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When mature sweet cherries (Prunus avium L.) came into contact with sweet cherry juice, cracking dramatically increased. The objectives of our study were: 1) to quantify the cracking of fruit in cherry juice, 2) to determine which constituent(s) of the juice especially promote cracking and, 3) to establish its/their mode of action in promoting cracking. Artificial juice was made up as an aqueous solution of the same five pure chemicals and at the same relative concentrations as the five major osmolytes of real sweet cherry juice. Artificial and real juice was used at half-isotonic concentrations as the real juice from that batch of fruit. Cracking of sweet cherries placed in either artificial or real juice was more rapid and occurred for lower net water uptakes than of fruit placed in half-isotonic polyethylene glycol 6000. The crack-promoting component in sweet cherry juice was malic acid. Further tests with malic acid, and other organic acids, and with different concentrations of malic acid, with and without pH control, and with the enantiomers of malic acid, showed the effects were primarily related to the pH of the incubation solution. Leakage of anthocyanin from discs of flesh was increased in the presence of malic acid and greater in hypotonic than hypertonic solutions, suggesting that malic acid increases the permeability of the plasma membrane and tonoplast and weakens the cell walls. Malic acid may be an important link (amplifier) in a reaction chain that begins with the bursting of individual epidermal cells and ends with the formation of macroscopic skin cracks.

Xylem flow is progressively shut down during maturation beginning with minor veins at the stylar end and progressing to major veins and finally to bundles at the stem end. This study investigates the functionality of the xylem vascular system in developing sweet cherry fruit (Prunus avium L.). The tracers acid fuchsin and gadoteric acid were fed to the pedicel of detached fruit. The tracer distribution was studied using light microscopy and magnetic resonance imaging. The vasculature of the sweet cherry comprises five major bundles. Three of these supply the flesh; two enter the pit to supply the ovules. All vascular bundles branch into major and minor veins that interconnect via numerous anastomoses. The flow in the xylem as indexed by the tracer distribution decreases continuously during development. The decrease is first evident at the stylar (distal) end of the fruit during pit hardening and progresses basipetally towards the pedicel (proximal) end of the fruit at maturity. That growth strains are the cause of the decreased conductance is indicated by: elastic strain relaxation after tissue excision, the presence of ruptured vessels in vivo, the presence of intrafascicular cavities, and the absence of tyloses.

Rain cracking severely affects the commercial production of many fleshy-fruit species, including of sweet cherries. The objectives were to investigate how the gaping macroscopic cracks (macrocracks) of a rain-cracked fruit can develop from microscopic cracks in the cuticle (microcracks). Incubating fruit in deionized water is well known to cause significant macrocracking. We found that after a lag phase of 2 h, the numbers and lengths of macrocracks increased. Macrocrack number approached an asymptote at 12 h, whereas macrocrack length continued to increase. The rate of macrocrack propagation (extension at the crack tip) was initially 10.8 mm h -1 but then decreased to a near-constant 0.5 mm h -1 . Light microscopy revealed three characteristic zones along a developing macrocrack. In zone I (ahead of the crack), the cuticle was intact, the epidermal cells were unbroken and their cell walls were thin. In zone II, the cuticle was fractured, the first epidermal cells died and their cell walls began to thicken (swell). In zone III, most epidermal cells had died, their cell walls were swollen and cell:cell separation began along the middle lamellae. The thickness of the anticlinal epidermal cell walls and the percentage of intact living cells along a crack were closely and negatively related. Cracks were stained by calcofluor white, but there was no binding of monoclonal antibodies (mAbs) specific for hemicelluloses (LM11, LM21, LM25). Strong binding was obtained with the anti-homogalacturonan mAb (LM19), indicating the presence of unesterified homogalacturonans on the crack surface. We conclude that macrocrack propagation is related to cell death and to cell wall swelling. Cell wall swelling weakens the cell:cell adhesion between neighbouring epidermal cells, which separate along their middle lamellae. The skin macrocrack propagates like a ‘run’ in a fine, knitted fabric.