The basis for salt tolerance is two-fold: first, the entry of ions, particularly sodium ions, into the xylem needs to be prevented as they would otherwise distribute in the aboveground tissues through the transpiration stream. This is achieved through transpiration-dependent salt tolerance, which involves the strengthening of the apoplastic barrier called the Casparian strip. Second, the cytoplasm of root cells needs to be detoxified by active export of sodium through the SOS pathway. The former pathway is induced by Casparian strip integrity factors that bind to the receptor-like kinase GSO1. Signalling downstream of GSO1 leads to formation and maintenance of the Casparian strip in the root endodermis.
The researchers found that GSO1 can also activate the SOS pathway through binding to and phosphorylation of SOS2. Co-expression of GSO1 with SOS pathway components in yeast further increases sodium efflux activity, suggesting that GSO1 contributes to SOS activation. This is corroborated by a genetic study, showing that salt-sensitive phenotypes of gso1 and sos3, but not of gso1 and sos2 mutants, are additive. Thus, GSO1 and SOS3 form two parallel pathways that converge on their common interactor SOS2. Interestingly, the strongest increase in GSO1 protein level upon salt stress is in the root apical meristem where it overlaps with SOS2 accumulation. This suggests that GSO1-induced SOS pathway activation is important for detoxification of the root stem cell niche. It is known that stem cells depend on calcium signals to establish cellular polarity. Hence, it is tempting to speculate that a calcium-independent mode of the SOS pathway may be necessary to uncouple sodium detoxification from developmentally regulated calcium signalling.
This is a preview of subscription content, access via your institution