# Signaling in the Tomato Immunity against _Fusarium oxysporum_
## 3 Discussion
All these results imply that the defensive tomato response against _Fol_ appears to be firstly associated with ET/JA-mediated genes, but this response appears not to be effective enough to stop the fungal colonization [26]. Our results suggest an accompaniment of ET in the SA signaling during the compatible interaction. In _Arabidopsis_, an antagonism between SA and ET/JA routes against _Fusarium oxysporum_ has been described [27]. Otherwise, ET has always been associated to symptoms [35] and senescence [36], therefore the _ACS2_ induction in susceptible tomato plants could involve ET not only in the gel formation within the xylem vessels to avoid the access to the pathogen, but also in the symptom development [37]. ABA is usually related to abiotic stress, although some defensive role in biotic interactions has also been observed [38]. Particularly, the ABA-mediated resistance against fungal pathogen has been associated to callose deposition [39]. In our study, a significant _LEA_ induction (Figure 2D), as well as an ABA accumulation at 7 dpi (Figure 3C), was measured in the susceptible MOM tomato plants. These results coincide with those obtained in _Arabidopsis_, in which ABA promotes _Fusarium oxysporum_ susceptibility [40]. Besides, the occlusion of the xylem vessels during the compatible tomato-_Fol_ interaction could resemble drought conditions, where a reduction of the transpiration rate and leaf expansion, as well as the ABA-mediated stomata closing, allow plants to survive [41]. All the above data indicate that the different accumulation patterns of these three signal molecules depend on the diversity of pathogens with a range of lifestyles. To our knowledge, this is the first study in which the levels of SA, JA, and ABA have been measured in two different isogenic tomato lines (susceptible and resistant) infected with _Fol_. Interestingly, we also observed divergences in volatile chemical composition upon fungal infection. Specifically, the VOC emission of a diseased leaf was enriched in C9 and C6 fatty acid derivatives, while that of a resisting leaf was characterized mainly by terpenes and C5 fatty acid derivatives (Figure 4). A significant production of oxidized compounds such as ketones and aldehydes, esters from the defensive SA response (MeSA, EtSA), and some compounds from fatty acid degradation (2-hexanone, 2-nonenal), were associated with susceptible tomato plants infected by _Fol_ (Table S3 and Figure 4). The differential 2-nonenal and 2-hexanone emission was in agreement with a significant induction of the relative expression levels of _TomloxA_ at 3 dpi (Figure 5B) and _TomloxF_ and _HPL_ at 7 dpi (Figure 5D,E), respectively. In contrast, VOCs involved in the early resistance of tomato MOV to _Fol_ were some monoterenes, apoc-arotenoids, and sesquiterpenes while some benzenoids (isobutylbenzene, methylbenzene, benzeneacetaldehyde) and fatty acid derivatives (2-ethylhexanoic acid, 5-ethyl-2-furanone, (_E_)-2-pentenal) were implicated in the late resistance (Table S2). The statistically significant induction of both _MTS1_ at any time point along with _TomloxC_ at 7 dpi matched with the specific monoterene and C5 volatiles emitted in the ETI establishment. Historically, VOCs have been associated with fruit quality and plant defense against herbivores. Recently, new plant-pathogen interactions have been studied to find novel biological properties of these compounds in the agrochemical industry. Compounds emitted that are related to phytophagous insects and wounding are mainly metabolites derived from fatty acid degradation and terpenoids [42; 43]. Fatty acids and their derivatives have been well studied due to their antimicrobial properties [44]. Hexanoic acid inhibits _Fol_ mycelia growth at high concentrations, and reduces its germination at low concentrations [45]. Its antifungal effect is due to the increase of the membrane hydrophobicity, destabilizing them and inhibiting the interaction with proteins and lipids in the cell surface [46].