Abstract

Tomato, like most species from tropical and subtropical regions, exhibits postharvest chilling injury (PCI) when stored at low temperatures. Because of its economic importance and the functional genomics tools available, we used tomato to investigate aspects of fruit PCI development. We asked two questions: first, are there spatial-temporal differences in the development of PCI that can be detected by magnetic resonance imaging (MRI)? Here, the aim was to use a non-invasive method to study PCI progression in vivo. At mature green and breaker, the pericarp, locular tissue and columella produced distinct D-values while in contrast, there was no such differentiation in riper fruit. Although the pericarp is where most PCI symptoms are visible, this tissue showed less dynamism upon cold exposure, compared to the inner tissues as detected by MRI. This suggests the occurrence of distinct, independently modulated mechanisms contributing to the development of PCI-symptomatology. Collectively our data showed that the MRI could detect fruit ripening, its attenuation by cold, and fruit tissue-specific responses to chilling stress. The second question we asked was if epigenetic modification of the tomato genome or transcriptome influences PCI response. We examined PCI severity in fruit injected with a demethylating agent, 5-azacytidine (AZA). Two tomato genotypes exposed to varying severities of cold-stress were studied. Results suggested that AZA was able to moderate PCI in ‘Micro-Tom’ after 3 weeks at 2.5°C, while different patterns were observed in ‘Sun Cherry’ across various cold treatments. The effects of AZA on PCI were complex, multilayered and highly context-dependent.