The MdSP1-MdANK immune module activated by effector SyCD1 enhances <i>Malus domestica</i> resistance <i>to Valsa mali</i>

Biological control offers an efficient and sustainable strategy for managing apple Valsa canker (AVC), caused by Valsa mali (syn. Cytospora mali), a major pathogen threatening global apple (Malus domestica) production. The actinomycete Saccharothrix yanglingensis Hhs.015 strain exhibits strong biocontrol efficacy by colonizing plant tissues and inducing resistance, but the underlying mechanisms remain insufficiently characterized. In the present study, the effector S. yanglingensis cupredoxin protein (SyCD1) was identified from the Hhs.015 strain. SyCD1 significantly enhanced resistance in multiple apple tissues by activating defense responses. Specifically, SyCD1 triggered the jasmonic acid (JA) signaling pathway, leading to the upregulation of M. domestica small peptide protein 1 (MdSP1) and M. domestica ankyrin repeat protein (MdANK). SyCD1 directly interacted with MdSP1, further strengthening immune responses. Moreover, MdSP1 interacted with MdANK, and this cooperative action enhanced apple resistance to V. mali. The present study systematically elucidated the mechanism by which SyCD1 activates the JA signaling pathway to engage the MdSP1-MdANK immune module.