Abstract
Rain cracking (hereinafter referred to as macrocracking) severely impacts the production of sweet cherry (Prunus avium). Calcium (Ca) sprays can reduce macrocracking, but the reported responses to Ca sprays are variable and inconsistent. The objective of this study was to establish the physiological mechanism through which Ca reduces macrocracking in sweet cherry fruit. Six spray applications of 50 mM CaCl2 had no effect on macrocracking (assessed using a standardized immersion assay) despite a 28% increase in the Ca-to-dry mass ratio. Similarly, during another experiment, there was no effect of up to nine Ca sprays on macrocracking, although the Ca-to-dry mass ratio increased as the number of applications increased. In contrast, CaCl2 spray applications during simulated rain (in a fog chamber) significantly reduced the proportion of macrocracked fruit. Additionally, immersion of fruit in CaCl2 decreased macrocracking in a concentration-dependent manner. Monitoring macrocrack extension using image analysis revealed that the rate of macrocrack extension decreased markedly as the CaCl2 concentration increased. This effect was significant at concentrations as low as 1 mM CaCl2. Decreased anthocyanin leakage, decreased epidermal cell wall swelling, and increased fruit skin stiffness and fracture force contributed to the decrease in macrocracking. There was no effect of CaCl2 on the cuticle deposition rate. Our results demonstrated that Ca decreased macrocracking when applied to a wet fruit surface either by spraying on wet fruit or by incubation in solutions containing CaCl2. Under these circumstances, Ca had direct access to the cell wall of an extending macrocrack. The mode of action of Ca in reducing macrocracking is primarily decreasing the rate of crack extension at the tip of a macrocrack.
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