EseG, an Effector of the Type III Secretion System of Edwardsiella tarda, Triggers Microtubule Destabilization

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	EseG, an Effector of the Type III Secretion System of Edwardsiella tarda, Triggers Microtubule Destabilization
	Xie, Hai Xia 2,3; Yu, Hong Bing 4; Zheng, Jun 2; Nie, Pin 3; Foster, Leonard J.5; Mok, Yu-Keung 2; Finlay, B. Brett 4; Leung, Ka Yin 1,2
刊名	INFECTION AND IMMUNITY
	2010-12-01
卷号	78 期号:12 页码:5011-5021
关键词	ENTEROPATHOGENIC ESCHERICHIA-COLI
ISSN号	0019-9567
通讯作者	Leung, KY, Trinity Western Univ, Fac Nat & Appl Sci, Dept Biol, 7600 Glover Rd, Langley, BC V2Y 1Y1, Canada
中文摘要	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 beta-lactamase as a fluorescence-based reporter showed that EseG was translocated into HeLa cells at 35 degrees 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 (EseG(142-192)), 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.
英文摘要	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 (LD(50)) 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 beta-lactamase as a fluorescence-based reporter showed that EseG was translocated into HeLa cells at 35 degrees 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 (EseG(142-192)), 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.
学科主题	Immunology; Infectious Diseases
WOS标题词	Science & Technology ; Life Sciences & Biomedicine
类目[WOS]	Immunology ; Infectious Diseases
研究领域[WOS]	Immunology ; Infectious Diseases
关键词[WOS]	ENTEROPATHOGENIC ESCHERICHIA-COLI ; SALMONELLA PATHOGENICITY ISLAND-2 ; INTRACELLULAR REPLICATION ; SHIGELLA-FLEXNERI ; PROTEINS ; VIRULENCE ; IDENTIFICATION ; CELLS ; TRANSLOCON ; CHAPERONE
收录类别	SCI
资助信息	Agency for Science, Technology, and Research (A*STAR), Singapore [04/1/21/19/346, 06/1/21/16/431, 07/1/21/19/495]; Natural Science and Engineering Research Council (NSERC) [372373-2010]; Trinity Western startup grant [0488]; Canadian Institutes of Health Research (CIHR) [MOP-77688]
语种	英语
WOS记录号	WOS:000284213600005
公开日期	2010-12-23
内容类型	期刊论文
源URL	[http://ir.ihb.ac.cn/handle/342005/13573]
专题	水生生物研究所_鱼类生物学及渔业生物技术研究中心_期刊论文
作者单位	1.Trinity Western Univ, Fac Nat & Appl Sci, Dept Biol, Langley, BC V2Y 1Y1, Canada 2.Natl Univ Singapore, Fac Sci, Dept Biol Sci, Singapore 117543, Singapore 3.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Hubei Province, Peoples R China 4.Univ British Columbia, Michael Smith Labs, Vancouver, BC V6T 1Z4, Canada 5.Univ British Columbia, Ctr High Throughput Biol, Dept Biochem & Mol Biol, Vancouver, BC V6T 1Z4, Canada
推荐引用方式 GB/T 7714	Xie, Hai Xia,Yu, Hong Bing,Zheng, Jun,et al. EseG, an Effector of the Type III Secretion System of Edwardsiella tarda, Triggers Microtubule Destabilization[J]. INFECTION AND IMMUNITY,2010,78(12):5011-5021.
APA	Xie, Hai Xia.,Yu, Hong Bing.,Zheng, Jun.,Nie, Pin.,Foster, Leonard J..,...&Leung, Ka Yin.(2010).EseG, an Effector of the Type III Secretion System of Edwardsiella tarda, Triggers Microtubule Destabilization.INFECTION AND IMMUNITY,78(12),5011-5021.
MLA	Xie, Hai Xia,et al."EseG, an Effector of the Type III Secretion System of Edwardsiella tarda, Triggers Microtubule Destabilization".INFECTION AND IMMUNITY 78.12(2010):5011-5021.