Open access peer-reviewed chapter

Role of Plant Hormones in Mitigating Abiotic Stress

Written By

Nazima Rasool

Submitted: 27 November 2022 Reviewed: 12 January 2023 Published: 20 February 2023

DOI: 10.5772/intechopen.109983

From the Edited Volume

Abiotic Stress in Plants - Adaptations to Climate Change

Edited by Manuel Oliveira and Anabela Fernandes-Silva

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Abstract

Agricultural productivity world over is threatened by abiotic stress, intensifying food security issues. The plant hormones play a significant role in mitigating abiotic stresses, including drought stress, salinity stress, heat stress, and heavy metal stress, faced by the plants. Considerable research has been conducted to understand hormone-mediated abiotic stress responses in plants and the underlying biosynthetic and regulatory pathways. Deciphering these pathways would allow their manipulation in the laboratory and possible extension to the field. In the present chapter, an overview of the role plant hormones play in mitigating abiotic stress, the underlying mechanisms of their action, and the cross-talk between their signaling pathways to mitigate abiotic stress is presented.

Keywords

  • abiotic stress
  • plant hormones
  • stress response
  • stress mitigation
  • plant productivity

1. Introduction

Plant hormones or phytohormones are biochemicals required for the normal growth and development of plants [1, 2, 3]. Plant hormones include auxins (IAA), gibberellins (GAs) cytokinins (CK), abscisic acid (ABA), ethylene (ET), besides jasmonates (JA), salicylic acid (SA), brassinosteroids (BR), strigolactones (SL), and nitric oxide (NO). Apart from their role in plant growth and development, hormones also mediate response to biotic (disease, pathogens, herbivores, etc.) and abiotic (drought, heat, salinity, heavy metals, etc.) stress [3, 4, 5, 6]. Hormones act at the site of their biosynthesis or some distance away from it [3, 6, 7, 8]. Hormone biosynthesis, distribution, and patterns of their signal transduction change under stress conditions [8, 9]. Ethylene and ABA play remarkable roles in regulating the abiotic stress response [8]. The exogenous supply of phytohormones also increases stress endurance in plants [10, 11]. Abiotic stress factors rarely occur individually, and many stresses produce the same effects at the cellular level with an overlap in the expression pattern of stress response genes [12]. In the current chapter, the hormone-mediated response of plants to the abiotic stress, including drought, heat, and salinity, is discussed.

1.1 What is abiotic stress?

Ecological factors favor plant growth at optimum levels and constitute stress at sub- or supra-optimal levels. Abiotic stress reduces crop productivity by about 50% (Table 1) [8, 29]. High temperatures lead to 20% decrease in the yield, low temperatures 7%, salinity 10%, drought 9% and other forms of stress cause 4% yield loss [30]. In grain crops, grain size, number, and dry weight are influenced by abiotic stress, especially if present during the reproductive phase [30]. Various aspects of plant growth as affected by abiotic stress are presented in Figure 1. Crop productivity may be reduced by 2.5–16% by a 1°C rise in seasonal temperature in tropical and subtropical regions [31]. The stress response depends on the genetic constitution and adaptive response of a plant [32].

CropAbiotic stress factorLoss in productivityReferences
WheatDrought27.5%Zhang et al., [13]
Temperature29–44%Djanaguiraman et al., [14]
Salinity45%Ali et al., [15]
RiceDrought25.4%Zhang et al., [13]
Temperature3.2%*Zhao et al., [16]
Salinity30–50%Eynard et al., [17]
MaizeDrought5–15%Campos et al., [18]
Temperature7.4%*Zhao et al., [16]
Salinity34%Cucci et al., [19]
ChickpeaDrought45–69%Nayyar et al., [20]
Temperature39%Devasirvatham et al., [21]
Salinity8–10%Zawude and Shanko, [22]
SoybeanDrought46–71%Samarah et al., [23]
Temperature42–64%Jumrani & Bhatia, [24]
Salinity66–86%Bustingorri & Lavado [25]
SunflowerDrought50%Hussain et al., [26]
Temperature*6%Rondanini et al., [27]
Salinity50%El-Kader et al., [28]

Table 1.

