Kuchin S, Carlson M
Department of Genetics and Development, Columbia University, New York, New York 10032, USA.
Mol Cell Biol. 1998 Mar;18(3):1163-71. doi: 10.1128/MCB.18.3.1163.
The Srb10-Srb11 protein kinase of Saccharomyces cerevisiae is a cyclin-dependent kinase (cdk)-cyclin pair which has been found associated with the carboxy-terminal domain (CTD) of RNA polymerase II holoenzyme forms. Previous genetic findings implicated the Srb10-Srb11 kinase in transcriptional repression. Here we use synthetic promoters and LexA fusion proteins to test the requirement for Srb10-Srb11 in repression by Ssn6-Tup1, a global corepressor. We show that srb10delta and srb11delta mutations reduce repression by DNA-bound LexA-Ssn6 and LexA-Tup1. A point mutation in a conserved subdomain of the kinase similarly reduced repression, indicating that the catalytic activity is required. These findings establish a functional link between Ssn6-Tup1 and the Srb10-Srb11 kinase in vivo. We also explored the relationship between Srb10-Srb11 and CTD kinase I (CTDK-I), another member of the cdk-cyclin family that has been implicated in CTD phosphorylation. We show that mutation of CTK1, encoding the cdk subunit, causes defects in transcriptional repression by LexA-Tup1 and in transcriptional activation. Analysis of the mutant phenotypes and the genetic interactions of srb10delta and ctk1A suggests that the two kinases have related but distinct roles in transcriptional control. These genetic findings, together with previous biochemical evidence, suggest that one mechanism of repression by Ssn6-Tup1 involves functional interaction with RNA polymerase II holoenzyme.
酿酒酵母的Srb10-Srb11蛋白激酶是一种细胞周期蛋白依赖性激酶(cdk)-细胞周期蛋白对,已发现其与RNA聚合酶II全酶形式的羧基末端结构域(CTD)相关联。先前的遗传学研究结果表明Srb10-Srb11激酶参与转录抑制。在这里,我们使用合成启动子和LexA融合蛋白来测试Ssn6-Tup1(一种全局共抑制因子)在抑制过程中对Srb10-Srb11的需求。我们发现,srb10δ和srb11δ突变会降低DNA结合的LexA-Ssn6和LexA-Tup1的抑制作用。激酶保守亚结构域中的一个点突变同样降低了抑制作用,表明需要催化活性。这些发现建立了体内Ssn6-Tup1与Srb10-Srb11激酶之间的功能联系。我们还探讨了Srb10-Srb11与CTD激酶I(CTDK-I)之间的关系,CTDK-I是cdk-细胞周期蛋白家族的另一个成员,与CTD磷酸化有关。我们发现,编码cdk亚基的CTK1突变会导致LexA-Tup1的转录抑制和转录激活出现缺陷。对srb10δ和ctk1A突变体表型及遗传相互作用的分析表明,这两种激酶在转录控制中具有相关但不同的作用。这些遗传学发现与先前的生化证据一起表明,Ssn6-Tup1的一种抑制机制涉及与RNA聚合酶II全酶的功能相互作用。