The SALT-OVERLY-SENSITIVE (SOS) pathway in Arabidopsis (Arabidopsis thaliana) functions to prevent the toxic accumulation of sodium in the cytosol when plants are grown in salt-affected soils. In this pathway, the CALCINEURIN B-LIKE10 (AtCBL10) calcium sensor interacts with the AtSOS2 kinase to activate the AtSOS1 plasma membrane sodium/proton exchanger. CBL10 has been duplicated in Eutrema (Eutrema salsugineum), a salt-tolerant relative of Arabidopsis. Because Eutrema maintains growth in salt-affected soils that kill most crop plants, the duplication of CBL10 provides a unique opportunity to functionally test the outcome of gene duplication and its link to plant salt tolerance. In Eutrema, individual down-regulation of the duplicated CBL10 genes (EsCBL10a and EsCBL10b) decreased growth in the presence of salt and, in combination, led to an even greater decrease, suggesting that both genes function in response to salt and have distinct functions. Cross-species complementation assays demonstrated that EsCBL10b has an enhanced ability to activate the SOS pathway while EsCBL10a has a function not performed by AtCBL10 or EsCBL10b Chimeric EsCBL10a/EsCBL10b proteins revealed that the specific functions of the EsCBL10 proteins resulted from changes in the amino terminus. The duplication of CBL10 increased calcium-mediated signaling capacity in Eutrema and conferred increased salt tolerance to salt-sensitive Arabidopsis.
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