A Molecular Target for Viral Killer Toxin: TOK1 Potassium Channels

Killer strains of S. cerevisiae harbor double-stranded RNA viruses and secrete protein toxins that kill virus-free cells. The K1 killer toxin acts on sensitive yeast cells to perturb potassium homeostasis and cause cell death. Here, the toxin is shown to activate the plasma membrane potassium channe...

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Bibliographic Details
Published in:Cell 1999-10, Vol.99 (3), p.283-291
Main Authors: Ahmed, Aamir, Sesti, Federico, Ilan, Nitza, Shih, Theodore M, Sturley, Stephen L, Goldstein, Steve A.N
Format: Article
Language:English
Subjects:
Animals
Cell Membrane - physiology
Coculture Techniques
Drug Resistance, Microbial - genetics
Female
Fungal Proteins - genetics
Gene Deletion
Killer Factors, Yeast
killer toxins
Membrane Potentials
Mycotoxins - genetics
Mycotoxins - metabolism
Oocytes - physiology
Polymerase Chain Reaction
potassium channels
Potassium Channels - genetics
Potassium Channels - physiology
Recombinant Proteins - metabolism
RNA Viruses - physiology
Saccharomyces cerevisiae
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae - physiology
Saccharomyces cerevisiae - virology
Saccharomyces cerevisiae Proteins
Spheroplasts - physiology
TOK1 gene
TOK1 protein
Xenopus laevis
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Summary:Killer strains of S. cerevisiae harbor double-stranded RNA viruses and secrete protein toxins that kill virus-free cells. The K1 killer toxin acts on sensitive yeast cells to perturb potassium homeostasis and cause cell death. Here, the toxin is shown to activate the plasma membrane potassium channel of S. cerevisiae, TOK1. Genetic deletion of TOK1 confers toxin resistance; overexpression increases susceptibility. Cells expressing TOK1 exhibit toxin-induced potassium flux; those without the gene do not. K1 toxin acts in the absence of other viral or yeast products: toxin synthesized from a cDNA increases open probability of single TOK1 channels (via reversible destabilization of closed states) whether channels are studied in yeast cells or X. laevis oocytes.
ISSN:0092-8674
1097-4172
DOI:10.1016/S0092-8674(00)81659-1