Abstract：
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.
摘要：
白桦树(白桦.）是重要的先锋树，在维持生态系统稳定和森林再生中起着至关重要的作用。桦树的生长受到盐胁迫的显著抑制,尤其是根抑制。盐过度敏感1（SOS1）是多种植物中唯一广泛表征的Na外排转运蛋白。盐过敏突变体,sos1，显示出NaCl对根系生长的显著抑制作用。然而,SOS1在桦树对盐胁迫的反应中的作用尚不清楚。这里,我们表征了桦树中推定的Na/H反转运蛋白BpSOS1，并通过CRISPR/Cas9方法产生了桦树BpSOS1的功能丧失突变体。bpsos1突变体表现出异常增加的盐敏感性，这与根中过量的Na积累有关，茎和老叶。我们观察到盐胁迫下bpsos1突变植物叶片中K含量的显着降低。此外，在盐胁迫下，bpsos1突变体的根和叶的Na/K比率显着高于野生型植物。发现根分生组织中Na外排的能力受到损害，这可能导致bpsos1突变体中Na和K的失衡。我们的发现表明，Na/H交换剂BpSOS1通过维持Na稳态在桦树耐盐性中起着关键作用，并为分子育种提高桦树和其他树木的耐盐性提供了证据。
