Phytoanticipins
Some of the best evidence for a role of phytoantici-
pins has come from studies of the take-all fungus of
cerealsGaeumannomyces graminis, and related studies on
the tomato pathogen Septoria lycopersici. As discussed
in Chapter 9 (see Fig. 9.12), these host-specialized
fungi can overcome the phytoanticipins of their
host plants by producing enzymes (avenacinase and
α-tomatinase) that detoxify the phytoanticipins,
whereas fungi that are not specifically adapted to
these host plants are killed by these compounds.
Phytoanticipins may be involved in several other
plant–fungus interactions. A classic example is the
resistance of red- and yellow-skinned onions to
Colletotrichum circinans, the cause of “onion smudge”
disease, whereas white-skinned onions are susceptible.
The pigments themselves are not important but they
are associated with high levels of the phenolic phyto-
anticipins, catecholand protocatechuic acid.
Phytoalexins (warding-off compounds)
Phytoalexins are distinct from phytoanticipins because
they are low-molecular-weight compounds produced
in response to infection. More than 350 phytoalexins
have been reported across a range of crop plants,
especially dicotyledonous plants such as beans, pota-
toes, peas, and cotton. Most of them are flavonoids,
phenolics, or terpenoids, synthesized by three major
secondary metabolic pathways: the acetate-malonate
route, the acetate-mevalonate route, and the shikimic
acid route, similar to the secondary metabolic path-
ways of fungi (Chapter 7). The structures of four
phytoalexins are shown in Fig. 14.11.
A substantial body of evidence suggests that phyto-
alexins act as defense compounds – at least in
protecting plants against general attack by fungi. These
compounds accumulate rapidly during the hyper-
sensitive response, and at growth-inhibitory levels in
or around the dead or dying tissues. However, they can
also be detoxified by pathogens that are specific to indi-
vidual plant species, so there is a dynamic interaction
between the speed of host response and the ability of
a fungus to detoxify the defense compounds.
A similar localized accumulation of phytoalexins
can often be induced by artificial wounding or appli-
cation of a toxic chemical to the plant surface. It is
always preceded by an oxidative burst, and H 2 O 2 is
thought to be one of the initial signals that activates
the defense genes involved in phytoalexin production.
The sequence of events leading to phytoalexin accu-
mulation has been studied by exploiting the discovery
that low-molecular-weight compounds consisting of a
few β-linked sugar residues can act as powerfulelicitors
of the hypersensitive response. These oligosaccharides
are released from the extracellular polysaccharides of
fungal hyphae, probably by the actions of β-glucanase
enzymes that reside in plant cell walls. When applied
to plant cells or tissues in vitro, the elicitors cause
an early oxidative burst and the induction of plant
enzymes of the phenylpropanoid pathway, including
phenylalanine ammonia lyasewhich is involved in
phytoalexin production, and synthesis by the plantFUNGI AS PLANT PATHOGENS 291
OH
CH 3 O O
O
O
O
Pisatin (isoflavonoid)Gossypol (dimeric sesquiterpene) Rishitin (bicyclic sesquiterpene)Wyerone acid (acetylene)O O
OH
O
HO
HO
CHO OH
OH
OH
OH CHO
CH 3
HO
HO
CH 2
Fig. 14.11Structures of four phytoalexins: pisatinfrom peas; wyerone acidfrom broad bean; gossypolfrom cotton;
rishitinfrom potato.