of chitinaseand ββ-1,3-glucanasewhich can degrade
fungal walls.
Clearly, this cascade of cellular responses creates a
hostile environment for a potential pathogen. So how
do host-adapted necrotrophic pathogens overcome or
avoid these defenses? Studies on the Botrytis–broad
bean interaction have shown that both B. fabaeand B.
cinereacan cause a hypersensitive response in appro-
priate conditions (see earlier) and the phytoalexin
wyerone acidaccumulates in the dead cells. But B. fabae
is more tolerant of wyerone acid than isB. cinerea in
vitro, and B. fabaealso causes less wyerone acid to accu-
mulate in the lesion, perhaps by detoxifying it. Thus,
B. cinereanever spreads further from the necrotic spot,
whereas B. fabaeis checked temporarily but then can
spread through the surrounding tissues, killing them
progressively. The resulting large brown lesions give
rise to the name for this disease – chocolate spot (see
Fig. 14.8).
The mechanisms of detoxification of phytoalexins
have been reported for some other fungi. The pathogen
of pea plants, Nectria haematococca, detoxifies pisatin
by demethylation (Fig. 14.12). Other strains of this
pathogen that infect bean plants detoxify one of the
bean phytoalexins kievitoneby hydration (Fig. 14.12).
In both cases the ability of the pathogen to infect
the plant is correlated with the ability to detoxify the
phytoalexin. Moreover, when the pisatin demethylase
gene from N. haematococca was transformed into
Cochliobolus heterostrophus, a maize pathogen, this
fungus became a pathogen of pea leaves. So, there is
strong evidence that host-adapted pathogens have
evolved mechanisms for overcoming the inhibitory
effects of their hosts’ phytoalexins, and even the
acquisition of a single phytoalexin-detoxifying gene can
change the host range of a fungus. There is, however,
a twist to this story. In the Nectria–bean interaction,
all strains of N. haematococcawere found to produce
the hydrating enzyme, kievitone hydratase, but some
strains did not secrete it from the hyphae. These
strains were nonpathogenic, in contrast to strains that
secreted the enzyme. In the Nectria–pea interaction
the relationship between pathogenicity and production
of the detoxifying enzyme was supported by many lines
of evidence, but targeted disruption of the gene for
pisatin demethylase led to strains that were still
pathogenic. Reviewing all the work on detoxification
of phytoanticipins and phytoalexins, VanEtten et al.
(1995) suggested that pathogens may have evolved
several mechanisms for overcoming the host defenses,
so that some of these mechanisms, although still
expressed, may be redundant.292 CHAPTER 14
Fig. 14.12Two examples of detoxification of phytoalexins (at the position marked *).