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Viral killer toxins induce caspase-mediated apoptosis in yeast

Jochen Reiter1, Eva Herker, Frank Madeo

  • 1Applied Molecular Biology, University of the Saarland, D-66041 Saarbrücken, Germany.

The Journal of Cell Biology
|January 26, 2005
PubMed

Insights

Killer toxins induce yeast apoptosis at low doses, requiring yeast caspase 1 and reactive oxygen species (ROS). High doses cause necrosis. Apoptosis aids toxin-mediated killing in natural killer yeast environments.

Area of Science:

  • * Cellular biology and microbiology, focusing on yeast apoptosis.
  • * Investigating programmed cell death mechanisms in Saccharomyces cerevisiae.

Background:

  • * Yeast apoptosis can be induced by various stressors like H2O2, aging, and acetic acid.
  • * Yeast caspase 1 (Yca1p) and reactive oxygen species (ROS) are critical regulators of yeast cell death pathways.

Purpose of the Study:

  • * To determine if virally encoded killer toxins induce apoptosis in yeast.
  • * To elucidate the roles of yeast caspase 1 and ROS in toxin-induced apoptosis.
  • * To differentiate between apoptotic and necrotic cell death responses to varying toxin concentrations.

Main Methods:

  • * Treatment of yeast cells with moderate and high doses of K1, K28, and zygocin killer toxins.
  • * Analysis of cell death pathways using Deltayca1 and Deltagsh1 deletion mutants.
  • * Monitoring of reactive oxygen species (ROS) accumulation and caspase activity.

Main Results:

  • * Moderate doses of killer toxins (K1, K28, zygocin) trigger an apoptotic response in yeast.
  • * High toxin concentrations lead to necrotic cell death, specific to each toxin.
  • * Yeast apoptosis induced by toxins requires both ROS accumulation and the presence of yeast caspase 1.

Conclusions:

  • * Apoptosis is a significant mechanism for toxin-mediated cell killing by killer yeasts at naturally low toxin concentrations.
  • * The dose-dependent switch from apoptosis to necrosis is a key feature of killer toxin activity.
  • * Yeast caspase 1 and ROS are essential mediators of toxin-induced programmed cell death.

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