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Induction of salt tolerance in salicylate-deficient NahG Arabidopsis transformants using the nitric oxide donor

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The effects of treatment with nitric oxide donor sodium nitroprusside (SNP, 0.5 mM) on salt tolerance of wild type (Col–0) Arabidopsis thaliana plants and Arabidopsis thaliana plants transformed with the bacterial salicylate hydroxylase gene (NahG) were compared. Basic salt tolerance level (200 mM NaCl) was higher in NahG transformants. Under salt stress conditions, these plants showed higher activity levels for antioxidant enzymes as well as higher content of sugars and anthocyanins. The treatment with NO donor induced salt tolerance in the plants of both genotypes, which could be observed as less strong growth inhibition, reduced oxidative damage, and preservation of chlorophyll pool in leaves. After the exposure to salt stress, the activity of both superoxide dismutase and guaiacol peroxidase was higher in SNP-treated wild type plants and NahG transformants than in the nontreated plants. After the imposition of salt stress, proline content in leaves of the wild type plants treated with the nitric oxide donor was lower than in the leaves of the nontreated plants. In contrast, SNP treatment of NahG transformants led to a significant increase in the proline content in leaves under the salt stress conditions. Conclusions have been made that wild type Col-0 plants and NahG transformants differ in how their systems of protection against salt stress are activated and that nitric oxideinduced mobilization of protection systems in A. thaliana may not require the presence of salicylate.

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Correspondence to T. O. Yastreb.

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Original Russian Text © T.O. Yastreb, Yu.V. Karpets, Yu.E. Kolupaev, A.P. Dmitriev, 2017, published in Tsitologiya i Genetika, 2017, Vol. 51, No. 2, pp. 73–82.

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Yastreb, T.O., Karpets, Y.V., Kolupaev, Y.E. et al. Induction of salt tolerance in salicylate-deficient NahG Arabidopsis transformants using the nitric oxide donor. Cytol. Genet. 51, 134–141 (2017). https://doi.org/10.3103/S0095452717020086

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