Interestingly, the inoculation with SA03 notably promoted the NO accumulation in the stress-treated plants accompanied by the increased cellular ABA levels. However, FLU exposure notably repressed the NO biosynthesis under saline–alkaline stress. It has previously been indicated that NO plays crucial roles in abiotic stress response and tolerance in plants, which is combined with ABA and other hormones (León et al., 2014). Moreover, NO acts as downstream signals of ABA to regulate salt tolerance in plants by activating antioxidant enzymatic activities and Na+/H+ antiporters (Zhang et al., 2009). Recently, NO has also been found to regulate Fe deficiency responses by remobilizing cell wall Fe and provoking the FIT1-mediated signaling pathways (Graziano and Lamattina, 2007; Chen et al., 2010; Wang et al., 2017). Thus, NO may function as a secondary messenger of ABA to activate diverse adaptive mechanisms that alleviate adverse effects caused by saline–alkaline stress. In this study, the inoculated plants treated with c-PTIO shared the resemblance in phenotypic traits and alteration of physiological parameters with the FLU-treated inoculated plants under the stress. Intriguingly, c-PTIO exposure did not markedly down-regulate the expression of Fe transport-related genes in the inoculated plants compared with the FLU-treated inoculated plants, although no significant difference in shoot Fe concentrations was observed between the c-PTIO- and FLU-treated plants under saline–alkaline stress. Previous studies have indicated that NO not only regulates FIT1-mediated IRT1 and FRO2, but also can chelate Fe from cell wall (Chen et al., 2010). It is well known that about 75% of Fe is deposited in root cell walls, which are severed as largest reservoir for apoplastic Fe (Bienfait et al., 1985). Fe deficiency can trigger rapid accumulation of NO to invoke Fe uptake and reutilize cell wall Fe (Graziano and Lamattina, 2007). These indicated that inhibition of NO biosynthesis blocked plant uptake of Fe from rhizosphere soils and remobilization of apoplastic Fe from roots to shoots under Fe deficient conditions. This may explain the reason that the FLU-treated inoculated plants had high-level expressions of Fe transport-related genes under saline–alkaline stress, which could not lead to the increase in shoot Fe concentrations. Therefore, the SA03-induced stress tolerance of plants mainly attributed to the ABA-mediated NO signaling pathways.