Plant–insect interactions are vital to agricultural productivity and ecosystem health, influencing biodiversity, ecosystem services, and food production. These interactions can be beneficial, e.g., pollination and natural pest control, or detrimental, e.g., herbivory and pathogen transmission (Shen and Ni, 2024). In agriculture, insect pollinators, including bees and butterflies, enhance crop yields, with 75% of food crops relying on insect-mediated pollination (Riffell, 2020; Jordan et al., 2021). Predatory and parasitic insects, like lady beetles and parasitoid wasps, help regulate pests, reducing pesticide reliance and fostering sustainability (Fei et al., 2023; Wu et al., 2022). Conversely, herbivorous insects cause crop damage, impose economic losses, and spread plant pathogens (Mostafa et al., 2022; Sarwar, 2020; Wielkopolan et al., 2021). In natural ecosystems, these interactions sustain biodiversity by regulating plant populations and preventing monocultures (Balmaki et al., 2022; Whitehill et al., 2023), and coevolution between plants and insects has driven the development of traits like plant defenses and insect’s detoxification abilities (Beran and Petschenka, 2022; Endara et al., 2023; Amezian et al., 2021). Managing these interactions is key to sustainable pest management ( Figure 1 ), integrating natural predators and advanced breeding or genetic approaches to reduce chemical pesticide dependence while supporting agricultural productivity and conservation (Boeraeve and Hatt, 2024).

The coevolution of plants and insects represents a dynamic evolutionary arms race shaping biodiversity and ecosystem functionality over millions of years (Mello and Silva-Filho, 2002). Reciprocal pressures drive plants to evolve defenses while insects develop counter-adaptations (Endara et al., 2017; Leite Dias and D’Auria, 2024). Plant defenses include physical barriers (e.g., thorns and trichomes), chemical toxins (e.g., alkaloids and terpenoids), and molecular responses like immune signaling and the production of volatile organic compound (VOC) to attract natural enemies (Salgado‐Luarte et al., 2023; Hu et al., 2024; Demis, 2024). Insects counter these defenses through detoxification systems, behavioral adaptations, and molecular effectors that suppress plant immunity (Boter and Diaz, 2023; Acevedo et al., 2015). For example, monarch butterflies exploit toxic cardenolides, using them for predator defense, while noctuid caterpillars use HARP1-like proteins to suppress plant defenses (Hoogshagen et al., 2024; Chen et al., 2019b). This coevolution drives innovation in plant immunity and insect counterstrategies, shaping both antagonistic (herbivory) and mutualistic (pollination) interactions (Bronstein et al., 2006; Nepi et al., 2018). Understanding these interactions is crucial for sustainable pest management (Dixon and Dickinson, 2024). Deciphering genetic and biochemical pathways in plant resistance and insect counter adaptation can inspire novel strategies to enhance plant immunity and disrupt insect defenses, reducing reliance on chemical pesticides and fostering agricultural resilience (Ahmad et al., 2024).

Research on plant immunity to insect herbivory is vital to addressing global food security challenges posed by climate change, pests, and diseases. Insect pests cause 20–40% of global crop losses annually, threatening food supplies and economic stability, especially in agriculture-dependent developing nations (Popp et al., 2013; Junaid and Gokce, 2024). The jasmonate signaling cascade plays a central role in mediating herbivore-induced defenses. Upon perception of damage, jasmonoyl-isoleucine (JA-Ile) accumulates and binds to the SCF^COI1 receptor complex, promoting degradation of JAZ and JAV1 repressors, thereby releasing transcription factors such as MYC2 to activate downstream defense genes, including those involved in secondary metabolite biosynthesis and protease inhibitor production (Hewedy et al., 2023; Macioszek et al., 2023; Ali et al., 2024a). This hormonal signaling cascade contributes to the synthesis of defense metabolites and structural reinforcements, such as lignin and cuticular waxes (Xiao et al., 2021; Bungala et al., 2024). Advances in breeding, genetic modification, and multi-omics integration further allow fine-tuning of these pathways for enhanced pest resilience under variable climatic conditions (Felton and Tumlinson, 2008; Soares et al., 2019; Skendžić et al., 2021). In addition, emerging studies highlight the involvement of other hormones such as abscisic acid (ABA), gibberellins (GA), and auxins in modulating plant responses to herbivory. ABA can influence stomatal regulation and drought-mediated defense trade-offs during herbivore attack. GA signaling often interacts antagonistically with JA to regulate resource allocation between growth and defense. Auxins may contribute to defense by modulating leaf morphology and influencing cross-talk with JA/SA pathways (Erb, 2018). Strengthening plant immunity reduces synthetic pesticide use, preserves beneficial insects, and fosters sustainable food systems (Sharma et al., 2021; Barbero and Maffei, 2023; da Silva Pinheiro et al., 2024) ( Figure 2 ).

