Journal
NEW PHYTOLOGIST
Volume 213, Issue 4, Pages 1802-1817Publisher
WILEY
DOI: 10.1111/nph.14302
Keywords
Arabidopsis thaliana; basal immunity; biotic stress network; effectortriggered; immunity (ETI); RNA-seq; transcriptional reprogramming
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Funding
- Max-Planck Society and an Alexander von Humboldt Foundation postdoctoral fellowship
- International Max-Planck Research School (IMPRS) doctoral fellowship
- China Scholarship Council
- Deutsche Forschungsgemeinschaft SFB 680 (Molecular Basis of Evolutionary Innovations)
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Plant defenses induced by salicylic acid (SA) are vital for resistance against biotrophic pathogens. In basal and receptor-triggered immunity, SA accumulation is promoted by Enhanced Disease Susceptibility1 with its co-regulator Phytoalexin Deficient4 (EDS1/PAD4). Current models position EDS1/PAD4 upstream of SA but their functional relationship remains unclear. In a genetic and transcriptomic analysis of Arabidopsis autoimmunity caused by constitutive or conditional EDS1/PAD4 overexpression, intrinsic EDS1/PAD4 signaling properties and their relation to SA were uncovered. A core EDS1/PAD4 pathway works in parallel with SA in basal and effector-triggered bacterial immunity. It protects against disabled SA-regulated gene expression and pathogen resistance, and is distinct from a known SA-compensatory route involving MAPK signaling. Results help to explain previously identified EDS1/PAD4 regulated SA-dependent and SAindependent gene expression sectors. Plants have evolved an alternative route for preserving SA-regulated defenses against pathogen or genetic perturbations. In a proposed signaling framework, EDS1 with PAD4, besides promoting SA biosynthesis, maintains important SA-related resistance programs, thereby increasing robustness of the innate immune system.
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