|Bakker, Matthew - University Of Manitoba|
|Moshe, Kafri - Princeton University|
|Patena, Weronika - Princeton University|
|Jonikas, Martin - Princeton University|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 10/16/2019
Publication Date: 10/16/2019
Citation: Bakker, M.G., Moshe, K., Patena, W., Vaughan, M.M., McCormick, S.P., Jonikas, M.C. 2019. Identification of Chlamydomonas reinhardtii genes involved in the toxicity of trichothecene mycotoxins [abstract].
Technical Abstract: The trichothecenes are a family of small molecules of fungal origin that are toxic to many eukaryotes and that create a safety risk when they contaminate food and feed. In the case of fusarium head blight of wheat, trichothecenes are also a virulence factor that promotes disease progression. This latter activity suggests that a detailed understanding of how these toxins impact plants may provide insights that are useful for improving disease management and plant health. We identified plant genes that may be related to the toxicity of trichothecenes, using a library of mutants of the model plant Chlamydomonas reinhardtii. Mutant strains were pooled and the mixed community was grown in the presence of 15-acetyldeoxynivalenol, in the presence of trichodermin, or in the absence of trichothecenes (reference condition). After incubation, the relative abundance of the C. reinhardtii strains was determined by sequencing the internal barcodes within the cassettes that had been used to generate mutants, binning reads across multiple mutants per gene. Genes linked to differential success in the presence of the toxin were identified by subjecting normalized read count ratios (abundance in the presence of toxin : abundance in the control) to Fisher’s exact tests with false discovery rate multiple testing correction. Genes whose disruption significantly impacted performance spanned diverse putative functions, and included protein kinases, transporters, pleiotropic drug resistance determinants, RNA helicase, and genes involved in cell signaling or in regulation of the plant cell death pathway. It was more common for gene knockouts to enhance susceptibility than to enhance resistance toward trichothecenes. This work provides candidate plant genes for further testing to determine the mechanism by which disrupting gene function alters susceptibility to trichothecene toxins.