Post harvest diseases fruits and vegetables - Xavier University ...

FREEDOM PALESTINE FREEDOM PALESTINE FREEDOM PALESTINE
264 Postharvest Diseases of Fruits and Vegetables
but not to Cercospora nicotianae, suggesting that other factors besides
chitinase, may be involved in disease resistance (BrogUe et al., 1991). A
later study describes enhanced resistance to fungal attack in transgenic
plants by co-expression of chitinase and glucanase genes (Zhu et al.,
1994). Other microbial enzymes normally induced in plants, such as
peroxidase and other pathogen-defense-related compounds, might also be
exploited for bioengineering (Bowles, 1990; Mohan and Kolattukudy,
1990).
The knowledge and understanding of postharvest disease etiology and
physiology may be of much help in selecting new genes and developing
new transgenic plants, resistant to postharvest diseases. For example,
the knowledge that wounding leads to fungal penetration into the host
and triggers postharvest disease development (Barkai-Golan and
Kopeliovitch, 1981; Brown, G.E. and Barmore, 1983; Eckert and
Ratnayake, 1994) may lead to genetic alteration of the plant to make it
more physically resistant to wounding or to enhance the production of
wound-healing compounds to shorten the time that the wounded tissue is
vulnerable to pathogen attack (Mount and Berman, 1994). Similarly,
understanding the role of the pathogen cell-wall-degrading enzymes in
plant tissue deterioration may lead to the creation of new transgenic
plants by which the pathogen polygalacturonase (PG) is suppressed.
Following the characterization of PG-inhibiting proteins from pears by
Stotz et al. (1993), it was suggested that the pear promoter might affect a
fruit-specific expression of the gene, resulting in the inhibition o£ Botrytis
cinerea. It was further suggested that the characterization of the protein
inhibitor from pears should lead to the expression of PG-inhibiting
proteins in transgenic plants and possibly to the inhibition of decay
development. In fact, Powell et al. (1994) reported that transgenic tomato
fruits expressing the gene of fungal PG-inhibiting glycoproteins of pears,
were more resistant to B. cinerea than the control fruits.
Using nor (non-ripening) or rin (ripening inhibitor) tomato mutants
that block many aspects of the ripening process of the fruit, including
softening of the tissues and color development, Barkai-Golan et al. (1986)
and Giovannoni et al. (1989) found that the tomato's own PG plays an
important part in the total PG activity in the host during pathogenesis,
and probably takes a major role in the degradation of cell wall pectic
substances. Following these findings, it was further suggested that the
suppression of fruit PG might be useful in increasing fruit shelf life
(Giovannoni et al., 1989). Bioengineering this enzyme has been
accomplished with tomatoes (Kramer et al., 1990; Smith et al., 1988) and
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