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J Bacteriol. 1979 Oct;140(1):301-5. doi: 10.1128/jb.140.1.301-305.1979.
2
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2
Mechanisms of microbial resistance and detoxification of mercury and organomercury compounds: physiological, biochemical, and genetic analyses.微生物对汞及有机汞化合物的抗性与解毒机制：生理学、生物化学及遗传学分析
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3
Physical and functional mapping of Tn2603, a transposon encoding ampicillin, streptomycin, sulfonamide, and mercury resistance.Tn2603转座子的物理和功能图谱，该转座子编码氨苄青霉素、链霉素、磺胺类药物和汞抗性。
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4
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J Bacteriol. 1987 Oct;169(10):4848-51. doi: 10.1128/jb.169.10.4848-4851.1987.
5
Constitutive synthesis of a transport function encoded by the Thiobacillus ferrooxidans merC gene cloned in Escherichia coli.在大肠杆菌中克隆的嗜铁氧化硫杆菌merC基因编码的转运功能的组成型合成。
J Bacteriol. 1990 May;172(5):2688-92. doi: 10.1128/jb.172.5.2688-2692.1990.
6
Transposon A-generated mutations in the mercuric resistance genes of plasmid R100-1.转座子A在质粒R100 - 1汞抗性基因中产生的突变。
J Bacteriol. 1979 Oct;140(1):167-81. doi: 10.1128/jb.140.1.167-181.1979.
7
Hypersensitivity to Hg2+ and hyperbinding activity associated with cloned fragments of the mercurial resistance operon of plasmid NR1.对Hg2+过敏以及与质粒NR1汞抗性操纵子的克隆片段相关的高结合活性。
J Bacteriol. 1979 Oct;140(1):161-6. doi: 10.1128/jb.140.1.161-166.1979.

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Site-specific DNA deletions occurring adjacent to the termini of a transposable ampicillin resistance element (Tn3).在一个可转移的氨苄青霉素抗性元件（Tn3）末端附近发生的位点特异性DNA缺失。
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Mapping of the drug resistance genes carried by the r-determinant of the R100.1 plasmid.对R100.1质粒r决定簇携带的耐药基因进行定位。
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在质粒R100 - 1的r - 决定子mer区域中发生的缺失是为了选择丧失汞超敏性的菌株而进行的。

Deletions in the r-determinant mer region of plasmid R100-1 selected for loss of mercury hypersensitivy.

作者信息

Foster T J, Nakahara H

出版信息

J Bacteriol. 1979 Oct;140(1):301-5. doi: 10.1128/jb.140.1.301-305.1979.

DOI:10.1128/jb.140.1.301-305.1979
PMID:387727
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC216811/
Abstract

A mutant of plasmid R100-1, which conferred cellular hypersensitivity to Hg2+ because of the insertion of Tn801 (TnA) into the gene determining synthesis of mercuric reductase enzyme, allowed further mutational events to be selected which resulted in either reversion to Hg2+ resistance (characteristic plasmid R100-1) or sensitivity at a level characteristic of plasmidless strains. Restriction endonuclease EcoRI and BamHI analysis showed that reversion to resistance resulted from loss of TnA from the R100-mer:Tn801 plasmid, whereas the change from hypersensitivity to sensitivity to Hg2+ usually resulted from deletion of part or all of Tn801 plus plasmid deoxyribonucleic acid sequences corresponding to the operator-proximal end of the mer operon.

摘要

质粒R100 - 1的一个突变体，由于Tn801（TnA）插入到决定汞还原酶合成的基因中，导致细胞对Hg2+超敏，该突变体使得进一步的突变事件得以被选择出来，这些突变事件要么导致回复到Hg2+抗性（典型的质粒R100 - 1），要么导致达到无质粒菌株特征水平的敏感性。限制性内切酶EcoRI和BamHI分析表明，抗性回复是由于R100 - mer:Tn801质粒上TnA的缺失，而从对Hg2+超敏到敏感的变化通常是由于部分或全部Tn801以及与mer操纵子操纵基因近端相对应的质粒脱氧核糖核酸序列的缺失所致。