**3.2. Signaling and defense response**

Recognition of pathogen elicitors that are released at the site of infection is rapidly followed by changes in ion flow and the production of reactive oxygen species. These events activate signaling cascades, which lead to the activation of the transcription factors involved in the activation of defense genes [66]. These responses are known to be regulated through complex signaling pathways involving various phytohormones. The FOL-activated signaling network integrates signals shared and mediated by synergistic or antagonistic interactions between salicylic acid (SA), jasmonic acid (JA), ethylene (ET), abscisic acid (ABA), and ROS [67, 68].

and ABA. Responses may be ethylene synthesis, ROS production, pathogenesis-related (PR)

A Molecular Vision of the Interaction of Tomato Plants and *Fusarium oxysporum* f. sp. *lycopersici*

http://dx.doi.org/10.5772/intechopen.72127

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On the other hand, jasmonates are involved in the reduction of FOL susceptibility in tomato plants, by increasing the activity of polyphenol oxidase [85]. Whereas in Arabidopsis plants, it has been observed that the response to *F. oxysporum* requires signaling pathways through ET, JA, SA, and the NPR1 gene, although it is independent of the function PAD4 and EDS1 [86]. The interactions between SA and JA signaling are complex, but research indicates an antagonistic relationship between them [87], while jasmonates and ET cooperate to synergistically induce defense genes such as PR1b, PR5, and PDF1.2 [88, 89]. Expression of the ERF1 gene responsive to ET and to JA is a common component in the pathways of both phytohormones [90]. It is suggested that ABA function affects disease resistance by suppressing basal and induced transcription of JA and ET response genes, which clarifies the antagonistic relationship between these hormones [91]. However, ABA has been reported to be involved in the production of callose for the early and efficient construction of papillae at sites of infection to counteract the pathogen [92]. On the other hand, signaling mediated by heterotrimer G proteins has been shown to suppress the induction of SA-, JA-, ET-, and ABA-dependent genes during the initial phase of infection with *F. oxysporum*, whereas at a later phase, it improves

The defense responses that are activated by these pathways in tomato plants involve the increase of defense enzymes such as phenylalanine ammonium lyase and peroxidase [94], as well as the synthesis and accumulation of proteins related to pathogenesis, such as chitinases and b 1–3 glucanases. These proteins act synergistically to inhibit the growth of the fungus [95]. Programmed cell death can be induced by α-tomatine, which has a fungicidal action, in addition to its potential role as an activator of tyrosine kinase signaling pathways and the monomeric GTP-binding protein (G protein) that leads to Ca elevation and the ROS burst in FOL cells [96]. The regulation of plant immune responses is mediated by transcription factors of the WRKY family, which are functionally connected by forming a transcriptional network composed of positive and negative feedback loops within a network of partially redundant elements, some of which hold central positions that allow the activation of fast and efficient

Once the first line of defense is activated through recognition of PAMPs, FOL employs mechanisms that allow it to suppress such activated responses. During the infection process, it secretes small proteins rich in cysteine (effector or virulence proteins). The function of these proteins is to promote infection and colonization in the host plant, by disrupting various cellular processes such as signal transduction or modifying the proteins in the host plant [98].

The set of these effectors determines the specificity of the host, as well as the ability of the pathogen to manipulate the host immunity [99, 100]. In FOL, these effectors are designated as proteins secreted in the xylem (SIX) and six genes have been reported to encode them [101].

protein expression, and cell death [83, 84].

the JA-/ET-dependent genes like PDF1.2 and PR4 [93].

defense programs [97].

**3.3. Effector protein recognition**

The SA plays an essential role in plant defense signaling since the recognition of FOL-derived components allows the accumulation of this phytohormone, with the subsequent establishment of local resistance in the infected region.

