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

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FREEDOM PALESTINE FREEDOM PALESTINE FREEDOM PALESTINE<br />

Physiological <strong>and</strong> Biochemical Changes 103<br />

The origin of PG in Rhizopus stolonifer-miected tomatoes has been<br />

studied in various tomato <strong>fruits</strong> (Barkai-Golan et al., 1986): (a) a non<br />

ripening nor tomato mutant, which contains no PG during any stages<br />

of development; (b) a green normal fruit, which does not contain PG<br />

while still unripe; <strong>and</strong> (c) a ripe red fruit, which contained PG of plant<br />

origin. Analysis by gel electrophoresis of Rhizopus PG, after in vitro<br />

growth, revealed the production of at least seven molecular forms of this<br />

enzyme. In each of the <strong>fruits</strong> tested, Rhizopus infection resulted in the<br />

accumulation of these typical PG isozymes, which are all of fungal<br />

origin; however, in the infected ripe tomato fruit, both fruit <strong>and</strong> fungal<br />

enzymes were found. An analysis by gel electrophoresis enabled<br />

differentiation between the isozyme b<strong>and</strong>s of the tomato <strong>and</strong> those of<br />

the fungus which migrated in the gel faster than those of the fruit PG.<br />

It could not, however, provide a clear differentiation between the<br />

slower-migrating fungal isozymes <strong>and</strong> the fruit isozymes (Barkai-Golan<br />

et al., 1986). The differentiation between these isozymes was completed<br />

by immunological analysis with antiserum against specific forms of<br />

tomato enzymes; this analysis demonstrated that the infected fruit<br />

contained a higher level of tomato enzyme than the uninfected fruit of<br />

similar maturity. It was concluded that infection by R, stolonifer<br />

enhanced PG production in the normally ripening fruit or, in other<br />

words, that the infection advanced the ripening process in genetically<br />

competent tomato tissue. The infection did not, however, induce PG in<br />

the non-ripening nor <strong>fruits</strong>, which lack an active ripening system <strong>and</strong><br />

are unable to produce PG naturally (Barkai-Golan et al., 1986).<br />

Clarification of the origin of PG in the infected tissue also suggests that<br />

the pectolytic enzymes of the mature tomato fruit can take an active<br />

part in fungal pathogenicity or contribute to disease development.<br />

D. STIMULATION OF FRUIT SOFTENING AND CHANGES<br />

IN THE PECTIC COMPOUND CONTENTS<br />

Examination of avocado <strong>fruits</strong> infected by Fusarium solani has<br />

revealed that their softening starts earlier than in uninfected <strong>fruits</strong>, <strong>and</strong><br />

that it occurs during the incubation period of the pathogen, before the<br />

appearance of decay symptoms (Zauberman <strong>and</strong> Schiffmann-Nadel,<br />

1974). Furthermore, softening does not begin at the point of infection<br />

<strong>and</strong> progress outwards from there, but occurs simultaneously in the<br />

whole fruit. This finding raised the suggestion that the advance in fruit<br />

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