| Project/Area Number |
06670291
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | Osaka University |
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Principal Investigator |
YAMAMOTO Koichiro Osaka Univ., Res.Inst.Microbial Dis., Associate Professor, 微生物病研究所, 助教授 (30158274)
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| Co-Investigator(Kenkyū-buntansha) |
IIDA Tetsuya Osaka Univ., Res.Inst.Microbial Dis., Research Associate, 微生物病研究所, 助手 (90221746)
HONDA Takeshi Osaka Univ., Res.Inst.Microbial Dis., Professor, 微生物病研究所, 教授 (60029808)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Vibrio cholerae / Hemolysin / DNA sequence / Enterotoxin / Phospholipase / Cholera toxin / Gene / Protein / トランスポゾン |
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| Research Abstract |
From the Tn5-inserted mutant library of Vibrio cholerae O1, we found a mutant, NF404, which lost the production of both hemolysin and cholera toxin (CT) even though the Tn5-insertion site was out side from the structural genes for hemolysin and CT.Cloning and sequencing analysis of the homologous region from the wild-type strain, revealed that the sequence spanning the coding region of an ORF1 nominated as lypA,encoding a 39.5 kDa protein. Deduced amino acid sequence of the lypA gene had 37.6% identity to the lysophospholipase L2 of Escherichia coli. Introduction of lypA into NF404 has lost cholera toxin and hemolysin productions, restored the lysophospholipase activity and CT production but not the hemolytic activity. Inactivation of lypA of the wild-type strains by single crossover insertion decreased the lysophospholipase L2 activity and cholera toxin production but not the hemolytic activity. These defective strains decreased enterotoxicity. These results suggest that lypA is possibly required for the expression of CT and may play a role in pathogenicity of Vibrio cholerae.
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