Kulkens T, van Heerikhuizen H, Klootwijk J, Oliemans J, Planta R J
Biochemisch Laboratorium, Vrije Universiteit, Amsterdam, The Netherlands.
Curr Genet. 1989 Dec;16(5-6):351-9. doi: 10.1007/BF00340714.
Using the gel retardation assay we have identified a protein that can specifically bind to a site within the enhancer of the 37S pre-ribosomal RNA operon in yeast, as well as to a site 210 bp upstream of the site of transcription initiation of this operon. This protein (RBP1) has been partially purified by means of heparin-agarose chromatography and protects 20 bp in the rDNA enhancer, and 25 bp in the initiation region, against DNase I in an in vitro footprinting assay. In vivo footprinting studies using methylation of intact yeast cells with dimethylsulphate, indicate that the same binding sites are occupied in vivo as well. Deletions that abolish binding of RBP1 to the enhancer in vitro, as well as linker insertions into the RBP1 binding site in the initiation region that strongly diminish in vitro binding of RBP1, have no effect whatsoever on the enhancement of rDNA transcription in vivo. This was studied by deletion/mutation of the RBP1 binding site in vitro in an artificial ribosomal minigene and measuring the effect on the minigene transcription in vivo in yeast cells, transformed with the deleted/mutated minigenes. It can therefore be concluded that binding of RBP1 is not an important parameter in the functioning of the rDNA enhancer in yeast. Using the same minigene system we also show that RBP1 is not involved in termination of RNA polymerase I (Pol I) transcription at the main terminator T2.
利用凝胶阻滞试验,我们鉴定出一种蛋白质,它能特异性结合酵母中37S前核糖体RNA操纵子增强子内的一个位点,以及该操纵子转录起始位点上游210 bp处的一个位点。这种蛋白质(RBP1)已通过肝素-琼脂糖层析进行了部分纯化,并且在体外足迹试验中,它能保护rDNA增强子中的20 bp以及起始区域中的25 bp不被DNase I降解。使用硫酸二甲酯对完整酵母细胞进行甲基化的体内足迹研究表明,体内同样的结合位点也被占据。在体外消除RBP1与增强子结合的缺失突变,以及在起始区域的RBP1结合位点插入接头从而强烈降低RBP1体外结合能力的突变,对体内rDNA转录的增强没有任何影响。这是通过在体外对人工核糖体小基因中的RBP1结合位点进行缺失/突变,并测量其对用缺失/突变小基因转化的酵母细胞体内小基因转录的影响来研究的。因此可以得出结论,RBP1的结合不是酵母中rDNA增强子功能的一个重要参数。使用相同的小基因系统,我们还表明RBP1不参与RNA聚合酶I(Pol I)在主要终止子T2处的转录终止。