**5. NO-phytohormone cross talk under temperature stress**

Temperature stress negatively influences the vegetative and reproductive growth phases of plants. Coordinated action between NO and plant hormones (ABA, JA, GA, CK) induce thermotolerance in plants by activating the antioxidant machinery and up-regulating the expression of genes encoding heat shock proteins [104–106]. Studies involving *Arabidopsis* mutants impaired in ABA biosynthesis (*aba1-1*) and signaling (*abi 1-1*) showed that drought and heat stress induced stomatal closure involved JA and H2 O2 signaling that triggered NO levels [106] and Ca2+ and SLAC1 function [107, 108]. However, SA antagonized JA function to induce stomatal opening in *abi1-1* [106]. In *Phragmites communis*, ABA treatment triggered NOS activity and increased NO levels that improved the thermotolerance of plant calluses [109]. Treatment of *Stylosanthes guianensis* seedlings with ABA stimulated the activities of CAT, SOD, and APX suggesting that ABA-induced NO generation leads to the production of antioxidant enzymes [110]. Evidence supports the antagonist relationship between SA and ET in improving heat tolerance in plants by increasing proline contents and enhancing photosynthetic-NUE [111]. SA cross talk with AUX, ET, JA, and BR has been demonstrated in specific bioassays [112]. SA triggered increase in GST activity was noted to induce heat stress tolerance in *Zea mays* [113]. Presumably, SA reduced H2 O2 accumulation through NO generation; however, direct evidences of NO interaction with plant hormones (SA, GA, AUX, BR, and JA) in improving plant heat stress tolerance are lacking. BRs are also thought to interact with ABA, SA, and ET to induce heat stress signaling through complex networks [114, 115]. BR treatment of *Brassica napus* seedlings subjected to short-term heat shocks was noted to enhance endogenous ABA concentration [116]. BR induced increase in ABA level has also been reported in cellular culture of *Chlorella vulgaris* [117].

Low temperature severely restricts plant growth and causes both structural and metabolic damages in plants [118]. Exposure to low temperature induces oxidative and nitrosative stress thereby promoting NO synthesis [119], which serves as a potential link between PA and ABA to induce stress responses in plants [120]. Literature indicated extensive cross talk among NO, ABA, PAs, and H2 O2 to modulate various physiological and stress responses under low temperature conditions [110, 121]. Interplay among NO, SA, and ABA was noted to enhance the antioxidative activities (CAT, SOD, POX) that contributed to improved chilling injury in *Zea mays* seedlings [122]. Guo et al. [123] found that coordinated action between NO and ABA up-regulated cold-induced *MfSAMS1* expression, resulting in enhanced acclimation against cold stress in *Medicago sativa* subsp*. falcata*. Moreover, expression of *MfSAMS1* altered the levels of Spm, Put, and Spd and activities of PAO and copper-containing amine oxidase, which regulate anti-oxidant machinery during cold acclimation. Exogenous NO supply increased Put and Spd levels and stimulated the expression of genes encoding Spd synthase (*LeSPDS*), arginine decarboxylase (*LeADC. LeADC1*), and ornithine decarboxylase (*LeODC*) to improve chilling stress tolerance in *Lycopersicon esculentum* leaves. However, the expression of genes encoding Spm synthase (*LeSPMS*) and *S*-adenosylmethionine decarboxylase (*LeSAMDC*) was not influenced by NO treatment [121]. Reports of Li et al. [124] showed that NO treatment converts Put into Spd or Spm to confer cold tolerance in *Zingiber officinale* seedlings. Pretreatment of *Orzya sativa* seedlings with various ammonium concentrations decreased the effects of cold stress by increasing Put and Spd contents [125], suggesting the possible involvement of NO in stress tolerance. In a recent article, Wang et al. [126] reported the coordinated action of NO and PAs to induce chilling tolerance in cold-stored banana. NO treatment increased the activities of PAO, diamine oxidase (DAO) and glutamate decarboxylase (GAD), leading to γ-aminobutyric acid (GABA) accumulation to prevent chilling injury in fruits.

NR and NOS pathway are the most widely known NO sources in plants [19, 127]. Evidence obtained by Aydin and Nalbantoğlu [128] showed that SA pretreatment of *Spinacia oleracea*

leaves influenced NR activity to induce chilling stress tolerance. A recent study indicated the involvement of JA in NO synthesis that increased CAT activity to scavenge H2 O2 , leading to reduced chilling injury in *Cucumis sativus* [129]. Therefore, it is concluded that NO cross talk with other hormones safeguards the quality of stored fruits and vegetables. Another study on NO revealed that it increases the expression of *MaCAT, MaPOD, MaSOD,* and *MaAPX* genes to alleviate damages caused by low temperature in banana (Wu et al. [75]). In *Elymus nutans*, interaction between NO and 5-aminolevulinic acid (ALA) stimulated antioxidant defense to reduce chilling injury [130]. Further investigations involving influence of NO on BR, CK, JA, and ET pathways are suggested which would provide important information about signaling cascades of these regulatory substances in cold stressed plants.
