• Studies with loss-of-function ABA signaling mutants support that ABA positively regulates Botrytis susceptibility and cuticle formation. However, due to the complex associations between ABA deficiency, cuticle permeability, Botrytis resistance, and cell death, we further addressed the relationships between these phenotypes using gain-of-function ABA signaling mutants.
• Botrytis sensitivities, cuticle permeability, and cell death were assayed, utilizing a genetic approach with the Arabidopsis thaliana (Arabidopsis) ABA hypersensitive mutants, protein phosphatase2c quadruple mutant (pp2c-q) and enhanced response to aba1 (era1-2), and their double mutants with botrytis susceptible1 (bos1), a mutant with deregulated cell death. RNA-seq analysis with cuticle permeable mutants of differing ABA sensitivities was employed.
• Neither pp2c-q nor era1-2 exhibited phenotypes predicted by known roles of ABA; conversely, era1-2 was cuticle permeable and Botrytis-resistant, while cuticle-biosynthesis gene expression was lower in both. RNA-seq from cuticle permeable mutants identified a core set of genes regulating Botrytis resistance and susceptibility to biotrophs independent of ABA signaling. Further, BOS1 was required for Botrytis resistance of era1-2.
• Our data uncoupled ABA sensitivity and cell death from Botrytis resistance of cuticle permeable mutants and indicated that ABA has both negative and positive roles in the regulation of cuticle formation.