Loss of productivity in the major staple crops due to abiotic stress.

Estimates for 1°C rise in temperature.


Figure 1.

Schematic presentation of impact of abiotic stress on growth & development of plants.

1.2 Drought

Drought has been defined as “a period of abnormally dry weather sufficiently prolonged for the lack of water to cause a serious hydrologic imbalance in the affected area” [33]. Drought is one of the dominant factors diminishing crop productivity [34, 35]. Drought has been called as “one of the world’s extreme weather-related natural hazards” [35, 36]. It threatens the sustainability of agricultural systems around the world [37]. From 1994 to 2013, it represented 5% of all natural disasters and affected one billion people [35, 38]. All aspects of plant growth, including photosynthesis, protein synthesis, water relations, cell turgidity, membrane integrity, and nutrient uptake, are affected by drought [8, 39, 40]. It causes oxidative stress and damages the biological molecules, including DNA, proteins, and photosynthetic pigments. [8, 35, 41, 42, 43, 44, 45]. Plants synthesize a whole range of molecules as protection against drought stress, for example, proline, glycine betaine, soluble sugars (mannitol, sorbitol, and trehalose), polyamines, and proteins [37, 46].

ABA levels increase in plants under drought stress [47, 48], inducing the expression of ABA-dependent genes [6, 49]. ABA signaling leads to the closure of stomata, reducing transpiration [48]. Expression levels of ZEP (Zeaxanthin Epoxidase) gene, AAO3 (Arabidopsis Aldehyde Oxidase) gene, NCED3 (Nine-Cis-Epoxycarotenoid Dioxygenase) gene, and the MCSU (Molybdenum Cofactor Sulfurase) Gene are increased upon osmotic stress [50]. Overexpression of NCED3 improves water use efficiency and its mutation causes drought susceptibility [49, 51, 52]. ABA is transported into the guard cells through passive diffusion via members of ABC (ABCG25 and ABCG40) and nitrate (AIT1/NRT1.2 and NPF4.6) transporter families. ABCG25 is an ABA exporter with tissue-specific expression induced by ABA and drought stress [49, 53]. ABCG40, AIT1/NRT1.2, and NPF4.6 import ABA into the guard cells. ABA also generates ROS, which leads to increased cytosolic Ca2+ levels and stomatal closure [54, 55, 56].

About 14 ABA receptor proteins mediate ABA signaling. Pyrabactin Resistance 1 (PYR1) and PYR1-like (PYL) regulatory elements undergo a conformational change after ABA binding and inactivate the clade A Serine/Threonine Protein Phosphatase 2C (PP2C) [48, 57, 58]. This in turn triggers the ABA signaling cascade by phosphorylation of serine/threonine kinases [48, 59]. Transcription of ABA-responsive genes is upregulated by binding of ABRE (ABA-Responsive Elements) to the ABRE-Binding Proteins (AREBs) or ABRE-Binding Factors (ABFs) [48, 60]. ABFs are activated by their ABA-mediated phosphorylation [48, 61]. AREB1/ABF2, AREB2/ABF4, and ABF3 are induced by abiotic stress, including dehydration and high salinity [48]. Transcription factors belonging to MYC, MYB, and NAC protein families are also known to work in an ABA-dependent manner [48, 62, 63]. Stress response improves in plants overexpressing RD26 (Responsive to Desiccation 26), a stress-inducible NAC transcription factor [48, 63]. Dehydration-Responsive Element (DRE)-Binding Protein (DREB) transcription factors are regulated by ABA-dependent pathways under osmotic stress [48, 64]. The binding of AREB1, AREB2, and ABF3 to the DREB2A promoter results in the activation of DREB2A in an ABA-dependent manner [48, 65].

