The F plasmid centromere, sopC, is required for full repression of the sopAB operon.

The F plasmid centromere, sopC, is required for full repression of the sopAB operon.
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F 质粒着丝粒 sopC 是完全抑制 sopAB 操纵子所必需的。

DOI:
10.1006/jmbi.1999.2909
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发表时间:
1999
期刊:
Journal of molecular biology.
影响因子:
--
通讯作者:
Biek,DP
Biek,DP
中科院分区:
--
文献类型:
--
作者:
Yates,P;Lane,D;Biek,DP

文献摘要

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F质粒的SopB蛋白在分裂前将F质粒拷贝分配给子细胞中具有双重作用。它与sopC着丝粒位点结合,形成稳定质粒所需的分区复合物,并与SopA相互作用,抑制sopAB操纵子的转录,从而防止过量SopB导致的不稳定。我们通过筛选诱变的mini-F DNA的不稳定遗传,分离出sop突变体。其中4个突变体来自sopB中不同的错义突变。所有四个缺陷,在不同程度上,在自动调节的SOP蛋白合成。突变体蛋白质显示减少连接数的mini-F和不稳定的质粒携带sopC的能力减弱,表明降低的能力,形成一个正常的复合物与sopC可能是自我调节缺陷的基础。抑制的转录的SOP启动子lacZ融合的SOPA和SOPB强烈增强SOPC的存在下,在顺式或反式,和增强减少或无效时,野生型SOPB被替换的突变体SOPB等位基因。一个单一的43 bp单位的sopC几乎是有效的sopC本身在增强阻遏。结果表明,sopC是完全阻遏sop启动子所必需的。因此,他们指出了一个以前未被怀疑的作用,这个着丝粒网站,并建议,自动调节和分区可能通常是协调的过程。
The SopB protein of the F plasmid has a dual role in the partition of F plasmid copies to daughter cells prior to division. It binds to the sopC centromere site to form the partition complex needed for stabilizing the plasmid, and it interacts with SopA to repress transcription of the sopAB operon, thus preventing the destabilization that results from excess SopB. We have isolated sop mutants by screening for unstable inheritance of mutagenized mini-F DNA. Four of the mutants resulted from different missense mutations in sopB. All four were deficient, to varying degrees, in autoregulation of Sop protein synthesis. The mutant proteins showed diminished capacity for reducing the linking number of mini-F and for destabilizing a plasmid carrying sopC, indicating that reduced ability to form a normal complex with sopC might underlie the autoregulation defect. Repression of the transcription of a sop promoter-lacZ fusion by SopA and SopB was strongly enhanced in the presence of sopC, in cis or in trans, and the enhancement was reduced or nullified when wild-type sopB was replaced by the mutant sopB alleles. A single 43 bp unit of sopC was almost as effective as sopC itself in enhancing repression. The results show that sopC is necessary for full repression of the sop promoter. They thus indicate a previously unsuspected role for this centromere site, and suggest that autoregulation and partition might normally be coordinated processes.