Genetic engineering of tomato with the objective of regulating PG activity has yielded
complex results. In the rin mutant of tomato, which lacks PG and does not soften, introduction
of a PG gene resulted in the synthesis of an active enzyme; however, this did not
cause fruit softening (Giovannoni et al., 1989). As a corollary to this, introduction of the
PG gene in the antisense orientation resulted in near total inhibition of PG activity (Smith
et al., 1988). In both these cases, there was very little effect on fruit softening, suggesting
that factors other than pectin depolymerization may play an integral role in fruit softening.
Further studies using tomato cultivar such as UC82B (Kramer et al., 1992) showed that
antisense inhibition of ethylene biosynthesis or PG did indeed result in lowered PG activity,
improved integrity of cell wall, and increased fruit firmness during fruit ripening. As
well, increased activity of pectin methylesterase, which removes the methyl groups from
esterified galacturonic acid moieties, may contribute to the fruit softening process.
The activities of pectin-degrading enzymes have been related to the incidence of physiological
disorders such as “mealiness” or “wooliness” in mature unripened peaches that
are stored at a low temperature. The fruits with such a disorder show a lack of juice and a
dry texture. Deesterification of pectin by the activity of pectin methyl esterase is thought
to be responsible for the development of this disorder. Pectin methyl esterase isozymes
with relative molecular masses in the range of 32 kDa have been observed in peaches, and
their activity increases after 2 weeks of low-temperature storage. Polygalacuronase activity
increases as the fruit ripens. The ripening fruits that possess both polygalacturonase and
pectin methyl esterase do not develop mealy symptoms when stored at low temperature,
implicating the potential role of pectin degradation in the development of mealiness in
peaches.