Ninfa A J, Magasanik B
Proc Natl Acad Sci U S A. 1986 Aug;83(16):5909-13. doi: 10.1073/pnas.83.16.5909.
Transcription from nitrogen-regulated promoters, such as glnAp2, requires the glnG gene product, NRI, as well as the rpoN(glnF) gene product, sigma60, and is regulated by the glnL gene product, NRII. We find that in a reaction mixture containing NRI, NRII, and ATP, NRII catalyzes the transfer of the gamma phosphate of ATP to NRI. This covalent modification of NRI occurs concurrently with the acquisition of the ability by the reaction mixture to activate transcription from glnAp2. In the presence of PII, the product of glnB, NRII catalyzes the removal of the phosphate from NRI-phosphate. This reaction occurs concurrently with the loss by the reaction mixture of the ability to activate transcription from glnAp2. On the basis of this evidence, we propose that NRI-phosphate activates transcription from nitrogen-regulated promoters and that the role of NRII is control of the formation and breakdown of NRI-phosphate in response to cellular signals of nitrogen availability.
来自氮调节启动子(如glnAp2)的转录需要glnG基因产物NRI以及rpoN(glnF)基因产物sigma60,并受glnL基因产物NRII的调节。我们发现,在含有NRI、NRII和ATP的反应混合物中,NRII催化ATP的γ磷酸基团转移至NRI。NRI的这种共价修饰与反应混合物获得激活glnAp2转录的能力同时发生。在PII(glnB的产物)存在的情况下,NRII催化从磷酸化NRI上去除磷酸基团。此反应与反应混合物失去激活glnAp2转录的能力同时发生。基于这些证据,我们提出磷酸化NRI激活氮调节启动子的转录,并且NRII的作用是响应细胞内氮可利用性信号控制磷酸化NRI的形成和分解。