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Water conductance of the cuticular membrane (CM) of mature sweet cherry fruit (Prunus avium L. cv. Sam) was investigated by monitoring water loss from segments of the outer pericarp excised from the cheek of the fruit. Segments consisted of epidermis, hypodermis and several cell layers of the mesocarp. Segments were mounted in stainless-steel diffusion cells with the mesocarp surface in contact with water, while the outer cuticular surface was exposed to dry silica (22 +/- 1 degrees C). Conductance was calculated by dividing the amount of water transpired per unit area and time by the difference in water vapour concentration across the segment. Conductance values had a log normal distribution with a median of 1.15 x 10(-4) m s(-1) (n=357). Transpiration increased linearly with time. Conductance remained constant and was not affected by metabolic inhibitors (1 mM NaN3 or 0.1 mM carbonylcyanide m-chlorophenylhydrazone) or thickness of segments (range 0.8-2.8 mm). Storing fruit (up to 42 d, 1 degrees C) used as a source of segments had no consistent effect on conductance. Conductance of the CM increased from cheek (1.16 +/- 0.10 x 10(-4) m s(-1)) to ventral suture (1.32 +/- 0.07 x 10(-4) m s(-1)) and to stylar end (2.53 +/- 0.17 x 10(-4) m s(-1)). There was a positive relationship (r2=0.066**; n=108) between conductance and stomatal density. From this relationship the cuticular conductance of a hypothetical astomatous CM was estimated to be 0.97 +/- 0.09 x 10(-4) m s(-1). Removal of epicuticular wax by stripping with cellulose acetate or extracting epicuticular plus cuticular wax by dipping in CHCl3/methanol increased conductance 3.6- and 48.6-fold, respectively. Water fluxes increased with increasing temperature (range 10-39 degrees C) and energies of activation, calculated for the temperature range from 10 to 30 degrees C, were 64.8 +/- 5.8 and 22.2 +/- 5.0 kJ mol(-1) for flux and vapour-concentration-based conductance, respectively.

The results support the view that the cessation of CM deposition during early sweet cherry fruit development is accounted for by a downregulation of genes involved in CM deposition. Genes that merit further investigation include PaWINA, PaWINB, PaLipase, PaLTPG1, PaATT1, PaLCR, PaGPAT4/8, PaLACS2, PaLACS1 and PaCER1.

Changes in surface area, deposition and elastic strain of the cuticular membrane (CM) were monitored during development of sweet cherry (Prunus avium L.) fruit. Fruit mass and surface area ('Sam') increased in a sigmoidal pattern between 16 and 85 days after full bloom (DAFB) with maximum rates of 0.35 g day(-1) and 0.62 cm(2) day(-1), respectively. Rates of total area strain, namely the sum of elastic plus plastic strain, were highest in cheek and stem cavity regions followed by stylar and suture regions. Rates of total uniaxial strain were higher in transverse, namely perpendicular to the stem/stylar axis, than in longitudinal direction, namely parallel to the stem/stylar axis. On a whole fruit basis CM mass remained essentially constant during fruit development. Mass of CM, dewaxed CM and wax per unit surface area decreased during development, particularly between 43 and 71 DAFB. There was no change in wax content of isolated CM. Up to 43 DAFB the surface area of isolated CM was similar to the area prior to excision indicating little elastic strain, but markedly decreased thereafter. Calculating elastic and plastic components of total strain of the CM revealed, that initial deformation up to 22 to 43 DAFB was mostly plastic. Thereafter, elastic strain was evident and both, elastic and plastic deformation, increased linearly with an increase in total strain. There was no consistent difference in the relative contribution of elastic strain to total strain between transverse and longitudinal directions, but both total and elastic strain were larger in the transverse direction. Abrading the CM had only little effect on fruit turgor. However, turgor decreased when the exocarp was cut indicating that the exocarp provided a significant structural shell of a mature sweet cherry fruit ('Regina'). Our data demonstrate, that (1) surface area expansion in sweet cherry fruit causes elastic and plastic strain of the CM, and (2) the onset of elastic strain coincided with the cessation of CM formation.