In Arabidopsis thaliana, many genes involved in ABA biosynthesis and signaling have been characterized [6, 66]. When A. thaliana is exposed to drought or salt stress, expression of the ABA3/LOS5 gene increases considerably [67]. Constitutive or drought-induced expression of this gene has been reported to increase rice yield [668]. AtNCED3 plays an important role in drought tolerance [6]. Higher expression of SgNCED1 in transgenic tobacco plants with this gene from Stylosanthes guianensis had improved drought and salinity tolerance and higher (51–77%) ABA content [6, 69]. In tomato plants, overexpression of LeNCED1 constitutively resulted in the accumulation of ABA [6, 70]. Drought-inducible rd29A promoter-driven gene construct in Brassica napus increased yield under mild drought conditions [6, 71]. The wild form of this gene codes for the b-subunit of farnesyltransferase, which is involved in ABA-dependent signal transduction [72]. Exogenous application of ABA enhances the activities of GT, CAT, APX, and SOD [31, 37]. ABA priming increases the relative water content in drought-stressed wheat cultivars [73].

ABA is negatively regulated by cytokinin receptor HKs, AHK2 (Arabidopsis histidine kinase 2), AHK3, and AHK4 mutations in these genes increase drought tolerance [49, 74, 75]. CK, being an ABA antagonist, is decreased in conditions of drought stress; however, CK has also been reported to increase proline levels, inhibit senescence, and promote survival under drought conditions [6, 76]. Exogenously applied 6-benzylaminopurine increased the photosynthetic rate and stimulated protective enzymes in the maize seedlings [77]. BRs increase drought tolerance in many plants when applied exogenously [6, 78]. However, some reports also suggest that endogenous BRs or their perception are not involved in the water stress response [6, 79]. Auxins regulate ABA [37, 80]; Indole-3-acetic acid (IAA)-amido synthetase encoding gene TLD1/OsGH3.13 increases expression of LEA (Late Embryogenesis Abundant) genes increasing drought tolerance in rice seedlings [6, 81]. Several studies indicate mitigating effects of SA on drought, salinity, and high-temperature stress [82, 83]. SA has been reported to increase catalase activity in wheat under drought stress [37, 84]. In Portulaca oleracea, SA improved photosynthetic pigments, secondary metabolites, and gas exchange [3785]. SA application increased water use efficiency, photosynthesis, and activity of antioxidant enzymes and also prevented cell damage under drought [86]. Ethylene activates DREB transcription factors [87]. Under mild drought stress shoot dry weight of six cultivars of wheat ranging from sensitive to tolerant was higher in the tolerant ones, which was related to higher ethylene content [37, 88]. Etol1 mutants of rice that accumulate more ethylene than OsETOL1 tolerate drought better.

1.3 Temperature

Temperature affects the distribution, phenology, and physiology of plants [89]. Temperature is increasing under dry as well as wet conditions in the changing global climate scenario [89, 90]. For 2081 – 2100, the IPCC has predicted average temperatures higher by 1.0°C to 1.8°C under very low, 2.1°C to 3.5°C under intermediate and 3.3°C to 5.7°C under very high GHG emission scenarios in comparison to 1850-1900 [91]. The crop productivity decreases by 6% for one degree rise in temperature beyond the optimum [8, 92]. Temperature stress causes accumulation of ROS, denaturation, misfolding, and aggregation of proteins, changes the membrane structure affecting permeability and raft distribution, besides its impact on leaf area, leaf retention, stomatal conductance, water potential, rate of transpiration, etc. [89, 90, 91, 93]. Photosynthetic capacity may be diminished or permanently damaged due to heat stress [91, 94].

