Nitrogen control in Salmonella: regulation by the glnR and glnF gene products.
Nitrogen control in Salmonella: regulation by the glnR and glnF gene products.
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沙门氏菌中的氮控制：glnR 和 glnF 基因产物的调节。
DOI：
10.1073/pnas.76.9.4576
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发表时间：
1979
影响因子：
11.1
通讯作者：
N. Mcfarland
中科院分区：
文献类型：
--
作者：
S. Kustu;D. Burton;E. García;L. McCarter;N. Mcfarland
glnR 基因的产物是沙门氏菌中谷氨酰胺合成（Gln 合成酶）[L-谷氨酸：氨连接酶（ADP 形成），EC 6.3.1.2] 和两种受氮控制的周质转运蛋白合成的氮调节所必需的。具有导致glnR产物功能丧失的突变的菌株[例如，具有Tn10插入的菌株或在glnR中具有ICR诱导的（移码）突变的菌株]与完全去阻抑的野生型菌株相比，其Gln合成酶的含量约为3%，并且不能响应氮限制而增加这种酶或周质转运蛋白的合成。谷氨酰胺合成酶、glnA 的结构基因和周质转运蛋白的结构基因在染色体上不相连；因此，glnR 似乎编码一种可扩散的正调控元件。与此一致，突变体glnR等位基因在glnA（Gln合成酶的合成）的表达方面是野生型等位基因的隐性。尽管glnR与glnA密切相关，但具有glnR产物功能完全丧失的突变的菌株可以通过其产生可检测的Gln合成酶以及在没有谷氨酰胺的情况下生长的能力来与glnA菌株区分开来。为了明确证明glnR与glnA不同，我们从glnR中插入Tn10的菌株中纯化并表征了Gln合成酶。由于插入突变体的谷氨酰胺合成酶的特性，最重要的是氨基酸的羧基末端序列，与野生型合成酶的特性相同，因此 Tn10 插入不能位于 glnA 中（如果是，则必须改变谷氨酰胺合成酶的羧基末端）；因此我们得出结论，Tn10 插入在调节基因 glnR 中，该基因与 glnA 不同。讨论了 glnR 产物与先前定义的 glnF 产物在介导氮控制中的功能模型。
The product of the glnR gene is required for nitrogen regulation of the synthesis of glutamine synthesis (Gln synthetase) [L-glutamate:ammonia ligase (ADP-forming), EC 6.3.1.2] and two periplasmic transport proteins that are subject to nitrogen control in Salmonella. Strains with mutations to loss of function of the glnR product [e.g., a strain with a Tn10 insertion or one with an ICR-induced (frameshift) mutation in glnR] have about 3% as much Gln synthetase as a fully derepressed wild-type strain and are unable to increase synthesis of this enzyme or periplasmic transport proteins in response to nitrogen limitation. The structural gene for Gln synthetase, glnA, and those for the periplasmic transport proteins are unlinked on the chromosome; thus, glnR appears to encode a diffusible positive regulatory element. Consistent with this, the mutant glnR allele is recessive to the wild-type allele with regard to expression of glnA (synthesis of Gln synthetase). Although glnR is closely linked to glnA, strains with mutations to complete loss of function of the glnR product can be distinguished from glnA strains by their ability to produce detectable Gln synthetase and to grow in the absence of glutamine. To demonstrate unequivocally that glnR is distinct from glnA, we have purified and characterized Gln synthetase from a strain with a Tn10 insertion in glnR. Because the properties of Gln synthetase from the insertion mutant, most importantly the carboxyl-terminal sequence of amino acids, are the same as those of synthetase from wild type, the Tn10 insertion cannot be in glnA (if it were, the carboxyl terminus of Gln synthetase would have to be altered); therefore we conclude that the Tn10 insertion is in a regulatory gene, glnR, which is distinct from glnA. A model for the function of the glnR product together with the previously defined glnF product in mediating nitrogen control is discussed.