The photochemical reactions occurring in the thylakoid membrane of the chloroplast are the primary site for ROS-mediated oxidative damages provoking inequality in the electron flow from oxygen-evolving complex (OEC) to photosystem II (PSII) (Janda et al., 2012). Inhibition/decrease in photosynthetic rate could be attributed to the reduction of Phospholipase D (PLD) activity which may ultimately affect Ribulose Bisphosphate Carboxylase/Oxygenase (RUBISCO) activity (Wani et al., 2017). Recent exploration demonstrated the involvement of SA in regulating PLD activity under stress conditions which sequentially activates phosphatidic acid (PA), thereby modulating vital metabolic processes (Janda et al., 2012). SA-mediated amelioration of photosynthesis and electron transfer by modulating the activity of either PLD or PA has been observed in Arabidopsis thaliana, Brassica napus, and Glycine max under stress conditions (Liu L. et al., 2016; Liu Z. et al., 2016; Wani et al., 2017). SA is believed to activate PLD or PA under stress conditions by triggering transcriptomic changes in the host organisms causing activation of several PLD-dependent genes such as PR-1 and NPR1 (Kalachova et al., 2013). Further, SA is also known to stimulate Phosphatidylinositol-4-Kinase (PI4K), resulting in the formation of Phosphatidylinositol-4-Phosphate (PI4P) and phosphatidylinositol-4-5-bisphosphate, thereby enabling the activity of RUBISCO (Kalachova et al., 2013). In several plants, including Arabidopsis thaliana, both endogenous and exogenous SA (0.5 and 1.0 mM) has modulated the expression of phosphatidylinositol-4-5-bisphosphate under heat stress resulting in enhanced accumulation of PLDs and RUBISCO synthesis (Janda et al., 2015).

Exogenous application of SNP has been reported to rebuild various physiological and biochemical processes in plants, including photosynthesis (Prochazkova et al., 2013). Foliar application of SNP at lower concentrations has stimulated chlorophyll synthesis in several crop plants, including Solanum lycopersicum, Solanum tuberosum, and Lactuca sativa (Prochazkova et al., 2013). Treating plants with a higher concentration of SNP has resulted in the decreased level of photosynthesis enzyme and thus limiting photosynthesis rates in Medicago sativa, Glycine max, and Phaseolus vulgaris (Liu et al., 2014). To decipher the mechanism of how exogenous NO regulate photosynthesis in plants, NO hypersensitive mutants were created and genetically screened in Arabidopsis thaliana (Lozano-Juste and León, 2010). Among all the mutants created, six exhibited mutation on single locus NOX1 (NADPH oxidase 1), a close homolog of CUE1 (Chlorophyll a/b binding unexpressed 1). The CUE1 is responsible for synthesizing chloroplast phosphoenolpyruvate/phosphate translocator, which is involved in various physiological processes and NO production in plants (Lechon et al., 2020). These NOX1 (CUE1) mutants displayed intense disorganization of chloroplast phosphoenolpyruvate/phosphate translocator, which suppressed vital physiological processes, including photosynthesis and electron transport system (Lechon et al., 2020). Additionally, NOX1 (CUE1) mutants exhibited late flowering compared to non-mutant counterparts, as the former have elevated NO levels due to increased synthesis (Yun et al., 2016). The NOX1 (CUE1) mutants generated in other model plants per se., Medicago truncatula and Lotus japonicus, have also shown reduced growth of floral meristem due to downregulation of key gene LFY (LEAFY) and CO (Co-regulator) (Parankusam et al., 2017). Recent findings in Arabidopsis thaliana have shown that the expression of both LFY and CO genes is in the same oscillatory circadian rhythm path as NOX1 and NOS1 (Parankusam et al., 2017). Thus, the above findings strongly indicate NO's involvement in the regulation of photosynthesis, flowering, and various other vital processes in plants.

