Minisymposium 22: Salinity

Abs # 43003: Interaction between sos1 mutation and AVP1 overexpression in Arabidopsis thaliana: Evidence for an epistatic effect and a role in potassium nutrition

Presenter:	Undurraga, Soledad F, soledad.f.undurraga@uconn.edu
Authors	Undurraga, Soledad F (A)   Gaxiola, Roberto A (A)
Affiliations:	(A): University of Connecticut

Cells expend as much as 50% of their total intracellular energy reserves to maintain gradients of ions across their membranes. The electrochemical potential of these ion gradients represents stored energy. Plants and fungi are similar in that they use proton (H⁺) gradients as the "currency" with which to mediate transport of ions. The simplicity of the vacuolar H⁺-PPase structure makes it an excellent candidate for manipulating the proton gradients in plants. Transgenic plants overexpressing AVP1 (AVP1OX) a gene that encodes the vacuolar H⁺-pyrophosphatase in Arabidopsis, are more salt- and drought-tolerant than their control counterparts. They accumulate higher Na⁺ and K⁺ contents than controls when grown in the presence of 100 mM NaCl. Transport evidence with isolated tonoplast vescicles indicated that AVP1OX plants have higher PPi-dependent H+-driving force that results in more efficient vacuolar cation sequestration. SOS1 has been identified as a plasma membrane Na⁺/H⁺ antiporter (PNAS 97:6896-6901). sos1 mutant plants are sensitive to low concentrations of Na⁺ (Plant Cell 8:617-627). SOS1 overexpression confers salt tolerance (Nature Biotech 21:81-85). In order to establish if there is an epistatic effect of AVP1 overexpression over the sos1 mutation, we crossed sos1-1 mutants with two AVP1OX lines. The driving hypothesis postulated that the enhanced vacuolar Na⁺ sequestration capacity displayed by AVP1OX plants could rescue the sos1 salt sensitivity. In order to test this hypothesis, homozygous AVP1OX/sos1 plants were gown under hydroponic conditions for 40 days and then transferred to a hydroponic media supplemented with 50 mM NaCl. All the AVP1OX/sos1-1 lines tested were as sensitive to 50 mM NaCl as the original sos1 mutants. These results are consistent with an epistatic effect of the sos1 mutation over AVP1 overexpression in regard to salt tolerance. Interestingly, the original reports of the sos1 mutation related the salt sensitivity to an impaired K⁺ acquisition capacity. The introduction of the sos1 loss-of-function mutation into the AVP1OX background did not show any apparent phenotype on plants grown in a normal K⁺ (20 mM) synthetic media. However, a dramatic reduction in shoot biomass and a total inhibition of root hair development resulted when AVP1OX/sos1 plants were transferred to synthetic media with limiting K⁺ (100 mM). These results suggest that the SOS1 antiporter plays an important role in high-affinity K⁺ uptake.