Chemical genetics reveals negative regulation of abscisic acid signaling by a plant immune response pathway

Tae Houn Kim, Felix Hauser, Tracy Ha, Shaowu Xue, Maik Böhmer, Noriyuki Nishimura, Shintaro Munemasa, Katharine Hubbard, Nora Peine, Byeong Ha Lee, Stephen Lee, Nadia Robert, Jane E. Parker, Julian I. Schroeder

Research output: Contribution to journalArticle

84 Citations (Scopus)

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 languageEnglish
Pages (from-to)990-997
Number of pages8
JournalCurrent Biology
Volume21
Issue number11
DOIs
Publication statusPublished - Jun 7 2011
Externally publishedYes

Fingerprint

Plant Immunity
Abscisic Acid
abscisic acid
immune response
Signal transduction
signal transduction
Signal Transduction
Chemical activation
Pathogens
abiotic stress
Small Molecule Libraries
piperidines
calcium
Chemical compounds
Disease Resistance
Salicylic Acid
plant adaptation
Genetics
pathogens
furans

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Kim, T. H., Hauser, F., Ha, T., Xue, S., Böhmer, M., Nishimura, N., ... Schroeder, J. I. (2011). Chemical genetics reveals negative regulation of abscisic acid signaling by a plant immune response pathway. Current Biology, 21(11), 990-997. https://doi.org/10.1016/j.cub.2011.04.045

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 journalArticle

Kim, TH, Hauser, F, Ha, T, Xue, S, Böhmer, M, Nishimura, N, Munemasa, S, Hubbard, K, Peine, N, Lee, BH, Lee, S, Robert, N, Parker, JE & Schroeder, JI 2011, 'Chemical genetics reveals negative regulation of abscisic acid signaling by a plant immune response pathway', Current Biology, vol. 21, no. 11, pp. 990-997. https://doi.org/10.1016/j.cub.2011.04.045
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. / Chemical genetics reveals negative regulation of abscisic acid signaling by a plant immune response pathway. In: Current Biology. 2011 ; Vol. 21, No. 11. pp. 990-997.
@article{9523c508a4714ef19c3d1cf4f828ba3e,
title = "Chemical genetics reveals negative regulation of abscisic acid signaling by a plant immune response pathway",
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.",
author = "Kim, {Tae Houn} and Felix Hauser and Tracy Ha and Shaowu Xue and Maik B{\"o}hmer and Noriyuki Nishimura and Shintaro Munemasa and Katharine Hubbard and Nora Peine and Lee, {Byeong Ha} and Stephen Lee and Nadia Robert and Parker, {Jane E.} and Schroeder, {Julian I.}",
year = "2011",
month = "6",
day = "7",
doi = "10.1016/j.cub.2011.04.045",
language = "English",
volume = "21",
pages = "990--997",
journal = "Current Biology",
issn = "0960-9822",
publisher = "Cell Press",
number = "11",

}

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 -