This review delves into the dynamic evolutionary arms races between plants and their insect herbivores, examining molecular, chemical, and physical plant defenses alongside insect counter adaptations. It emphasizes the role of environmental factors, such as climate change, in shaping these interactions. Cutting-edge biotechnological advancements, including genetic engineering and metabolic enhancement, are explored as tools to bolster plant immunity for sustainable pest management. By identifying key knowledge gaps, the review advocates for future research integrating multi-omics approaches and innovative strategies to address global agricultural and food security challenges.

Plants deploy highly coordinated signaling pathways to mount rapid defense responses against herbivores, wherein jasmonic acid (JA), salicylic acid (SA), and ethylene (ET) function as primary regulators (Romero et al., 2023). Upon herbivory, signaling cascades are activated almost immediately after damage through wounding perception and herbivore-associated molecular pattern (HAMP) recognition, leading to early hormone production within minutes (Machado et al., 2016; Pandey et al., 2017; Zafeiriou et al., 2022). These hormonal networks regulate both direct defenses, such as protease inhibitors (PIs), oxidative enzymes, and secondary metabolites that impair herbivore digestion, and indirect defenses including herbivore-induced plant volatiles (HIPVs) that recruit natural predators (Sultana et al., 2024; Upadhyay et al., 2024). Recent studies have highlighted that indole-3-acetic acid (IAA) plays a pivotal role in the early systemic signaling following herbivore attack, especially during insect wounding (Singh et al., 2024a). IAA accumulation is often triggered within minutes after herbivore perception, preceding the JA burst, and coordinates auxin-responsive gene expression that modulates downstream defense amplification and tissue remodeling (Machado et al., 2016; Ali et al., 2024c).

Trichomes, cuticle layers, and waxes act as critical mechanical barriers against herbivory ( Figure 9 ). Nonglandular trichomes prevent insect attachment, while glandular trichomes secrete toxic metabolites including terpenoids and alkaloids (Wang et al., 2021a, b; Balaji and Jambagi, 2024). Trichome development is controlled by the GL1–GL3–TTG1 (GL1–GL3–TTG1 complex) and downstream targets like GL2, modulated by feedback (Pattanaik et al., 2014; Pei et al., 2024; Zumajo-Cardona et al., 2023). JA and gallic acid influence trichome density via MYC2, integrating light and wound signals (Brian and Bergelson, 2003). JA–ET crosstalk further enhances glandular secretion and patterning in Arabidopsis through GL3 (Yoshida et al., 2009; Song et al., 2022). Cuticular waxes, composed of Very-Long-Chain Fatty Acids (VLCFAs), alkanes, and esters, minimize desiccation and deter insect feeding (Zeisler-Diehl et al., 2018; Batsale et al., 2021). VLCFAs are derived from C16/C18 fatty acids and elongated in the ER by the FAE complex (Batsale et al., 2023). Export to the surface is mediated by ABC (ATP-Binding Cassette Transporters) such as ABCG12 (CER5), reinforcing the cuticle barrier (Pighin et al., 2004). Wax layers also trap VOCs that repel herbivores or attract predators (Camacho-Coronel et al., 2020; Xue et al., 2017). ABA signaling enhances wax biosynthesis under herbivory (Lewandowska et al., 2024; Joubès and Domergue, 2018).

