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Published on: August 4, 2019
Viral induced yeast apoptosis
Manfred J Schmitt1, Jochen Reiter
1Molecular and Cell Biology, FR 8.3 Biosciences, Saarland University, Saarbrücken, Germany. mjs@microbiol.uni-sb.de
Abstract:
In an analogous system to mammals, induction of an apoptotic cell death programme (PCD) in yeast is not only restricted to various exogenous factors and stimuli, but can also be triggered by viral killer toxins and viral pathogens. In yeast, toxin secreting killer strains are frequently infected with double-stranded (ds)RNA viruses that are responsible for killer phenotype expression and toxin secretion in the infected host. In most cases, the viral toxins are either pore-forming proteins (such as K1, K2, and zygocin) that kill non-infected and sensitive yeast cells by disrupting cytoplasmic membrane function, or protein toxins (such as K28) that act in the nucleus by blocking DNA synthesis and subsequently causing a G1/S cell cycle arrest. Interestingly, while all these virus toxins cause necrotic cell death at high concentration, they trigger caspase- and ROS-mediated apoptosis at low-to-moderate concentration, indicating that even low toxin doses are deadly by triggering PCD in enemy cells. Remarkably, viral toxins are not solely responsible for cell death induction in vivo, as killer viruses themselves were shown to trigger apoptosis in non-infected yeast. Thus, as killer virus-infected and toxin secreting yeasts are effectively protected and immune to their own toxin, killer yeasts bear the intrinsic potential to dominate over time in their natural habitat.
Insights
Yeast programmed cell death (PCD) can be triggered by viral killer toxins and pathogens. These toxins, even at low doses, induce apoptosis, conferring a survival advantage to killer yeast strains.
Area of Science:
- * Microbiology and molecular biology
- * Cellular biology and programmed cell death (PCD)
- * Virology and yeast genetics
Background:
- * Yeast programmed cell death (PCD) is induced by various factors, including viral agents.
- * Killer yeast strains harbor double-stranded RNA viruses, enabling toxin production and secretion.
- * These viral toxins exhibit diverse mechanisms, targeting cell membranes or nuclear functions.
Purpose of the Study:
- * To investigate the role of viral killer toxins and pathogens in inducing PCD in yeast.
- * To elucidate the mechanisms by which viral toxins trigger cell death pathways.
- * To understand the ecological implications of viral-induced PCD in yeast populations.
Main Methods:
- * Analysis of yeast strains infected with dsRNA viruses.
- * Characterization of viral toxin structures and functions (e.g., pore-forming, nuclear-acting).
- * Assessment of cell death induction (necrosis vs. apoptosis) at varying toxin concentrations.
Main Results:
- * Viral toxins induce necrotic cell death at high concentrations and caspase- and ROS-mediated apoptosis at lower concentrations.
- * Killer yeast strains are immune to their own secreted toxins.
- * Killer viruses themselves can induce apoptosis in non-infected yeast cells.
Conclusions:
- * Viral toxins are potent inducers of PCD in sensitive yeast cells, even at sub-lethal doses.
- * Viral-induced PCD provides a competitive advantage to killer yeast, facilitating dominance.
- * Yeast-pathogen interactions involving viral toxins and PCD are crucial for microbial ecology.
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