缺乏磷酸烯醇丙酮酸羧激酶活性的大肠杆菌突变体的遗传和生理学特征
Genetic and physiological characterization of Escherichia coli mutants deficient in phosphoenolpyruvate carboxykinase activity.
作者信息
Goldie A H, Sanwal B D
出版信息
J Bacteriol. 1980 Mar;141(3):1115-21. doi: 10.1128/jb.141.3.1115-1121.1980.
Abstract
Mutants doubly deficient in phosphoenolpyruvate carboxykinase (pck) and phosphoenolpyruvate synthetase (pps) were unable to grow with succinate as the sole carbon source. A number of pck mutations isolated from pps strains by penicillin selection mapped at 74 min on the Escherichia coli chromosome, between glpD and aroB. Several of the strains containing these mutations had a protein antigenically related to phosphoenolpyruvate carboxykinase, and therefore, the mutations probably represented mutations in the structural gene for this enzyme. Phosphoenolpyruvate carboxykinase was regulated at the level of transcription by catabolite repression. Enzyme levels also increased in stationary-phase cultures by a mechanism independent of cyclic adenosine monophosphate or the product of the relA gene.
摘要
磷酸烯醇式丙酮酸羧激酶（pck）和磷酸烯醇式丙酮酸合成酶（pps）双缺陷的突变体无法以琥珀酸盐作为唯一碳源生长。通过青霉素选择从pps菌株中分离出的一些pck突变位于大肠杆菌染色体上74分钟处，在glpD和aroB之间。含有这些突变的几个菌株有一种与磷酸烯醇式丙酮酸羧激酶抗原相关的蛋白质，因此，这些突变可能代表该酶结构基因中的突变。磷酸烯醇式丙酮酸羧激酶在转录水平受分解代谢物阻遏调控。在稳定期培养物中，酶水平也通过一种独立于环磷酸腺苷或relA基因产物的机制增加。
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