Schreier H J, Brown S W, Hirschi K D, Nomellini J F, Sonenshein A L
Department of Microbiology, Arizona State University, Tempe 85287.
J Mol Biol. 1989 Nov 5;210(1):51-63. doi: 10.1016/0022-2836(89)90290-8.
Transcription of the Bacillus subtilis gene coding of glutamine synthetase (glnA) is regulated by the nitrogen source. The glnA gene lies in an operon in which it is preceded by an open reading frame with the potential to encode a polypeptide of approximately 16,000 Mr. We have now shown that this open reading frame is utilized in vivo, that its product (GlnR) acts as a diffusible, negative regulator of gln transcription, and that GlnR is likely to be a DNA-binding protein. Certain mutations in glnR, including a large, in-frame deletion and a start codon mutation, led to high-level constitutivity of the operon; other mutations caused low-level constitutivity. These latter mutations, which affected the C terminus of GlnR, seemed to disrupt response to the nitrogen source without eliminating the ability of GlnR to bind to DNA. Wild-type GlnR by itself, however, did not impose nitrogen-dependent regulation; such regulation also required the product of glnA. A model is presented in which glutamine synthetase monitors the availability of nitrogen and imposes negative regulation by interaction with or modification of GlnR.
枯草芽孢杆菌谷氨酰胺合成酶（glnA）编码基因的转录受氮源调控。glnA基因位于一个操纵子中，在它之前有一个开放阅读框，有可能编码一个分子量约为16,000的多肽。我们现已表明，这个开放阅读框在体内被利用，其产物（GlnR）作为gln转录的一种可扩散的负调节因子，并且GlnR可能是一种DNA结合蛋白。glnR中的某些突变，包括一个大的框内缺失和一个起始密码子突变，导致操纵子的高水平组成型表达；其他突变导致低水平组成型表达。这些影响GlnR C末端的后一类突变，似乎破坏了对氮源的反应，但没有消除GlnR与DNA结合的能力。然而，野生型GlnR本身并不施加氮依赖性调节；这种调节还需要glnA的产物。提出了一个模型，其中谷氨酰胺合成酶监测氮的可用性，并通过与GlnR相互作用或修饰GlnR来施加负调节。
