TY - JOUR
T1 - Chemical genetics reveals negative regulation of abscisic acid signaling by a plant immune response pathway
AU - Kim, Tae Houn
AU - Hauser, Felix
AU - Ha, Tracy
AU - Xue, Shaowu
AU - Böhmer, Maik
AU - Nishimura, Noriyuki
AU - Munemasa, Shintaro
AU - Hubbard, Katharine
AU - Peine, Nora
AU - Lee, Byeong Ha
AU - Lee, Stephen
AU - Robert, Nadia
AU - Parker, Jane E.
AU - Schroeder, Julian I.
N1 - Funding Information:
We thank Chris Somerville (UC Berkeley/Energy Biosciences Institute) for providing access to the chemical library. We also thank Jane Glazebrook (University of Minnesota), William Gray (University of Minnesota), Jeff Dangl (University of North Carolina), Xin Li (University of British Columbia), Erwin Grill (Technische Universität München), and Taku Demura (RIKEN) for providing mutants and materials and Yunde Zhao (UCSD) and Aurelien Boisson-Dernier for helpful discussions. This research was supported by the National Institutes of Health (R01GM060396), the National Science Foundation (MCB0918220), and in part by the Chemical Sciences, Geosciences, and Biosciences Division of the Office of Basic Energy Sciences of the Department of Energy (DE-FG02-03ER15449) grants (J.I.S.) and a Deutsche Forschungsgemeinschaft (DFG) SFB 670 grant (J.E.P.). F.H. received support from a SNF fellowship, and M.B. received support from a DFG fellowship. The University of California, San Diego, has submitted a patent form on behalf of T.H.K. and J.I.S. on aspects of the findings.
PY - 2011/6/7
Y1 - 2011/6/7
N2 - Coordinated regulation of protection mechanisms against environmental abiotic stress and pathogen attack is essential for plant adaptation and survival. Initial abiotic stress can interfere with disease-resistance signaling [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, we identified a small molecule [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-resistance responses, including EDS1, PAD4, RAR1, and SGT1b, are required for DFPM - and notably also for Pseudomonas - interference with ABA signal transduction, 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-dependent manner. 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.
AB - Coordinated regulation of protection mechanisms against environmental abiotic stress and pathogen attack is essential for plant adaptation and survival. Initial abiotic stress can interfere with disease-resistance signaling [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, we identified a small molecule [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-resistance responses, including EDS1, PAD4, RAR1, and SGT1b, are required for DFPM - and notably also for Pseudomonas - interference with ABA signal transduction, 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-dependent manner. 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.
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U2 - 10.1016/j.cub.2011.04.045
DO - 10.1016/j.cub.2011.04.045
M3 - Article
C2 - 21620700
AN - SCOPUS:79958069055
VL - 21
SP - 990
EP - 997
JO - Current Biology
JF - Current Biology
SN - 0960-9822
IS - 11
ER -