Rebekah DeVinney

Associate Professor, Department of Microbiology, Immunology & Infectious Diseases

Microbiology, Immunology & Infectious Diseases (MIID)

Alberta Heritage Foundation for Medical Research Scholar

Address:  2C68 Health Research Innovation Centre

                  3280 Hospital Drive N.W., Calgary, AB T2N 4N1

Phone: (403) 220-4095

Lab Phone: (403) 220-8303

Fax: (403) 210-7882

Email: rdevinne@ucalgary.ca

Curriculum Vitae

B.A., Chemistry, University of California, San Diego, 1979

Ph.D. Biology, University of California, Santa Cruz, 1996

Postdoctoral Fellowship, Biotechnology Laboratory, University of British Columbia, 2000

Potential Graduate Supervisor

Research

Bacterial pathogens have evolved mechanisms to exploit essential host cell functions. This has led to the emergence of a; new discipline, cellular microbiology, which uses microbial pathogens as tools to address important issues in cell biology. An important target is the actin cytoskeleton. In epithelial cells, the actin cytoskeleton plays an important role in modulating cell shape, barrier function, cell signaling and motility. Research in the DeVinney lab is focused on understanding the mechanisms used by the human enteric pathogens, enterohemorrhagic E. coli (EHEC), enteropathogenic E. coli (EPEC) and Vibrio parahaemolyticus to alter the epithelial cell actin cytoskeleton. Infection with EHEC or EPEC leads to a dramatic reorganization of the actin cytoskeleton of intestinal epithelial cells, and the formation of pedestals beneath the adherent bacteria. We are interested in determining the bacterial factors required for these events, and elucidating their host cell targets. Current projects include investigating the role of the lipid microenvironment in bacterial-induced actin dynamics, and the contribution of other signaling pathways, including PI-3 kinase, to cytoskeletal disruption.  

A second area of interest is in the diarrheal pathogen Vibrio parahaemolyticus . In contrast to EHEC and EPEC, V. parahaemolyticus infection results in the disruption of the actin cytoskeleton in the absence of stable bacterial adherence. Recent work in our lab has indicated that V. parahaemolyticus can disrupt intestinal barrier function. Ongoing projects include determining the mechanism of barrier function disruption, and identifying the bacterial factors required for this effect.

Photo: Vibrio parahaemolyticus disruption of epithelial cell tight junctions. Left: Uninfected Caco2 cells. Right: V. parahaemoltyicus infected cells. Red: ZO-1, Green: Actin.

Keywords: Cellular microbiology, actin cytoskeleton, enterohemorrhagic E. coli, Vibrio parahaemolyticus, signal transduction, cell biology