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FREEDOM PALESTINE FREEDOM PALESTINE FREEDOM PALESTINE Physiological and Biochemical Changes 103 The origin of PG in Rhizopus stolonifer-miected tomatoes has been studied in various tomato fruits (Barkai-Golan et al., 1986): (a) a non ripening nor tomato mutant, which contains no PG during any stages of development; (b) a green normal fruit, which does not contain PG while still unripe; and (c) a ripe red fruit, which contained PG of plant origin. Analysis by gel electrophoresis of Rhizopus PG, after in vitro growth, revealed the production of at least seven molecular forms of this enzyme. In each of the fruits tested, Rhizopus infection resulted in the accumulation of these typical PG isozymes, which are all of fungal origin; however, in the infected ripe tomato fruit, both fruit and fungal enzymes were found. An analysis by gel electrophoresis enabled differentiation between the isozyme bands of the tomato and those of the fungus which migrated in the gel faster than those of the fruit PG. It could not, however, provide a clear differentiation between the slower-migrating fungal isozymes and the fruit isozymes (Barkai-Golan et al., 1986). The differentiation between these isozymes was completed by immunological analysis with antiserum against specific forms of tomato enzymes; this analysis demonstrated that the infected fruit contained a higher level of tomato enzyme than the uninfected fruit of similar maturity. It was concluded that infection by R, stolonifer enhanced PG production in the normally ripening fruit or, in other words, that the infection advanced the ripening process in genetically competent tomato tissue. The infection did not, however, induce PG in the non-ripening nor fruits, which lack an active ripening system and are unable to produce PG naturally (Barkai-Golan et al., 1986). Clarification of the origin of PG in the infected tissue also suggests that the pectolytic enzymes of the mature tomato fruit can take an active part in fungal pathogenicity or contribute to disease development. D. STIMULATION OF FRUIT SOFTENING AND CHANGES IN THE PECTIC COMPOUND CONTENTS Examination of avocado fruits infected by Fusarium solani has revealed that their softening starts earlier than in uninfected fruits, and that it occurs during the incubation period of the pathogen, before the appearance of decay symptoms (Zauberman and Schiffmann-Nadel, 1974). Furthermore, softening does not begin at the point of infection and progress outwards from there, but occurs simultaneously in the whole fruit. This finding raised the suggestion that the advance in fruit http://arab2000.forumpro.fr
FREEDOM PALESTINE FREEDOM PALESTINE FREEDOM PALESTINE 104 Postharvest Diseases of Fruits and Vegetables softening is not related to the local effect of the fungus but to its ability to induce a softening mechanism similar to that of the healthy fruit. The inducement of this mechanism may be directly related to the enhanced ethylene emission typical of infected fruit, and to the ability of the 'infection ethylene', similarly to exogenic ethylene, to enhance fruit softening and lead to earlier senescence. Earlier studies of apples infected with various pathogens had already shown a considerable reduction in the insoluble pectin in their tissues, particularly in those cases where the pathogen was responsible for fruit soft rot (Cole and Wood, 1961). Studies with F, soZaAii-inoculated avocados indicated that fungal infection affected the rates of changes in the pectic substances: the increase in the soluble pectin and the reduction in the insoluble protopectin are more rapid in the infected than the uninfected fruit, even though the final values of each of the fractions are similar in the two cases. Since fruit softening starts with the increase in the soluble pectin and the decrease in the protopectin, it is clear that it occurs earlier in the infected fruit (Zauberman and Schiffmann-Nadel, 1974). Cell disintegration and tissue maceration were followed by an increase in soluble pectin in grapefruit peel treated with endo-PG produced by Penicillium italicum (Barmore and Brown, 1980). The increase in soluble pectin was recorded after 3-5 h incubation of the enzyme with host tissue, as presented in Table 6: TABLE 6 Maceration of grapefruit peel mesocarp by endo-polygalacturonase from fruits infected with Penicillium italicum^ Treatment time Maceration Pectin solubilization^ (h) index2 (mg/g of peel) 1 1 0.47 3 3 0.88 5 5 1.02 1 Reproduced from Barmore and Brown (1980) with permission of the American Phytopathological Society. 2 0 = no maceration; 5 = complete maceration 3 Soluble pectin content resulting from the action of endopolygalacturonase http://arab2000.forumpro.fr
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Post harvest diseases fruits and vegetables - Xavier University ...

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