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`Galia' (Cucumis melo var. reticulatus L. Naud. `Galia') melons exhibit relatively short postharvest longevity, limited in large part by the rapid softening of this high quality melon. The present study was performed to characterize the physiological responses of `Galia' fruit harvested at green (preripe) and yellow (advanced ripening) stages and treated with 1-methylcyclopropene (1-MCP) before storage at 20 °C. Treatment with 1.5 μL·L-1 1-MCP before storage delayed the climacteric peaks of respiration and ethylene production of green fruit by 11 and 6 d, respectively, and also significantly suppressed respiration and ethylene production maxima. Softening of both green and yellow fruit was significantly delayed by 1-MCP. During the first 5 d at 20 °C, the firmness of green control fruit declined 66% while 1-MCP-treated fruit declined 46%. By day 11, firmness of control and 1-MCP-treated green fruit had declined about 90% and 75%, respectively. The firmness of control yellow fruit stored at 20 °C declined 70% within 5 d while 1-MCP-treated fruit declined 30%. The 1-MCP-induced firmness retention was accompanied by significant suppression of electrolyte leakage of mesocarp tissue, providing evidence that membrane dysfunction might contribute to softening of `Galia' melons. The mesocarp of fruit harvested green and treated with 1-MCP eventually ripened to acceptable quality; however, under the treatment conditions (1.5 μL·L-1 1-MCP, 24 h) used in this study, irreversible suppression of surface color development was noted. The disparity in ripening recovery between mesocarp versus epidermal tissue was considerably less evident for fruit harvested and treated with 1-MCP at an advanced stage of development. The commercial use of 1-MCP with `Galia'-type melons should prove of immense benefit in long-term storage and/or export situations, and allow for retention of quality and handling tolerance for fruit harvested at more advanced stages of ripening.

Pectin depolymerization during fruit ripening has been shown to be largely due to pectinolytic enzymes, including polygalacturonases (E.C. 3.2.1.15) and pectinmethylesterases (E.C. 3.2.1.11). Studies have shown that these enzymes are not the primary determinants of softening, although participation in texture changes during the late stages of ripening seems evident. Pectin depolymerization differs significantly between various fruit types, notably avocado and tomato, even though levels of extractable PG activity in these fruits are similar. Collective evidence indicates that the activities of some cell wall enzymes are restricted in vivo, with maximum hydrolytic potential expressed only in response to tissue disruption or wounding. In contrast, other enzymes reported to participate in pectin degradation, notably beta-galactosidases/exo-galactanases, exhibit in vitro activity far below that anticipated to be required for the loss of cell wall galactosyl residues during ripening. Factors controlling in vivo hydrolysis have not been fully explored but might include apoplastic pH, cell wall inorganic ion levels, non-enzymic proteins including the noncatalytic beta-subunit and expansins, wall porosity, and steric hindrances. Recent studies of cell wall metabolism during ripening have demonstrated an orderly process involving, in the early stages, cell wall relaxation and hemicellulose degradation followed, in the later stages, by pectin depolymerization. A limited number of studies have indicated that radical oxygen species generated either enzymically or non-enzymically might participate in scission of pectins and other polysaccharides during ripening and other developmental processes. Similar mechanisms might also occur in response to wounding, an event typically followed by an oxidative burst. Cell wall degradation as influenced by physical wounding could be of particular relevance to the deterioration of lightly processed fruits.

Pre-ripe `Booth 7' avocado (Persea americana Mill.) fruit, a cross of West Indian and Guatemalan strains, were treated with 0.9 μL·L-1 1-methylcyclopropene (1-MCP) for 12 hours at 20 °C. After storage for 18 days in air at 13 °C, at which time whole fruit firmness values averaged about 83 N, half of the 1-MCP-treated fruit were treated with 100 μL·L-1 ethylene for 12 hours and then transferred to 20 °C. 1-MCP delayed softening, and fruit treated with 1-MCP retained more green color than air-treated fruit when full ripe (firmness 10 to 15 N). 1-MCP affected the activities of pectinmethylesterase (EC 3.2.1.11), α-(EC 3.2.1.22) and β-galactosidases (EC 3.2.1.23), and endo-β-1,4-glucanase (EC 3.2.1.4). The appearance of polygalacturonase (EC 3.2.1.15) activity was completely suppressed in 1-MCP-treated fruit for up to 24 days, at which time the firmness of 1-MCP-treated fruit had declined nearly 80% compared with initial values. The effect of exogenous ethylene applied to partially ripened 1-MCP-treated fruit differed for different ripening parameters. Ethylene applied to mid-ripe avocado exerted no effect on the on-going rate or final extent of softening of 1-MCP-treated fruit, even though polygalacturonase and endo-1,4-β-glucanase activities increased in response to ethylene. β-galactosidase decreased in 1-MCP-treated fruit in response to ethylene treatment. 1-MCP delayed the increase in solubility and depolymerization of water- and CDTA (1,2-cyclohexylenedinitrilotetraacetic acid)-soluble polyuronides, likely due to reduced polygalacturonase activity. At the full-ripe stage, the levels of arabinose, galactose, glucose, mannose, rhamnose, and xylose associated with the CDTA-soluble polyuronide fraction were similar among all treatments. In contrast, the galactose levels of water-soluble polyuronides declined 40% and 17% in control and 1-MCP treated fruit, respectively. Hemicellulose neutral sugar composition was unaffected by 1-MCP or ethylene treatment. The data indicate that the capacity of avocado fruit to recover from 1-MCP-mediated suppression of ripening can be only partially amended through short-term ethylene application and differs significantly for different ripening parameters.