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Transcriptional enhancement by upstream activators is brought about by different molecular mechanisms for class I and II RNA polymerase genes.

机译:上游激活剂的转录增强是通过I类和II类RNA聚合酶基因的不同分子机制实现的。

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摘要

Ribosomal gene transcription requires the functional interplay of at least two promoter elements, the upstream control element (UCE) and the start site proximal core, which operate in concert to promote efficient and accurate transcription initiation by RNA polymerase I (pol I). Because this bipartite organization of the rDNA promoter is formally analogous to the organization of a typical pol II promoter, we have examined whether transcriptional activation by upstream activating sequences is brought about by similar molecular mechanisms for both classes of genes. We have replaced the UCE of the mouse rDNA promoter by three different pol II activating sequences (the yeast GAL4 binding sites, the target sequence of the enhancer binding protein E2 from bovine papilloma virus type 1 and the octamer motif), and measured the template activity of these chimeric promoters in the presence of the trans-activating proteins either in a cell free transcription system or in vivo after transfection into mouse cells. In the context of the pol I promoter none of these transcriptional activators enhanced rDNA transcription. The results indicate that activation by UCEs is not interchangeable between genes transcribed by RNA pol I and II, respectively, and suggest that different molecular mechanisms mediate the synergistic action of distant control sequences of different classes of genes.
机译:核糖体基因转录需要至少两个启动子元件的功能相互作用,即上游控制元件(UCE)和起始位点近端核心,它们协同工作以促进RNA聚合酶I(pol I)高效而准确的转录起始。因为rDNA启动子的这种两部分组织形式上与典型的pol II启动子的组织形式相似,所以我们检查了上游激活序列的转录激活是否是由两类基因的相似分子机制引起的。我们用三个不同的pol II激活序列(酵母GAL4结合位点,来自牛乳头瘤病毒1型的增强子结合蛋白E2的目标序列和八聚体基序)取代了小鼠rDNA启动子的UCE,并测量了模板活性在无细胞转录系统中或在转染入小鼠细胞后体内在反式激活蛋白存在下这些嵌合启动子的表达。在pol I启动子的背景下,这些转录激活因子均未增强rDNA转录。结果表明,UCEs的激活在分别由RNA pol I和II转录的基因之间是不可互换的,并且表明不同的分子机制介导了不同类别基因的远距离控制序列的协同作用。

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