Ausubel F M, Bird S C, Durbin K J, Janssen K A, Margolskee R F, Peskin A P
J Bacteriol. 1979 Nov;140(2):597-606. doi: 10.1128/jb.140.2.597-606.1979.
Previous studies have implicated glutamine synthetase (L-glutamate:ammonia ligase [adenosine diphosphate for-ing], EC 6.6.1.2) as a major controlling element of the nitrogen fixation (nif) genes in Klebsiella pneumoniae. We report here the isolation of a new class of K. pneumoniae mutants which exhibit altered patterns of nif and hut (histidine utlization) regulation. The expression of nif in these mutants, which were isolated as Gln+ (glutamine nonrequiring) revertants of a particular glnA mutation, is extremely sensitive to ammonia repression. These mutants have a Nif- Hut- phenotype at external ammonia concentrations at which wild-type strains are Nif+ Hut+. On the other hand, these mutants can be fully derepressed for nif at very low ammonia concentrations. We adopted the nomenclature "GlnR- (Nif- Hut-)" to facilitate discussion of the phenotype of these mutant strains. The mutations in these strains which confer the GlnR- phenotype map at or near glnA, the structural gene for glutamine synthetase.
以往的研究表明,谷氨酰胺合成酶(L-谷氨酸:氨连接酶[生成二磷酸腺苷],EC 6.6.1.2)是肺炎克雷伯菌中固氮(nif)基因的主要调控元件。我们在此报告分离出一类新型的肺炎克雷伯菌突变体,其固氮和hut(组氨酸利用)调控模式发生了改变。这些突变体是作为特定glnA突变的Gln +(无需谷氨酰胺)回复突变体分离得到的,其nif的表达对氨抑制极为敏感。在外部氨浓度下,这些突变体具有Nif - Hut - 表型,而野生型菌株在此浓度下为Nif + Hut +。另一方面,在极低的氨浓度下,这些突变体的nif可以完全去阻遏。我们采用“GlnR - (Nif - Hut - )”这一命名法,以便于讨论这些突变菌株的表型。赋予GlnR -表型的这些菌株中的突变定位在谷氨酰胺合成酶的结构基因glnA处或其附近。