Fröhler J, Rechenmacher A, Thomale J, Nass G, Böck A
J Bacteriol. 1980 Sep;143(3):1135-41. doi: 10.1128/jb.143.3.1135-1141.1980.
Mutations leading to borrelidin resistance in Escherichia coli by overproduction of threonyl-transfer ribonucleic acid synthetase were anaylzed genetically. The regulatory mutations were closely linked to the treonyl-transfer ribonucleic acid synthetase structural gene (thrS), located clockwise to it. The mutation that causes the threefold-increased enzyme level was more distant from thrS than the mutation responsible for the ninefold overproduction. Both mutations were cis dominant in merodiploid strains, indicating that they affected promoter-operator-like control elements. Overproduction was restricted to threonyl-transfer ribonucleic acid synthetase and was not observed for the products of genes neighboring thrS (e.g., infC, pheS, pheT, and argS), providing evidence that thrS is transcribed singly and that gene amplificationis not a likely basis for increased thrS experession.
对通过苏氨酰 - 转移核糖核酸合成酶过量产生导致大肠杆菌对硼relidin产生抗性的突变进行了遗传分析。调控突变与苏氨酰 - 转移核糖核酸合成酶结构基因（thrS）紧密连锁，位于其顺时针方向。导致酶水平增加三倍的突变比导致九倍过量产生的突变距离thrS更远。这两个突变在部分二倍体菌株中都是顺式显性的，表明它们影响启动子 - 操纵子样控制元件。过量产生仅限于苏氨酰 - 转移核糖核酸合成酶，在thrS相邻基因（如infC、pheS、pheT和argS）的产物中未观察到，这证明thrS是单独转录的，并且基因扩增不太可能是thrS表达增加的基础。