Researchers have shown that an increase in auxin level or signaling decreases SA signaling and vice-versa (Iglesias et al., 2011; Miura and Tada, 2014). Krizek et al. (2016) further validated this hypothesis, who observed improved photosynthesis and relative water content in auxin-insensitive mutant's arx2-1 and double mutant's aintegumenta-like 6 (ail6) exhibiting increased SA levels. Furthermore, Arabidopsis thaliana plants with altered Wallsarethin 1 (WAT1) protein synthesis improved secondary cell wall and development due to enhanced SA in both roots and shoots compared to auxin level (Miedes et al., 2014). Similarly, cotton plants mutated for WAT1, WAT2, and WAT3 genes showed robust expression of ICS1, resulting in enhanced accumulation of SA under pathogen attack (Tang et al., 2019). Arabidopsis thaliana plants over-expressing SA-inducible DNA binding with One Finger (DOF) protein stimulated OBF Binding Protein (OBP3) TF that significantly improved root and shoot growth by preventing membrane damage and maintaining ion/osmotic homeostasis (Song et al., 2016). SA signaling can also activate the Target of Rapamycin (TOR) signaling pathways, which are highly conserved in plants associated with growth and developmental processes (Schepetilnikov and Ryabova, 2018). TOR signaling pathways have been widely reported to improve ion transition, nutrient transition, and protein synthesis, thus improving the growth and reproduction of crop plants (Schepetilnikov and Ryabova, 2018).

In plants, cGMP has been widely reported to perform a central role in the growth and developmental pathways, including NO signaling (Silveira et al., 2016). Researchers have actively documented NO-mediated cGMP synthesis modulated the expression of defense-related genes including PR-1 and PAL in transgenic tobacco plants under pathogen attack (Charrier et al., 2012; Chun et al., 2012). Recently, studies have also postulated that cGMP and cyclic adenosine 5'-diphosphoribose (cADPR) strongly influence NO synthesis in plants (Sanz et al., 2015). The exogenous application of SNP showed prevention toward membrane damage by regulating the level of thiobarbituric acid reactive substances and plant relative water contents under stress conditions (Rai et al., 2018a,b, 2020a). The cGMP-cADPR-NO triad has been shown to participate in various signaling pathways, including the abscisic acid pathway, which modulates vacuolar ryanodine receptor (RYR) like proteins to stimulate the biosynthesis of membrane proteins (Khan et al., 2014). Additionally, both cGMP and cADPR pathways function synergistically to regulate the NO biosynthesis to activate RYR like proteins and other genes/proteins of the defense pathway.

A large body of literature has documented the role of SA (low concentration) in stimulating growth-related processes and immunity in plants either independently or by interacting/modulating with other phytohormones and signaling molecules. Interestingly, studies have also postulated that most SA regulators do not have a specific DNA/protein motif to stimulate SA biosynthesis. How these regulators regulate SA biosynthesis still seems farfetched (An and Mou, 2011). Which raises a big question how SA-mediated growth-immunity trade-off can be circumvented in a way that makes it possible to breed disease resistance plants without causing a significant reduction of their growth? To answer this question, a forward genetics approach was undertaken by creating loss of function mutants for SA-analog benzothiadiazole non-responsive to bth (nrb) in Arabidopsis thaliana (van Butselaar and Van den Ackerveken, 2020). These SA-analog suppressor mutants showed increased growth but lost their immune response to specific pathogens (Caarls et al., 2017). A similar observation was made for Hydroxycinnamoyl Transferase (HCT)-RNAi sid2-1 and TOR-overexpression lines in Oryza sativa. The SA deficient mutants also exhibited enhanced performance growth and productivity by compromising their innate immune response (van Butselaar and Van den Ackerveken, 2020).

Additionally, studies have also indicated the role of NPR1 in stimulating the growth, productivity, and immunity of rice plants by modulating endogenous SA levels in response to pathogen attacks (Dinler and Tasci, 2020). However, NPR1 independent SA signaling requires activation of WRKY TFs to induce defense response in plants (Gao et al., 2018). The mechanism by which SA activates WRKY TFs is still unclear; however, it has been postulated that the master regulator of SA signaling, i.e., NPR1 undergoes a series of redox-dependent modifications (Li et al., 2020). One such modification involves the activation of thioredoxins which reduces intermolecular disulfide bonds in NPR1, thus causing a conformational change in its monomeric form and activating the expression of WRKY and other TFs (Gao et al., 2018). Another aspect by which SA modulates the growth and yield of crop plants without imperiling immunity is activating the Ideal Plant Architecture 1 (IPA1) gene that encodes squamosa binding protein (Zhang et al., 2020a,b). In rice and Arabidopsis thaliana, site-directed mutagenesis of Os-Sporocyteless 14 (OsSPL14) variant downregulated the expression of miRNA156, which in turn activated the transcription of Isopentenyl Adenine 1D (IPA1D) that improved the immunity, and yield of rice plants against biotic stress (Yin et al., 2019).

