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Bacterial porin disrupts mitochondrial membrane potential and sensitizes host cells to apoptosis

Vera Kozjak-Pavlovic1, Elke A Dian-Lothrop, Michael Meinecke

  • 1Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany.

Plos Pathogens
|October 24, 2009
PubMed

Insights

The pathogenic Neisseria gonorrhoeae PorB porin enters host mitochondria, disrupting membrane potential and inducing apoptosis. ATP binding by PorB is crucial for this cell death process.

Area of Science:

  • Microbiology
  • Cell Biology
  • Biochemistry

Background:

  • Neisseria gonorrhoeae is a pathogen that causes the sexually transmitted infection gonorrhea.
  • The bacterial PorB porin is implicated in triggering host cell apoptosis.
  • The precise mechanism by which PorB induces apoptosis remains unclear.

Purpose of the Study:

  • To elucidate the mechanism by which the PorB porin of Neisseria gonorrhoeae induces host cell apoptosis.
  • To investigate the role of mitochondrial targeting and the mitochondrial membrane potential in PorB-mediated apoptosis.

Main Methods:

  • Tracking PorB import into host cell mitochondria.
  • Assessing mitochondrial membrane potential (DeltaPsi(m)) using fluorescent probes.
  • Analyzing mitochondrial morphology and cristae structures.
  • Utilizing an ATP-binding deficient PorB mutant to assess its role in apoptosis induction.

Main Results:

  • PorB is imported into host mitochondria via the TOM translocase but bypasses the SAM machinery.
  • PorB integrates into the mitochondrial inner membrane, leading to the loss of mitochondrial membrane potential (DeltaPsi(m)).
  • PorB induces mitochondrial matrix condensation and loss of cristae, sensitizing cells to apoptosis.
  • A PorB mutant lacking ATP-binding capability failed to induce DeltaPsi(m) loss and apoptosis.

Conclusions:

  • PorB-mediated disruption of mitochondrial membrane potential is essential for inducing apoptosis in host cells.
  • ATP binding is critical for PorB's function in dissipating DeltaPsi(m) and triggering cell death.
  • PorB's unique import pathway and inner membrane integration highlight novel mechanisms of bacterial pathogenesis.

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