The Plasmodiophora brassicae effector PbEGF1 manipulates plant immunity and regulate primary infection
Plasmodiophora brassicae causes a significant global threat to cruciferous vegetables and crops. However, the current comprehensions of its pathogenic ways is still unclear. This study identified a P. brassicae effector, called PbEGF1, which strongly induces cell death in N. benthamiana. Notably, PbEGF1 was significantly up-regulated in seedlings inoculated with highly virulent P. brassicae, indicating a pivotal role for PbEGF1 in pathogenicity. Furthermore, overexpression of PbEGF1 in hosts enhanced susceptibility to P. brassicae, and promoted elongation of root hairs, thus creating favorable conditions for root hair infection. Silencing of PbEGF1 reduced the pathogenicity of P. brassicae. This finding confirms the significance of primary infection in host recognition and interaction with P. brassicae. To further elucidate the virulence function of PbEGF1, we identified BnNHL13 (nonrace-specific disease resistance 1/harpin-induced 1-like 13) as its target protein. Silencing BnNHL13 enhanced host susceptibility to P. brassicae, and promoted root hairs elongation, indicating that down-regulation of BnNHL13 was more conducive to establishing P. brassicae infection. Subsequent investigation revealed that PbEGF1 has the ability to induce degradation of the BnNHL13 protein, thereby disrupting the host defense response and facilitating P. brassicae infection. Our findings provide novel insights into genetic strategies for enhancing plant resistance against clubroot disease.