Abstract
Study of Saccharomyces cerevisiae killer toxin-sensitive strains with the Δkre2 phenotype (resistant to toxin K1, sensitive to toxin K2) showed that the phenotype is complemented by the KRE2 gene not only in intact cells but also in spheroplasts, and resistance to K1 thus resides very probably in the plasma membrane. Δkre1 deletant displays a faulty interaction with both K1 and K2 toxin. Hence, Kre1p probably serves as plasma membrane receptor for both toxins. Deletants in seven other genes (GDA1, SAC1, LUV1, KRE23, SAC2, KRE21, ERG4) exhibit different degrees of the Δkre2-like resistance pattern, but the phenotype in Δgda1 and Δsac1 is not connected with a defect in K1 toxin interaction with the plasma membrane, similarly as in Δkre6 and Δkre11 strains with a higher resistance to K2 toxin. Differences between the K1 and K2 killer toxin thus occur on the level of both the plasma membrane and the cell wall.
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