Chemical Genetics Reveals Negative Regulation of Abscisic Acid Signaling by a Plant Immune Response Pathway

Coordinated regulation of protection mechanisms against environmental abiotic stress and pathogen attack is essential for plant adaptationandsurvival. Initial abioticstresscaninterfere with disease-resistancesignaling[1-6].Conversely, initial plant immune signaling may interrupt subsequent abscisic acid (ABA)signal transduction [7, 8]. However, the processes involved in this crosstalk between these signaling networks have not been determined. By screening a 9600-compound chemical library,weidentifiedasmallmolecule [5-(3,4-dichlorophenyl)furan-2-yl]-piperidine-1-ylmethanethione (DFPM)that rapidly downregulates ABA-dependent gene expression and also inhibits ABA-induced stomatal closure. Transcriptome analyses show that DFPM also stimulates expression of plant defense-related genes.Major early regulators of pathogen- resistanceresponses, includingEDS1,PAD4,RAR1,and SGT1b, are required for DFPM-and notably also for Pseudomonas- interference with ABA signal ansduction, whereas salicylic acid, EDS16, and NPR1 are not necessary. Although DFPM does not interfere with early ABA perception by PYR/RCAR receptors or ABA activation of SnRK2 kinases, it disrupts cytosolic Ca2+ signaling and downstream anion channel activation in a PAD4-dependentmanner. Our findings provide evidence that activation of EDS1/PAD4-dependent plant immune responses rapidly disrupts ABA signal transduction and that this occurs at the level of Ca2+ signaling, illuminating how the initial biotic stress pathway interferes with ABA signaling.