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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.

Watermelon fruit have been shown to be extremely sensitive to exogenous ethylene, exhibiting acute symptoms of whole‐fruit softening and placental‐tissue water‐soaking following short periods of exposure to the gas. This study addressed the firmness, specific activities of cell wall hydrolases, and solubility and molecular mass properties of polyuronides in placental tissue in response to treatment of intact fruit with ethylene. Watermelon fruit were harvested at the immature and full‐ripe stages and exposed to 50 µl l−1 ethylene for 6 days at 20°C. The firmness of placental tissue from ethylene‐treated ripe and immature fruit decreased nearly 80% during 6 days of ethylene exposure, whereas the firmness of placental tissue from fruit maintained in air remained relatively constant up to day 3 and then decreased slightly (12%) during the following 3 days of storage. Although ethylene treatment in some cases influenced the levels of extractable placental‐tissue polygalacturonase (EC 3.2.1.15), pectinmethylesterase (EC 3.2.1.11), and α‐(EC 3.2.1.22) and β‐galactosidase (EC 3.2.1.23) specific activities, these effects were not observed for fruit of both developmental stages and appeared not to be directly involved in the water–soaking syndrome. Symptoms of water‐soaking were accompanied by increases in the levels of water‐ and CDTA (trans‐1,2‐cyclohexanediamine‐N,N,N',N′‐tetraacetic acid)‐soluble polyuronides and significant molecular mass downshifts in polyuronides in both immature and ripe watermelon fruit. Polyuronide depolymerization in ethylene‐treated ripe fruit was extensive. The parallel trends of enzyme changes in ethylene‐ compared with air‐treated fruit indicate that extractable enzyme levels are not associated with development of the water‐soaking disorder. The potential involvement of membrane dysfunction in the water‐soaking phenomenon is discussed.