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首页> 外文期刊>Molecular and Cellular Biology >Distinct properties of c-myc transcriptional elongation are revealed in Xenopus oocytes and mammalian cells and by template titration, 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), and promoter mutagenesis.
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Distinct properties of c-myc transcriptional elongation are revealed in Xenopus oocytes and mammalian cells and by template titration, 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), and promoter mutagenesis.

机译：在非洲爪蟾卵母细胞和哺乳动物细胞中以及通过模板滴定，5,6-二氯-1-β-D-核呋喃呋喃糖基苯并咪唑（DRB）和启动子诱变揭示了c-myc转录延伸的独特特性。

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A block to c-myc transcription elongation has been observed in Xenopus oocytes and mammalian cells. Here, we show that the distribution of RNA polymerase II transcription complexes in the c-myc promoter proximal region in Xenopus oocytes is different from that observed previously in mammalian cells. Thus, there are major differences in the c-myc elongation block observed in the two systems. In addition, as first reported for a Xenopus tubulin gene (K. M. Middleton and G. T. Morgan, Mol. Cell. Biol. 10:727-735, 1990). c-myc template titration experiments reveal the existence of two classes of RNA polymerase II transcription complexes in oocytes: one (at low template concentration) that is capable of reading through downstream sites of premature termination, and another (high template concentration) that does not. We show that these classes of polymerases are distinct from those previously identified by 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB), which distinguishes transcription complexes on the basis of transcribed distance, rather than on the basis of differential elongation through sites of premature termination. We also show that mutations that affect the efficiency of initiation of transcription from the c-myc P2 promoter can influence premature termination by at least two mechanisms: TATA box mutations function by the titration effect (decrease in transcription initiation results in a relative decrease in premature termination), while an upstream activator (E2F) site functions by contributing to the assembly of polymerase complexes competent to traverse the downstream sites of premature termination.
机译：在非洲爪蟾卵母细胞和哺乳动物细胞中观察到了对c-myc转录延伸的阻滞。在这里，我们显示爪蟾卵母细胞的c-myc启动子近端区域中的RNA聚合酶II转录复合物的分布与以前在哺乳动物细胞中观察到的不同。因此，在两个系统中观察到的c-myc延伸区存在主要差异。另外，如关于非洲爪蟾微管蛋白基因的首次报道（K.M.Middleton和G.T.Morgan，Mol.Cell.Biol.10：727-735，1990）。 c-myc模板滴定实验揭示了卵母细胞中存在两类RNA聚合酶II转录复合体：一种（低模板浓度）能够读取过早终止的下游位点，另一种（高模板浓度）不能读取。我们表明，这些类型的聚合酶与先前由5,6-二氯-1-β-D-呋喃呋喃基糖基苯并咪唑（DRB）鉴定的聚合酶不同，DRB在转录距离的基础上而不是在差异延伸的基础上区分了转录复合物通过提前终止的站点。我们还显示，影响c-myc P2启动子转录起始效率的突变可通过至少两种机制影响过早终止：TATA盒突变通过滴定作用起作用（转录起始的减少导致过早发生的相对减少）上游激活子（E2F）位点通过有助于聚合酶复合物的组装而起作用，这些复合物能够穿过过早终止的下游位点。

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