Introduction to Fungi, Third Edition

DIAPORTHALES
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enveloped by hyphae which proliferate to form
the wall (peridium) of the perithecium, and
by others which form the pseudoparenchymatous
centrum and paraphyses. A neck lined by
periphyses is formed relatively early in perithecium
development. The ascogenous hyphae
arising from the ascogonial coils form a bowlshaped
hymenium in the base of the perithecium.
Shortly before maturity of the
perithecium, the ascogenous hyphae produce
croziers. Karyogamy, meiosis and mitosis all
occur in the usual way, giving rise to eight
nuclei which divide once more, so that eight
bicellular ascospores are produced in each ascus.
A typical feature of Diaporthe is that the asci often
become detached from the hymenium before or
after the ascospores are ripe, so that the cavity of
the perithecium is filled with loose asci or free
ascospores. Ascospores are usually discharged
non-violently as sticky tendrils exuding from the
ostiole of the perithecium. The ascus has a
prominent apical apparatus which stains with
iodine.
Ecology
Species of Phomopsis and Diaporthe cause serious
plant diseases of commercial significance,
such as pod and stem blight of soybeans
and other pulse fruits (D. phaseolorum, anamorph
P. phaseoli) or stem canker and leaf necrosis of
sunflower (D. helianthi, anamorph P. helianthi).
Many Phomopsis diseases are caused by species
complexes, i.e. different Phomopsis spp. can be
isolated from the same diseased plant in the
field. All species associated with a given disease
may not be equally pathogenic. A good example
is dead arm of vines, which is caused primarily
by P. viticola. Several other Phomopsis species
which can also be isolated from vines are only
weakly pathogenic or entirely non-pathogenic
(Mostert et al., 2001). Fungi colonizing the living
plant host as permanently asymptomatic infections
are termed endophytes. The example of
P. viticola illustrates the diffuse boundary
between endophytism and parasitism; some
Phomopsis strains are entirely endophytic whereas
others initially cause latent infections but later
become pathogenic (Mostert et al., 2000). Another
example is provided by Diaporthe toxica
(anamorph formerly called P. leptostromiformis)
which infects living lupins as coralloid hyphae
with a limited spread beneath the cuticle.
Such latent infections can persist for many
months until death of the colonized host
organs occurs by natural causes, e.g. senescence
at the end of the growing season. Within
1 2 days of host death, large-scale colonization
of the infected tissue occurs (Shankar et al., 1998).
Colonization by saprotrophic and pathogenic
Phomopsis spp. can be accompanied by the secretion
of large amounts of cell wall-degrading
enzymes which indiscriminately macerate the
plant tissue (Heller & Gierth, 2001). This accounts
for the strongly necrotic nature of many
Phomopsis diseases. Toxins may also be produced
by phytopathogenic species, and these may facilitate
rapid colonization by killing host cells and
preventing an immune response. The Phomopsis
state of D. toxica produces phomopsins, which are
cyclic peptides comprising six unusual amino
acids. These can accumulate in lupin stems and
seeds to such high levels that they cause a serious
toxicosis called lupinosis in sheep grazing on
lupin stubble, or fed with lupin seeds (Culvenor
et al., 1977). They seem to act mainly on the
microtubular cytoskeleton, and their primary
effect is on the liver of affected sheep (Edgar
et al., 1986). Another example is the toxin phomozin
which is produced by P. helianthi and has
been shown to be capable of killing host tissue
(Mazars et al., 1991).
Recently, Diaporthe ambigua, the cause of
cankers on roots and stems of fruit trees,
has been found to be infected by a mycovirus
which reduces the ability of its fungal host to
cause disease on plants (Preisig et al., 2000).
Hypovirulence-causing fungal viruses and their
implications for biological control are discussed
in the following section on Cryphonectria
parasitica.
12.8.2 Cryphonectria parasitica
Readable accounts of various aspects of
C. parasitica have been written by Nuss (1992),
Heiniger and Rigling (1994) and Dawe and
Nuss (2001). The origin of C. parasitica is uncertain.
It was first reported in 1904 as a sudden and