Osorio A V, Servín-González L, Rocha M, Covarrubias A A, Bastarrachea F
Mol Gen Genet. 1984;194(1-2):114-23. doi: 10.1007/BF00383506.
Mutants resistant to 80 microM L-methionine-DL-sulfoximine (MS) were isolated on glucose-minimal 15 mM NH4+ medium plates from Escherichia coli cells which were hypersensitive to this concentration of the analogue by virtue of their harboring glnG mutations. MS-resistant mutants derived from strain MX902 carried, in addition to its glnG74 ::Tn5 allele, mutations tightly linked to glnA, as shown by P1-mediated transduction experiments. One particular allele, gln-76, which suppressed the MS-sensitivity conferred by glnG74 ::Tn5 but not its Ntr- phenotype (inability to transport and utilize compounds such as arginine or proline as the only nitrogen sources), was shown to allow constitutive expression of glutamine synthetase in the absence not only of a functional glnG product but also of a functional glnF product. This behavior was found to be cis-dominant in complementation experiments with F'14 merogenotes . In an otherwise wild-type genetic background as in MX929 (gln-76 glnA+ glnL+ glnG+ glnF +), however, normal activation, mediated by the glnG and glnF products was preferred over that mediated by gln-76.
从因携带glnG突变而对该浓度类似物高度敏感的大肠杆菌细胞中，在葡萄糖-基本培养基（含15 mM NH4+）平板上分离出对80 microM L-甲硫氨酸-DL-亚砜亚胺（MS）具有抗性的突变体。如P1介导的转导实验所示，源自菌株MX902的MS抗性突变体除了其glnG74::Tn5等位基因外，还携带与glnA紧密连锁的突变。一个特定的等位基因gln-76，它抑制了glnG74::Tn5赋予的MS敏感性，但不抑制其Ntr表型（无法转运和利用精氨酸或脯氨酸等化合物作为唯一氮源的能力），被证明不仅在缺乏功能性glnG产物而且在缺乏功能性glnF产物的情况下允许谷氨酰胺合成酶的组成型表达。在与F'14部分二倍体的互补实验中发现这种行为是顺式显性的。然而，在如MX929（gln-76 glnA+ glnL+ glnG+ glnF +）这样的其他方面为野生型的遗传背景中，由glnG和glnF产物介导的正常激活优于由gln-76介导的激活。
