Knight Janine P, Daly Thomas M, Bergman Lawrence W
Department of Microbiology and Immunology, Drexel University College of Medicine, 2900 Queen Lane, Philadelphia, PA 19129, USA.
Curr Genet. 2004 Jul;46(1):10-9. doi: 10.1007/s00294-004-0502-z. Epub 2004 May 4.
Cyclins, cyclin-dependent kinases (CDK) and their inhibitors play a critical role in many biological processes. In yeast, the ankyrin repeat protein Pho81p, by being an inhibitor of the Pho85p-Pho80p cyclin-dependent protein kinase complex, transcriptionally regulates the production of repressible acid phosphatase, encoded by the PHO5 gene. Recent studies in our laboratory showed that Pho81p is phosphorylated by the Pho80p-Pho85p CDK complex in vitro; and, to determine the significance of the phosphorylation, we used site-directed mutagenesis to alter the potential phosphorylation sites for this kinase complex. The resulting mutations were introduced into a yeast strain containing a deletion of PHO81 and the effect of the mutation on PHO5 expression was assayed. Results suggest that phosphorylation of particular residues within Pho81p is crucial for its activity as an inhibitor. Studies using a green fluorescent protein-Pho81p fusion and Western analysis indicate that the localization and half-life of the mutants are similar to wild-type Pho81 proteins. However, an in vivo binding assay indicates that the mutant Pho81p is deficient in binding to the Pho80p-Pho85p kinase complex. These findings support the observation that the mutant fails to inhibit kinase activity in low phosphate. These studies provide insight into the mechanism of regulation of CDK inhibitor activity.
细胞周期蛋白、细胞周期蛋白依赖性激酶(CDK)及其抑制剂在许多生物学过程中发挥着关键作用。在酵母中,锚蛋白重复序列蛋白Pho81p作为Pho85p - Pho80p细胞周期蛋白依赖性蛋白激酶复合物的抑制剂,可转录调控由PHO5基因编码的可阻遏酸性磷酸酶的产生。我们实验室最近的研究表明,Pho81p在体外被Pho80p - Pho85p CDK复合物磷酸化;并且,为了确定磷酸化的意义,我们使用定点诱变来改变该激酶复合物的潜在磷酸化位点。将产生的突变引入到含有PHO81缺失的酵母菌株中,并检测突变对PHO5表达的影响。结果表明,Pho81p内特定残基的磷酸化对其作为抑制剂的活性至关重要。使用绿色荧光蛋白 - Pho81p融合蛋白和蛋白质免疫印迹分析的研究表明,突变体的定位和半衰期与野生型Pho81蛋白相似。然而,体内结合试验表明,突变型Pho81p与Pho80p - Pho85p激酶复合物的结合存在缺陷。这些发现支持了突变体在低磷酸盐条件下无法抑制激酶活性的观察结果。这些研究为CDK抑制剂活性的调控机制提供了深入了解。