A RALF-brassinosteroid signaling circuit regulates Arabidopsis hypocotyl cell shape.

Abstract

Plant cells survey and modulate their cell walls to control their shape and anisotropic growth. Signaling mediated by the plant steroid hormones brassinosteroids (BR) plays a central role in coordinating cell wall status and cell growth, and alterations in the cell wall-BR feedback loop leads to life-threatening defects in tissue and cellular integrity. How the status of the cell wall is relayed to BR signaling remains largely unclear. Increasing evidence shows that RAPID ALKALANIZATION FACTORs (RALFs), a class of secreted peptides, play structural and signaling roles at the cell surface. Here, we show that loss of RALF signaling mediated by the plasma membrane-localized RALF receptor complex FERONIA (FER)-LORELEI-LIKE GPI-anchor protein 1 (LLG1) leads to defects in cell morphology, organization, and composition of the cell wall-including pectin methylation status-and to an increase in BR signaling. We observed that increase in BR signaling mitigates the cellular defects associated with the loss of FER-mediated RALF signaling. We show that perception of RALF23 promotes the formation and signaling activity of the main BR receptor complex formed by BRASSINOSTEROID INSENSITIVE 1 (BRI1) and BRI1-ASSOCIATED KINASE 1 (BAK1) and that its bioactivity relies on pectin status. Our observations suggest a model in which RALF peptides operate at the nexus between cell wall status and BR signaling, capable of inducing changes in the cell wall as well as functioning as a cell-wall-informed signaling cues initiating a feedback loop that solicits BR signaling and coordinates cell morphogenesis.