An ethylene response factor negatively regulates red light induced resistance of melon to powdery mildew by inhibiting ethylene biosynthesis.

Powdery mildew is a common serious disease threatening global melon production. Red light can improve plant resistance to powdery mildew by inducing endogenous ethylene synthesis; however, the underlying molecular mechanism requires elucidation. In this study, an ERF transcription factor CmRAP2-13 was identified, silencing it significantly improved melon seedlings resistance to powdery mildew. Further research found that CmRAP2-13 inhibited the expression of key ethylene synthesis genes CmACS10 and CmERF27 by binding to GCC-box in the promoters, thus inhibiting ethylene biosynthesis. At the same time, protein-level interaction between CmRAP2-13 and CmERF27 also occurred. When CmRAP2-13 existed, the transcriptional activation of CmERF27 on CmACS10 was interfered and weakened. However, red light pretreatment notably decreased the expression of CmRAP2-13, and this process was influenced by phytochrome B, the red light receptor. Analysis of defence-related gene expression following ethephon application and CmRAP2-13 silencing revealed that CmRAP2-13 acted as a negative regulator of melon seedling resistance to powdery mildew, functioning as a convergence point for red light and ethylene signalling. Taken together, red light induced CmRAP2-13 and played a negative role in regulating Podosphaera xanthii infection in melons. Powdery mildew infection produced ethylene, which further inhibited CmRAP2-13 expression and formed a feedback regulation loop to participate in disease resistance. Our research on CmRAP2-13 deciphers the important regulatory network of red light-induced ethylene production in melon powdery mildew resistance, which can be used as a potential target of genetic engineering to enhance plant protection against powdery mildew.