Mating-type locus control of killer toxins from Kluyveromyces lactis and Pichia acaciae

Killer-toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their actions in haploid MAT[alpha] cells revealed that introduction of the opposite mating-type locus (MATa) significantly suppressed antizymosis. Together...

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Published inFEMS yeast research Vol. 6; no. 3; pp. 404 - 413
Main Authors Klassen, Roland, Jablonowski, Daniel, Stark, Michael J.R, Schaffrath, Raffael, Meinhardt, Friedhelm
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.05.2006
Oxford University Press
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Abstract Killer-toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their actions in haploid MAT[alpha] cells revealed that introduction of the opposite mating-type locus (MATa) significantly suppressed antizymosis. Together with resistance expressed by MATa/MAT[alpha] diploids, the reciprocal action of MATa or MAT[alpha] in haploids of opposite mating types suggests that these killer toxins may be subject to MAT locus control. Congruently, derepressing the silent mating-type loci, HMR and HML, by removing individual components of the histone deacetylase complex Sir1[-]4, either by transposon-tagging or by chemically inactivating the histone deacetylase catalytic subunit Sir2, yields toxin resistance. Consistent with MAT control of toxin action, killer-toxin-insensitive S. cerevisiae mutants (kti) become mating-compromised despite resisting the toxins' cell-cycle effects. Mating inhibition largely depends on the time point of toxin application to the mating mixtures and is less pronounced in Elongator mutants, whose resistance to the toxins' cell-cycle effects is the result of toxin-target process deficiencies. In striking contrast, non-Elongator mutants defective in early-response events such as toxin import/activation hardly recover from toxin-induced mating inhibition. This study reveals a novel effect of yeast killer toxins on mating and sexual reproduction that is independent of their impact on cellular proliferation and cell-cycle progression.
AbstractList Killer-toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their actions in haploid MAT[alpha] cells revealed that introduction of the opposite mating-type locus (MATa) significantly suppressed antizymosis. Together with resistance expressed by MATa/MAT[alpha] diploids, the reciprocal action of MATa or MAT[alpha] in haploids of opposite mating types suggests that these killer toxins may be subject to MAT locus control. Congruently, derepressing the silent mating-type loci, HMR and HML, by removing individual components of the histone deacetylase complex Sir1[-]4, either by transposon-tagging or by chemically inactivating the histone deacetylase catalytic subunit Sir2, yields toxin resistance. Consistent with MAT control of toxin action, killer-toxin-insensitive S. cerevisiae mutants (kti) become mating-compromised despite resisting the toxins' cell-cycle effects. Mating inhibition largely depends on the time point of toxin application to the mating mixtures and is less pronounced in Elongator mutants, whose resistance to the toxins' cell-cycle effects is the result of toxin-target process deficiencies. In striking contrast, non-Elongator mutants defective in early-response events such as toxin import/activation hardly recover from toxin-induced mating inhibition. This study reveals a novel effect of yeast killer toxins on mating and sexual reproduction that is independent of their impact on cellular proliferation and cell-cycle progression.
Abstract Killer-toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their actions in haploid MATα cells revealed that introduction of the opposite mating-type locus (MATa) significantly suppressed antizymosis. Together with resistance expressed by MATa/MATα diploids, the reciprocal action of MATa or MATα in haploids of opposite mating types suggests that these killer toxins may be subject to MAT locus control. Congruently, derepressing the silent mating-type loci, HMR and HML, by removing individual components of the histone deacetylase complex Sir1−4, either by transposon-tagging or by chemically inactivating the histone deacetylase catalytic subunit Sir2, yields toxin resistance. Consistent with MAT control of toxin action, killer-toxin-insensitive S. cerevisiae mutants (kti) become mating-compromised despite resisting the toxins' cell-cycle effects. Mating inhibition largely depends on the time point of toxin application to the mating mixtures and is less pronounced in Elongator mutants, whose resistance to the toxins' cell-cycle effects is the result of toxin-target process deficiencies. In striking contrast, non-Elongator mutants defective in early-response events such as toxin import/activation hardly recover from toxin-induced mating inhibition. This study reveals a novel effect of yeast killer toxins on mating and sexual reproduction that is independent of their impact on cellular proliferation and cell-cycle progression.
