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Sodium chloride (NaCl) induced expression of a jacalin-related mannose-binding lectin (<i>JRL</i>) gene in leaves, roots, and callus cultures of <i>Populus euphratica</i> (salt-resistant poplar). To explore the mechanism of the <i>PeJRL</i> in salinity tolerance, the full length of <i>PeJRL</i> was cloned from <i>P. euphratica</i> and was transformed into Arabidopsis. PeJRL was localized to the cytoplasm in mesophyll cells. Overexpression of <i>PeJRL</i> in Arabidopsis significantly improved the salt tolerance of transgenic plants, in terms of seed germination, root growth, and electrolyte leakage during seedling establishment. Under NaCl stress, transgenic plants retained K⁺ and limited the accumulation of Na⁺. <i>PeJRL</i>-transgenic lines increased Na⁺ extrusion, which was associated with the upward regulation of <i>SOS1</i>, <i>AHA1</i>, and <i>AHA2</i> genes encoding plasma membrane Na⁺/proton (H⁺) antiporter and H⁺-pumps. The activated H⁺-ATPases in <i>PeJRL</i>-overexpressed plants restricted the channel-mediated loss of K⁺ that was activated by NaCl-induced depolarization. Under salt stress, <i>PeJRL</i>&#8315;transgenic Arabidopsis maintained reactive oxygen species (ROS) homeostasis by activating the antioxidant enzymes and reducing the production of O₂^&#8722; through downregulation of NADPH oxidases. Of note, the <i>PeJRL-</i>transgenic Arabidopsis repressed abscisic acid (ABA) biosynthesis, thus reducing the ABA-elicited ROS production and the oxidative damage during the period of salt stress. A schematic model was proposed to show the mediation of PeJRL on ABA response, and ionic and ROS homeostasis under NaCl stress.