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FII型IncR质粒NR1的不相容性产物控制着质粒复制区域中的基因表达。

The incompatibility product of IncFII R plasmid NR1 controls gene expression in the plasmid replication region.

作者信息

Easton A M, Rownd R H

出版信息

J Bacteriol. 1982 Nov;152(2):829-39. doi: 10.1128/jb.152.2.829-839.1982.

DOI:10.1128/jb.152.2.829-839.1982
PMID:6290455
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC221537/
Abstract

The incompatibility properties of IncFII R plasmid NR1 were compared with those of two of its copy number mutants, pRR12 and pRR21. pRR12 produced an altered incompatibility product and also had an altered incompatibility target site. The target site appeared to be located within the incompatibility gene, which is located more than 1,200 base pairs from the plasmid origin of replication. The incompatibility properties of pRR21 were indistinguishable from those of NR1. Lambda phages have been constructed which contain the incompatibility region of NR1 or of one of its copy mutants fused to the lacZ gene. In lysogens constructed with these phages, beta-galactosidase was produced under the control of a promoter located within the plasmid incompatibility region. Lysogens containing prophages with the incompatibility regions from pRR12 and pRR21 produced higher levels of beta-galactosidase than did lysogens containing prophages with the incompatibility region from the wild-type NR1. The introduction into these inc-lac lysogens of pBR322 plasmids carrying the incompatibility regions of the wild-type or mutant plasmids resulted in decreased levels of beta-galactosidase production. For a given lysogen, the decrease was greater when the pBR322 derivative expressed a stronger incompatibility toward the plasmid from which the fragment in the prophage was derived. This suggested that the incompatibility product acts on its target to repress gene expression in the plasmid replication region.

摘要

将IncFII R质粒NR1的不相容性特性与其两个拷贝数突变体pRR12和pRR21的不相容性特性进行了比较。pRR12产生了一种改变的不相容性产物,并且其不相容性靶位点也发生了改变。靶位点似乎位于不相容性基因内,该基因位于距质粒复制起点1200多个碱基对的位置。pRR21的不相容性特性与NR1的无法区分。已经构建了λ噬菌体,其包含与lacZ基因融合的NR1或其拷贝突变体之一的不相容区域。在用这些噬菌体构建的溶原菌中,β-半乳糖苷酶在位于质粒不相容区域内的启动子控制下产生。含有来自pRR12和pRR21的不相容区域的原噬菌体的溶原菌产生的β-半乳糖苷酶水平高于含有来自野生型NR1的不相容区域的原噬菌体的溶原菌。将携带野生型或突变体质粒不相容区域的pBR322质粒导入这些inc-lac溶原菌中导致β-半乳糖苷酶产生水平降低。对于给定的溶原菌,当pBR322衍生物对原噬菌体中片段所源自的质粒表现出更强的不相容性时,降低幅度更大。这表明不相容性产物作用于其靶标以抑制质粒复制区域中的基因表达。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d6/221537/06c5e37cce79/jbacter00252-0291-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d6/221537/06c5e37cce79/jbacter00252-0291-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/60d6/221537/06c5e37cce79/jbacter00252-0291-a.jpg

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The incompatibility product of IncFII R plasmid NR1 controls gene expression in the plasmid replication region.FII型IncR质粒NR1的不相容性产物控制着质粒复制区域中的基因表达。
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引用本文的文献

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Suppression of replication-deficient mutants of IncFII plasmid NR1 can occur by two different mechanisms that increase expression of the repA1 gene.FII型质粒NR1复制缺陷型突变体的抑制可通过两种不同机制发生,这两种机制均可增加repA1基因的表达。
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2
Insertion and deletion mutations in the repA4 region of the IncFII plasmid NR1 cause unstable inheritance.IncFII质粒NR1的repA4区域中的插入和缺失突变导致遗传不稳定。
J Bacteriol. 1993 Sep;175(17):5350-8. doi: 10.1128/jb.175.17.5350-5358.1993.
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Analysis of functional domains of Rts1 RepA by means of a series of hybrid proteins with P1 RepA.

本文引用的文献

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J Bacteriol. 1984 Oct;160(1):28-35. doi: 10.1128/jb.160.1.28-35.1984.
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Regulation of plasmid replication.质粒复制的调控
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