A Biostimulant Obtained from the Seaweed Ascophyllum nodosum Protects Arabidopsis thaliana from Severe Oxidative Stress.
Mohammad Amin OmidbakhshfardNeerakkal SujeethSaurabh GuptaNooshin OmranianKieran J GuinanYariv BrotmanZoran NikoloskiAlisdair R FernieBernd Mueller-RoeberTsanko S GechevPublished in: International journal of molecular sciences (2020)
Abiotic stresses cause oxidative damage in plants. Here, we demonstrate that foliar application of an extract from the seaweed Ascophyllum nodosum, SuperFifty (SF), largely prevents paraquat (PQ)-induced oxidative stress in Arabidopsis thaliana. While PQ-stressed plants develop necrotic lesions, plants pre-treated with SF (i.e., primed plants) were unaffected by PQ. Transcriptome analysis revealed induction of reactive oxygen species (ROS) marker genes, genes involved in ROS-induced programmed cell death, and autophagy-related genes after PQ treatment. These changes did not occur in PQ-stressed plants primed with SF. In contrast, upregulation of several carbohydrate metabolism genes, growth, and hormone signaling as well as antioxidant-related genes were specific to SF-primed plants. Metabolomic analyses revealed accumulation of the stress-protective metabolite maltose and the tricarboxylic acid cycle intermediates fumarate and malate in SF-primed plants. Lipidome analysis indicated that those lipids associated with oxidative stress-induced cell death and chloroplast degradation, such as triacylglycerols (TAGs), declined upon SF priming. Our study demonstrated that SF confers tolerance to PQ-induced oxidative stress in A. thaliana, an effect achieved by modulating a range of processes at the transcriptomic, metabolic, and lipid levels.
Keyphrases
- arabidopsis thaliana
- cell death
- oxidative stress
- reactive oxygen species
- dna damage
- signaling pathway
- single cell
- hydrogen peroxide
- genome wide
- diabetic rats
- gene expression
- magnetic resonance
- anti inflammatory
- fatty acid
- magnetic resonance imaging
- cell proliferation
- endoplasmic reticulum stress
- cell cycle arrest
- mouse model
- dna methylation
- nitric oxide
- poor prognosis
- computed tomography
- genome wide identification
- heat shock protein