The initial phase in mycoparasitism is Trichoderma spp. detecting or identifying R. solani as prey. Trichoderma spp. recognize the oligopeptide and oligosaccharide compounds produced by R. solani in reaction to hydrolytic enzymes, such as proteases and chitinases (Druzhinina et al., 2011; Sood et al., 2020). A signaling cascade is activated when these molecules attach to receptors on Trichoderma spp. hyphae. This causes transcription factors to be activated, which govern production of secondary metabolite (SM) production and lysis of cell wall (Harman et al., 2004; Druzhinina et al., 2011; Table 1). Many Trichoderma spp. express genes encoding proteases and oligopeptide transporters before and during interaction with R. solani, according to a recent study. The bulk of proteases are subtilisin-like serine proteases, and genes for these enzymes may be found in abundance in expressed sequence tags (ESTs). For example, a review of the ESTs collected at the start of the T. atroviridis-R. solani interaction revealed many genes that produce subtilisin-like serine proteases. The prb1 gene encodes these proteases, and overexpression of these proteases boosted mycoparasitic activity. The action of these proteases on R. solani may result in the release of oligopeptide molecules that bind to receptors on Trichoderma spp. Using T. atroviride EST libraries, a preliminary transcriptome research revealed considerable alterations in T. atroviride gene expression, including changes that resembled a response to nitrogen restriction, lipid metabolism adjustments, and signaling changes (Seidl et al., 2009; Kaur et al., 2021).

G protein-coupled receptors (GPCRs) of biocontrol agents act as a sensor for the oligopeptides secreted by plant pathogens (Daguerre et al., 2014). They are the most frequent cell surface receptors for detecting environmental signals at the plasma membrane. These receptors sense ligands, such as nutrients, oligopeptides, sex pheromones, oxylipins. They frequently use heterotrimeric G proteins to connect with downstream signaling pathways including the mitogen-activated protein kinase (MAPK) and cAMP-protein kinase A (PKA) cascades (Table 1; Figure 3). In response to R. solani, several GPCR-encoding genes were expressed in Trichoderma spp. showing that GPCRs play a role in detecting and triggering the mycoparasitic response. The three primary components of heterotrimeric G protein signaling are a GPCR, a heterotrimeric G protein (made up of G and G subunits), and an effector. G protein activation (exchange of GDP for GTP on the G subunit) and dissociation of the GTP-bound subunit from the associated dimer occur as a result of the ligand contact, allowing both units to govern downstream effectors. In fungus, the cAMP-PKA pathway and MAPK cascades are typical effectors of heterotrimeric G protein. Both routes are substantially conserved and linked. Transmembrane G protein-coupled receptor signals are channeled by heterotrimeric G proteins to various intracellular destinations via activating effectors, such as adenylate cyclase or the MAPK cascades (Kaziro et al., 1991; Daguerre et al., 2014; Segreto et al., 2021). Trichoderma spp. require G proteins, GPCRs, and adenylate cyclase receptors to synthesize external cell wall lytic enzymes, release antifungal chemicals, and produce infection structures (Figure 3). Trichoderma hyphae were prevented from connecting to R. solani cell surfaces by inhibiting the gene encoding the T. atroviride seven-transmembrane receptor Gpr1, as well as upregulation of two chitinase genes (nag1 and ech42) and the protease gene prb1. Due to the importance of these genes in mycoparasitism, their downregulation in T. atroviride results in pathogen survival (Omann et al., 2012). Two G protein subunits identified in T. atroviride are Tga1 and Tga3. During direct fight with R. solani, the tga1 mutant completely lost its mycoparasitic activity (Reithner et al., 2011). Infection structure development remained steady, while production of 6-pentyl-pyrone and sesquiterpene-derived antifungal metabolites reduced (Rocha-Ramírez et al., 2002; Reithner et al., 2011). Similarly, when addressed directly, the tga3 mutant was unable to build infection structures or mycoparasitize R. solani (Zeilinger et al., 1999). In fungus, the MAPK pathways are well-known signal transduction systems (Schmoll et al., 2016). Trichoderma’s genome contains genes for three pathogenicity MAPKs: (1) TmKA (also known as Tvk1 and Tmk1), (2) cell integrity kinase (TmkB), and (3) osmoregulatory MAPK (Hog1; Schmoll et al., 2016). TmkA gene mutation in T. virens strain “P” had no effect on biocontrol efficacy against R. solani (Zeilinger et al., 1999; Viterbo et al., 2004; Mukherjee et al., 2011, 2012). However, deletion of the same gene TmkA in the T. virens strain “Q” drastically lowered the Trichoderma’s biocontrol efficacy against R. solani (Mendoza-Mendoza et al., 2003). Trichoderma virens tvk1 mutants secreted more lytic enzymes and were far more efficient in disease control than the wild-type strain (Mukherjee et al., 2003). Trichoderma atroviride tmk1 mutants displayed decreased mycoparasitism activity against R. solani in direct mycoparasite–host interactions, as well as against R. solani specific control of ech42 gene transcription (Reithner et al., 2011). Furthermore, deletion of a Tmk1 homologue in T. atroviridis resulted in decreased mycoparasitic activity against R. solani, as well as increased synthesis of chitinase and other antifungal chemicals (Reithner et al., 2011).

