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 in | FEMS yeast research Vol. 6; no. 3; pp. 404 - 413 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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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. |
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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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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16630280$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1002_yea_1725 crossref_primary_10_1134_S0026261713030065 crossref_primary_10_1016_j_dnarep_2007_07_010 crossref_primary_10_1002_yea_1321 crossref_primary_10_1007_s13213_011_0256_z crossref_primary_10_1111_j_1365_2958_2008_06319_x crossref_primary_10_1042_BST0351533 crossref_primary_10_1111_j_1574_6968_2005_00082_x crossref_primary_10_1371_journal_pone_0075512 crossref_primary_10_1134_S0026261713010025 |
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Copyright | 2005 Federation of European Microbiological Societies Published by Blackwell Publishing Ltd. All rights reserved 2005 2005 Federation of European Microbiological Societies Published by Blackwell Publishing Ltd. All rights reserved |
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Keywords | zymocin killer linear plasmid silencing |
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Notes | http://dx.doi.org/10.1111/j.1567-1364.2005.00006.x These two authors contributed equally. * Editor: Lex Scheffers |
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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 |
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