Interplay between JA, SA and ABA signalling during basal and induced resistance against <i>Pseudomonas syringae</i> and <i>Alternaria brassicicola</i>

We have examined the role of the callose synthase PMR4 in basal resistance and β-aminobutyric acid-induced resistance (BABA-IR) of <i>Arabidopsis thaliana</i> against the hemi-biotrophic pathogen <i>Pseudomonas syringae</i> and the necrotrophic pathogen <i>Alternaria brassicicola</i>. Compared to wild-type plants, the <i>pmr4-1</i> mutant displayed enhanced basal resistance against <i>P. syringae</i>, which correlated with constitutive expression of the <i>PR-1</i> gene. Treating the <i>pmr4-1</i> mutant with BABA boosted the already elevated levels of PR-1 gene expression, and further increased the level of resistance. Hence, BABA-IR against P. syringae does not require PMR4-derived callose. Conversely, <i>pmr4-1</i> plants showed enhanced susceptibility to <i>A. brassicicola</i>, and failed to show BABA-IR. Wild-type plants showing BABA-IR against <i>A. brassicicola</i> produced increased levels of JA. The <i>pmr4-1</i> mutant produced less JA upon <i>A. brassicicola</i> infection than the wild-type. Blocking SA accumulation in <i>pmr4-1</i> restored basal resistance, but not BABA-IR against <i>A. brassicicola</i>. This suggests that the mutant's enhanced susceptibility to <i>A. brassicicola</i> is caused by SA-mediated suppression of JA, whereas the lack of BABA-IR is caused by its inability to produce callose. <i>A. brassicicola</i> infection suppressed ABA accumulation. Pre-treatment with BABA antagonized this ABA accumulation, and concurrently potentiated expression of the ABA-responsive <i>ABI1</i> gene. Hence, BABA prevents pathogen-induced suppression of ABA accumulation, and sensitizes the tissue to ABA, causing augmented deposition of PMR4-derived callose.