ena-STUDY-Molecular and Cell Biology-18-09-2018-13:10:08:660-1285
Transcriptome kinetics of Saccharomyces cerevisiae strain BY4742 in response to viral killer toxin K1
The A/B toxin K1 secreted by virus-infected Saccharomyces cerevisiae strains kills sensitive cells via disturbance of cytoplasmic membrane function. Despite decades of research, the mechanisms underlying K1 toxicity and immunity have not been elucidated yet. In a novel approach, this study aimed to characterize transcriptional changes of K1-treated sensitive yeast cells in a time-dependent manner. Global transcriptional profiling revealed substantial cellular adaptations in target cells resulting in 1189 differentially expressed genes in total. Killer toxin K1 induced oxidative, cell wall and hyperosmotic stress responses as well as rapid down-regulation of transcription and translation. Essential pathways regulating energy metabolism were also significantly affected by the toxin. Remarkably, a futile cycle of the osmolytes trehalose and glycogen was identified probably representing a critical feature of K1 intoxication. In silico analysis suggested several transcription factors involved in K1-triggered signal transduction. The identified transcriptional changes implicate an evolutionary conserved response at least initially counteracting ionophoric toxin action, and provide valuable hints to elucidate the still unknown molecular events leading to K1 toxicity and immunity.
The A/B toxin K1 secreted by virus-infected Saccharomyces cerevisiae strains kills sensitive cells via disturbance of cytoplasmic membrane function. Despite decades of research, the mechanisms underlying K1 toxicity and immunity have not been elucidated yet. In a novel approach, this study aimed to characterize transcriptional changes of K1-treated sensitive yeast cells in a time-dependent manner. Global transcriptional profiling revealed substantial cellular adaptations in target cells resulting in 1189 differentially expressed genes in total. Killer toxin K1 induced oxidative, cell wall and hyperosmotic stress responses as well as rapid down-regulation of transcription and translation. Essential pathways regulating energy metabolism were also significantly affected by the toxin. Remarkably, a futile cycle of the osmolytes trehalose and glycogen was identified probably representing a critical feature of K1 intoxication. In silico analysis suggested several transcription factors involved in K1-triggered signal transduction. The identified transcriptional changes implicate an evolutionary conserved response at least initially counteracting ionophoric toxin action, and provide valuable hints to elucidate the still unknown molecular events leading to K1 toxicity and immunity.