Plants produce transcription factors, heat signaling proteins, and molecular chaperones to prevent protein misfolding and aggregation after heat shock (HS) [95, 96]. In response to HS, the endogenous ABA levels increase transiently increasing the antioxidant capacity [47, 97, 98], for example, by inducing RBOH-NADPH oxidases. Out of 10 different RBOH genes identified in Arabidopsis, only AtRBOHD is upregulated in response to heat stress [91, 99]. The mutants for this gene show low germination and seedling survival at higher temperatures [91, 97, 100]. ABA biosynthesis inhibitors and ABA signaling mutants have impaired heat stress tolerance [91, 97]. Both the heat shock proteins and their transcription factors are regulated by ABA. Expression levels of ABA1/ZEP and NCED2/5/9 increase in Arabidopsis at 32°C increasing the ABA levels. Cucumbers and red-skinned grapes show higher ABA levels at 35°C [98, 101]. Drought priming in Festuca arundinacea and Arabidopsis increases their heat tolerance. Arabidopsis ABA biosynthesis mutants or plants treated with ABA biosynthesis inhibitors lack the drought priming effect [91, 102]. ABA treatment increases the expression of tall fescue heat stress transcription factor A2c (FaHSFA2c). ABA may also modulate carbohydrate and energy status to strengthen the heat stress response [103].

Auxins play an important role in thermomorphogenesis [91, 98, 104]. Auxin biosynthesis genes TAA1, CYP79B2, and YUCCA8 are upregulated at higher temperatures; thermomorphogenesis response is abolished in shy2–2 (short hypocotyl) mutation affecting the auxin-responsive IAA3 gene [98, 105, 106]. Auxin-mediated thermomorphogenesis is regulated through phytochrome interacting factors (PIFs) and bHLH transcriptional regulators. PIFs also upregulate auxin biosynthesis; HDA9 (histone deacetylase 9), a chromatin-modifying enzyme, facilitates the binding of PIF4 to the promoter of YUCCA8 [91, 98, 106, 107]. pif4 mutants have very low levels of enzymes of the YUCCA family, aminotransferase, and cytochrome P450s, which are involved in the heat stress response [91, 105, 106]. In pif4 plants, ectopic expression of PIF4 under an epidermis-specific promoter restores hypocotyl elongation induced by heat stress [91, 98, 108]. PIF4 and PIF7 loss of function mutants lose their heat stress-induced thermomorphogenesis. Thermomorphogenesis also requires HSP90. Thermomorphogenesis also involves brassinosteroids through phyB-PIF4 [98, 109, 110]; the temperature-sensitivity of hypocotyl elongation is inhibited by the application of PPZ (propiconazole), a BR biosynthesis inhibitor [109, 111].

BRs increase the production of HSPs [91, 112] and regulate the heat-induced accumulation of proton–pumping ATPase and aquaporins [91, 113], besides inducing the expression and activity of ROS scavenging enzymes under heat stress [91, 114]. In tomatoes, BR treatment increases the expression of RBOH1 and apoplast H2O2 levels [115]. Interestingly, H2O2 activates MPK2, which in turn enhances RBOH1 expression [91, 116]. Heat stress causes the accumulation of BZR1 (Brassinazole-resistant 1), an important transcription factor in BR signaling, in the nucleus [110].

Ethylene is another hormone involved in heat stress tolerance. EIN2 and ER1 mutants have poor survival rates under heat stress [95, 97]. Arabidopsis plants overexpressing ERF1 are more tolerant to heat stress than the control plants; ERF-1 overexpressing plants have higher transcript levels of HsfA3 and HSP70. Studies have indicated increased synthesis of ET under heat stress [98, 117]. However, in Arabidopsis, ein2–1 mutants exhibit greater tolerance to heat stress [91, 118]. ET is involved in CO2-induced heat stress responses in tomatoes [11] and increased thermotolerance in rice [91, 95].