In addition to, GPCRs, another importance receptors for signaling transduction are Cyclic adenosine monophosphate (cAMP) receptors. They are involved in the growth, condition, development, and biocontrol efficiency in Trichoderma spp. (Brunner et al., 2008; Table 1; Figure 3). Adenylate cyclase converts ATP to cAMP and is present on the inner side of the plasma membrane and at several sites throughout the fungal cell. Adenylate cyclase is triggered by a multitude of signaling molecules that activate G (Gs) protein-coupled receptors that stimulate adenylate cyclase. cAMP activates a cAMP-dependent protein kinase (PKA) that phosphorylates proteins like transcription factors to regulate gene expression (Dickman and Yarden, 1999). Tac1, an adenylate cyclase gene in T. virens, was deleted, which not only removed biocontrol efficacy against R. solani but also lowered secondary metabolite synthesis (Mukherjee et al., 2007).

In addition to cAMP and MAPK, the target of rapamycin (TOR) pathway is a critical regulator of Trichoderma spp. cell proliferation in response to nutrient availability (Table 1; Figure 3). In response to a lack of carbon and nitrogen, this pathway is triggered, resulting in anabolic activities and development (Schmoll et al., 2016). The TOR kinase is inhibited by rapamycin, and nutritional deficiency enhances the expression of genes involved in alternate nitrogen absorption. A growing body of evidence suggests that TOR has a role in nitrogen signaling and pathogenicity-related activities in fungal plant diseases. The Trichoderma genomes also encode single TOR kinase-like the fungal plant pathogens. In a recent study, the activity of TOR1, that is, T. atroviride’s solitary and crucial TOR kinase, was suppressed by chemical TOR inhibitors or genetic alteration. TSC2 and TSC1, which are negative regulators of TOR complex 1 (TORC1) in human cells, resulting in altered nitrogen source-dependent growth of T. atroviride, decreased generation of numerous secondary metabolites, and decreased mycoparasitic overgrowth on R. solani (Segreto et al., 2021). Transcription factors (TFs), which regulate gene transcription at the cellular level during antagonism, are currently understudied (Table 1). Specific motifs in the promoters of Trichoderma spp. biocontrol genes may bind transcription factors involved in nitrogen repression, stress responses, and the regulation of plant cell wall-degrading enzymes. There is no indication, however, that they have a role in antifungal activity. For example, T. atroviride’s xylanase transcriptional regular Xyr1 has a role in mycoparasitism and is essential to trigger the plant defense response (Reithner et al., 2014). When xyr1 was eliminated, R. solani competed more effectively. Plant defense responses were similarly delayed during the T. atroviride/Arabidopsis thaliana interaction.