Plants produce diverse chemical compounds including phenolics, alkaloids, terpenoids, VOCs, and protease inhibitors (Divekar et al., 2023a, 2022; Vasantha-Srinivasan et al., 2024). Their synthesis is induced by HAMPs or wounding and regulated by JA and SA signaling (Sharma et al., 2017; Malik et al., 2021; Nguyen et al., 2022). Phenolic compounds such as flavonoids, tannins, and lignins act through multiple mechanisms digestive inhibition, nutrient sequestration, or cell wall reinforcement (Kumar et al., 2020; Singh et al., 2021; Iqbal and Poór, 2024; Balakrishnan et al., 2024). Flavonoids and tannins interfere with enzymes or form indigestible complexes, while lignins strengthen tissue resistance. Alkaloids like nicotine and caffeine disrupt herbivore neural and metabolic pathways (Matsuura and Fett-Neto, 2015; Steppuhn et al., 2004; Garvey et al., 2020; Abernathy et al., 2023; Raisch and Raunser, 2023; Mostafa et al., 2022). Nicotine overstimulates nicotinic receptors; caffeine inhibits phosphodiesterase. Their biosynthesis is JA-dependent, involving Putrescine N-Methyltransferase (PMT) and caffeine synthase (Yang et al., 2016). Terpenoids-monoterpenes, sesquiterpenes, and diterpenes exert toxicity by disrupting membranes, mimicking hormones, or inhibiting neural enzymes (Konuk and Ergüden, 2020; Tsang et al., 2020; Zielińska-Błajet and Feder-Kubis, 2020; Câmara et al., 2024). Diterpenes target mitochondrial function (Yang et al., 2022). Their synthesis is upregulated via the Mevalonate Pathway (MVA) and Methylerythritol Phosphate (MEP) pathways (Opitz et al., 2014; Singh et al., 2024c; Ghorbel et al., 2021). VOCs, especially Green Leaf Volatiles (GLVs) and Herbivore-Induced Plant Volatiles (HIPVs), deter herbivores and attract predators (Mortensen, 2013; Allmann et al., 2013; Ameye et al., 2018; Jones et al., 2022a, b; Zhang et al., 2017; Frago et al., 2022; Matsui and Engelberth, 2022). Hexenal disrupts olfactory cues; methyl jasmonate recruits parasitoids. VOCs also prime systemic defense in neighboring tissues. Protease inhibitors (PIs) and tannins impair digestion by targeting gut proteases and binding proteins (Divekar et al., 2023b; Cid-Gallegos et al., 2022; Molino et al., 2021; Iqbal and Poór, 2024; Mora et al., 2022). JA and SA regulate the expression of key defense genes such as Proteinase Inhibitor II (PI-II) from S. lycopersicum and Phenylalanine Ammonia-Lyase (PAL), which is conserved across several species including Arabidopsis and Nicotiana, providing rapid and localized resistance against herbivores (Farmer and Ryan, 1992). Table 1 systematically summarizes various induced defense compounds and their specific actions against herbivores.

Herbivores engage in finely tuned behaviors that limit exposure to inducible plant defenses. For example, leaf miners such as Liriomyza spp. feed internally, avoiding detection by external pattern recognition receptors and minimizing activation of systemic hormonal cascades (Hamza et al., 2023). Gall-inducing insects hijack developmental signaling to create nutrient-rich microenvironments shielded from chemical defenses (Mishra et al., 2024b). Additionally, many insects exploit phenological windows targeting young, less lignified tissues with lower concentrations of phenolics and VOCs (Milton, 1979). Physical adaptations, such as hydrophobic tarsal pads in thrips and beetles, allow navigation across resinous or trichome-dense surfaces, mitigating mechanical restriction and enhancing feeding efficiency (Voigt et al., 2017).

At the molecular level, insects have developed specific mutations and regulatory mechanisms to resist plant defenses. Resistance to plant toxins often arises from genetic mutations that can alter the target sites of these compounds (Petschenka and Dobler, 2009). Some insects, such as milkweed bugs and monarch butterflies, exhibit remarkable adaptations through mutations in the sodium–potassium ATPase gene. These mutations reduce the binding affinity of cardenolides, which are toxic steroids produced by milkweed plants, to the enzyme and effectively neutralize their inhibitory effects. This molecular modification enables these insects to not only tolerate high levels of cardenolides but also sequester these compounds for use as a chemical defense against predators (Aardema et al., 2012). In the Colorado potato beetle L. decemlineata, the production of digestive enzymes, including lipases and cellulases, is upregulated to break down structural components of plants, such as waxes and cellulose. This enzymatic plasticity helps in coping with different plant species or varying environmental conditions (Wilhelm et al., 2024).

