A salt stress‐activated GSO1‐SOS2‐SOS1 module protects the Arabidopsis root stem cell niche by enhancing sodium ion extrusion

Abstract

Soil salinity impairs plant growth reducing crop productivity. Toxic accumulation of sodium ions is counteracted by the Salt Overly Sensitive (SOS) pathway for Na + extrusion, comprising the Na + transporter SOS1, the kinase SOS2, and SOS3 as one of several Calcineurin‐B‐like (CBL) Ca 2 + sensors. Here, we report that the receptor‐like kinase GSO1/SGN3 activates SOS2, independently of SOS3 binding, by physical interaction and phosphorylation at Thr16. Loss of GSO1 function renders plants salt sensitive and GSO1 is both sufficient and required for activating the SOS2‐SOS1 module in yeast and in planta . Salt stress causes the accumulation of GSO1 in two specific and spatially defined areas of the root tip: in the endodermis section undergoing Casparian strip (CS) formation, where it reinforces the CIF‐GSO1‐SGN1 axis for CS barrier formation; and in the meristem, where it creates the GSO1‐SOS2‐SOS1 axis for Na + detoxification. Thus, GSO1 simultaneously prevents Na + both from diffusing into the vasculature, and from poisoning unprotected stem cells in the meristem. By protecting the meristem, receptor‐like kinase‐conferred activation of the SOS2‐SOS1 module allows root growth to be maintained in adverse environments. image Salt extrusion through the SOS (salt overly sensitive) pathway is essential for plant salt tolerance. This study identifies the receptor‐like kinase GSO1 as a direct activator of the protective SOS2‐SOS1 module that promotes cellular Na + extrusion from the meristem to maintain root growth. The receptor‐like kinase mutant gso1 is hypersensitive to salt stress. GSO1 expression is strongly upregulated in the meristem under salt stress. GSO1 phosphorylates SOS2 at T16 to activate the SOS2‐SOS1 module for salt extrusion. The GSO1‐SOS2‐SOS1 axis promotes salt extrusion for meristem protection.