Auxins-Interkingdom Signaling Molecules

*Aqsa Tariq and Ambreen Ahmed*

### **Abstract**

Phytohormones play a fundamental role in the development of plants. Among various phytohormones produced by the plants, Auxins act as a master hormone that plays a major role during plant development and differentiation through cell division. Besides plants, many rhizospheric microorganisms are also capable of producing auxins specifically indole-3-acetic acid (IAA), that act as signaling molecules for the regulation of gene expressions in plants. However, bacterial IAA is majorly linked with the modulation of plant roots architecture and developing positive plant-microbe interactions. Bacterial auxin modifies root morphology by enhancing root length, forming adventitious root and root hair, thereby, increasing surface area for water and nutrient absorption affecting various aspects of plant biology in a number of ways. Bacteria mostly utilize tryptophan, present in plant root exudates, to synthesize IAA that eventually helps bacteria to colonize roots by establishing beneficial associations with plant roots. Auxins also stimulate the formation of exopolysaccharides and biofilms that help bacterial root colonization. Auxins have given the survival benefit to rhizobacteria that make them more competent to establish symbiotic interaction with plants. Synergistic and antagonistic interactions of auxins (both interkingdom and Intrakingdom) with other phytohormones play a key role in plant development and growth improvement.

**Keywords:** Auxins, bacterial IAA, phytostimulation, Indole-3-acetamide, Tryptophan

### **1. Introduction**

Auxins are mainly synthesized in meristematic tissues and transported to other plant parts. Auxins play a critical role in controlling various processes during growth and development across variable environmental conditions, even at lower concentrations, these can modulate gene expression by interacting with specific proteins involved in the transcription process [1]. The plant rhizosphere is enriched with a diversity of microflora that directly contributes to their growth. The rhizosphere microbiota has the ability to produce phytohormones as a signaling molecule for inter and intraspecies communications. The synthesis and release of auxins establish a mutualistic or morbific link between organisms. Indole-3-acetic acid (IAA) is a widely produced rhizobacterial signaling phytohormone. Primarily, auxin controls various physiological processes, such as cell division, elongation, phototactic, and geotactic responses, in plants [2]. Thus, in nature, plants are receiving endogenous and exogenous signals simultaneously influencing their developmental patterns. Endogenous auxin can either be free (active auxin) or act as storage intermediates

as conjugated compounds with amino acids and sugars [3]. Since higher auxin levels cause inhibitory effects, therefore, homeostasis and coordination of auxin signaling within plants and their surroundings are necessary for their regular growth and development. Endogenous auxin levels suggest the type of interactions between plant and rhizobacteria. Generally, three possible plant-bacterial IAA associations have been stated so far, first, due to direct transfer of bacterial IAA genes into host cell; second, due to bacteria living and releasing IAA within plant tissues and lastly, due to bacteria colonizing plant surfaces and producing IAA [4]. The first two associations usually result from pathogenic interactions. The knowledge of deciphering these signals and their outcomes is critical for the development of strategies for sustainable agricultural practices. Thus, the present chapter highlights the significant role of bacterial IAA as a potent microbial signaling molecule regarding beneficial plant-rhizobacterial interactions which are important for ecological resilience and sustainability.

### **2. Biosynthetic pathways of auxins**

Conferring to key intermediate compounds, five different pathways for IAA synthesis have been reported in bacteria using tryptophan precursors [5]. Rhizobacteria use tryptophane either from plant root exudates or synthesize through chorismate precursor using trp gene by shikimate pathway [6, 7]. Rhizobia are an example of rhizobacteria that utilize host tryptophan for IAA synthesis [8]. Zhang *et al*. [9] analyzed 7282 prokaryotic genomes and revealed that 82.2% were efficient IAA producers from tryptophan precursors. However, Brown and Burlingham [10] observed a low amount of auxin in bacterial cultures without tryptophan indicating the fact that bacteria might have the ability to synthesize auxin without using tryptophan [11, 12]. Later, this was confirmed by the studies of Prinsen *et al*. [13] who reported the ability of IAA production by *Azospirillum brasilense* following tryptophan-independent pathway. However, there is a lack of information regarding genes, enzymes, or proteins involved. Recently, Li *et al*. [14] and Ahmad *et al*. [15] have also reported IAA biosynthesis in the absence of an exogenous tryptophan supply in Arthrobacter pascens ZZ21 and *Micrococcus aloeverae* DCB-20, respectively, however, no genetic evidence has been provided so far. Moreover, more than one auxin biosynthetic pathway functions within plants and bacteria together [9, 14].

*In vitro* production of IAA was observed to be highly influenced by bacterial growth conditions and the presence of tryptophan [16–18]. Higher auxin production by bacterial strains has been observed under increasing tryptophan concentrations [19]. Moreover, the genetic elements involved in the regulation of bacterial IAA have been demonstrated in *A. brasilense*. The key gene involved in this process is *ipdC* gene. Moreover, increased expression of *ipdC* gene was observed under increasing IAA levels indicating the involvement of auxin signaling in regulating its biosynthesis, a positive-feedback regulation. *In silico* analysis revealed that *RpoN* binding site is responsible for regulating the expression of *ipdC* gene [20]. Various transcriptional factors influencing *ipdC* gene expression have been identified in different bacterial species. Patten and Glick [21] described RpoS to regulate ipdC transcription in *Pseudomonas putida* and *P*. *agglomerans*, respectively. Similarly, *GacS/GacA* system has been identified in *Pseudomonas chlororaphis* as a negative regulator of tryptophan-dependent routes of IAA production [22]. Ryu and Patten [23] identified *TyrR* protein to regulate the induction of *ipdC* gene expression in Enterobacter cloacae in response to tryptophan. A high similarity of various auxin synthetic pathways has been observed between plants and bacteria with slightly

#### *Auxins-Interkingdom Signaling Molecules DOI: http://dx.doi.org/10.5772/intechopen.102599*

different intermediate products. An overview of various auxin biosynthetic pathways has been given below:

**Indole-3-acetamide (IAM) pathway**: It involves two steps, conversion of tryptophan to Indole-3-acetamide by tryptophan-2-monooxygenase followed by conversion to IAA by IAM hydrolase [4]. The phytopathogens, such as *Agrobacterium tumefaciens*, *Pantoea agglomerans,* and *Pseudomonas syringae,* and some plant growthpromoting rhizobacterial (PGPR) genera, such as Rhizobium and Bradyrhizobium, have exhibited this pathway [7, 24].

**Indole-3-pyruvic acid (IPyA) pathway**: It involves three steps, first formation of Indole-3-pyruvic acid by aminotransferase occurs followed by decarboxylation into indole-3-acetaldehyde which is finally oxidized into IAA (**Figure 1**). The key enzyme in this pathway is identified as indole-3-pyruvate decarboxylase (encoded by ipdC gene) [4]. This pathway is present in a broad range of bacterial species from phytopathogenic bacteria (*P. agglomerans*) to PGPR (*Pseudomonas*, *Azospirillum*, *Enterobacter*, *Bacillus*, *Paenibacillus*, *Bradyrhizobium*, and *Rhizobium*) and even in cyanobacteria [7, 25].

