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

FREEDOM PALESTINE FREEDOM PALESTINE FREEDOM PALESTINE
64 Postharvest Diseases of Fruits and Vegetables
25°C. However, in spite of the differences in the amounts of toxin
produced, no significant differences in pathogenicity were recorded
among fungal strains, as determined by lesion diameter on each of the
fruits. In other words, no correlation was found between patulin
production and disease development. Even strains that did not produce
patulin at 0° and 25°C infected the fruits to the same degree as strains
capable of growth and patulin production at these temperatures.
Furthermore, patulin production was totally inhibited when inoculated
apples were held in a 3%C02/2%02 atmosphere (25''C), although the level
of infection under the controlled atmosphere conditions was fairly high,
reaching 70% of that of the control.
Non-host-specific toxins are generally acknowledged to be an element
of virulence for many bacteria as well. Most of the known bacterial toxins
are produced by various pathovars of Pseudomonas syringae (Scheffer,
1983; Gross, 1991). These toxins constitute a family of structurally
diverse compounds, usually peptide in nature, that, in some cases,
display wide-spectrum antibiotic activity. Progress has been made in
identifsdng gene clusters associated with toxin production, and there is
some evidence that toxin genes may be activated in response to specific
plant signals (Gross, 1991).
C. DETOXIFICATION OF HOST DEFENSE COMPOUNDS
BY PATHOGENS
In addition to the activities of cell-wall-degrading enzymes and toxins
of the pathogen, the ability to degrade plant chemical defense
compounds, such as the tomato a-tomatine, has also been discussed as a
potential pathogenicity determinant (Staples and Mayer, 1995).
The saponin, a-tomatine is a steroidal glyco-alkaloid that occurs in
many plant species and provides a preformed barrier to fungal invasion
(Verhoeff and Liem, 1975; Osbourn, 1996). It is found in all parts of
tomato plants but is especially plentiful in the peel of green tomato fruits
(see the chapter on Host Protection and Defense Mechanisms -
Preformed Inhibitory Compounds). The toxicity of a-tomatine to fungi is
due to its ability to interact with membrane sterols, and thus cause
membrane leakage (Fenwick et al., 1992; Quidde et al., 1998).
Tomato pathogens have developed two primary strategies to overcome
this chemical defense (Osbourn et al., 1994): either they are resistant to
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