Abstract

      Salinty is one of the abiotic stresses which most affects crop productivity, especially in semiarid regions like the mediterranean zone where the Valencian Community is located. In order to be able to mitigate the detrimental effects of abiotic stresses it is necessary to know the molecular basis of the plant physiological responses; then these could be manipulated in a sensible way. In the case of salinity tolerance, actually are known a group of key aspects that have contributed to improve the cultivated plants, but more investigation is necessary to be able to obtain results adapted for agricultural practices.
      
      This work proposed a new approach using norspermidine, a non-metabolize polyamine, as seleccion agent to find Arabidopsis lines resistant to toxic cations. A genetic screen of the Arabidopsis “activation-tagging” mutant collection based on tolerance to the toxic cation norspermidine resulted in a dominant mutant par1-1D (polyamine resistant) with increased expression of the QSO2 gene (At1g15020), encoding a member of the quiescin-sulfhydryl oxidase family. The par1-1D mutant plants, and transgenic plants overexpressing QSO2 cDNA, are more tolerant than wild type Arabidopsis to polyamines, Li+ and Na+. This seems to be explained by a decrease in the accumulation of these toxic cations in xylem and shoots. On the other hand, the accumulation of K+ in xylem and shoots is increased in the par1-1D mutant. A loss-of-function mutant of the QSO2 gene (par1-2) exhibits phenotypes opposites to those of par1-1D mutant. The QSO2 gene is mostly expressed in roots and pollen and the predicted QSO2 protein has a signal peptide. Accordingly, a QSO2::GFP fusion expressed in Nicotiana benthamiana is localized at the cell surface. The recombinant QSO2 protein expressed in yeast has disulphydryl oxidase activity.
      
      A plausible mechanism for QSO2 action consists of the activation of K+ loading into the xylem independent of SKOR, which is not necessary to QSO2 function. This would produce an increase in the membrane potential in the interface symplast:xylem, decreasing therefore the toxic cations entrance into xylem and its traslocation to the aerial part. This work demonstrates the function of the sulfhydryl oxidases in regulating ionic homeostasis and shows the importance of the regulation of the cation loading into xylem in the tolerance to toxic cations.