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大肠杆菌钠敏感突变体中磷脂代谢的改变。

Altered phospholipid metabolism in a sodium-sensitive mutant of Escherichia coli.

作者信息

Lusk J E, Kennedy E P

出版信息

J Bacteriol. 1972 Mar;109(3):1034-46. doi: 10.1128/jb.109.3.1034-1046.1972.

Abstract

A mutant of Escherichia coli has been isolated, the growth of which is inhibited by low concentrations (1 mm) of NaCl. High levels of magnesium, calcium, or strontium in the medium permit growth in the presence of sodium. The metal content of the inhibited mutant is normal, but the strain is unable to tolerate levels of sodium to which the wild type is indifferent. Immediately after the addition of sodium to cultures of the mutant, rates of synthesis of protein, ribonucleic acid, deoxyribonucleic acid, and total lipid are unchanged, but more cardiolipin and less phosphatidylethanolamine are produced. The direct enzymatic cause of this change, which affects membrane function, is not known. Studies of the metabolism of phosphatidylglycerol in vivo after pulse-labeling with [2-(3)H]glycerol reveal that a major pathway both in wild-type and mutant strains involves the cleavage of labeled glycerol from phosphatidylglycerol.

摘要

已分离出一种大肠杆菌突变体,其生长受到低浓度(1 mM)氯化钠的抑制。培养基中高水平的镁、钙或锶可使该突变体在有钠存在的情况下生长。受抑制的突变体的金属含量正常,但该菌株无法耐受野生型无动于衷的钠水平。向突变体培养物中添加钠后,蛋白质、核糖核酸、脱氧核糖核酸和总脂质的合成速率立即没有变化,但会产生更多的心磷脂和更少的磷脂酰乙醇胺。影响膜功能的这种变化的直接酶促原因尚不清楚。在用[2-(3)H]甘油进行脉冲标记后,对体内磷脂酰甘油代谢的研究表明,野生型和突变体菌株中的一条主要途径都涉及从磷脂酰甘油中裂解标记的甘油。

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