MdLYK7 enhances resistance to Valsa canker by activating salicylic acid signaling and PbeBGLU12-mediated fungal cell wall stress.

Valsa canker (VC), caused by necrotrophic fungi in genus Valsa, is a devastating disease that threatens apple and pear production in China and other regions of East Asia. Receptor-like kinases (RLKs) play crucial roles in pathogen signal perception and the initiation of immune responses. However, key members of RLKs contribute to VC resistance and potential functions remain largely elusive. In this study, we identified a Malus domestica lysin-motif RLK gene, MdLYK7, whose overexpression substantially enhanced the VC resistance in apple and pear fruits and in suspension cells of Pyrus betulifolia 'Duli-G03'. Heterologous overexpression of MdLYK7 in P. betulifolia significantly induced PbeBGLU12, which encodes the β-glucosidase 12-like protein. Among them, Yeast two-hybrid (Y2H) library screening, bimolecular fluorescence complementation, luciferase complementation imaging, and co-immunoprecipitation assays showed that MdLYK7 interacted with PbeBGLU12. Functional analysis further demonstrated that PbeBGLU12 is required for MdLYK7-mediated immune response, promotes salicylic acid (SA) accumulation and SA-responsive gene expression, and increases fungal cell wall stress in Valsa pyri. Transcriptome analysis indicated that overexpression of MdLYK7 resulted in differential expression of genes associated with phenylpropanoid biosynthesis and starch and sucrose metabolism in 'Duli-G03' cells in response to Valsa pyri (Vp) signals. Collectively, these results reveal an MdLYK7-PbeBGLU12 module that enhances Valsa canker resistance by activating SA-associated defense responses and imposing stress on the fungal cell wall. This study provides new insight into the molecular basis of Valsa canker resistance and identifies candidate targets for resistance breeding in apple and pear.