**Tryptamine (TAM) pathway**: It involves decarboxylation of tryptophan to tryptamine which is then converted into indole-3-acetaldehyde by amine oxidase

#### **Figure 1.**

*Various tryptophan-dependent and -independent pathways for auxin (IAA) synthesis. Red lines indicate the tryptophan-independent pathway of IAA synthesis. Black lines show tryptophan-dependent pathways. Chorismate is the precursor of both mechanisms. [A- trans - aminotransferase; Trp dec - tryptophan decarboxylase; Am oxi - amine-oxidase; IPDC - Indole-3-pyruvate decarboxylase; IAM-hyd - Indole-3 acetamide hydrolase; Nitril - Nitrilase; IAAid dehyd – Indole-3-acetaldehyde dehydrogenase].*

followed by its oxidation to IAA [4]. This has been reported in Bacillus cereus and *Azospirillum* [7, 24].

**Indole-3-acetonitrile (IAN) pathway**: In this pathway, tryptophan is converted into Indole-3-acetonitrile either by indolic glucosinolates or indole-3-acetaldoxime which is then further converted into IAA by nitrilase. This pathway has also been reported in *Alcaligenes faecalis*, *A*. *tumefaciens*, and *Rhizobium* spp. [7, 24].

**Tryptophan side-chain oxidase (TSO) pathway**: This is found in Pseudomonas fluorescens CHA0 and involves direct conversion of tryptophan to indole-3-acetaldehyde which then oxidizes to IAA. This mechanism is only found in bacteria and has not been studied in plants (**Figure 1**) [7, 24].

### **3. IAA – Signaling molecule**

a.Intrakingdom Signaling

Auxins modulate the gene expression making it inter and intrakingdom communicating chemical messenger and quorum-sensing molecule. Scott *et al*. [26] observed bacterial chemotaxis toward IAA in *P. putida*. This movement is mediated by methyl-accepting proteins that receive and transmit IAA signals to flagellar machinery [26]. Hence, the movement of PGPR toward plant roots might be due to IAA present in root exudates. This IAA also acts as a nutrient pool, thereby, chemotaxis toward IAA ensures bacterial survival within the plant environment. Moreover, the fact that most of the plant-associated rhizobacteria produce IAA indicates that IAA might have some crucial role in bacterial cells other than interacting with plants [27]. From an evolutionary perspective, bacteria gain this ability for their survival and persistence within the plant environment [28]. IAA producers are more environmentally adaptive and competitive as compared to non-producers. Studies by Bianco *et al*. [29] showed that IAA confers protection to bacteria under various abiotic conditions, such as acidity, UV, salt, and heat stress. The author observed higher production of extracellular polysaccharides (EPS), lipopolysaccharides, and biofilms in IAA overproducers that improved bacterial adherence to plant surfaces which ultimately protect bacterial cells from various environmental stresses. Moreover, overproduction of trehalose in IAA producers has been observed indicating the accumulation of osmolytes within the bacterial cell to confer osmotic protection [29]. This was further confirmed by the studies of Donati *et al*. [30]. They reported a higher survival rate of IAA-treated bacteria under oxidative, desiccation, and osmotic stress and observed increased production of EPS and biofilm. Under various stress conditions, increased IAA levels were observed within bacterial cells indicating the fact that IAA plays important role in modulating gene expression of bacterial cells and making them more competitive [31]. However, the exact mechanism is still unknown and needed to be explored. IAA also acts as a signaling molecule for various metabolic processes within bacterial cells. Van Puyvelde *et al*. [32] observed the overall changes in gene expression of a mutant strain of *A. brasilense* and noted the decreased expression of 39 genes, including the genes involved in bacterial cell respiration by affecting the expression of NADH dehydrogenase. However, on the other hand, increased expression of the nitratereducing system involved in aerobic denitrification and ATP-binding cassette transporters and tripartite ATP-independent periplasmic (TRAP) transporters was also observed. Van Puyvelde *et al*. [32] also noted increased expression of T6SS (Type VI Secretion System) by exogenous IAA induction which is involved in the transport of various components via injection tube from a bacterial cell to

#### *Auxins-Interkingdom Signaling Molecules DOI: http://dx.doi.org/10.5772/intechopen.102599*

plants cell (the mechanism by which bacteria interact directly to plant signaling pathways). Moreover, IAA also enhances the expression of genes involved in the formation of effector proteins of T3SS (Type III Secretion System) required for injection of pathogenicity within plant cells [33].

### b.Interkingdom Signaling

Signal exchange between plant and rhizospheric bacteria occurs through the release of root exudates [34]. This signaling is key for developing and determining the nature of plant-bacterial interactions (symbiotic or pathogenic). PGPR colonization is the result of these signaling activities. Besides IAA synthesis, many rhizobacterial species have the ability to degrade IAA. This IAA degrading ability has given the advantage to bacteria for rhizospheric colonization and manipulating plant physiology for their survival. However, the mechanism of how IAA degradation is beneficial for plants and bacteria is not well studied and needed to be explored. Zuniga *et al*. [35] observed that IAA degradation by *Burkholderia phytofirmans* is key for efficient rhizosphere colonization and subsequent plant growth promotion. Any mutation in IAA degrading gene (iacC) also affects the growth promotional activity of the bacteria. In addition, auxin also interferes with the developmental pathways of the host. So, it is hypothesized that rhizobacteria synthesize and secrete auxin that is taken up by plants in such quantities that alter normal plant developmental pathways [36]. The principal feature of bacterial IAA reported by researchers is to manipulate the plant root growth (**Figure 2**). It induces the formation of root hair and enhances the growth of primary and lateral roots within their optimum range. However, at higher concentrations, it causes inhibitory effects and ceases the primary root growth [37]. It is suggested that this larger root system besides helping the host plant, also benefits its associated bacterial species and a larger root system absorbs more nutrients and strengthens the bacterial survival within the plant vicinity [38]. Moreover, IAA is considered to have a parallel role in developing and maintaining plant-rhizobacterial interactions [39]. In the

