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转座子Tn501的汞离子转运蛋白MerT的过表达及汞超敏突变的遗传筛选。

Overexpression of MerT, the mercuric ion transport protein of transposon Tn501, and genetic selection of mercury hypersensitivity mutations.

作者信息

Hobman J L, Brown N L

机构信息

School of Biological Sciences, University of Birmingham, Edgbaston, UK.

出版信息

Mol Gen Genet. 1996 Jan 15;250(1):129-34. doi: 10.1007/BF02191833.

DOI:10.1007/BF02191833
PMID:8569683
Abstract

The small (116 amino acids) inner membrane protein MerT encoded by the transposon Tn501 has been overexpressed under the control of the bacteriophage T7 expression system. Random mutants of MerT were made and screened for loss of mercuric ion hypersensitivity. Several mutant merT genes were selected and sequenced: Cys24Arg and Cys25Tyr mutations abolish mercury resistance, as do charge-substitution mutations in the first predicted transmembrane helix (Gly14Arg, Gly15Arg, Gly27Arg, Ala18Asp), and the termination mutations Trp66Ter and Cys82Ter.

摘要

由转座子Tn501编码的小的(116个氨基酸)内膜蛋白MerT已在噬菌体T7表达系统的控制下过表达。制备了MerT的随机突变体,并筛选汞离子超敏性丧失的突变体。选择了几个突变的merT基因并进行测序:Cys24Arg和Cys25Tyr突变消除了汞抗性,第一个预测的跨膜螺旋中的电荷取代突变(Gly14Arg、Gly15Arg、Gly27Arg、Ala18Asp)以及终止突变Trp66Ter和Cys82Ter也消除了汞抗性。

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本文引用的文献

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