Interplay between secondary metabolites and plant hormones in silver nitrate-elicited Arabidopsis thaliana plants
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Updated: Jul 1, 2025

Pattern-Triggered Oxidative Burst and Seedling Growth Inhibition Assays in Arabidopsis thaliana
Published on: May 21, 2019
Eva Cañizares1, Juan Manuel Acién1, Berivan Özlem Gumuş1
1Dept. Biologia, Bioquímica I Ciències Naturals, Universitat Jaume I, Castelló de La Plana, Spain.
Abstract:
Plants produce a myriad of specialized compounds in response to threats such as pathogens or pests and different abiotic factors. The stress-related induction of specialized metabolites can be mimicked using silver nitrate (AgNO3) as an elicitor, which application in conservation agriculture has gained interest. In Arabidopsis thaliana, AgNO3 triggers the accumulation of indole glucosinolates (IGs) and the phytoalexin camalexin as well as pheylpropanoid-derived defensive metabolites such as coumaroylagmatins and scopoletin through a yet unknown mechanism. In this work, the role of jasmonic (JA) and salicylic acid (SA) signaling in the AgNO3-triggered specialized metabolite production was investigated. To attain this objective, AgNO3, MeJA and SA were applied to A. thaliana lines impaired in JA or SA signaling, or affected in the endogenous levels of IGs and AGs. Metabolomics data indicated that AgNO3 elicitation required an intact JA and SA signaling to elicit the metabolic response, although mutants impaired in hormone signaling retained certain capacity to induce specialized metabolites. In turn, plants overproducing or abolishing IGs production had also an altered hormonal signaling response, both in the accumulation of signaling molecules and the molecular response mechanisms (ORA59, PDF1.2, VSP2 and PR1 gene expression), which pointed out to a crosstalk between defense hormones and specialized metabolites. The present work provides evidence of a crosstalk mechanism between JA and SA underlying AgNO3 defense metabolite elicitation in A. thaliana. In this mechanism, IGs would act as retrograde feedback signals dampening the hormonal response; hence, expanding the signaling molecule concept.
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