The protist ubiquitin ligase effector PbE3-2 targets RD21A to impede plant immunity

Clubroot caused by the soil-borne protist pathogenPlasmodiophora brassicaeis one of the most devastating diseases of Brassica oil and vegetable crops worldwide. Understanding the pathogen infection strategy is crucial for the development of disease control. However, the molecular mechanism by which this pathogen promotes infection remains largely unknown. Here, we identified aP. brassicae-secreted effector PbE3-2 that impedes plant immunity by ubiquitinating the immune regulator RD21A for degradation. Overexpression ofPbE3-2inArabidopsis thalianaresulted in higher susceptibility toP. brassicaeand decreases in chitin-triggered reactive oxygen species burst and expression of marker genes in salicylic acid signaling. PbE3-2 interacted with and ubiquitinated RD21Ain vitroandin vivo. Mutant plants deficient inRD21Aexhibited similar susceptibility and compromsied immune responses as inPbE3-2overexpression plants. These results suggest thatP. brassicaepromotes clubroot disease through RD21A degradation mediated by the effector PbE3-2. As PbE3-2 is widely conserved across differentP. brassicaepathotypes, the degradation of RD21A by PbE3-2 might be a prevalent infection strategy in this pathogen.