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Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells
09:25

Implementation of a Permeable Membrane Insert-based Infection System to Study the Effects of Secreted Bacterial Toxins on Mammalian Host Cells

Published on: August 19, 2016

Cellular and molecular action of the mitogenic protein-deamidating toxin from Pasteurella multocida

Brenda A Wilson1, Mengfei Ho

  • 1Department of Microbiology and Host-Microbe Systems Theme of the Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. bawilson@life.illinois.edu

The FEBS Journal
|May 17, 2011
PubMed

Insights

The Pasteurella multocida toxin (PMT) uniquely targets G-protein signaling pathways, distinct from other dermonecrotic toxins. This action drives cellular proliferation and inhibits differentiation, explaining infection effects.

Area of Science:

  • Microbiology
  • Cellular Biology
  • Toxicology

Background:

  • Pasteurella multocida toxin (PMT) belongs to the dermonecrotic toxin family.
  • Dermonecrotic toxins modulate host G-protein targets via deamidation/transglutamination, activating GTPase activity.

Purpose of the Study:

  • To elucidate the unique structural and functional mechanisms of PMT compared to other dermonecrotic toxins.
  • To investigate PMT's specific G-protein targets and downstream cellular effects.

Main Methods:

  • Comparative analysis of toxin structures and biochemical activities.
  • Experimental investigation of PMT interactions with G-protein families (G(q), G(i), G(12/13)).
  • Assessment of PMT's impact on mitogenic, survival, and differentiation signaling pathways.

Main Results:

  • PMT uniquely targets heterotrimeric G(q)-, G(i)-, and G(12/13)-protein α subunits, unlike other dermonecrotic toxins acting on Rho GTPases.
  • PMT potently stimulates mitogenic and survival pathways via G(q) and G(12/13) activation, promoting cellular proliferation.
  • PMT strongly inhibits differentiation pathways through G(i) signaling activation.

Conclusions:

  • PMT's distinct mechanism of G-protein activation explains cellular proliferation and inhibited differentiation observed during P. multocida infections.
  • PMT's effects on host cell signaling contribute to the pathogenesis of P. multocida infections.
  • PMT exposure may lead to potential long-term physiological sequelae.

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