In their arms race with plants, herbivorous insects have evolved the ability to suppress plant immune responses by using specialized proteins known as effectors. These molecules, secreted in the saliva or other oral secretions of insects, can directly interfere with the immune signaling pathways of plants, enabling successful colonization and feeding (Wang et al., 2023). Herbivores use effectors to manipulate plant immune signaling systems, such as those regulated by JA, SA, and ET. These phytohormones orchestrate plant defense responses against different types of attackers (Caarls et al., 2015). The primary goal of herbivore effectors is to suppress recognition by plants and prevent the downstream activation of these pathways. Herbivorous insects secrete effectors that suppress plant PTI, which is activated upon recognition of HAMPs, thereby facilitating successful feeding (Basu et al., 2018). For example, Helicoverpa zea secretes glucose oxidase (GOX), which disrupts ROS signaling in the plant host, weakening defense activation (Tian et al., 2012), and aphids deliver salivary effectors to inhibit R-proteins and suppress ETI cascades (Elzinga et al., 2014). Some insects, like weevils, modulate polygalacturonase inhibitors to suppress cell wall-based defenses, facilitating feeding with minimal resistance (Kalunke et al., 2015; Gong et al., 2023). Through such diverse adaptations, herbivorous insects effectively navigate plant defenses. Understanding these mechanisms is vital for developing innovative pest management strategies in agricultural systems.

Herbivorous insects can manipulate plant hormonal crosstalk to circumvent defenses by exploiting the antagonistic interaction between JA and SA. Aphids and whiteflies stimulate SA accumulation while suppressing JA-mediated defenses, resulting in reduced synthesis of JA-regulated compounds such as PIs and secondary metabolites (Zarate et al., 2007; Zhang et al., 2013; Xu et al., 2019). This hormonal manipulation facilitates phloem feeding, thereby promoting insect colonization and reproduction (VanDoorn et al., 2015; Zhang et al., 2018). Whiteflies (Bemisia tabaci) secrete salivary effectors to activate SA signaling, dampening JA-mediated defenses in host plants like tomato (Zhang et al., 2018), and aphids use similar strategies, activating SA and suppressing JA to weaken defenses, facilitating efficient feeding (Zhang et al., 2023a; 2024c). The tobacco hornworm (Manduca sexta) secretes GOX to interfere with the oxidative burst associated with JA signaling, reducing overall plant defense and enhancing feeding efficiency (Bari and Jones, 2009). These examples illustrate the intricate strategies by which herbivorous insects manipulate plant hormonal crosstalk, thereby enhancing their ability to overcome plant defenses.

Insect herbivores have evolved intricate countermeasures to overcome plant defenses mediated by ABA, a key hormone involved in stress adaptation (Park et al., 2019). One such strategy involves the secretion of salivary effector proteins that disrupt ABA signaling to suppress plant defensive responses. These effectors may target crucial components of the ABA pathway, including ABA receptors (PYR/PYL/RCAR), protein phosphatases (PP2Cs), or transcriptional regulators, effectively modulating guard cell behavior and secondary metabolite production (Korek and Marzec, 2023). Such interference can compromise stomatal closure, leading to enhanced water loss and weakened physical barriers, ultimately increasing insect feeding efficiency. Additionally, certain insect salivary proteins have been shown to mimic phosphatases, potentially dephosphorylating key signaling proteins involved in ABA cascades, thereby dampening the transcription of ABA-responsive genes that are otherwise critical for defense reinforcement under combined drought and herbivore pressure (Khan et al., 2015). Beyond signaling disruption, insects may enzymatically degrade or detoxify ABA through metabolic conversion pathways, reducing the hormone’s bioavailability. Some evidence suggests that insect species may upregulate specific oxidases or transferases that modify plant-derived ABA into inactive forms (Kosma et al., 2009). While such detoxification pathways remain underexplored, they represent a compelling frontier in plant-insect interaction research. Moreover, plant biotechnology research suggests that enhancing ABA pathway robustness through genetic engineering can mitigate such insect manipulations. For instance, transgenic lines with fortified ABA signaling components have shown improved resilience to both abiotic and biotic stress, although precise gene targets and field validation remain critical (Dhariwal et al., 1998). These multifaceted counter-adaptations reflect the dynamic co-evolution between plants and insect herbivores, underscoring the need for integrated pest management strategies that consider both plant resistance and insect plasticity in manipulating defense signaling networks.