#### **Figure 2.**

*Interaction of root exudates to attract various auxin-producing plant beneficial bacteria leading to various metabolic activities within bacteria and making them more competent to colonize rhizosphere. Plants also uptake bacterial auxin that interacts with other phytohormones to control overall plant development.*

symbiotic association between rhizobia and legumes, the formation of macroscopic nodular structures on the roots of the host plant is considered to be formed by the action of auxin signals. Flavonoids accumulated at the sites of rhizobial entry to plant roots, inhibit auxin efflux resulting in auxin accumulation that causes excessive cell division leading to the formation of root nodules. Hence, the initiation of nodule formation is triggered by auxin signaling. Moreover, the specification of founder cells for nodule formation is also triggered by inhibition of auxin transport. Similarly, the formation of vascular bundles and the number of nodules also depend on long-distance auxin signaling. Hence, it has been hypothesized that auxin signaling triggers the formation of nodules on roots of host plants [38, 40]. Besides initiation of root nodules, IAA also modulates bacterial metabolic pathways involved in the conversion of bacteria to bacteroids for nitrogen fixation within nodules. For example, Bianco *et al*. [29] observed the activation of tricarboxylic acid and polyhydroxybutyrate cycle in *Sinorhizobium meliloti* by exogenous IAA application and in IAA-overproducer mutants (RD64). Theunis [41] observed high auxin levels in nodulated roots than in non-nodulated roots. High IAA levels also interact with nitrogen-fixing bacterial ability and enhance the nitrogen levels in nodules. In addition, the studies of Huo *et al*. [42] experimentally proven that reduction of IAA transporter genes (PIN) results in reduced nodulation. Moreover, rhizobacterial IAA also interacts with the hormonal metabolism of its associated plants. It is reported to promote the transcription of 1-aminocyclopropane-l-carboxylic acid (ACC) synthase enzyme in plants to catalyze the production of ACC deaminase enzyme which converts ACC to ammonia and α-ketobutyrate resulting in lower ethylene levels of plants. Consequently, by lowering plant ethylene levels, rhizobacteria can reduce the effect of ethylene on root growth causing plants to get nutrients and water under a wide range of stress conditions [43]. In addition, auxin signals also influence other phytohormones to regulate various plant processes. Auxin and brassinosteroids coordinate and interact to regulate the development of plant roots. Similarly, it also regulates gibberellin responses by interfering with the stability of DELLA proteins. Lower auxin levels caused reduced synthesis of gibberellins due to stabilization of DELLA proteins. Cytokinins, contrarily, have been known to suppress root formation. Therefore, overall plant growth and development depends on signaling crosstalk between auxin and other phytohormones to determine the final physiology of plants [37].

The role of bacterially produced IAA has been very significant in plant growth promotion and has been investigated by various researchers. Ahmed and Hasnain [19] studied auxin production ability and potential plant growth promotional activity of two gram-positive *Bacillus* strains and noted enhanced growth parameters, including root system and auxin content of treated plants. In another study, Fatima and Ahmed [44] investigated the role of IAA producing chromium resistant Sporosarcina saromensis and two species of Bacillus cereus on the growth of *Helianthus annuus* L. and observed an increase in plant growth parameters (shoot length, root length, fresh weight, and a number of leaves) and auxin content in treated plants. Auxin-producing bacteria stimulate seed germination and root proliferation leading to the enhanced and well-developed root system of the host plant to have greater access to water and nutrients [45]. IAA facilitates cell elongation by losing plant cell walls, thereby, increasing root length, nutrient uptake, and the release of root exudates. Enhancement in the root system of plants by exogenous application of IAA was elaborated by Vacheron *et al*. [46]. The author observed that exogenous IAA application significantly alters the root architecture of plants in a dose-dependent manner. Root growth is enhanced under optimum auxin conditions; however, higher IAA levels cease primary root growth and stimulate lateral

#### *Auxins-Interkingdom Signaling Molecules DOI: http://dx.doi.org/10.5772/intechopen.102599*

#### **Figure 3.**

*Root growth responses to various auxin levels.*


#### **Table 1.**

*Various signaling interactions of IAA.*

root growth and root hair formation. In Arabidopsis sp. greater number of lateral roots have been found in the presence of high auxin-producing *Phyllobacterium brassicacearum*, however, no effect on primary root was present. Higher levels of auxins trigger lateral root formation and initiate root hair formations. However, if the auxin concentrations in plant root do not reach optimum levels even after uptake of bacterial IAA, root growth remains unaffected. Low auxin-producing *A. brasilense* has not shown any improvement in the root growth of its associated plants [47]. Recent studies have also proven the hypothesis that bacterially produced IAA contributes toward phenotypic changes in the root architecture of treated plants (**Figure 3**) (**Table 1**) [54–56].

### **4. Conclusions**

Auxin is a key phytohormone controlling the whole physiology of plants by interacting and regulating other phytohormones as well. Besides plants, various rhizobacteria have the ability to produce auxins. Various auxin biosynthetic pathways act simultaneously to regulate auxin formation. These pathways in plants and bacteria are highly similar, however, the tryptophan side chain oxidase pathway is the mechanism found only in bacteria. The main precursor for auxin synthesis is tryptophan, however, tryptophan-independent routes are also present but these routes are not well described and need to be studied. Auxin besides controlling plant growth and development, also affects various regulatory processes in bacteria as well, making inter and intrakingdom cross-signaling interactions. In bacteria, auxin primarily supports bacterial survival by strengthening their stress tolerance mechanism and also enhancing colonizing ability. This also helps in bacterial rhizospheric competence making them more adaptive to the environment. As an interkingdom signaling molecule, auxins interact with various plant signaling mechanisms and coordinate various plant growth processes. Auxins directly affect plant root architecture helping plants for enhanced nutrient and water uptake even under various stress conditions. Plants under optimum auxin levels showed enhanced and prolonged root systems but higher levels of auxin do not increase root length instead initiate the formation of lateral roots and root hair. However, very low auxin levels do not show any effect on root growth. Thus, auxins exert a significant impact (either directly or indirectly) on the healthy development and growth of the plants in a coordinated manner.

### **Conflict of interest**

The authors declare no conflict of interest.

*Auxins-Interkingdom Signaling Molecules DOI: http://dx.doi.org/10.5772/intechopen.102599*

### **Author details**

Aqsa Tariq and Ambreen Ahmed\* Institute of Botany, University of the Punjab, Quaid-e-Azam Campus, Lahore, Pakistan

\*Address all correspondence to: ambreenahmed1@hotmail.com

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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#### *Auxins-Interkingdom Signaling Molecules DOI: http://dx.doi.org/10.5772/intechopen.102599*

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### **Chapter 2**

## Plant Hormones: Role in Alleviating Biotic Stress

*Nazima Rasool*

### **Abstract**

Plant hormones play a critical role in regulating plant developmental processes. Jasmonic acid, salicylic acid and brassinosteroids have been recently added to the list of plant hormones apart from auxins, gibberellins, cytokinins, abscisic acid and volatile hormone ethylene. Besides their regulatory role in plant development, plant hormones, ethylene, Jasmonic acid and salicylic acid play key roles in the plant defense response while as auxins, gibberellins, abscisic acid, cytokinins and brassinosteroids are known to modulate their effects. For an effective response to biotic stresses, the signaling pathways of different hormones are integrated at different levels enabling crosstalk between them. In this chapter, I will analyze how plant hormones signal defense response and interact with each other through crosstalk to regulate plant defense.

