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The softening of fruits during ripening is accompanied by changes in the texture of fruits ( Tucker et al. 2017 ) and is mainly caused by cell wall polysaccharide degradation, pectin solubilization, and cell structure destruction. Peach fruits are

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al., 2005 ; Newhouse et al., 2007 ), and small-scale field tests of transgenic elms have been established ( Merkle et al., 2007 ). Determination of the chemical attributes of plant cell walls is of great importance for evaluating both the effects of

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Abstract

Fruit extracts of Lycopersicon esculentum cv. Tiny Tim were found to contains α- and β-galactosidase, a- and β-glucosidase, α- and β-mannosidase, and α- and β-xylosidase activities. All of these enzymes either declined or remained constant in concentration during fruit development and ripening. Activities of β-glucosidase and α-galactosidase were found to be associated with isolated cell wall fragments. No evidence was found for an increase in concentration of the enzymes in the cell wall during ripening. The probability that these enzymes are not involved in fruit softening is discussed.

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Abstract

Ca2+ content in cell wall-middle lamella (CW–ML) areas of outer and inner pericarp, placenta, and gel parenchyma of ripening tomato (Lycopersicon esculentum Mill. cvs. Celebrity and Jumbo) and mesocarp of ripening peach [Prunus persica (L.) Batsch cv. Georgia Belle] was determined by energy dispersive (EDS) X-ray microanalysis. Ca2+ increased from 1.50 to 6.95 mg·g–1 dry weight in CW–ML of outer pericarp and 0.98 to 2.60 mg·g–1 dry weight in CW–ML of inner pericarp during ripening. Ca2+ content remained constant in tomato placenta and peach mesocarp, and was undetectable in tomato gel parenchyma throughout ripening. CW–ML of peach mesocarp had lower Ca2+ content than tomato pericarp and placenta at all ripening stages, but total peach uronic acid content was 2.5 times greater. Pectin methylesterase (PME) activity increased in tomato pericarp as fruit ripened, but remained low and unchanged in placenta and gel parenchyma. PME treatment of pericarp increased amounts of CW–ML Ca2+ in the breaker stage but not in the green mature stage. The results indicate that increased amounts of Ca2+ are bound to CW–ML of tomato pericarp as ripening occurs but not in placenta or peach mesocarp. Pectin deesterification and wall softening during ripening may in part be factors that control the presence and amount of CW–ML Ca2+.

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Abstract

Normal and collapsed juice vesicles were removed from stored late-harvested grapefruit segments (Citrus paradisi Macf. cv. Marsh) and the cell wall anatomy of epidermal and internal parenchyma was compared with light, scanning electron, and transmission electron microscopy. Normal juice vesicles were turgid and elongate, and epidermal cells and internal parenchyma were intact. Collapsed juice vesicles appeared flattened, and internal parenchyma were compressed. Cell wall thickening occurred in internal parenchyma and single or clustered epidermal cells of collapsed vesicles. Cell walls of the same cells in normal vesicles were thin. Epidermal and internal parenchyma cell walls of collapsed vesicles were 10 to 50 to 10 to 20 times the thickness, respectively, of corresponding normal cell walls. Lignin was detected in thickened cell walls of epidermal and internal parenchyma of collapsed vesicles. The results suggest that cell wall synthesis in vesicles is a symptom of section drying in grapefruit.

Open Access

Changes in texture, cell wall structure and composition during storage of Ca-treated and untreated `Golden Delicious' apple fruit (Malus domestics Borkh.) were investigated. The cell wall region of Ca-treated fruit showed no swelling during storage and cell-to-cell contact was maintained, whereas regions of the middle lamella in untreated tissue stained lightly, appeared distended, and eventually separated. In control fruit, microfibril orientation was lost in distended regions of the cell wall, especially in the outer wall region adjacent to the middle lamella. Furthermore, the middle lamella was fenestrated and in some cases was completely degraded. These changes during storage of control fruit were accompanied by a decrease in arabinose and galactose moieties of the cell wall and an increase in soluble pectin. Calcium treatment of fruit inhibited solubilization of polyuronide and arabinose moieties and reduced the loss in galactose content during storage. Tensile strength and firmness were positively correlated to Ca content of the fruit cortex. Excessive tensile stress caused tissue failure in control fruit when cells of the cortical tissue separated at the middle lamella. In contrast, cylinders of Ca-treated fruit fractured through cortical cell walls.