CKs play an important role in heat stress responses in plants [91, 119, 120]. They increase the activities of APX, SOD, and GP and also upregulate genes responsible for photosynthesis and carbohydrate metabolism under heat stress [91, 121]. CK oxidase/dehydrogenase inhibitors improve heat stress tolerance [91, 122]. Heat stress tolerance is also increased in plants with ectopic expression of isopentenyl transferase (ipt) from Agrobacterium tumefaciens [91, 123]. In Arabidopsis, rice, and passion fruit, external CK application decreased the negative effects of heat stress [124, 125].

In Medicago sativa, plant height, photosynthetic efficiency, and plant biomass were improved by pre-treatment with SA [126]. SA promotes the activities of CAT, SOD, and POX, which improve photosynthetic efficiency, ROS scavenging, and HSP21 levels [83, 95]. Under heat stress, it protects photosystem II and maintains high Rubisco activity [95, 127]. SA application in tomatoes under heat stress decreased oxidative damage and significantly improved gas exchange, proline content, and water use efficiency [83]. ET and JA accumulate in Arabidopsis after heat stress [97]. Plants with constitutive expression of PR1 (cpr5–1) have higher heat stress tolerance [95, 118]. Exogenous JA application reduced the negative effects of heat stress [95118]. External application of strigolactone to SL biosynthesis mutants restores seed thermo-inhibition [98, 128].

GA biosynthesis and accumulation increase under elevated temperatures in Carrizo citrange seedlings, wheat, and soybean hypocotyl [98, 129]. PIF4 upregulates the GA20ox1 gene [130]. PIF4 transcription factors Class I TCP14 and TCP15 (Teosinte Branched 1, Cycloidea, and PCF) play an important role during this process; TCP14 and TCP15 mutants have reduced temperature sensitivity [130]. Seeds at 32°C have lower expression of GA20ox1, GA20ox2, GA20ox3, GA3ox1, and GA3ox2 in comparison to those kept at 28–29°C [98, 131].

SA biosynthesis is suppressed at higher temperatures in tobacco after TMV infection and in Arabidopsis after Pst 350 DC3000 infection [132]. High temperatures suppress the expression of Isochorismate Synthase 1 (ICS1), and ics1do not show temperature sensitivity to infection [132]. JA biosynthesis genes are upregulated by moderately higher (29–30°C) temperatures after wounding or Pst DC3000 infection in Arabidopsis [132, 133]. High temperatures have a tissue-specific effect on JA systemic transport in plants [122].

1.4 Salinity

Soils with electric conductivity higher than 4 dS/m at 25°C are classified as saline [134]. Salinity has affected more than 800 million hectares of land globally, decreasing potential agricultural land by 1–2% per year [8, 135]. More than 50% of the land in developing countries, particularly that falling in the arid region, is affected by salinity, causing yield losses to the tune of 40%, for example, in the case of wheat [8136]. It decreases the quantity as well as the quality of the produce [8, 137]. Salinity impairs water uptake and causes ion toxicity, osmotic stress, nutrient deficiency, and oxidative stress [138]. Salt stress causes physiological drought impairing protein and photosynthesis [8, 137]. Changes in the intracellular Ca2+ levels, excess Na+, and ROS accumulation are the signals that trigger the salt stress response [139].

