# Signaling in the Tomato Immunity against _Fusarium oxysporum_
## 1 Introduction  
Tomatoes (_Solanum locyersicum_) are an important crop, whose cultivation and consumption are both constantly increasing, reaching a worldwide production of more than 180 million tons on a cultivated area of almost 4.8 million hectares in 2018 [1]. In addition, the tomato is an excellent model plant for studying plant-pathogen interactions, and the results of such research can be scaled-up to other ones. For its economic importance worldwide, the control of main pests or diseases becomes essential to prevent yield and productivity losses in tomato crops. Among the most common tomato diseases, there are those caused by bacteria such as _Pseudomonas syringae_, viruses like tomato mosaic virus (ToMV), and pathogenic fungi such as _Bports cinerea_, _Phytophthora infestants_, and _Fusarium oxysporum_. Specifically, _F. oxysporum_ f. sp. _locyersici (Fol_) is the form specialis that affects tomato plants [2] and represents the fifth most important plant pathogenic fungus around the world responsible for economic losses around 14% in tomato crops [3]. _Fol_ has hemibiotrophic behavior, living in soil during long periods before infecting a new host. The pathogenic isolates are able to reach the central cylinder of the roots through centripetal intracellular growth by digestion of the cell wall, mainly via intercellular progress [4]. Once _Fol_ reaches the xylem, its growth within the xylem vessels goes through the hypocotyl and the petioles. This mycelia growth and the defensive system of the plant bring about a progressive obstruction of the vessels and the consecutive collapse of the water and nutrient supply. In tomato plants, _Fol_ causes a yellowing and withering of the upper leaves, browning of the hypocotyl vessels, and death in long term infection [5]. The use of fungicides against fusarium wilt during cropping is ineffective, and therefore prevention is necessary. Besides, due to its persistence in soil and its easy dissemination through seeds and wind, fusarium wilt is difficult to control, with the possibility of scaling up as a consequence of global warming. Nowadays, the most effective means of control is the use of resistant cultivars, but the co-evolution of resistant genes and different formae speciales makes this interaction very complex [6]. There are eleven candidates for effectors or avirulence genes in _Fol_, denominated SIX (secreted in xylem), which contribute to the pathogen virulence [7]. Among them, _Avr1_, _Avr2_, and _Avr3_ are widely described [8]. Tomato plants containing the \(I\) (immunity) resistance genes (_I_, \(I\)2, \(I\)3 and \(I\)7) become resistant to fungal infection after the corresponding _Avr_ recognition, therefore activating the effector-triggered immunity (ETI), which is characterized by the development of the so-called systemic acquired resistance (SAR), and resulting in an incompatible interaction [9]. The complexity of this interaction lays on the suppression by _Avr1_ of \(I\)2 and \(I\)3 mediated resistance in tomato plants [8]. Besides, there is no further knowledge about the pathogenic action of the other SIX effectors [10]. In contrast, tomato plants deficient in the \(I\) resistance genes are susceptible to fungal infection by a lack of \"gene for gene\" recognition, resulting in a compatible interaction. Different phytohormones such as salicylic acid (SA), jasmonic acid (JA), abscisic acid (ABA), and ethylene (ET) have been involved in tomato plant response against different pathogens [11; 12]. However, the contribution of these signal molecules in both compatible and incompatible tomato-_Fol_ interaction has not yet been explored. Metabolomics has emerged as a powerful platform for both understanding the complex plant-pathogen interactions and unraveling new strategies for chemical control.