**Keywords:** plant hormones, disease response, biotic stress, hormone cross-talk

### **1. Introduction**

Plant productivity is threatened by biotic and abiotic stress. In order to feed the world population of over 7 billion at the moment, productivity needs to be safeguarded against biotic and abiotic stresses. Biotic stress is caused due to attacks of viruses, bacteria, fungi, nematodes and other pathogens and pests. Pathogens are usually categorized into biotrophs and necrotrophs. Although the former penetrate the epidermal cells, multiply inside the intercellular spaces and feed on the living host tissue the latter kill the host cells and then feed on the cell remains. Biotrophs are mostly host-specific, the nectrophs have a broader host range [1]. Agricultural intensification has already led to increased soil pollution and land degradation problems. Therefore, understanding the natural mechanisms of defense in plants against various kinds of stresses is important to exploit it in a sustainable and environment-friendly manner. Of the various mechanisms plants have developed to combat biotic stress, hormones are of primary importance. Plant hormones are biochemicals that are synthesized at one location in plants and bring about the desired effect at the same or different location, at unimaginably low concentrations. Plant hormones are diverse in their chemical nature and biological functions derived from amino acids (IAA, ethylene), lipids (Jasmonic acid), from the isoprenoid (cytokinins, gibberellins, abscisic acid etc) and chorismate (salicylic acid) pathways (**Figure 1**). There are many biomolecules that have been added to the list of plant or phytohormones of late, which include jasmonic acid (JA), salicylic acid (SA), strigolactones (SL), brassinosteroids (BR) and peptides, besides auxins (IAA), gibberellins (GA), abscisic acid (ABA), cytokinins (CK) and ethylene (ET) that have been there since a long time. Salicylic acid, jasmonic acid and ethylene play very important roles

#### *Plant Hormones - Recent Advances, New Perspectives and Applications*

#### **Figure 1.** *Pathways of hormone biosynthesis.*


*Plant Hormones: Role in Alleviating Biotic Stress DOI: http://dx.doi.org/10.5772/intechopen.102689*


**Table 1.**

*Role of various plants hormones in biotic and abiotic stress response.*

in plant biotic stress response [2] while as, auxins, abscisic acid and gibberellins etc. modulate it. An overview of the important roles of major plant hormones is presented in **Table 1**. The role of hormones in plant growth and development is largely known and mechanisms of their biosynthesis have been elucidated in the majority of the cases, what remains to be fully understood is their mediation of the defense response in plants. In this chapter, I discuss how these hormones mediate the plant defense response and also assess how their effects are modulated by other hormones.

### **2. The major players in the plant defense**

**Ethylene (ET)**: This is a gaseous hormone that is responsible for various functions in plants notably fruit ripening, flower senescence and abscission of leaves etc. In dark-grown seedlings ET causes inhibition of hypocotyls and root elongation, radial swelling of hypocotyls and exaggeration of the apical hook this is commonly called as the triple response [15, 16]. The role of ET in plant stress is very well known [17–19], it favors stress resistance over growth thereby increasing stress tolerance [20–23]. ET acts in cooperation with JA to present an effective defense response against necrotrophic and chewing insects [1, 24]. ET response involves a battery of ET receptors which, for example, in *Arabidopsis* (*Arabidopsis thaliana*) include ETHYLENE RESPONSE 1 (ETR1), ETR2, ETHYLENE RESPONSE SENSOR 1 (ERS1), ERS2 and ETHYLENE INSENSITIVE 4 (EIN4) [24–28]. Mutations in these lead to ET insensitivity and increased susceptibility to the necrotrophic pathogens [24, 29, 30]. ein3 and eil1 (ETHYLENE INSENSITIVE LIKE) double mutants are completely ethylene insensitive and these lacks the triple response, pathogen resistance and the ability to fully suppress ctr1 mutation [15, 31, 32]. CONSTITUTIVE TRIPLE RESPONSE (CTR) is the negative regulator of the ET pathway in absence of ET. When ET binds to ER anchored EIN2-protein

receptors, it causes dephosphorylation of the latter. This leads to cleavage of the C-terminal domain (EIN2-C) of the EIN2 [1, 15, 33, 34]. EIN2-C moves to the nucleus and triggers EIN3 and EIN3-like transcription factors, eliciting ET-mediated response [15]. Transcription of *ETHYLENE INSENSITIVE3* (EIN3) activates defense response by inducing expression of *ERF1* [19, 35]. Repression of EIN2 by CONSTITUTIVE TRIPLE RESPONSE (CTR1) is released after perception of ET by ETHYLENE RESPONSE 1 (ETR1) [19, 36]. ET release stabilizes EIN3/EIL1 levels [15]. At the same time, ET also decreases levels of EBF1/2 (EIN3 BINDING F-BOX 1) protein through suppression of translation of its mRNA in the cytosol promoted by EIN2-C [15, 37, 38] and by EIN2-dependent proteasomal degradation of EBF1/2 proteins [15, 39]. EIN3 leads to EBF1/2 expression providing a negative feedback loop to the ET signaling [1].

**Jasmonic acid ( JA):** Methyl jasmonate and its free acid jasmonic acid are collectively known as jasmonates. Jasmonic acid is the better known of the two while JA-Ile is the active form [1]. JA is a cyclopentane fatty acid that is synthesized from linolenic acid which is a common constituent of plant cell membranes [40]. JAs play a vital role in the various plant developmental processes including flowering, fruiting, senescence and secondary metabolism. These are known to be critically important in plant defense and abiotic stress response [41–43]. JA activates the antioxidant system, causes the accumulation of amino acids, and soluble sugars and regulates the stomatal opening and closing during abiotic stress [6, 44]. JA interacts with SA, ET and ABA during plant defense response [1, 4, 45]; its interactions with auxins, gibberellins and cytokinins during important development processes like root, stamen, hypocotyl, xylem development etc. are also well known [40]. The JAs affect both plant development and plant stress-resistance [46, 47].

Coronatine Insensitive Receptor (COI1) and JAZ (Jasmonate-ZIM domain) proteins mediate JA-signaling pathway [24, 48, 49]. The others involved in JA signaling include JASMONATE INSENSITIVE 1/MYC2 (JIN1/MYC2) and several members of the APETALA2/ETHYLENE-RESPONSIVE FACTOR (AP2/ERF) family [19, 50]. COI1 forms a part of the E3 –ubiquitin degradation complex as SCF COI1 complex. The SCF consists of Skp-1/Cullin/F-box. JAZ is a repressor of the JA response. SCF COI1 complex binds with JAZ repressors at higher JA concentrations and this leads to ubiquitination and degradation of JAZ mediated by 26S proteasome [1]. The JA signaling pathway may follow two paths one is the MYC pathway and another is the ERF pathway. Wounding and insect feeding induces the MYC branch which further involves MYC2, MYC3 and MYC4 - basic helix–loop–helix leucine zipper transcription factors [1]. In absence of JA-Ile JAZ proteins interact with JIN1/MYC2 and inhibit transcriptional regulation of JA-responsive genes [19]. Interaction of JAZ with MYC proteins competitively inhibits their interaction with the MED25 subunit of the Transcriptional Mediator Complex [1, 51]. This causes the expression of several JA responsive genes including VSP2 (vegetative storage protein), JA synthesis gene LOX2 and JA signaling repressor JAZ genes. ERF pathway is stimulated by necrotrophic pathogens. As the name indicates this branch is regulated by ET; AP2/ERF-domain transcription factors ORA59 and ERF (ERF1, ERF2, ERF5 and ERF6) control this branch. ORA59 and ERF1 bind to GCC-box motif through ERF domain and activate the expression of PDF1.2 which is the marker gene of this pathway [1, 19, 52–55]. The mode of interaction between JAZ and ERFs is not known. EIN3 directly interacts with JAZ which represses the expression of *ORA59* and *ERF1* [1, 56]. Given the two branches MYC and ERF are induced under different kinds of pathogen attacks these two are mutually antagonistic [1].

