Wei G R, Kustu S
Mol Gen Genet. 1981;183(2):392-9. doi: 10.1007/BF00270646.
Some mutations to glutamine auxotrophy in the 86 unit region of the Salmonella chromosome lie within the nitrogen regulatory gene, ntrC, rather than the structural gene encoding glutamine synthetase, glnA, Assignment of mutations to ntrC is based on fine structure mapping by P22-mediated transduction and on complementation analysis. Strains with ntrC lesions that cause glutamine auxotrophy (NtrCrepressor) have very low levels of glutamine synthetase (lower than those of strains that completely lack ntrC function and comparable to those of strains that lack ntrA function). NtrCrep strains fail to increase synthesis of glutamine synthetase or several amino acid transport components under nitrogen limiting conditions. Thus, like ntrA strains, they appear to repress glnA transcription and fail to activate transcription of glnA or other nitrogen controlled genes. Mutations that suppress the glutamine requirement caused by NtrCrep lesions arise at high frequency; these mutations also suppress the glutamine requirement caused by ntrA lesions. Several suppressor mutations result in loss of function of ntrC.
沙门氏菌染色体86单位区域内谷氨酰胺营养缺陷型的一些突变位于氮调节基因ntrC内，而非编码谷氨酰胺合成酶的结构基因glnA内。将突变定位到ntrC是基于P22介导的转导精细结构图谱和互补分析。导致谷氨酰胺营养缺陷型的ntrC损伤菌株（NtrC阻遏物）的谷氨酰胺合成酶水平非常低（低于完全缺乏ntrC功能的菌株，与缺乏ntrA功能的菌株相当）。NtrCrep菌株在氮限制条件下无法增加谷氨酰胺合成酶或几种氨基酸转运成分的合成。因此，与ntrA菌株一样，它们似乎抑制glnA转录，并且无法激活glnA或其他氮控制基因的转录。抑制由NtrCrep损伤引起的谷氨酰胺需求的突变高频出现；这些突变也抑制由ntrA损伤引起的谷氨酰胺需求。几个抑制突变导致ntrC功能丧失。