Similarly, a large body of evidence has confirmed that S-nitrosoglutathione (GSNO) is considered NO reservoir in plants that can modulate a variety of peptide and protein nitrosylation (Gupta et al., 2011; Corpas et al., 2013; Begara-Morales et al., 2018). This S-nitrosylation, in turn, affects the expression of various downstream genes, TFs, and activity of different intracellular and extracellular enzymes (Corpas et al., 2013). To decipher NO's role in stimulating growth-immunity trade-off, NO deficient mutants were created in Arabidopsis thaliana that showed impaired growth and development and early senescence compared to wild plants. Intriguingly, exogenous NO application to the above mutants markedly improved their growth by regulating the expression of SAG12 and SAG13 compared to their wild counterparts (Shanmugam et al., 2015). The increased accumulation of SAG proteins could be due to the increased nitrosylation of GSNO reductase (GSNOR), leading to enhanced GSNO production (Lindermayr et al., 2010). Again, to test this hypothesis, Antisense RNA-mediated silencing of GSNOR was executed in Arabidopsis thaliana. Their results showed that the lower production of S-nitrosothiols (SNO) was responsible for decreased growth and enhanced susceptibility to pathogenic attack (Bogdan, 2015). Furthermore, in Pisum sativum and Oryza sativa, NO is also known to stimulate growth and yield by regulating the level of methyl-jasmonate (Fancy et al., 2017). Most recently, researchers have confirmed that sequential reduction of NO in Pisum sativum plants showed decreased accumulation of NOS gene, which ultimately resulted in reduced growth and yield (Yadu et al., 2017). Additionally, NO deficient Arabidopsis thaliana mutants created for Nitric Oxide Synthase and Nitric Oxide-Associated 1 (NOS1/NOA1) showed stunted growth and early senescence wild plants as a result of increased accumulation of SAGs (Shen et al., 2013). Recent findings have indicated that NO also acts as a negative regulator of ABA biosynthesis genes such as 9-cis-epoxycarotenoid dioxygenase (NCED9) and a positive regulator of cytokinin biosynthetic genes such as isopentenyl adenine (IPT1) and zeaxanthin reductase (ZR) (Kong et al., 2016). Evidence has also documented the role of both SA and NO in stimulating pollen growth and in flowering by modulating the transcription of Constans (CO), Leafy (LFY), and Flowering Locus C (FLC). Previous findings have reported that NO can regulate the expression of the above genes by activating several TFs, including MADS-box TFs (Falak et al., 2021). These MADS-box TFs orchestrate Ca²⁺ level, which triggers calmodulin (CaM) protein, thus oscillating growth and natural circadian rhythm in plants under stress conditions (Falak et al., 2021).

Raymond F. White first incepted involvement of SA in plant immunity in 1979, where he demonstrated that the application of acetyl-SA (aspirin) protected Nicotiana tabacum plants against viral infection. Further, in-depth characterization revealed that the SA-mediated accumulation of PR proteins boosted Nicotiana's innate immunity (Fragniere et al., 2011). Later, researchers advocated that plant defense response against pathogen attack is mediated by developing a hypersensitive reaction that triggers the release of SA, thus curbing pathogen penetration and spread (Wani et al., 2017). Controversially, some researchers have postulated that plants over-accumulating a salicylate hydroxylase (NahG) encoding gene negatively regulates SAR and causes SA depletion in plant tissues (Janda and Ruelland, 2015). Likewise, a study conducted by Vos et al. (2015) also confirmed that SA failed to induce insect resistance in plants as an egg laid by an insect on a plant's leaf dramatically accelerated SA accumulation that impaired Jasmonic acid (JA) mediated resistance against pathogens. However, some studies have disapproved the above notion and concluded that insect' egg could stimulate the development of SAR, which helps control microbial populations associated with plant roots, thus boosting plant immunity (Cui et al., 2019). SAR development is often positively regulated by SA-mediated signal perception proteins NPR1 and NPR2 and negatively regulated by NPR3 and NPR4. Recently, Li et al. (2021) reported that priming Vitis vinifera plants with β-aminobutyric acid (BABA) induces the expression of NPR1, NPR3, and Heat Shock Proteins 24 (HSP24), thus providing defense against the necrotrophic fungus Botrytis cinerea.

