Abstract
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.
| Original language | English |
|---|---|
| Pages (from-to) | 990-997 |
| Number of pages | 8 |
| Journal | Current Biology |
| Volume | 21 |
| Issue number | 11 |
| DOIs | |
| Publication status | Published - Jun 7 2011 |
| Externally published | Yes |
Fingerprint
ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Chemical genetics reveals negative regulation of abscisic acid signaling by a plant immune response pathway. / Kim, Tae Houn; Hauser, Felix; Ha, Tracy; Xue, Shaowu; Böhmer, Maik; Nishimura, Noriyuki; Munemasa, Shintaro; Hubbard, Katharine; Peine, Nora; Lee, Byeong Ha; Lee, Stephen; Robert, Nadia; Parker, Jane E.; Schroeder, Julian I.
In: Current Biology, Vol. 21, No. 11, 07.06.2011, p. 990-997.Research output: Contribution to journal › Article
}
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.
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.
UR - http://www.scopus.com/inward/record.url?scp=79958069055&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=79958069055&partnerID=8YFLogxK
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 -