Introduction to Fungi, Third Edition

SCLEROTINIACEAE
433
Fig15.3 Monilinia fructigena. (a) Apple showing brown rot caused by this fungus, and bearing conidial pustules.The wound serving
as entry point is indicated by an arrow. (b) Blastoconidia of the Monilia type.
Purdy (1979), Hegedus and Rimmer (2005) and
Bolton et al. (2006).
Sclerotinia sclerotiorum can infect pollen grains
of crop plants but can also become genuinely
seed-borne, surviving systemically in the embryo
for several years and replacing the rotten tissues
with mycelium and sclerotia (Tu, 1988). Such
seed-borne infections are readily eliminated by
fungicidal seed-dressings, but infections of growing
crops are less easily controlled. Hence,
biological control of S. sclerotiorum has been
attempted. A promising biocontrol agent is the
pycnidial fungus Coniothyrium minitans which
infects and parasitizes hyphae and sclerotia of
S. sclerotiorum in the soil and in plant tissue
(Tribe, 1957; de Vrije et al., 2001). The ability of
C. minitans to destroy dormant S. sclerotiorum
sclerotia in the soil is particularly interesting, as
it offers a chance to decontaminate infected soil
on which susceptible crop plants could not
otherwise be grown for several years. Gerlagh
et al. (2003) have demonstrated that one or two
conidia of C. minitans are sufficient to initiate
infection of a sclerotium. Conidia of C. minitans
can be spread rapidly by the activity of soil
invertebrates, including mites (Williams et al.,
1998). These properties have led to the registration
of C. minitans as a commercial biocontrol
agent against S. sclerotiorum. Since C. minitans
colonizing the soil can tolerate many fungicides
used against S. sclerotiorum, the integrated
control of Sclerotinia rot is also possible in some
crops (Budge & Whipps, 2001).
Oxalic acid and pH regulation
Like other fungi such as Botrytis cinerea (see
p. 435) and brown-rot basidiomycetes (p. 527),
S. sclerotiorum releases large amounts of oxalic
acid into the infected plant tissue, and this is an
important pathogenicity factor (Godoy et al.,
1990). Oxalic acid may chelate Ca 2þ ions released
from cell wall degradation, and it also suppresses
the host’s hypersensitive response (Cessna et al.,
2000). Most importantly, however, it acidifies the
infected plant tissue. There is good evidence that
S. sclerotiorum can sense the pH of its environment,
and that it can adjust the production rate
of oxalic acid accordingly. In this way, optimum
conditions are created for the activity of its
pectin-degrading enzymes, especially endopolygalacturonases,
which macerate colonized host
tissues (Rollins & Dickman, 2001). A transcription
factor encoded by the pac1 gene seems to be
involved in regulating the expression of genes
controlled by external pH (Rollins, 2003).
Transgenic sunflower or soybean plants
containing an oxalate oxidase gene from
cereals show good resistance to infection by
S. sclerotiorum. This appears to be a promising
control strategy for the future, but is currently
still slow in gaining public acceptance (Lu, 2003).
Conventional resistance breeding is also possible,