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Enzymically active cell wall isolated from mature-green and ripening tomato (Lycopersicon esculentum Mill cv. `Rutgers') fruit was employed to investigate the mobility of the enzyme polygalacturonase (PG, EC 3.2.1.15). Cell walls from mature-green `Rutgers' fruit or from the ripening mutant rin, which alone exhibits little or no release of pectin, were unaffected by the addition of enzymically active cell wall from ripening `Rutgers' fruit, indicating that PG is either not transferred at all or is not transferred to sites of pectin hydrolysis. The quantity of pectin released by the addition of soluble PG to enzymically active wall depended on the quantity of enzyme added. Similar data were obtained using purified PG2. Pectin solubilization from all wall isolates exhibiting enzymically mediated pectin release diminished with time; however, transfer to fresh buffer initiated a resumption of autolytic activity, indicating that an inhibitor is released during the course of pectin hydrolysis.

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Cell wall changes in `Fantasia' nectarines [Prunus persica (L) Batsch var. nectarina (Ait) maxim] were determined after storage at 0C with or without intermittent warming (at 20C at 2-week intervals) and after ripening. For comparison, fruit were examined at harvest and after ripening without storage. Fruit stored continuously at 0C for 6 weeks became mealy during ripening, whereas fruit subjected to intermittent warming ripened normally. Ripening immediately after harvest was associated with solubilization and subsequent depolymerization of pectic polymers and a net loss of galactosyl residues from the cell wall. No solubilization of pectic polymers from the cell wall occurred during storage of fruit at 0C. Mealy fruit, ripened after continuous storage at 0C, showed only limited solubilization of pectins and depolymerization, high relative molecular weight (M) polymers being predominant. During ripening after storage, pectic polymer solubilization was not as extensive in intermittently warmed fruit as in fruit undergoing normal ripening but solubilized polymers were depolymerized, low M uronic acid-rich polymers becoming predominant. Intermittent warming of fruit resulted in significant softening during storage, alleviating the development of mealiness by promotion of cell wall changes associated with normal ripening.

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Most `Flavortop' nectarines [Prunus persica (L.) Batsch (Nectarine Group)] that were placed directly into 0 °C storage developed chilling injury after removal, while preconditioning fruit for 2 days at 20 °C (delayed storage) reduced chilling injury substantially. Chilling injury was expressed as the development of a dry, woolly flesh texture during ripening. Delayed-storage fruit were as firm as control fruit when placed in storage, but softened more during storage. Analysis of cell wall components showed that in woolly fruit a higher percentage of pectin was retained in the sodium carbonate fraction, although during ripening polymers in this fraction decreased in molecular mass (Mr). In the guanidine thiocyanate hemicellulose fraction of woolly fruit, the associated pectin and hemicellulose remained as large polymers, while in delayed-storage fruit they decreased in Mr during ripening. Endo-polygalacturonase (PG), pectin esterase (PE), and endo-glucanase (EGase) activities of delayed-storage fruit were the same as control fruit at the beginning of storage, although exo-PG was higher. However, differences were observed at the end of storage. Endo-PG activity was lower in control than delayed-storage fruit at the end of storage while PE activity was higher, and exo-PG and EGase activities were similar. These differences in activity were not reflected in the mRNA abundance of the respective enzymes. Endo-PG and PE message was similar in all fruit at the end of storage and increased during ripening, while EGase message was low at all times except in control fruit after storage and development of woolliness. Prevention of chilling injury by delayed storage appears to be due to the ability of the fruit to continue a progressive, slow cell wall degradation in storage which allows normal ripening to proceed when the fruit are rewarmed. Regulation of the softening process did not appear to be by enzyme synthesis, since mRNA levels of the enzymes did not correspond with enzyme activity.

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`Keitt' and `Tommy Atkins' mango (Mangifera indica L.) fruit were evaluated for selected ripening criteria at six ripening stages, from mature green to overripe. `Tommy Atkins' mangos developed more red and yellow pigmentation (CIE a* and b*) in peel and mesocarp tissues than `Keitt'. The outer mesocarp of `Keitt' remained firm longer than `Tommy Atkins', and the inner mesocarp was softer than the outer at each stage in both cultivars. Cell wall neutral sugars, particularly arabinosyl, rhamnosyl, and galactosyl residues, decreased with ripening in both cultivars. `Keitt' had more loosely associated, chelator-soluble pectin, accumulated more soluble polyuronides, and retained more total pectin at the ripe stage than `Tommy Atkins'. Both cultivars had similar polygalacturonase (EC 3.2.1.15) activity which increased with ripening. The amount and molecular weight of cell wall hemicellulose decreased with ripening in both cultivars. These data indicate that enzymatic and/or nonenzymatic processes, in addition to polygalacturonase activity, are involved in the extensive softening of mango fruit.

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