A STRUBBELIG–NHL3 cell surface receptor complex mediates the response to cellulose deficiency in Arabidopsis

Abstract

Plant cells are enclosed by a semi-rigid cell wall with a complex biochemical composition and architecture. The poorly understood process of remodelling the cell wall is crucial for controlling growth and development and for regulating abiotic and biotic stress responses. Cell wall remodelling upon disruption of cell wall integrity through inhibition of cellulose biosynthesis depends on the receptor kinase STRUBBELIG (SUB) and its binding partner QUIRKY (QKY). Here, we identify NON-RACE SPECIFIC DISEASE RESISTANCE/HIN1 HAIRPIN-INDUCED-LIKE protein 3 (NHL3) as an additional factor involved in the SUB-dependent cellulose biosynthesis inhibition response. Collectively, our data indicate that NHL3 maintains SUB at the plasma membrane by physically interacting with SUB. SUB signalling is attenuated by receptor-mediated endocytosis initiated by release of first the SUB–NHL3 and later the SUB–QKY interaction. Our results further suggest a diverse set of biochemically and functionally distinct SUB complexes involved in regulating cell wall integrity and development. This study shows that signalling by the multifunctional receptor kinase SUB in cell wall integrity involves two functionally distinct cell surface complexes whose activities are attenuated by sequential endocytosis, revealing a stress–growth trade-off.