bak1-5 mutation uncouples tryptophan-dependent and independent postinvasive immune pathways triggered in Arabidopsis by multiple fungal pathogens

Robust nonhost resistance of Arabidopsis thaliana against the nonadapted hemibiotrophic fungus Colletotrichum tropicale requires PEN2-dependent preinvasive and CYP71A12/CYP71A13-dependent postinvasive resistance, which both rely on tryptophan (Trp) metabolism. Here we report that CYP71A12 and CYP71A13 are critical for Arabidopsis postinvasive resistance toward both the necrotrophic Alternaria brassicicola and the adapted hemibiotrophic C. higginsianum fungi. Metabolite analyses suggest that the production of indole-3-carboxylic acid derivatives (ICAs) and camalexin is induced upon pathogen invasion, while phenotypic comparison of cyp79B2 cyp79B3 and pen2 cyp71A12 cyp71A13 plants indicates that the contribution of ICAs to postinvasive resistance is dose-dependent. We also found that the disruption of intact pattern recognition receptor complex caused by bak1-5 mutation significantly reduced postinvasive resistance against C. tropicale and A. brassicicola, indicating that pattern recognition commonly contributes to this second defense-layer against pathogens with distinct infection strategies. However, the bak1-5 mutation had no detectable effects on Trp-metabolite accumulation triggered by pathogen invasion. Together with this, further comparative gene expression analyses suggested that pathogen invasion in Arabidopsis activates (i) bak1-5 insensitive Trp-metabolism that leads to antimicrobial secondary metabolites, and (ii) a bak1-5 sensitive immune pathway that activates the expression of antimicrobial proteins.