**6. NO-phytohormone cross talk under other abiotic stresses**

stomatal closure involved JA and H2

reduced H2

O2

NO, ABA, PAs, and H2

O2

O2

126 Phytohormones - Signaling Mechanisms and Crosstalk in Plant Development and Stress Responses

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

tion 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

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

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*

increase in ABA level has also been reported in cellular culture of *Chlorella vulgaris* [117].

accumulation through NO generation; however, direct evidences of NO interac-

to modulate various physiological and stress responses under low

signaling that triggered NO levels [106] and Ca2+ and

Ever increasing human population and industrial productivity has resulted in alarming rise in air pollutants, causing extensive damages to natural habitats of plant [131]. Ozone is characterized as one of the most phytotoxic air pollutants severely restricting plant growth and development [132]. Plants use many transportable chemical signals such as NO to turn the sensing of ozone from guard cells to adjacent epidermal and mesophyll cells [133]. Presumably, NO generation in relation to ozone stress induces ET and ABA synthesis and interferes with stomatal ABA response, potentially by inhibiting K+ efflux at the guard cells [134]. The involvement of alternative oxidase (*AOX*) in the inhibition of ozone-induced toxicity has also been demonstrated to require both NO- and ET-dependent pathways [135]. Interestingly, Rao and Davies [136] observed that NO treatment caused leaf injury due to increased levels of ozoneinduced ET production. Both SNP and ozone treatment up-regulated the expression of the ET biosynthesis related genes (*ACS6* and *ACC oxidase*), which correlates with ET formation [137]. In *Arabidopsis*, exogenous NO supply in combination with ozone stress was noted to attenuate the induction of SA biosynthesis and other defense-related genes [132].

Destruction of ozone layer in upper atmosphere, as a result of increased concentrations of air pollutants, has exposed living organisms to UV-radiation particularly UV-B that induces oxidative stress in plants [138, 139]. Although it is well known that NO interacts with ABA, ET, MeJA to control guard cell signaling in response to various environmental stresses [140, 141], only few reports are available with regard to NO, ET, and ABA cross talk in stomatal regulation under UV-B stress [142]. Studies involving *Lactuca sativa* seedlings showed that exogenous NO supply (using SNP as a NO donor) prevented UV-B induced inhibition of GA and IAA synthesis [143]. NO stimulated decrease in SA and ABA levels was found to be associated with reduced H2 O2 and malondialdehyde contents. In contrast, coordinated action of NO and SA was observed to reduce UV-B stress in *Triticum aestivum* seedlings [144].

A transient NO burst is among the earliest responses to wounding [145]. NO production in wounded parts involves several pathways including cross talk with signaling cascades of hormones and endogenous signals [146, 147]. It was shown that NO and AUX actively take part in wound-healing response in plants [145, 148]. Imanishi et al. [149] presented evidence for the involvement MeJA and mechanical wounding in expression of the *Ipomoelin* gene (*IPO*) in sweet potato. Later, Jih et al. [150] demonstrated that SNP-derived NO delayed wounding-induced *IPO* expression, providing evidence for antagonistic association between NO and JA. In *Arabidopsis*, NO treatments led to elevated expression of key enzymes of the octadecanoid pathway, like *LOX2, AOS, or OPR3,* in wounded leaf epidermis [151]. However, this induction did not influence JA responsible genes, like PDF*1.2*, hence supporting the earlier evidences about NO and JA association. NO-induced wound-responses could act as a modulator of cell death initiation together with H2 O2 accumulation, and delay of IPO-expression [152]. Contrasting reports in *Lycopersicon esculentum* demonstrated neither wound-induced NO burst, nor NO-induced elevation of endogenous SA levels [153]. Moreover, SNP-derived NO inhibited the expression of the proteinase inhibitors *Inh1, Inh2*, cathepsin D inhibitor (*CDI*), and metallocarboxypeptidase inhibitor (*CPI*) and increased *AOS* or *LOX* activity. Nevertheless, these studies demonstrate clearly that induction of a wound-response in plants involve cross talk among various stress signaling molecules.

Initiation of senescence in plants is controlled by various factors such as nutrient supply, light conditions, leaf age, and environmental stress [154]. Plant hormones such as ET and CK influence senescence by either promoting or delaying the process, respectively [155, 156]. Evidence supports the interaction of NO with other plant hormones to floral senescence and fruit maturation [157]. Recently, Ji et al. [158] demonstrated that SA treatment at low concentrations induced NOA1-dependent NO signaling and activated antioxidant defense to counteract MeJA-induced leaf senescence. NO plays a conceivable role to counteract the ABA- and jasmonate-induced senescence in rice by inhibiting H2 O2 accumulation and lipid peroxidation [159]. Mishina et al. [160] found that delayed leaf senescence in *Arabidopsis* involves NO-induced reduction in SA levels. During fruit ripening, NO cross talk with SA and ET involves the regulation of levels of secondary metabolites such as anthocyanins [161]. NO-induced suppression of cell wall softening related enzymes such as polygalacturonase (PG), pectin methylesterase (PME), and pectate lyase (PL) was found to delay softening and ripening of stored *Carica papaya* by reducing ABA, IAA and zeatin ribose (ZR) levels [123].