Ethylene is the major hormone in the salt stress response [138]. The levels of ET as well as its precursor ACC (1-aminocyclopropane-1-carboxylate) increase under salt stress [138, 140]. While salt tolerance can be increased by the application of ET or its precursor ACC [141, 142], inhibition of ET synthesis or signaling may increase salt sensitivity [138]. Ethylene signaling involves five ethylene receptors [ETR1 (Ethylene Response 1), ERS1 (Ethylene Response Sensor 1), ETR2, EIN4 (Ethylene Insensitive 4), and ERS2], a protein kinase, CTR1 (Constitutive Triple Response 1—a negative regulator) and a key positive regulator EIN2, which signals primary transcription factors EIN3, EIL1 (Ethylene Insensitive Like 1) and EIL2 and many downstream ethylene response factors. Osmotic stress, induced by many abiotic stresses, including salinity, suppresses the expression of ETR1 [138, 143]. During short- and long-term salt stress, ethylene receptor genes (ETR1, ETR2, and EIN4), signaling genes (CTR1, EIN3, ERF1, and ERF2), and MAPK cascade genes (MEKK1-MKK2-MPK4/6), are upregulated in cotton [144]. Many ERF (Ethylene-Responsive Element Binding Factor) genes ESE1ESE3 are induced by ethylene and salt stress. Accumulation and transcriptional activity of EIN3 and EBF1/EBF2 degradation are promoted under salt stress [144]. The levels of 1-aminocyclopropane-1-carboxylic acid synthases (ACSs) increase significantly under salinity stress [138, 144, 145]. ACC pretreatment increases salt stress tolerance in Arabidopsis seedlings [138, 141, 142, 146]. Salinity induces ACS1 transcription in tobacco [138, 147]. Salt stress given to salt-acclimated and non-acclimated plants upregulated four ACSs [138, 148]. In the post-transcriptional regulation of ACSs, stress-induced MAPK cascades phosphorylate CSs, preventing their 26S proteasome-mediated degradation [138, 149]. The effect of salt acclimation is diminished by the loss of function of MAPK6 [148]. Stabilization of ACSs apparently needs MPK6 to maintain high ethylene levels [138, 148]. ACSs are also stabilized by CDPKs (Calcium-Dependent Protein Kinases) in tomatoes [138]. ACC content and activity of 1-aminocyclopropane-1-carboxylic acid oxidase (ACO) is increased under salt stress in Cicer arietinum roots [138].

200 mM NaCl induces the expression of ETOL1 in rice [138, 150]. ETO1’s loss of function promotes ethylene production in Arabidopsis. Root-to-shoot delivery of Na+ is restricted in the absence of ETO1, which also increases RBOHF-dependent ROS accumulation in root stele tissue. Loss of ETO1 also increases K+ levels by increasing K+-transporter HAK5 transcripts [138]. Arabidopsis etr1 loss-of-function mutants have increased salt tolerance [141, 142, 151]. ET sensitivity decreases and salt sensitivity increases in tobacco and Arabidopsis on overexpression of NTHK1 [138, 147]. Loss of function of CTR1 increases salinity tolerance [142, 145]. Arabidopsis loss-of-function EIN2 mutants are salt sensitive; overexpression of the C-terminus of EIN2 in ein2–5 mutants decreases salt sensitivity [138, 141, 142  152]. ein3eil1 double mutants of Arabidopsis are highly sensitive to salinity. Also, ein3–1 mutants are highly salt-sensitive whereas plants overexpressing EIN3 are salt tolerant [138, 142, 145, 152].

An array of stress-responsive genes is regulated by ABA [153]. ABA coordinates with ET in mediating salt stress. On exposure to salt, many genes involved in ABA biosynthesis, including ZEP, AAO, and MCSU, are stimulated through Ca2+ −dependent phosphorylation events and their downstream signaling pathways [153, 154]. Increased ABA levels have been reported in many plants, including Oryza sativa [155], Brassica [156], Phaseolus vulgaris [157], and Zea mays [158]. Higher ABA levels help accumulate proteins for osmotic adjustment and also cause stomatal closure. High accumulation of ABA due to ectopic expression of drought-responsive GenesOsDSM2 (Drought-Hypersensitive Mutant 2) and OsCam11 (Oryza Sativa Calmodulin1–1) in rice increases salt stress tolerance [153]. Salt stress as well as ABA treatment upregulates several MAPKs [153], and plants with higher expression levels of MAPKs have higher salt stress tolerance [153, 159]. ABA-regulated Ca2+-dependent kinases and SnRks phosphorylate ABA-related transcription factors, affect gene expression, and modulate salt stress [12, 153, 159]. Promoters of stress-responsive genes contain many regulatory sequences (DRE/CRT, ABRE, MYC recognition sequence (MYCRS), and MYB recognition sequence (MYBRS)). Activation of salt stress-responsive genes is stimulated by ABA-dependent transcription factors ABFs, MYCs, and MYBs, which directly bind to these sequences on the promoters [153]. Promoters of all LEA genes have ABRE motifs that bind ABF [153]. ABFs and DREB2 regulate the drought-inducible Dihydroorotate Dehydrogenase1 gene, which is important in salt and drought stress responses [153]. Since ABA and ET enter into crosstalk during the stress response, tolerance to salt, osmotic, and heat stresses is alleviated by a mutation in ACS7 [138].

