Jovanovic G, Model P
Laboratory of Genetics, The Rockefeller University, New York, NY 10021, USA.
Mol Microbiol. 1997 Aug;25(3):473-81. doi: 10.1046/j.1365-2958.1997.4791844.x.
PspF bound to the psp enhancer activates E sigma54 holoenzyme-dependent transcription of the Escherichia coli phage-shock protein (psp) operon and autogenously represses its own sigma70-dependent transcription, thereby keeping its concentration at a low level. It has been demonstrated previously that integration host factor (IHF) bound to a DNA site located between the psp core promoter and the PspF binding sites stimulates psp expression. We show here that wild-type IHF strongly retards DNA containing the psp promoter region. In vitro, PspF binding to the psp enhancer facilitates IHF binding, while IHF binding to the pspF-pspA-E promoter-regulatory region increases the efficacy of PspF binding to the upstream activating sequences (UASs). This is the first demonstration of co-operative binding of an activator and IHF in a sigma54-dependent system. In the absence of IHF, in vivo autoregulation of pspF transcription is lifted and, consequently, PspF production is increased, indicating that IHF enhances PspF binding to the psp enhancer in vivo.
结合到psp增强子上的PspF激活大肠杆菌噬菌体休克蛋白（psp）操纵子的E σ54全酶依赖性转录，并自身抑制其自身的σ70依赖性转录，从而使其浓度保持在较低水平。先前已经证明，结合到位于psp核心启动子和PspF结合位点之间的DNA位点上的整合宿主因子（IHF）刺激psp表达。我们在此表明，野生型IHF强烈阻滞含有psp启动子区域的DNA。在体外，PspF与psp增强子的结合促进IHF结合，而IHF与pspF-pspA-E启动子调控区域的结合增加了PspF与上游激活序列（UASs）结合的效力。这是在σ54依赖性系统中激活剂与IHF协同结合的首次证明。在没有IHF的情况下，体内pspF转录的自动调节被解除，因此，PspF的产生增加，表明IHF在体内增强了PspF与psp增强子的结合。
