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

FREEDOM PALESTINE FREEDOM PALESTINE FREEDOM PALESTINE
Host Protection and Defense Mechanisms 87
days prior to removal to cold storage (5°C) results in the suberization of
cells at the wound area, and the formation of a barrier against Botrytis
cinerea and other pathogens. Such a treatment considerably reduces the
incidence of decay at the end of prolonged storage (Heale and Sharman,
1977).
Studies with cultured carrot cells indicated that phenolic compounds
with low molecular weight, which are a link in lignin biosynthesis, and
free radicals produced during its polymerization, may take part in
resistance inducement by damaging fungal cell membranes, fungal
enzymes or toxins (Kurosaki et al., 1986a; Vance et al., 1980).
Accumulation of phenolic compounds and callose deposition in cell walls
of young tomato fruits, following inoculation with B. cinerea, were found
to arrest fungal development, thus retarding or preventing decay
(Glazener, 1982). The mechanism by which phenolic compounds
accumulate in the host is not yet clear, but research carried out with
wheat leaves suggested that the chitin in the fungal cell walls acts as a
stimulator to lignification in the leaves (Pearce and Ride, 1982).
Curing, involving the use of warmth and high humidity to harden
wounds and promote the development of resistance to infection, was long
ago recommended for control of Penicillium decay in sweet oranges
(Tindale and Fish, 1931). Since then, the efficiency of curing in protecting
against infection by various wound pathogens has been described for
several citrus fruits. It was thus found that holding wounded citrus fruits
for several days at 30-36°C and high relative humidity (90-96%)
markedly suppressed decay development during storage (Baudoin and
Eckert, 1985; Brown, G.E., 1973; Hopkins and Loucks, 1948). The
resistance of the fruits developed under these conditions has been
attributed to the deposit of lignin or lignin-like material by the living
cells of the flavedo (the external, colored layer of the peel) adjacent to the
injury, leading to the formation of a barrier which prevents fungal
penetration and restricts its growth (Brown, G.E. and Barmore, 1983). In
addition, lignification of cell walls at the site of infection protects them
against the activity of cell-wall-degrading pectolytic enzymes produced
by the fungus, and prevents degradation of the middle lamella of cell
walls (Ismail and Brown, 1979; Vance et al., 1980).
The combination of moderate temperatures with high relative
humidity was found to be suitable for rapid production of lignin at the
wounded area, while such a temperature was too high for Penicillium
digitatum development (Brown, G.E., 1973), but lowering the
temperature to 2TC allowed rapid fungal development, which preceded
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