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β-Aminobutyric Acid (BABA)-Induced Resistance in Arabidopsis thaliana: Link with Iron Homeostasis

¹Université de Bourgogne, UMR 1347 Agroécologie, BP 86510, F-21000 Dijon, France; ²ERL CNRS 6300, BP 86510, 21000 Dijon, France; ³AgroParisTech, ENGREF, 75015 Paris, France; ⁴INRA, UMR 1347 Agroécologie, BP 86510, F-21000 Dijon, France; ⁵Laboratoire de Biologie Moléculaire et Cellulaire, Institut de Biologie, Université de Neuchâtel, 2009 Neuchâtel, Switzerland; ⁶Institut de Chimie Moléculaire de l'Université de Bourgogne–UMR CNRS 6302, BP 47870, 21000 Dijon, France; ⁷Chemical Analytical Service of the Swiss Plant Science Web, University of Neuchâtel, 2000 Neuchâtel, Switzerland

β-Aminobutyric acid (BABA) is a nonprotein amino acid inducing resistance in many different plant species against a wide range of abiotic and biotic stresses. Nevertheless, how BABA primes plant natural defense reactions remains poorly understood. Based on its structure, we hypothesized and confirmed that BABA is able to chelate iron (Fe) in vitro. In vivo, we showed that it led to a transient Fe deficiency response in Arabidopsis thaliana plants exemplified by a reduction of ferritin accumulation and disturbances in the expression of genes related to Fe homeostasis. This response was not correlated to changes in Fe concentrations, suggesting that BABA affects the availability or the distribution of Fe rather than its assimilation. The phenotype of BABA-treated plants was similar to those of plants cultivated in Fe-deficient conditions. A metabolomic analysis indicated that both BABA and Fe deficiency induced the accumulation of common metabolites, including p-coumaroylagmatine, a metabolite previously shown to be synthesized in several plant species facing pathogen attack. Finally, we showed that the protective effect induced by BABA against Botrytis cinerea was mimicked by Fe deficiency. In conclusion, the Fe deficiency response caused by BABA could bring the plant to a defense-ready state, participating in the plant resistance against the pathogens.