According to Jiang et al. [54], in fruits stored at low temperatures, chilling injuries are due to the reduction in the ability to respond to the ethylene signal, and it has an impact on an abnormal maturation of the fruit.
Our RNAi predictably prevented recovery from heat shock and, in addition, negatively influenced repair of chilling injuries caused by cold stress.
In addition to this neuromuscular perturbation, chilling injuries accumulate at low temperatures as a result of various physiological dysfunctions (see ref [3] for review).
Preharvest hormone application has been demonstrated to reduce chilling injuries a reduced number of cultivars, such as Chimarrita and Chiripá [ 3, 5, 6].
Peaches are susceptible to chilling injuries, such as 'woolliness' that is caused by juice loss leading to a 'wooly' fruit texture.
Previously, we have demonstrated that exogenous application of GA at the initial stages of pit hardening effectively reduces the incidence of chilling injuries in responsive cultivars [ 5, 6].
Overall, our results provide insights on the mechanisms controlling the complex phenotypes associated to postharvest textural changes in peach and suggest that hormone mediated reprogramming previous to pit hardening affects the onset of chilling injuries.
In the current work, we have investigated the factors underlying the prevention of chilling injuries in peaches by the application of GA at the initial stages of pit hardening, coupling physiological analyses of a responsive cultivar to global transcriptional profiling.
This gene indeed represents an intriguing connection between ROS-associated signalling, low temperature-dependent PCD and cold stress tolerance [[ 91]], and it is thought to limit cell death via up-regulation of Cu-Zn-superoxide dismutase acting as protection against uncontrolled oxidative processes during chilling injuries [[ 92]].
