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首页> 外文期刊>Journal of bacteriology >A Dual Binding Site for Integration Host Factor and the Response Regulator CtrA inside the Caulobacter crescentus Replication Origin
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A Dual Binding Site for Integration Host Factor and the Response Regulator CtrA inside the Caulobacter crescentus Replication Origin

机译：整合整合因子和Caulobacter crescentus复制起源内的响应调节剂CtrA的双重结合位点。

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The response regulator CtrA controls chromosome replication by binding to five sites, a, b, c, d, and e, inside the Caulobacter crescentus replication origin (Cori). In this study, we demonstrate that integration host factor (IHF) binds Cori over the central CtrA binding site c. Surprisingly, IHF and CtrA share DNA recognition sequences. Rather than promoting cooperative binding, IHF binding hinders CtrA binding to site c and nearby site d. Unlike other CtrA binding sites, DNA mutations in the CtrA c/IHF site uniquely impair autonomous Cori plasmid replication. These mutations also alter transcription from distant promoters more than 100 bp away. When the CtrA c/IHF site was deleted from the chromosome, these cells grew slowly and became selectively intolerant to a CtrA phosphor-mimic allele (D51E). Since CtrA protein concentration decreases during the cell cycle as IHF protein concentration increases, we propose a model in which IHF displaces CtrA in order to bend Cori and promote efficient chromosome replication.
机译：响应调节剂CtrA通过与 Caulobacter crescentus 复制起点（ Cori ）内部的五个位点a，b，c，d和e结合来控制染色体复制。在这项研究中，我们证明了整合宿主因子（IHF）在中央CtrA结合位点c上结合 Cori 。出乎意料的是，IHF和CtrA共享DNA识别序列。 IHF结合不促进协同结合，而是阻碍CtrA与位点c和附近位点d结合。与其他CtrA结合位点不同，CtrA c / IHF位点的DNA突变会独特地损害自主 Cori 质粒的复制。这些突变还会改变距离超过100 bp的启动子的转录。当从染色体上删除CtrA c / IHF位点时，这些细胞生长缓慢，并选择性地不耐受CtrA磷模拟等位基因（D51E）。由于CtrA蛋白浓度在细胞周期中会随着IHF蛋白浓度的增加而降低，因此我们提出了一个模型，其中IHF取代CtrA以弯曲 Cori 并促进有效的染色体复制。

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