Schneider R, Travers A, Muskhelishvili G
Institut für Genetik und Mikrobiologie, LMU München, Maria-Ward-Str. 1a, 80638 München, Germany.
Mol Microbiol. 2000 Oct;38(1):167-75. doi: 10.1046/j.1365-2958.2000.02129.x.
The Escherichia coli DNA architectural protein FIS is a pleiotropic regulator, which couples the cellular physiology with transitions in the superhelical density of bacterial DNA. Recently, we have shown that this effect is in part mediated via DNA gyrase, the major cellular topoisomerase responsible for the elevation of negative supercoiling. Here, we demonstrate that, in turn, the expression of the fis gene strongly responds to alterations in the topology of DNA in vivo, being maximal at high levels of negative supercoiling. Any deviations from these optimal levels decrease fis promoter activity. This strict dependence of fis expression on the superhelical density suggests that fis may be involved in 'fine-tuning' the homeostatic control mechanism of DNA supercoiling in E. coli.
大肠杆菌DNA结构蛋白FIS是一种多效性调节因子，它将细胞生理与细菌DNA超螺旋密度的转变联系起来。最近，我们已经表明，这种效应部分是通过DNA促旋酶介导的，DNA促旋酶是负责增加负超螺旋的主要细胞拓扑异构酶。在这里，我们证明，反过来，fis基因的表达在体内对DNA拓扑结构的改变有强烈反应，在高水平负超螺旋时达到最大值。任何偏离这些最佳水平的情况都会降低fis启动子活性。fis表达对超螺旋密度的这种严格依赖性表明，fis可能参与了大肠杆菌DNA超螺旋稳态控制机制的“微调”。
