Use of controlled atmosphere in Prunus persica postharvest for chilling injuries mitigation: A multi-omics approach

Chilling injury (CI) limits the storage and marketability of peaches and nectarines, especially late-season cultivars like Prunus persica ‘Fantasia’. Symptoms include internal breakdown, mealiness, and flesh reddening, which compromise quality. While physiological aspects of CI are well studied, its molecular and regulatory bases remain unclear. Recent evidence indicates that postharvest performance depends not only on storage but also on transcriptional, epigenetic, and developmental programs established earlier. This thesis addresses CI through (i) transcriptomic reprogramming under controlled atmosphere (CA) storage, (ii) epigenetic regulation of gene expression during cold and CA storage, and (iii) developmental signals from the bud stage. Physiological analyses showed that CA reduced internal breakdown and reddening while maintaining firmness, juiciness, and ripening. Transcriptomics revealed that CA attenuated stress-related genes (peroxidases, polyphenol oxidases, heat shock proteins), stabilized redox balance, and modulated cell wall genes: repression of polygalacturonases prevented mealiness, while regulation of expansins and galactosidases allowed softening without juice loss. Hormonal regulation included reduced ethylene biosynthesis and activation of auxin-responsive genes, suggesting a balanced ethylene–auxin interplay. A cluster of six NAC transcription factors on chromosome 2 was induced under CA, with one gene maintaining expression after shelf life, linking stress buffering and ripening control. Epigenetic analyses showed widespread methylation changes, particularly in the CHH context, with differentially methylated regions overlapping stress, hormone, and cell wall genes. Eighty-three chromatin-related genes (methyltransferases, acetyltransferases, histone modifiers) were differentially expressed, especially late in storage, indicating that CA also stabilizes transcriptional landscapes via epigenetic mechanisms. Finally, using the slow-ripening (SR) mutant, genomic analysis confirmed a deletion in a NAC gene underlying its ripening defect. Bud transcriptomes revealed organ-specific networks involving hormones and chromatin regulators, supporting that early developmental programs precondition fruit physiology and stress responses. Together, these studies show that CA mitigates CI by modulating transcriptional and epigenetic networks, with stress attenuation, cell wall remodeling, hormonal tuning, and NAC transcription factors as key regulators. Evidence from SR further highlights developmental contributions. This multidimensional view of CI integrates developmental, transcriptional, and epigenetic processes with storage conditions, providing molecular bases for breeding and management strategies to enhance postharvest performance in peach and related stone fruits.