5,6-Dichloro-1-beta-D-ribofuranosylbenzimidazole inhibits transcription elongation by RNA polymerase II in vitro.
5,6-Dichloro-1-beta-D-ribofuranosylbenzimidazole inhibits transcription elongation by RNA polymerase II in vitro.
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发表时间：
1989-02
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通讯作者：
L. Chodosh;A. Fire;M. Samuels;P. Sharp
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作者：
L. Chodosh;A. Fire;M. Samuels;P. Sharp
嘌呤核苷类似物5，6-dichloro-1-beta-D-ribofuranosylbenzimidazole是核糖核酸聚合酶II的选择性转录抑制物。尽管大量体内研究表明，它通过促进延长的聚合酶分子的提前终止来抑制转录，但到目前为止的体外研究表明，DRB在转录启动水平上起作用。我们在体外分析了在HeLa全细胞提取物和部分纯化的转录系统中DRB介导的转录抑制的机制。结果表明，DRB抑制RNA转录本合成的程度与其长度成正比。例如，DRB被发现在体外优先抑制腺病毒主要晚期转录单位的启动子-远端相对于启动子-近端部分的转录。确定了一个可能参与调节这种抑制效应的因素。我们认为DRB在体内和体外抑制转录的机制是相似的。
The purine nucleoside analog 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) is a selective inhibitor of transcription by RNA polymerase II. Although a wealth of in vivo studies have suggested that DRB inhibits transcription by enhancing the premature termination of elongating polymerase molecules, in vitro studies to date have been interpreted to suggest that DRB acts at the level of transcription initiation. We have analyzed the mechanism of DRB-mediated transcription inhibition in vitro both in HeLa whole cell extracts and in a partially purified transcription system. The results indicate that the extent to which DRB inhibits the synthesis of a RNA transcript is directly proportional to its length. For example, DRB was found to preferentially inhibit transcription in vitro of promoter-distal relative to promoter-proximal portions of the adenovirus major late transcription unit. A factor potentially involved in mediating this inhibitory effect is identified. We conclude that the mechanism of DRB inhibition of transcription in vivo and in vitro are similar.