Coi1 mutants lacking JA response are more susceptible to necrotrophic pathogens including *Botrytis cinerea*, *Pythium irregulare*, *Alternaria brassicicola* and other pathogens [24, 57–60]. Susceptibility to herbivores is increased by mutations stabilizing JA e.g., JAZ1∆3A mutation increases susceptibility to *Spodoptera exigua* [24, 61]. The fine-tuning of JA-mediated defense response mediated via MYC2 is achieved by post-translational phosphorylation at thr328 residue that makes it unstable leading to its degradation by plant Ubox protein (PUB10) that works as E3 ligase facilitating MYC2 turn over [19, 62].

**Salicylic acid (SA):** this is a phenolic acid hormone that plays important role in the regulation of plant growth, fruit ripening and development. It is involved in pathogenesis-related protein expression [63, 64]. It may be synthesized through the shikimic acid pathway either via the isochorismate branch or phenylalanine ammonia-lyase branch. Salicylic acid regulates the expression of genes encoding molecular chaperones, heat shock proteins, antioxidants and those involved in the biosynthesis of secondary metabolites, alcohol dehydrogenases and cytochrome P450 [64, 65]. In recent years, SA has been increasingly implicated in the plant defense response [10, 66]. Increased SA biosynthesis improves plant tolerance to salt, oxidative and heat stress [10] and it is synthesized in response to pathogen attack [19]. Meaning thereby it has a role to play in biotic as well as the abiotic stress response. SA also leads to systemic acquired resistance (SAR) - defense response to a secondary pathogen infection far and wide in the plant after it has been exposed to a pathogen previously [19]. SA is accumulated in the plant tissue before SAR is initiated [24]. During SAR there is oxidative burst which is followed by increased levels of antioxidants to neutralize the harmful effects of the reactive oxygen species [24]. Mutations in SA-related genes compromise plant immunity to pathogens and diminish the expression of anti-microbial proteins [19, 67]. sid2–1 *Arabidopsis* mutants with impaired SA biosynthesis show reduced pathogen resistance [68]. In transgenic *Arabidopsis* plants expressing bacterial SA hydroxylase gene nahG, which causes the conversion of SA to catechol, SAR is not activated instead PR gene expression is activated [24, 69, 70]. SA effects SAR by affecting the expression of various genes including PAL and priming genes, it activates phytoalexin and auxin signaling-related pathways, it also effects the deposition of callose and phenolic products [46, 71]. SA induces resistance against biotrophic and hemibiotrophic pathogens including *Hyaloperonospora arabidopsidis* and *Pseudomonas syringae*.

SA signaling involves NPR1 (non-expressor of pathogenesis-related (PR) genes, a protein with ankyrin repeat [8, 72]. NPR1 is an oligomer formed by intramolecular disulfide bridges under uninduced conditions [8, 73]. SA induces de-oligomerization of NPR1 releasing active monomers which migrate to the cell's nucleus inducing expression of PR genes [8, 74]; only the monomeric forms can interact with the TGA (TGACG binding) transcription factors which are bZIP proteins [8, 19, 75]. This facilitates the binding of TGA transcription factors with promoters of NPR1 dependent genes [8, 76]. The triple mutant tga2 tga5 tga6 does not respond to SA and does not have SAR [8, 77]. Both NPR1 and TGA undergo nitrosylation which increases the DNA binding ability of the latter. Thiol S-nitrosylation on the other hand causes oligomerization of the NPR1 leading to its inactivation [8, 74]. NPR1 undergoes phosphorylation and proteasome-degradation thereby allowing its turnover [78]. NRR3/4 also interacts with TGA and mutants nrp3/4 over accumulate NPR1 leading to faulty SAR [8]. The binding of NPR3 and NPR4 with Cullin 3 ubiquitin E3 ligase causes SA-dependent NPR1 degradation [8, 79]. The binding of NPR with SA causes a conformational change in the NPR1 required for NPR1 dependent PR gene expression. NPR is also important in epigenetic effect-dependent trans-generational immunity in plants [8, 80]. Pathogen resistance in Monocots is enhanced by over expression of NPR1 [8, 81].

### **3. The modulators of the plant defense**

**Auxins (IAA)**: The role auxins play in plant growth and development is very well known however, their involvement in plants' response to the biotic stress has only begun to be elucidated [64, 82]. Auxins control apical dominance, tropic responses, development of vascular cambium, organ patterning, flower and fruit development [13]. Auxin/indole acetic acid (Aux/IAA), Auxin response factors (ARF), TOPLESS (TL) proteins are the transcriptional regulators that affect cell-specific transcription of auxins and are involved in auxin signaling [83–87]. Research on ARF has led to their identification and characterization from several pants including *Arabidopsis* [88], maize [89], rice [85, 90], poplar [91], tomato [87, 92, 93], Chinese cabbage [94], sorghum [95] and banana [83, 96].

Important auxin-responsive genes include *Aux/IAA*, *GH3* and *SAUR* gene families. In a study by Ghanshyam and Jain [13], 154 auxin-induced and 161 auxinrepressed genes were reported to express differentially under the biotic stressinduced by *Magnaporthe grisea* and *Striga hermonthica*. 62 of the auxin-induced genes were common to both the pathogens while others showed a specific response, 55 to *M. grisea* and 37 to *S. hermonthica*. In the category of auxin-repressed genes, 16 genes showed response to both the pathogens while others showed a specific response, 10 to *M. grisea* and 35 to *S. hermonthica*. Altered expression in auxin genes has also been reported in cotton in response to *Fusarium oxysporum* f. sp. vasinfectum infection [13, 97]. *Botrytis cinerea* infection in arabidopsis causes down-regulation of all the auxin-responsive genes [98]. Repression of auxin-mediated signaling through micro-RNAs leads to resistance against *P. syringae* in arabidopsis. Various pathogens operate by modulating auxin levels *in planta* to enhance the host susceptibility [99, 100]. Exogenous IAA increased susceptibility to *Xanthomonas oryzae* pv. oryzae due to cell wall loosening effects of auxins [101]. The *P. syringae* type III effector AvrRpt2 causes altered auxin levels and modified auxin-related phenotypes and decreases resistance against Pst DC3000 in *Arabidopsis* plants lacking expression of *RPS2* [24, 102]. In this case, susceptibility was found to be directly related to the auxin levels. Another study conducted by Naseem et al. [103], also supports that auxins, JA and ABA increase the host's susceptibility. Naseem and Dandekar, [104] propose a working model of the interaction between auxins and CK stating that the pathogens increase auxin levels increasing disease susceptibility by decreasing SAand CK-based disease response while as CK pretreatment influences auxin synthesis and transport thereby increasing resistance [24].

