<i>Arabidopsis</i> ABCG34 contributes to defense against necrotrophic pathogens by mediating the secretion of camalexin.

Abstract

Plant pathogens cause huge yield losses. Plant defense often depends on toxic secondary metabolites that inhibit pathogen growth. Because most secondary metabolites are also toxic to the plant, specific transporters are needed to deliver them to the pathogens. To identify the transporters that function in plant defense, we screened <i>Arabidopsis thaliana</i> mutants of full-size ABCG transporters for hypersensitivity to sclareol, an antifungal compound. We found that <i>atabcg34</i> mutants were hypersensitive to sclareol and to the necrotrophic fungi <i>Alternaria brassicicola</i> and <i>Botrytis cinerea</i><i>AtABCG34</i> expression was induced by <i>A</i><i>brassicicola</i> inoculation as well as by methyl-jasmonate, a defense-related phytohormone, and AtABCG34 was polarly localized at the external face of the plasma membrane of epidermal cells of leaves and roots. <i>atabcg34</i> mutants secreted less camalexin, a major phytoalexin in <i>A</i><i>thaliana</i>, whereas plants overexpressing AtABCG34 secreted more camalexin to the leaf surface and were more resistant to the pathogen. When treated with exogenous camalexin, <i>atabcg34</i> mutants exhibited hypersensitivity, whereas BY2 cells expressing AtABCG34 exhibited improved resistance. Analyses of natural <i>Arabidopsis</i> accessions revealed that AtABCG34 contributes to the disease resistance in naturally occurring genetic variants, albeit to a small extent. Together, our data suggest that AtABCG34 mediates camalexin secretion to the leaf surface and thereby prevents <i>A</i><i>brassicicola</i> infection.