Herbivorous insects have evolved precise delivery systems to deploy effector molecules that interfere with host immunity at the cellular and molecular levels. Piercing–sucking insects, including aphids and whiteflies, utilize slender stylets to navigate intercellular spaces and deliver salivary effectors directly into the cytoplasm of phloem and mesophyll cells, where they disrupt host immune signaling (Wang et al., 2023; Naalden et al., 2021). For instance, Myzus persicae secretes Mp10, which suppresses callose deposition at sieve plates, thereby maintaining phloem conductivity for sustained nutrient uptake (Bos et al., 2010). Bemisia tabaci releases the effector BtE1 that interferes with SA-mediated defense cascades, leading to reduced expression of defense-related genes and enhanced phloem extraction efficiency (van Kleeff et al., 2024). Similarly, rice planthoppers like Nilaparvata lugens translocate effectors such as NlNSE1 and NlNSE2 into host tissues to suppress JA biosynthetic and downstream signaling pathways, thereby diminishing the accumulation of phenolic and flavonoids essential for herbivore deterrence (Lou et al., 2005). These strategies facilitate long-term colonization and reproductive success. Chewing insects, such as caterpillars and coleopterans, also employ salivary effectors during feeding to suppress localized immune responses. Helicoverpa armigera secretes GOX, which attenuates the oxidative burst by downregulating NADPH oxidase activity and interfering with ROS-dependent amplification of JA signaling (Tian et al., 2012). Likewise, L. decemlineata produces polygalacturonase (LDPG1), which degrades homogalacturonan in the plant cell wall matrix, thereby weakening structural integrity and facilitating herbivore feeding (Gosset et al., 2009). Other herbivores have evolved enzymatic adaptations that modulate secondary metabolite activation. N. lugens secretes β-glucosidases that hydrolyze glucosylated precursors, preventing the activation of toxic glucosinolates and reducing defense metabolite pools (Wang et al., 2008). Similarly, sawflies feeding on Brassicaceae manipulate the glucosinolate–myrosinase system to suppress the release of isothiocyanates, diminishing plant chemical deterrence (Ahuja et al., 2011). The diversification of effector repertoires across insect taxa illustrates a sophisticated evolutionary response to host immunity, reflecting the coevolutionary pressure exerted by plant surveillance systems. While plants continuously evolve novel receptors and immune modulators to recognize and neutralize insect effectors, herbivores reciprocally fine-tune effector specificity, expression timing, and delivery routes to evade detection and maintain feeding success (Wang et al., 2023). Understanding these dynamic molecular dialogues offers promising avenues for engineering crops with enhanced recognition capacity or effector-triggered resistance, laying the foundation for next-generation pest management strategies.

The intricate interplay between plants and herbivorous insects involves signaling molecules and genes orchestrating both plant defenses and insect counterstrategies (Zebelo and Maffei, 2015; Pang et al., 2021). The JA derivative JA-Ile, in particular, is central to plant defenses against chewing insects. It binds to the COI1–JAZ receptor complex, degrading JAZ repressors and activating transcription factors like MYC2, which, in turn, induces PIs and secondary metabolites, such as glucosinolates and alkaloids (Kumar et al., 2024). SA plays a pivotal role in plant defense against phloem-feeding insects by activating PR genes through the SA signaling pathway (Fang et al., 2025). Systemin and ET amplify local and systemic defenses by interacting with the JA and SA pathways, while VOCs further enhance resistance (Erb, 2018). Insect-derived elicitors, or HAMPs, refine plant responses. For instance, fatty acid–amino acid conjugates from S. frugiperda and β-glucosidase from Pieris brassicae activate MAPK cascades via plant LRR-RLK receptors, boosting secondary metabolite production (Vidhyasekaran, 2016). In contrast, insect salivary effectors such as aphid Mp55 suppress plant defenses by reducing the accumulation of defense-related compounds, thereby facilitating infestation (Elzinga et al., 2014). In addition to Mp55, several candidate salivary effectors have been identified from M. persicae, including Mp10, Mp42, and MpC002, which are predicted to interfere with plant immune responses (Bos et al., 2010). Rapid plant defense signaling involves ROS and calcium ion (Ca²⁺), which activate transcription factors like WRKY through MAPK and CDPK pathways, further amplifying stress-responsive gene expression (Adachi et al., 2015). Additionally, jasmonate signaling activates MYC transcription factors, such as MYC2, to regulate defense responses (Lorenzo et al., 2004).

