Pectin degradation in ripening and wounded fruits

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 b-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 b-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.