A Plasmodiophora Brassicae Effector PbCBM1 Promotes Clubroot Susceptibility by Competitively Binding to AtPHB3 to Disrupt Salicylic Acid Biosynthesis in Plants.

Plasmodiophora brassicae poses a severe threat to rapeseed (Brassica napus) production worldwide. As an obligate biotrophic pathogen, it deploys effectors to suppress host immunity, yet how these effectors manipulate plant defence, particularly salicylic acid (SA)-b-mediated immunity, remains largely unknown. In this study, a CBM1 (carbohydrate-binding module)-containing effector, PbCBM1, from P. brassicae was identified, which is secreted and suppresses INF1/BAX-induced cell death. PbCBM1-overexpressing Arabidopsis showed significantly elevated susceptibility to P. brassicae. AtPHB3 (Prohibitin 3), a key regulator of SA biosynthesis, was identified as the interactor of PbCBM1 both in vivo and in vitro. The phb3 mutant also exhibited increased susceptibility, suggesting that PbCBM1 may promote plant susceptibility by targeting AtPHB3 during pathogen infection. The subsequent results showed that PbCBM1-overexpressing plants reduced SA pathway gene expression and isochorismate/SA accumulation upon chitin treatment. Furthermore, LUC and competitive Co-IP assays revealed that PbCBM1 competes with AtICS1 (Isochorismate synthase 1) for AtPHB3 binding. Collectively, P. brassicae secretes the effector PbCBM1 to competitively target AtPHB3, disrupting AtPHB3-AtICS1 complex integrity, thereby suppressing SA biosynthesis and immunity. This study reveals a novel molecular mechanism by which a biotrophic pathogen subverts plant defence and provides potential targets for breeding clubroot-resistant rapeseed varieties.