GSBS Dissertations and Theses

Publication Date

2003-05-22

Document Type

Doctoral Dissertation

Academic Program

Molecular Genetics and Microbiology

Department

Molecular Genetics & Microbiology

First Thesis Advisor

John M. Leong

Keywords

Actins, Adhesins, Escherichia coli, Escherichia coli Proteins, Receptors, Cell Surface

Abstract

Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli O157:H7 (EHEC) form characteristic lesions on infected mammalian cells called actin pedestals. Each of these two pathogens injects its own translocated intimin receptor (Tir) molecule into the plasma membranes of host cells. Interaction of translocated Tir with the bacterial outer membrane protein intimin is required to trigger the assembly of actin into focused pedestals beneath bound bacteria. Despite similarities between the Tir molecules and the host components that associate with pedestals, recent work indicates that EPEC and EHEC Tir are not functionally interchangeable. For EPEC, Tir-mediated binding of Nck, a host adaptor protein implicated in actin signaling, is both necessary and sufficient to initiate actin assembly. In contrast, for EHEC, pedestals are formed independently of Nck, and require translocation of bacterial factors in addition to Tir to trigger actin signaling.

Comments

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DOI

10.13028/bgmm-dh06

Rights and Permissions

Copyright is held by the author, with all rights reserved.

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