Dissecting oligogalacturonide-mediated pathogen resistance and root development

Oligogalacturonides (OGs) are damage-associated molecular patterns (DAMPs) generated during cell wall pectin degradation and are well-established signaling molecules in plant immunity and development. Their production depends on the interplay between polygalacturonases (PGs), which hydrolyze homogalacturonan, and PG-inhibiting proteins (PGIPs), which modulate OG accumulation towards the size classes that most strongly activate immune responses. To study OG function in planta with temporal control, we generated transgenic Arabidopsis thaliana lines expressing a β-estradiol-inducible PGIP-PG chimera (“OG machine,” OGM) that enables on- demand OG production. Upon induction, OGM plants display enhanced resistance to microbial pathogens and elevated salicylic acid (SA) levels, but also show root growth inhibition and reduced biomass, consistent with a role for OGs in the growth–defense trade-off. To dissect the molecular mechanisms underlying these phenotypes, we expressed OGM in mutant backgrounds defective in key immune components. Using these crosses, we show that OGM- induced root growth inhibition requires the NADPH oxidase RBOHD and JAR1, which is necessary for synthesis of bioactive jasmonate, and depends largely on the immune regulator EDS1. In contrast, this phenotype is independent of SA and other factors such as NDR1, and does not require MPK3 or MPK6 individually. Notably, the enhanced resistance of OGM plants to the necrotrophic fungus Botrytis cinerea is JAR1-dependent, but does not require RBOHD or EDS1. Together, these results indicate that OGs engage distinct hormone-linked signaling modules to differentially regulate immunity and development. Ongoing transcriptomic analyses will further clarify the pathways activated downstream of OGs that lead to resistance to B. cinerea.