Similarly, Yildiz et al. (2021) confirmed that the mobile SAR signal induced by treating Arabidopsis thaliana plants with N-hydroxypipecolic acid (NHP) stimulated NPR1 mediated transcriptional reprogramming of Flavin-dependent Monooxygenase 1 (FMO1) and other downstream genes, thus systematically activating an immune response against pathogenic attack. The role of plant natural product NHP in activating immune response has been identified more recently (Yildiz et al., 2021), which is synthesized directly from pipecolic acid catalyzed by FMO1 in a series of transamination/reduction steps mediated by SARD-4 and AGD2-like defense response protein (ALD1). SA-mediated activation of NPR1 has also been shown to stimulate the ubiquitination of several cytoplasmic proteins by forming SA-induced condensates (SINC). These SINCs are rich in stress proteins that trigger ETI by facilitating programmed cell death and SAR (Li et al., 2021). The fundamental role of NPR1 and NPR2 homologs in conferring viral resistance have also been identified and characterized in Cymbidium orchids (Ren et al., 2020), thus indicating SA-induced NPR proteins act as a central hub for modulating the expression of defense-related genes.

NO has also been shown to induce PTI and ETI, thereby stimulating programmed cell death, causing inactivation of pathogenic proteins by increasing the synthesis of cryptogenic and initiating global reprogramming of gene expression (Martínez-Medina et al., 2019a). Researchers have well-corroborated that NO and RNS mediated S-nitrosylation of cysteines residues unequivocally control NO function (Nurnberger and Kemmerling, 2018). In plants, S-Nitrosylation is either catalyzed by thioredoxin or the GSNOR system, both of which strengthen the plant's immune response (Martínez-Medina et al., 2019a). Studies have also confirmed that plants displaying higher GSNOR activity are more resistant to powdery or downy mildew pathogens (Jahnova et al., 2020). In addition, treating potato plants with the inducers of SAR showed a steep increase in GSNOR activity and increased immunity against hemibiotrophic oomycete Phytophthora infestans (Jedelska et al., 2021). Another study has been undertaken to validate the role of GSNOR in imparting pathogenic resistance by generating GSNOR/NOX1 mutant in Arabidopsis thaliana. The mutants showed decreased basal resistance to Pseudomonas syringae and increased S-nitrosothiol levels which could be the main reason behind the abolition of NO-mediated resistance (Xu et al., 2013). RNA interference (RNAi) studies have also confirmed that the higher NO levels have a growth stimulatory effect on a fungal pathogen such as Aspergillus niger, Monilinia fructicola, and Penicillium italicum (Thalineau et al., 2016). Recently, researchers have confirmed the synergistic relation between NO and phytoglobins in plants exposed to pathogenic attacks. They concluded that an increase in NO levels induces the expression of phytoglobins 1 (PHYTGOB1) in tomato roots, thus generating immune system and defense response (Martínez-Medina et al., 2019a). Further, exogenous application of pipecolic acid (Pip) to barley leaves, in turn, activates GSNOR activity leading to the development of SAR, thereby reducing the toxic effect of P. syringae (Lenk et al., 2019).

The function of master regulator NPR1 has been extensively implicated in regulating SA/JA mediated redox signaling, which is known to suppress the JA-responsive pathway at the level of initiation of gene transcription (Van der Does et al., 2013; Caarls et al., 2015). Several recent studies have indicated that SA induced monomerization, reduction, and translocation of NPR1 to the nucleus can suppress JA signaling by differentially regulating F-box protein Coronatine-insensitive-Isoleucine 1 (COI1) and Jasmonate ZIM domain (JAZ) repressor proteins (Van der Does et al., 2013; Song et al., 2015). The activated JAZ repressor proteins in the absence of JA get associated with Topless (TPL) repressor protein by novel interactor of JAZ (NINJA) or Histone Deacetylase 6 (HDA6) adaptor protein causing transcriptional inactivation of MYC, Ethylene Insensitive 3 (EIN3), and EIN Like 1 (EIL1) (Vos et al., 2013). However, in the presence of bioactive JA, the master regulator COI1 binds with JA-Ile that initiates proteolytic degradation of JAZ repressor proteins, thereby activating JA-responsive genes (Van der Does et al., 2013). Conversely, researchers have documented SA receptors activated JA signaling to stimulate effectors triggered immunity via the non-canonical pathway (Liu L. et al., 2016). They further indicated that the canonical pathway was established upon SA accumulation sensed by NPR3 and NPR4, thus activating JA signaling by differentially regulating the expression of JAZ repressor proteins and COI1-mediated genes (Liu L. et al., 2016). Additionally, Kloth et al. (2016) performed transcriptome analysis to decipher the role of WRKY22 TF in regulating SA/JA signaling. Their results indicated that ectopic expression of WRKY22 and WRKY 29 induces SA/JA signaling, thereby conferring resistance to Arabidopsis thaliana against the biotrophic pathogen. Similarly, a study conducted by De Vleesschauwer et al. (2016) also corroborated the above notion where the role of DELLA protein Slender Rice 1 (SLR1) stimulated SA/JA-mediated defense signaling, which conferred hemibiotrophic resistance to rice plants. Recently, integrated transcriptome analysis revealed the coordinated role of SA/JA-mediated defense signaling regulated growth and immunity in poplar plants against Melampsora larici-populina, Septoria musiva, and Marssonina brunnea (Luo et al., 2019).