Trichoderma spp. coil and generate helix-shaped hyphae around R. solani shortly after recognition, and this phenomenon is dependent on lectin recognition from R. solani’s cell wall. Conversely, plant lectins also cause coiling, demonstrating that lectins do not determine specificity in Trichoderma spp. Additionally, coiling is not always associated with mycoparasitism, as some Trichoderma spp. do exhibit this characteristic. Besides, hyphae of Trichoderma spp. become spiral or helical in shape and are considered diagnostic features in some Trichoderma spp. Trichoderma spp. often precede mycoparasitic attack by growing alongside the host hyphae and forming papilla-like structures. At the places where papilla-like structures form, the cell wall is degraded, and the lumen is penetrated. These papilla-like structures are identical to the appressorium of plant pathogenic fungi and those generated. Recent study suggests the presence of essential components of the cAMP and MAP kinase signaling pathways, such as G protein subunits (G), which govern extracellular enzyme synthesis, antibiotic production, and coil formation surrounding R. solani and T. atroviride expressed the G-gene (tga1) under the control of its promoter or the promoter of the proteinase gene (prb1; Reithner et al., 2005). All mutants showed an increase in coiling. Furthermore, T. viride overexpressing tga1 exhibited a greater capacity to outgrow R. solani. Induction of genes encoding ABC efflux transporters, pleiotropic and multidrug resistance transporters, and detoxification mechanisms (such as those encoding ABC efflux transporters and pleiotropic and multidrug resistance transporters) and detoxification mechanisms (such as those encoding ABC efflux transporters and pleiotropic and multidrug resistance transporters) in the presence of R. solani is a distinctive feature of Trichoderma spp. When R. solani develops sclerotia, it signals with radical oxygen species and excretes antifungal chemicals into the environment. Both radical oxygen species and antifungal drugs have been demonstrated to promote Trichoderma spp. stress’s response. The deletion of one of the genes in T. atroviridis that produces an ABC transporter (Abc2) resulted in poor biocontrol of R. solani, demonstrating that detoxification plays a role in mycoparasitism.

Secondary antifungal metabolites, such as NRPs (peptaibols, gliotoxin, gliovirin, etc.), polyketides, isoprenoid-derived metabolites, pyrones, and cell wall-hydrolytic enzymes or degrading enzymes (CWDEs) eventually kill the prey (Table 2; Figure 3). Trichoderma spp. genomes contain many genes for the synthesis of antifungal metabolites and CWDEs. Trichoderma virens, for example, possess the most non-ribosomal peptide synthesis of any plant pathogenic fungus. The cell wall of any fungus is composed of 30% dry weight chitin, -1,3-glucans, -1,3-glucans, and -1,4-glucans. Cellulases, polygalacturonases (PG), chitinases, glucanases, and proteinase are only a few of the CWDEs found in Trichoderma spp.

Pyrones are a good example of secondary metabolites produced by Trichoderma spp. that have strong biocontrol activity against R. solani. They have numerous antagonistic activities against R. solani were isolated from several Trichoderma spp. For example, a characteristic aromatic odor resembling coconut was observed in a T. harzianum and T. viride due to 6-pentyl-α-pyrone (6-PP). Pyrones with significant antifungal action against R. solani were observed as one of the paramount secondary metabolites produced by Trichoderma spp. (Kotasthane et al., 2015).

Gliotoxins are mycotoxins that contain sulfur have antimicrobial, antiviral, and immunomodulatory activities (Vey et al., 2001). The cell wall-degrading enzymes of Trichoderma spp. augment their antifungal activity synergistically (Lorito et al., 1998). Several genes of T. virens that encode gliotoxins, such as gliI, gliC, gliF, and gliG, appear to be important in antifungal action against R. solani (Atanasova et al., 2013a,b). However, these genes transcription is regulated by a number of factors, including pH, temperature, culture medium composition, and aeration (McDonagh et al., 2008; Table 3).

