Search for killer phenotypes with potential for biological control

Antunes, Jorge T.; Aguiar, Cristina Almeida

doi:10.1007/s13213-011-0256-z

Cited by 16 publications

(8 citation statements)

References 32 publications

(51 reference statements)

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“…The size of the lysis zones formed was converted to the relative toxin activity and subtracted from the total activity to calculate the binding efficiency. The level of the ␤-1,3-and ␤-1,6-glucans (increased [1], decreased [2], or wt) is indicated for each mutant. (B) The level of alkali-insoluble ␤-1,6-and ␤-1,3-glucans in each mutant was estimated by the phenol-sulfuric acid method.…”

Section: Dynamics Of K2 Toxin Binding To Yeast Cellsmentioning

confidence: 99%

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Yeast β-1,6-Glucan Is a Primary Target for the Saccharomyces cerevisiae K2 Toxin

et al. 2015

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b Certain Saccharomyces cerevisiae strains secrete different killer proteins of double-stranded-RNA origin. These proteins confer a growth advantage to their host by increasing its survival. K2 toxin affects the target cell by binding to the cell surface, disrupting the plasma membrane integrity, and inducing ion leakage. In this study, we determined that K2 toxin saturates the yeast cell surface receptors in 10 min. The apparent amount of K2 toxin, bound to a single cell of wild type yeast under saturating conditions, was estimated to be 435 to 460 molecules. It was found that an increased level of ␤-1,6-glucan directly correlates with the number of toxin molecules bound, thereby impacting the morphology and determining the fate of the yeast cell. We observed that the binding of K2 toxin to the yeast surface receptors proceeds in a similar manner as in case of the related K1 killer protein. It was demonstrated that the externally supplied pustulan, a poly-␤-1,6-glucan, but not the glucans bearing other linkage types (such as laminarin, chitin, and pullulan) efficiently inhibits the K2 toxin killing activity. In addition, the analysis of toxin binding to the intact cells and spheroplasts confirmed that majority of K2 protein molecules attach to the ␤-1,6-glucan, rather than the plasma membrane-localized receptors. Taken together, our results reveal that ␤-1,6-glucan is a primary target of K2 toxin and is important for the execution of its killing property.T he production of antimycotic killer toxins has been observed in several yeast genera and proved to be a widespread phenomenon (1, 2). Killer strains of Saccharomyces cerevisiae secrete protein toxins derived from a family of double-stranded RNAs (dsRNAs). The toxins have been grouped into four types (K1, K2, K28, and Klus) based on their killing profiles and lack of crossimmunity (3, 4). Such proteins are able to kill the nonkiller yeast, as well as yeast of other killer types, while the toxin-producing cells remain immune to their own or to the same type of killers (4, 5). K1 toxin disrupts the regulated ion flux across the plasma membrane, leading to the death of sensitive yeast strains (6, 7). The killing action of K1 toxin involves at least two steps. During the first step, the toxin binds to the cell wall, whereas the second step leads to the translocation and insertion of the toxin into the plasma membrane (6). Beta-1,6-glucan was originally proposed to be a cell wall receptor for K1 (8). Analysis of several kre mutants demonstrated that decrease of the cell wall ␤-1,6-glucan level leads to K1 resistance, thus confirming the involvement of this type of glucan in toxin binding (9). During the second step, K1 toxin interacts with plasma membrane receptors and disrupts the functional integrity of the plasma membrane either by inducing the formation of new ion channels (7) or through the activation of existing potassium channels (10). Products of TOK1 (protein, forming the potassium ion channel) and KRE1 (glycoprotein, involved in ␤-glucan assembly) have be...

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Section: Dynamics Of K2 Toxin Binding To Yeast Cellsmentioning

confidence: 99%

“…T he production of antimycotic killer toxins has been observed in several yeast genera and proved to be a widespread phenomenon (1,2). Killer strains of Saccharomyces cerevisiae secrete protein toxins derived from a family of double-stranded RNAs (dsRNAs).…”

mentioning

confidence: 99%

Yeast β-1,6-Glucan Is a Primary Target for the Saccharomyces cerevisiae K2 Toxin

et al. 2015

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“…Microorganisms frequently compete with each other for resources in the environment, leading to the evolution of a variety of toxins to inhibit their competitors [9]. S. cerevisiae has evolved robust resistance to mycotoxins produced by other fungal species [10].…”

Section: The Role Of Master Regulators Pdr1 and Pdr3 In Multidrug Resmentioning

confidence: 99%

Transcription factors and ABC transporters: from pleiotropic drug resistance to cellular signaling in yeast

Buechel

Pinkett

2020

FEBS Letters

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Budding yeast S. cerevisiae survives in microenvironments utilizing networks of regulators and ATPbinding cassette (ABC) transporters to circumvent toxins and a variety of drugs. Our understanding of transcriptional regulation of ABC transporters in yeast is mainly derived from the study of multidrug resistance protein networks. Over the past two decades, this research has not only expanded the role of transcriptional regulators in pleiotropic drug resistance (PDR) but evolved to include the role that regulators play in cellular signaling and environmental adaptation. Inspection of the gene networks of the transcriptional regulators and characterization of the ABC transporters has clarified that they also contribute to environmental adaptation by controlling plasma-membrane composition, toxic-metal sequestration, and oxidative-stress adaptation. Additionally, ABC transporters and their regulators appear to be involved in cellular signaling for adaptation of S. cerevisiae populations to nutrient availability. In this review we summarize the current understanding of the S. cerevisiae transcriptional regulatory networks and highlight recent work in other notable fungal organisms, underlining the expansion of the study of these gene networks across the kingdom fungi.

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“…A produção de toxina killer foi indicada pela presença de um halo de inibição de crescimento ao redor do ponto de inoculação, acompanhado de uma região azul adjacente, que representa as células mortas coradas pelo azul de metileno. Para ser considerada killer, a levedura deve apresentar essa característica contra, pelo menos, uma das cepas sensíveis de referência (OLIVEIRA, 2009;ANTUNES & AGUIAR, 2012). A cepa killer padrão Saccharomyces cerevisiae NCYC232, produtora da toxina K1, foi utilizada como controle positivo.…”

Section: Fenótipo Killerunclassified

Isolamento E Caracterização De Leveduras De Caldo De Cana De Uma Indústria De Fermentação Alcoólica No Nordeste Brasileiro

Martins¹,

Lima²,

Martins³

2015

Enciclopédia Biosfera

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Search for killer phenotypes with potential for biological control

Cited by 16 publications

References 32 publications

Yeast β-1,6-Glucan Is a Primary Target for the Saccharomyces cerevisiae K2 Toxin

Yeast β-1,6-Glucan Is a Primary Target for the Saccharomyces cerevisiae K2 Toxin

Transcription factors and ABC transporters: from pleiotropic drug resistance to cellular signaling in yeast

Isolamento E Caracterização De Leveduras De Caldo De Cana De Uma Indústria De Fermentação Alcoólica No Nordeste Brasileiro

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