聚(C)和肝素对大肠杆菌转录终止蛋白ϱ的抑制作用

Susan L. Bektesh , John P. Richardson
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引用次数: 1

摘要

在大肠杆菌RNA聚合酶催化的T7噬菌体DNA生物合成RNA过程中,低浓度Poly(C)和肝素(1 μg/ml)可抑制RNA合成终止蛋白ϱ的功能。这两种多阴离子都抑制ϱ与分离T7 RNA的结合。当分离的RNA转录物用作辅助因子时,肝素也抑制ϱATPase。结论是,聚阴离子通过结合ϱ上的位点来抑制终止,该位点通常用于在ϱ-mediated释放RNA时与新生RNA转录物的初始相互作用。由于其中一种抑制剂poly(C)本身是ϱATPase的有效激活剂,因此还得出结论,ϱ终止所需的ATP水解步骤必须与ϱ对RNA分子的作用相结合,才能从转录复合体中释放出来。
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Inhibition of the action of Escherichia coli transcription termination protein ϱ by poly(C) and heparin

Poly(C) and heparin at low concentrations (1 μg/ml) prevent the RNA synthesis termination protein ϱ from functioning during the biosynthesis of RNA from bacteriophage T7 DNA catalyzed by Escherichia coli RNA polymerase. Both of these polyanions inhibit the binding of ϱ to isolated T7 RNA. Heparin also inhibits ϱATPase when isolated RNA transcripts are used as cofactors. It is concluded that the polyanions inhibit termination by binding to the site on ϱ that is normally used for the initial interaction with a nascent RNA transcript in the ϱ-mediated release of RNA. Since one of the inhibitors, poly(C), is itself a potent activator for ϱATPase, it is also concluded that the ATP hydrolysis step that is required for ϱ termination has to be coupled to an action of ϱ on the RNA molecule to be released from the transcription complex.

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