Abstract
AbstractPlasmodiophora brassicaecauses a significant global threat to cruciferous vegetables and crops. However, the current comprehensions of its pathogenic ways is still unclear. This study identified aP. brassicaeeffector, called PbEGF1, which strongly induces cell death inN. benthamiana.Notably,PbEGF1was significantly up-regulated in seedlings inoculated with highly virulentP. brassicae, indicating a pivotal role for PbEGF1 in pathogenicity. Furthermore, overexpression of PbEGF1 in hosts enhanced susceptibility toP. brassicae,and promoted elongation of root hairs, thus creating favorable conditions for root hair infection. Silencing ofPbEGF1reduced the pathogenicity ofP. brassicae. This finding confirms the significance of primary infection in host recognition and interaction withP. 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. SilencingBnNHL13enhanced host susceptibility toP. brassicae,and promoted root hairs elongation, indicating that down-regulation ofBnNHL13was more conducive to establishingP. brassicaeinfection. Subsequent investigation revealed that PbEGF1 has the ability to induce degradation of the BnNHL13 protein, thereby disrupting the host defense response and facilitatingP. brassicaeinfection. Our findings provide novel insights into genetic strategies for enhancing plant resistance against clubroot disease.
Publisher
Cold Spring Harbor Laboratory