Molecular mechanisms underlying ClO₂-mediated disease resistance and delayed ripening in postharvest apricot fruit

Both postharvest black spot disease, caused by pathogenic infections, and the rapidity of ripening and senescence processes are major challenges in apricot fruit storage, in combination leading to quality deterioration and economic losses. Herein, we elucidated the molecular mechanism by which chlorine dioxide (ClO₂) inhibits postharvest black spot disease and delays ripening and senescence in apricot fruit through comprehensive analysis of postharvest gene expression profiles and metabolite changes. Results showed that ClO₂ treatment reduced the incidence of black spot by 46 % and the lesion diameter by 46 % during storage. At the molecular level, ClO₂ treatment up-regulated the expression of disease resistance-related genes ( WRKY33, WRKY2 ) while inhibiting the transcription of ethylene synthesis genes ( ACO1, ACS1 ). It also regulated hormone signaling pathways involving jasmonic acid, auxin, and gibberellin. Metabolomic analysis revealed that ClO₂ treatment led to accumulations of terpenoids (platycodin C), sulfur-containing amino acids (homocysteine), as well as elevated levels of jasmonic acid and melatonin. Furthermore, ClO₂ activated key metabolic pathways including plant-pathogen interaction, ascorbic acid (ASA) and aldehyde acid metabolism, and α-linoleic acid metabolism. It also enhanced cell wall integrity via the regulation of CES1 and BGAL1 , and coordinated the synthesis of defense-related metabolites such as ASA. This study provides compelling molecular evidence supporting the application of ClO₂ as a green preservation strategy for postharvest apricots, and offers valuable insights into the hormone-metabolite crosstalk mechanisms governing postharvest disease resistance and senescence regulation.