<i>AcJAZ2L2</i> confers resistance to kiwifruit bacterial canker <i>via</i> regulation of JA signaling and stomatal immunity

Kiwifruit bacterial canker, caused by <i>Pseudomonas syringae</i> pv. actinidiae, poses a critical threat to global kiwifruit production. Previous studies implicated jasmonic acid (JA) signaling in kiwifruit responses to this pathogen; however, the molecular mechanisms underlying JA-mediated regulation remain largely unclear. Here, we identified and characterized AcJAZ2L2, a pivotal jasmonate-signaling regulator that confers substantial resistance against <i>P. syringae</i> pv. actinidiae. Transcriptomic profiling coupled with consensus co-expression network analysis revealed that AcJAZ2L2 expression is uniquely up-regulated in resistant kiwifruit cultivars after pathogen infection. Functional validation through genome editing with the clustered regularly interspaced short palindromic repeat-associated protein 9 nuclease and, through transgenic overexpression, confirmed the essential role of AcJAZ2L2 in resistance. Specifically, lines overexpressing AcJAZ2L2 displayed markedly reduced disease symptoms, lower pathogen colonization, and decreased stomatal density, whereas knockout lines exhibited increased susceptibility. Mechanistically, AcJAZ2L2 directly interacts with AcMYC2-like transcription factors, repressing downstream JA-responsive genes (AcVSP2L1 and AcVSP2L2) and maintaining stomatal closure to prevent pathogen entry. Promoter analysis further revealed cultivar-specific allelic divergence that drives differential AcJAZ2L2 transcriptional activation, explaining genotype-dependent resistance levels. Our findings establish a novel JAZ-MYC regulatory module that links JA signaling to stomatal immunity in kiwifruit and provide precise genetic targets for breeding cultivars with enhanced resistance to bacterial canker.