Auxins down-regulate jasmonic acid biosynthesis genes in *Arabidopsis* [13, 105]. GH3.5 acts as a bifunctional modulator in auxin and SA signaling [106]. Overexpression of *GH3.5* leads to accumulation of SA and accumulation of pathogenesis-related −1 gene (PR-1 gene) product while the capacity of systemic acquired resistance (SAR) is compromised in gh3.5 mutants [106]. Resistance of arabidopsis against *X. oryzae* is increased due to the over expression of *GH3–8* [101].

**Abscisic acid (ABA):** ABA is a sesquiterpene that is synthesized from carotenoids [107]. ABA is usually known as "stress hormone", it regulates a wide range of processes to increase a plant's stress tolerance [23, 108, 109]. It is known to influence the expression of 10% of the protein-coding genes in the events of stress [64, [110]. Important components in ABA signaling include PYR/PYL/RCAR etc. [107]. This hormone oversees important functions in plants that include, seed dormancy, accumulation of nutrient reserves in the developing seeds, desiccation tolerance and arrest of embryonic development during seed maturation [111]. It also plays important role in the protein synthesis and synthesis of some osmolytes [112]. ABA may positively or negatively modulate defense response depending on the type of the pathogen [113–116]. Impaired biosynthesis or signaling ABA mutants in *Arabidopsis*

*Plant Hormones: Role in Alleviating Biotic Stress DOI: http://dx.doi.org/10.5772/intechopen.102689*

(*abi1–1*, *abi2–1*, *aba1–6*, *aba2–12*, *aao3–2*, and *pyr1pyl1pyl2pyl4*) and tomato (*sitiens)* showed increased resistance to *B. cinerea, P. syringae*, *Fusarium oxysporum*, *Plectosphaerella cucumerina* and *Hyaloperonospora parasitica* [117–122]. Antagonistic interactions between ABA and major plant defense hormones including ET, JA and SA have been reported and it has been found that 65% of the genes upregulated and 30% of the genes down-regulated in aba1–6 mutants are those that are affected (upor down-regulated) by ET, JA or SA treatment [119, 122, 123]. The genes constitutively up/down-regulated in these mutants were also found to differentially express upon infection by *P. cucumerina*, indicating their role in the defense. ABA also plays role in expression of R genes [124]. ABA deficient plants are more susceptible than wild types to pathogens *Alternaria brassicicola*, *Ralstonia solanacearum* and *Pythium irregulare* [57, 125, 126]. JA biosynthesis needs ABA in *Arabidopsis* for *P. irregulare* resistance [57]. However, negative interaction between the two is known in the case of the *P. cucumerina* [122]. It has been reported that inoculation of *Arabidopsis* with avirulent strains of *R. solanacearum* makes the plant resistant to the virulent strains of the bacterium and the resistance is mediated through ABA, hence, this hormone could be used for controlling wilt induced by this pathogen [114].

**Cytokinins (CK)**: The most important aspect of cytokinin function in plants is the maintenance of the identity of stem cells thus cytokinins affect the basic aspects of the growth and development of plants [40, 127]. CK was first identified as a hormone affecting cell division in tissue culture conditions and now its role in regulating the cell cycle is well known [23, 128]. Various functions regulated by cytokinins include inhibition of lateral root initiation and leaf senescence [23, 129–132] differentiation of vascular tissue (phloem and metaxylem in roots [23, 133, 134], morphogenic differentiation in expanding leaves and regulation of their cell division [23, 135–137] Cytokinins are derivatives of isopentenyladenine; zeatin is a common CK [40, 127, 138] which exists in two forms -cis and trans-zeatin. Trans-zeatin is more active [40, 139, 140] and is produced by isopentenyl transferases and cytochrome P450CYP735A1 and CYP735A2 [40, 127]. Activity and homeostasis of cytokinins are regulated by their degradation or conjugation with glucose and amino acids, and CK oxidase which cleaves cytokinins [40, 139, 140].

The role of cytokinins in plant defense was first recorded from tobacco plants with down-regulated S-adenosyl homocysteine hydrolases; the plants had higher resistance to tobacco mosaic virus, cucumber mosaic virus, potato virus X, and potato virus Y and also showed increased levels of CK and higher levels CK-related developmental defects [24, 141]. Cytokinin deficient plants have higher stress tolerance [40, 43, 142–144]. Several cytokinin receptors, histidine phosphotransfer proteins and transcription factors mediate CK signaling. Three histidine kinases (AHK2, AHK3, and AHK4/WOODEN LEG) working as cytokinin receptors have been identified in *Arabidopsis* [127, 145]. Cytokinins cause autophosphorylation of the conserved histidine residues in these kinases [40]. The phosphate is transferred to the histidine phosphotransfer proteins (AHPs) through aspartate residue. Phosphorylated AHPs move to the cellular nucleus activating B-TYPE ARABIDOPSIS RESPONSE REGULATOR (ARR) transcription factors causing transcription of cytokinin response genes [146, 147]. Both the environmental factors as well as the JA levels in plants affect the components of the cytokinin response system [40, 148–151]. It is believed that JA may be controlling CK response through MYC2 by promoting AHP expression [40]. Thus interactions between JA and CK might occur at the levels of signaling response elements [40]. Many studies indicate that CKs affect the plant defense response mediated by SA and JA. CK is believed to affect priming in SAR and affects the synthesis of SA and PR proteins [24, 152–154]. Exogenous supply and internal increased levels of CK increase

the JA levels to hasten the defense reaction in wounded plants [24, 155, 156]. The mechanism employed by CK for disease protection is different in different plants e.g., in solanaceous plants, it increases the ratio of phytoalexin to pathogen restricting pathogen development [24]. JA accumulation increases CK ribosides in potato [24, 157]. Several genes involved in regulating CK levels in plants including IPT and CKX are seen as purported targets in enhancing plant disease resistance [24, 143, 158, 159]. Stabilized CK levels in transgenic arabidopsis plants lead to improved resistance to *Verticillium longispoum* [19, 160]. The interaction of ARABIDOPSIS RESPONSE REGULATOR 2 (ARR2), with TGA3 to promote plant defense response in an NPR 1 dependent manner is known [19, 160]. Likewise, rice resistance to *M. grisea* increases due to interaction between SA and CK in an OsNPR1 and WRKY45-dependent manner [14, 19]. Thus the role of cytokinins in the plant disease response cannot be over-emphasized [19, 152, 160, 161].

