Killer strains of S. cerevisiae harbor double-stranded RNA viruses and secr
ete 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
l of S. cerevisiae, TOK1. Genetic deletion of TOK1 confers toxin resistance
; overexpression increases susceptibility. Cells expressing TOK1 exhibit to
xin-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 cDN
A increases open probability of single TOK1 channels (via reversible destab
ilization of closed states) whether channels are studied in yeast cells or
X. laevis oocytes.