MYC2‐LNC86472‐miR166a‐HB15 Module Mediates the Effect of Jasmonic Acid on Soft Rot Resistance in Colored Calla Lily

ABSTRACT Soft rot is a major disease restricting the production of colored calla lily, with severe impacts on their ornamental, commercial, and market value, caused by infection with Pectobacterium carotovorum . This study investigated the involvement of long noncoding RNAs (lncRNAs) in the soft rot response of colored calla lily leaves. Transcriptome sequencing of infected leaves identified 35,175 potential lncRNAs. Differential expression analysis revealed significant upregulation or downregulation of numerous lncRNAs following infection, indicating their potential involvement in the plant's immune response to P. carotovorum . Among these, LNC86472 was identified as a differentially expressed lncRNA that functions as a potential endogenous target mimic (eTM) for miR166a. Meanwhile, miR166a directly targets homeodomain‐leucine zipper 15 ( HB15 ) transcripts, which activates immune responses and restricts pathogen invasion. Functional studies involving the transient expression and silencing of LNC86472 and HB15 in colored calla lily leaves demonstrated that overexpression resulted in enlarged lesion sizes and compromised plant immune responses, while silencing them led to the opposite effect. Notably, infection‐induced increases in jasmonic acid levels were associated with the downregulation of LNC86472. Further analysis showed that MYC2 directly binds to the LNC86472 promoter to repress its expression. These results suggest that jasmonic acid (JA)‐mediated downregulation of LNC86472 releases miR166a, thereby facilitating miR166a‐mediated cleavage of HB15 transcripts. This study provides new insights into the role of lncRNAs in the soft rot infection process of colored calla lily.