P-228 - The SCHENGEN receptor signaling module regulates lignin barrier formation to restrict bacterial pathogens

Plants have evolutionarily developed sophisticated immune systems during the course of the arms race with pathogens. Recently, we demonstrated that the lignin acts as a physical anti-bacterial structure for invading pathogens. Upon challenging with pathogens, hypersensitive-response programmed cell death (HR-PCD) is accompanied by the formation of the lignin, which restricts bacterial pathogens. Despite the importance of the lignin barrier, how plants regulate the signaling pathway for lignin formation remains elusive. In this study, we demonstrate that the receptor-like kinase SGN3/GSO1 (SCHENGEN3/GASSHO1), previously reported to be involved in the formation of the Casparian strip in roots, plays a crucial role in the formation of lignin barrier during plant immunity. During effector-triggered immunity (ETI), the expression of SGN3 and CIFs (CASPARIAN STRIP INTEGRITY FACTORs, the ligand of SGN3) was upregulated. sgn3-4 and cif1/2 knockout mutants showed decreased lignification upon challenging with the avirulent pathogen Pst DC3000 (AvrRpm1). Furthermore, CIFs-SGN3 complexes interacted / phosphorylated BIK1 (BOTRYTIS-INDUCED KINASE1) in vitro and in vivo. Our findings demonstrate that the SCHENGEN pathway is critical for the formation of lignin barrier during ETI, highlighting an additional role of CIFs-SGN3 receptor complex.