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

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 signalling nodes in Arabidopsis, EDS1-PAD4-ADR1 and EDS1-SAG101-NRG1. Genetic and transcriptomic analyses show that EDS1-PAD4-ADR1 primarily enhances the immune component abundance and is critical for limiting pathogen growth, whereas EDS1-SAG101-NRG1 mainly activates the hypersensitive cell death response (HR) but is dispensable for immune priming. This study enhances our understanding of the distinct contributions of these two signalling modules to ETI and suggests potential strategies for improving disease resistance in crops without compromising yield.