Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Micro-managing the executioner: pathogen targeting of mitochondria.

Steven R Blanke1

  • 1Department of Microbiology and Molecular Genetics, University of Illinois, 302 Burrill Hall, Urbana-Champaign, IL 61801, USA. sblanke@uh.edu

Trends in Microbiology
|February 1, 2005
PubMed
Summary

Helicobacter pylori's toxin VacA targets mitochondria, disrupting cell viability. This pathogen exploits mitochondrial membrane permeabilization to induce apoptosis, bypassing normal cell death pathways.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A bacterial genotoxin reveals a p53-proteasome-LC3 regulatory axis that drives the suppression of autophagy in cells experiencing sublethal DNA damage.

iScience·2025
Same author

Autophagy suppression in DNA damaged cells occurs through a newly identified p53-proteasome-LC3 axis.

bioRxiv : the preprint server for biology·2024
Same author

Corrigendum: Revisiting bacterial cytolethal distending toxin structure and function.

Frontiers in cellular and infection microbiology·2024
Same author

Revisiting bacterial cytolethal distending toxin structure and function.

Frontiers in cellular and infection microbiology·2023
Same author

Host cell sensing and restoration of mitochondrial function and metabolism within <i>Helicobacter pylori</i> VacA intoxicated cells.

mBio·2023
Same author

Restoration of mitochondrial structure and function within <i>Helicobacter pylori</i> VacA intoxicated cells.

Advances in microbiology·2023

Area of Science:

  • Cell biology
  • Mitochondrial function
  • Pathogen-host interactions

Background:

  • Eukaryotic cell viability is primarily regulated by mitochondria.
  • Mitochondrial membrane permeabilization is a key step in programmed cell death.
  • Pathogenic microbes can hijack host cell machinery to induce cell death.

Purpose of the Study:

  • To investigate the mechanism by which Helicobacter pylori toxin VacA affects mitochondrial membranes.
  • To understand how VacA induces cell death in epithelial cells.
  • To explore the role of mitochondrial targeting in pathogen-induced apoptosis.

Main Methods:

  • Localization studies of VacA within epithelial cells.
  • In vitro transport assays of VacA into isolated mitochondria.

Related Experiment Videos

  • Analysis of mitochondrial membrane changes induced by VacA.

    • Main Results:

    • VacA was shown to localize to mitochondria in epithelial cells.
    • VacA rapidly transported into mitochondria in vitro.
    • VacA induced mitochondrial membrane permeabilization dependent on cellular entry and toxin channel activity.

    Conclusions:

    • Helicobacter pylori utilizes the pro-apoptotic toxin VacA to target and permeabilize mitochondrial membranes.
    • This mechanism allows the pathogen to control host cell viability and evade host defenses.
    • Mitochondrial membrane targeting is an emerging microbial strategy for manipulating host cell fate.