## 3 Discussion
At the same time, our data also highlight the putative signaling pathways of DYE responses by identifying several transcription factors, some of which appear to be ROS-responsive, that may be responsible for the downstream regulation of specific metabolic genes. In addition, our data would support the hypothesis that the berries of plants subjected to DYE treatment display increased resilience to abiotic stress. This effect may be accomplished through a finer regulation of ROS levels and a reduced oxidative stress that may be testified by a diminished proline content, assumed as a proxy for oxidative stress [102], and by the upregulation of the _VviCCD4a_ encoding gene, most likely not involved in ABA biosynthesis but rather in the generation of signaling molecules [77]. In fact, preventing the oxidation of aroma precursors in grapevine berry fruits, especially when they are exposed to heat or drought, either alone or in combination, has been claimed by several authors to be essential to favor better later maintenance in the wine [4; 5; 14]. Moreover, we found that the treatment with DYE specifically induced a subset of hormonal responses, a novel, unpredicted aspect that has not been evidenced by previous studies dealing with DYE. In particular, the upregulation of several genes encoding key enzymes of the main biosynthetic steps of jasmonic acid (JA) and ethylene strengthens the hypothesis of a selective \"priming\" action of DYE. This priming action depends on the increase of these two stress hormones, which notoriously act in synergism in the regulation of stress responses. It can be speculated that these hormones may be possibly involved in reinforcing those responses falling within the functional categories of \"response to chitin\" and \"response to pathogen\", while leaving unaffected the main ripening processes. Regarding JA biosynthesis, the upregulation of three types of lipases (_Vitri09g00038, Vitvi10g00669, and Vitvi15g00298_, group 1) [48; 49; 50] and of two LOX genes (_Vitvi13g01780, Vitvi09g00085_, group 1) [44; 45] supports the view of stimulation of several key biosynthetic steps of the hormone. The upregulation of JA-responsive genes like hydroxy-JA sulfotransferase 2A (_Vitvi13g00864_, group 1) [51] may be a feedback control response induced by the increased JA levels. The activation of JA responses was also confirmed by the downregulation of negative regulators of JA signaling (Table 1). The co-regulation of the ethylene biosynthetic gene ACO4 (_Vitvi10g02409_, group 1) [55] as well as various ethylene and JA inducible ERF transcription factors encoding genes (ERF4 (_Vitvi19g01784_, group 1) [59], ERF5 (_Vitvi16g01438_, group 1) [56; 57], ERF9 (_Vitvi12g00274_, group 1), and ERF105 (_Vitvi16g01444, Vitvi17g00787, Vitvi16g01434, Vitvi16g01432, Vitvi18g00295_ and _Vitvi16g01423_, group 1) [66]) further suggests the simultaneous enhanced action of the two hormones induced by DYE treatment. It is interesting to note that some of these genes, together with WRKY encoding genes (WRKY22 (_Vitvi15g01090_, group 1) and WRKY33 (_Vitvi08g00793_, group 1)) [63; 64; 65], were reported in Arabidopsis to be putatively associated with hypoxia responses and with JA- and ethylene-inducible resistance to necrotrophic pathogens (_Botrytis_), further supporting the hypothesis of a \"priming\" effect exerted by DYE. ABA responses appeared to also be affected, although the final readout of such effects seems less univocally interpretable since both positive and negative regulators were induced by the treatment. The upregulation of ABA responsive genes (Table 1), as well as the increased transcription of a sulphate transporter gene (_Vitvi05g00548_, group 1) required for ABA biosynthesis [78] and of an SNF1-related kinase gene (_Vitvi17g00116_, group 1) [68], and the downregulation of a gene encoding a cytokinin receptor histidine kinase (_Vitvi12g00685_, group 4) negatively regulating ABA sensitivity, would support an overall positive regulation of ABA responses by DYE supply.