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Analysis of Yersinia enterocolitica Effector Translocation into Host Cells Using Beta-lactamase Effector Fusions
Published on: October 13, 2015
Yersinia enterocolitica differentially modulates RhoG activity in host cells
Bernhard Roppenser1, Anja Röder, Moritz Hentschke
1Institut für Medizinische Mikrobiologie, Virologie und Hygiene, Universitätsklinikum Hamburg-Eppendorf, Martinistrabetae 52, 20246 Hamburg, Germany.
Journal of Cell Science
|February 12, 2009
Summary
Yersinia bacteria manipulate host cells using virulence factors that control RhoG, a key regulator of cell invasion. This study reveals how Yersinia enterocolitica activates and deactivates RhoG to manage host cell interactions during infection.
Area of Science:
- Microbiology
- Cell Biology
- Molecular Biology
Background:
- Pathogenic Yersinia species employ diverse virulence factors to subvert host cell functions.
- Rho GTPases are critical regulators of cellular processes, frequently targeted by bacterial pathogens.
Purpose of the Study:
- To investigate the role of RhoG, a Rho GTPase regulator, in the context of Yersinia enterocolitica infection.
- To elucidate the mechanisms by which Yersinia manipulates RhoG activity during host cell interaction.
Main Methods:
- Live-cell imaging to visualize RhoG activation and deactivation at bacterial contact sites.
- Analysis of bacterial effector proteins, Invasin and YopE, and their impact on RhoG and downstream signaling.
- Investigating the localization of YopE and its specificity for Rho GTPases.
Main Results:
- Yersinia enterocolitica activates RhoG via Invasin to promote bacterial invasion.
- The type III secretion system effector YopE deactivates RhoG, acting as a GTPase-activating protein (GAP).
- YopE's localization to the Golgi and endoplasmic reticulum dictates its specificity for RhoG and other Rho GTPases, influencing Rac1 activity.
Conclusions:
- RhoG is a central target in the Yersinia virulence strategy.
- Yersinia manipulates RhoG to control Rac1 activity during different infection stages, impacting host cell dynamics.
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