Terpenes are natural compounds having the formula (C₅H₈). There are various classes of terpenes and classification is based on the number of carbon (C) atoms as; C15; sesquiterpenes, C5; hemiterpenes, C20; diterpenes, C10; monoterpenes, C30; triterpenes, C40; tetraterpenes, C25; sesquiterpenes, or polyterpenes (Daguerre et al., 2014). In Trichoderma spp. a gene hmgR that codes for hydroxy-methylglutaryl-coenzyme has been identified. An enzyme reductase (HMGR) converts hydroxy-methylglutaryl-coenzyme into mevalonate. Mevalonate is than required for the formation of terpene compounds, such as terpene cyclases, trichodermin, triterpene viridin, and trichothecenes (Figures 2, 3). Some of these compounds, such as trichothecenes and trichodermin produced by Trichoderma spp., have antifungal activity against R. solani. Other terpenes compounds, such as triterpene ergosterol, are required for cell membrane fluidity. Trichoderma harzianum antifungal activity was diminished when hmgR was largely silenced, demonstrating that terpenoid chemicals are important in antagonism (Cardoza et al., 2007; Table 3). Harzianum A is an example of trichothecene, which inhibits fungal plant infections, such as R. solani, and induces genes involved in plant defense. Harzianum A synthesis is regulated by the tri gene cluster, which was recently identified in T. arundinaceum (Cardoza et al., 2007; Malmierca et al., 2013). When the genes tri5 and tri4 were disrupted, the generation of Harzianum A ceased, and the biocontrol activity of the transformants against R. solani was diminished.

Oxidases are crucial to Trichoderma spp.’ antagonistic activities against R. solani. During oxidation of glucose by oxidases, hydrogen peroxide (H₂O₂) is produced. Hydrogen peroxide inhibits sclerotia and subsequent hyphal growth of fungi when glucose is present. T. harzianum ETS 323 extracellular proteins recently yielded a new L-amino oxidase (Th-LAAO; Yang et al., 2011). In the presence of Th-LAAO, hyphal lysis of R. solani was seen in vitro. The efficiency of fungal antagonism against soil-borne pathogens is based not only on the production and release of antimicrobial components but also on antagonistic fungi’s capacity to protect themselves against toxins. To defend themselves from toxins generated by infections or themselves, biocontrol agents have many genes that encode ABC transporters and detoxifying enzymes. T. atroviride Taabc2 deletion mutants, for example, were less resistant to fungal inhibitory compounds, including their own, and performed less well in defending tomato plants against R. solani assaults (Ruocco et al., 2009).

Microorganisms require nutrients to survive, so competition for nutrient constraints and the colonization of plant tissues results in pathogens control (Sarma et al., 2014). When resources are few, microorganisms with the same ecological niche and physiological requirements struggle for nourishment (de Boer et al., 2003). Trichoderma spp., compete with R. solani for nutrients, mainly carbon (Sivan and Harman, 1991; Sarrocco et al., 2009). Comparatively to other fungi, they are better at mobilizing and absorbing soil nutrients (Sood et al., 2020). Moreover, in comparison to other fungi, they have a remarkable ability for ATP through the sugars metabolism including cellulose, hemicelluloses, glucans, and chitin (Oszust et al., 2020). Biomass components, mainly cellulose and hemicelluloses, are thought to be significant determinants of biocontrol fungi’s antagonistic activity. They are intended to be part of the saprophytic lifestyle and plant pathogen competition. Trichoderma spp., undoubtedly the most investigated fungal biocontrol agent, contain bulk of the genes encoding biomass-degrading hydrolytic enzymes found so far. Proteases, cellulases, hemicelluloses and amylases, are biological substrates degrading hydrolytic enzymes. As a result, Trichoderma spp. aid in carbon recycling. Trichoderma spp. and R. solani’s competitive capacity for cellulose utilization on wheat straw was assessed in a prior research (Sarrocco et al., 2009). Because wheat straw is the primarily source of cellulose and hemicelluloses, cellulolytic activity levels measured as mechanism in the straw possession competition. Fungus competition may also be influenced by the prompt uptake of nitrogen and carbon molecules that are either naturally present or released in the soil. Overexpression has been linked to the absorption of nutrients produced through the destruction of pathogenic fungi’s fungal cell walls, as well as direct nutrients competition in the soil, according to many transcriptome investigations. So far, only Gtt1, a high-affinity glucose transporter discovered in T. harzianum, has been examined, and its mRNA level rose in response to R. solani (Delgado-Jarana et al., 2003; Table 4). Competition for micronutrients can also arise in the soil. The most well-known example is competition for iron, which is essential for fungal pathogen development and pathogenicity. Trichoderma spp. secrete a number of siderophores that chelate iron and alter its availability to other bacteria. T. harzianum produced the most siderophores and had potent antifungal properties. A paucity of iron in the environment causes siderophore development and iron competition. Trichoderma spp. biocontrol ability against R. solani is influenced by iron competition (Table 4). As compared to R. solani and Trichoderma spp. can more effectively access the limited amounts of iron available. A peptide synthetase gene, Psy1, has been discovered. Psy1 disruptants generated normal levels of gliotoxin but struggled to grow in low-iron environments, indicating that Psy1 is involved in siderophore synthesis (Wilhite et al., 2001). Harzianic acid is a siderophore released by T. harzianum that promotes plant development while also acting as an antifungal against R. solani (Vinale et al., 2013).

