Transcription-coupled DNA supercoiling in defined protein systems and in E. coli topA mutant strains.
Transcription-coupled DNA supercoiling in defined protein systems and in E. coli topA mutant strains.
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作者：
Fulcrand G;Zhi X;Leng F
RNA聚合酶的转录可以在体外和大肠杆菌topA菌株中刺激（−）DNA超卷曲。这种现象已经被“双超螺旋结构域”转录模型成功地解释了，其中（+）超螺旋在转录RNA聚合酶的前面产生，（−）超螺旋在转录RNA聚合酶的后面产生。先前，已经证明某些序列特异性DNA结合蛋白在体外蛋白质系统中有效地刺激转录偶联DNA超卷曲（TCDS）。这些结果与拓扑屏障模型一致，其中某些核蛋白复合物可以形成拓扑屏障，阻碍独立染色体超螺旋结构域的扩散和合并。事实上，最近的生物化学和单分子结果证明了基于核蛋白的DNA拓扑屏障的存在，它能够将DNA分子划分为不同的拓扑结构域。此外，最近的体内研究表明，仅一个转录集合（包括转录RNA聚合酶和RNA转录物）就足以引起局部DNA超螺旋度的变化。这种局部染色体结构的拓扑变化应该会对关键DNA序列元件的构象和功能产生重大影响，例如启动子和DNA复制起点。在本文中，我们还将回顾TCDS是激活弱启动子（如鼠伤寒沙门氏菌leu-500启动子）转录起始的关键刺激力的最新进展。
Transcription by RNA polymerases can stimulate (−) DNA supercoiling both in vitro and in E. coli topA strains. This phenomenon has been successfully explained by a "twin-supercoiled-domain" model of transcription in which (+) supercoils are produced in front of the transcribing RNA polymerase and (−) supercoils behind it. Previously, it has been shown that certain sequence-specific DNA-binding proteins potently stimulate transcription-coupled DNA supercoiling (TCDS) in an in vitro protein system. These results are consistent with a topological barrier model where certain nucleoprotein complexes can form topological barriers that impede the diffusion and merger of independent chromosomal supercoil domains. Indeed, recent biochemical and single molecule results demonstrated the existence of nucleoprotein-based DNA topological barriers, which are capable of dividing a DNA molecule into different topological domains. Additionally, recent in vivo studies showed that a transcriptional ensemble (including the transcribing RNA polymerase and the RNA transcript) alone is sufficient to cause a change in local DNA superhelicity. This topological change in local chromosome structure should have a great impact on the conformation and function of critical DNA sequence elements, such as promoters and DNA replication origins. In this paper, we will also review recent progress by which TCDS is a critical stimulating force to activate transcription initiation from weak promoters, such as the S. typhimurium leu-500 promoter.
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DOI：
10.2741/968
发表时间：
2003-01-01
期刊：
FRONTIERS IN BIOSCIENCE
影响因子：
--
作者：
Chen, CC;Wu, HY
通讯作者：
Wu, HY
DOI：
10.1073/pnas.142002099
发表时间：
2002-07-09
影响因子：
11.1
作者：
Leng, FF;McMacken, R
通讯作者：
McMacken, R
DOI：
10.1073/pnas.89.18.8784
发表时间：
1992-09-15
影响因子：
11.1
作者：
CHEN, DR;BOWATER, R;LILLEY, DMJ
通讯作者：
LILLEY, DMJ
DOI：
10.1073/pnas.96.25.14342
发表时间：
1999-12-07
影响因子：
11.1
作者：
Nelson, P
通讯作者：
Nelson, P
影响因子：
4.4
作者：
Mielke, SP;Fink, WH;Benham, CJ
通讯作者：
Benham, CJ