Different action of killer toxins K1 and K2 on the plasma membrane and the cell wall of

Novotná, Drahomíra; Flegelová, H.; Janderová, B.

doi:10.1016/j.femsyr.2004.04.007

Cited by 35 publications

(19 citation statements)

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“…Similar observations were made previously for several kre mutants with increased resistance to K2 toxin and therefore decreased survival (20), but this phenomenon was not correlated with changes in ␤-1,6-glucan level. Still, we cannot exclude the possibility that in addition to the altered level of this glucan in the tested mutants, the survival of cells may be modulated by other cellular processes due to changed cellular levels of the tested proteins.…”

Section: Discussionsupporting

confidence: 87%

“…Analysis of the sensitivity of a ⌬kre1 mutant to either K1 or K2 toxin demonstrated total resistance in both cases, suggesting that Kre1p serves as plasma membrane receptor (19,20). Also, it was shown that both K1 and K2 bind less efficiently to a set of mutants featuring a decreased level of ␤-1,6-glucan, implying that it serves as a cell wall receptor for both proteins (9,19,20). Despite the similarities between the K1 and K2 toxins and taking into account the abovementioned differences among them, the details of killer protein interactions with the target cells and immunity mechanisms remain to be uncovered.…”

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confidence: 99%

“…Distinct sets of host factors affecting resistance and sensitivity toward K1 and K2 killer toxins were identified, revealing functional discrepancies between these toxins as well (9,19). Analysis of the sensitivity of a ⌬kre1 mutant to either K1 or K2 toxin demonstrated total resistance in both cases, suggesting that Kre1p serves as plasma membrane receptor (19,20). Also, it was shown that both K1 and K2 bind less efficiently to a set of mutants featuring a decreased level of ␤-1,6-glucan, implying that it serves as a cell wall receptor for both proteins (9,19,20).…”

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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: Discussionsupporting

confidence: 87%

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confidence: 99%

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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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“…There are two kinds of killer toxin receptors: the primary, usually located on the cell wall, and the secondary receptor, that exist on the plasma membrane of the sensitive cells. The interaction with the first receptor within the cell wall of a sensitive target cell involves a fast and energy-independent binding [20,49,75,76,95,96,97,98,99]. Cell walls are mainly composed by carbohydrates, some of them free and some linked to proteins.…”

Section: Killing Mechanism Of Actionmentioning

confidence: 99%

“…Mutational analyses reveal that solely α subunit interacts with Kre1p. Δ KRE1 mutants show complete resistance to K1, indicating that Kre1p acts as a receptor in the cytoplasmic membrane [21,98,99,103,112]. …”

Section: Killing Mechanism Of Actionmentioning

confidence: 99%

The Biology of Pichia membranifaciens Killer Toxins

Belda

Ruíz

Alonso

et al. 2017

Toxins

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The killer phenomenon is defined as the ability of some yeast to secrete toxins that are lethal to other sensitive yeasts and filamentous fungi. Since the discovery of strains of Saccharomyces cerevisiae capable of secreting killer toxins, much information has been gained regarding killer toxins and this fact has substantially contributed knowledge on fundamental aspects of cell biology and yeast genetics. The killer phenomenon has been studied in Pichia membranifaciens for several years, during which two toxins have been described. PMKT and PMKT2 are proteins of low molecular mass that bind to primary receptors located in the cell wall structure of sensitive yeast cells, linear (1→6)-β-d-glucans and mannoproteins for PMKT and PMKT2, respectively. Cwp2p also acts as a secondary receptor for PMKT. Killing of sensitive cells by PMKT is characterized by ionic movements across plasma membrane and an acidification of the intracellular pH triggering an activation of the High Osmolarity Glycerol (HOG) pathway. On the contrary, our investigations showed a mechanism of killing in which cells are arrested at an early S-phase by high concentrations of PMKT2. However, we concluded that induced mortality at low PMKT2 doses and also PMKT is indeed of an apoptotic nature. Killer yeasts and their toxins have found potential applications in several fields: in food and beverage production, as biocontrol agents, in yeast bio-typing, and as novel antimycotic agents. Accordingly, several applications have been found for P. membranifaciens killer toxins, ranging from pre- and post-harvest biocontrol of plant pathogens to applications during wine fermentation and ageing (inhibition of Botrytis cinerea, Brettanomyces bruxellensis, etc.).

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Current awareness on yeast

2005

Yeast

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In order to keep subscribers up‐to‐date with the latest developments in their field, this current awareness service is provided by John Wiley & Sons and contains newly‐published material on yeasts. Each bibliography is divided into 10 sections. 1 Books, Reviews & Symposia; 2 General; 3 Biochemistry; 4 Biotechnology; 5 Cell Biology; 6 Gene Expression; 7 Genetics; 8 Physiology; 9 Medical Mycology; 10 Recombinant DNA Technology. Within each section, articles are listed in alphabetical order with respect to author. If, in the preceding period, no publications are located relevant to any one of these headings, that section will be omitted. (4 weeks journals ‐ search completed 8th. Dec. 2004)

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Different action of killer toxins K1 and K2 on the plasma membrane and the cell wall of

Cited by 35 publications

References 41 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

The Biology of Pichia membranifaciens Killer Toxins

Current awareness on yeast

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