Killer-toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their actions in haploid MATalpha cells revealed that introduction of the opposite mating-type locus (MATa) significantly suppressed antizymosis. Together with resistance expressed by MATa/MATalpha diploids, the reciprocal action of MATa or MATalpha in haploids of opposite mating types suggests that these killer toxins may be subject to MAT locus control. Congruently, derepressing the silent mating-type loci, HMR and HML, by removing individual components of the histone deacetylase complex Sir1-4, either by transposon-tagging or by chemically inactivating the histone deacetylase catalytic subunit Sir2, yields toxin resistance. Consistent with MAT control of toxin action, killer-toxin-insensitive S. cerevisiae mutants (kti) become mating-compromised despite resisting the toxins' cell-cycle effects. Mating inhibition largely depends on the time point of toxin application to the mating mixtures and is less pronounced in Elongator mutants, whose resistance to the toxins' cell-cycle effects is the result of toxin-target process deficiencies. In striking contrast, non-Elongator mutants defective in early-response events such as toxin import/activation hardly recover from toxin-induced mating inhibition. This study reveals a novel effect of yeast killer toxins on mating and sexual reproduction that is independent of their impact on cellular proliferation and cell-cycle progression.
Killer‐toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their actions in haploid MATα cells revealed that introduction of the opposite mating‐type locus (MATa) significantly suppressed antizymosis. Together with resistance expressed by MATa/MATα diploids, the reciprocal action of MATa or MATα in haploids of opposite mating types suggests that these killer toxins may be subject to MAT locus control. Congruently, derepressing the silent mating‐type loci, HMR and HML, by removing individual components of the histone deacetylase complex Sir1−4, either by transposon‐tagging or by chemically inactivating the histone deacetylase catalytic subunit Sir2, yields toxin resistance. Consistent with MAT control of toxin action, killer‐toxin‐insensitive S. cerevisiae mutants (kti) become mating‐compromised despite resisting the toxins' cell‐cycle effects. Mating inhibition largely depends on the time point of toxin application to the mating mixtures and is less pronounced in Elongator mutants, whose resistance to the toxins' cell‐cycle effects is the result of toxin‐target process deficiencies. In striking contrast, non‐Elongator mutants defective in early‐response events such as toxin import/activation hardly recover from toxin‐induced mating inhibition. This study reveals a novel effect of yeast killer toxins on mating and sexual reproduction that is independent of their impact on cellular proliferation and cell‐cycle progression.
Author Stark, Michael J.R.
Meinhardt, Friedhelm
Klassen, Roland
Schaffrath, Raffael
Jablonowski, Daniel
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Copyright 2005 Federation of European Microbiological Societies Published by Blackwell Publishing Ltd. All rights reserved 2005
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Keywords zymocin
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Snippet Killer-toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their actions in...
Abstract Killer-toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their...
Killer‐toxin complexes produced by Kluyveromyces lactis and Pichia acaciae inhibit cell proliferation of Saccharomyces cerevisiae. Analysis of their actions in...
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SubjectTerms cell cycle
Cell proliferation
Diploids
diploidy
Genes, Mating Type, Fungal
haploidy
Heterozygote
Histone deacetylase
Histone Deacetylase Inhibitors
Histone Deacetylases - genetics
Histone Deacetylases - physiology
killer
Killer Factors, Yeast
Kluyveromyces lactis
Kluyveromyces marxianus var. lactis
linear plasmid
loci
Mating
Mating Factor
Mating types
Mutagenesis, Insertional
Mutants
Mutation
Mycotoxins - toxicity
Peptides - genetics
Peptides - physiology
Pichia
protein subunits
Saccharomyces cerevisiae
Saccharomyces cerevisiae - genetics
Saccharomyces cerevisiae - growth & development
Saccharomyces cerevisiae Proteins - genetics
Saccharomyces cerevisiae Proteins - physiology
Sexual reproduction
silencing
Silent Information Regulator Proteins, Saccharomyces cerevisiae - genetics
Silent Information Regulator Proteins, Saccharomyces cerevisiae - physiology
Sirtuin 2
Sirtuins - genetics
Sirtuins - physiology
Toxins
Yeast
yeasts
zymocin
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Title Mating-type locus control of killer toxins from Kluyveromyces lactis and Pichia acaciae
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1567-1364.2005.00006.x
https://www.ncbi.nlm.nih.gov/pubmed/16630280
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