| Project/Area Number |
20390465
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Osaka University |
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Principal Investigator |
KAWABATA Shigetada Osaka University, 大学院・歯学研究科, 教授 (50273694)
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| Co-Investigator(Kenkyū-buntansha) |
TERAO Yutaka 大阪大学, 大学院・歯学研究科, 准教授 (50397717)
NAKATA Masanobu 大阪大学, 大学院・歯学研究科, 助教 (90444497)
SUMITOMO Tomoko 大阪大学, 大学院・歯学研究科, 助教 (50423421)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥19,370,000 (Direct Cost: ¥14,900,000、Indirect Cost: ¥4,470,000)
Fiscal Year 2010: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2009: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2008: ¥9,620,000 (Direct Cost: ¥7,400,000、Indirect Cost: ¥2,220,000)
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| Keywords | レンサ球菌 / 線毛 / 付着因子 / 定着因子 / 組織指向性 |
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| Research Abstract |
The human pathogen Streptococcus pyogenes produces diverse pili depending on the serotype. In a serotype M49 S. pyogenes strain, we demonstrate that FctA is the pilus backbone protein, and FctB and Cpa, a collagen-binding adhesin, are ancillary proteins. We also found that both Cpa and FctA are trypsin-resistant T antigens. Mutagenesis assays and eukaryotic cell adherence tests revealed that FctB and housekeeping sortase SrtA contribute to the cell wall anchoring of pili, whereas Cpa functions as a pilus adhesin to human keratinocytes. Sortase C2 and putative signal peptidase LepA enzymes were crucial for polymerization of FctA. The pilus expression increased with lower temperature. The ability to form biofilms was not affected by the mutation of the pilus genes. In contrast to the M49 pili, pili of a serotype M6 S. pyogenes strain were found to be assembled from two proteins, i.e. the backbone protein T6 and ancillary protein FctX, in a manner that requires both SrtA and pilus-associated sortase SrtB. We found that T6 pili contribute to biofilm formation, but not to adherence to human keratinocytes under the condition used in this study. These data suggest the serotype-dependent pilus assembly mechanism and contribution of S. pyogenes pili to the tissue tropism.
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