Raetz C R
J Biol Chem. 1976 Jun 10;251(11):3242-9.
Mutants of Escherichia coli K-12 defective in CDP-diglyceride:L-serine phosphatidyltransferase (phosphatidylserine synthetase) can be isolated by a rapid autoradiographic screening assay described previously (Raetz, C. R. H. (1975) Proc. Natl. Acad. Sci. U. S. A. 72, 2274-2278). Four organisms of this kind have now been characterized. The gene (designated pss) which is altered in these mutants is closely linked to the nadB locus near minute 49 on the E. coli chromosome. Strains carrying the pss-8 mutation do not grow at elevated temperatures and have low levels of an altered synthetase in cell extracts. An analysis of several hundred transductants and temperature-resistant revertants reveals that the pss-8 mutation is responsible both for the enzyme defect and for the phenotype. When a pss-8 mutant is shifted to the nonpermissive temperature, the cells stop dividing and form long filaments. After 3 hours at 44 degrees the level of phosphatidylethanolamine drops from 66 to 32% (percentage of the total lipid phosphorus), while the combined levels of phosphatidylglycerol and cardiolipin rise from 34 to 68%.
利用先前描述的快速放射自显影筛选试验（雷茨，C.R.H.（1975年）《美国国家科学院院刊》72卷，2274 - 2278页），可以分离出在CDP - 二甘油酯：L - 丝氨酸磷脂酰转移酶（磷脂酰丝氨酸合成酶）方面有缺陷的大肠杆菌K - 12突变体。现已对四种这类生物体进行了表征。在这些突变体中发生改变的基因（命名为pss）与大肠杆菌染色体上49分钟附近的nadB位点紧密连锁。携带pss - 8突变的菌株在高温下无法生长，并且细胞提取物中一种改变的合成酶水平较低。对数百个转导子和温度抗性回复体的分析表明，pss - 8突变既导致了酶缺陷，也导致了该表型。当一个pss - 8突变体转移到非允许温度时，细胞停止分裂并形成长丝。在44摄氏度下3小时后，磷脂酰乙醇胺的水平从66%降至32%（占总脂质磷的百分比），而磷脂酰甘油和心磷脂的总水平从34%升至68%。
