中文摘要：

为夫酸安合成酶的结构基因， glnA，从 Amycolatopsismediterranei， U32 经由从 Streptomycescoelicolor.The 用模拟基因屏蔽一个 genomic 图书馆被克隆克隆被在一个紫胶倡导者的控制下面为 anEscherichia 关口 i glnA 0 异种的夫酸安要求补充机能上地验证。顺序分析显示出编码 466 氨基酸残余的蛋白质的一个开的读物框架。推出的氨基酸顺序忍受重要相同到另外的细菌的类型我夫酸安合成酶，明确地与 5 .coelicolor 和 Mycobacterium 肺结核的酶相同的71%and72%，在 A.mediterranei U32 的这 glnA 基因导致了的 respectively.Disruptionof 没有在 vivo.In 的可检测的夫酸安合成酶活动的夫酸安营养缺陷型对比，为两显型 intrans.It 的克隆的glnA~+基因罐头补充因此建议在 A.mediterranei U32 ，编码夫酸安合成酶的 glnA 基因是特别地负责的因为在 vivo 夫酸安在我们的实验室下面的合成定义生理的条件。

英文摘要：

The structural gene for glutamine synthetase, glnA, from Amycolatopsis mediterranei U32 was cloned via screening a genomic library using the analog gene from Streptomyces coelicolor. The clone was functionally verified by complementing for glutamine requirement of an Escherichia coli glnA null mutant under the control of a lac promoter. Sequence analysis showed an open reading frame encoding a protein of 466 amino acid residues. The deduced amino acid sequence bears significant homologies to other bacterial type I glutamine synthetases, specifically, 71% and 72% identical to the enzymes of S. coelicolor and Mycobacterium tuberculosis, respectively. Disruption of this glnA gene in A. mediterranei U32 led to glutamine auxotrophy with no detectable glutamine synthetase activity in vivo. In contrast, the cloned glnA^＋ gene can complement for both phenotypes in trans. It thus suggested that in A. mediterranei U32, the glnA gene encoding glutamine synthetase is uniquely responsible for in vivo glutamine synthesis under our laboratory defined physiological conditions.