The wheat NHX antiporter gene TaNHX2 confers salt tolerance in transgenic alfalfa by increasing the retention capacity of intracellular potassium

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Abstract
Previous studies have shown that TaNHX2 transgenic alfalfa (Medicago sativa L.) accumulated more K+ and less Na+ in leaves than did the wild-type plants. To investigate whether the increased K+ accumulation in transgenic plants is attributed to TaNHX2 gene expression and whether the compartmentalization of Na+ into vacuoles or the intracellular compartmentalization of potassium is the critical mechanism for TaNHX2-dependent salt tolerance in transgenic alfalfa, aerated hydroponic culture was performed under three different stress conditions: control condition (0.1 mM Na+ and 6 mM K+ inside culture solution), K+-sufficient salt stress (100 mM NaCl and 6 mM K+) and K+-insufficient salt stress (100 mM NaCl and 0.1 mM K+). The transgenic alfalfa plants had lower K+ efflux through specific K+ channels and higher K+ absorption through high-affinity K+ transporters than did the wild-type plants. Therefore, the transgenic plants had greater K+ contents and [K+]/[Na+] ratios in leaf tissue and cell sap. The intracellular compartmentalization of potassium is critical for TaNHX2-induced salt tolerance in transgenic alfalfa.

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