The signaling molecule NO has also been reported to induce JA signaling in plants by activating key JA biosynthesis enzymes such as Allene Oxide Synthase (AOS) and Lipoxygenase 2 (LOX2), thereby triggering a cascade of defense response (Huang et al., 2004). Furthermore, researchers have also well-indicated NO-mediated elicitation of jasmonate biosynthesis stimulated the expression of a wide range of JA-responsive genes such as LOX3, 12-oxophytodienoate reductase 1, 2, and 3 (Mur et al., 2013). Additionally, NO is integrated into JA signaling either by NO-mediated initiation of SA biosynthesis or by activating the ICS1 gene and TGA TFs. Subsequently, SA induces the production of thioredoxins that causes monomerization of NPR1 within the nucleus and, after binding to TGA via ORA59 promoter, suppresses JA signaling (Mur et al., 2013). Another notion is upon infection with necrotrophic pathogen or attacker, enhanced endogenous level of NO induces the expression of LOX3 and 12-oxo-phytodienoic acid (OPDA) reductase (OPR) 1,2, and 3, which causes transcriptional activation of JA biosynthetic genes (Mur et al., 2013). Correspondingly, NO-mediated activation of the ascorbate-glutathione cycle upon exogenous application of JA conferred drought stress tolerance in wheat seedlings, thereby confirming the synergistic interaction of NO/JA signaling in improving plant growth and immunity (Shan et al., 2015). NO-mediated stimulation of jasmonate-dependent basal defense response conferred resistance to tomato plants against root-knot nematode (RKN) by increasing the expression of Protease Inhibitor 2 (Zhou et al., 2015). Studies have also shown that enhanced endogenous levels of NO causes downregulation of JAZ repressor proteins JAZ1 and JAZ10 in the meristematic root regions, thereby improving root architecture and stomatal apparatus in transgenic Arabidopsis thaliana (Barrera-Ortiz et al., 2018; Yastreb et al., 2018). Recently, a study conducted by Avila et al. (2019) confirmed the synergistic role of NO/JA in stimulating defense response in Solanum quitoense plants against F. oxysporum, thereby suggesting the activation of the corresponding signaling pathway by both defense priming compounds.

Elucidation of crosstalk between SA and ABA in stress signaling pathways has become the center of attraction among plant biologists. Increasing evidence has well-recognized ABA stimulates defense response and improves growth and developmental processes in plants (Jiang et al., 2010). Congruently, SA also boosts plant immunity against many biotic/abiotic stresses, thereby positively impacting plant growth and development. However, researchers have demonstrated SA and ABA work antagonistically where SA antagonizes ABA signaling components at both cellulars and transcriptional levels by regulating the activity of Pyrabactin Resistance 1/PYR1-Like Regulatory Component of ABA Receptor (PYR/PYL/RCAR) (Manohar et al., 2017). Further, studies have shown that SA antagonizes ABA signaling by differentially regulating type 2C Protein Phosphatase (PP2C), PP2A, and SnRK2s (Sucrose nonfermenting 1-Related subfamily 2 protein Kinase) which are essential for initiating ABA signaling in plants under stress conditions (Manohar et al., 2017). A large body of literature has revealed the antagonistic relationship between SA and ABA signaling pathway. For example, Meguro and Sato (2014) reported that exogenous application of SA inhibited ABA signaling, affecting shoot growth by downregulating the genes involved in the cell cycle in rice plants.

