Espin G, Alvarez-Morales A, Merrick M
Mol Gen Genet. 1981;184(2):213-7. doi: 10.1007/BF00272907.
A number of mutants have been isolated which affect regulation of the nitrogen fixation (nif) gene cluster in Klebsiella pneumoniae and all of which are linked to glnA, the structural gene for glutamine synthetase (G.S.). These mutants were classified on the basis of their G.S. and nitrogenase activities in conditions of nitrogen limitation and excess. The plasmid R68.45 was then used to generate a number of R-primes carrying the glnA region of the K. pneumoniae chromosome. One of these R-primes (pGE10) was subsequently used in complementation analysis and by isolation of transposon-induced insertion mutations in pGE10 we have demonstrated the existence of a gene, glnG, closely linked to glnA. Mutations in glnG have a similar phenotype to glnG mutants described in Escherichia coli (Pahel and Tyler 1979) and Salmonella typhimurium (Kustu et al. 1979) in that substantially reduce G.S. activity but are not glutamine auxotrophs. GlnG mutants have very low nitrogenase activity indicating that the glnG product may be involved regulation of the nif gene cluster in K. pneumoniae.
已经分离出许多影响肺炎克雷伯菌中固氮（nif）基因簇调控的突变体，并且所有这些突变体都与谷氨酰胺合成酶（G.S.）的结构基因glnA相连。这些突变体根据它们在氮限制和过量条件下的G.S.和固氮酶活性进行分类。然后使用质粒R68.45产生一些携带肺炎克雷伯菌染色体glnA区域的R-prime。随后，其中一个R-prime（pGE10）用于互补分析，并且通过在pGE10中分离转座子诱导的插入突变，我们证明了存在一个与glnA紧密相连的基因glnG。glnG中的突变具有与大肠杆菌（Pahel和Tyler，1979年）和鼠伤寒沙门氏菌（Kustu等人，1979年）中描述的glnG突变体相似的表型，即显著降低G.S.活性，但不是谷氨酰胺营养缺陷型。GlnG突变体具有非常低的固氮酶活性，表明glnG产物可能参与肺炎克雷伯菌中nif基因簇的调控。
