基因表达所必需的。先前的证据表明SNF5蛋白参与转录激活,并且一种与DNA结合的LexA-SNF5融合蛋白被证明可激活附近启动子的表达。在此,我们研究了SNF2、SNF5和SNF6蛋白之间的功能关系。在snf2和snf6突变体中,与DNA结合的LexA-SNF5融合蛋白的激活作用大大降低,这表明LexA-SNF5的激活需要SNF2和SNF6的功能。一个抑制由snf2引起的转录缺陷的spt6突变,恢复了snf2突变体中LexA-SNF5的激活作用。对SNF2基因进行测序,发现它编码一种靶向细胞核的194-kDa蛋白。与DNA结合的LexA-SNF2融合蛋白也能激活转录,且依赖于SNF5和SNF6。这些发现表明,SNF2、SNF5和SNF6在转录激活中相互依赖发挥作用,可能形成一个异源复合物。