Modular mechanisms of immune priming and growth inhibition mediated by plant effector-triggered immunity

Himanshu Chhillar; Hoang Hung Nguyen; Pei-Min Yeh; Jonathan D. G. Jones; Pingtao Ding

doi:10.1016/j.celrep.2025.115394

Modular mechanisms of immune priming and growth inhibition mediated by plant effector-triggered immunity

Himanshu Chhillar, Hoang Hung Nguyen, Pei-Min Yeh, Jonathan D. G. Jones, Pingtao Ding

Research output: Contribution to journal › Article › peer-review

Abstract

Excessive activation of effector-triggered immunity (ETI) in plants inhibits plant growth and activates cell death. ETI mediated by intracellular Toll/interleukin-1 receptor/resistance protein (TIR) nucleotide-binding, leucine-rich repeat receptors (NLRs) involves two partially redundant signaling nodes in Arabidopsis, ENHANCED DISEASE SUSCEPTIBILITY 1-PHYTOALEXIN DEFICIENT 4-ACTIVATED DISEASE RESISTANCE 1 (EDS1-PAD4-ADR1) and EDS1-SENESCENCE-ASSOCIATED GENE 101-N REQUIREMENT GENE 1 (EDS1-SAG101-NRG1). Genetic and transcriptomic analyses show that EDS1-PAD4-ADR1 primarily enhances immune component abundance and is critical for limiting pathogen growth, whereas EDS1-SAG101-NRG1 mainly activates the hypersensitive response (HR) cell death but is dispensable for immune priming. This study enhances our understanding of the distinct contributions of these two signaling modules to ETI and suggests molecular principles and potential strategies for improving disease resistance in crops without compromising yield.

Original language	English
Article number	115394
Journal	Cell Reports
Volume	44
Issue number	3
Early online date	8 Mar 2025
DOIs	https://doi.org/10.1016/j.celrep.2025.115394
Publication status	Published - 25 Mar 2025

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1-s2.0-S2211124725001652-mainFinal published version, 4.06 MBLicence: CC BY

Cite this

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title = "Modular mechanisms of immune priming and growth inhibition mediated by plant effector-triggered immunity",

abstract = "Excessive activation of effector-triggered immunity (ETI) in plants inhibits plant growth and activates cell death. ETI mediated by intracellular Toll/interleukin-1 receptor/resistance protein (TIR) nucleotide-binding, leucine-rich repeat receptors (NLRs) involves two partially redundant signaling nodes in Arabidopsis, ENHANCED DISEASE SUSCEPTIBILITY 1-PHYTOALEXIN DEFICIENT 4-ACTIVATED DISEASE RESISTANCE 1 (EDS1-PAD4-ADR1) and EDS1-SENESCENCE-ASSOCIATED GENE 101-N REQUIREMENT GENE 1 (EDS1-SAG101-NRG1). Genetic and transcriptomic analyses show that EDS1-PAD4-ADR1 primarily enhances immune component abundance and is critical for limiting pathogen growth, whereas EDS1-SAG101-NRG1 mainly activates the hypersensitive response (HR) cell death but is dispensable for immune priming. This study enhances our understanding of the distinct contributions of these two signaling modules to ETI and suggests molecular principles and potential strategies for improving disease resistance in crops without compromising yield.",

author = "Himanshu Chhillar and Nguyen, {Hoang Hung} and Pei-Min Yeh and Jones, {Jonathan D. G.} and Pingtao Ding",

year = "2025",

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doi = "10.1016/j.celrep.2025.115394",

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T1 - Modular mechanisms of immune priming and growth inhibition mediated by plant effector-triggered immunity

AU - Chhillar, Himanshu

AU - Nguyen, Hoang Hung

AU - Yeh, Pei-Min

AU - Jones, Jonathan D. G.

AU - Ding, Pingtao

PY - 2025/3/25

Y1 - 2025/3/25

N2 - Excessive activation of effector-triggered immunity (ETI) in plants inhibits plant growth and activates cell death. ETI mediated by intracellular Toll/interleukin-1 receptor/resistance protein (TIR) nucleotide-binding, leucine-rich repeat receptors (NLRs) involves two partially redundant signaling nodes in Arabidopsis, ENHANCED DISEASE SUSCEPTIBILITY 1-PHYTOALEXIN DEFICIENT 4-ACTIVATED DISEASE RESISTANCE 1 (EDS1-PAD4-ADR1) and EDS1-SENESCENCE-ASSOCIATED GENE 101-N REQUIREMENT GENE 1 (EDS1-SAG101-NRG1). Genetic and transcriptomic analyses show that EDS1-PAD4-ADR1 primarily enhances immune component abundance and is critical for limiting pathogen growth, whereas EDS1-SAG101-NRG1 mainly activates the hypersensitive response (HR) cell death but is dispensable for immune priming. This study enhances our understanding of the distinct contributions of these two signaling modules to ETI and suggests molecular principles and potential strategies for improving disease resistance in crops without compromising yield.

AB - Excessive activation of effector-triggered immunity (ETI) in plants inhibits plant growth and activates cell death. ETI mediated by intracellular Toll/interleukin-1 receptor/resistance protein (TIR) nucleotide-binding, leucine-rich repeat receptors (NLRs) involves two partially redundant signaling nodes in Arabidopsis, ENHANCED DISEASE SUSCEPTIBILITY 1-PHYTOALEXIN DEFICIENT 4-ACTIVATED DISEASE RESISTANCE 1 (EDS1-PAD4-ADR1) and EDS1-SENESCENCE-ASSOCIATED GENE 101-N REQUIREMENT GENE 1 (EDS1-SAG101-NRG1). Genetic and transcriptomic analyses show that EDS1-PAD4-ADR1 primarily enhances immune component abundance and is critical for limiting pathogen growth, whereas EDS1-SAG101-NRG1 mainly activates the hypersensitive response (HR) cell death but is dispensable for immune priming. This study enhances our understanding of the distinct contributions of these two signaling modules to ETI and suggests molecular principles and potential strategies for improving disease resistance in crops without compromising yield.

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