Abstract
K1 represents a heterodimeric A/B toxin secreted by virus-infected Saccharomyces cerevisiae strains. In a two-staged receptor-mediated process, the ionophoric activity of K1 leads to an uncontrolled influx of protons, culminating in the breakdown of the cellular transmembrane potential of sensitive cells. K1 killer yeast necessitate not only an immunity mechanism saving the toxin-producing cell from its own toxin but, additionally, a molecular system inactivating the toxic α subunit within the secretory pathway. In this study, different derivatives of the K1 precursor were constructed to analyze the biological function of particular structural components and their influence on toxin activity as well as the formation of protective immunity. Our data implicate an inactivation of the α subunit during toxin maturation and provide the basis for an updated model of K1 maturation within the host cell's secretory pathway.IMPORTANCE The killer phenotype in the baker's yeast Saccharomyces cerevisiae relies on two double-stranded RNA viruses that are persistently present in the cytoplasm. As they carry the same receptor populations as sensitive cells, killer yeast cells need-in contrast to various bacterial toxin producers-a specialized immunity mechanism. The ionophoric killer toxin K1 leads to the formation of cation-specific pores in the plasma membrane of sensitive yeast cells. Based on the data generated in this study, we were able to update the current model of toxin processing, validating the temporary inactivation of the toxic α subunit during maturation in the secretory pathway of the killer yeast.
Highlights
K1 represents a heterodimeric A/B toxin secreted by virus-infected Saccharomyces cerevisiae strains
Mature K1 and K28 toxin molecules resemble classical A/B toxins consisting of one toxic ␣ subunit and one  subunit, which is essential for target cell binding [3]
We have previously shown that the posttranslational import of K28 pptox into the secretory pathway has direct implications for the immunity mechanism, saving the toxin-producing cell from its own reinternalized toxin [14]
Summary
K1 represents a heterodimeric A/B toxin secreted by virus-infected Saccharomyces cerevisiae strains. IMPORTANCE The killer phenotype in the baker’s yeast Saccharomyces cerevisiae relies on two double-stranded RNA viruses that are persistently present in the cytoplasm As they carry the same receptor populations as sensitive cells, killer yeast cells need—in contrast to various bacterial toxin producers—a specialized immunity mechanism. Based on the data generated in this study, we were able to update the current model of toxin processing, validating the temporary inactivation of the toxic ␣ subunit during maturation in the secretory pathway of the killer yeast. In the case of the baker’s yeast Saccharomyces cerevisiae, four virally encoded killer toxins (K1, K2, K28, and Klus) have been described based on their killing properties and the lack of cross-immunity [1] Killer yeast secreting these toxins are infected with two distinct double-stranded RNA viruses, M and L-A, persistently present in the cytoplasm of the host cell. Despite their different modes of action, the structural compositions as well as the processing of these killer toxin
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