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A Genetic Screen to Isolate Toxoplasma gondii Host-cell Egress Mutants
14:56

A Genetic Screen to Isolate Toxoplasma gondii Host-cell Egress Mutants

Published on: February 8, 2012

Rapid membrane disruption by a perforin-like protein facilitates parasite exit from host cells

Björn F C Kafsack1, Janethe D O Pena, Isabelle Coppens

  • 1Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.

Science (New York, N.Y.)
|December 20, 2008
PubMed

Insights

Toxoplasma gondii perforin-like protein 1 (TgPLP1) is crucial for parasite egress from host cells. Lacking TgPLP1 prevents host cell permeabilization, impairing parasite exit and significantly reducing virulence.

Area of Science:

  • Microbiology
  • Parasitology
  • Cell Biology

Background:

  • Perforin-like proteins are found in various pathogens but their functions remain largely unknown.
  • Toxoplasma gondii is an intracellular protozoan pathogen that utilizes secreted proteins for host cell manipulation.

Purpose of the Study:

  • To investigate the function of Toxoplasma perforin-like protein 1 (TgPLP1) in the lifecycle and virulence of Toxoplasma gondii.
  • To determine the role of TgPLP1 in parasite egress from host cells.

Main Methods:

  • Genetic ablation of TgPLP1 in Toxoplasma gondii.
  • Microscopy to observe parasite egress and host cell integrity.
  • Assessment of parasite growth in vitro and virulence in vivo.

Main Results:

  • TgPLP1-deficient parasites were unable to efficiently permeabilize the parasitophorous vacuole and host plasma membranes during egress.
  • Ablation of TgPLP1 led to parasite entrapment within host cells.
  • TgPLP1 deficiency resulted in a >10^5-fold reduction in acute virulence in a mouse model.

Conclusions:

  • TgPLP1 is essential for the rapid membrane permeabilization required for normal parasite egress from host cells.
  • TgPLP1 plays a critical role in the virulence of Toxoplasma gondii.
  • Perforin-like proteins may be a conserved mechanism for microbial egress and virulence in intracellular pathogens.

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