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Phospholipid-Dependent Biogenesis and Function of Bacterial Flagella. Elucidation of Their Molecular Mechanisms

细菌鞭毛的磷脂依赖性生物发生和功能。

基本信息

批准号：
06453165
负责人：
SHIBUYA Isao
金额：
$ 4.74万
依托单位：
Saitama University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1994
资助国家：
日本
起止时间：
1994 至 1995
项目状态：
已结题

项目摘要

The biological roles of membrane phospholipids in gene expression was studied with Escherichia coli and the following results were obtained.1. The primary structure of the pgsA3 allele that causes acidic-phospholipid deficiency was determined and the structure-function relationships of the gene product, phosphatidylglycerophosphate synthase, was elucidated.2. Flagellar synthesis and cell motility was severely inhibited by the pgsA3 mutation. This was due to a severe transcriptional repression of the flagellar master operon, flhD-flhC.The upstream locus of the flhD coding region required for this repression was identified.3. The pgsA3 mutation also caused reduction of the outer-membrane OmpF protein. The translational, not the transcriptional, expression of the ompF gene was inhibited by the enhanced formation of the micF RNA that is antisense to the ompF.4. A pssA null mutant in which zwitterionic phospholipids were completely absent was constructed. Despite its phospholipid composition radically different from that of pgsA3 mutants, this null allele also repressed the flagellar master operon and activated the micF expression.5. The results imply that an unbalanced phospholipid composition, rather than the decrease or increase of specific phospholipid species, induces a phospholipid-specific stress signal to which certain regulatory genes respond positively or negatively according to their intrinsic mechanisms.

本研究以大肠杆菌为材料，研究了膜磷脂在基因表达中的生物学作用，得到以下结果.确定了引起酸性磷脂缺乏症的pgsA 3等位基因的一级结构，并阐明了该基因产物磷脂酰甘油磷酸合酶的结构与功能关系.鞭毛的合成和细胞运动性受到严重抑制的pgsA 3突变。这是由于鞭毛主操纵子flhD-flhC的严重转录抑制所致，并鉴定了flhD编码区的上游位点. pgsA 3突变也引起外膜OmpF蛋白的减少。ompF基因的翻译，而不是转录，表达受到抑制的增强形成的micF RNA是反义的ompF。4。构建了其中完全不存在两性离子磷脂的pssA无效突变体。尽管其磷脂组成与pgsA 3突变体完全不同，但该无效等位基因也抑制鞭毛主操纵子并激活micF表达。结果表明，一个不平衡的磷脂组合物，而不是减少或增加特定的磷脂种类，诱导磷脂特异性应激信号，某些调控基因积极或消极地响应，根据其内在机制。