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    Role of EspZ in Enteropathogenic Escherichia coli Virulence

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    Name:
    azu_etd_15203_sip1_m.pdf
    Embargo:
    2025-12-31
    Size:
    1.855Mb
    Format:
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    Author
    Ramamurthy, Shylaja
    Issue Date
    2016
    Advisor
    Viswanathan, V.K.
    
    Metadata
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    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Embargo
    Release after 31-Dec-2025
    Abstract
    Enteropathogenic Escherichia coli (EPEC) is a leading cause of infantile diarrhea, particularly in developing countries. EPEC belongs to the attaching and effacing (A/E) family of pathogens. All A/E pathogens harbor a type III secretion system (T3SS) that delivers virulence proteins directly into host epithelial cells. These proteins mediate diverse structural and functional alterations that likely facilitate pathogenesis. We recently demonstrated that EspZ, a secreted protein unique to A/E pathogens, is a critical virulence factor and that mutant strains lacking espZ are impaired for pathogenesis in both mouse and rabbit models of infection. EspZ prevents premature death of cultured intestinal epithelial cells by inhibiting intrinsic apoptosis. We hypothesized that EspZ promotes cell survival by engaging host proteins. Yeast two-hybrid studies identified the mitochondrial fission protein, hFis1, as a putative EspZ interactor. Co-immunoprecipitation studies confirmed EspZ-hFis1 interaction, and hFis1 was shown to be re-distributed in infected cells. These observations are consistent with the established role of hFis1 in intestinal cell survival pathways. The goal of my studies is to validate hFis1-EspZ interactions in epithelial cell cyto-protection and, eventually, to establish the significance of this pathway in EPEC virulence.
    Type
    text
    Electronic Thesis
    Degree Name
    M.S.
    Degree Level
    masters
    Degree Program
    Graduate College
    Microbiology
    Degree Grantor
    University of Arizona
    Collections
    Master's Theses

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