Apoplastic Sensing of the Microbial Elicitor CfCorE1 by Pear PbrPGIP1 Orchestrates a Molecular Booster Effect to Enhance Disease Resistance

Pear anthracnose caused by Colletotrichum fructicola poses a significant threat to global pear industry, and deciphering how plant perceives this fungus is critical for effective disease control. Apoplastic immunity serves as a critical frontline against phytopathogens, where plant polygalacturonase-inhibiting proteins (PGIPs) traditionally function by counteracting microbial polygalacturonases (PGs). However, whether PGIPs possess sensory functions for direct pathogen monitoring beyond passive inhibition remains a fundamental question in crop biotechnology. Here, we characterize CfCorE1, a conserved microbial elicitor from C. fructicola that triggers pear immunity and disease resistance, as a ligand perceived by the pear PbrPGIP1 protein. We demonstrate that PbrPGIP1 plays dual-function in plant immunity: it not only inhibits fungal CfPG(s) but also directly hijacks CfCorE1 to potentiate defense responses. Using CRISPR/Cas9-mediated gene editing, we generated PbrPGIP1 mutants which exhibited significantly compromised resistance to fungal infection and diminished sensitivity to CfCorE1, confirming its essential role in pathogen perception. Structural and biochemical analyses identified four key residues (Ala103, Thr104, His115, and Arg116) in CfCorE1 required for the PbrPGIP1 interaction. Remarkably, we illustrated that CfCorE1 binding creates a synergistic booster effect, significantly strengthening the PbrPGIP1-CfPG(s) complex and enhancing the inhibitory capacity of PbrPGIP1 against fungal PG(s). Crucially, exogenous application of CfCorE1 confers broad-spectrum disease resistance across multiple crop species. Our findings uncover a novel mechanistical layer of apoplastic surveillance and provide a high-efficiency molecular strategy for developing sustainable, broad-spectrum disease resistance in plants including horticultural crops.