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Updated: May 22, 2026

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
Pasteurella multocida toxin interaction with host cells: entry and cellular effects
1Department of Microbiology and the Host-Microbe Systems Theme of the Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. bawilson@life.illinois.edu
Abstract:
The mitogenic dermonecrotic toxin from Pasteurella multocida (PMT) is a 1285-residue multipartite protein that belongs to the A-B family of bacterial protein toxins. Through its G-protein-deamidating activity on the α subunits of heterotrimeric G(q)-, G(i)- and G(12/13)-proteins, PMT potently stimulates downstream mitogenic, calcium, and cytoskeletal signaling pathways. These activities lead to pleiotropic effects in different cell types, which ultimately result in cellular proliferation, while inhibiting cellular differentiation, and account for the myriad of physiological outcomes observed during infection with toxinogenic strains of P. multocida.
Insights
Pasteurella multocida toxin (PMT) stimulates cell growth by altering G-protein signaling. This bacterial toxin promotes proliferation while inhibiting differentiation, impacting infection outcomes.
Area of Science:
- Microbiology
- Molecular Biology
- Toxicology
Background:
- Pasteurella multocida is a bacterial pathogen.
- The mitogenic dermonecrotic toxin (PMT) is a key virulence factor produced by P. multocida.
- PMT is a large, multipartite A-B family toxin.
Purpose of the Study:
- To elucidate the molecular mechanism of PMT action.
- To understand how PMT influences cellular signaling pathways.
- To correlate PMT activity with disease outcomes in P. multocida infections.
Main Methods:
- Biochemical assays to determine G-protein deamidation activity.
- Cell-based assays to assess downstream signaling.
- Analysis of cellular proliferation and differentiation markers.
Main Results:
- PMT deamidates α subunits of G(q)-, G(i)-, and G(12/13)-proteins.
- This activity potently stimulates mitogenic, calcium, and cytoskeletal signaling.
- PMT induces cellular proliferation and inhibits differentiation.
Conclusions:
- PMT's G-protein deamidating activity is central to its virulence.
- PMT disrupts normal cellular functions, leading to pleiotropic effects.
- Understanding PMT's mechanism is crucial for addressing P. multocida infections.
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