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The succulent xerophyte Zygophyllum xanthoxylum (Bunge) Engl. can absorb Na+ from the soil as an osmoticum in order to resist osmotic stress. The tonoplast Na+/H+ antiporter ZxNHX1 is essential for maintaining the salt-accumulation characteristics of Z. xanthoxylum by compartmentalizing Na+ into vacuoles. Previous results revealed that the silencing of ZxNHX1 greatly decreased Na+ accumulation in Z. xanthoxylum under 50 mM NaCl due to the weakened compartmentalisation; in addition, K+ concentration also significantly reduced in ZxNHX1 -RNAi lines. Yet, whether the reduction of K+ concentration was directly triggered by the silencing of ZxNHX1 remains unclear. In this study, the growth parameters and expression levels of ZxSOS1 , ZxHKT1 ; 1 , ZxAKT1 and ZxSKOR were measured in wild-type and ZxNHX1 -RNAi lines under control or –0.5 MPa osmotic stress. The results showed that the silencing of ZxNHX1 inhibited the plant growth, decreased Na+ concentration in leaves, reduced the transcript abundance of ZxSOS1 and dramatically increased that of ZxHKT1 ; 1 in roots of Z. xanthoxylum under osmotic stress; whereas tissue K+ concentrations and the expression level of ZxSKOR displayed no significant variations, and the expression of ZxAKT1 were significantly reduced in ZxNHX1 -RNAi lines under osmotic stress, compared with the wild type. These results suggest that in Z. xanthoxylum , ZxNHX1 can maintain the normal growth by compartmentalizing Na+ into vacuoles, and regulate the spatial distribution of Na+ indirectly by affecting the expressions of ZxSOS1 and ZxHKT1 ; 1. Moreover, the silencing of ZxNHX1 is not the main reason that led to the reduction of K+ concentration in ZxNHX1 -RNAi lines under 50 mM NaCl, and ZxNHX1 might be indirectly involved in regulating K+ homeostasis. In Zygophyllum xanthoxylum , a xerophytic shrub, the silencing of ZxNHX1 (tonoplast Na +/ H + antiporter) triggered the reduction of Na+ and K+ concentration under 50 mM NaCl treatment. In this work, the K+ concentration displayed no significant variation in ZxNHX1 -RNAi lines compared with the wild type under osmotic stress, indicating that ZxNHX1 might not directly participate in controlling K+ homeostasis. The results provide a basis for further researches on the transport of Na+ and K+ in Z. xanthoxylum. [ABSTRACT FROM AUTHOR]

The succulent xerophyte Zygophyllum xanthoxylum (Bunge) Engl. can absorb Na+ from the soil as an osmoticum in order to resist osmotic stress. The tonoplast Na+/H+ antiporter ZxNHX1 is essential for maintaining the salt-accumulation characteristics of Z. xanthoxylum by compartmentalizing Na+ into vacuoles. Previous results revealed that the silencing of ZxNHX1 greatly decreased Na+ accumulation in Z. xanthoxylum under 50 mM NaCl due to the weakened compartmentalisation; in addition, K+ concentration also significantly reduced in ZxNHX1-RNAi lines. Yet, whether the reduction of K+ concentration was directly triggered by the silencing of ZxNHX1 remains unclear. In this study, the growth parameters and expression levels of ZxSOS1, ZxHKT1;1, ZxAKT1 and ZxSKOR were measured in wild-type and ZxNHX1-RNAi lines under control or -0.5 MPa osmotic stress. The results showed that the silencing of ZxNHX1 inhibited the plant growth, decreased Na+ concentration in leaves, reduced the transcript abundance of ZxSOS1 and dramatically increased that of ZxHKT1;1 in roots of Z. xanthoxylum under osmotic stress; whereas tissue K+ concentrations and the expression level of ZxSKOR displayed no significant variations, and the expression of ZxAKT1 were significantly reduced in ZxNHX1-RNAi lines under osmotic stress, compared with the wild type. These results suggest that in Z. xanthoxylum, ZxNHX1 can maintain the normal growth by compartmentalizing Na+ into vacuoles, and regulate the spatial distribution of Na+ indirectly by affecting the expressions of ZxSOS1 and ZxHKT1;1. Moreover, the silencing of ZxNHX1 is not the main reason that led to the reduction of K+ concentration in ZxNHX1-RNAi lines under 50 mM NaCl, and ZxNHX1 might be indirectly involved in regulating K+ homeostasis.