| Project/Area Number |
14571749
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Showa University |
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Principal Investigator |
GOTO Nobuichi Showa University, School of Dentistry, Professor, 歯学部, 教授 (10077175)
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| Co-Investigator(Kenkyū-buntansha) |
MORISAKI Hirobumi Showa University, School of Dentistry, Research Associate, 歯学部, 助手 (30317581)
IGARASHI Takeshi Showa University, School of Dentistry, Associate Professor, 歯学部, 助教授 (10159585)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2003: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Sortase / Biofilm / Streptococcus mutans / Dextranase / Glucan-binding protein C / Surface protein antigen / LPXTG motif / Cell wall anchoring / Cell Wall Anchoring / デンタルプラーク |
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| Research Abstract |
We analyzed surface proteins of Streptococcus mutans responsible for formation of plaque biofilm and obtained the following results. The sortase gene (srtA) of S. mutans 109c was amplified by PCR and inverse PCR and cloned into pT7 blue T-vector. The complete nucleotide sequence was then determined. A srtA-deficient mutant (SrtA^-) of S.mutans 109c was constructed by insertional inactivation on the basis of the nucleotide sequence. Western blot analysis with specific antiserum demonstrated that the SrtA mediated cell localization of surface proteins such as a surface protein antigen (PAc), a glucan-binding protein C (GbpC) and a dextranase (Dex). The ability of plaque-biofilm formation of the wild type (109c) and the SrtA^-of S.mutans was then compared. The SrtA^-lost the abilities for both glucan-dependent aggregation under the presence of dextran and formation of water-insoluble adhesive glucan. These results suggested that the SrtA mediates cell-localization of at least 3 surface proteins (PAC, GbpG, Dex) of S.mutans and controls physiological functions (formation of caries-inducible biofilm) of those proteins. These phenomena appear to expect not only as the result of inactivation of the srtA gene but also due to the inhibition of the SrtA enzyme of S.mutans. SrtA of S.mutans could therefore be an attractive target for the prevention of biofilm formation and subsequent dental caries.
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