Thermostable Elicitor from <i>Colletotrichum fructicola</i> Interacts with PbrPOD1 to Promote Pear Resistance and Protect against Bitter Rot Disease

Exploitation of elicitor-induced resistance represents a promising strategy for crop disease management. Although numerous elicitors have been identified, the mechanisms by which they trigger crop resistance have remained largely uncharacterized. Pear anthracnose (pear bitter rot), caused by the broad-host-range pathogen <i>Colletotrichum fructicola</i>, results in significant economic losses. In this study, we functionally characterized CfCE61, an elicitor secreted by <i>C. fructicola</i>. Deletion of <i>CfCE61</i> increased fungal virulence in the pear fruit, suggesting that CfCE61 may activate pear immunity. Consistent with this, the recombinant CfCE61 protein enhanced fruit immunity and resistance against <i>C. fructicola</i>. Notably, heat treatment did not impair CfCE61-triggered immunity, indicating its thermostability. Through immunoprecipitation-mass spectrometry (IP-MS) and protein-protein interaction assays, we demonstrated that CfCE61 associates with the peroxidase PbrPOD1 <i>in vivo</i> and <i>in vitro</i>. Transient overexpression of PbrPOD1 significantly enhanced the resistance against <i>C. fructicola</i> in pear leaves. Further analysis revealed that CfCE61 promotes PbrPOD1 enzyme activity without altering its protein abundance. Co-treatment with CfCE61 and PbrPOD1 synergistically improved the pear resistance to <i>C. fructicola</i>. Our findings illustrate that CfCE61 acts as a thermostable elicitor by interacting with PbrPOD1 and enhancing peroxidase activity to protect against pear bitter rot disease.