A noncanonical TNL immune hub defines separable recognition and signaling modules for clubroot resistance

Plant immunity mediated by nucleotide-binding leucine-rich repeat (NLR) receptors often relies on canonical EDS1 / NDR1 signaling, but alternative mechanisms are emerging. We uncover a novel modular, noncanonical immune hub orchestrated by Rcr1 , a TIR-NLR (TNL) gene conferring clubroot resistance in Brassica napus against the root-infecting protist Plasmodiophora brassicae . Unlike typical TNLs, Rcr1 engages non-NLR partners in two separable modules: a CP1 (cysteine protease)–WRKY-based recognition module, likely monitoring a pathogen virulence target, and an AP (ankyrin-repeat protein)–ERF-based signaling module, driving jasmonic acid/ethylene-mediated defense. This architecture functions without detectable EDS1 / NDR1 involvement, challenging salicylic acid-dominant models of biotrophic immunity and expanding current views of how TNLs can be wired in plant defense. Using high-throughput interactor screening and CRISPR/Cas9 knockouts, we validate these modules, while heat-inducible gene excision reveals Rcr1 ’s critical early role (0–14 days post-inoculation). Together, our findings position Rcr1 as an exemplar of modular TNL architecture, suggesting that separable recognition and signaling branches may represent a broader principle of immune flexibility in plants. This study redefines TNL flexibility, offering a blueprint for breeding durable disease-resistant crops via modular immune engineering, with clubroot resistance as a model.