Ahmad and Baker (1987) coined the term rhizosphere competence for Trichoderma spp. which they described as the capacity of these fungi to grow and operate in the growing rhizosphere. The rhizosphere is a common ecological habitat for Trichoderma spp. and it provides saprotrophy and biotrophy possibilities on plant root exudates. Mucigel is a slimy gel-like capsule that covers plant root terminals (Oszust et al., 2020; Vinale and Sivasithamparam, 2020; Yu et al., 2022). The outermost cells of the root cap expel highly hydrated polysaccharides, such as pectins and hemicelluloses (arabinoxylans and rhamnogalacturonans). Trichoderma spp. produce hemicellulases (hemicellulolytic) and cellulases (cellulolytic) to utilize polysaccharides more effectively than R. solani secreted by plant root tips (Guzmán-Guzmán et al., 2017). For example, an endopolygalacturonase expressing gene, is required for the effective establishment of T. harzianum in the tomato rhizosphere, and this gene is also useful in root colonization and the induction of plant defenses. Plants also excrete saccharides, such as monosaccharides, disaccharides, and sucrose, which offer essential carbon substrate for Trichoderma spp. rhizosphere establishment (Oszust et al., 2020). Trichoderma spp. have also genes that encode intracellular invertases; for example, sucrose permease takes up sucrose before being hydrolyzed. Trichoderma spp. also have particular sucrose transporter and have biochemical properties similar to plant sucrose transporters (Sood et al., 2020). Sucrose is actively transmitted from plant to fungus, according to these shards of evidence. Furthermore, several Trichoderma spp. express a large number of important solute transporters, the functions of which to acquire additional root exudates are unclear (Zhang and Zhuang, 2020). In conclusion, the presence of pathogens and root-derived nutrients may have been significant attractants for Trichoderma spp. to establish themselves in the rhizosphere and create relationships with plant roots.

The ability to recognize and cling to roots, penetrate the plant, and endure toxic compounds released by the plant in reaction to invasion is necessary for root colonization. Trichoderma spp. colonize the intercellular spaces of the first or second layer of root cells (Brotman et al., 2008). The hyphal and conidial cell walls contain several proteins that aid Trichoderma spp. in attaching to the roots via appressorium-like structures (Steindorff et al., 2012; Table 4). Enzymes, such as cellulase, hemicellulase, and protease, are subsequently secreted and employed to enter the roots (Viterbo et al., 2004). Trichoderma spp. proliferation is further aided by the highly hydrated polysaccharides of the root-secreted mucigel layer, as well as the mono- and disaccharides discharged into the rhizosphere by plant roots. According to research, root colonization, defense mechanism coordination, and leaf photosynthetic rate enhancement are all facilitated by plant-derived sucrose. To obtain root exudates, Trichoderma spp. have a variety of transporters/carriers, such as permease/intracellular invertase system and a di/tripeptide transporter. Hydrophobins are tiny proteins secreted by Trichoderma spp. that have recently been discovered. These proteins aid Trichoderma spp. in the attachment of fungal roots. These proteins feature a unique domain with eight cysteine residues in conserved positions. Based on their hydropathy patterns and solubility, hydrophobins were initially classified as class I and II. Furthermore, phytopathogenic fungi also rely on them to attach to the surface of the host plant (Talbot et al., 1996). Recently, a gene tvhydii1 that belong to class II hydrophobin, was isolated and characterized from T. virens (Guzmán-Guzmán et al., 2017). Overexpression of the gene tvhydii1 increases T. virens’ antagonistic activity against R. solani as well as the colonization of plant roots. Furthermore, deletion of tvhydii1 reduces antagonistic activity against R. solani and plant root colonization. Trichoderma spp. also encode expansin-like proteins, such as Swollenin TasSwo, which loosen, expand, or disrupt plant cell wall elements including cellulose and hemicellulose. Although their exact mechanism of action is unclear, it is thought that expansin-like proteins break into the crevices generated by interlacing microfibers in the cell wall, causing a conformational shift that causes the cell wall to expand, assisting root colonization. Plant CWDEs are also engaged in active root colonization, in addition to expansin and hydrophobin proteins. Many plants showed the strengthening of epidermal and cortical cell walls, as well as the deposition of considerable quantities of callose and cellulose, 72 h following root colonization. Callose-enriched cell walls limit Trichoderma spp. to the epidermis and cortical intercellular gaps, preventing Trichoderma spp. from entering the vascular stele. Antimicrobial chemicals are also synthesized and accumulated by plants in response to Trichoderma spp. invasion. To a large extent, the ability to colonize plant roots is determined by the strain’s ability to withstand environmental stresses. Several ATP-binding cassette (ABC) transporter genes have been discovered and described in Trichoderma spp., and they have been linked to the transfer of a variety of substrates, including phytotoxins, mating factors, antibiotics, pesticides, and heavy metals. The rapid degradation of phenolic compounds exuded by plants and the suppression of phytoalexin production, as detected in Trichoderma spp. is due to ABC transport systems (Cheng et al., 2011). ABC transport systems are key factors in the multiple interactions established by Trichoderma spp. with other microbes in a potentially toxic or antagonistic environment. Trichoderma spp. has been shown to contribute to biocontrol through small cysteine-rich proteins. These small proteins bind to chitin of plants and fungi and prevent Trichoderma spp. from chitinases (Stergiopoulos and de Wit, 2009).

