Please use this identifier to cite or link to this item:https://hdl.handle.net/20.500.12259/46782
Type of publication: research article
Type of publication (PDB): Straipsnis Clarivate Analytics Web of Science / Article in Clarivate Analytics Web of Science (S1)
Field of Science: Chemija / Chemistry (N003)
Author(s): Servienė, Elena;Lukša, Juliana;Orentaitė, Irma;Lafontaine, Denis;Urbonavičius, Jaunius
Title: Screening the budding yeast genome reveals unique factors affecting K2 toxin susceptibility
Is part of: PLoS ONE [elektroninis išteklius]. San Francisco, USA : Public Library of Science, 2012, vol. 7, iss. 12
Extent: p. 1-12
Date: 2012
Keywords: K2 toxin;Biotoxins;Genome
Abstract: Background: Understanding how biotoxins kill cells is of prime importance in biomedicine and the food industry. The budding yeast (S. cerevisiae) killers serve as a convenient model to study the activity of biotoxins consistently supplying with significant insights into the basic mechanisms of virus-host cell interactions and toxin entry into eukaryotic target cells. K1 and K2 toxins are active at the cell wall, leading to the disruption of the plasma membrane and subsequent cell death by ion leakage. K28 toxin is active in the cell nucleus, blocking DNA synthesis and cell cycle progression, thereby triggering apoptosis. Genome-wide screens in the budding yeast S. cerevisiae identified several hundred effectors of K1 and K28 toxins. Surprisingly, no such screen had been performed for K2 toxin, the most frequent killer toxin among industrial budding yeasts. Principal Findings: We conducted several concurrent genome-wide screens in S. cerevisiae and identified 332 novel K2 toxin effectors. The effectors involved in K2 resistance and hypersensitivity largely map in distinct cellular pathways, including cell wall and plasma membrane structure/biogenesis and mitochondrial function for K2 resistance, and cell wall stress signaling and ion/pH homeostasis for K2 hypersensitivity. 70% of K2 effectors are different from those involved in K1 or K28 susceptibility. Significance: Our work demonstrates that despite the fact that K1 and K2 toxins share some aspects of their killing strategies, they largely rely on different sets of effectors. Since the vast majority of the host factors identified here is exclusively active towards K2, we conclude that cells have acquired a specific K2 toxin effectors set. Our work thus indicates that K1 and K2 have elaborated different biological pathways and provides a first step towards the detailed characterization of K2 mode of action
Internet: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0050779
Affiliation(s): Biochemijos katedra
Botanikos institutas
Vilniaus Gedimino technikos universitetas
Vytauto Didžiojo universitetas
Appears in Collections:Universiteto mokslo publikacijos / University Research Publications

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