1995 Fiscal Year Final Research Report Summary
Phospholipid-Dependent Biogenesis and Function of Bacterial Flagella. Elucidation of Their Molecular Mechanisms
| Project/Area Number |
06453165
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
応用微生物学・応用生物化学
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| Research Institution | Saitama University |
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Principal Investigator |
SHIBUYA Isao Saitama University, Dept.Biochem.& Mol.Biol., Professor, 理学部, 教授 (60013306)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUZAKI Hiroshi Saitama University, Dept.Biochem.& Mol.Biol., Associate Professor, 理学部, 助教授 (80008870)
MSTSUMOTO Kouji Saitama University, Dept.Biochem.& Mol.Biol., Professor, 理学部, 教授 (00119140)
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| Project Period (FY) |
1994 – 1995
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| Keywords | Escherichia coli / Phospholipid Composition / Flagellar Master Operon / OmpF / Transcriptional regulation / Operon Fusion / DNA Functional Region |
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| Research Abstract |
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.
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