Funanage V L, Brenchley J E
Genetics. 1977 Jul;86(3):513-26. doi: 10.1093/genetics/86.3.513.
A number of glutamine auxotrophs of Salmonella typhimurium were isolated and characterized genetically. Three of the mutations appear to be closely linked and are complemented by episomes carrying the glnA region of Escherichia coli. The lesions in these strains are approximately 20% linked by P1 transduction with a mutation in the rha gene, but are unlinked to ilv. Another mutation causing glutamine auxotrophy in strain JB674 is genetically distinct from the others. Strain JB674 grown in glucose medium containing ammonia as the nitrogen source has reduced levels of glutamine synthetase that is more adenylylated than in the parent strain, suggesting that the enzyme can not be deadenylylated normally. The lesion causing glutamine auxotrophy in JB674 lies in the region corresponding to the glnB and glnE genes affecting glutamine synthetase modification in Klebsiella areogenes. Four Gln+ revertants of JB674 have glutamine synthetase activities 4 to 6 fold higher than normal. One mutation causing this increased enzyme synthesis has been shown by three-factor crosses with the glnA mutations to lie near or within the glnA gene.
分离并对鼠伤寒沙门氏菌的多个谷氨酰胺营养缺陷型进行了遗传学表征。其中三个突变似乎紧密连锁,并由携带大肠杆菌谷氨酰胺合成酶基因(glnA)区域的附加体互补。这些菌株中的损伤通过P1转导与rha基因突变有大约20%的连锁,但与ilv不连锁。在菌株JB674中导致谷氨酰胺营养缺陷的另一个突变在遗传上与其他突变不同。在以氨作为氮源的葡萄糖培养基中生长的菌株JB674,其谷氨酰胺合成酶水平降低,且比亲本菌株有更多的腺苷酸化,这表明该酶不能正常去腺苷酸化。在JB674中导致谷氨酰胺营养缺陷的损伤位于与影响产气克雷伯菌谷氨酰胺合成酶修饰的glnB和glnE基因相对应的区域。JB674的四个谷氨酰胺合成酶阳性(Gln+)回复突变体的谷氨酰胺合成酶活性比正常高4至6倍。通过与glnA突变进行三因子杂交表明,导致这种酶合成增加的一个突变位于glnA基因附近或内部。