**2.2. Signaling by MAPK**

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

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

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

It is known that FOL can produce three types of asexual spores: (i) microconidia, (ii) macroconidia, and (iii) chlamydospores; while the sexual or teleomorphic phase is unknown. FOL can survive saprophytically in soil and organic waste in the absence of a host, either as mycelium or in all types of spores mentioned [14]. Chlamydospores are resistance structures capable of

available once the plants are infected and have *Fusarium* vascular wilt.

80 Fusarium - Plant Diseases, Pathogen Diversity, Genetic Diversity, Resistance and Molecular Markers

different stages of plant infection or under various conditions.

**2.** *F. oxysporum* **f. sp.** *lycopersici* **(FOL)**

**2.1. Host recognition by FOL**

tomato plant [13].

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

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].
