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Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
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Published on: January 3, 2012

Inactivation of small Rho GTPases by the multifunctional RTX toxin from Vibrio cholerae

Kerri-Lynn Sheahan1, Karla J Fullner Satchell

  • 1Department of Microbiology-Immunology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.

Cellular Microbiology
|May 4, 2007
PubMed

Insights

The Vibrio cholerae RTX toxin reversibly inactivates Rho GTPases, impacting the actin cytoskeleton. This novel mechanism differs from other bacterial toxins that modify Rho GTPases.

Area of Science:

  • Microbiology
  • Cell Biology
  • Biochemistry

Background:

  • Bacterial toxins frequently target Rho GTPases to disrupt the actin cytoskeleton.
  • The Vibrio cholerae RTX toxin was known to cross-link actin, causing depolymerization.
  • Further investigation revealed RTX toxin possesses additional cell rounding activity beyond actin cross-linking.

Purpose of the Study:

  • To elucidate the mechanism behind the RTX toxin's cell rounding activity.
  • To identify the specific Rho GTPases targeted by the RTX toxin.
  • To characterize the RTX toxin's novel mechanism of Rho GTPase inactivation.

Main Methods:

  • Deletion analysis of the RTX toxin to isolate functional domains.
  • Cell-based assays to assess actin cytoskeleton integrity and Rho GTPase activity.
  • Biochemical assays to determine the enzymatic activity of the identified RTX domain.

Main Results:

  • The RTX toxin inactivates Rho GTPases, including Rho, Rac, and Cdc42, disrupting the actin cytoskeleton.
  • This inactivation is reversible and independent of the previously identified actin cross-linking domain.
  • A novel 548-amino-acid region of RTX mediates Rho GTPase inactivation without GAP or phosphatase activity.

Conclusions:

  • The RTX toxin employs a distinct mechanism to reversibly inactivate Rho GTPases, contributing to cell rounding.
  • This study identifies a new mode of bacterial toxin action on host cell signaling pathways.
  • Understanding this mechanism provides insights into bacterial pathogenesis and host-pathogen interactions.

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