Abstract
Rosa chinensis is an important economic and ornamental crop, but powdery mildew greatly reduces its ornamental and economic value. The RcCPR5 gene, encoding a constitutive expressor of pathogenesis-related genes, has two splicing variants in R. chinensis. Compared with RcCPR5-1, RcCPR5-2 has a large C-terminal deletion. During disease development, RcCPR5-2 responded quickly and coordinated with RcCPR5-1 to resist the invasion of the powdery mildew pathogen. In virus-induced gene silencing experiments, down-regulation of RcCPR5 improved the resistance of R. chinensis to powdery mildew. This was confirmed to be broad-spectrum resistance. In the absence of pathogen infection, RcCPR5–1 and RcCPR5–2 formed homodimers and heterodimers to regulate plant growth; but when infected by the powdery mildew pathogen, the RcCPR5–1 and RcCPR5–2 complexes disassociated and released RcSIM/RcSMR to induce effector-triggered immunity, thereby inducing resistance to pathogen infection.
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