|Duenas, Marco - UNIVERSITY OF CALIFORNIA|
|Boparai, Ajareshwar - UNIVERSITY OF CALIFORNIA|
|Kaundal, Amita - UNIVERSITY OF CALIFORNIA|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 3/12/2019
Publication Date: N/A
Technical Abstract: Salinity negatively affects plant growth and development. Plants deploy many means and strategies to cope with salinity stress. One is to control ion movement from root to shoot by controlling the loading of Na+ in the transpiration stream. The HKT1 gene is known to play a role in the removal of Na+ from the xylem back into the root that protects shoot from toxic salt concentrations. Almond is a salt-sensitive crop and the rootstock is vital in almond cultivation in salt-affected regions. In this study, we complemented the Arabidopsis athkt1 knockout mutant with HKT1 ortholog (PpHKT1) from the almond rootstock ‘Nemaguard’to see if the function of atHKT1 could be restored. PpHKT1 gene was transformed into the Arabidopsis athkt1 mutant under the constitutive promoter (PpHKT1OE2.2) and the native promoter (PpHKT1NP6). Transgenic lines were then tested for their salt tolerance. Both transgenic lines tolerated salt concentrations up to 120 mM NaCl. However, the mutant athkt1 failed to survive 18 days under 120 mM NaCl. The relative dry weight and the lateral root growth were much larger in the transgenic lines when compared to athkt1 under 80 mM NaCl solutions. The transgenic lines showed lower electrolyte leakage and higher relative water content compared to athkt1, suggesting that transgenic plants performed better in conditions of increased salt concentration due to the maintenance of the integrity of the membranes. Expression analyses showed that PpHKT1 was inducted under salinity, which confirmed that over-expression and native expression of PpHKT1 can complement salt function in hkt1 Arabidopsis mutants.