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.

Apoplastic barrier establishment in roots and nodules of Lotus japonicus is essential for root-shoot signaling and N-fixation

“…Based on our work, these defects can be due to defective CS establishment. This agrees with several studies showing that disrupted CS formation leads intolerance to abiotic stresses ( 16 , 46 ). Defect in root apoplastic barrier also affects root exudation ( 47 ).…”

Integrative physiology and transcriptome reveal salt-tolerance differences between two licorice species: Ion transport, Casparian strip formation and flavonoids biosynthesis

“…Unlike in G. uralensis , in G. inflata the significant upregulation of the ABC, PER, and CASP families and LAC3 in roots suggests that salt stress may easily promote the translocation of lignin precursors, oxidative deposition, and the development of CS formation (Fig. 11 ), which enhances the blockade of Na + and allows more Na + to be trapped in the roots, resulting in better protection of the aboveground parts of G. inflata against Na + poisoning [ 60 ].…”

“…Suberin is stored within the interior of the cell wall to develop suberin lamellae, which contain phenolic monomers, aliphatic monomers, and glycerol monomers and play an important role in the response of plants to stress [ 60 – 63 ]. CYP86A1, which regulates the synthesis of aliphatic suberin monomers, catalyses the formation of short-chain ω-hydroxy fatty acids, ranging from C12 to C18 fatty acids, and CYP86B1 catalyses the formation of long-chain ω-hydroxy fatty acids from C22 to C24 fatty acids, which is particularly important during the early deposition of suberin [ 64 , 65 ], whereas LACS2 efficiently catalyses the synthesis of long-chain fatty acyl-CoA [ 66 ].…”

Designing salt stress‐resilient crops: Current progress and future challenges

“…In maize, Enhanced Suberin Like (ZmESBL) mediates the salt-induced reprogramming of CS development, and mutants lacking ZmESBL have up to five-fold higher shoot Na + contents (Wang et al, 2022d). Under salt stress, the receptor-like kinase GASSHO 1/SCHENGEN 3 (GSO1/SGN3) accumulates in the meristem zone, where the GSO1-SOS2-SOS1 axis promotes Na + exclusion to prevent Na + from poisoning stem cells, and in the endodermis, where it reinforces the CS integrity factor (CIF)-GSO1-SGN1 axis for CS formation to prevent Na + from diffusing into the vascular tissue (Chen et al, 2023).…”