**3.5 Ethylene**

Ethylene is an important signaling molecule and a gaseous phytohormone. Its coordination with downstream signaling components has been reported to help plants in varyingly tolerating salinity stress [104–106]. Induction of ethylene generation in salinity-exposed plants is indicative of its significance as a downstream signal and modulation of gene expression [104]. Ethylene-homeostasis and ethylene signaling have been argued as an important factor required for plant-salinity tolerance [107, 108]. The maintenance of cellular ethylene (via endogenous productioninduced accumulation and/or by exogenously supplied of ethylene precursor, 1-aminocyclopropane-1-carboxylic acid) has been reported to enhance Na<sup>+</sup> and K<sup>+</sup> homeostasis and induce downstream signaling for ROS-homeostasis; and eventually to improve plant salt tolerance [109–111]. Earlier, ethylene-mediated improvement in *Arabidopsis* salt tolerance mainly involved enhanced retention of K<sup>+</sup> in shoots and roots rather than decrease in tissue Na<sup>+</sup> content [112]. Ethylene (or its biochemical precursor, 1-aminocyclopropane-1-carboxylic acid) supplies improved plant tolerance to high salinity [110, 113–115]. Ethylene can trigger plant salt tolerance by modulating polyamine catabolism enzymes associated with H2O2 production [116]. S-nitrosylation of ACO homolog 4 (1-aminocyclopropane-1-carboxylate oxidase homolog 4; ACOh4) improved ethylene synthesis and improved salt tolerance in salinity-exposed tomato plants [117]. The roles of S-adenosylmethionine (SAM, involved in ethylene biosynthesis) and its derivatives in plant salt tolerance have also been recently discussed [118].

Molecular studies have unveiled the 'MdNAC047-ETHYLENE RESPONSE FACTOR (MdERF3)-ethylene-salt tolerance' regulatory pathway in apple [108]. Apple *MdERF4* was reported to negatively regulate salt tolerance by inhibiting *MdERF3* transcription [119]. *MdMYB46* enhanced salt (and osmotic) stress tolerance in apple by directly activating stress-responsive signals [120]. Additionally, plant responses to salt stress may also involve EIN3/EIL1-dependent genes and other ROS scavenger-coding genes [110]. The outcomes of crosstalk between *miR319* and ethylene contribute to plant-salinity tolerance. To this end, overexpression of *Osa-MIR319b* and targeting mimicry form of *miR319 (MIM319*) confirmed the role of *miR319*-mediated positive regulation of ethylene synthesis, and eventually improved salinity tolerance in switchgrass (*Panicum virgatum*) [121]. However, negative roles of ethylene have also been reported in salinity-exposed plants, where enhanced ethylene levels did not help plants in counteracting salinity stress impacts [122–124]. Thus, the reported few ambiguous roles of ethylene in plant-salinity stress responses require further explanations.

## **3.6 Gibberellins**

Gibberellins (gibberellic acid, GA), a large family of tetracyclic di-terpenoid compounds, are classical plant hormones denoted largely by 'gibberellin numbers' (GAn) in order of discovery, such as GA1, GA2, …, GAn. In general, GAs are involved in growth and development [125, 126]. However, the literature is full on the involvement of GA in plant tolerance to a number of abiotic stresses [96, 126, 127]. In salinity-exposed barley, exogenous GA3 increased the shoot and root length of germinated barley seeds; significantly reduced ion-leakage, osmolyte (proline) accumulation; and thereby rescued the expression of the *HvABI5*, *HvABA7,* and *HvKO1* by 3, 10, and 33 fold, respectively [128]. Exogenously applied GA enhanced growth and salinity stress tolerance in *Z. mays* by modulating the morpho-physiological, biochemical, and molecular attributes [129]. Moreover, GA3-supply improved pigment content, plant growth, and development, reduced Na+ concentration in shoots and roots, increased the water absorption and metabolic activities in seeds, uplifted the seed dormancy, modulated cell division, and cell elongation. In this way, GA3-supply increased the growth of root, shoot, and number of leaves; increased photosynthetic activities and the dry matter production; maintained a fine-tuning among AsA-GSH cycle components; improved the plant height, yield, and yield-related traits, Ca2+ and K<sup>+</sup> concentrations, and transpiration rates; and decreased Na<sup>+</sup> concentrations in different test plants under salinization [129–133].

As reported in plants under most abiotic stresses, a higher accumulation of DELLA proteins was reported in salinity-exposed plants, which in turn was argued to restrain growth and enhance stress tolerance through reducing GA signaling activity [134, 135]. Seed priming with GA was reported to induce high salinity tolerance in *Pisum sativum*, where the applied GA modulated antioxidants, secondary metabolites, and upregulated antiporter genes [136]. Moreover, pre-treating/soaking of seeds with GAs was widely evidenced to improve increased α-amylase; salinity-caused nutritional disorders; decreased Na+ content; enhanced ion uptake, photosynthesis, and redox homeostasis; improved coordination among CAT, APX, and SOD, as an adaptive mechanism to salt stress [137–140].

