Reitzer L J, Magasanik B
Cell. 1986 Jun 20;45(6):785-92. doi: 10.1016/0092-8674(86)90553-2.
Transcription of the Escherichia coli glnALG operon, whose products are glutamine synthetase and the regulatory proteins NRII and NRI, is activated by nitrogen deprivation. Initiation of transcription at the nitrogen-regulated promoter glnAp2 requires sigma 60, the product of rpoN (glnF, ntrA), and NRI, the product of glnG (ntrC). We have now shown that the ability of this promoter to be activated by a low intracellular concentration of NRI depends on two binding sites for NRI located approximately 110 and 140 bp, respectively, upstream of the start of transcription. Moving these binding sites more than 1000 bp does not diminish the ability of NRI to stimulate transcription at glnAp2. Thus, the NRI binding sites resemble enhancers in eukaryotic cells.
大肠杆菌谷氨酰胺合成酶操纵子(glnALG operon)的转录产物包括谷氨酰胺合成酶以及调节蛋白NRII和NRI,该操纵子的转录受氮缺乏激活。在氮调节启动子glnAp2处的转录起始需要σ60(rpoN(glnF,ntrA)的产物)和NRI(glnG(ntrC)的产物)。我们现已表明,该启动子被低细胞内浓度的NRI激活的能力取决于两个NRI结合位点,它们分别位于转录起始点上游约110和140 bp处。将这些结合位点移动超过1000 bp不会削弱NRI刺激glnAp2转录的能力。因此,NRI结合位点类似于真核细胞中的增强子。