Abstract
In rice, the OsHKT1;5 gene has been reported to be a critical determinant of salt tolerance. This gene is harbored by the SKC1 locus, and its role was attributed to Na+ unloading from the xylem. No direct evidence, however, was provided in previous studies. Also, the reported function of SKC1 on the loading and delivery of K+ to the shoot remains to be explained. In this work, we used an electrophysiological approach to compare the kinetics of Na+ uptake by root xylem parenchyma cells using wild type (WT) and NIL(SKC1) plants. Our data showed that Na+ reabsorption was observed in WT, but not NIL(SKC1) plants, thus questioning the functional role of HKT1;5 as a transporter operating in the direct Na+ removal from the xylem. Instead, changes in the expression level of HKT1;5 altered the activity of membrane transporters involved in K+ and Ca2+ acquisition and homeostasis in the rice epidermis and stele, explaining the observed phenotype. We conclude that the role of HKT1;5 in plant salinity tolerance cannot be attributed to merely reducing Na+ concentration in the xylem sap but triggers a complex feedback regulation of activities of other transporters involved in the maintenance of plant ionic homeostasis and signaling under stress conditions.
Highlights
The exposure of plants to high levels of salt in the rhizosphere results in the accumulation of toxic levels of Na+ and Cl- in the cellular and extracellular compartments affecting cellular metabolic activity and, overall plant performance
In addition to genes controlling K+ and Na+ homeostasis (e.g., SOS1 for Na+/H+ exchange; GORK channel for K+ efflux; HAK5 for high affinity K+ uptake), we looked at the changes in the expression levels of RBOHD, a gene that encodes an NADPH oxidase and mediates stress-induced Ca2+ signaling in plants by controlling operation of the “ROS-Ca2+ hub” at the plasma membrane [35])
The magnitude of NaCl-induced K+ efflux was strongest in NIL (SKC1) plants (Figure 6C–E), explaining its salt-sensitive phenotype. These results could not be explained by transcriptional changes in the expression levels of GORK and
Summary
The exposure of plants to high levels of salt in the rhizosphere results in the accumulation of toxic levels of Na+ and Cl- in the cellular and extracellular compartments affecting cellular metabolic activity and, overall plant performance. In addition to genes controlling K+ and Na+ homeostasis (e.g., SOS1 for Na+/H+ exchange; GORK channel for K+ efflux; HAK5 for high affinity K+ uptake), we looked at the changes in the expression levels of RBOHD, a gene that encodes an NADPH (nicotinamide adenine dinucleotide phosphate) oxidase and mediates stress-induced Ca2+ signaling in plants by controlling operation of the “ROS-Ca2+ hub” at the plasma membrane [35]). The magnitude of NaCl-induced K+ efflux was strongest in NIL (SKC1) plants (Figure 6C–E), explaining its salt-sensitive phenotype These results could not be explained by transcriptional changes in the expression levels of GORK and HAK5 transporters in the mature root zone (Figure 5), implying some operational regulation. More emphasis needs to be put, on in planta functional assays
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