# Signaling in the Tomato Immunity against _Fusarium oxysporum_
## 3 Discussion  
Fusarium wilt is one of the most important diseases in tomato crops, which is caused by the soil-borne fungus _Fusarium oxysporum_ f. sp. _yocorsici_[2]. Nowadays, neither fungicide treatments nor culture methods are proven to be effective. The discovery and subsequent introgressive hybridization of resistance genes (_l_) in tomato plants has resulted in better crop development as well as yield improvement [6]. Hence, the main goal of this study was to explore the volatile chemical composition and the main defensive phytohormones involved in the resistant Movione (MOV) and susceptible MOM (MOM) isogenic lines of Moneymaker tomato plants, carrying or not carrying the \(l\) resistance gene, upon fungal infection. Specifically, the identification of the VOCs emitted by tomato leaves after ETI establishment could provide us with new resistance inducers for the treatment of fusarium wilt. To characterize both compatible and incompatible interactions, the gene activation of some defensive routes together with the levels of different signal molecules, e.g., SA, JA, and ABA, were measured at several time points (Figures 2 and 3). The analysis of SA accumulation showed higher SA levels in susceptible _Fol_-infected MOM plants when compared to resistant MOV plants (Figure 3A), which is in accordance with higher _PRI_ expression observed in these isogenic lines (Figure 2A). In agreement with our results, accumulation of SA in virulent infections, such as those produced by _Fol_, CEVd, tomato spotted wilt virus, _Xanthomonas campestris_, or _Pseudomonas syringae_, has also been described in tomato plants [11; 14; 24; 25]. An SA signaling positive regulation was described in the compatible interaction between _Fusarium oxysporum_ and _Arabidopsis thaliana_[26], which was confirmed by the hyper susceptibility of _NahG_ transgenic plants unable to accumulate this hormone [27]. Besides, exogenous application of SA through root feeding and foliar spray induced resistance against _Fol_ in tomatoes [28]. These results point to the defensive role of this phenolic compound in the tomato-_Fol_ interaction. However, the endogenous accumulation of SA in virulent infections suggests that its presence is not sufficient to generate resistance. The low _PRI_ expression with the minimal SA levels measured during the incompatible interaction suggests that the resistance of tomato plants to _Fol_ is not mediated by SA, pointing out some antagonism with other defensive routes, such as the JA-mediated pathway [29]. In this sense, a statistically significant activation of both the JA marker gene _JAZ7_ (Figure 2B), and the _TomloxD_ and _AOS_ genes involved in JA biosynthesis (Figure 5C,F) was found during the ETI establishment, indicating that tomato plants' resistance to fusarium wilt could be mediated by this phytohormone at the onset of the infection process. In fact, JA perception, but not its biosynthesis, is critical to the fusarium wilt development in _Arabidopsis thaliana_[30]. Besides, jasmonate-deficient tomato mutants showed hypersusceptibility to the pathogen [31], and exogenous JA treatments in wheat reduced both the symptoms of fusarium wilt and mycelia growth [32]. Most recent studiessuggest that host-_Fusarium_ interaction is governed by JA, and that compromised JA levels are associated with increased susceptibility [33]. Generally, ET and JA are associated with plant resistance mechanisms against recrotrophic pathogens [12]. A higher induction of the _ACS2_ gene was observed in susceptible MOM plants when compared to resistant MOV plants after fungal infection at all times analyzed (Figure 2C), showing a maximum at 14 dpi. Transcriptomic studies point out the ET-mediated activation of isolated genes during the first steps of the infection, prior to the signaling of other hormones such as JA, SA, or ABA [34].