Cuticular Properties and Postharvest Calcium Applications Influence Cracking of Sweet Cherries

Abstract

Abstract The influence of stomata, the stylar scar, cuticular fractures, and Ca2+ on susceptibility of ‘Bing’ sweet cherry fruit (Prunus avium L.) to water injury was studied. Water injury was first detected as an increase in cell turgor. Water penetration caused separation of the cuticle from the epidermal cell wall. Swelling in the epidermal cell wall region resulted in cuticular fracturing that generally preceded fruit cracking. Uncracked fruit that had cuticular fractures softened rapidly. Stomata were sparsely distributed on the fruit surface and were often fixed in an open or partially open position. Water injury was not visible at stomata even when injury occurred adjacent to the stomatal region. Initial signs of injury were commonly visible near the stylar scar. Histochemical studies revealed that the surface of the stylar scar was devoid of a cuticle covering and was rich in insoluble carbohydrates. Greater penetration of solute containing 45Ca2+ occurred at the stylar scar. Fine fractures in the cuticle surface were observed in fruit at harvest time in 1985 and 1986. Cherry fruit with cuticular fractures had a higher water absorption rate than unfractured fruit. In immersion tests, Ca2+ reduced cherry cracking. EGTA increased fruit cracking; this increase was negated by adding Ca2+. Neither Ca2+ nor EGTA affected the water absorption rate of the fruit. EGTA decreased the cracking threshold of the fruit, while Ca2+ increased it. Soluble pectin content of the immersion solution rose with increasing incubation times. EGTA increased while Ca2+ markedly decreased soluble pectin concentration in the immersion solution. Histochemical studies indicated a breakdown of the cell wall structure in the epidermal region of water-injured fruit. Autoradiographs of fruit immersed in a solution containing 45Ca2+ showed the epidermal region to be the site of Ca2+ action in altering fruit cracking. Chemical name used: Ethyleneglycol-bis-(β-aminoethyl ether) N,N,N,N-tetraacetic acid (EGTA)