Rain cracking is a problem for sweet cherry production in all countries where this very high-value crop is grown (Christensen, 1996). Despite considerable research effort the mechanistic basis of the phenomenon is still poorly understood. The fruit’s water relations are thought to play a critical role in cracking (Considine and Kriedemann, 1972; Measham et al., 2009; Sekse, 1995, 2008; Sekse et al., 2005). Recent investigations have established that stage III sweet cherry fruit have a surprisingly low turgor (Knoche et al., 2014; Schumann et al., 2014). The mechanism by which low turgor is maintained despite a massive accumulation of carbohydrates and, hence, a very negative osmotic potential is at present unknown. Barring the pit, a sweet cherry has a similar mechanical constitution as a grape (Vitis vinifera L., Vitis labrusca L.), which is also very vulnerable to rain cracking (Considine and Brown, 1981). As in sweet cherries, grape turgor is very low in postveraison fruit (Lang and Düring, 1990; Wada et al., 2008, 2009). The low turgor in grapes is accounted for by the accumulation in the apoplast of solutes at osmotic concentrations closely matching those in the symplast. The rough balance in the osmotic potentials in symplast and apoplast results in similar pressures in these two compartments and thus flaccidity (Wada et al., 2008). This conclusion is based on the following experimental evidence. First, at harvest maturity there is no significant difference in osmolarity between apoplastic fluid extracted from grapes via the stalk using a pressure bomb and that of the expressed juice of crushed fruit (almost totally symplastic in origin—very large, thin-walled flesh cells), whereas in immature grapes they are substantially different (Lang and Düring, 1991). This finding is interpreted as being the result of a loss of compartmentation during maturation (Lang and Düring, 1991). Second, Tilbrook and Tyerman (2008) observed significant cell death within an intact, mature grape berry using microscopy and vitality staining. The membrane’s loss of osmotic competence allows diffusion of symplastic solutes into the apoplast. Third, using tissue centrifugation (Wada et al., 2008) and a pressure plate apparatus (Wada et al., 2009) the grape apoplast was selectively sampled. The subsequent compositional analyses also revealed that symplastic solutes accumulate in the apoplast of mature grapes (Wada et al., 2008, 2009).
For sweet cherries, comparable, direct evidence for the presence of apoplastic solutes that would account for the lack of turgor is not yet available. However, grape berry and sweet cherry are morphologically and physiologically similar with respect to cracking and therefore the above explanation may also apply to sweet cherry. First, the bursting of cells as a consequence of excessive water uptake possibly through microcracks (Glenn and Poovaiah, 1989; Peschel and Knoche, 2005) and of significant cell-wall degradation during maturation (Kondo and Danjo, 2001) would result in solute leakage into the apoplast. Second, we observed macerated tissue surrounding the pit of many sweet cherry cultivars at maturity (M. Knoche, unpublished data). We interpret this observation as the loss of compartmentation in this region of the fruit.
The question arises what would be the consequences of such leakage? In the work we report here, we observe a surprising and dramatic increase in cracking when sweet cherry fruit are brought into direct contact with the expressed juice of sweet cherries.
The objectives of this study were to investigate what consequences the leakage of cell contents into the fruit’s apoplast might have. We were particularly interested in 1) quantifying cracking of sweet cherry fruit when incubated in different osmotica, including in artificial sweet cherry juice containing the same five dominant chemical moieties found in real cherry juice; 2) identifying any “active,” crack-promoting constituent in real cherry juice; and 3) establishing its mode of action in increasing cracking.
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