### **3.7 Jasmonic acid**

Important critical signaling molecule jasmonic acid (JA) is among the most abundant members of the jasmonate class of plant hormones. Derived from linolenic acid (as cyclopentanone) and lipids, JA is known to regulate plant growth, development, and stress responses [45, 141]. Extensive reports are available on the role (and underlying mechanisms) of JA-mediated plant-salinity tolerance. Methyl jasmonic acid supply shifted the endogenous fatty acid levels and supported *O. sativa* growth in saline soil [142]. Transcriptomic analysis has revealed methyl jasmonate-mediated salt tolerance in alfalfa (*Medicago sativa*) as a result of antioxidant activity regulation and ion homeostasis [99]. JA-supply mediated mitigation of the inhibitory effect of salt stress in *T. aestivum* by increasing the endogenous levels of CK and IAA, reducing ABA contents, increasing α-tocopherol, phenolics, and flavonoids levels, and triggering SOD and APX activity [143]. In salinity-exposed *Anchusa italica*, methyl jasmonate improved test plant-salinity tolerance by enhancing contents of photosynthetic pigment, soluble sugars, K+ and Ca2+, declining Na+ content, and eventually improving the major growth attributes [144]. Salinity stress-mediated induction in endogenous JA is also known in plants [145, 146]. Interaction outcomes of JA with ABA can also improve plant-salinity tolerance [141, 147]. JA-mediated saline stress tolerance in *O. sativa* involved autophagy and programmed cell death as critical pathways [148]. Jasmonate biosynthesis gene *OsOPR7* was involved in the mitigation of salinityinduced mitochondrial oxidative stress [149]. Conferment of a greater cell elongation under salt stress was achieved with mutations of JA-receptor CORONATINE

INSENSITIVE1 (COI1) and MYC2/3/4 along with the stabilized JASMONATE ZIM mutant jaz3-1 [150].

## **3.8 Nitric oxide**

A highly versatile gaseous, free-radical, redox-signaling molecule, nitric oxide (NO), has been widely reported to perform diverse functions in plants [15, 151]. In a wide range of studies on salinity-exposed plants, exogenous supply of NO (or sodium nitroprusside, SNP; a NO donor) improved seed vigor, germination, and plant health and productivity through alleviating oxidative damage as a result of decreased levels of electrolyte leakage, MDA, and H2O2, improving antioxidant defense mechanism, decreasing methylglyoxal toxicity, and upregulating the glyoxalase system, adjusting the levels of osmolytes, and maintaining ionic balance [16, 152–154]. NO-supply can also reverse the glucose-mediated photosynthetic repression in plants under salinity exposure [154]. In NO (0.1 mM SNP)-mediated *T. aestivum* seed priming (for 20 h) helped improve germination rate, the weight of radical and coleoptile, and K+ ion and Na<sup>+</sup> ion homeostasis [155, 156]. Exogenous application of NO (or its donor, SNP) can increase leaf area, plant dry mass, and the lengths of shoot and root in NaCl-stressed plants [157, 158]. Additionally, the maintenance of ion homeostasis (via enhanced K+ uptake and reduced Na+ uptake) and the modulation of the Na+ /H+ antiporter enzyme were also reported in salinity-exposed and NO (or its donor, SNP)-supplemented test plants [159]. NO-mediated high salt tolerance in plants may also involve a NO-accrued increase in H<sup>+</sup> -ATPase activity and eventual reduced leakage-mediated maintenance of high cytosolic K+ /Na+ ratio [156, 160]. NO-mediated improved defense against saltinduced stress also involves NO's interaction with signaling molecules [15]. In earlier studies, NO (or its donor, SNP)-supply mediated improvements in the photosynthetic capacity involved NO-mediated protection of photosynthetic pigments; maintenance of normal shape of thylakoids and increase in chloroplast size; enhancement in the quenching of additional energy and quantum-yield of photosystem II; increase in ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCO) activity; induction in the influx and efflux of Ca2+; regulation of stomatal behavior and guard cells-ABA concentration; and efficient energy dissipation [158, 161–163].

The asA-GSH cycle is a central modulator of the plant stress responses and defense, ROS metabolism, and cellular redox balance [26, 164]. A plethora of reports supports the role of NO in the maintenance of the cellular redox balance via regulation of AsA-GSH cycle components (enzymatic and non-enzymatic) in salinityimpacted plants [123, 165, 166]. In different salinity-exposed plants, NO (or its donor, SNP)-supply resulted in significantly decreased cellular O2 •− generation, H2O2, MDA content, and electrolyte leakage via maintaining a fine-tuning among antioxidant enzymes (including SOD, CAT, APX a H2O2-scavenging enzyme, MDHAR, DHAR, GR, GST, GPX, and CAT) and non-enzymatic antioxidants (including GSH and AsA) [15, 16, 151, 167].
