Chemical Genetics Reveals Negative Regulation of Abscisic Acid Signaling by a Plant Immune Response Pathway
Chemical Genetics Reveals Negative Regulation of Abscisic Acid Signaling by a Plant Immune Response Pathway
- Current Biology, 21(7), p.990-997, 2011 .
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.
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.