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Soil salinity affects plant growth and development, which directly impact yield. Plants deploy many mechanisms to cope with, or mitigate, salt stress. One of such mechanism is to control movement of ions from root to shoot by regulating the loading of Na +  in the transpiration stream. The high-affinity K +  transporter 1 (HKT1) is known to play a role in the removal of Na +  from the xylem and bring it back to the root. As almond is a salt-sensitive crop, the rootstock plays an important role in successful almond cultivation in salt-affected regions. We currently lack knowledge on the molecular mechanisms involved in salt tolerance of almond rootstocks. In this study, we complemented the Arabidopsis  athkt1  knockout mutant with  HKT1  ortholog ( PpHKT1)  from the almond rootstock ‘Nemaguard’. Arabidopsis transgenic lines that were generated in  athkt1  background with the constitutive promoter (PpHKT1OE2.2) and the native promoter (PpHKT1NP6) were subjected to different salt treatments. Both transgenic lines survived salt concentrations up to 120 mM NaCl, however, the mutant  athkt1  died after 18 days under 120 mM NaCl. At 90 mM NaCl, the dry weight of  athkt1  decreased significantly compared to the transgenic lines. Both transgenic lines showed significantly longer lateral roots compared to the  athkt1  mutant at 80 mM NaCl treatment. The transgenic lines, PpHKT1OE2.2 and PpHKTNP6 had lower electrolyte leakage and higher relative water content compared to  athkt1 , suggesting that transgenic plants coped well with increased salt concentration by maintaining the integrity of the membranes. The expression analyses showed that  PpHKT1  was induced in PpHKT1OE2.2 and PpHKTNP6 lines under salt treatment, which confirmed that both over-expression and native expression of  PpHKT1  in the Arabidopsis mutant can complement salt tolerance function.

Expression of the high-affinity K+ transporter 1 (PpHKT1) gene from almond rootstock ‘Nemaguard’ improved salt tolerance of transgenic Arabidopsis