**Gibberellins (GA)**: Plant developmental processes including, seed development and seed germination, seedling growth, root proliferation, trichome initiation, determination of leaf size and shape, flower induction and development, pollination, fruit expansion etc. are mediated by gibberellins [162, 163]. Gibberellins are tetracyclic diterpenoid carboxylic acids; only a few of many known GAs, notably GA1 and GA4 act as plant hormones [164]. Gibberellins help plants to maintain their internal homeostasis by enabling control over their osmotic and water levels [162]. The mechanism of gibberellin action is relatively better understood in comparison to the other phytohormones. These work by bringing about the degradation of DELLA transcription factors via E3-ubiquitin-ligase [10, 165, 166]. In some plants loss of function mutations in DELLAs has been reported to improve the resistance of plants to biotic stress through SA dependent pathways, meaning thereby GAs, work in biotic as well as an abiotic stress response [10, 11, 167]. During seed germination and seedling establishment, exogenous GA reverses the inhibitory effect of the different stress factors and it also improves SA biosynthesis thereby, improving plant stress response [10]. GA antagonistically interacts with JA to mediate plant growth and defense response which involves direct interaction between DELLA and JAZ proteins [40, 168, 169]. Of the various JAZ proteins, osJAZ9 has been reported to be the key protein in mediating these interactions [40, 170]. The overall plant growth is the result of the fine balance between stress response and developmental process which is mediated through well-regulated JA/ GA balance [34, 150, 171]. The "relief of repression" model explains this antagonistic interaction very well. It postulates that DELLAs and JAZ interact with each other leaving MYC2 free to mediated JA-dependent response under conditions of low GA while in presence of an adequate concentration of GA, DELLA is degraded by E3-ubiquitinylation mediated by GA leaving JAZ free to interact with MYC2 and attenuating the JA-mediated response [46]. Thus, JA/GA interact antagonistically [168]. The fact that JA promotes transcription of RGA3 (Repressor of GA1–3) and that MYC2 directly binds to their promoter further lends support to this model [40, 172].

**Brassinosteroids (BR):** First discovered from *Brassica napus*, BRs are polyhydroxy steroidal compounds about 70 different types of which have been isolated so far [46, 173]; only a few of them including brassinolide, 28-homobrassnolide and 24-epibrassinolide are actively engaged in the plant development [64, 174]. These are widely distributed in different plant organs including pollen, flower buds, vascular cambium, fruits, leaves, roots and shoots [64, 175]. These are also involved in modulating JA signaling and in the JA-dependent plant defense response. These affect many plant functions and alleviate the effects of hypoxia and unfavorable effects of various environmental stressors [46]. BRs are mainly seen as the hormones that alleviate

abiotic stress, however, there are reports that these modulate the pattern-triggered immunity (PTI) (discussed in the next section) in *Arabidopsis* [176, 177].

### **4. Pathogen recognition reactions**

A set of conserved pathogen proteins are important for plants to recognize the infection, these Microbe-Associated Molecular Patterns (MAMP), also called as Pathogen-Associated Molecular Patterns (PAMP), are recognized and bound by Pattern Recognition Receptors (PRRs) present in the host cell plasma membrane. This MAMP-PRR binding triggers an immune response called as MAMP Triggered Immunity (MTI) [24, 178, 179]. Microbes synthesize effectors which interfere with MTI and help pathogens evade recognition by the host immune system increasing their virulence and making plants susceptible to the pathogen and deregulating the host immunity, this process is known as Effector Triggered Susceptibility (ETS) [24, 180]. Bacteria acquire large repertoires of type III Effectors (T3E) and inject them through a syringe-like type III secretion system into their host plant. *Xanthomonas* sp. secretes Transcription activator-like (TAL) effectors, such as AvrBs3 secreted by *Xanthomonas axonopodis* pv. Vesicatoria, which after finding their way into the plant cell nucleus affects host gene expression [177, 181–183]. Auxin is a potential target for bacterial effectors. Effector proteins AvrBs3 1–5 have been reported to upregulate UPA1–5 [177, 184]. Induction of UPA20, a TAL target leads to cell hypertrophy indicating auxin accumulation [177, 185]. In *Arabidopsis* lines lacking the gene that recognizes T3E the bacterial effector AvrRpt2, a cysteine protease, triggers the auxin signaling pathway. Transgenic plants expressing AVrRpt2 accumulate higher auxin levels and constitutively express auxin signaling [177]. Thus, AVrRpt2 enhances bacterial virulence by affecting auxin signaling [177, 186]. An auxin signaling pathway is the preferred target of phytoplasmas [177, 187]. *Candidatus phytoplasma* asteris effector TENGU leads to dwarfism and abnormal organogenesis in reproductive parts leading to flower sterility. In transgenic *Arabidopsis* plants, many auxin-related genes including *Aux/IAA, SAUR, GH3* and *PIN* families were found to be downregulated indicating TENGU effector mediated disruption in the auxin signaling in the host plants [177, 188]. Similarly, *Ustilago maydis* hijacks the SA biosynthesis pathway in the maize plants to express its virulence [177]. Effector– triggered immunity (ETI) counters ETS in a gene-for-gene resistance mechanism [24, 189]. This leads to hypersensitivity response i.e., localized cell death in the infected region [24, 190, 191]. Hypersensitivity response leads to the activation of SAR [24]. The type of defense response depends upon the type of pathogens e.g., biotrophic pathogens are contained by programmed cell death which is mediated by SA [24]. On the other hand, the necrotrophs benefit from the cell death, the defense response, in this case, entails secretion of antibacterial/fungal compounds and accumulation of proteins that have antimicrobial properties such as defensins [24, 192–194]. JA-ET and SA, because of the inherent difference in the defense response these engage in, are antagonistic [24, 195, 196].

### **5. Hormone crosstalk in defense**

Hormone crosstalk is the interaction of various plant hormones in a highly complex yet ordered manner [197, 198]. Crosstalk between various hormones is intensive in defense response [1, 5, 40, 45, 199]; it is mediated through regulatory proteins, hormone receptors, protein kinases, transcription factors etc. involved in hormone

biosynthesis, degradation or signaling [5, 10, 40, 200, 201]. Hormonal cross-talk becomes increasingly important when plants are exposed to multiple pathogen stress simultaneously. Plants have to trade-off between defense and growth, therefore, the impact of individual hormones may not be as important as the overall interaction (positive or negative) among them. Numerous studies bring to light the flexible and coordinated interplay between growth and stress-related hormones especially JA and GA in regulating plant defense response [40, 150, 171, 202]; antagonistic interaction between SA and JA has been well researched [177, 203], the crosstalk between GA and SA was known only recently [10, 167]. Crosstalk enables pathogenesis-related genes affect response to abiotic stress [10, 204]. Crosstalk aids plants to gear up their defense system against various kinds of pathogens; however, all the aspects of this phenomenon in plant defense are not known.

