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moulds” Penicillium italicumandP. digitatum which
commonly cause the rotting of oranges, P. expansum
which commonly rots apples in storage (Fig. 14.5),
Sclerotinia fructigenawhich rots apples, peaches, and
some other fruits, often through wounds caused by
birds and wasps before the fruit is harvested (Figs 14.5,
14.6),and species of Rhizopuswhich rot many types of
fruit, including pears (Fig. 14.6).
The interesting feature of these fungi is that they cause
different types of rot, ranging from fast-spreading
watery rots to firm, dry rots. In all cases they are
unable to rot the fruit until it passes through the
phase termed climacteric, when the fruit begins to
ripen. This is the stage at which the acid content
declines and sugar levels start to rise.

The roles of pectic enzymes in

pathogenesis

The common feature of all fruit-rot diseases is that the

tissues are rotted by pectic enzymesthat degrade the

middle lamella(the cementing layer) between adja-

cent plant cell walls (Fig. 14.7). The pectin of the middle

lamella consists of chains of α-linked galacturonic acid

residues, some of which are methylated, and mixed

polymers of galacturonic acid, mannose, and lesser

amounts of other sugars. The pectic enzymesare of

three major types.

1 Pectin methyl esterase (PME) is often produced by

the plant itself and it demethylates pectin. PME

seems to play little role in the breakdown of pectin,

but the methanol released by this enzyme can act

as a germination trigger and potential carbon source

forAthelia rolfsii(see earlier).

2 Pectic lyase(PL) is a chain-splitting enzyme with

both endo- and exo-acting forms. It cleaves the

bonds between the sugar residues in a characteristic

way, eliminating water during the process.

3 Polygalacturonase(PG) is another chain-splitting

enzyme with both endo- and exo-forms. Unlike PL,

this enzyme is a hydrolase – it uses water to add H+

to one sugar residue and OH−to the adjacent residue

during cleavage of the bond.

Fungi are induced to synthesize pectic enzymes in

the presence of pectic compounds, and the enzymes

probably act in concert. This was shown when the genes

encoding the equivalent enzymes of the bacterium

Erwinia carotovora (the cause of potato black-leg disease)

were engineered separately intoE. coli. The recipient

cells required a minimum of one exo-PL, two endo-PLs,

and one endo-PG in order to rot the potato tissues.

Pectic enzymes of fungi exist as a range of isomers which

separate according to size and net charge during gel

electrophoresis. The resulting pectic zymograms can be

used to distinguish population subgroups of fungi (see

Fig. 9.8), but the isomers may not differ significantly

in function.

Initially it was thought that the principal role of

pectic enzymes in pathogenesis was to separate cells,

causing disruption of the fine protoplasmic bridges

(plasmodesmata) that link cells through their walls.

More recent studies suggest other roles. Pectic enzymes

can be directly toxic to plant protoplasts in vitro, and

286 CHAPTER 14

Fig. 14.6(a,b) Wounded apple naturally contaminated by airborne spores of Rhizopus(mucorales), producing a fast-
spreading, watery rot that collapses and liquefies the tissues. Dark, spreading hyphae and sporangiophores are seen on
the fruit surface. (c) Apple infected by Sclerotinia fructigenain field conditions, showing pustules of spores on the fruit
surface. The fruit progressively dries out and mummifies.

(a) (b) (c)