The mechanism of rain cracking of sweet cherry fruit

Moritz Knoche [Institute for Horticultural Production Systems, Leibniz-University Hannover, Germany]
Andreas Winkler [Institute for Horticultural Production Systems, Leibniz-University Hannover, Germany]

Sweet cherry (Prunus avium L.) cracking is a severe limitation in production worldwide. It is thought to be caused by excessive water uptake and a subsequent increase in turgor. When a critical threshold is exceeded (‘critical turgor’) the fruit is believed to crack. Experimental evidence supporting this wide spread concept is lacking. Instead, published data question the critical turgor hypothesis and an alternative explanation must be thought of. This mini review summarizes experimental research published in the last two decades that resulted in an alternative explanation of sweet cherry fruit cracking, the so called Zipper hypothesis. According to this hypothesis, cracking is the result of a series of events that ultimately propagate a crack through skin and flesh and ‘unzip’ the fruit. It is based on the following sequence of events: Tension (stress) develops in the skin during stage III growth and particularly in the cuticle due to a downregulation of genes involved in cutin and wax synthesis. Stress in the skin results in strain and microcracks in the cuticle. Furthermore, surface wetness on and high humidity above the strained cuticle aggravates microcracking. Microcracking impairs the cuticle’s barrier function and focuses water uptake in a particular region of the fruit surface. Water bypasses the cuticle, penetrates into the fruit and moves to sites where water potential is most negative. These are the large thin-walled parenchyma cells of the outer mesocarp that have a more negative osmotic potential than the small thick walled epidermal and hypodermal cells. Water uptake causes individual cells to burst. As a consequence, cell content leaks into the apoplast. Major constituents of sweet cherry such as glucose, fructose and malic acid now occur in the apoplast at comparable concentrations as in the symplast. The consequences are several fold: First, cell turgor decreases and is entirely lost when epidermal cells plasmolyse in the juice from the flesh. Second, malic acid extracts cell wall bound Ca, weakens cell walls and increases the permeability of plasma membranes causing a chain reaction of leakage of adjacent cells. The leakage of cells and the loss of the (low) turgor results in swelling of cell walls, in particular of the pectin middle lamella. Swollen cell walls have decreased stiffness, fracture tension and cell adhesion resulting in the separation of neighbouring cells along their cell walls. The tension generated by the strain of the skin is now sufficient to cause the cells to separate along their swollen walls and to rupture the skin. This process continues at the crack tip where the stress concentrates and causes the crack to elongate. The skin ‘unzips’ in the same way like a ‘zipper’ or a ‘ladder’ that propagates in a piece of knitted fabric.

DOI: 10.26353/j.itahort/2019.1.5965

Keywords: cracking, fruit growth, cherry, Prunus avium, fruit water relations


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Knoche, M. and Winkler, A. (2019) 'The mechanism of rain cracking of sweet cherry fruit', Italus Hortus, 26(2), pp. 59-65. doi: 10.26353/j.itahort/2019.1.5965