Small RNAs, including miRNAs and siRNAs, regulate plant defenses by fine-tuning gene expression post-transcriptionally. Both miR393 and miR319 enhance JA defenses by suppressing auxin signaling and modulating JA biosynthesis, promoting secondary metabolite production (Schommer et al., 2008; Iglesias et al., 2014; Jacob et al., 2021), and siRNAs, such as phasiRNAs derived from miRNA-targeted NLR transcripts, silence genes that negatively regulate JA signaling, ensuring resource-efficient defenses during herbivore attacks (Liao et al., 2022). Cross-kingdom RNA transfer adds complexity to plant-insect interactions. Plants can deliver small RNAs via extracellular vesicles to insects, targeting genes involved in detoxification or digestion, such as cytochrome P450s in H. armigera, thereby disrupting insect physiology (Zhao et al., 2024). Conversely, H. armigera miRNAs, such as miR854, manipulate plant defenses by targeting JA-signaling regulators like WRKY, shifting the JA–SA balance to weaken resistance (Tan et al., 2012; Chen et al., 2019a). Small RNAs secreted by insect saliva can target key plant defense genes, including those involved in lignin biosynthesis (e.g., MYB transcription factors), RLK signaling pathways, and ROS generation, thereby attenuating both structural and biochemical defenses (Han et al., 2025). For example, siRNAs from aphids and whiteflies interfere with NADPH oxidases, reducing the oxidative bursts crucial for secondary metabolite production (Hu et al., 2020). These RNA-mediated interactions highlight the sophistication and complexity of the co-evolutionary arms race between plants and herbivores.

Symbiotic microbes critically influence plant–insect dynamics by either enhancing plant immunity or facilitating herbivore adaptation. In the rhizosphere, arbuscular mycorrhizal fungi (AMF) and nitrogen-fixing rhizobia prime plant defenses by modulating phytohormonal pathways. AMF enhance JA-dependent synthesis of terpenoids and phenolics that deter insect feeding (Sharma et al., 2017; Boyno et al., 2023). Sinorhizobium meliloti, which forms nodules in legumes like Medicago truncatula, not only improves nitrogen status but also strengthens aphid resistance through JA-mediated induction of deterrent metabolites (Pandharikar et al., 2020). Endophytic fungi and bacteria within plant tissues also contribute to insect resistance. Fusarium solani-derived endophytes in rice upregulate phenolic biosynthesis and PR gene expression, reducing stem borer infestation (De Lamo and Takken, 2020; Xia et al., 2022). Similarly, Epichloë fungi in grasses produce defensive alkaloids—peramine and lolines regulated by JA, SA, and ET signaling crosstalk (Bharadwaj et al., 2020). Recent work has shown that plant-associated microbiomes directly modulate hormone-regulated defenses in plant–insect interactions (Théatre et al., 2021). A meta-analysis revealed that inoculation with PGPR (e.g., Pseudomonas fluorescens, Bacillus subtilis) enhances resistance to chewing insects by inducing JA- and ET-mediated defense responses, including elevated PIs and phenolic accumulation in leaves demonstrated under greenhouse conditions in cabbage and maize (Ruiz-Santiago et al., 2025). Endophytic Trichoderma asperellum M2RT4 induces systemic resistance against Tuta absoluta in tomato by activating both SA and JA signaling pathways and altering volatile emissions to reduce oviposition and larval survival (Agbessenou et al., 2022). Moreover, Root herbivory by insects alters rhizosphere microbial communities, which feeds back to influence aboveground plant defense via ISR-like mechanisms (Friman et al., 2021). These studies highlight direct and indirect hormone-pathway modulation by microbes, contextualized in eco-physiological setups. Additionally, microbes appear to subtly influence IAA- and JA-hormone balance: PGPR-induced auxin changes may prime downstream defense cascades (root-shoot signaling), aligning with the timing and strength of systemic responses (Rashid and Chung, 2017). It is important to emphasize that these effects, though robust in controlled environments, vary significantly with plant genotype, microbial consortia, environmental factors, and insect feeding strategies (Tronson and Enders, 2025). These examples illustrate how microbial partnerships facilitate plant defense suppression via detoxification, hormonal modulation, and nutritional support.

