Suppression of LjBAK1-mediated immunity by SymRK promotes rhizobial infection in Lotus japonicus

Abstract An important question in biology is how organisms can associate with different microbes that pose no threat (commensals), pose a severe threat (pathogens) and those that are beneficial (symbionts). The root nodule symbiosis serves as important model system to address such questions in the context of plant-microbe interactions. It is now generally accepted that rhizobia have the abilities to actively suppress host immune responses during the infection process, analogous to the way in which plant pathogens can evade immune recognition. However, much remains to be elucidated with regard to the mechanisms by which the host recognizes the rhizobia as pathogens and how, subsequently, these pathways are suppressed to allow establishment of the nitrogen fixing symbiosis. In this study, we found that SymRK (Symbiosis Receptor-like Kinase) is required for rhizobial suppression of plant innate immunity in Lotus japonicus. SymRK associates with LjBAK1 (BRASSINOSTEROID INSENSITIVE 1-Associated receptor Kinase 1), a well characterized, positive regulator of plant innate immunity, and directly inhibits LjBAK1 kinase activity. Rhizobial inoculation enhances the association between SymRK and LjBAK1 in planta. LjBAK1 is required to regulate plant innate immunity and plays a negative role in mediating rhizobial infection in L. japonicus. The data indicate that the protein complex of SymRK-LjBAK1 serves as an intersection point between rhizobial symbiotic signaling pathways and innate immunity pathways, which provides an evidence that rhizobia might actively suppress the host’s ability to mount a defense response in the legume-rhizobium symbiosis.