|Kaundal, Amita - University Of California - Cooperative Extension Service|
|Duenas, Marco - University Of California|
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 11/1/2018
Publication Date: N/A
Technical Abstract: Soil salinity affects plant growth and development, which directly impact yield. One of the mechanisms that a plant deploys to cope with stress is to control the movement of ions from root to shoot by regulating 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. 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’. The transgenic lines expressing PpHKT1 under 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. The fresh weight of athkt1 decreased significantly under 90 mM of NaCl compared to the control; however, transgenic lines showed no significant decrease under salt treatment. The transgenic lines displayed significantly longer lateral roots, relatively lower electrolyte leakage, and high relative water content compared to athkt1 under salinity stress. The expression analyses revealed that PpHKT1 was induced in both transgenic lines under salt treatment, confirming that over-expression and native expression of PpHKT1 in the Arabidopsis mutant can complement the salt tolerance function.