sharp eyespot disease, Fusarium culmorumwhich causes
fusarium foot rot, and Tapesia yallundaewhich causes
“true” eyespot disease. When these fungi were grown
on cereal cell walls in laboratory culture, all three fungi
produced arabinase, xylanase, and β-1,3-glucanase, but
only small amounts of pectic enzymes. By contrast, when
pathogens of nongrass plants (Fusarium oxysporum,
Verticillium albo-atrum) were grown on walls of their
hosts they produced large amounts of pectic enzymes.
So, the cereal pathogens seem to be adapted to
degrade the typical wall components of their hosts. But
the surprising feature in this study was that the cereal
pathogens produced arabinase and glucanase consti-
tutively, in the absence of host wall material, and the
production of these enzymes was not repressed by
sugars. These are unusual features because polymer-
degrading enzymes in general are both inducible and
repressible. The likely explanation is that these host-
specialized fungi grow only on cereals, so they have
adapted to produce the necessary wall-degrading
enzymes constitutively.
Plant defense against host-specialized
necrotrophic pathogens
Plants have several potential lines of defense against
invading pathogens. These defenses include both
physical barriers and fungitoxic compounds in the
plant tissues.
The main physical barrier to infection of many
plants is the cuticle on the leaf or stem surface, and in
this regard the enzyme cutinasehas been thought to
be important for fungal infection. There is circumstantial
and correlative evidence for this. However, when targeted
gene disruption was used to block cutinase production
by three leaf pathogens, there was no reduction in
pathogenicity of two of the fungi and only a partial
reduction in a third fungus (VanEtten et al. 1995). A
possible explanation is that some of the pathogenicity
genes might only be expressed during infection and
not in laboratory culture. Alternatively, there might
be multiple forms of these genes, some of which
are expressed in vitroand others only in the host
environment. This example illustrates the difficulty of
unravelling the often-complex host defense systems
of plants.
In addition to preformed physical barriers, plants
can respond to infection by developing a papilla– a
localized thickening of the cell wall at the point of
attempted invasion. In extreme cases the papilla con-
tinues to develop as the hypha grows (Fig. 14.10),
so that it encases the penetrating hypha. In electron
micrographs, papillae are seen as massive localized
accumulations of wall material in which membranes
and other degenerate cytoplasmic components have
been trapped. Cytochemical stains usually reveal the
presence of callose in papillae, but in the Gramineae
the papillae often show staining reactions for lignin and
suberin.FUNGI AS PLANT PATHOGENS 289
Fig. 14.9Log dose/probit response plots of infection of broad bean leaves by Botrytis fabaeand B. cinerea. See text for
details. (Based on Wastie 1960.)