Schneider R, Travers A, Kutateladze T, Muskhelishvili G
Institut für Genetik und Mikrobiologie, LMU München, Maria-Ward-Str. 1a, 80638 München, Germany.
Mol Microbiol. 1999 Dec;34(5):953-64. doi: 10.1046/j.1365-2958.1999.01656.x.
In Escherichia coli, the transcriptional activity of many promoters is strongly dependent on the negative superhelical density of chromosomal DNA. This, in turn, varies with the growth phase, and is correlated with the overall activity of DNA gyrase, the major topoisomerase involved in the elevation of negative superhelicity. The DNA architectural protein FIS is a regulator of the metabolic reorganization of the cell during early exponential growth phase. We have previously shown that FIS modulates the superhelical density of plasmid DNA in vivo, and on binding reshapes the supercoiled DNA in vitro. Here, we show that, in addition, FIS represses the gyrA and gyrB promoters and reduces DNA gyrase activity. Our results indicate that FIS determines DNA topology both by regulation of topoisomerase activity and, as previously inferred, by directly reshaping DNA. We propose that FIS is involved in coupling cellular physiology to the topology of the bacterial chromosome.
在大肠杆菌中,许多启动子的转录活性强烈依赖于染色体DNA的负超螺旋密度。而负超螺旋密度又随生长阶段而变化,并且与DNA促旋酶的整体活性相关,DNA促旋酶是参与增加负超螺旋的主要拓扑异构酶。DNA结构蛋白FIS是细胞在指数生长早期阶段代谢重组的调节因子。我们之前已经表明,FIS在体内调节质粒DNA的超螺旋密度,并且在结合时会在体外重塑超螺旋DNA。在此,我们还表明,FIS会抑制gyrA和gyrB启动子,并降低DNA促旋酶活性。我们的结果表明FIS通过调节拓扑异构酶活性以及如之前所推断的通过直接重塑DNA来决定DNA拓扑结构。我们提出FIS参与将细胞生理与细菌染色体的拓扑结构联系起来。