A conserved virulence strategy in which multiple rice-infecting fungal pathogens employ a subtilisin-like protease effector, SBT1, to suppress host immunity is identified and OsMAPKKKα is identified as a promising target for engineering disease-resistant crops.
Abstract
Rice (Oryza sativa) is highly susceptible to a variety of devastating fungal diseases. However, whether these phylogenetically distinct fungal pathogens employ conserved effectors to disrupt common immune hubs remains unclear. Here, we identify a conserved virulence strategy in which multiple rice-infecting fungal pathogens employ a subtilisin-like protease effector, SBT1, to suppress host immunity. Upon secretion into plant cells, SBT1 directly targets the key immune signaling component OsMAPKKKα and mediates its degradation in a proteolytic activity-dependent manner. OsMAPKKKα acts in a linear signaling cascade: it is phosphorylated and stabilized by OsRLCK185 at Thr493, and subsequently phosphorylates OsMKK4 to activate downstream MAPK signaling. By degrading OsMAPKKKα, SBT1 disrupts the chitin-triggered immune signaling transduced through the OsCERK1–OsRLCK185–OsMAPKKKα–OsMKK4 module. Importantly, host-induced gene silencing (HIGS) targeting SBT1 confers broad-spectrum resistance against multiple fungal pathogens. Our study unveils a previously unexplored pathogen strategy wherein a secreted effector protease dismantles a central signaling node, and identifies OsMAPKKKα as a promising target for engineering disease-resistant crops.
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