Janssen K A, Magasanik B
J Bacteriol. 1977 Feb;129(2):993-1000. doi: 10.1128/jb.129.2.993-1000.1977.
Mutations resulting in defects in the adenylylation system of glutamine synthetase (GS) affect the expression of glnA, the structural gene for GS. Mutants with lesions in glnB are glutamine auxotrophs and contain repressed levels of highly adenylylated GS. Glutamine-independent revertants of the glnB3 mutant have acquired an additional mutation at the glnE site. The glnE54 mutant is incapable of adenylylating GS and produces high levels of enzyme, even when ammonia is present in the growth medium. The fact that mutations in glnB and glnE simultaneously disturb both the normal adenylylation and repression patterns of GS in Klebsiella aerogenes indicates that the adenylylation system, or adenylylation state, of GS is critical for the regulation of synthesis of GS.
导致谷氨酰胺合成酶（GS）腺苷酸化系统缺陷的突变会影响GS结构基因glnA的表达。glnB有损伤的突变体是谷氨酰胺营养缺陷型，且含有高度腺苷酸化的GS的受抑制水平。glnB3突变体的谷氨酰胺非依赖回复突变体在glnE位点获得了额外的突变。glnE54突变体无法对GS进行腺苷酸化，即使生长培养基中存在氨，也会产生高水平的酶。glnB和glnE中的突变同时干扰产气克雷伯菌中GS的正常腺苷酸化和抑制模式，这一事实表明GS的腺苷酸化系统或腺苷酸化状态对GS合成的调节至关重要。
