**1. Introduction**

Microorganisms have interacted with plants for millions of years. However, for these to be pathogenic, they must have virulence factors, secondary metabolites, and exoenzymes that allow them to access the interior of the plant through the leaves, root or wounds, or natural openings, to establish an interaction of compatibility with the host [1, 2]. One of the pathogens

© 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

that affect a considerable number of plant species is the fungus of the genus *Fusarium*, which causes the disease known as vascular wilt [3]. This genus is made up of a large set of species that possess many biological properties. In addition, it is characterized by the production of fusiform macroconidia that are widely distributed in soil and on organic substrates [4]. The species known as *Fusarium oxysporum* causes large losses to vegetable crops both in open field and in greenhouse production [5]. Special forms (f. sp.) have been assigned according to the specificity of the host, of which about 70 have been described f. sp. [6]. Among these special forms*, F. oxysporum* f. sp. *lycopersici* (FOL) affects the tomato crop (*Solanum lycopersicum*) and is one of the main limiting factors for its production. FOL is divided into physiological races based on its ability to infect specific cultivars [7]. Regardless of biological, chemical, or cultural measures, adequate management strategies to eliminate this pathogen are not currently available once the plants are infected and have *Fusarium* vascular wilt.

remaining viable in the soil for several years according to environmental conditions, and this allows this pathogen to be dispersed rapidly with the movement of water, soil, or air [15, 16]. The presence of these reproductive structures of FOL in the development medium of tomato plant allows the plant-pathogen interaction to be initiated with a preinfection state, where the host recognition is carried out, and subsequently the germination of the spores, which will

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

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In this stage, the identification of the host is vital for the initiation of the infection process, and this is done through the release of exudates from the host roots, as these compounds represent a carbon source for the fungus [18]. Its composition includes sugars, polysaccharides, amino acids, aliphatic, aromatic and fatty acids, sterols, phenolic compounds, enzymes, vitamins,

The specific compounds that FOL recognizes in its host have not been characterized. To initiate spore germination, it is known that exudates from the root of tomato plants stimulate the germination of FOL microconidia. In addition, a relationship was found between the stimulation of germination and the age of plants. The highest stimulation of germination was observed when the plants were 70 to 90 days old. Changes were also observed in root exudates such as the concentration of phenolic compounds and flavonoids or induced changes in the exudates by the degree of colonization of the arbuscular mycorrhizal fungus Glomus

Mitogen-activated protein kinases (MAPKs) are proteins that have been evolutionarily conserved using cycles of phosphorylation and dephosphorylation for signal transduction. Activated MAPK kinase kinases (MAP3Ks) first phosphorylate two serine and/or threonine residues located within the activation loop of MAPK kinases (MAP2Ks). Activated MAP2Ks in turn trigger MAPK activation through dual phosphorylation of a highly conserved activation loop. Sequential activation of this pathway (MAP3Ks-MAP2Ks-MAPK) plays an essential role during the development of FOL. Activation of this signaling pathway will result in the expression of genes and transcripts necessary to regulate the infection process and the development of the disease, such as the expression of pathogenicity, infectious growth, or root

Recent studies report that the physiological and developmental processes of FOL are regulated by three signaling pathways identified as *Fusarium oxysporum* MAP K (Fmk1), MAP kinase (Mpk1), and high-osmolarity glycerol response (Hog1) and are mediated by MAPKs. Each of these pathways has specific roles; in the case of Fmk1, it has functions related to virulence and fusion of hyphae. Mpk1 is related to characteristics of the cell wall as its integrity and remodeling, the growth and fusion of vegetative hyphae. Finally, Hog1 is linked to osmoregulation responses and stress responses. The three pathways are involved in the pathogenesis of FOL and in the development of the disease [24]. This was demonstrated by using RNA interference (RNAi) to silence these signaling pathways, which caused loss of surface hydrophobicity, reduction of invasion, hypovirulence, conidial size alteration, growth

reduction, and a significant decrease in pathogenesis in tomato seedlings [25].

mosseae, modifying the spore germination and the degree of colonization [20, 21].

continue with the tissue infection [17].

**2.2. Signaling by MAPK**

attachment, once FOL identifies the host [22, 23].

plant growth regulators, and other secondary metabolites [19].

The disease development in susceptible tomato plants requires that FOL pass through a series of transitions, beginning with spore germination and culminating in the establishment of a systemic infection [8]. However, to reach this point, FOL requires avoiding the defense mechanisms that activate the plant-pathogen interaction [4]. The protection mechanism in tomato plants requires the perception of the pathogen through receptors of pathogen-associated molecular patterns (PAMPs) located in the plasma membrane, which triggers the basal defense system. This includes the influx of extracellular calcium (Ca) and mobilization of intracellular Ca to the cytosol, generation of reactive oxygen species (ROS), activation of mitogen-activated protein kinases (MAPKs) as well as calcium-dependent protein kinases (CDPKs) [9], and finally the induction of defense-related genes [10]. To avoid this defense system, FOL has the ability to secrete effectors such as the so-called proteins secreted in the xylem (SIX), which allows the infection to continue [11]. This implies the presence of avirulence (Avr) genes in the fungus, which is recognized by the products of the corresponding genes in the tomato, called R genes [12]. The interaction and compatibility of the Avr genes and R genes will result in the successful FOL infection or the survival of the tomato plant [13].

Despite the importance and necessity of controlling this disease, the molecular mechanisms of pathogenesis in tomato and the genetic basis for host specificity are still poorly understood.

This chapter presents the information necessary to obtain an understanding of fungal pathogenesis at the molecular level, allowing the characterization of actively expressed genes at different stages of plant infection or under various conditions.