Natural predators and parasitoids regulate herbivore populations, indirectly enhancing plant immunity through trophic cascades. By reducing herbivore pressure, they allow plants to allocate resources toward growth and reproduction, making predator–prey interactions important to sustaining plant health (Silliman and Angelini, 2012). Predators like lady beetles (Coccinellidae) prey on aphids, reducing aphid populations and thereby diminishing the secretion of salivary effectors that suppress plant defenses. This predation enables plants to maintain their natural immune responses (Elzinga and Jander, 2013). Parasitoids, such as Trichogramma species, parasitize pest eggs and disrupt the host’s ability to produce salivary effectors, similarly reducing herbivore-induced plant-defense suppression and allowing stronger immune activation (Martel et al., 2021). Plants also detect insect oviposition and initiate defenses against subsequent herbivory (Wang et al., 2021c). In A. thaliana, for example, oviposition by P. brassicae activates an SA-dependent signaling pathway, inducing PR protein expression and enhancing systemic resistance (Gouhier-Darimont et al., 2013). This response involves the recognition of egg-associated elicitors, similar to PAMPs, triggering localized and systemic defense mechanisms to prepare for future attacks.

Despite advancements, critical gaps remain in understanding the complexity of plant immunity to herbivores. Hormonal crosstalk between JA, SA, and ET pathways under field conditions, where biotic and abiotic stresses co-occur, is not fully elucidated (Ku et al., 2018; Ament et al., 2010), and trade-offs in JA-SA antagonism, dynamically modulated by herbivore pressures, environmental fluctuations, and genotype-specific regulatory networks, continue to complicate precise predictions in defense allocation (Samanta and Roychoudhury, 2024). Also, the roles of resistance genes, miRNAs, and Long non-coding RNAs (lncRNAs) in herbivore defense are largely unexplored and require functional studies to reveal their precise behaviors (Huang et al., 2023). Newly identified herbivore effectors, such as those found in P. rapae and M. sexta, demonstrate their ability to manipulate plant defenses, yet their mechanisms and targets need deeper investigation. Additionally, the temporal dynamics of defense activation and specificity under multi-herbivore attacks remain poorly understood (Croy et al., 2021). Addressing these gaps demands integrative approaches that incorporate ecological conditions, coevolutionary pressures, and pest adaptation mechanisms.

In field production systems, plant defense mechanisms operate alongside and often interact with common agronomic practices such as chemical applications and IPM. While agrochemicals (e.g., synthetic insecticides) are effective in reducing pest pressures, they can disrupt hormonal signaling, harm non-target organisms, and promote resistance (Zhou et al., 2024; Ahmad et al., 2024). Conversely, IPM strategies that combine monitoring, biological control, cultural practices, and targeted chemical interventions can support natural plant defense pathways while reducing reliance on pesticides, though adoption and implementation remain highly context-dependent due to economic and logistical challenges (Grasswitz, 2019; Wyckhuys et al., 2023). Incorporating discussions on these practical challenges is essential for aligning mechanistic insights with real-world crop protection, ensuring that laboratory-based discoveries translate effectively into field-resilient plant immunity.

