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Ripe sweet cherry fruit (Prunus avium L.) are susceptible to cracking during and after rainfall. Cracking is the final step in a series of events. According to the ‘Zipper model’, a localized bursting of cells causes swelling of cell walls. Swelling - in turn – reduces cell-to-cell adhesion thereby weakening the strained fruit skin. This – in turn - results in rupture of the skin and development of macroscopically visible cracks. Little is known about the mechanism of swelling and the factors affecting swelling. The objectives of the present study were to (1) identify the part of the cell wall that fails during formation of a crack, (2) establish methods to quantify cell wall swelling and identify the underlying mechanisms, (3) characterize cell wall swelling during fruit development and identify the cell wall fraction responsible for swelling, and (4) manipulate cell wall swelling using Ca salts. Light microscopy studies of macroscopically cracked fruit surfaces revealed, that cell wall swelling reduced cell-to-cell adhesion and caused cells to separate along their cell walls. When the surface of cracks was stained with monoclonal antibodies against specific polysaccharide epitopes, only LM19 that stains unesterified homogalacturonans strongly bound indicating exposure of pectins on the crack surface. Thus, failure of the pectin middle lamella caused the separation of adjacent cells. In vivo experiments on excised epidermal segments and in vitro studies using extracted cell walls revealed that swelling is a physical process that is completely reversible. The pressure exerted by the swelling cell wall was low and within the range of turgor values reported for sweet cherry. Swelling increased in the course of fruit development, particularly during early development (stage I and II). The cell wall fraction with the highest swelling ability were the pectins. Within the pectins, the hydrochloric acid-soluble fraction and the sodium hydroxide-soluble fraction were the most susceptible fractions for swelling. Ca2+, ...