Depending on the pathosystem, plant defense responses are usually triggered by activation of a complex signal transduction network that includes salicylic acid (SA), jasmonic acid (JA), either with or without ethylene (ET), and abscisic acid (ABA) as important plant immunity regulators. Checker et al. (2018), SA-mediated signaling pathways in plants result in systemic acquired resistance (SAR) against biotrophic and hemibiotrophic diseases. JA/ET-mediated signaling pathways, on the other hand, result in induced systemic resistance (ISR) in plants against necrotrophic diseases (Pieterse et al., 2014). According to a recent research, Trichoderma spp. induce a hybrid ISR/SAR type of resistance in plants against fungal pathogens including R. solani known as Trichoderma-induced systemic resistance (TISR; Leonetti et al., 2017; Figure 4). Hence, resistance in plants is increased by Trichoderma spp. against R. solani, which can be activated through signaling pathways that involve both SA and JA/ET-mediated signal transduction. Even still, scientists disagree on the method by which Trichoderma spp. activate defensive responses and the sort of resistance they induce in plants. Furthermore, there are significant gaps and differences when it comes to explaining the crosstalk of signaling molecules involved in Trichoderma-induced defense responses in plants. Other chemicals that may reduce or increase the synthesis and activity of signaling molecules must also be considered in order to better comprehend the crucial interactions between JA, SA, ET, and their derivatives in the intricate signaling network (Figure 4).