Pest adaptation, a significant impediment in plant protection, involves evolutionary shifts that undermine the long-term efficacy of biotechnological interventions. For instance, B. thuringiensis (Bt) cotton, initially celebrated for its effectiveness in reducing lepidopteran pest infestations in India, has increasingly faced challenges due to the development of resistant pest populations under continuous selection pressure (Karimi et al., 2012; Xing and Wang, 2024). This resistance emergence underscores the necessity for robust resistance management strategies such as refuge planting and gene pyramiding to maintain the sustainability of Bt technologies (Bravo et al., 2015). Concurrently, the ecological implications of these interventions require comprehensive scrutiny. The deployment of biocontrol agents and their derivatives, aimed at suppressing pest populations below economic thresholds, contributes to maintaining ecosystem equilibrium by preserving beneficial arthropods (Patil et al., 2021). However, realizing the full potential of such biotechnological tools necessitates integrative frameworks that consider agroecological complexities. While initial field deployments like Bt cotton demonstrated reduced pesticide reliance and increased yield (Sánchez et al., 2018; Singh et al., 2019), challenges such as RNAi variability under field conditions and poor farmer access to information persist (Ramírez-Pool et al., 2024; Shields et al., 2018). The broader shift toward environmentally benign practices, aligned with green chemistry principles, emphasizes reduced toxicity, target specificity, and biodegradability, supporting IPM strategies. Nonetheless, the continued use of synthetic pesticides raises environmental and public health concerns, with mounting evidence of their contribution to soil, water, and air pollution and their bioaccumulative impacts on biodiversity and human health (Lahlali et al., 2022; Antoszewski et al., 2022). Ultimately, translating laboratory innovations into sustainable field solutions will require not only adaptive resistance management and regulatory coherence but also farmer-centric knowledge dissemination and ecosystem-based monitoring for long-term agricultural resilience.

Despite their precision, the deployment of biotechnological tools, such as CRISPR/Cas9 and RNAi, raises ethical and ecological concerns. Genetically modified plants with enhanced resistance may disrupt natural pest–predator dynamics and affect nontarget species via unintended RNAi effects (Lundgren and Duan, 2013; Diaz et al., 2025). Public apprehensions about GM crops, as seen with Bt brinjal in India and stringent GM organism policies in the EU, emphasize the need for transparent risk assessments and stakeholder engagement (Singh, 2018; European Commission, 2024). Ecological concerns, including pest adaptation, gene flow to wild relatives, and the disruption of plant–microbe interactions, necessitate rigorous long-term studies (Mandal et al., 2020). Strategies integrating genetic engineering with agroecological practices can mitigate environmental impacts and foster sustainable pest management (Anderson et al., 2019). Additionally, robust governance frameworks and ecological risk assessments are critical for deploying engineered plants ethically and sustainably, ensuring their role in climate-resilient agriculture while preserving ecosystem integrity (Hilbeck et al., 2011).

Recent changes in regulatory landscapes have started to differentiate genome-edited crops from conventional GMOs. For example, countries like the US, Brazil, and Japan have streamlined regulations for CRISPR-based edits that do not introduce foreign DNA, considering them equivalent to conventional breeding outcomes (EFSA Panel on Genetically Modified Organisms, 2010; Anderson et al., 2019). In contrast, the European Union continues to apply stringent GMO regulations to genome-edited plants, limiting their adoption and research potential (Voigt, 2023). These discrepancies influence global trade, technology diffusion, and food security policy, highlighting the urgent need for harmonized international biosafety standards.

Furthermore, climate change amplifies the complexity of these challenges. Elevated CO₂ levels, extreme weather patterns, and altered pest pressures may unpredictably interact with transgenic traits, affecting efficacy and stability (Liu et al., 2020). For instance, RNAi-based insecticidal crops may exhibit variable gene silencing efficiency under fluctuating temperatures, potentially compromising pest control and increasing resistance risk (Fletcher et al., 2020). Additionally, CRISPR-driven traits targeting susceptibility (S)-genes may influence unintended pathways under abiotic stress, necessitating context-specific ecological modeling before field deployment. To address these emerging concerns, a new paradigm of “precautionary innovation governance” is recommended (Nascimento et al., 2023). This includes public–private collaborations, real-time monitoring of gene flow, off-target effects, and ecosystem-level feedback mechanisms. Implementing gene-drive containment strategies, temporal deployment limits, and trait-reversal mechanisms (e.g., CRISPR-off switches) can provide adaptive safety controls while ensuring continued innovation (Pawluk et al., 2016). Lastly, multi-stakeholder dialogue involving farmers, ecologists, ethicists, and regulators is essential to develop trust and social license for genome-edited agricultural solutions (Lindberg et al., 2023).