GSBS Dissertations and Theses

Approval Date

May 2003

Document Type

Doctoral Dissertation

Department

Graduate School of Biomedical Sciences, Molecular Genetics & Microbiology

Subjects

Actins; Adhesins, Escherichia coli; Escherichia coli Proteins; Receptors, Cell Surface; Academic Dissertations; Dissertations, UMMS

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

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