Figure 4.

Regulatory aspects of inducible tocopherol biosynthesis. A, The Psm-triggered induction of γ-tocopherol biosynthesis in Arabidopsis leaves is dependent on EDS1 and PAD4 but independent of SA signaling. Accumulation of γ-tocopherol is shown in the leaves of wild-type Col-0 and different mutant plants impaired in defense- or stress hormone-related signaling at 48 h after Psm inoculation or mock treatment: etr1 (not responsive to ET), dde2 (deficient in JA biosynthesis), aba2-1 (deficient in ABA biosynthesis), cpr5-2 (constitutive defense responses and ROS production), coi1-35 (JA insensitive), rbohD (deficient in oxidative burst-associated O₂⁻ production), ald1 (deficient in Pip and NHP biosynthesis), sid2-1 (deficient in SA biosynthesis), npr1-3 (deficient in SA signal transduction), eds1-2 (defective in EDS1), pad4-1 (defective in PAD4), and NahG (deficient in SA accumulation). Different letters above the bars denote statistically significant differences (P < 0.05, ANOVA and posthoc Tukey’s honestly significant difference [HSD] test). Other details are as described in Figure 3. B, Psm-inducible accumulation of the tocopherol precursor amino acid Tyr is promoted by EDS1 and PAD4 signaling. Levels of Tyr are shown in control (MgCl₂-infiltrated) leaves and Psm-inoculated leaves of Col-0, eds1-2, and pad4-1 plants at 24 h post infiltration. Details are as described in (A). C and D, Exogenous treatment with flagellin and generation of O₂⁻ both trigger the induction of γ-tocopherol biosynthesis. C, Leaves of Col-0 plants were infiltrated with 100 nm flg22 peptide or water (mock). D, A mixture of 0.5 units mL⁻¹ XO and 0.5 mm X or 0.5 mm X without enzyme (mock treatment) was infiltrated into leaves. Leaves were harvested 48 h post treatment for analyses. Other details are as described in Figure 3. FW, Fresh weight.