2005 Fiscal Year Final Research Report Summary
Analysis of regulatory mechanisms for bacterial invasion into host cell on Shigella sonnei.
| Project/Area Number |
16590377
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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 |
Bacteriology (including Mycology)
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| Research Institution | Department of Bacteriology, National Institute of Infectious Diseases |
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Principal Investigator |
WATANABE Haruo National Institute of Infectious Diseases, Department of Bacteriology, chief director or the department & sub-chairman of the institution., 細菌第一部・副所長, 細菌第一部長 (70142130)
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| Co-Investigator(Kenkyū-buntansha) |
MITOBE Jiro National Institute of Infectious Diseases, Department of Bacteriology, Investigator, 細菌第一部, 主任研究官 (40333364)
MASHASI Miura Tokyo Metropolitan Univ., Department of Biology
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| Project Period (FY) |
2004 – 2005
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| Keywords | Shigellae / Cell invasion / ospE2 gene / Actin / Talin / FAK / Cell morphology / focal-contact |
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| Research Abstract |
The chief function of the Cpx two-component system of perceiving various cell envelope stresses, but CpxR is also known to regulate the expression of the type III secretion system (TTSS) of Shigella sonnei through the transcription of the primary regulator virF. We have isolated novel cpxA mutants that exhibited decreased TTSS expression from Escherichia coliHW1273, which carries the virulence plasmid of S. sonnei. The cpxA deletion strain of HW1273 expressed β-galactosidase activity levels from the virF-lacZ fusion, similar to those of HW1273. However, protein expression of the second regulator InvE (VirB) and the TTSS component IpaB proteins were apparently at a low level. In addition, the cpxA deletion strain of S. sonnei showed the same phenotype. These results indicate that the Cpx two-component system is involved in the virulence expression through the post-transcriptional process of the regulatory protein InvE-a novel feature of the Cpx-two component system on the post-transcrip
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tional process and virulence expression of Shigella
The OspE2 product of Shigella spp., the expression of which is regulated by the mxiE gene, is secreted through a type III secretion system into host cell. We investigated the function of OspE2 of Shigella sonnei by using cultured epithelial cells. Cells invaded by an ospE2 deletion mutant altered their morphology into the rounding shape, which was not due to cell death, whereas cells invaded by the wild-type strain kept their cell shape intact. The ospE2 mutation did not affect initial cell entry and multiplication in cells, but the mutant formed smaller-than-normal plaques on cell monolayers, indicating a deficiency in cell-to-cell spread by the bacteria. A mxiE deletion mutant also showed changed in cell morphology and deficiency in bacteria spread to adjacent cells. In cells invaded by the ospE2 mutant, disturbance of actin stress fibers was prominent at 3 h after invasion. Analysis of OspE2 localization indicated that the OspE2 protein accumulated on focal contact-like structures in the infected host cells. These results suggest that colocalization of the OspE2 protein in the focal contact of infected cells may function to maintain an intact cell morphology. The morphological change induced by invasion of the ospE2 mutant may affect secondary bacterial transmission. Less
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Research Products
(4 results)
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[Journal Article] OspE2 of Shigella sonnei is required for the maintenance of cell architecture of bacterium-infected cells.2006
Author(s)
Miura, M., Terajima, J., Izumiya, H., Mitobe, J., Komano, T., Watanabe, H.
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Journal Title
Infection and Immunity 74
Pages: 2587-2595
Description
「研究成果報告書概要(和文)」より
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