Introduction to Fungi, Third Edition

PLEOSPORALES
477
1999). Victorin binds to mitochondrial proteins,
and it is possible that it initiates cell death via
mitochondrial dysfunction (Curtis & Wolpert,
2002). Intriguingly, in the mammalian equivalent
of the hypersensitive response (i.e. apoptosis),
mitochondria are also among the first
organelles to break down.
Mitochondria are also the target of the
specific toxin produced by C. heterostrophus
(B. maydis), which caused the well-described
southern leaf blight of corn in the United
States in 1970 (Ullstrup, 1972; Schuman, 1991).
Prior to that epidemic, maize breeders had relied
heavily on male-sterile cultivars, i.e. cultivars
which do not produce viable pollen and are
therefore dependent on pollen from another
cultivar for seed production. This facilitated
the production of hybrids, i.e. the F1 progeny of
genetically dissimilar parents. These often
produce particularly high yields, a phenomenon
known as hybrid vigour. Male sterility was
achieved by a mitochondrial mutation called
cms-T (cytoplasmic male sterility). The plant line
used as the pollen donor did not contain the
cms-T mutation, so that the hybrid seeds grew
into plants capable of producing pollen in the
field of the farmers. In 1970, about 80% of the
maize crop contained cms-T cytoplasm. At about
the same time a mutation in a minor leaf
spot pathogen, C. heterostrophus race O, spread
in the field. This new race produced several
related polyketides collectively called T-toxin
(Fig. 17.15c), which specifically affected the
mitochondria of hybrid maize. The epidemic
of 1970 resulted in crop losses totalling over
US $1 billion for that year. The target site of
T-toxin in cms-T maize mitochondria is now
known to reside in a small protein present
as a tetramer in the outer mitochondrial membrane.
T-toxin binds directly to this protein,
causing conformational changes which open
up pores and render mitochondria leaky
(Levings et al., 1995; Wolpert et al., 2002). Race O
causes only minor leaf spots on cms-T as well as
other cultivars of maize.
Cochliobolus carbonum is the cause of northern
leaf spot and ear rot of maize. There are three
races, of which only race 1 is a serious pathogen
on all those cultivars of maize containing two
recessive alleles of the Hm1 resistance gene. This
strongly enhanced pathogenicity is caused by a
group of cyclic tetrapeptides collectively called
HC-toxin (Fig. 17.15d), where HC stands for
Helminthosporium carbonum, the former name of
the anamorph. Resistant cultivars produce an
enzyme which detoxifies HC-toxin. The susceptibility
of certain maize cultivars was caused
by a simultaneous inactivation of both duplicate
genes encoding the enzyme, HC-toxin reductase
(Multani et al., 1998). The mode of action of HCtoxin
is not yet clear; it seems to inhibit, rather
than induce, defence responses (Wolpert et al.,
2002).
As we have seen, certain strains of
C. carbonum, C. heterostrophus and C. victoriae have
caused catastrophic epidemics on particular
cereal hosts employing biochemically unrelated
toxins. This specificity of action i.e. a specific
pathogen race being pathogenic only against
certain host cultivars paved the way towards
an understanding of the gene-for-gene concept
(see pp. 112 and 397). A further question of
interest is the origin of these highly aggressive
strains. A partial answer was found somewhat
fortuitously by an examination of the mating
type genes in all three pathogens. Both idiomorphs
MAT-1 and MAT-2 have been found in
various field isolates of C. heterostrophus and
C. carbonum, but all known isolates of C. victoriae
belong to MAT-2. Further, C. victoriae and MAT-1
strains of C. carbonum are interfertile. These
observations have led to the suggestion that
C. victoriae arose from a MAT-2 strain of C.
carbonum which received the gene cluster for
pathogenicity on oats (i.e. the genes encoding the
enzymes necessary for toxin synthesis) by horizontal
gene transfer (Christiansen et al., 1998).
The integration of this gene cluster must have
been close to the MAT-2 locus, so that it did
not spread to MAT-1 strains of C. carbonum by
crossing-over.
17.2.8 Pyrenophora (anamorph Drechslera)
In its taxonomically restricted use, the Drechslera
state (Fig. 17.16b) is the conidial form of
Pyrenophora and is clearly defined as a monophyletic
group (Zhang & Berbee, 2001). Drechslera