Low temperatures induce numerous cellular and physiological disorders, such as an increase in respiratory rate, reduction of photosynthetic activity and generation of reactive oxygen species causing a set of visible symptoms known as chilling injury in crops that are susceptible to cold. To overcome these alterations, fruit activate a number of defense mechanism that includes synthesis of pigments to protect from photoxidative stress, enzymes to reduce oxidative stress and an increase in the levels of cryoprotective and antifreezing proteins. Although table grape is classified as tolerant to chilling injury, non-treated grapes responded to temperature shifts in the first stage of storage at 0ºC activating defense responses related to the phenylpropanoid pathway, whereas the application of high CO2 levels reduced these responses. In addition, previous studies indicate that the efficacy of gaseous treatment reducing decay in table grapes was not mediated by the induction of pathogenesis-related proteins (PRs), such as chitinase and β-1,3-glucanase. All these seem to indicate that although table grape is tolerant to cold injury it senses temperature shifts triggering a stress response, and the treatment with high CO2 levels could be participating in the perception of low temperature by the fruit, alleviating partially this stress and improving fruit quality. However, very little is known about the biochemical and molecular mechanisms involved. Thus, having as a final goal the improvement of the quality of table grapes during the postharvest period, we aim to obtain a comprehensive understanding of the molecular mechanisms involved in the differences observed in response to low-storage temperature between table grape bunches non-treated and treated with high levels of CO2. Concretely, we will focus on the study of two types of transcription factors (CBFs and ERFs) and their putative target genes (dehydrins and PRs).
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