Document Detail

The pathogenic E. coli type III effector EspZ interacts with host CD98 and facilitates host cell prosurvival signalling.
MedLine Citation:
PMID:  20374249     Owner:  NLM     Status:  MEDLINE    
Enterohaemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC respectively) are diarrhoeal pathogens that cause the formation of attaching and effacing (A/E) lesions on infected host cells. These pathogens encode a type III secretion system (T3SS) used to inject effector proteins directly into host cells, an essential requirement for virulence. In this study, we identified a function for the type III secreted effector EspZ. Infection with EPEC DeltaespZ caused increased cytotoxicity in HeLa and MDCK cells compared with wild-type EPEC, and expressing espZ in cells abrogated this effect. Using yeast two-hybrid, proteomics, immunofluorescence and co-immunoprecipitation, it was demonstrated that EspZ interacts with the host protein CD98, which contributes to protection against EPEC-mediated cytotoxicity. EspZ enhanced phosphorylation of focal adhesion kinase (FAK) and AKT during infection with EPEC, but CD98 only appeared to facilitate FAK phosphorylation. This study provides evidence that EspZ and CD98 promote host cell survival mechanisms involving FAK during A/E pathogen infection.
Stephanie R Shames; Wanyin Deng; Julian A Guttman; Carmen L de Hoog; Yuling Li; Philip R Hardwidge; Ho Pan Sham; Bruce A Vallance; Leonard J Foster; B Brett Finlay
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-03-31
Journal Detail:
Title:  Cellular microbiology     Volume:  12     ISSN:  1462-5822     ISO Abbreviation:  Cell. Microbiol.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-08-18     Completed Date:  2011-01-10     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100883691     Medline TA:  Cell Microbiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  1322-39     Citation Subset:  IM    
Michael Smith Laboratories, University of British Columbia, Vancouver, British Columbia, Canada.
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MeSH Terms
Antigens, CD98 / metabolism*
Bacterial Secretion Systems
Cell Line
Enteropathogenic Escherichia coli / metabolism*,  pathogenicity
Escherichia coli Infections / metabolism*,  microbiology*
Escherichia coli Proteins / metabolism,  physiology*
Focal Adhesion Protein-Tyrosine Kinases / metabolism
Hela Cells
Protein Binding
Proto-Oncogene Proteins c-akt / metabolism
Grant Support
//Canadian Institutes of Health Research; //Howard Hughes Medical Institute
Reg. No./Substance:
0/Antigens, CD98; 0/Escherichia coli Proteins; 0/SepZ protein, E coli; EC Adhesion Protein-Tyrosine Kinases; EC Proteins c-akt

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