In the same way as the systemic resistance of the whole plant [69], the biosynthesis of SA is regulated by the Arabidopsis defense-related gene (SID2) [70]. This pathway requires the high-affinity protein SABP2, responsible for the conversion of methyl salicylic acid to SA [71], as well as the nonexpresser of pathogenesis-related (PR) genes positive regulator (NPR1) [72], which is regulated by the transcription factors of the TGA and WRKY family [73, 74]. On the other hand, the function of Ca as a second messenger has been characterized in numerous signaling pathways of plants, transporting a wide range of environmental and developmental stimuli to the physiological response [75]. An example is its participation in the regulation of SA levels through the interaction of a Ca/calmodulin with the transcription factor–enhanced disease susceptibility 1 (EDS1), through the activation of the Ca channels for the influx and subsequent mobilization of the intracellular Ca stores [76]. The increase of Ca in the cytoplasm is the first step in the signaling pathway of PAMP-triggered immunity (PTI). This elevation may occur in response to the perception of PAMPs, interactions of the R gene due to phosphorylation events, G protein signaling, and/or cyclic nucleotide increase [77].

The SA is crucial to induce the production of superoxide anion and hydrogen peroxide, by the activation of apoplastic peroxidase, and subsequently NADPH oxidase of the plasma membrane [78], which are connected to each other through the activation of Ca channels, as it has been pointed out that the increase of the cytoplasmic Ca coincides with the concomitant increase of ROS, or by the phosphorylation of proteins [79]. ROS are known for their direct antimicrobial role against pathogens as well as their relation to the activation of second messengers related to the expression of genes related to the production of response proteins [80], such as the peroxidases of class III, which are important due to their involvement in the reinforcement of the cell wall in the site of interaction with the pathogen, through catalysis of the reticulation of cell wall components including glycoproteins, lignin, and suberin [81]. Also, the oxidative burst is associated with the hypersensitivity response or programmed cell death, processes that inhibit the invasion of the pathogen through isolation [82].

Activation of MAPKs is critical in components of basal defense pathways as well as in more specific interactions involving R-gene–mediated resistance. The oxidative burst activates an MAPK cascade that induces the downstream defensive mechanisms regulated by SA, ET, JA, and ABA. Responses may be ethylene synthesis, ROS production, pathogenesis-related (PR) protein expression, and cell death [83, 84].

On the other hand, jasmonates are involved in the reduction of FOL susceptibility in tomato plants, by increasing the activity of polyphenol oxidase [85]. Whereas in Arabidopsis plants, it has been observed that the response to *F. oxysporum* requires signaling pathways through ET, JA, SA, and the NPR1 gene, although it is independent of the function PAD4 and EDS1 [86]. The interactions between SA and JA signaling are complex, but research indicates an antagonistic relationship between them [87], while jasmonates and ET cooperate to synergistically induce defense genes such as PR1b, PR5, and PDF1.2 [88, 89]. Expression of the ERF1 gene responsive to ET and to JA is a common component in the pathways of both phytohormones [90]. It is suggested that ABA function affects disease resistance by suppressing basal and induced transcription of JA and ET response genes, which clarifies the antagonistic relationship between these hormones [91]. However, ABA has been reported to be involved in the production of callose for the early and efficient construction of papillae at sites of infection to counteract the pathogen [92]. On the other hand, signaling mediated by heterotrimer G proteins has been shown to suppress the induction of SA-, JA-, ET-, and ABA-dependent genes during the initial phase of infection with *F. oxysporum*, whereas at a later phase, it improves the JA-/ET-dependent genes like PDF1.2 and PR4 [93].

The defense responses that are activated by these pathways in tomato plants involve the increase of defense enzymes such as phenylalanine ammonium lyase and peroxidase [94], as well as the synthesis and accumulation of proteins related to pathogenesis, such as chitinases and b 1–3 glucanases. These proteins act synergistically to inhibit the growth of the fungus [95]. Programmed cell death can be induced by α-tomatine, which has a fungicidal action, in addition to its potential role as an activator of tyrosine kinase signaling pathways and the monomeric GTP-binding protein (G protein) that leads to Ca elevation and the ROS burst in FOL cells [96]. The regulation of plant immune responses is mediated by transcription factors of the WRKY family, which are functionally connected by forming a transcriptional network composed of positive and negative feedback loops within a network of partially redundant elements, some of which hold central positions that allow the activation of fast and efficient defense programs [97].
