2005 Volume 22 Issue 5 Pages 477-487
Salt stress in plant cells is mainly caused by a combination of hyperosmotic stress resulting from a high concentration of Na+ in the environment and ionic stress resulting from the toxicity of cytosolic Na+. Thus, salt tolerance in plants can be improved by expressing genes involved in compatible-solute biosynthesis to increase hyperosmotic tolerance, and/or by expressing vacuolar and plasma membrane ion transporters to re-establish intracellular Na+ homeostasis under salt stress. To increase the salt tolerance of plants, we have identified and characterized genes that can confer increased hyperosmotic- and ionic-stress tolerance to plant cells.
We identified three paralogues of the HAL3 gene in tobacco (NtHAL3a, NtHAL3b, and NtHAL3c) that encode putative 4′-phosphopantothenoylcysteine decarboxylases. We found that overexpression of NtHAL3a in tobacco BY2 cells increased the level of proline, a major compatible solute in plants, and improved the salt tolerance of these cells. We also found that tolerance to ionic stress can be improved in plants by the expression of the yeast ENA1 gene, which encodes a sodium efflux pump that is present in fungi but not in plants. Furthermore, to understand the molecular mechanisms underlying Na+ and K+ homeostasis in rice (Oryza sativa L.), we identified two rice HKT transporters, OsHKT1 and OsHKT2, with different properties of Na+ and K+ transport. Finally, we investigated the role of the conserved glycine filter residue in the K+ selectivity of the two OsHKTs.