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Silicon ameliorates clubroot responses in canola (Brassica napus): A “multi-omics”-based investigation into possible mechanisms

ABSTRACT: Clubroot disease, caused by Plasmodiophora brassicae Woronin results in severe yield losses in Brassica crops, including canola. Silicon (Si) mitigates several stresses and enhances plant resistance to phytopathogens. We investigated the effects of Si on clubroot disease symptoms in canola at two concentrations of Si (Si1.0 and Si0.5). In addition, the effects of Si on P. brassicae-induced gene expression, endogenous levels of phytohormones and metabolites were also studied. Si application reduced clubroot symptoms and improved plant growth under greenhouse conditions. Pathogen-induced transcript-level changes were affected by Si treatment to P. brassicae with genes related to antioxidant activity, phytohormone biosynthesis and signalling, nitrogen metabolism and secondary metabolism exhibiting differential expression. Endogenous levels of several phytohormones (e.g., auxin, cytokinin, salicylic acid and abscisic acid), amino acids and secondary metabolites (e.g., glucosinolates) were affected by Si. This is the first report that Si ameliorates clubroot symptoms and its possible mode of action.

ORGANISM(S): Brassica Napus Canola

TISSUE(S): Plant

DISEASE(S): Clubroot Disease

SUBMITTER: Anna Kisiala

PROVIDER: ST002406 | MetabolomicsWorkbench | Mon Dec 12 00:00:00 GMT 2022

REPOSITORIES: MetabolomicsWorkbench

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Project description:This model is from the article: Mathematical modeling elucidates the role of transcriptional feedback in gibberellin signaling. Middleton AM , Úbeda-Tomás S , Griffiths J , Holman T , Hedden P , Thomas SG , Phillips AL , Holdsworth MJ , Bennett MJ , King JR, Owen MR Proc. Natl. Acad. Sci. U.S.A. 2012 May; 109(19): 7571-6 22523240 , Abstract: The hormone gibberellin (GA) is a key regulator of plant growth. Many of the components of the gibberellin signal transduction [e.g., GIBBERELLIN INSENSITIVE DWARF 1 (GID1) and DELLA], biosynthesis [e.g., GA 20-oxidase (GA20ox) and GA3ox], and deactivation pathways have been identified. Gibberellin binds its receptor, GID1, to form a complex that mediates the degradation of DELLA proteins. In this way, gibberellin relieves DELLA-dependent growth repression. However, gibberellin regulates expression of GID1, GA20ox, and GA3ox, and there is also evidence that it regulates DELLA expression. In this paper, we use integrated mathematical modeling and experiments to understand how these feedback loops interact to control gibberellin signaling. Model simulations are in good agreement with in vitro data on the signal transduction and biosynthesis pathways and in vivo data on the expression levels of gibberellin-responsive genes. We find that GA-GID1 interactions are characterized by two timescales (because of a lid on GID1 that can open and close slowly relative to GA-GID1 binding and dissociation). Furthermore, the model accurately predicts the response to exogenous gibberellin after a number of chemical and genetic perturbations. Finally, we investigate the role of the various feedback loops in gibberellin signaling. We find that regulation of GA20ox transcription plays a significant role in both modulating the level of endogenous gibberellin and generating overshoots after the removal of exogenous gibberellin. Moreover, although the contribution of other individual feedback loops seems relatively small, GID1 and DELLA transcriptional regulation acts synergistically with GA20ox feedback.

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Silicon ameliorates clubroot responses in canola (Brassica napus): A “multi-omics”-based investigation into possible mechanisms

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