Cell wall damage attenuates root hair patterning and tissue morphogenesis mediated by the receptor kinase STRUBBELIG.

Cell wall remodeling is essential for the control of growth and development as well as the regulation of stress responses. However, the underlying cell wall monitoring mechanisms remain poorly understood. Regulation of root hair fate and flower development in Arabidopsis thaliana requires signaling mediated by the atypical receptor kinase STRUBBELIG (SUB). Furthermore, SUB is involved in cell wall integrity signaling and regulates the cellular response to reduced levels of cellulose, a central component of the cell wall. Here, we show that continuous exposure to sub-lethal doses of the cellulose biosynthesis inhibitor isoxaben results in altered root hair patterning and floral morphogenesis. Genetically impairing cellulose biosynthesis also results in root hair patterning defects. We further show that isoxaben exerts its developmental effects through the attenuation of SUB signaling. Our evidence indicates that downregulation of SUB is a multi-step process and involves changes in SUB complex architecture at the plasma membrane, enhanced removal of SUB from the cell surface, and downregulation of SUB transcript levels. The results provide molecular insight into how the cell wall regulates cell fate and tissue morphogenesis.

Arabidopsis MCTP family member QUIRKY regulates the formation of the STRUBBELIG receptor kinase complex.

Intercellular communication plays a central role in organogenesis. Tissue morphogenesis in Arabidopsis (Arabidopsis thaliana) requires signaling mediated by a cell surface complex containing the atypical receptor kinase STRUBBELIG (SUB) and the multiple C2 domains and transmembrane region protein QUIRKY (QKY). QKY is required to stabilize SUB at the plasma membrane. However, it is unclear what the in vivo architecture of the QKY/SUB signaling complex is, how it is controlled, and how it relates to the maintenance of SUB at the cell surface. We addressed these questions using a combination of genetics, yeast 2-hybrid assays, and Förster resonance energy transfer (FRET)/fluorescence lifetime imaging microscopy (FLIM) in epidermal cells of seedling roots. We found that QKY promotes the formation of SUB homooligomers in vivo. Homooligomerization of SUB appeared to involve its extracellular domain. We also showed that QKY and SUB physically interact and form a complex at the cell surface in vivo. In addition, the data showed that the N-terminal C2A-B region of QKY interacts with the intracellular domain of SUB. They further revealed that this interaction is essential to maintain SUB levels at the cell surface. Finally, we provided evidence that QKY forms homomultimers in vivo in a SUB-independent manner. We suggest a model in which the physical interaction of QKY with SUB mediates the oligomerization of SUB and attenuates its internalization, thereby maintaining sufficiently high levels of SUB at the cell surface required for the control of tissue morphogenesis.