Martin R G, Rosner J L
Laboratory of Molecular Biology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0560, USA.
Curr Opin Microbiol. 2001 Apr;4(2):132-7. doi: 10.1016/s1369-5274(00)00178-8.
The AraC family of bacterial transcriptional activators regulate diverse genetic systems. Recent X-ray diffraction studies show that the monomeric MarA and Rob activators bind to their asymmetric degenerate DNA sites via two different helix-turn-helix elements. Activation by MarA, SoxS or Rob requires a particular orientation of the asymmetric binding sequence (and hence the activator), depending on its distance from the -10 RNAP signal. Genetic studies are beginning to clarify how the activators interact with RNAP. Growing evidence suggests that for the sugar metabolism activators, multiple binding sites upstream of the promoter anchor the activator in a repressing or nonactivating configuration. By interaction with the sugar and/or CRP, the activator is allosterically altered so it can bind a new set of sites that enable it to activate the promoter. Surprisingly, the virulence activator, Rns, must bind to both upstream and downstream sites in order to activate the rns promoter.
细菌转录激活因子的AraC家族调控多种遗传系统。最近的X射线衍射研究表明，单体形式的MarA和Rob激活因子通过两个不同的螺旋-转角-螺旋元件与其不对称简并DNA位点结合。MarA、SoxS或Rob的激活作用需要不对称结合序列（以及激活因子）的特定取向，这取决于其与-10 RNA聚合酶信号的距离。遗传学研究开始阐明激活因子如何与RNA聚合酶相互作用。越来越多的证据表明，对于糖代谢激活因子，启动子上游的多个结合位点将激活因子锚定在抑制或非激活构型中。通过与糖和/或CRP相互作用，激活因子发生变构改变，从而能够结合一组新的位点，使其能够激活启动子。令人惊讶的是，毒力激活因子Rns必须与上游和下游位点都结合才能激活rns启动子。