Similarly, many researchers have also implicated that exogenous application of SA antagonizes ABA-responsive genes by suppressing key ABA signaling components such as ABA1, ABA2, RD29A, thereby suppressing the growth of mutant plants compared to their broad type (Manohar et al., 2017). Correspondingly, several studies have also demonstrated a synergistic relationship between SA/ABA where Horváth et al. (2015) observed upregulation of ABA biosynthesis genes such as Zeaxanthin Epoxidase (SlZEP1), 9-Cis-Epoxycarotenoid Dioxygenase (SlNCED1), and Aldehyde Oxidases (SlAO1 and AlAO2) in SA treated plants exposed to salt stress. Likewise, Saleh et al. (2020) reported that both SA and ABA modulate the expression of various stress-responsive genes and TFs, thereby conferring salt stress tolerance to Vitis vinifera plants. Similarly, co-ordinated signaling of both SA and ABA was found to activate the Ca²⁺/CPK-dependent mechanism that triggers an immune response in Arabidopsis thaliana plants exposed to a biotrophic pathogen, thereby preventing stomatal closure (Prodhan et al., 2018). Recently, Park et al. (2021) observed that SA-stimulated ROS accumulation in drought exposed plants stimulated ABA signaling genes such as MYC2 and NCED3, activating Ca²⁺dependent defense response in a distinct phase of drought exposure.

NO metabolism instigates cellular and biochemical reactions to mechanistically regulate ABA homeostasis by modulating ABA-responsive genes such as PYR/PYL/RCAR, PP2C, and SnRK2 (Neill et al., 2002). Additionally, NO-mediated PTMs such as tyrosine nitration and S-nitrosylation have been positively correlated with the regulation of the NCED enzyme, which is central for ABA biosynthesis and NO accumulation (Lozano-Juste and León, 2010). Furthermore, in Arabidopsis thaliana, the cytochrome P450-707A2 (CYP707A2) gene has been well-documented to regulate ABA catabolism and NO biosynthesis, thereby releasing seed dormancy (Lozano-Juste and León, 2010). However, researchers have also corroborated that NO might negatively modulate ABA signaling in guard cells by down-regulating Open Stomata 1 (OST1) and SnRK2 genes via NO-mediated PTMs (Wang et al., 2015). Further, they also concluded that impairment of NO-mediated PTMs in gsnor1-3 mutant exaggerated NO accumulation in guard cells leading to S-nitrosylation of SnRK2 and dysfunction of ABA signaling (Wang et al., 2015). Likewise, Wang et al. (2015) reported that exogenous application of NO breaks seed dormancy and was also influential in alleviating the inhibitory effect of ABA on seed germination by simulating NO-mediated PTMs, which may have resulted in the inactivation of SnRK2. Phytoglobins inactivation in drought-stressed Zea mays plants exhibited low ABA levels that induced cell death in developing embryos. However, exogenous application of ABA reverses this effect causing activation of phytoglobins in Zmpgb1.1 suppressing line with increased accumulation of NO (Kapoor et al., 2018). Conversely, exogenous application of NO and ABA coordinatively regulated various defense-related genes/TFs, thereby conferring PEG-induced drought stress tolerance in Brassica plants (Sahay et al., 2019).

Low molecular weight organic compound polyamines are ubiquitously present in all lifeforms. They can induce a hypersensitive response in plants upon interaction with the pathogenic attacker and stress conditions (Szepesi, 2011). The PAs which are most commonly accumulated in the plant kingdom are putrescine (Put), spermidine (Spd), and spermine (Spm). Several studies have demonstrated that PA biosynthesis and signaling are regulated upon interaction with other phytohormones perse, SA, and NO (Szepesi, 2011). For example, exogenous application of SA modulated PA biosynthesis in maize and tomato plants by increasing the activities of crucial biosynthesis enzymes arginine decarboxylase (ADC) and ornithine decarboxylase (ODC) (Zhang et al., 2011). Likewise, exogenous application of SA and Spm compellingly enhanced the expression of several antioxidant enzymes, metabolites, and defense-related genes that ultimately improved photosynthesis, root/shoot dry weight, and growth of Echinacea purpurea, tomato, maize, oat, and plum plants (Szalai et al., 2016; Takács et al., 2016; Darvizheh et al., 2018, 2019; Canales et al., 2019; Koyuncu et al., 2019). Recently, Pal et al. (2019) also reported that treating wheat dwarf mutant created for reduced height (Rht1 and Rht3) with exogenous polyamine significantly boosted polyamine metabolism, growth, and development of mutant plants by stimulating SA and ABA signaling. Likewise, Liu et al. (2020) also confirmed the above notion where Put was responsible for ROS-mediated activation of SA-signaling, which triggered ETI and SAR in Arabidopsis thaliana by enhancing the accumulation of EDS1 and NPR1 genes in response to pathogen attack.