The information available on the mechanism of salt stress response via auxins is scarce [153]. YUCCA3, a gene involved in auxin biosynthesis, causes hypersensitivity to salt stress, leading to increased auxin production [160]. Auxin accumulation and redistribution in response to salt stress change the root architecture [161]. Salt stress in tomatoes decreases auxin levels by 75% [162]. The reduced growth under salt stress is a manifestation of altered levels of IAA biosynthesis and its distribution [8]. The salinity stress in wheat decreases CKs biosynthesis [8]. In Arabidopsis, wild-type plants were not as tolerant to salt stress as CK-deficient mutants [75]. Mutants with decreased CK levels had higher expression of the HKT1–1 gene, which encodes a Na+ transporter [75]. Salt tolerance was reduced in Arabidopsis plants overexpressing IPT8 genes [163]. However, the positive role of CK in salinity stress has also been reported. Applying cytokinin oxidase inhibitor (INCYDE) to salt-stressed tomato plants improved flower production and photosynthesis [164].

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2. Conclusions

Plant hormones play an important role in the growth and development of plants and also represent an important line of defense against abiotic stress. Hormones change the pattern of growth to enable the plants to withstand stress. The plant stress response involves many hormones, their downstream response factors, associated gene networks, and transcription factors. The crosstalk between hormones and their synergistic or antagonistic interactions play central role in phytohormone-mediated abiotic stress tolerance [165]. Understanding the molecular level interaction between elements of different pathways controlling stress response is critical to allow their manipulation to improve stress tolerance. This is important, as the diversity, duration, and intensity of abiotic stresses are increasing in the changing global climate scenario. Plant hormones are an important target for better management of abiotic stress, especially, in view of the limited success of conventional breeding techniques in dealing with it. Phytohormone pathways and the intermediaries therein can go a long way in the production of climate-resilient crops.

New technologies to bioengineer plants have proven useful in achieving this end; examples include soybean [166], maize [167], rice [168], and potato [169]. Techniques including transcriptome analysis, next-generation sequencing analysis, transgenic plants, genome editing, etc. are being used to identify the hormone-mediated regulatory mechanisms of the plant stress response. Transcriptome analysis using microarrays, a survey of transcriptome profiles, and levels of microRNAs in plants under stress using RNA-seq have helped understand the mechanism of stress tolerance in plants [170]. With genome editing technology, genomes can now be modified in a site-specific manner using specifically designed endonucleases like zinc finger nucleases (ZFN) or TAL effector nucleases (TALEN; [49, 171]) and the CRISPR/CAS system [49, 172].

In a nutshell, new pathways are already emerging. However, the complex interactions between the hormones and their ability to regulate a wide array of plant developmental and physiological processes complicate teasing out the effect of an individual hormone. Lack of information about the tissue-specific stress response and genetic plasticity as well as the extreme complexity of thresholds for different stress responses makes mechanistic understanding of abiotic stress tolerance difficult [173]. In order to better understand the hormone mediated abiotic stress response, the future research should focus on identifying the antagonistic and synergistic interactions between various hormones and the critical regulatory junctures in the hormone crosstalk.

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Written By

Nazima Rasool

Submitted: 27 November 2022 Reviewed: 12 January 2023 Published: 20 February 2023