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. 2023 Mar 14;23:139. doi: 10.1186/s12870-023-04152-8

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© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 1 — The suggested model depicts melatonin’s signaling function in conferring salt stress resistance in plants. By being exposed to salinity, Na⁺ produces ROS, which activates antioxidant and non-antioxidant enzymes as well as melatonin. Melatonin activates antioxidant and non-antioxidant enzymes, as well as, increases SOS and NHX activities. SOS transports excess Na⁺ to the extracellular space using the plasma membrane proton gradient. NHX on the vacuole tonoplast contributes to Na⁺ homeostasis (created using Inkscape software ver.1.2.2). Na⁺/H⁺ exchanger1 (NHX1); Salt overly sensitive1 (SOS1); Salt overly sensitive2 (SOS2); Ascorbate peroxidase (APX); Superoxide dismutase (SOD); Catalase (CAT); Peroxidase (POD); Glutathione peroxidase (GPX); Glutathione reductase (GR); Glutathione transferase (GST)