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

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FREEDOM PALESTINE FREEDOM PALESTINE FREEDOM PALESTINE<br />

Attack Mechanisms of the Pathogen 57<br />

The virulence of a pathogen has been related to the total PG activity or<br />

to specific PG isozymes. The production of PG isozymes may be<br />

influenced by various factors, such as growth conditions of the pathogen,<br />

nutrients <strong>and</strong> fungal strains (Clevel<strong>and</strong> <strong>and</strong> Cotty, 1991; Tobias et al.,<br />

1993). Recently an increase in total PG activity <strong>and</strong> in that of PG<br />

isozymes has also been correlated with reactivation of latent infections<br />

<strong>and</strong> the beginning of tissue maceration by the reactivated pathogen<br />

(Zhang et al., 1997).<br />

Endo-pectate lyase, which attacks the pectic acid at r<strong>and</strong>om, is<br />

produced by various pectolytic bacteria <strong>and</strong> is probably the major cause<br />

of cell wall decomposition of potatoes infected by these bacteria (Hall <strong>and</strong><br />

Wood, 1973), but enzymes of the endo-PG group may also be involved in<br />

tuber maceration (Beraha et al., 1974). The involvement of pectate lyase<br />

(PL) in fungal decay has been described for anthracnose (Colletotrichum<br />

gloeosporioides) in stored avocados (Wattad et al., 1994); PL was found to<br />

cause softening in unripe avocado <strong>fruits</strong>, whereas the addition of<br />

antibodies to this enzyme inhibited tissue maceration.<br />

Saprophytic fungi <strong>and</strong> bacteria, which are not included in the<br />

post<strong>harvest</strong> pathogens' category, may also produce pectolytic enzymes on<br />

various substrates; some of these are capable of macerating discs of<br />

potato tuber or of other plant organs (Ishii, 1977). Therefore, the fact<br />

that a given microorganism can produce pectolytic enzymes in vitro<br />

cannot serve, by itself, as evidence of pathogenic capability. To determine<br />

the capability of a pathogen to decompose the pectic compounds of plant<br />

cell walls, its pectolytic activity should be examined in the host tissues<br />

themselves.<br />

Simmonds (1963) suggested that the failure of the pathogen to produce<br />

adequate levels of pectolytic enzymes in the host may be related to the<br />

establishment of infections that remain quiescent until the ripening<br />

process leads to suitable changes in the cell wall structure. An<br />

inadequate level of pectolytic activity in the plant tissue may be caused<br />

by several factors (Swinburne, 1983): (1) Pectolytic enzymes are not all<br />

constitutive <strong>and</strong> they may need inducers for their production (Bateman<br />

<strong>and</strong> Basham, 1976); the inducing substrates could be supplied to the<br />

pathogen only as the fruit ripens. (2) Even if such enzymes were<br />

produced, access to the labile sites within the wall could be blocked by<br />

cation cross-linking. (3) Enzymes may be inactivated by inhibitors<br />

present at higher levels in the immature fruit than in the mature one<br />

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