**2.3. Pathogenesis and virulence**

The concepts of pathogenicity and virulence are often erroneously considered as synonyms. Its definition initially focused on the intrinsic properties of the pathogen. However, currently, the definition of these characteristics considers the contributions of the pathogen and the host in the development of the disease. Based on this, the concept of pathogenicity is described as the ability of a microorganism to cause damage in a host, while virulence is defined as the relative ability of a microorganism to cause damage in a host [26]. Following these definitions, we next describe the genes required for the development of the disease caused by FOL (**Figure 1**).

pathogen growth, as well as secretion of pectinolytic enzymes and fusion of vegetative hyphae [28]. The Fmk1 MAPK cascade critically depends on the transcription factor Ste12, which controls the invasive growth and virulence downstream of the Fmk1 MAPK cascade. However, it is not linked to the regulation of root adhesion, suggesting that activation of Ste12 is independent of the MAPK pathway and that multiple pathways may converge on

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

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

83

The participation of *Fusarium oxysporum* FOW2 gene, a type Zn(II) 2Cys6 transcription factor encoded by the gene designated by the same name, has also been indicated. It is highly conserved in the special forms of FOL, and its expression is essential for pathogenicity [30]. On the other hand, extracellular pH has been shown to act as a key signal for growth, differentiation, and virulence in pathogens [31]. Gene expression in fungi by environmental pH is regulated by a conserved signaling pathway, whose terminal component is the PacC/Rim1p zinc finger transcription factor. PacC is considered to act as a negative virulence regulator in FOL. Expression of this transcription factor is pH dependent, with high transcription levels under alkaline growth conditions and low transcription levels under acidic growth conditions. There was also a clear effect of pH and PacC on the expression of two genes that encode

The genes described related to the pathogenesis of FOL control various processes in the development of the pathogen. Such is the case of the cyclic AMP-dependent protein kinase A of *F. oxysporum* (FoCPKA) gene, which regulates multiple traits related to growth, microconidia formation, germ-tube shape, septation, and branching of hyphae by means of a cyclic adenosine monophosphate-dependent protein kinase A (cAMP) [33]. On the other hand, the Fgb1 gene encodes the β-subunit of the G protein that controls hyphae growth, development, and virulence through pathways dependent and independent of cAMP signals, while the α subunit is encoded by the Fga1 gene, whose silencing reduces the conidiation and pathogenicity

In a study on the cloning of the Fga2 gene, it was shown that the functions of the two Gα proteins overlap but are distinct. On the one hand, the Fga1 pathway regulates the growth and development of fungi, including morphogenesis and conidiation. In contrast, the Fga2 pathway plays a more crucial role in pathogenicity [37]. In addition, the loss of function of the Fgas1 gene, responsible for the expression of β-1,3-glucosyltransferases, dramatically affects

Another gene related to the cell wall characteristics of FOL is Rho1, responsible for the coding of a putative Rho-type GTPase. It plays a crucial role in infection, avoiding recognition by the host defense system since its deletion in FOL leads to changes such as an increase in the amount of polymers in the cell wall, which serve as response activators in plants [39]. The Fow1 gene encodes a protein with high similarity to mitochondrial carrier proteins, which is specifically required for colonization in plant tissue since its absence generates a reduction in the virulence of FOL [40]. Likewise, the involvement of the Fpd1 gene has been described, which has as its possible function the coding for a transmembrane protein whose deficiency

the virulence of FOL, since it is linked to structural alterations of the cell wall [38].

this transcription factor [29].

endopolygalacturonases [32].

of the fungus [34–36].

reduces the pathogenicity of FOL [41].

FOL infection process begins with the germination of spores on the host surface. It begins with the emergence of the germinal tube through the wall of the spore followed by the emergence of ramifications of this structure giving rise to fungal hyphae [27], which adhere to the root and continue with invasive growth and penetration of plant tissue. In this stage of penetration and colonization of the host, FOL requires expression of the Fmk1 gene. It is responsible for the coding of an MAPK, required for root adhesion and penetration, invasive

**Figure 1.** Relationship of genes and transcription factors activated during disease development of FOL.

pathogen growth, as well as secretion of pectinolytic enzymes and fusion of vegetative hyphae [28]. The Fmk1 MAPK cascade critically depends on the transcription factor Ste12, which controls the invasive growth and virulence downstream of the Fmk1 MAPK cascade. However, it is not linked to the regulation of root adhesion, suggesting that activation of Ste12 is independent of the MAPK pathway and that multiple pathways may converge on this transcription factor [29].

