Figure 5.

MYB51, MYB122, and WRKY33 regulate metabolic flux through camalexin and 4OH-ICN pathways. (A, B) LC-DAD analysis of camalexin (top), ICN (center), and 4OH-ICN (bottom) in 9-day-old seedlings elicited with Psta (A) or co-elicited with 20 μM Dex and Psta (B) for 24 h. Data represent mean ± SE of four replicates of 13–17 seedlings each. The rpm1 mutant is ETI-deficient when elicited with Psta (Bisgrove et al., 1994; Barco et al., 2019b). The cyp82C2 mutant is impaired in 4-hydroxylation of ICN (Rajniak et al., 2015). Different letters denote statistically significant differences (P < 0.05, one-factor ANOVA coupled to Tukey's test). Experiments in (A) were performed twice, producing similar results. Experiments in (B) were performed three times, producing a range of results ( Supplementary Image 6 ), the average outcome of which is shown. ICN totals consist of the sum of ICN and methanolic degradation product indole-3-carboxylic acid methyl ester (ICA-ME). 4OH-ICN totals consist of the sum of methanolic and aqueous degradation products 4-hydroxyindole-3-carboxylic acid methyl ester (4OH-ICA-ME) and 4-hydroxyindole-3-carboxylic acid (4OH-ICA), respectively. DW, dry weight.