Rain cracking in sweet cherry (Prunus avium L.) imposes a severe limitation on commercial producers of this high value fruit. In recent years, considerable progress has been made in unraveling the mechanistic basis of fruit cracking in sweet cherry. In this mini review we discuss the so-called Zipper hypothesis that explains the events leading up to the ‘unzipping’ of the fruit skin and ultimately to cracking. Using the Zipper model, we then explore the reasons why fruits may sometimes crack under rain shelters or postharvest in the box, in transit, and why the measured response of fruit cracking to Ca sprays is so frustratingly inconsistent. Based on the Zipper hypothesis, cracking is the result of a series (causal chain) of events that ultimately ‘unzip’ the fruit. Tension (stress) develops in the skin during stage III growth. Stress results in microcracks in the cuticle. Microcracking is exacerbated by surface wetness and high humidity. Microcracks focus subsequent water uptake into particular regions on the fruit surface. Here, they allow water to bypass the cuticle and to penetrate through to the cells of the skin and flesh. Ultimately, water causes the large, thin-walled parenchyma cells to burst. This allows their cell contents (including malic acid) to leak into the apoplast. The malic acid causes the neighboring cells also to leak and it also extracts Ca from the cell walls. The cell walls then swell and cell-to-cell adhesion decreases. In this way a crack forms and propagates, ‘unzipping’ the skin in a way somewhat analogous to that in which a ‘ladder’ will propagate from a small area of damage in a knitted fabric.
Keywords: cuticle, Prunus avium, microcrack, calcium, rain shelter, review, xylem, water uptake