Like fungi and mammals, plants activate possible defense systems in response to the presence of other species. This is best appreciated in the context of pathogens that induce a two-branched inborn immune response. PAMP-triggered immunity (PTI) is the first stage in which plants use pattern recognition receptors to recognize and respond to pathogen-associated molecular patterns (PAMPs) or microorganism-associated molecular patterns (MAMPs). Plants respond to pathogen virulence factors in the second step known as effector-triggered immunity (ETI). MAMPs are molecular signatures that are extremely conserved, such as fungi’s chitin and xylanase and oomycetes’ heptaglucan. After PRR activation, changes in ion fluxes across the plasma membrane, the oxidative burst (production of nitric oxide and reactive oxygen species), activation of MAPK cascades, and callose deposition are all downstream defensive activation events. Many breakthroughs have been made in identifying the pathways involved in this resistance; in many cases, SA or JA, when combined with ET, ROS, or NO, causes a cascade of processes that culminate in the synthesis of a range of metabolites and proteins with varied roles (Bellin et al., 2013). ABA, auxins, gibberellins, cytokinins, and brassinosteroids have also been demonstrated to play essential roles in recent studies (Pieterse et al., 2009). Although there appears to be crosstalk or competition between the pathways, different stresses stimulate distinct routes (Durrant and Dong, 2004). SAR confers long-term disease resistance by accumulating genes that produce pathogenesis-related (PR) proteins against pathogens that are either biotrophic or hemibiotrophic (Pieterse et al., 2009). However, rather than directly initiating PR gene transcription, ISR enhances plants’ defenses against a future onslaught by necrotrophic pathogen like R. solani. Overall, the JA/ET and SA pathways are thought to be mutually special. However, other investigations have found a synergistic effect between these routes. According to recent advances, Trichoderma spp. simultaneously induces plant SAR-related genes as well as ISR-related genes during plant root colonization, providing protection against R. solani with various lifestyles (Salas-Marina et al., 2011). Recent research has shown that Trichoderma spp. may cause biochemical and molecular alterations in SAR, which are mostly linked to the production of PR proteins, such as PR1, PR5, and PR2 (Zhang and Zhuang, 2020). The activation of the mutually antagonistic SA and JA pathways by Trichoderma spp. results in a loss of plant ecological fitness, a process known as crosstalk (Van Oosten et al., 2008). Trichoderma–plant interactions take place predominantly in the rhizosphere, where resistance development is driven by the interchange of microbial and plant elicitors required for organism-to-organism interactions. Depending on the involved elicitors created by Trichoderma hyphae, the interaction of these molecules with plant receptors may influence Trichoderma adhesion and identification, and hence the induction of resistance in plants. Secondary metabolites produced by Trichoderma spp., such as proteins with enzymatic activity, as well as Trichoderma spp. and plant cell wall components, are all implicated in the development of plant resistance. Pathogen defenses have been activated by plant components, such as pectins, phospholipids, and saccharides. Some Trichoderma elicitors, include proteins produced by avirulence genes and MAMPs, which are slow-evolving molecules. Trichoderma spp. secrete low molecular weights (6–42 kDa) enzymes or peptides which act as elicitors, such as serine xylanases, proteases, chitinases, cellulases, or glucanases. Other Trichoderma spp. compounds which act as elicitors are indole compounds, fatty acids, lipids and their derivatives (glycosphingolipids etc.), saccharides (polysaccharides or oligosaccharides) and chitin or chitin-like compounds (Djonović et al., 2007; da Silva Aires et al., 2012; Tables 4 and 5).

Small proteins like cerato-platanins, hydrophobins, swollenins, and expansins are vital between Trichoderma spp. and plants. Host presence stimulates secretion of these proteins by Trichoderma spp. These proteins are also involved in mycoparasitism and induction of plants resistance against pathogens. For example, Cerato-platanins (Sm1/Epl1), which are tiny secreted proteins with four cysteines linked together by two disulfide linkages are necessary for T. atroviride and T. virens mediated cotton resistance to R. solani. They trigger systemic and local resistance in plants for R. solani (Djonović et al., 2006; Seidl et al., 2009). Hydrophobins are a group of other small proteins which are secreted from the Trichoderma spp. cell wall. They help Trichoderma spp. to adhere to the root surface. Local defense in plants is stimulated by Swollenin, expansin-like proteins with a cellulose-binding domain (Guzmán-Guzmán et al., 2017; Table 5). Swollenin disrupt plant cell walls’ crystalline cellulose structure and aid in Trichoderma spp. colonization of plants roots (Saloheimo et al., 2002). Root colonization by T. asperellum stimulates the production of swollenin to induce local defense in plant (Brotman et al., 2008). In the rhizosphere, Trichoderma spp. use swollenin to establish themselves by increase root surface area. Plant protein for expansion of root and root hair cell wall is expansins which has sequence similarity to Swollenin (Guo et al., 2011).

