Bender R A, Magasanik B
J Bacteriol. 1977 Oct;132(1):100-5. doi: 10.1128/jb.132.1.100-105.1977.
Glutamine synthetase could be repressed several hundredfold rather than 6- to 10-fold as previously reported. Ammonia was not the primary repression signal for glutamine synthetase. Repression appeared to be mediated by a high level of glutamine and probably by a high ratio of glutamine to alpha-ketoglutarate. Mutations in glnA (the structural gene for glutamine synthetase) were seen to fall into three phenotypic groups: glutamine auxotrophs that produced no detectable glnA product; glutamine auxotrophs that produced a glnA product lacking enzymatic activity (and hence repressibility by ammonia) but were repressible under appropriate conditions; and glutamine synthetase regulatory mutants, whose glnA product was enzymatically active and not repressible under any conditions.
谷氨酰胺合成酶的表达可能被抑制数百倍，而不是如先前报道的6至10倍。氨不是谷氨酰胺合成酶的主要抑制信号。这种抑制似乎是由高水平的谷氨酰胺介导的，可能还与谷氨酰胺与α-酮戊二酸的高比例有关。谷氨酰胺合成酶结构基因（glnA）的突变可分为三个表型组：不产生可检测到的glnA产物的谷氨酰胺营养缺陷型；产生缺乏酶活性（因此不受氨抑制）但在适当条件下可被抑制的glnA产物的谷氨酰胺营养缺陷型；以及谷氨酰胺合成酶调节突变体，其glnA产物具有酶活性且在任何条件下都不可被抑制。
