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Molecular Genetic Analyses of the Physiological Role of Acidic Phospholipids in Escherichia coli Cell Growth

酸性磷脂在大肠杆菌细胞生长中生理作用的分子遗传学分析

基本信息

批准号：
10640598
负责人：
MATSUMOTO Kouji
金额：
$ 2.18万
依托单位：
Saitama University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10640598/
关键词：
Escherichia coli Acidic phospholipids phosphatidylglycerol lpp-mutation rcs mutation 1pp欠損変異

项目摘要

Two plans were enforced. The plans were resulted from the discovery that Escherichia coli cells lacking the major acidic phospholipids was viable if it harbored a defective lpp allele.1) One is to clarify the lethality of acidic-phospholipid deficiency in the cells having wild type lpp allele. For this purpose we have constructed an lpp inducible system and examined the localization of proLPP protein in the membranes during its retarded growth after induction of lpp.2) The other is to clarify the reason for the temperature-sensitivity of the cells lacking the major acidic phospholipids. The temperature-sensitivity suggest that at temperatures above 40 the acidic phospholipid, phosphatidylglycerol, plays an indispensable role(s). For this purpose we have isolated 48 clones of temperature-resistant suppressor mutants and identified the loci of suppressor mutations. Half of the clones were revealed to have mutations in rcsC and rcsF genes. Introduction of rcsB mutation made the PG-deficient cells temperature-resistant. These suppressor analyses suggested that an over-expression of a certain gene(s) under the control of rcsC-rcsB regulatory system might be responsible for the temperature-sensitivity. However, introduction of cpsB mutation that interrupts capsular polysaccharide synthesis did not suppress the temperature-sensitivity of the PG-deficient cells. The result indicated that synthesis of capsular polysaccharide per se is not responsible for the temperature-sensitivity but that a certain gene(s) under the control of the regulatory system is responsible for the temperature-sensitivity of the PG-deficient cells.

两个计划被执行。这些计划是由于发现缺乏主要酸性磷脂的大肠杆菌细胞如果具有缺陷的lpp等位基因则是可行的。1）一个是澄清具有野生型lpp等位基因的细胞中酸性磷脂缺乏的致死性。为此，我们构建了一个lpp诱导系统，并研究了lpp诱导后proLPP蛋白在细胞膜上的定位。2）二是阐明缺乏主要酸性磷脂的细胞对温度敏感的原因。温度敏感性表明，在40 ℃以上的温度下，酸性磷脂（磷脂酰甘油）起着不可或缺的作用。为此目的，我们分离了48个耐温抑制突变体的克隆，并确定了抑制突变的位点。一半的克隆被发现在rcsC和rcsF基因中具有突变。rcsB突变的引入使PG缺陷细胞具有耐温性。这些抑制基因的分析表明，rcsC-rcsB调控系统控制下的某些基因的过表达可能是导致温度敏感性的原因。然而，引入cpsB突变，中断荚膜多糖合成没有抑制PG缺陷细胞的温度敏感性。结果表明，PG缺陷型细胞的温度敏感性不是由荚膜多糖的合成本身决定的，而是由调控系统控制的某个基因决定的。