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首页> 外文期刊>Journal of Molecular Biology >KID, A SMALL PROTEIN OF THE PARD STABILITY SYSTEM OF PLASMID R1, IS AN INHIBITOR OF DNA REPLICATION ACTING AT THE INITIATION OF DNA SYNTHESIS
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KID, A SMALL PROTEIN OF THE PARD STABILITY SYSTEM OF PLASMID R1, IS AN INHIBITOR OF DNA REPLICATION ACTING AT THE INITIATION OF DNA SYNTHESIS

机译：KID是PLASMID R1板稳定性系统的小蛋白，是DNA合成开始时DNA复制的抑制剂。

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摘要

The Kid and Ks proteins are the killer component and the antagonist belonging to parD, a killer stability system of plasmid R1. The Kid and Ks proteins have been purified, the second one as a C-LYT-Kis fusion that conserves the antagonistic activity of the Kis protein, but not its auto-regulatory potential. Kid inhibits in vitro replication of CoEl to a basal level without altering the superhelicity of the template but it does not substantially affect in vitro replication of P4, a DnaA, DnaB, DnaC and DnaG-independent replicon. Kid inhibits lytic induction of a lambda, prophage, but this inhibition can be neutralized by excess DnaB. In addition, a multicopy dnaB recombinant, but not a multicopy dnaG recombinant, prevents the toxicity associated with this protein. Inhibition of ColE1 replication by Kid in vitro is prevented by the C-LYT-Kis protein. Functional analysis indicates that the antagonistic activity of Ks is independent of its activity as a co-regulator of the parD promoter. It is also;shown that C-LYT-Kis and Kid interact, forming a tight complex. These results strongly suggest that the toxicity of the kid protein is due to inhibition of DnaB-dependent DNA replication, and that direct protein-protein interactions are involved in the neutralization of the activity of the killer protein by the antagonist. [References: 30]
机译：Kid和Ks蛋白是杀手成分和拮抗剂，属于parD（质粒R1的杀手稳定性系统）。 Kid和Ks蛋白已经纯化，第二种是C-LYT-Kis融合蛋白，保留了Kis蛋白的拮抗活性，但没有其自动调节的潜力。 Kid可以将CoEl的体外复制抑制到基础水平，而不会改变模板的超螺旋性，但它基本上不会影响P4，DnaA，DnaB，DnaC和不依赖DnaG的复制子的体外复制。 Kid抑制λ噬菌体的裂解诱导，但是这种抑制作用可以被过量的DnaB中和。此外，多拷贝的dnaB重组体，而不是多拷贝的dnaG重组体，可防止与此蛋白相关的毒性。 C-LYT-Kis蛋白阻止了Kid在体外对ColE1复制的抑制。功能分析表明，Ks的拮抗活性独立于其作为parD启动子协同调节剂的活性。它还表明，C-LYT-Kis和Kid相互作用，形成紧密的复合物。这些结果有力地表明，kid蛋白的毒性归因于DnaB依赖的DNA复制的抑制，并且直接的蛋白-蛋白相互作用与拮抗剂对杀手蛋白活性的中和有关。 [参考：30]

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