A putative Na⁺/H⁺ antiporter BpSOS1 contributes to salt tolerance in birch

White birch (Betula platyphylla Suk.) is an important pioneer tree which plays a critical role in maintaining ecosystem stability and forest regeneration. The growth of birch is dramatically inhibited by salt stress, especially the root inhibition. Salt Overly Sensitive 1 (SOS1) is the only extensively characterized Na⁺ efflux transporter in multiple plant species. The salt-hypersensitive mutant, sos1, display significant inhibition of root growth by NaCl. However, the role of SOS1 in birch responses to salt stress remains unclear. Here, we characterized a putative Na⁺/H⁺ antiporter BpSOS1 in birch and generated the loss-of-function mutants of the birch BpSOS1 by CRISPR/Cas9 approach. The bpsos1 mutant exhibit exceptional increased salt sensitivity which links to excessive Na⁺ accumulation in root, stem and old leaves. We observed a dramatic reduction of K⁺ contents in leaves of the bpsos1 mutant plants under salt stress. Furthermore, the Na⁺/K⁺ ratio of roots and leaves is significant higher in the bpsos1 mutants than the wild-type plants under salt stress. The ability of Na⁺ efflux in the root meristem zone is found to be impaired which might result the imbalance of Na⁺ and K⁺ in the bpsos1 mutants. Our findings indicate that the Na⁺/H⁺ exchanger BpSOS1 plays a critical role in birch salt tolerance by maintaining Na⁺ homeostasis and provide evidence for molecular breeding to improve salt tolerance in birch and other trees.