CERK1 compromises Fusarium solani resistance by reducing jasmonate level and undergoes a negative feedback regulation via the MMK2‐WRKY71 module in apple.

Fusarium spp., a necrotrophic soil‐borne pathogen, causes root rot disease on many crops. CERK1, as a typical pattern recognition receptor, has been widely studied. However, the function of CERK1 during plant–Fusarium interaction has not been well described. We determined that MdCERK1 is a susceptibility gene in the apple‐Fusarium solani (Fs) interaction, and jasmonic acid (JA) plays a crucial role in this process. MdCERK1 directly targets and phosphorylates the lipoxygenase MdLOX2.1, an enzyme initiating the JA biosynthesis, at positions Ser326 and Thr327. These phosphorylations inhibit its translocation from the cytosol to the chloroplasts, leading to a compromised JA biosynthesis. Fs upregulates MdCERK1 expression during infection. In turn, when the JA level is low, the apple MdWRKY71, a transcriptional repressor of MdCERK1, is markedly upregulated and phosphorylated at Thr99 and Thr102 residues by the MAP kinase MdMMK2. The phosphorylation of MdWRKY71 enhances its transcription inhibition on MdCERK1. Taken together, MdCERK1 plays a novel role in limiting JA biosynthesis. There seems to be an arms race between apple and Fs, in which Fs activates MdCERK1 expression to reduce the JA level, while apple senses the low JA level and activates the MdMMK2‐MdWRKY71 module to elevate JA level by inhibiting MdCERK1 expression. Summary Statement: Chitin Elicitor Receptor Kinase 1, CERK1 plays a well‐known role in plants to initiate the primary defence upon pathogens infection. In addition to this, this study discovered that apple CERK1 interacts with and phosphorylates the lipoxygenase MdLOX2.1 to block the JA biosynthesis. Moreover, the apple MMK2‐WRKY71 module negatively regulates MdCERK1 expression to maintain the JA level. [ABSTRACT FROM AUTHOR]