Ripening-related firmness loss shortens considerably the storage potential of sweet cherry (Prunus avium L.), thus limiting postharvest handling, transportation, and commercialisation. The biochemical mechanisms underlying this process in cherries are not fully understood, and the mechanisms operating in a given fruit may be not extrapolated to a different species. Cell wall materials obtained from untreated and calcium-treated 'Celeste' sweet cherries were fractionated and analysed after cold storage, and related enzyme activities and gene expression were assessed. Calcium-treated fruit were firmer, with lower weight loss and decay incidence than the controls. The accumulation of PaβGal and PaEXP1 transcripts was strongly inhibited in cold-stored fruit, although expression levels recovered largely after three days of shelf life. Data suggest that pectin methylesterase, β-galactosidase and expansin activities may control the access of additional proteins to their substrates. A possible role for the apoplastic redox status in the modulation of the process is also discussed