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A ‘cool’ mechanism of salicylic acid-mediated defense and growth tradeoff

Chung-Jui Tsai: University of Georgia

<div>Crop protection based on induced resistance via treatment with salicylic acid (SA) or SA analogs offers the prospect of broad-spectrum disease control, but often comes with yield loss due to as yet poorly understood mechanisms. Mechanistic investigation of SA inhibition on plant growth has been challenging, in part because many SA-elevated <em>Arabidopsis</em> mutants are perturbed in immune signaling pathways with pleiotropic effects. We generated a novel suite of transgenic <em>Arabidopsis</em> that hyperaccumulates SA and SA-conjugates, not because of a mutation, but by ectopic expression of a bacterial SA synthase. These “biosynthetic mutants” exhibited enhanced disease resistance to <em>Pseudomonas syringae</em> pv. tomato DC3000, and enhanced tolerance to salinity and osmotic stresses. Plant growth was inhibited in an SA-dependent manner, and the effect was exacerbated at cool temperatures. Transcriptomics analysis revealed an inhibitory effect of SA on a group of cold-regulated (COR) genes implicated in membrane protection against abiotic stresses. Constitutive expression of COR genes rescued the growth phenotype in high-SA plants without affecting disease resistance. Elucidating the growth-immunity-temperature interplay promises to improve crop protection strategies that deploy SA-based disease resistance without yield penalty under fluctuating environments.</div>

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