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  • Author or Editor: Christine Schumann x
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Susceptibility of sweet cherry (Prunus avium L.) fruit to rain cracking increases toward maturity and is thought to be related to increases in both tissue pressure ( ) and cell pressure ( ). Furthermore, at a given water potential ( ), one might expect the increase in and the to balance the decrease in osmotic potential ( ). The objectives of our study were to quantify and in developing sweet cherry using vapor pressure osmometry (VPO), compression plate (CP), and the cell pressure probe (CPP). In addition, the tissue water potential was determined by quantifying the bending of strips of fruit skin and the change in projected area of discs excised from the flesh when incubated in a range of sucrose solutions of varying osmotic potentials ( ). Fruit growth followed a sigmoid pattern with time with the Stage II/Stage III transition occurring at ≈55 days after full bloom (DAFB). The and the were constant up to ≈55 DAFB but decreased to –2.8 MPa at maturity. The calculated by subtracting the from averaged ≈350 kPa up to 48 DAFB and then decreased at a decreasing rate to ≈21 kPa toward maturity. The determined from bending assays using excised skin strips or from water uptake of excised flesh discs was essentially constant up to ≈48 DAFB, then decreased until ≈75 DAFB and remained constant thereafter. These values were in good agreement with those determined by VPO. The as determined by CP passed through a transient peak at ≈41 DAFB, then decreased until ≈63 DAFB and remained constant and low until maturity. Similarly, by CPP increased from 27 to 48 DAFB, remained constant until ≈55 DAFB, and then decreased until maturity. Our data demonstrate a consistent decrease in and that coincides with a decrease in of sweet cherry during Stage III. Because and are low relative to , the change in parallels that in . The reason for the low turgor most likely lies in the accumulation of apoplastic solutes. These prevent a catastrophic increase in pressure that would otherwise lead to the bursting of individual cells and the cracking of entire fruit.

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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.

Open Access