### **6. Molecular Mechanism of hormone crosstalk**

Phosphorylation Cascade is a common second messenger which integrates various hormone responses. JAZ and DELLA proteins mediate the antagonistic interactions between JA and GA [198, 205, 206]. A great deal of information exists on how DELLAs interact with JAZ proteins [168, 169]. GA response in *Arabidopsis* is suppressed by direct interaction of its transcription-factors-like PIF (phytochrome interacting factors) with the DELLAs including GIBBERELLIC ACID INSENSITIVE (GAI), REPRESSOR OF GA (RGA), RGA-like1 (RGL1), RGL2 and RGL3 thus, DELLAs act as negative regulators of the GA response [198, 207]. DELLAs binding with JAZ1 leaves MYC2 free to initiate JA signal response thereby enabling JA-responsive transcription [19, 168]. In a contrary situation, higher GA levels attenuate JA signaling by degrading DELLAs thereby allowing interaction of MYC2 with JAZ1 [40, 198, 208]. GA-related transcription factors like PIF3 are repressed at higher JA levels as JA stabilizes DELLA proteins through JAZ degradation [169, 198]. JA/GA antagonism in rice is mediated by an interaction between OsJAZ9 and DELLA proteins, namely, SLENDER RICE 1 (SLR1) [170, 198]. DELLAs also repress SA biosynthesis as well signaling affecting the balance between JA and SA [10, 167]. JA leads to selection of defense overgrowth in the events of pathogen attack by interfering with GA-mediated degradation of DELLAs [19, 169, 209]. In DELLA quadruple mutants (mutant lacking GAI, RGA, RGL1 and RGL2 proteins) expression of PR1 and PR2 is increased which makes them more resistant to hemibiotrophs, however, delayed induction of PDF1.2 a JA/ET dependent gene marker in such mutants leaves them susceptible to necrotrophs [19, 167]. By way of controlling DELLAs GAs indirectly control the SA/JA balance. The molecular mechanism of antagonistic interaction of SA with ET and JA pathways is largely unknown [1]. NPR1, however, is at the core of most of these antagonistic interactions. A WRKY70 transcription factor is another key player in the hormone crosstalk. WRKY33 is a positive regulator of JA-dependent genes but a repressor of SA pathway, therefore, wrky33 mutants show upregulated expression of several SA-regulated genes including SID2/ICS1, EDS5/SID1, PAD4, EDS1, NIMIN1, PR1, PR2, PR3. SA induction leads to down-regulated JA signaling and increased susceptibility of these mutants to necrotrophic fungi [177, 210]. When over-expressed it leads to constitutive expression of SA-responsive PR genes and repression of JA responsive PDG1.2 gene [19, 211]. Likewise, *Arabidopsis* mpk4 (MAP kinase 4) knockout mutants exhibit constitutive SAR, higher expression of PR genes but an impaired expression of JA-responsive *PDF1.2* and *THI2.1* genes [19, 196]. Synergistic interactions between SA and JA have also been reported especially at their lower concentrations and when both the defense responses are triggered together [19, 196, 211]. MED16 which

*Plant Hormones: Role in Alleviating Biotic Stress DOI: http://dx.doi.org/10.5772/intechopen.102689*

positively regulates SA-induced defense response negatively regulates JA/ET signaling pathway [177, 212]. Some strains of *P. syringae* produce phytotoxin coronatine (COR), a mimic of the JA-Ile and this suppresses SA signaling [177, 213, 214]. This is the reason for the lower virulence of the strains of *P. syringae* that have impaired production of COR on wild *Arabidopsis* plants but not on SA deficient plants [177, 215]. JA and ET cooperate in comparison with the JA and SA where interactions are mostly antagonistic, e.g., JA and ET both stabilize EIN3 thereby leading to the defense of roots against necrotrophic pathogens [19, 56]. Both JA and ET activate the expression of ERF1 which in turn activates PR genes [19, 216]. However, in cases of herbivore and insect attacks the two pathways may interact antagonistically e.g., JA–activated MYC2 interacts with ET-stabilized EIN3 and represses its downstream activity. In turn, EIN3 represses MYC2 thereby repressing JA-mediated defense response against herbivores [19, 217].

#### **7. Concluding remarks and future perspectives**

Allocation of resources and energy to defense in absence of threat would constrain growth and developmental processes [177, 218–220]. Therefore, a hormonebased defense mechanism in plants evolved to prevent loss of resources in absence of stress [177, 220] slowing down the potential adaptation of putative attackers to the biochemical defense system of plants [177, 220]. During priming plants subjected to pathogen attack respond more strongly to subsequent pathogen attacks, resources here are not committed until the threat returns making priming a relatively cost-effective defense strategy [177, 221]. Moreover, the primed plants treated with a low, non-effective concentration of defense hormones also respond better to the pathogen attack than the non-primed ones [177, 221]. Priming has parallels with the trans-generational defense in plants, such as SA-dependent SAR and JA-dependent inherited defense as trans-generational priming has been described in some plants [80, 177, 214]. Epigenetically inherited changes can strongly affect the defense response including priming in plants [80, 177, 222].

Our understanding of plant defense response has considerably improved in the past few years due to modified and transgenic plants species [177]. Transgenic plants constitutively expressing some hormones have been reported to show improved resistance to pathogens [177, 223, 224]. But, such an "effective" resistance response is also known to incur the costs paid in terms of altered development e.g. dwarfism, development of spontaneous lesions in different organs, accelerated pace of senescence, delayed flowering, sterility and lower seed output [177, 223–225].

Dissecting hormone response specifically in the event of a pathogen attack is complicated by the complex regulatory pathways interconnecting at several different levels. In nature, a plant has to deal with both abiotic and biotic stresses therefore, its response to the environment, in general, has to be concerted and balanced. Ideally, a plant resistant to biotic or abiotic stress should not be hampered in terms of its growth, development and overall productivity. It is a generally conceded fact that the traditional methods of crop improvement have reached their peak and are now leveling off. Thus, molecular and genetic engineering methods provide reliable alternative means of crop improvement. Phytohormone engineering is seen as a new opportunity to maintain susceptible crop production, especially in the climate change scenario. Elucidating the path of signal transduction in stress response is an important step in manipulating the role of phytohormones in stress response. In the future plant defense response mediated by hormones should be studied under field conditions with model crop plants so that a better picture of the effectiveness of the hormone-mediated disease control, associated trade-offs in growth and

development parameters, and impact on the performance of the plants are brought to light. A clear understanding of the hormone homeostasis at the molecular level is required to manipulate it and use it as a tool for effective defense against crop pathogens.

### **Author details**

Nazima Rasool University of Kashmir, Kargil Campus, India

\*Address all correspondence to: rasoolnazima@gmail.com

© 2022 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

*Plant Hormones: Role in Alleviating Biotic Stress DOI: http://dx.doi.org/10.5772/intechopen.102689*

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### **Chapter 3**
