The receptor kinase NILR1 confers nematode resistance through developmental rather than canonical immune signaling

NILR1 contributes to quantitative resistance against Heterodera schachtii and signals through a brassinosteroid-type kinase cascade, but whether its contribution engages canonical immune signaling or follows a distinct, developmentally biased logic has remained unclear.

We profiled early transcriptional responses of wild-type and nilr1 roots to H. schachtii by RNA-seq at 30 min and 3 h post inoculation and analyzed them using a genotype × treatment interaction model, complemented by gene set enrichment and integration with cell-type-resolved, brassinosteroid-responsive regulatory networks.

We found that canonical PTI marker transcription and flg22-induced ROS production were preserved or even elevated in nilr1 , indicating that the tested PTI outputs are largely maintained despite increased susceptibility. Instead, genes whose nematode-induced responses showed NILR1-sensitive interaction effects were enriched for a HAT7/GTL1 centred cortex developmental module, and genetic disruption of GTL1/DF1 moderately altered H. schachtii parasitism, consistent with a role for this module in shaping host permissiveness.

Our data support a model in which NILR1 contributes to nematode resistance primarily via developmental, brassinosteroid-type signaling rather than via the canonical PTI outputs assayed here, consistent with a co-option of BRI1 clade (LRR-RLK-Xb) architecture — a receptor family classically associated with development — into a pathway that modulates susceptibility to a plant-parasitic nematode.