**2.3. Pathogenesis and virulence**

(**Figure 1**).

The concepts of pathogenicity and virulence are often erroneously considered as synonyms. Its definition initially focused on the intrinsic properties of the pathogen. However, currently, the definition of these characteristics considers the contributions of the pathogen and the host in the development of the disease. Based on this, the concept of pathogenicity is described as the ability of a microorganism to cause damage in a host, while virulence is defined as the relative ability of a microorganism to cause damage in a host [26]. Following these definitions, we next describe the genes required for the development of the disease caused by FOL

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

FOL infection process begins with the germination of spores on the host surface. It begins with the emergence of the germinal tube through the wall of the spore followed by the emergence of ramifications of this structure giving rise to fungal hyphae [27], which adhere to the root and continue with invasive growth and penetration of plant tissue. In this stage of penetration and colonization of the host, FOL requires expression of the Fmk1 gene. It is responsible for the coding of an MAPK, required for root adhesion and penetration, invasive

**Figure 1.** Relationship of genes and transcription factors activated during disease development of FOL.

The participation of *Fusarium oxysporum* FOW2 gene, a type Zn(II) 2Cys6 transcription factor encoded by the gene designated by the same name, has also been indicated. It is highly conserved in the special forms of FOL, and its expression is essential for pathogenicity [30].

On the other hand, extracellular pH has been shown to act as a key signal for growth, differentiation, and virulence in pathogens [31]. Gene expression in fungi by environmental pH is regulated by a conserved signaling pathway, whose terminal component is the PacC/Rim1p zinc finger transcription factor. PacC is considered to act as a negative virulence regulator in FOL. Expression of this transcription factor is pH dependent, with high transcription levels under alkaline growth conditions and low transcription levels under acidic growth conditions. There was also a clear effect of pH and PacC on the expression of two genes that encode endopolygalacturonases [32].

The genes described related to the pathogenesis of FOL control various processes in the development of the pathogen. Such is the case of the cyclic AMP-dependent protein kinase A of *F. oxysporum* (FoCPKA) gene, which regulates multiple traits related to growth, microconidia formation, germ-tube shape, septation, and branching of hyphae by means of a cyclic adenosine monophosphate-dependent protein kinase A (cAMP) [33]. On the other hand, the Fgb1 gene encodes the β-subunit of the G protein that controls hyphae growth, development, and virulence through pathways dependent and independent of cAMP signals, while the α subunit is encoded by the Fga1 gene, whose silencing reduces the conidiation and pathogenicity of the fungus [34–36].

In a study on the cloning of the Fga2 gene, it was shown that the functions of the two Gα proteins overlap but are distinct. On the one hand, the Fga1 pathway regulates the growth and development of fungi, including morphogenesis and conidiation. In contrast, the Fga2 pathway plays a more crucial role in pathogenicity [37]. In addition, the loss of function of the Fgas1 gene, responsible for the expression of β-1,3-glucosyltransferases, dramatically affects the virulence of FOL, since it is linked to structural alterations of the cell wall [38].

Another gene related to the cell wall characteristics of FOL is Rho1, responsible for the coding of a putative Rho-type GTPase. It plays a crucial role in infection, avoiding recognition by the host defense system since its deletion in FOL leads to changes such as an increase in the amount of polymers in the cell wall, which serve as response activators in plants [39]. The Fow1 gene encodes a protein with high similarity to mitochondrial carrier proteins, which is specifically required for colonization in plant tissue since its absence generates a reduction in the virulence of FOL [40]. Likewise, the involvement of the Fpd1 gene has been described, which has as its possible function the coding for a transmembrane protein whose deficiency reduces the pathogenicity of FOL [41].
