Abstract
The pale potato cyst nematode (PCN), Globodera pallida, is one of the most economically important pests to potato worldwide. In general, cyst nematodes engaged in prolonged and intimate interactions with host root cells, which is a dynamic process circling between nematode infection and the activation of host immune systems. Plants deploy multiple immune-related receptors to recognize invaders and activate defense responses against them. Here, we report that NILR1, a plant cell membrane-localized leucine-rich repeat receptor-like kinase (LRR-RLK), cooperating with the BRASSINOSTEROID INSENSITIVE- associated receptor kinase 1 (BAK1), confers basal resistance to PCN (G. pallida). Overexpression of NILR1 or BAK1 resulted in resistance to PCN, whereas knockdown of either of them led to greater susceptibility to PCN. Phytohormones play critical roles in the outcome of plant-pathogen interactions. We found that the brassinosteroid (BR) signaling positively regulates immune response to PCN in potato by hindering the generation of reactive oxygen species (ROS). Additionally, BR application stabilized NILR1 in the cell membrane and NILR1- or BAK1- knockdown potato plants were less sensitive to BR treatment than wild-type potato plants, suggesting the NILR1-BAK1 complex also plays a significant role in BR signaling in potato, likely acting as a surface-localized receptor or co-receptor for perception of BR hormone and PCN infection. On the other hand, G. Pallida has evolved a mechanism to overcome the NILR1-mediated immune response using the effector RHA1B. RHA1B is a functional ubiquitin ligase that is capable of targeting subtracts for ubiquitination and degradation. We show that RHA1B directly targets the NILR1-BAK1 complex and promotes its degradation, thereby interfering with the host immune response. Collectively, our results reveal a novel NILR1-BAK1 complex functions a positive regulatory hub with a central role in linking the BR signaling and nematode immune response. Significantly, successful parasitic PCN utilizes the effector RHA1B to destroy NILR1-BAK1 complex promoting parasitism.