Magasanik B
Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.
Biochimie. 1989 Sep-Oct;71(9-10):1005-12. doi: 10.1016/0300-9084(89)90104-1.
The transcription of glnA, the structural gene for glutamine synthetase in enteric bacteria, is regulated by the phosphorylation and dephosphorylation of an effector protein, NRI. In its phosphorylated form the effector activates the initiation of transcription at promoters specific of sigma 54, rather than the abundant sigma 70. The ability of NRI-phosphate to stimulate the formation of open promoter-sigma 54 RNA polymerase complexes is enhanced by specific binding sites, located in the case of glnA 100 and 130 base pairs upstream from the transcriptional start site. These sites can be moved more than 1000 base pairs upstream or downstream without losing their effectiveness. The phosphorylation and dephosphorylation of NRI-NRI-phosphate is catalyzed by the modulator protein NRII. Its activity is controlled by an intracellular signal, the ratio of glutamine to 2-ketoglutarate, which is generated by glutamine synthetase in response to the environmental stimulus, the availability or lack of ammonia. The signal is transduced to the modulator by means of 2 additional proteins: uridylytransferase and PII.
肠道细菌中谷氨酰胺合成酶的结构基因glnA的转录受效应蛋白NRI的磷酸化和去磷酸化调节。效应蛋白以磷酸化形式激活σ54特异性启动子处的转录起始，而非丰富的σ70。磷酸化的NRI刺激开放启动子-σ54 RNA聚合酶复合物形成的能力，因位于glnA转录起始位点上游100和130个碱基对处的特异性结合位点而增强。这些位点可在上游或下游移动超过1000个碱基对而不丧失其有效性。NRI-NRI磷酸化和去磷酸化由调节蛋白NRII催化。其活性受细胞内信号谷氨酰胺与2-酮戊二酸的比例控制，该比例由谷氨酰胺合成酶响应环境刺激（氨的可利用性或缺乏）产生。该信号通过另外两种蛋白质：尿苷酰转移酶和PII传递给调节蛋白。
