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Abscisic Acid–Cytokinin Antagonism Modulates Resistance Against Pseudomonas syringae in Tobacco

First, second, and third authors: Department of Plant and Environmental Sciences, Copenhagen Plant Science Centre, University of Copenhagen, Højbakkegård Allé 13, 2630 Taastrup, Denmark, and Institute of Plant Sciences, Department of Plant Physiology, University of Graz, Schubertstraße 51, 8010 Graz, Austria; and third author: Global Change Research Centre, Czech Globe AS CR, v.v.i., Drásov 470, Cz-664 24 Drásov, Czech Republic.

Phytohormones are known as essential regulators of plant defenses, with ethylene, jasmonic acid, and salicylic acid as the central immunity backbone, while other phytohormones have been demonstrated to interact with this. Only recently, a function of the classic phytohormone cytokinin in plant immunity has been described in Arabidopsis, rice, and tobacco. Although interactions of cytokinins with salicylic acid and auxin have been indicated, the complete network of cytokinin interactions with other immunity-relevant phytohormones is not yet understood. Therefore, we studied the interaction of kinetin and abscisic acid as a negative regulator of plant immunity to modulate resistance in tobacco against Pseudomonas syringae. By analyzing infection symptoms, pathogen proliferation, and accumulation of the phytoalexin scopoletin as a key mediator of kinetin-induced resistance in tobacco, antagonistic interaction of these phytohormones in plant immunity was identified. Kinetin reduced abscisic acid levels in tobacco, while increased abscisic acid levels by exogenous application or inhibition of abscisic acid catabolism by diniconazole neutralized kinetin-induced resistance. Based on these results, we conclude that reduction of abscisic acid levels by enhanced abscisic acid catabolism strongly contributes to cytokinin-mediated resistance effects. Thus, the identified cytokinin–abscisic acid antagonism is a novel regulatory mechanism in plant immunity.

Additional keywords: Nicotiana tabacum, plant–pathogen interaction.