Salt intolerance in Arabidopsis: shoot and root sodium toxicity, and inhibition by sodium-plus-potassium overaccumulation
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Arabidopsis plants in NaCl suffering half growth inhibition do not suffer osmotic stress and seldom shoot Na + toxicity; overaccumulation of Na + plus K + might trigger the inhibition.
It is widely assumed that salinity inhibits plant growth by osmotic stress and shoot Na+ toxicity. This study aims to examine the growth inhibition of Arabidopsis thaliana by NaCl concentrations that allow the completion of the life cycle. Unaffected Col-0 wild-type plants were used to define nontoxic Na+ contents; Na+ toxicities in shoots and roots were analyzed in hkt1 and sos1 mutants, respectively. The growth inhibition of Col-0 plants at 40 mM Na+ was mild and equivalent to that produced by 8 and 4 mM Na+ in hkt1 and sos1 plants, respectively. Therefore, these mutants allowed to study the toxicity of Na+ in the absence of an osmotic challenge. Col-0 and Ts-1 accessions showed very different Na+ contents but similar growth inhibitions; Ts-1 plants showed very high leaf Na+ contents but no symptoms of Na+ toxicity. Ak-1, C24, and Fei-0 plants were highly affected by NaCl showing evident symptoms of shoot Na+ toxicity. Increasing K+ in isotonic NaCl/KCl combinations dramatically decreased the Na+ content in all Arabidopsis accessions and eliminated the signs of Na+ toxicity in most of them but did not relieve growth inhibition. This suggested that the dominant inhibition in these conditions was either osmotic or of an ionic nature unspecific for Na+ or K+. Col-0 and Ts-1 plants growing in sorbitol showed a clear osmotic stress characterized by a notable decrease of their water content, but this response did not occur in NaCl. Overaccumulation of Na+ plus K+ might trigger growth reduction in NaCl-treated plants.
KeywordsArabidopsis Osmotic inhibition Salt tolerance Sodium toxicity
We thank Carlos Alonso-Blanco, Rhonda Meyer, and José Manuel Pardo for kindly providing seeds of the Arabidopsis accession, and gl1, hkt1-4, and sos1-1 mutants. This work was supported by the Spanish Ministerio de Economía y Competitividad, Grant number AGL2012-36174 and fellowship to RA-A.
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