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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 391-399 |
| Number of pages | 9 |
| Journal | Journal of Cell Biology |
| Volume | 170 |
| Issue number | 3 |
| DOIs | |
| State | Published - Sep 1 2005 |
Fingerprint
ASJC Scopus subject areas
- Cell Biology
Cite this
Viruses activate a genetically conserved cell death pathway in a unicellular organism. / Ivanovska, Iva; Hardwick, J Marie.
In: Journal of Cell Biology, Vol. 170, No. 3, 01.09.2005, p. 391-399.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Viruses activate a genetically conserved cell death pathway in a unicellular organism
AU - Ivanovska, Iva
AU - Hardwick, J Marie
PY - 2005/9/1
Y1 - 2005/9/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=23744458531&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=23744458531&partnerID=8YFLogxK
U2 - 10.1083/jcb.200503069
DO - 10.1083/jcb.200503069
M3 - Article
C2 - 16061692
AN - SCOPUS:23744458531
VL - 170
SP - 391
EP - 399
JO - Journal of Cell Biology
JF - Journal of Cell Biology
SN - 0021-9525
IS - 3
ER -