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dc.contributor.advisorViswanathan, V.K.en
dc.contributor.authorRamamurthy, Shylaja
dc.creatorRamamurthy, Shylajaen
dc.date.accessioned2017-04-20T00:06:12Z
dc.date.available2017-04-20T00:06:12Z
dc.date.issued2016
dc.identifier.urihttp://hdl.handle.net/10150/623145
dc.description.abstractEnteropathogenic 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.
dc.language.isoen_USen
dc.publisherThe University of Arizona.en
dc.rightsCopyright © 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.en
dc.titleRole of EspZ in Enteropathogenic Escherichia coli Virulenceen_US
dc.typetexten
dc.typeElectronic Thesisen
thesis.degree.grantorUniversity of Arizonaen
thesis.degree.levelmastersen
dc.contributor.committeememberViswanathan, V.K.en
dc.contributor.committeememberVedantam, Gayatrien
dc.contributor.committeememberCampos, Samuelen
dc.description.releaseRelease after 31-Dec-2025en
thesis.degree.disciplineGraduate Collegeen
thesis.degree.disciplineMicrobiologyen
thesis.degree.nameM.S.en
dc.description.admin-noteOriginally set to release after 13-Dec-2018; contacted by Graduate College 29-Nov-2018 to extend embargo through 30-Dec-2020. Kimberly Contacted again 13-Jan-2021 to extend embargo through 31-Dec-2025 Lauren
html.description.abstractEnteropathogenic 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.


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