PRRs recognize MAMPs released by Trichoderma spp. By signaling molecules within the plants, these MAMPs contribute to the signal cascade. Trichoderma MAMPs transiently promote Ca²⁺ and H⁺ influx and K⁺ and Cl⁻ ejection in response to suitable plant receptors. Variations in the plasma membrane potential (Vm) occur often because of ion imbalances and changes in the channel activity (Liu et al., 2010). Plant cells undergo fast ROS, RNS and pH changes during depolarization. In addition to changes in ion absorption, Trichoderma spp. releases organic acids (gluconic or citric acid) into the soil, which lowers the soil pH. ROS and RNS are released during cell wall expansion and lignification. Furthermore, cell wall peroxidases and calcium channels become active. Many secondary metabolites and signaling molecules, including as H₂O₂ and NO, as well as SA and its derivatives, and JA/ET are generated and accumulated in response to Trichoderma spp. (Harman et al., 2004). Trichoderma spp. MAMPS and other effector molecules bind to PRRs and intracellular receptors in plants, triggering MTI (MAMPS-triggered) and ETI (effector-triggered) immunity. This interaction between Trichoderma spp. and plants produces ROS and RNS, which act as signaling molecules and initiate a defensive response in plants by synthesizing antifungal molecules, such as phytoalexins, VOCs (volatile organic compounds), PRs proteins, such as CWDEs, and so on. Trichoderma spp. has a local and systemic action that involves a signaling cascade and activation, as well as the accumulation of antimicrobial compounds and enzymes, such as polyphenol oxidase, peroxidase, lipoxygenase and PAL. PR proteins, terpenoids, phytoalexins (rishitin, phytosterol, lubimin, coumarin, resveratrol, solavetivone, and others), and antioxidants (glutathione, ascorbic acid, and others) are produced. Plants respond to fungal invasion by producing and concentrating defensive molecules, such as phytoalexins, aglycones, flavonoids, phenolic byproducts, terpenoids, and other antimicrobial substances. Trichoderma spp. on the other hand, are typically resistant to plant defense compounds and colonize plant root due to presence of ABC transport systems. Recent studies show that plants employ ROS and RNS as messengers to control the interplay between secondary messengers, MAPKs, and hormones, which are crucial in the induction of plant resistance SAR (Sami et al., 2018). An enzyme system known as the MAPKs kinase pathway may be activated by extracellular Trichoderma MAMPs, when they connect with plant receptors. The first step in triggering MPKKK kinase activity is a ligand–receptor contact. In the next step, MPK kinase is phosphorylated by MPKKKs, which in turn activates MPKK kinases, which phosphorylate MPKs (Sami et al., 2018).

In oxidative signaling, reactive oxygen (RO) and reactive nitrogen (RN) species interact with multiple hormonal signaling pathways. When plants were challenged with necrotrophic fungi, such as R. solani, among all RO and RN species, H₂O₂ and nitric oxide (NO) were shown to be quickly produced and were considered primary defensive activators. The processes by which NO may influence defensive signaling cascades were well investigated. S-nitrosylation and tyrosine-rich group nitration have emerged as significant NO-dependent protein regulatory mechanisms. Protein cysteine-rich thiol groups react with NO to create S-nitrosothiols so-called “reversible S-nitrosylation of proteins.” S-nitrosylation plays an important role in defensive responses, as shown by its effects on the SA signaling protein NPR1 and the ROS-generating NADPH oxidase complex AtRBOHD. NO has been shown to work with ROS and SA to establish SAR in plants (Sami et al., 2018). NO is also linked to other resistance-inducing signaling pathways, such as JA and ET. NO via S-nitrosylation has been shown in recent research to be one of the key regulators of SA-dependent systemic defensive responses in T. atroviride-treated plants. SA play an important part in the systemic defense responses elicited by T. atroviride in cucumber plants, protecting them from R. solani. SA or increasing the quantity of H₂O₂ or NO could promote the synthesis of active NPR1 proteins, which regulate the expression of genes that code for plant defense proteins. NPR1, which resides as an oligomer in the cytoplasm and is held together by intermolecular disulfide bonds, is susceptible to changes in redox status. By modifying the state of cell reduction, accumulated SA, H₂O₂ and NO might diminish disulfide bonds, leading NPR1 to degrade into monomers, which, when transferred into a nucleus to induce TISR by activating pathogenesis-related (PR) genes (Nawrocka et al., 2019). The mitogenic kinase pathways are also activated, resulting in the activation of transcription factors against R. solani (Nawrocka et al., 2019).