Action of yeast Killer factor: a resistant mutant with sensitive spheroplasts

Journal of Bacteriology (Impact Factor: 2.81). 04/1973; 113(3):1193-7.
Source: PubMed


Yeast killer factor proteins bind to cells of both sensitive and killer-producing strains, although the latter are immune to killer action. Spheroplasts prepared from sensitive cells bind less than 1% of the killer bound to whole cells, but remain fully sensitive to killer. This finding and those obtained from binding studies of partially purified, radioactive killer protein suggest that most of the toxins remain bound to the yeast cell wall and do not function further in the killing process. A killer-resistant mutant R(18) was isolated from a sensitive strain. Whole cells of the mutant were unable to bind killer and were fully resistant. In contrast, spheroplasts of R(18) were fully sensitive to killer. These data suggest that the sites exposed to killer in spheroplasts are distinct from those on the cell wall. These wall sites appear to be necessary for killer action in whole cells.

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    • "A carboxypeptidase is involved in the processing of precursors to secret the mature proteins (Cooper and Bussey, 1989). The toxin binds to a glucan receptor on the cell wall (Al-Aidroos and Bussey, 1978; Bussey, 1991) and to the sites on the membrane (Bussey et al., 1973a) of target yeast. Therefore, the susceptible yeast cells are killed in a two-step receptor-mediated manner. "
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    ABSTRACT: The aim of this work was to study the production of functional protein in yeast culture. The cells of Saccharomyces cerevisiae Embrapa 1B (K+R+) killed a strain of Saccharomyces cerevisiae Embrapa 26B (K-R-)in grape must and YEPD media. The lethal effect of toxin-containing supernatant and the effect of aeration upon functional killer production and the correlation between the products of anaerobic metabolism and the functional toxin formation were evaluated. The results showed that at low sugar concentration, the toxin of the killer strain of Sacch. cerevisiae was only produced under anaerobic conditions . The system of killer protein production showed to be regulated by Pasteur and Crabtree effects. As soon as the ethanol was formed, the functional killer toxin was produced. The synthesis of the active killer toxin seemed to be somewhat associated with the switch to fermentation process and with concomitant alcohol dehydrogenase (ADH) activity.
    Brazilian Archives of Biology and Technology 05/2011; 54(3):601-612. DOI:10.1590/S1516-89132011000300022 · 0.55 Impact Factor
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    • "These findings suggest that the cell wall receptor for K1 toxin could be some cross-linked glucan/ glycoprotein [15]. The existence of another K1 toxin receptor localised on the plasma membrane was predicted on the basis of indirect proofs [16] [17]. The products of two different genes – TOK1 and KRE1 – have recently been suggested as membrane receptors for toxin K1 [18] [19]. "
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    ABSTRACT: Study of Saccharomyces cerevisiae killer toxin-sensitive strains with the deltakre2 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. deltakre1 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 deltakre2-like resistance pattern, but the phenotype in deltagda1 and deltasac1 is not connected with a defect in K1 toxin interaction with the plasma membrane, similarly as in deltakre6 and deltakre11 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.
    FEMS Yeast Research 10/2004; 4(8):803-13. DOI:10.1016/j.femsyr.2004.04.007 · 2.82 Impact Factor
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    • "Mutants with a reduced amount of L-1,6-glucan (kre mutants) are resistant to killer toxin K1 [6]. The cell wall is not necessarily needed for the next step, toxin interaction with the plasma membrane, since wallless spheroplasts of sensitive strains but also of kre mutants succumb to the toxin as well [7]. These ¢ndings, together with kinetic studies indicating that susceptible cells contain two populations of toxin-binding sites [8], suggest that there are also some receptors for killer toxins on the plasma membrane. "
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    ABSTRACT: Killer toxin K1 of Saccharomyces cerevisiae kills sensitive cells of the same species by disturbing the ion gradient across the plasma membrane after binding to the receptor at cell wall β-1,6-glucan. Killer protein K2 is assumed to act by a similar mechanism. To identify the putative plasma membrane receptors for both toxins we mutagenized three sensitive S. cerevisiae strains and searched for clones with killer-resistant spheroplasts. The well diffusion assay identified three phenotypically different groups of clones: clones resistant simultaneously to both toxins, clones with lowered sensitivity to only K1 toxin and those with strongly lowered sensitivity to K2 and partially lowered sensitivity to K1 toxin. These phenotypes are controlled by recessive mutations that belong to at least four different complementation groups. This indicates certain differences at the level of interaction of K1 and K2 toxin with sensitive cells.
    FEMS Yeast Research 02/2002; 2(1):73 - 79. DOI:10.1111/j.1567-1364.2002.tb00070.x · 2.82 Impact Factor
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