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J. Cell Biol. 170 (3): 391-399

Copyright © 2005 by the Rockefeller University Press.


Viruses activate a genetically conserved cell death pathway in a unicellular organism

Iva Ivanovska1, and J. Marie Hardwick1,2

1 Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine
2 Department of Molecular Microbiology and Immunology, Johns Hopkins University School of Public Health, Baltimore, MD 21205

Correspondence to J. Marie Hardwick: hardwick{at}

Abstract: Given the importance of apoptosis in the pathogenesis of virus infections in mammals, we investigated the possibility that unicellular organisms also respond to viral pathogens by activating programmed cell death. The M1 and M2 killer viruses of Saccharomyces cerevisiae encode pore-forming toxins that were assumed to kill uninfected yeast cells by a nonprogrammed assault. However, we found that yeast persistently infected with these killer viruses induce a programmed suicide pathway in uninfected (nonself) yeast. The M1 virus–encoded K1 toxin is primarily but not solely responsible for triggering the death pathway. Cell death is mediated by the mitochondrial fission factor Dnm1/Drp1, the K+ channel Tok1, and the yeast metacaspase Yca1/Mca1 encoded by the target cell and conserved in mammals. In contrast, cell death is inhibited by yeast Fis1, a pore-forming outer mitochondrial membrane protein. This virus–host relationship in yeast resembles that of pathogenic human viruses that persist in their infected host cells but trigger programmed death of uninfected cells.

Abbreviations used in this paper: cfu, colony forming units; dsRNA, double-stranded RNA; YPD, yeast peptone dextrose.

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