Recently, NO and PA has emerged as an essential player in regulating growth and defense signaling pathways in plants (Wimalasekera et al., 2011). Studies have concluded that exogenous application of PA-induced NO signaling via unknown mechanisms, thereby stimulating a plethora of physiological and biochemical responses to ameliorate stress-induced oxidative damage in wheat and Arabidopsis thaliana (Diao et al., 2017). Additionally, the concerted action of NO and PA stimulates biosynthesis of various metabolites, antioxidants, and ROS and RNS, thereby regulating plant responses against environmental alterations (Wimalasekera et al., 2011). One of the possible mechanisms by which PA induces NO biosynthesis was deciphered by Agurla et al. (2018), where NO and ROS were over accumulated in response to PA-induced stomatal closure in Arabidopsis thaliana. They identified that PA-induced oxidative burst resulted from enhanced activity of NADPH oxidase and amine oxidase where ROS acted as upstream of NO production by modulating NOS-like activity, thereby completely reversing the inhibitory effect of PA on stomatal closure (Agurla et al., 2018). Similarly, exogenous application of melatonin, a pleiotropic signaling molecule, regulated PA metabolism and NO biosynthesis, and all three in a coordinative manner alleviated heat-induced oxidative damage in tomato seedlings (Jahan et al., 2019b). Likewise, Tailor et al. (2019) also reported that exogenous application of NO significantly enhanced intracellular Spm as evidenced by upregulation of PA biosynthetic enzymes arginine decarboxylase, S-adenosylmethionine decarboxylase, thereby conferring salt tolerance to sunflower seedlings.

Methylglyoxal is a short-oxygenated aldehyde released as a by-product of aerobic metabolisms such as glycolysis and the pentose phosphate pathway (Li, 2016). When synthesized at a higher level, MG can disrupt the array of physiological and biochemical processes in plants leading to loss of critical cellular functions and, in some cases, may induce a detrimental effect on plant survival (Li, 2016). MG detoxification is catalyzed by the glyoxalase (Gly) pathway, i.e., Gly I and Gly II, that efficiently convert MG into non-toxic molecules, reducing its adverse effect on plant growth and development (Li, 2016). Fewer studies have been conducted to analyze crosstalk between SA and MG detoxification signaling in regulating plant growth and immunity against environmental cues (Kaur et al., 2016). A study indicated that SA antagonizes selenium-induced oxidative damage in rice plants by stimulating the activities of enzymatic and non-enzymatic antioxidants along with GlyI and GlyII enzymes that limited the detrimental effect of MG on rice plants (Mostofa et al., 2020). Likewise, exogenous application of SA improves the growth and immunity of Brassica rapa plants under salt stress conditions by regulating the ASH-GSH cycle and MG detoxification system (Kamran et al., 2020). Similarly, SA mediated NO accumulation and signaling counters As-induced toxicity in maize plants by modulating enzymatic and non-enzymatic defense systems and glyoxalase pathway enzymes (Kaya et al., 2020).

NO crosstalk with MG involves the regulatory function of GSH, where increased synthesis of GSH due to enhanced accumulation of NO may be involved differential regulation of MG detoxification system and consequently enhancing oxidative stress tolerance in plants (Mostofa et al., 2018). Increasing evidence has corroborated the above notion. Researchers have observed and linked NO-mediated GSH signaling to play a critical regulatory role in modulating MG and glyoxalase systems in plants (Mostofa et al., 2018). For example, exogenous application of NO enhances antioxidative defense response and methylglyoxal detoxification system in wheat seedlings, thereby improving their growth and development under salinity stress (Hasanuzzaman et al., 2011, 2017). Moreover, Nahar et al. (2016) reported that crosstalk between PA and NO exerted an antagonistic effect on cadmium-induced oxidative stress in mung bean plants by modulating defense-related pathways' critical enzymes glyoxalase defense system.

