Localized bursting of mesocarp cells triggers catastrophic fruit cracking

Abstract

The so-called rain-cracking of sweet cherry fruit severely threatens commercial production. Simple observation tells us that cuticular microcracking (invisible) always precedes skin macrocracking (visible). The objective here was to investigate how a macrocrack develops. Incubating detached sweet cherry fruit in deionized water induces microcracking. Incubating fruit in D2O and concurrent magnetic resonance imaging demonstrates that water penetration occurs only (principally) through the microcracks, with nondetectable amounts penetrating the intact cuticle. Optical coherence tomography of detached, whole fruit incubated in deionized water, allowed generation of virtual cross-sections through the zone of a developing macrocrack. Outer mesocarp cell volume increased before macrocracks developed but increased at a markedly higher rate thereafter. Little change in mesocarp cell volume occurred in a control zone distant from the crack. As water incubation continued, the cell volume in the crack zone decreased, indicating leaking/bursting of individual mesocarp cells. As incubation continued still longer, the crack propagated between cells both to form a long, deep macrocrack. Outer mesocarp cell turgor did not differ significantly before and after incubation between fruit with or without macrocracks; nor between cells within the crack zone and those in a control zone distant from the macrocrack. The cumulative frequency distribution of the log-transformed turgor pressure of a population of outer mesocarp cells reveals all cell turgor data followed a normal distribution. The results demonstrate that microcracks develop into macrocracks following the volume increase of a few outer mesocarp cells and is soon accompanied by cell bursting.