Kuchin S, Yeghiayan P, Carlson M
Department of Genetics and Development, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Proc Natl Acad Sci U S A. 1995 Apr 25;92(9):4006-10. doi: 10.1073/pnas.92.9.4006.
The SSN3 and SSN8 genes of Saccharomyces cerevisiae were identified by mutations that suppress a defect in SNF1, a protein kinase required for release from glucose repression. Mutations in SSN3 and SSN8 also act synergistically with a mutation of the MIG1 repressor protein to relieve glucose repression. We have cloned the SSN3 and SSN8 genes. SSN3 encodes a cyclin-dependent protein kinase (cdk) homolog and is identical to UME5. SSN8 encodes a cyclin homolog 35% identical to human cyclin C. SSN3 and SSN8 fusion proteins interact in the two-hybrid system and coimmunoprecipitate from yeast cell extracts. Using an immune complex assay, we detected protein kinase activity that depends on both SSN3 and SSN8. Thus, the two SSN proteins are likely to function as a cdk-cyclin pair. Genetic analysis indicates that the SSN3-SSN8 complex contributes to transcriptional repression of diversely regulated genes and also affects induction of the GAL1 promoter.
通过抑制SNF1缺陷的突变鉴定出酿酒酵母的SSN3和SSN8基因，SNF1是从葡萄糖阻遏中释放所必需的一种蛋白激酶。SSN3和SSN8中的突变还与MIG1阻遏蛋白的突变协同作用以解除葡萄糖阻遏。我们已经克隆了SSN3和SSN8基因。SSN3编码一种细胞周期蛋白依赖性蛋白激酶（cdk）同源物，并且与UME5相同。SSN8编码一种与人类细胞周期蛋白C有35%同一性的细胞周期蛋白同源物。SSN3和SSN8融合蛋白在双杂交系统中相互作用，并从酵母细胞提取物中共免疫沉淀。使用免疫复合物测定法，我们检测到了依赖于SSN3和SSN8的蛋白激酶活性。因此，这两种SSN蛋白可能作为一个cdk-细胞周期蛋白对发挥作用。遗传分析表明，SSN3-SSN8复合物有助于对多种调控基因的转录抑制，并且还影响GAL1启动子的诱导。
