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Edwardsiella tarda type III effector EseG triggers host microtubule destabilization
Hai Xia Xie1,2; Hong Bing Yu3; Jun Zheng1; Pin Nie2; Leonard J. Foster4; Yu-Keung Mok1; B. Brett Finlay3; Ka Yin Leung1,5
2010
Source PublicationINFECTION AND IMMUNITY
ISSN0019-9567
Volume78Issue:12Pages:5011-5021
Abstract

Edwardsiella tarda is a Gram-negative enteric pathogen that causes hemorrhagic septicemia in fish and both gastrointestinal and extraintestinal infections in humans. A type III secretion system (T3SS) was recently shown to contribute to pathogenesis, since deletions of various T3SS genes increased the 50% lethal dose (LD50) by about 1 log unit in the blue gourami infection model. In this study, we report EseG as the first identified effector protein of T3SS. EseG shares partial homology with two Salmonella T3SS effectors (SseG and SseF) over a conserved domain (amino acid residues 142 to 192). The secretion of EseG is dependent on a functional T3SS and, in particular, requires the chaperone EscB. Experiments using TEM-1 -lactamase as a fluorescence-based reporter showed that EseG was translocated into HeLa cells at 35°C. Fractionation of infected HeLa cells demonstrated that EseG was localized to the host membrane fraction after translocation. EseG is able to disassemble microtubule structures when overexpressed in mammalian cells. This phenotype may require a conserved motif of EseG (EseG142–192), since truncated versions of EseG devoid of this motif lose their ability to cause microtubule destabilization. By demonstrating the function of EseG, our study contributes to the understanding of E. tarda pathogenesis. Moreover, the approach established in this study to identify type III effectors can be used to identify and characterize more type III and possible type VI effectors in Edwardsiella.

DOIhttps://doi.org/10.1128/IAI.00152-10
Indexed BySCI
Language英语
WOS Research AreaImmunology ; Infectious Diseases
WOS SubjectImmunology ; Infectious Diseases
WOS IDWOS:000284213600005
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Cited Times [WOS]:40   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionFaculty of Health Sciences
Corresponding AuthorKa Yin Leung
Affiliation1.Department of Biological Sciences, Faculty of Science, National University of Singapore, Singapore 117543
2.State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, Hubei Province, China 430072
3.Michael Smith Laboratories, 2185 East Mall
4.3 Department of Biochemistry and Molecular Biology, Centre for High-Throughput Biology, 2125 East Mall, University of British Columbia, Vancouver, BC, Canada V6T 1Z4
5.Department of Biology, Faculty of Natural and Applied Sciences, Trinity Western University, 7600 Glover Road, Langley, BC, Canada V2Y 1Y1
Recommended Citation
GB/T 7714
Hai Xia Xie,Hong Bing Yu,Jun Zheng,et al. Edwardsiella tarda type III effector EseG triggers host microtubule destabilization[J]. INFECTION AND IMMUNITY,2010,78(12):5011-5021.
APA Hai Xia Xie.,Hong Bing Yu.,Jun Zheng.,Pin Nie.,Leonard J. Foster.,...&Ka Yin Leung.(2010).Edwardsiella tarda type III effector EseG triggers host microtubule destabilization.INFECTION AND IMMUNITY,78(12),5011-5021.
MLA Hai Xia Xie,et al."Edwardsiella tarda type III effector EseG triggers host microtubule destabilization".INFECTION AND IMMUNITY 78.12(2010):5011-5021.
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