Furthermore, NO's exogenous application mitigates nickel-induced oxidative damage in eggplants by regulating antioxidant defense system, osmolyte accumulation, and MG detoxification system (Soliman et al., 2019). The study analyzed crosstalk between NO and hydrogen sulfide to stimulate resilience in maize plants exposed to heavy metal stress. The researchers observed that both NO and hydrogen sulfide effectively ameliorated chromium-induced oxidative damage in maize plants by controlling excess ROS generation, MG production, improving membrane integrity, and enzymatic and glyoxalase system (Kharbech et al., 2020).

Strigolactones, a butanolide-class of multifunctional phytohormones derived from the carotenoid catabolism pathway, regulate many plant functions under stress conditions (Torres-Vera et al., 2014). SL is exclusively synthesized in roots and the shoot downstream of carotenoid catabolism, where carlactone is the critical precursor for its biosynthesis (Torres-Vera et al., 2014). Strikingly, researchers have also documented the involvement of SL in regulating nodule formation, mycorrhizal colonization, and mediating plant-microbe interaction (Marzec and Muszynska, 2015). Conversely, Marzec and Muszynska (2015) highlighted the first report for SL's possible involvement in conferring stress tolerance. They observed that SL biosynthesis was enhanced upon pathogen infection, which differentially modulated defense response in Arabidopsis thaliana and O. sativa plants by activating the defense system under the tight control of SA and JA signaling. Later, several researchers indicated that SA acts synergistically to SL and initiates SL biosynthesis by stimulating the expression of critical genes [More Axillary Growth (MAX1, MAX3, and MAX4)] involved in SL production. Various researchers corroborated the above notion. They identified that mutant plants infected with Rhodococcus fascians showed decreased accumulation of SL, causing leafy gall syndrome compared to wild-type plants (Stes et al., 2015).

Interestingly, studies have shown that enhanced expression of MAX2 was observed upon ROS accumulation, thereby inducing oxidative damage in mutant plants compared to wild-type plants where the level of MAX2 was in control (Walter, 2020). Similarly, exogenous application of SA and GR24 (a synthetic analog of SL) stimulated transcriptional activation of SL biosynthetic genes, thereby conferring drought tolerance in wheat cultivars by regulating the antioxidative defense system (Sedaghat et al., 2017, 2020). Moreover, the positive role of SL in stimulating plant defense against fungal pathogens such as Botrytis cinerea, Alternaria alternata, and Meloidogyne incognita has also been demonstrated in SL biosynthetic mutant tomato plants upon interacting with other phytohormones such as ABA, SA, and JA (Aliche et al., 2020).

The interplay between NO and SL was deciphered only recently by Bharti and Bhatla (2015). They treated sunflower seedlings with GR24 that causing a significant reduction in lateral and adventitious root formation, calcium signal, PIN protein distribution, and root NO level. In addition, they also observed a two-fold increase in SL-biosynthetic enzymes in the presence of NO scavenger cPTIO, thus suggesting antagonistic relation between NO and SL. This hypothesis was further confirmed by Manoli et al. (2016). They also observed that exogenous application of NO down-regulates SL-biosynthetic genes by stimulating S-nitrosylation of NO biosynthetic enzymes, thereby activating PIN-dependent auxin regulation and cell differentiation. In this continuation, Sun et al. (2016) demonstrated that NO was the critical signaling mediator in regulating root growth and SL signaling in rice plants grown under nitrogen and phosphorus limiting conditions. They confirmed that SL inhibitor abamine significantly reduced root length in wild-type plants which were reversed by applying NO.

Moreover, the implication of SL and NO in regulating important plant function was also observed by Lv et al. (2018). They confirmed SL signaling played a significant role in stimulating NO and H₂O₂ production, thereby initiating stomatal closure in the Arabidopsis thaliana in an ABA-dependent manner. They further concluded that SL-related mutants showed an enhanced stomatal opening. In contrast, exogenous application of SL could induce stomatal closure by regulating essential genes of guard cell ABA signaling such as MAX2 and Slow Anion Channel-Associated 1 (SLAC1) (Lv et al., 2018). The interactive role of SL and NO was also recently analyzed by Olah et al. (2020), where they reported that mutant Arabidopsis thaliana plants (max1-1 and max2-1) showed reduced SL synthesis and enhanced NO and S-nitrosothiol levels due to reduced expression of GSNOR protein, thus strengthening root architectural system of Arabidopsis thaliana.