| Project/Area Number |
17590387
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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 | The University of Tokushima |
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Principal Investigator |
TOMOYASU Toshifumi The University of Tokushima, Institute of Technology and Science, Associate Professor, 大学院ソシオテクノサイエンス研究部, 助教授 (20323404)
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| Co-Investigator(Kenkyū-buntansha) |
NAGAMUNE Hideaki The University of Tokushima, Institute of Technology and Science, Professor, 大学院ソシオテクノサイエンス研究部, 教授 (40189163)
TABATA Atsushi The University of Tokushima, Institute of Technology and Science, Assistant Professor, 大学院ソシオテクノサイエンス研究部, 助手 (10432767)
TAKAYA Akiko Chiba University, Graduate School of Pharmaceutical Sciences, Department of Microbiology and Molecular Genetics, Lecturer, 大学院薬学研究院, 講師 (80334217)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2005: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Enterohemorrhagic E.coli / EHEC / LEE / Type III secretion system / AAA protease / ClpXP / Lon / GrlR / 腸管病原性大腸菌 / ClpX / GrlR / H-NS |
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| Research Abstract |
1. Enterohemorrhagic Escherichia coli (EHEC) and Enteropathogenic E. coli (EPEC) cause histopathological lesions of the intestinal epithelial cells that are known as attaching and effacing (A/E) lesions. Both strains carry a unique region of chromosomal DNA known as the locus for enterocyte effacement (LEE) that encodes a type III secretion system (TTSS) and virulence proteins. We have recently reported that AAA proteases (CIpXP, Lon) and molecular chaperones control 2 TTSSs in Salmonella Typhimurium: (i) flagellum biogenesis and (ii) the expression of the Pathogenicity Island 1. We demonstrated that the EHEC and EPEC clpPX mutants strongly impaired the secretion of virulence proteins by TTSS and repressed transcription from all the LEE promoters. The rpoS mutation in EHEC enhanced transcription from all the LEE promoters and the secretion of virulence proteins, and it could partially suppress the defects of the clpPX mutation. These data indicate that the EHEC ClpXP protease is a posi
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tive regulator for LEE expression, and this regulation occurs via 2 pathways: the o^<S->dependent and os-independent pathways.
2. Recently, 2 LEE-encoded regulators-GrlA (global regulator of LEE activator) and GrlR (Grl repressor)-were identified. Iyoda et al. reported that ClpXP protease controls the expression of LEEpromoters via the regulation of GrlR levels in EHEC (J.Bacteriol. 2005. 187: 4086-94). However, the control mechanisms underlying the expression of LEEpromoters by Gr1A, GrlR, and AAA proteases remain unclear. Therefore, we established an assay system using nonpathogenic E. coli that enables analysis of the interaction among these proteins by measuring the activities of the LEE2, LEE3, and LEE5promoters. Our data revealed that the activation of ler (LEE-encoded regulator) expression by Gr1A entailed the participation of the domain that exists for a length of 131 base pairs downstream from the ler stop codon. Presently, we are analyzing the LEE expression control mechanisms exerted by Gr1R, Gr1A, and AAA proteases in detail. Less
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