Abstract

Biotrophic pathogens depend on host carbon sources for proliferation. Here, we identified BnaA07.SUC2 in oilseed rape ( Brassica napus cv. Westar), which encodes a plasma membrane-localized proton-dependent sucrose transporter. Its expression is markedly induced in roots during the late stages of Plasmodiophora brassicae infection. The Arabidopsis thaliana suc2 mutant exhibited a strong clubroot-resistant phenotype, and functional complementation with BnaA07.SUC2 restored susceptibility to P. brassicae . Overexpression of BnaA07.SUC2 in oilseed rape significantly increased sucrose accumulation and disease susceptibility, whereas CRISPR/Cas9-mediated knockout of BnaA07.SUC2 enhanced clubroot resistance. Furthermore, yeast one-hybrid, dual-luciferase, and electrophoretic mobility shift assays showed that BnaA05.MYC2 directly binds to the BnaA07.SUC2 promoter and represses its expression. Overexpression of BnaA05.MYC2 in oilseed rape enhanced clubroot resistance, which was accompanied by reduced BnaA07.SUC2 transcript levels. Conversely, co-overexpression of BnaA07.SUC2 in the BnaA05.MYC2 -overexpressing oilseed rape background restored susceptibility, indicating that BnaA05.MYC2 promotes clubroot resistance by repressing BnaA07.SUC2 . BnaA05.MYC2 expression is induced by jasmonate (JA) signaling. JA signaling is activated during early infection but suppressed in later stages, and accordingly, BnaA05.MYC2 expression is upregulated initially but downregulated later. This downregulation relieves the repression of BnaA07.SUC2 , thereby enhancing sucrose supply to the pathogen. Our study identifies the SUC transporter BnaA07.SUC2 and its regulator BnaA05.MYC2 as key susceptibility components in P. brassicae pathogenesis, providing important insights into the interaction between P. brassicae and its host plant. Plasmodiophora brassicae is an obligate biotrophic pathogen that causes severe yield losses in cruciferous plants. Its life cy